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4
Pathophys.
65
Phenotypes
5
Pathograph
6
Genes
4
Medical Actions
6
References
2
Deep Research
🏷

Classifications

Harrison's Chapter
IMMUNE_RHEUMATOLOGIC

Pathophysiology

4
B Cell Autoreactivity and ANCA Production
Autoreactive B cells produce anti-proteinase 3 (PR3-ANCA) antibodies, the defining upstream event in GPA pathogenesis. Genetic predisposition (HLA-DP alleles) and environmental triggers (S. aureus, silica) drive loss of tolerance to PR3, leading to sustained autoantibody production.
B cell CL:0000236
B Cell Activation GO:0042113
Show evidence (2 references)
PMID:39257888 SUPPORT
"Granulomatosis with polyangiitis (GPA) is a rare systemic disease characterized by granulomatous inflammation of the respiratory tract and necrotizing vasculitis of small and medium vessels often associated with the production of anti-neutrophil cytoplasmic antibodies (ANCA) directed mainly..."
Confirms that GPA is defined by production of ANCA directed against PR3, establishing B cell-mediated autoantibody production as the upstream event.
PMID:36315063 SUPPORT Human Clinical
"Exposure to silica dust, farming and chronic nasal Staphylococcus aureus carriage are associated with increased risk of developing AAV."
Environmental triggers (silica, S. aureus) contribute to loss of B cell tolerance and ANCA production.
ANCA-Mediated Neutrophil Activation
Anti-proteinase 3 (PR3) antibodies bind to primed neutrophils, causing activation, degranulation, and release of reactive oxygen species and lytic enzymes. This causes direct endothelial damage and vessel wall necrosis. Neutrophil extracellular trap (NET) formation further amplifies vascular injury.
Neutrophil CL:0000775 Endothelial Cell CL:0000115
Neutrophil Activation GO:0042119 Neutrophil Extracellular Trap Formation GO:0140645
Show evidence (2 references)
PMID:37781373 SUPPORT
"The pathogenesis of AAV includes ANCA-mediated neutrophil activation, subsequent release of inflammatory cytokines and reactive oxygen species (ROS), and formation of neutrophil extracellular traps (NETs)."
This review confirms that ANCA-mediated neutrophil activation is a central pathogenic mechanism in AAV, leading to ROS release and NET formation.
PMID:38791316 SUPPORT
"Mechanisms involving ANCA and anti-GBM autoantibodies, neutrophil activation, and neutrophil extracellular trap (NETs) formation are discussed, along with the role of the complement system in inducing pulmonary injury."
Confirms neutrophil activation and NET formation as key mechanisms in pulmonary injury in GPA.
Granuloma Formation
Granulomatous inflammation with multinucleated giant cells, epithelioid macrophages, and necrosis affects the respiratory tract. CD4+ T cells and macrophages organize into granulomas that destroy tissue, a hallmark distinguishing GPA from other ANCA-associated vasculitides.
Macrophage CL:0000235 CD4-positive T cell CL:0000624
Granuloma Formation GO:0002432 Inflammatory Response GO:0006954
Show evidence (2 references)
ORPHA:900 SUPPORT
"HP:0002955 | Granulomatosis | Very frequent (99-80%)"
Orphanet classifies granulomatosis as a very frequent feature of GPA, consistent with granuloma formation being a hallmark pathological process.
PMID:39257888 SUPPORT
"Granulomatosis with polyangiitis (GPA) is a rare systemic disease characterized by granulomatous inflammation of the respiratory tract and necrotizing vasculitis of small and medium vessels"
Confirms granulomatous inflammation of the respiratory tract as a defining feature of GPA.
Complement Alternative Pathway Activation
The alternative complement pathway amplifies inflammation in GPA. C5a recruits and activates neutrophils, creating a positive feedback loop of vascular damage. This mechanism is the therapeutic target of avacopan (C5a receptor inhibitor).
Complement Activation GO:0006956
Show evidence (2 references)
PMID:37781373 SUPPORT
"Mechanistically, cytokines or complement factors activate and prime neutrophils for ANCA-binding; thus, C5a receptor blocker has garnered attention as potential replacement for glucocorticoids in clinical settings."
Confirms complement factors prime neutrophils for ANCA binding, and that C5a receptor blockade is a validated therapeutic target.
PMID:38791316 SUPPORT
"Mechanisms involving ANCA and anti-GBM autoantibodies, neutrophil activation, and neutrophil extracellular trap (NETs) formation are discussed, along with the role of the complement system in inducing pulmonary injury."
Confirms the complement system plays a role in amplifying ANCA-mediated pulmonary injury.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Granulomatosis with Polyangiitis Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.

Phenotypes

65
Blood 4
Epistaxis VERY_FREQUENT Epistaxis HP:0000421
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000421 | Epistaxis | Very frequent (99-80%)"
Orphanet classifies epistaxis as very frequent in GPA.
Diffuse Alveolar Hemorrhage OCCASIONAL Diffuse alveolar hemorrhage HP:0025420
Life-threatening complication requiring urgent treatment.
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0025420 | Diffuse alveolar hemorrhage | Occasional (29-5%)"
Orphanet classifies diffuse alveolar hemorrhage as occasional in GPA.
Purpura OCCASIONAL Purpura HP:0000979
Palpable purpura from leukocytoclastic vasculitis.
Show evidence (2 references)
ORPHA:900 SUPPORT
"HP:0000979 | Purpura | Occasional (29-5%)"
Orphanet classifies purpura as occasional in GPA.
PMID:36315063 SUPPORT Human Clinical
"chronic recurrent rhinosinusitis, cavitated lung nodules, palpable purpura or acute kidney injury"
Palpable purpura is listed as a key feature prompting AAV investigation.
Granulomatosis VERY_FREQUENT Granulomatosis HP:0002955
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0002955 | Granulomatosis | Very frequent (99-80%)"
Orphanet records granulomatosis as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis.
Cardiovascular 3
Pericarditis OCCASIONAL Pericarditis HP:0001701
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0001701 | Pericarditis | Occasional (29-5%)"
Orphanet classifies pericarditis as occasional in GPA.
Hypertension OCCASIONAL Hypertension HP:0000822
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000822 | Hypertension | Occasional (29-5%)"
Orphanet classifies hypertension as occasional in GPA.
Vasculitis VERY_FREQUENT Vasculitis HP:0002633
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0002633 | Vasculitis | Very frequent (99-80%)"
Orphanet records vasculitis as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis.
Digestive 1
Nausea and Vomiting FREQUENT Nausea and vomiting HP:0002017
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0002017 | Nausea and vomiting | Frequent (79-30%)"
Orphanet classifies nausea and vomiting as frequent in GPA.
Ear 3
Otitis Media VERY_FREQUENT Otitis media HP:0000388
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000388 | Otitis media | Very frequent (99-80%)"
Orphanet classifies otitis media as very frequent in GPA.
Sensorineural Hearing Impairment OCCASIONAL Sensorineural hearing impairment HP:0000407
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000407 | Sensorineural hearing impairment | Occasional (29-5%)"
Orphanet classifies sensorineural hearing loss as occasional in GPA.
Chronic otitis media OCCASIONAL Chronic otitis media HP:0000389
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0000389 | Chronic otitis media | Occasional (29-5%)"
Orphanet records chronic otitis media as an occasional (5-29%) phenotype of granulomatosis with polyangiitis.
Eye 4
Scleritis FREQUENT Scleritis HP:0100532
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0100532 | Scleritis | Frequent (79-30%)"
Orphanet classifies scleritis as frequent in GPA.
Proptosis OCCASIONAL Proptosis HP:0000520
Due to retro-orbital granulomatous mass formation.
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000520 | Proptosis | Occasional (29-5%)"
Orphanet classifies proptosis as occasional in GPA.
Keratitis OCCASIONAL Keratitis HP:0000491
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000491 | Keratitis | Occasional (29-5%)"
Orphanet classifies keratitis as occasional in GPA.
Retinopathy OCCASIONAL Retinopathy HP:0000488
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0000488 | Retinopathy | Occasional (29-5%)"
Orphanet records retinopathy as an occasional (5-29%) phenotype of granulomatosis with polyangiitis.
Genitourinary 3
Hematuria VERY_FREQUENT Hematuria HP:0000790
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000790 | Hematuria | Very frequent (99-80%)"
Orphanet classifies hematuria as very frequent in GPA.
Proteinuria FREQUENT Proteinuria HP:0000093
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000093 | Proteinuria | Frequent (79-30%)"
Orphanet classifies proteinuria as frequent in GPA.
Renal Insufficiency OCCASIONAL Renal insufficiency HP:0000083
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000083 | Renal insufficiency | Occasional (29-5%)"
Orphanet classifies renal insufficiency as occasional in GPA.
Head and Neck 2
Sinusitis VERY_FREQUENT Sinusitis HP:0000246
Temporal: CHRONIC
Chronic destructive sinusitis is one of the most common presenting features, often with bloody or purulent nasal discharge.
Show evidence (2 references)
ORPHA:900 SUPPORT
"HP:0000246 | Sinusitis | Very frequent (99-80%)"
Orphanet classifies sinusitis as very frequent in GPA.
PMID:28881446 SUPPORT Human Clinical
"In GPA, the most common disease features at diagnosis were otorhinolaryngological (74%), followed by "general" (57%) and pulmonary (48%) manifestations."
Olmsted County cohort confirms ENT manifestations (including sinusitis) as the most common presenting feature of GPA at 74%.
Saddle Nose Deformity OCCASIONAL Depressed nasal bridge HP:0005280
Due to nasal cartilage destruction from granulomatous inflammation.
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000366 | Abnormality of the nose | Very frequent (99-80%)"
Orphanet reports nasal abnormalities as very frequent; saddle nose deformity from cartilage destruction is a classic late finding.
Immune 3
Recurrent Respiratory Infections VERY_FREQUENT Recurrent respiratory infections HP:0002205
Reflects mucociliary dysfunction and mucosal destruction from chronic sinonasal granulomatous disease.
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0002205 | Recurrent respiratory infections | Very frequent (99-80%)"
Orphanet classifies recurrent respiratory infections as very frequent in GPA.
Skin Rash FREQUENT Skin rash HP:0000988
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000988 | Skin rash | Frequent (79-30%)"
Orphanet classifies skin rash as frequent in GPA.
Autoimmunity VERY_FREQUENT Autoimmunity HP:0002960
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0002960 | Autoimmunity | Very frequent (99-80%)"
Orphanet records autoimmunity as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis.
Integument 1
Skin Ulcer OCCASIONAL Skin ulcer HP:0200042
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0200042 | Skin ulcer | Occasional (29-5%)"
Orphanet classifies skin ulcers as occasional in GPA.
Metabolism 1
Fever VERY_FREQUENT Fever HP:0001945
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0001945 | Fever | Very frequent (99-80%)"
Orphanet classifies fever as very frequent in GPA.
Musculoskeletal 1
Arthritis FREQUENT Arthritis HP:0001369
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0001369 | Arthritis | Frequent (79-30%)"
Orphanet classifies arthritis as frequent in GPA.
Nervous System 3
Peripheral Neuropathy FREQUENT Peripheral neuropathy HP:0009830
Mononeuritis multiplex is the characteristic pattern.
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0009830 | Peripheral neuropathy | Frequent (79-30%)"
Orphanet classifies peripheral neuropathy as frequent in GPA.
Cranial Nerve Paralysis OCCASIONAL Cranial nerve paralysis HP:0006824
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0006824 | Cranial nerve paralysis | Occasional (29-5%)"
Orphanet classifies cranial nerve paralysis as occasional in GPA.
Headache OCCASIONAL Headache HP:0002315
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0002315 | Headache | Occasional (29-5%)"
Orphanet classifies headache as occasional in GPA.
Respiratory 6
Pulmonary Infiltrates VERY_FREQUENT Pulmonary infiltrates HP:0002113
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0002113 | Pulmonary infiltrates | Very frequent (99-80%)"
Orphanet classifies pulmonary infiltrates as very frequent in GPA.
Hemoptysis FREQUENT Hemoptysis HP:0002105
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0002105 | Hemoptysis | Frequent (79-30%)"
Orphanet classifies hemoptysis as frequent in GPA.
Cough FREQUENT Cough HP:0012735
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0012735 | Cough | Frequent (79-30%)"
Orphanet classifies cough as frequent in GPA.
Pulmonary Fibrosis FREQUENT Pulmonary fibrosis HP:0002206
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0002206 | Pulmonary fibrosis | Frequent (79-30%)"
Orphanet classifies pulmonary fibrosis as frequent in GPA.
Respiratory Insufficiency FREQUENT Respiratory insufficiency HP:0002093
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0002093 | Respiratory insufficiency | Frequent (79-30%)"
Orphanet classifies respiratory insufficiency as frequent in GPA.
Chronic Pulmonary Obstruction FREQUENT Chronic pulmonary obstruction HP:0006510
Airway obstruction from endobronchial granulomatous disease.
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0006510 | Chronic pulmonary obstruction | Frequent (79-30%)"
Orphanet classifies chronic pulmonary obstruction as frequent in GPA.
Constitutional 5
Chest Pain FREQUENT Chest pain HP:0100749
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0100749 | Chest pain | Frequent (79-30%)"
Orphanet classifies chest pain as frequent in GPA.
Fatigue VERY_FREQUENT Fatigue HP:0012378
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0012378 | Fatigue | Very frequent (99-80%)"
Orphanet classifies fatigue as very frequent in GPA.
Arthralgia VERY_FREQUENT Arthralgia HP:0002829
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0002829 | Arthralgia | Very frequent (99-80%)"
Orphanet classifies arthralgia as very frequent in GPA.
Myalgia OCCASIONAL Myalgia HP:0003326
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0003326 | Myalgia | Occasional (29-5%)"
Orphanet classifies myalgia as occasional in GPA.
Abdominal Pain FREQUENT Abdominal pain HP:0002027
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0002027 | Abdominal pain | Frequent (79-30%)"
Orphanet classifies abdominal pain as frequent in GPA.
Growth 1
Weight Loss VERY_FREQUENT Weight loss HP:0001824
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0001824 | Weight loss | Very frequent (99-80%)"
Orphanet classifies weight loss as very frequent in GPA.
Other 24
Nasal Septum Perforation OCCASIONAL Nasal septum perforation HP:0033434
Due to granulomatous destruction of nasal cartilage and septum.
Subglottic Stenosis OCCASIONAL Subglottic stenosis HP:0001607
Can cause stridor and airway compromise; may require surgical intervention.
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0001607 | Subglottic stenosis | Occasional (29-5%)"
Orphanet classifies subglottic stenosis as occasional in GPA.
Oral Cavity Abnormality VERY_FREQUENT Abnormal oral cavity morphology HP:0000163
Includes strawberry gingivitis, oral ulcers, and palatal perforation.
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000163 | Abnormal oral cavity morphology | Very frequent (99-80%)"
Orphanet classifies oral cavity abnormalities as very frequent in GPA.
Pulmonary Nodules OCCASIONAL Pulmonary nodule HP:0033608
May cavitate; cavitated lung nodules are highly suggestive of GPA.
Show evidence (2 references)
ORPHA:900 SUPPORT
"HP:0033608 | Pulmonary nodule | Occasional (29-5%)"
Orphanet classifies pulmonary nodules as occasional in GPA.
PMID:36315063 SUPPORT Human Clinical
"chronic recurrent rhinosinusitis, cavitated lung nodules, palpable purpura or acute kidney injury"
Cavitated lung nodules are listed as a key diagnostic feature prompting investigation for AAV.
Recurrent Intrapulmonary Hemorrhage FREQUENT Recurrent intrapulmonary hemorrhage HP:0006535
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0006535 | Recurrent intrapulmonary hemorrhage | Frequent (79-30%)"
Orphanet classifies recurrent intrapulmonary hemorrhage as frequent.
Glomerulonephritis FREQUENT Glomerulonephritis HP:0000099
Rapidly progressive pauci-immune crescentic glomerulonephritis.
Show evidence (2 references)
ORPHA:900 SUPPORT
"HP:0000099 | Glomerulonephritis | Frequent (79-30%)"
Orphanet classifies glomerulonephritis as frequent in GPA.
PMID:36315063 SUPPORT Human Clinical
"chronic recurrent rhinosinusitis, cavitated lung nodules, palpable purpura or acute kidney injury"
Acute kidney injury (from glomerulonephritis) is listed as a key presentation prompting AAV investigation.
Nasolacrimal Duct Obstruction FREQUENT Nasolacrimal duct obstruction HP:0000579
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000579 | Nasolacrimal duct obstruction | Frequent (79-30%)"
Orphanet classifies nasolacrimal duct obstruction as frequent in GPA.
Abnormality of the Hypothalamus-Pituitary Axis FREQUENT Abnormality of the hypothalamus-pituitary axis HP:0000864
Pituitary and hypothalamic granulomas are a documented manifestation of GPA.
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0000864 | Abnormality of the hypothalamus-pituitary axis | Frequent (79-30%)"
Orphanet classifies hypothalamus-pituitary axis abnormalities as frequent in GPA.
Anti-PR3 Antibody Positivity FREQUENT Anti-proteinase 3 antibody positivity HP:0033557
Present in 80-90% of patients with active generalized disease.
Show evidence (2 references)
ORPHA:900 SUPPORT
"HP:0033557 | Anti-proteinase 3 antibody positivity | Frequent (79-30%)"
Orphanet classifies anti-PR3 antibody positivity as frequent in GPA.
PMID:28881446 SUPPORT Human Clinical
"Thirty-four patients (61%) had myeloperoxidase (MPO)-ANCAs, and 17 (30%) were positive for proteinase 3 (PR3)-ANCAs; 5 (9%) were ANCA-negative."
Olmsted County cohort shows 30% PR3-ANCA positivity among all AAV patients, though GPA specifically has higher rates.
c-ANCA Positivity FREQUENT Cytoplasmic antineutrophil antibody positivity HP:0032230
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0032230 | Cytoplasmic antineutrophil antibody positivity | Frequent (79-30%)"
Orphanet classifies c-ANCA positivity as frequent in GPA.
Elevated ESR FREQUENT Elevated erythrocyte sedimentation rate HP:0003565
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0003565 | Elevated erythrocyte sedimentation rate | Frequent (79-30%)"
Orphanet classifies elevated ESR as frequent in GPA.
Anti-Neutrophil Elastase Antibody Positivity FREQUENT Anti-neutrophil elastase antibody positivity HP:0034104
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0034104 | Anti-neutrophil elastase antibody positivity | Frequent (79-30%)"
Orphanet classifies anti-neutrophil elastase antibody positivity as frequent in GPA.
Elevated CRP FREQUENT Elevated circulating C-reactive protein concentration HP:0011227
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0011227 | Elevated circulating C-reactive protein concentration | Frequent (79-30%)"
Orphanet classifies elevated CRP as frequent in GPA.
Cerebral ischemia OCCASIONAL Cerebral ischemia HP:0002637
Show evidence (1 reference)
PMID:11493161 SUPPORT Human Clinical
"in 9 cases the central nervous system was involved"
In a prospective cohort of 128 patients with generalized granulomatosis with polyangiitis, central nervous system involvement occurred in only 9 cases (~7%); cerebral ischemia is a subset of CNS disease, so it is far below the Orphanet "very frequent (80-99%)" band, supporting an OCCASIONAL primary frequency.
Context-specific annotations (1)
VERY_FREQUENT
Source-specific assertion from the Orphanet product4 dataset, which assigns a higher frequency band than clinical cohorts. Retained for provenance; the primary frequency above reflects clinical-literature estimates.
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0002637 | Cerebral ischemia | Very frequent (99-80%)"
Orphanet records cerebral ischemia as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis.
Glomerulopathy VERY_FREQUENT Glomerulopathy HP:0100820
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0100820 | Glomerulopathy | Very frequent (99-80%)"
Orphanet records glomerulopathy as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis.
Polyarticular arthritis FREQUENT Polyarticular arthritis HP:0005764
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0005764 | Polyarticular arthritis | Frequent (79-30%)"
Orphanet records polyarticular arthritis as a frequent (30-79%) phenotype of granulomatosis with polyangiitis.
Increased inflammatory response FREQUENT Increased inflammatory response HP:0012649
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0012649 | Increased inflammatory response | Frequent (79-30%)"
Orphanet records increased inflammatory response as a frequent (30-79%) phenotype of granulomatosis with polyangiitis.
Anti-myeloperoxidase antibody positivity FREQUENT Anti-myeloperoxidase antibody positivity HP:0033559
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0033559 | Anti-myeloperoxidase antibody positivity | Frequent (79-30%)"
Orphanet records anti-myeloperoxidase antibody positivity as a frequent (30-79%) phenotype of granulomatosis with polyangiitis.
Inflammatory abnormality of the eye FREQUENT Inflammatory abnormality of the eye HP:0100533
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0100533 | Inflammatory abnormality of the eye | Frequent (79-30%)"
Orphanet records inflammatory abnormality of the eye as a frequent (30-79%) phenotype of granulomatosis with polyangiitis.
Periorbital edema FREQUENT Periorbital edema HP:0100539
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0100539 | Periorbital edema | Frequent (79-30%)"
Orphanet records periorbital edema as a frequent (30-79%) phenotype of granulomatosis with polyangiitis.
Papule FREQUENT Papule HP:0200034
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0200034 | Papule | Frequent (79-30%)"
Orphanet records papule as a frequent (30-79%) phenotype of granulomatosis with polyangiitis.
Prostatitis OCCASIONAL Prostatitis HP:0000024
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0000024 | Prostatitis | Occasional (29-5%)"
Orphanet records prostatitis as an occasional (5-29%) phenotype of granulomatosis with polyangiitis.
Ureteral stenosis OCCASIONAL Ureteral stenosis HP:0000071
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0000071 | Ureteral stenosis | Occasional (29-5%)"
Orphanet records ureteral stenosis as an occasional (5-29%) phenotype of granulomatosis with polyangiitis.
Hydronephrosis OCCASIONAL Hydronephrosis HP:0000126
Show evidence (1 reference)
ORPHA:900 SUPPORT Other
"HP:0000126 | Hydronephrosis | Occasional (29-5%)"
Orphanet records hydronephrosis as an occasional (5-29%) phenotype of granulomatosis with polyangiitis.
🧬

Genetic Associations

6
HLA-DPB1 (Risk Factor)
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HLA-DPB1 | major histocompatibility complex, class II, DP beta 1 | hgnc:4940 | Major susceptibility factor in"
Orphanet identifies HLA-DPB1 as a major susceptibility factor in GPA.
HLA-DPA1 (Risk Factor)
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HLA-DPA1 | major histocompatibility complex, class II, DP alpha 1 | hgnc:4938 | Major susceptibility factor in"
Orphanet identifies HLA-DPA1 as a major susceptibility factor in GPA.
PRTN3 (Risk Factor)
Show evidence (1 reference)
ORPHA:900 SUPPORT
"PRTN3 | proteinase 3 | hgnc:9495 | Major susceptibility factor in"
Orphanet identifies PRTN3 as a major susceptibility factor. PRTN3 encodes proteinase 3, the target autoantigen of PR3-ANCA.
CTLA4 (Risk Factor)
Show evidence (1 reference)
ORPHA:900 SUPPORT
"CTLA4 | cytotoxic T-lymphocyte associated protein 4 | hgnc:2505 | Major susceptibility factor in"
Orphanet identifies CTLA4 as a major susceptibility factor in GPA.
PTPN22 (Risk Factor)
Show evidence (1 reference)
ORPHA:900 SUPPORT
"PTPN22 | protein tyrosine phosphatase non-receptor type 22 | hgnc:9652 | Major susceptibility factor in"
Orphanet identifies PTPN22 as a major susceptibility factor in GPA.
SERPINA1 (Risk Factor)
Show evidence (1 reference)
PMID:16859601 SUPPORT Human Clinical
"Genetic investigations have identified various candidate genes, with alpha1-antitrypsin deficiency being the most consistently reported genetic susceptibility factor to date."
Epidemiology review confirms alpha-1 antitrypsin deficiency (SERPINA1) as the most consistently reported genetic susceptibility factor for GPA.
💊

Medical Actions

4
Rituximab
Action: Pharmacotherapy NCIT:C15986
Agent: rituximab NCIT:C1702
Anti-CD20 monoclonal antibody; first-line for both induction and maintenance of remission in GPA.
Show evidence (1 reference)
PMID:36315063 SUPPORT Human Clinical
"Recent data favour rituximab as a preferable option for both induction and maintenance of remission."
Recent clinical review confirms rituximab as the preferred option for both induction and maintenance therapy in AAV.
Cyclophosphamide
Action: Pharmacotherapy NCIT:C15986
Agent: cyclophosphamide CHEBI:4027
Alkylating immunosuppressant; alternative for severe disease induction, particularly organ-threatening or life-threatening disease.
Show evidence (1 reference)
PMID:1739240 SUPPORT Human Clinical
"One hundred and thirty-three patients (84%) received "standard" therapy with daily low-dose cyclophosphamide and glucocorticoids."
Landmark NIH cohort demonstrates cyclophosphamide plus glucocorticoids as the standard induction therapy for GPA.
Corticosteroids
Action: Pharmacotherapy NCIT:C15986
Agent: corticosteroid CHEBI:50858
High-dose for induction, with subsequent taper. Glucocorticoid-sparing strategies are increasingly preferred.
Show evidence (1 reference)
PMID:36315063 SUPPORT Human Clinical
"regimens with less glucocorticoids are equally effective and safer in inducing remission compared with conventional regimens"
Recent evidence supports reduced glucocorticoid regimens as equally effective and safer than conventional high-dose protocols.
Avacopan
Action: Pharmacotherapy NCIT:C15986
Agent: avacopan NCIT:C174788
Oral C5a receptor inhibitor; allows glucocorticoid reduction or elimination during induction therapy by blocking complement-mediated neutrophil priming.
Mechanism Target:
Complement Alternative Pathway Activation
Show evidence (2 references)
PMID:36315063 SUPPORT Human Clinical
"avacopan is an effective glucocorticoid-sparing option."
Clinical review confirms avacopan as an effective glucocorticoid-sparing treatment option in AAV.
PMID:37781373 SUPPORT
"Mechanistically, cytokines or complement factors activate and prime neutrophils for ANCA-binding; thus, C5a receptor blocker has garnered attention as potential replacement for glucocorticoids in clinical settings."
Confirms the mechanistic rationale for avacopan as a C5a receptor blocker targeting complement-mediated neutrophil priming.
🌍

Environmental Factors

2
Silica Dust Exposure
Occupational exposure to crystalline silica is the most consistently reported environmental risk factor for GPA.
Show evidence (2 references)
PMID:16859601 SUPPORT Human Clinical
"evidence has grown for a possible relationship between WG and occupational exposure to crystalline silica."
Epidemiology review identifies crystalline silica as a putative environmental risk factor for GPA.
PMID:36315063 SUPPORT Human Clinical
"Exposure to silica dust, farming and chronic nasal Staphylococcus aureus carriage are associated with increased risk of developing AAV."
Clinical practice review confirms silica dust as an established risk factor.
Staphylococcus aureus Nasal Carriage
Chronic nasal carriage of S. aureus is associated with increased risk of developing GPA and with disease relapse.
Show evidence (1 reference)
PMID:36315063 SUPPORT Human Clinical
"Exposure to silica dust, farming and chronic nasal Staphylococcus aureus carriage are associated with increased risk of developing AAV."
Confirms nasal S. aureus carriage as an established risk factor for AAV.
🔬

Biochemical Markers

4
PR3-ANCA (c-ANCA) (Elevated)
Context: Present in 80-90% of active generalized disease
Show evidence (1 reference)
PMID:35479831 SUPPORT
"There is also evidence for classification of patients based on ANCA subtype; those with anti-proteinase 3 antibodies (PR3) or anti-myeloperoxidase antibodies (MPO) have differences in response to treatment and clinical outcomes."
Confirms PR3-ANCA subtyping has clinical and prognostic significance in GPA.
MPO-ANCA (p-ANCA) (Variable)
Context: Present in 10-20% of patients
Show evidence (1 reference)
ORPHA:900 SUPPORT
"HP:0033559 | Anti-myeloperoxidase antibody positivity | Frequent (79-30%)"
Orphanet classifies anti-MPO antibody positivity as frequent in GPA, reflecting the minority of GPA patients who are MPO-ANCA positive.
ESR (Elevated)
Context: Marker of systemic inflammation and disease activity.
CRP (Elevated)
Context: Correlates with disease activity.
{ }

Source YAML

click to show
name: Granulomatosis with Polyangiitis
creation_date: '2025-12-19T01:12:52Z'
updated_date: '2026-05-01T18:00:00Z'
category: Autoimmune
parents:
- Autoimmune Disease
- Vasculitis
disease_term:
  preferred_term: Granulomatosis with Polyangiitis
  term:
    id: MONDO:0012105
    label: granulomatosis with polyangiitis
description: >-
  A rare anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis
  characterized by necrotizing granulomatous inflammation of small and medium
  vessels (capillaries, venules, and arterioles), resulting in tissue ischemia.
  Strongly associated with anti-PR3 (c-ANCA) antibodies. The classic triad involves
  the upper respiratory tract, lungs, and kidneys, though any organ may be affected.
  Formerly known as Wegener's granulomatosis.
pathophysiology:
- name: B Cell Autoreactivity and ANCA Production
  description: >-
    Autoreactive B cells produce anti-proteinase 3 (PR3-ANCA) antibodies,
    the defining upstream event in GPA pathogenesis. Genetic predisposition
    (HLA-DP alleles) and environmental triggers (S. aureus, silica) drive
    loss of tolerance to PR3, leading to sustained autoantibody production.
  cell_types:
  - preferred_term: B cell
    term:
      id: CL:0000236
      label: B cell
  biological_processes:
  - preferred_term: B Cell Activation
    term:
      id: GO:0042113
      label: B cell activation
  evidence:
  - reference: PMID:39257888
    reference_title: "Granulomatosis with polyangiitis: clinical characteristics and updates in diagnosis."
    supports: SUPPORT
    snippet: >-
      Granulomatosis with polyangiitis (GPA) is a rare systemic disease characterized
      by granulomatous inflammation of the respiratory tract and necrotizing
      vasculitis of small and medium vessels often associated with the production of
      anti-neutrophil cytoplasmic antibodies (ANCA) directed mainly against leukocyte
      proteinase 3 (PR3).
    explanation: >-
      Confirms that GPA is defined by production of ANCA directed against PR3,
      establishing B cell-mediated autoantibody production as the upstream event.
  - reference: PMID:36315063
    reference_title: "Diagnosing and treating ANCA-associated vasculitis: an updated review for clinical practice."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Exposure to silica
      dust, farming and chronic nasal Staphylococcus aureus carriage are associated
      with increased risk of developing AAV.
    explanation: >-
      Environmental triggers (silica, S. aureus) contribute to loss of B cell
      tolerance and ANCA production.
  downstream:
  - target: ANCA-Mediated Neutrophil Activation
- name: ANCA-Mediated Neutrophil Activation
  description: >-
    Anti-proteinase 3 (PR3) antibodies bind to primed neutrophils, causing
    activation, degranulation, and release of reactive oxygen species and
    lytic enzymes. This causes direct endothelial damage and vessel wall
    necrosis. Neutrophil extracellular trap (NET) formation further amplifies
    vascular injury.
  cell_types:
  - preferred_term: Neutrophil
    term:
      id: CL:0000775
      label: neutrophil
  - preferred_term: Endothelial Cell
    term:
      id: CL:0000115
      label: endothelial cell
  biological_processes:
  - preferred_term: Neutrophil Activation
    term:
      id: GO:0042119
      label: neutrophil activation
  - preferred_term: Neutrophil Extracellular Trap Formation
    term:
      id: GO:0140645
      label: neutrophil extracellular trap formation
  evidence:
  - reference: PMID:37781373
    reference_title: The involvement of NETs in ANCA-associated vasculitis.
    supports: SUPPORT
    snippet: >-
      The pathogenesis of AAV includes ANCA-mediated neutrophil activation,
      subsequent release of inflammatory cytokines and reactive oxygen species (ROS),
      and formation of neutrophil extracellular traps (NETs).
    explanation: >-
      This review confirms that ANCA-mediated neutrophil activation is a central
      pathogenic mechanism in AAV, leading to ROS release and NET formation.
  - reference: PMID:38791316
    reference_title: Pathogenesis of Pulmonary Manifestations in ANCA-Associated Vasculitis and Goodpasture Syndrome.
    supports: SUPPORT
    snippet: >-
      Mechanisms involving ANCA and anti-GBM autoantibodies, neutrophil activation,
      and neutrophil extracellular trap (NETs) formation are discussed, along with
      the
      role of the complement system in inducing pulmonary injury.
    explanation: >-
      Confirms neutrophil activation and NET formation as key mechanisms in
      pulmonary injury in GPA.
  downstream:
  - target: Granuloma Formation
  - target: Complement Alternative Pathway Activation
- name: Granuloma Formation
  description: >-
    Granulomatous inflammation with multinucleated giant cells, epithelioid
    macrophages, and necrosis affects the respiratory tract. CD4+ T cells and
    macrophages organize into granulomas that destroy tissue, a hallmark
    distinguishing GPA from other ANCA-associated vasculitides.
  cell_types:
  - preferred_term: Macrophage
    term:
      id: CL:0000235
      label: macrophage
  - preferred_term: CD4-positive T cell
    term:
      id: CL:0000624
      label: CD4-positive, alpha-beta T cell
  biological_processes:
  - preferred_term: Granuloma Formation
    term:
      id: GO:0002432
      label: granuloma formation
  - preferred_term: Inflammatory Response
    term:
      id: GO:0006954
      label: inflammatory response
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002955 | Granulomatosis | Very frequent (99-80%)"
    explanation: >-
      Orphanet classifies granulomatosis as a very frequent feature of GPA,
      consistent with granuloma formation being a hallmark pathological process.
  - reference: PMID:39257888
    supports: SUPPORT
    snippet: >-
      Granulomatosis with polyangiitis (GPA) is a rare systemic disease characterized
      by granulomatous inflammation of the respiratory tract and necrotizing
      vasculitis of small and medium vessels
    explanation: >-
      Confirms granulomatous inflammation of the respiratory tract as a defining
      feature of GPA.
- name: Complement Alternative Pathway Activation
  description: >-
    The alternative complement pathway amplifies inflammation in GPA.
    C5a recruits and activates neutrophils, creating a positive feedback
    loop of vascular damage. This mechanism is the therapeutic target of
    avacopan (C5a receptor inhibitor).
  biological_processes:
  - preferred_term: Complement Activation
    term:
      id: GO:0006956
      label: complement activation
  evidence:
  - reference: PMID:37781373
    reference_title: The involvement of NETs in ANCA-associated vasculitis.
    supports: SUPPORT
    snippet: >-
      Mechanistically, cytokines or complement factors activate and prime neutrophils
      for ANCA-binding; thus, C5a receptor blocker has garnered attention as potential
      replacement for glucocorticoids in clinical settings.
    explanation: >-
      Confirms complement factors prime neutrophils for ANCA binding, and that
      C5a receptor blockade is a validated therapeutic target.
  - reference: PMID:38791316
    reference_title: Pathogenesis of Pulmonary Manifestations in ANCA-Associated Vasculitis and Goodpasture Syndrome.
    supports: SUPPORT
    snippet: >-
      Mechanisms involving ANCA and anti-GBM autoantibodies, neutrophil activation,
      and neutrophil extracellular trap (NETs) formation are discussed, along with
      the
      role of the complement system in inducing pulmonary injury.
    explanation: >-
      Confirms the complement system plays a role in amplifying
      ANCA-mediated pulmonary injury.
phenotypes:
# === ENT / Upper Respiratory ===
- name: Sinusitis
  category: ENT
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Sinusitis
    term:
      id: HP:0000246
      label: Sinusitis
    temporality: CHRONIC
  notes: >-
    Chronic destructive sinusitis is one of the most common presenting features,
    often with bloody or purulent nasal discharge.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000246 | Sinusitis | Very frequent (99-80%)"
    explanation: Orphanet classifies sinusitis as very frequent in GPA.
  - reference: PMID:28881446
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      In GPA, the most common disease features at diagnosis were
      otorhinolaryngological (74%), followed by "general" (57%) and pulmonary (48%)
      manifestations.
    explanation: >-
      Olmsted County cohort confirms ENT manifestations (including sinusitis)
      as the most common presenting feature of GPA at 74%.
- name: Epistaxis
  category: ENT
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Epistaxis
    term:
      id: HP:0000421
      label: Epistaxis
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000421 | Epistaxis | Very frequent (99-80%)"
    explanation: Orphanet classifies epistaxis as very frequent in GPA.
- name: Nasal Septum Perforation
  category: ENT
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Nasal septum perforation
    term:
      id: HP:0033434
      label: Nasal septum perforation
  notes: Due to granulomatous destruction of nasal cartilage and septum.
- name: Saddle Nose Deformity
  category: ENT
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Saddle Nose Deformity
    term:
      id: HP:0005280
      label: Depressed nasal bridge
  notes: Due to nasal cartilage destruction from granulomatous inflammation.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000366 | Abnormality of the nose | Very frequent (99-80%)"
    explanation: >-
      Orphanet reports nasal abnormalities as very frequent; saddle nose deformity
      from cartilage destruction is a classic late finding.
- name: Otitis Media
  category: ENT
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Otitis media
    term:
      id: HP:0000388
      label: Otitis media
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000388 | Otitis media | Very frequent (99-80%)"
    explanation: Orphanet classifies otitis media as very frequent in GPA.
- name: Sensorineural Hearing Impairment
  category: ENT
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Sensorineural hearing impairment
    term:
      id: HP:0000407
      label: Sensorineural hearing impairment
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000407 | Sensorineural hearing impairment | Occasional (29-5%)"
    explanation: Orphanet classifies sensorineural hearing loss as occasional in GPA.
- name: Subglottic Stenosis
  category: ENT
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Subglottic stenosis
    term:
      id: HP:0001607
      label: Subglottic stenosis
  notes: Can cause stridor and airway compromise; may require surgical intervention.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0001607 | Subglottic stenosis | Occasional (29-5%)"
    explanation: Orphanet classifies subglottic stenosis as occasional in GPA.
- name: Oral Cavity Abnormality
  category: ENT
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Oral cavity abnormality
    term:
      id: HP:0000163
      label: Abnormal oral cavity morphology
  notes: Includes strawberry gingivitis, oral ulcers, and palatal perforation.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000163 | Abnormal oral cavity morphology | Very frequent (99-80%)"
    explanation: Orphanet classifies oral cavity abnormalities as very frequent in GPA.
# === Pulmonary ===
- name: Recurrent Respiratory Infections
  category: Respiratory
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Recurrent respiratory infections
    term:
      id: HP:0002205
      label: Recurrent respiratory infections
  notes: >-
    Reflects mucociliary dysfunction and mucosal destruction from chronic
    sinonasal granulomatous disease.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002205 | Recurrent respiratory infections | Very frequent (99-80%)"
    explanation: Orphanet classifies recurrent respiratory infections as very frequent in GPA.
- name: Pulmonary Infiltrates
  category: Respiratory
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Pulmonary infiltrates
    term:
      id: HP:0002113
      label: Pulmonary infiltrates
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002113 | Pulmonary infiltrates | Very frequent (99-80%)"
    explanation: Orphanet classifies pulmonary infiltrates as very frequent in GPA.
- name: Pulmonary Nodules
  category: Respiratory
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Pulmonary nodule
    term:
      id: HP:0033608
      label: Pulmonary nodule
  notes: May cavitate; cavitated lung nodules are highly suggestive of GPA.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0033608 | Pulmonary nodule | Occasional (29-5%)"
    explanation: Orphanet classifies pulmonary nodules as occasional in GPA.
  - reference: PMID:36315063
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      chronic recurrent rhinosinusitis, cavitated lung nodules, palpable purpura or
      acute kidney injury
    explanation: >-
      Cavitated lung nodules are listed as a key diagnostic feature prompting
      investigation for AAV.
- name: Hemoptysis
  category: Respiratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Hemoptysis
    term:
      id: HP:0002105
      label: Hemoptysis
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002105 | Hemoptysis | Frequent (79-30%)"
    explanation: Orphanet classifies hemoptysis as frequent in GPA.
- name: Cough
  category: Respiratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Cough
    term:
      id: HP:0012735
      label: Cough
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0012735 | Cough | Frequent (79-30%)"
    explanation: Orphanet classifies cough as frequent in GPA.
- name: Diffuse Alveolar Hemorrhage
  category: Respiratory
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Diffuse alveolar hemorrhage
    term:
      id: HP:0025420
      label: Diffuse alveolar hemorrhage
  notes: Life-threatening complication requiring urgent treatment.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0025420 | Diffuse alveolar hemorrhage | Occasional (29-5%)"
    explanation: Orphanet classifies diffuse alveolar hemorrhage as occasional in GPA.
- name: Recurrent Intrapulmonary Hemorrhage
  category: Respiratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Recurrent intrapulmonary hemorrhage
    term:
      id: HP:0006535
      label: Recurrent intrapulmonary hemorrhage
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0006535 | Recurrent intrapulmonary hemorrhage | Frequent (79-30%)"
    explanation: Orphanet classifies recurrent intrapulmonary hemorrhage as frequent.
- name: Pulmonary Fibrosis
  category: Respiratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Pulmonary fibrosis
    term:
      id: HP:0002206
      label: Pulmonary fibrosis
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002206 | Pulmonary fibrosis | Frequent (79-30%)"
    explanation: Orphanet classifies pulmonary fibrosis as frequent in GPA.
- name: Respiratory Insufficiency
  category: Respiratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Respiratory insufficiency
    term:
      id: HP:0002093
      label: Respiratory insufficiency
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002093 | Respiratory insufficiency | Frequent (79-30%)"
    explanation: Orphanet classifies respiratory insufficiency as frequent in GPA.
- name: Chronic Pulmonary Obstruction
  category: Respiratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Chronic pulmonary obstruction
    term:
      id: HP:0006510
      label: Chronic pulmonary obstruction
  notes: Airway obstruction from endobronchial granulomatous disease.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0006510 | Chronic pulmonary obstruction | Frequent (79-30%)"
    explanation: Orphanet classifies chronic pulmonary obstruction as frequent in GPA.
- name: Chest Pain
  category: Respiratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Chest pain
    term:
      id: HP:0100749
      label: Chest pain
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0100749 | Chest pain | Frequent (79-30%)"
    explanation: Orphanet classifies chest pain as frequent in GPA.
# === Renal ===
- name: Glomerulonephritis
  category: Renal
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Glomerulonephritis
    term:
      id: HP:0000099
      label: Glomerulonephritis
  notes: Rapidly progressive pauci-immune crescentic glomerulonephritis.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000099 | Glomerulonephritis | Frequent (79-30%)"
    explanation: Orphanet classifies glomerulonephritis as frequent in GPA.
  - reference: PMID:36315063
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      chronic recurrent rhinosinusitis, cavitated lung nodules, palpable purpura or
      acute kidney injury
    explanation: >-
      Acute kidney injury (from glomerulonephritis) is listed as a key
      presentation prompting AAV investigation.
- name: Hematuria
  category: Renal
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Hematuria
    term:
      id: HP:0000790
      label: Hematuria
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000790 | Hematuria | Very frequent (99-80%)"
    explanation: Orphanet classifies hematuria as very frequent in GPA.
- name: Proteinuria
  category: Renal
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Proteinuria
    term:
      id: HP:0000093
      label: Proteinuria
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000093 | Proteinuria | Frequent (79-30%)"
    explanation: Orphanet classifies proteinuria as frequent in GPA.
- name: Renal Insufficiency
  category: Renal
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Renal insufficiency
    term:
      id: HP:0000083
      label: Renal insufficiency
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000083 | Renal insufficiency | Occasional (29-5%)"
    explanation: Orphanet classifies renal insufficiency as occasional in GPA.
# === Constitutional ===
- name: Fever
  category: Constitutional
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Fever
    term:
      id: HP:0001945
      label: Fever
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0001945 | Fever | Very frequent (99-80%)"
    explanation: Orphanet classifies fever as very frequent in GPA.
- name: Weight Loss
  category: Constitutional
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Weight loss
    term:
      id: HP:0001824
      label: Weight loss
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0001824 | Weight loss | Very frequent (99-80%)"
    explanation: Orphanet classifies weight loss as very frequent in GPA.
- name: Fatigue
  category: Constitutional
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Fatigue
    term:
      id: HP:0012378
      label: Fatigue
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0012378 | Fatigue | Very frequent (99-80%)"
    explanation: Orphanet classifies fatigue as very frequent in GPA.
# === Musculoskeletal ===
- name: Arthralgia
  category: Musculoskeletal
  frequency: VERY_FREQUENT
  phenotype_term:
    preferred_term: Arthralgia
    term:
      id: HP:0002829
      label: Arthralgia
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002829 | Arthralgia | Very frequent (99-80%)"
    explanation: Orphanet classifies arthralgia as very frequent in GPA.
- name: Myalgia
  category: Musculoskeletal
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Myalgia
    term:
      id: HP:0003326
      label: Myalgia
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0003326 | Myalgia | Occasional (29-5%)"
    explanation: Orphanet classifies myalgia as occasional in GPA.
- name: Arthritis
  category: Musculoskeletal
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Arthritis
    term:
      id: HP:0001369
      label: Arthritis
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0001369 | Arthritis | Frequent (79-30%)"
    explanation: Orphanet classifies arthritis as frequent in GPA.
# === Ocular ===
- name: Scleritis
  category: Ophthalmologic
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Scleritis
    term:
      id: HP:0100532
      label: Scleritis
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0100532 | Scleritis | Frequent (79-30%)"
    explanation: Orphanet classifies scleritis as frequent in GPA.
- name: Proptosis
  category: Ophthalmologic
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Proptosis
    term:
      id: HP:0000520
      label: Proptosis
  notes: Due to retro-orbital granulomatous mass formation.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000520 | Proptosis | Occasional (29-5%)"
    explanation: Orphanet classifies proptosis as occasional in GPA.
- name: Nasolacrimal Duct Obstruction
  category: Ophthalmologic
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Nasolacrimal duct obstruction
    term:
      id: HP:0000579
      label: Nasolacrimal duct obstruction
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000579 | Nasolacrimal duct obstruction | Frequent (79-30%)"
    explanation: Orphanet classifies nasolacrimal duct obstruction as frequent in GPA.
- name: Keratitis
  category: Ophthalmologic
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Keratitis
    term:
      id: HP:0000491
      label: Keratitis
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000491 | Keratitis | Occasional (29-5%)"
    explanation: Orphanet classifies keratitis as occasional in GPA.
# === Dermatologic ===
- name: Skin Rash
  category: Dermatologic
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Skin rash
    term:
      id: HP:0000988
      label: Skin rash
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000988 | Skin rash | Frequent (79-30%)"
    explanation: Orphanet classifies skin rash as frequent in GPA.
- name: Purpura
  category: Dermatologic
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Purpura
    term:
      id: HP:0000979
      label: Purpura
  notes: Palpable purpura from leukocytoclastic vasculitis.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000979 | Purpura | Occasional (29-5%)"
    explanation: Orphanet classifies purpura as occasional in GPA.
  - reference: PMID:36315063
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      chronic recurrent rhinosinusitis, cavitated lung nodules, palpable purpura or
      acute kidney injury
    explanation: >-
      Palpable purpura is listed as a key feature prompting AAV investigation.
- name: Skin Ulcer
  category: Dermatologic
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Skin ulcer
    term:
      id: HP:0200042
      label: Skin ulcer
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0200042 | Skin ulcer | Occasional (29-5%)"
    explanation: Orphanet classifies skin ulcers as occasional in GPA.
# === Neurologic ===
- name: Peripheral Neuropathy
  category: Neurologic
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Peripheral neuropathy
    term:
      id: HP:0009830
      label: Peripheral neuropathy
  notes: Mononeuritis multiplex is the characteristic pattern.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0009830 | Peripheral neuropathy | Frequent (79-30%)"
    explanation: Orphanet classifies peripheral neuropathy as frequent in GPA.
- name: Cranial Nerve Paralysis
  category: Neurologic
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Cranial nerve paralysis
    term:
      id: HP:0006824
      label: Cranial nerve paralysis
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0006824 | Cranial nerve paralysis | Occasional (29-5%)"
    explanation: Orphanet classifies cranial nerve paralysis as occasional in GPA.
- name: Headache
  category: Neurologic
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Headache
    term:
      id: HP:0002315
      label: Headache
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002315 | Headache | Occasional (29-5%)"
    explanation: Orphanet classifies headache as occasional in GPA.
# === Cardiovascular ===
- name: Pericarditis
  category: Cardiovascular
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Pericarditis
    term:
      id: HP:0001701
      label: Pericarditis
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0001701 | Pericarditis | Occasional (29-5%)"
    explanation: Orphanet classifies pericarditis as occasional in GPA.
- name: Abnormality of the Hypothalamus-Pituitary Axis
  category: Endocrine
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Abnormality of the hypothalamus-pituitary axis
    term:
      id: HP:0000864
      label: Abnormality of the hypothalamus-pituitary axis
  notes: Pituitary and hypothalamic granulomas are a documented manifestation of GPA.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000864 | Abnormality of the hypothalamus-pituitary axis | Frequent (79-30%)"
    explanation: Orphanet classifies hypothalamus-pituitary axis abnormalities as frequent in GPA.
- name: Hypertension
  category: Cardiovascular
  frequency: OCCASIONAL
  phenotype_term:
    preferred_term: Hypertension
    term:
      id: HP:0000822
      label: Hypertension
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0000822 | Hypertension | Occasional (29-5%)"
    explanation: Orphanet classifies hypertension as occasional in GPA.
# === Gastrointestinal ===
- name: Abdominal Pain
  category: Gastrointestinal
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Abdominal pain
    term:
      id: HP:0002027
      label: Abdominal pain
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002027 | Abdominal pain | Frequent (79-30%)"
    explanation: Orphanet classifies abdominal pain as frequent in GPA.
- name: Nausea and Vomiting
  category: Gastrointestinal
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Nausea and vomiting
    term:
      id: HP:0002017
      label: Nausea and vomiting
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0002017 | Nausea and vomiting | Frequent (79-30%)"
    explanation: Orphanet classifies nausea and vomiting as frequent in GPA.
# === Laboratory / Serologic ===
- name: Anti-PR3 Antibody Positivity
  category: Laboratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Anti-proteinase 3 antibody positivity
    term:
      id: HP:0033557
      label: Anti-proteinase 3 antibody positivity
  notes: Present in 80-90% of patients with active generalized disease.
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0033557 | Anti-proteinase 3 antibody positivity | Frequent (79-30%)"
    explanation: Orphanet classifies anti-PR3 antibody positivity as frequent in GPA.
  - reference: PMID:28881446
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Thirty-four patients (61%) had myeloperoxidase (MPO)-ANCAs, and 17 (30%) were
      positive for proteinase 3 (PR3)-ANCAs; 5 (9%) were ANCA-negative.
    explanation: >-
      Olmsted County cohort shows 30% PR3-ANCA positivity among all AAV patients,
      though GPA specifically has higher rates.
- name: c-ANCA Positivity
  category: Laboratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Cytoplasmic ANCA positivity
    term:
      id: HP:0032230
      label: Cytoplasmic antineutrophil antibody positivity
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0032230 | Cytoplasmic antineutrophil antibody positivity | Frequent (79-30%)"
    explanation: Orphanet classifies c-ANCA positivity as frequent in GPA.
- name: Elevated ESR
  category: Laboratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Elevated erythrocyte sedimentation rate
    term:
      id: HP:0003565
      label: Elevated erythrocyte sedimentation rate
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0003565 | Elevated erythrocyte sedimentation rate | Frequent (79-30%)"
    explanation: Orphanet classifies elevated ESR as frequent in GPA.
- name: Anti-Neutrophil Elastase Antibody Positivity
  category: Laboratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Anti-neutrophil elastase antibody positivity
    term:
      id: HP:0034104
      label: Anti-neutrophil elastase antibody positivity
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0034104 | Anti-neutrophil elastase antibody positivity | Frequent (79-30%)"
    explanation: Orphanet classifies anti-neutrophil elastase antibody positivity as frequent in GPA.
- name: Elevated CRP
  category: Laboratory
  frequency: FREQUENT
  phenotype_term:
    preferred_term: Elevated CRP
    term:
      id: HP:0011227
      label: Elevated circulating C-reactive protein concentration
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0011227 | Elevated circulating C-reactive protein concentration | Frequent (79-30%)"
    explanation: Orphanet classifies elevated CRP as frequent in GPA.
- name: "Vasculitis"
  category: Cardiovascular
  frequency: VERY_FREQUENT
  description: "Vasculitis is reported as a very frequent (80-99%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Vasculitis"
    term:
      id: HP:0002633
      label: "Vasculitis"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0002633 | Vasculitis | Very frequent (99-80%)"
    explanation: "Orphanet records vasculitis as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis."
- name: "Cerebral ischemia"
  category: Neurologic
  frequency: OCCASIONAL
  description: >-
    Cerebral ischemia is a rare central-nervous-system manifestation of
    granulomatosis with polyangiitis. The Orphanet product4 dataset assigns a
    "very frequent" band, but CNS involvement of any kind affects only a small
    minority of patients, and cerebral ischemia is a subset of that. The primary
    OCCASIONAL band reflects the clinical literature; the Orphanet band is
    retained below as a source-specific context.
  phenotype_term:
    preferred_term: "Cerebral ischemia"
    term:
      id: HP:0002637
      label: "Cerebral ischemia"
  evidence:
  - reference: PMID:11493161
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "in 9 cases the central nervous system was involved"
    explanation: >-
      In a prospective cohort of 128 patients with generalized granulomatosis
      with polyangiitis, central nervous system involvement occurred in only 9
      cases (~7%); cerebral ischemia is a subset of CNS disease, so it is far
      below the Orphanet "very frequent (80-99%)" band, supporting an OCCASIONAL
      primary frequency.
  phenotype_contexts:
  - frequency: VERY_FREQUENT
    notes: >-
      Source-specific assertion from the Orphanet product4 dataset, which
      assigns a higher frequency band than clinical cohorts. Retained for
      provenance; the primary frequency above reflects clinical-literature
      estimates.
    evidence:
    - reference: ORPHA:900
      supports: SUPPORT
      evidence_source: OTHER
      snippet: "HP:0002637 | Cerebral ischemia | Very frequent (99-80%)"
      explanation: "Orphanet records cerebral ischemia as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis."
- name: "Granulomatosis"
  category: Systemic
  frequency: VERY_FREQUENT
  description: "Granulomatosis is reported as a very frequent (80-99%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Granulomatosis"
    term:
      id: HP:0002955
      label: "Granulomatosis"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0002955 | Granulomatosis | Very frequent (99-80%)"
    explanation: "Orphanet records granulomatosis as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis."
- name: "Autoimmunity"
  category: Immunologic
  frequency: VERY_FREQUENT
  description: "Autoimmunity is reported as a very frequent (80-99%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Autoimmunity"
    term:
      id: HP:0002960
      label: "Autoimmunity"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0002960 | Autoimmunity | Very frequent (99-80%)"
    explanation: "Orphanet records autoimmunity as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis."
- name: "Glomerulopathy"
  category: Renal
  frequency: VERY_FREQUENT
  description: "Glomerulopathy is reported as a very frequent (80-99%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Glomerulopathy"
    term:
      id: HP:0100820
      label: "Glomerulopathy"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0100820 | Glomerulopathy | Very frequent (99-80%)"
    explanation: "Orphanet records glomerulopathy as a very frequent (80-99%) phenotype of granulomatosis with polyangiitis."
- name: "Polyarticular arthritis"
  category: Musculoskeletal
  frequency: FREQUENT
  description: "Polyarticular arthritis is reported as a frequent (30-79%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Polyarticular arthritis"
    term:
      id: HP:0005764
      label: "Polyarticular arthritis"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0005764 | Polyarticular arthritis | Frequent (79-30%)"
    explanation: "Orphanet records polyarticular arthritis as a frequent (30-79%) phenotype of granulomatosis with polyangiitis."
- name: "Increased inflammatory response"
  category: Systemic
  frequency: FREQUENT
  description: "Increased inflammatory response is reported as a frequent (30-79%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Increased inflammatory response"
    term:
      id: HP:0012649
      label: "Increased inflammatory response"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0012649 | Increased inflammatory response | Frequent (79-30%)"
    explanation: "Orphanet records increased inflammatory response as a frequent (30-79%) phenotype of granulomatosis with polyangiitis."
- name: "Anti-myeloperoxidase antibody positivity"
  category: Immunologic
  frequency: FREQUENT
  description: "Anti-myeloperoxidase antibody positivity is reported as a frequent (30-79%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Anti-myeloperoxidase antibody positivity"
    term:
      id: HP:0033559
      label: "Anti-myeloperoxidase antibody positivity"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0033559 | Anti-myeloperoxidase antibody positivity | Frequent (79-30%)"
    explanation: "Orphanet records anti-myeloperoxidase antibody positivity as a frequent (30-79%) phenotype of granulomatosis with polyangiitis."
- name: "Inflammatory abnormality of the eye"
  category: Ophthalmologic
  frequency: FREQUENT
  description: "Inflammatory abnormality of the eye is reported as a frequent (30-79%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Inflammatory abnormality of the eye"
    term:
      id: HP:0100533
      label: "Inflammatory abnormality of the eye"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0100533 | Inflammatory abnormality of the eye | Frequent (79-30%)"
    explanation: "Orphanet records inflammatory abnormality of the eye as a frequent (30-79%) phenotype of granulomatosis with polyangiitis."
- name: "Periorbital edema"
  category: Ophthalmologic
  frequency: FREQUENT
  description: "Periorbital edema is reported as a frequent (30-79%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Periorbital edema"
    term:
      id: HP:0100539
      label: "Periorbital edema"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0100539 | Periorbital edema | Frequent (79-30%)"
    explanation: "Orphanet records periorbital edema as a frequent (30-79%) phenotype of granulomatosis with polyangiitis."
- name: "Papule"
  category: Dermatologic
  frequency: FREQUENT
  description: "Papule is reported as a frequent (30-79%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Papule"
    term:
      id: HP:0200034
      label: "Papule"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0200034 | Papule | Frequent (79-30%)"
    explanation: "Orphanet records papule as a frequent (30-79%) phenotype of granulomatosis with polyangiitis."
- name: "Prostatitis"
  category: Genitourinary
  frequency: OCCASIONAL
  description: "Prostatitis is reported as an occasional (5-29%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Prostatitis"
    term:
      id: HP:0000024
      label: "Prostatitis"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0000024 | Prostatitis | Occasional (29-5%)"
    explanation: "Orphanet records prostatitis as an occasional (5-29%) phenotype of granulomatosis with polyangiitis."
- name: "Ureteral stenosis"
  category: Renal
  frequency: OCCASIONAL
  description: "Ureteral stenosis is reported as an occasional (5-29%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Ureteral stenosis"
    term:
      id: HP:0000071
      label: "Ureteral stenosis"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0000071 | Ureteral stenosis | Occasional (29-5%)"
    explanation: "Orphanet records ureteral stenosis as an occasional (5-29%) phenotype of granulomatosis with polyangiitis."
- name: "Hydronephrosis"
  category: Renal
  frequency: OCCASIONAL
  description: "Hydronephrosis is reported as an occasional (5-29%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Hydronephrosis"
    term:
      id: HP:0000126
      label: "Hydronephrosis"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0000126 | Hydronephrosis | Occasional (29-5%)"
    explanation: "Orphanet records hydronephrosis as an occasional (5-29%) phenotype of granulomatosis with polyangiitis."
- name: "Chronic otitis media"
  category: Otologic
  frequency: OCCASIONAL
  description: "Chronic otitis media is reported as an occasional (5-29%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Chronic otitis media"
    term:
      id: HP:0000389
      label: "Chronic otitis media"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0000389 | Chronic otitis media | Occasional (29-5%)"
    explanation: "Orphanet records chronic otitis media as an occasional (5-29%) phenotype of granulomatosis with polyangiitis."
- name: "Retinopathy"
  category: Ophthalmologic
  frequency: OCCASIONAL
  description: "Retinopathy is reported as an occasional (5-29%) manifestation of granulomatosis with polyangiitis in the Orphanet clinical phenotype dataset."
  phenotype_term:
    preferred_term: "Retinopathy"
    term:
      id: HP:0000488
      label: "Retinopathy"
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "HP:0000488 | Retinopathy | Occasional (29-5%)"
    explanation: "Orphanet records retinopathy as an occasional (5-29%) phenotype of granulomatosis with polyangiitis."
biochemical:
- name: PR3-ANCA (c-ANCA)
  presence: Elevated
  context: Present in 80-90% of active generalized disease
  evidence:
  - reference: PMID:35479831
    reference_title: ANCA Associated Vasculitis Subtypes.
    supports: SUPPORT
    snippet: >-
      There is also evidence for classification of patients based on ANCA subtype;
      those with anti-proteinase 3 antibodies (PR3) or anti-myeloperoxidase antibodies
      (MPO)
      have differences in response to treatment and clinical outcomes.
    explanation: >-
      Confirms PR3-ANCA subtyping has clinical and prognostic significance in GPA.
- name: MPO-ANCA (p-ANCA)
  presence: Variable
  context: Present in 10-20% of patients
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HP:0033559 | Anti-myeloperoxidase antibody positivity | Frequent (79-30%)"
    explanation: >-
      Orphanet classifies anti-MPO antibody positivity as frequent in GPA,
      reflecting the minority of GPA patients who are MPO-ANCA positive.
- name: ESR
  presence: Elevated
  context: Marker of systemic inflammation and disease activity.
- name: CRP
  presence: Elevated
  context: Correlates with disease activity.
genetic:
- name: HLA-DPB1
  association: Risk Factor
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HLA-DPB1 | major histocompatibility complex, class II, DP beta 1 | hgnc:4940 | Major susceptibility factor in"
    explanation: Orphanet identifies HLA-DPB1 as a major susceptibility factor in GPA.
- name: HLA-DPA1
  association: Risk Factor
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "HLA-DPA1 | major histocompatibility complex, class II, DP alpha 1 | hgnc:4938 | Major susceptibility factor in"
    explanation: Orphanet identifies HLA-DPA1 as a major susceptibility factor in GPA.
- name: PRTN3
  association: Risk Factor
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "PRTN3 | proteinase 3 | hgnc:9495 | Major susceptibility factor in"
    explanation: >-
      Orphanet identifies PRTN3 as a major susceptibility factor. PRTN3
      encodes proteinase 3, the target autoantigen of PR3-ANCA.
- name: CTLA4
  association: Risk Factor
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "CTLA4 | cytotoxic T-lymphocyte associated protein 4 | hgnc:2505 | Major susceptibility factor in"
    explanation: Orphanet identifies CTLA4 as a major susceptibility factor in GPA.
- name: PTPN22
  association: Risk Factor
  evidence:
  - reference: ORPHA:900
    supports: SUPPORT
    snippet: "PTPN22 | protein tyrosine phosphatase non-receptor type 22 | hgnc:9652 | Major susceptibility factor in"
    explanation: Orphanet identifies PTPN22 as a major susceptibility factor in GPA.
- name: SERPINA1
  association: Risk Factor
  evidence:
  - reference: PMID:16859601
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Genetic investigations have identified various candidate genes,
      with alpha1-antitrypsin deficiency being the most consistently reported genetic
      susceptibility factor to date.
    explanation: >-
      Epidemiology review confirms alpha-1 antitrypsin deficiency (SERPINA1)
      as the most consistently reported genetic susceptibility factor for GPA.
environmental:
- name: Silica Dust Exposure
  notes: >-
    Occupational exposure to crystalline silica is the most consistently
    reported environmental risk factor for GPA.
  evidence:
  - reference: PMID:16859601
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      evidence has grown for a possible relationship
      between WG and occupational exposure to crystalline silica.
    explanation: >-
      Epidemiology review identifies crystalline silica as a putative
      environmental risk factor for GPA.
  - reference: PMID:36315063
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Exposure to silica
      dust, farming and chronic nasal Staphylococcus aureus carriage are associated
      with increased risk of developing AAV.
    explanation: >-
      Clinical practice review confirms silica dust as an established risk factor.
- name: Staphylococcus aureus Nasal Carriage
  notes: >-
    Chronic nasal carriage of S. aureus is associated with increased risk
    of developing GPA and with disease relapse.
  evidence:
  - reference: PMID:36315063
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Exposure to silica
      dust, farming and chronic nasal Staphylococcus aureus carriage are associated
      with increased risk of developing AAV.
    explanation: >-
      Confirms nasal S. aureus carriage as an established risk factor for AAV.
treatments:
- name: Rituximab
  description: >-
    Anti-CD20 monoclonal antibody; first-line for both induction and
    maintenance of remission in GPA.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: rituximab
      term:
        id: NCIT:C1702
        label: Rituximab
  evidence:
  - reference: PMID:36315063
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Recent data favour rituximab as a preferable option for both induction and
      maintenance of remission.
    explanation: >-
      Recent clinical review confirms rituximab as the preferred option for both
      induction and maintenance therapy in AAV.
- name: Cyclophosphamide
  description: >-
    Alkylating immunosuppressant; alternative for severe disease induction,
    particularly organ-threatening or life-threatening disease.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: cyclophosphamide
      term:
        id: CHEBI:4027
        label: cyclophosphamide
  evidence:
  - reference: PMID:1739240
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      One hundred and thirty-three patients (84%) received "standard" therapy
      with daily low-dose cyclophosphamide and glucocorticoids.
    explanation: >-
      Landmark NIH cohort demonstrates cyclophosphamide plus glucocorticoids
      as the standard induction therapy for GPA.
- name: Corticosteroids
  description: >-
    High-dose for induction, with subsequent taper. Glucocorticoid-sparing
    strategies are increasingly preferred.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: corticosteroid
      term:
        id: CHEBI:50858
        label: corticosteroid
  evidence:
  - reference: PMID:36315063
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      regimens with less glucocorticoids are equally
      effective and safer in inducing remission compared with conventional regimens
    explanation: >-
      Recent evidence supports reduced glucocorticoid regimens as equally effective
      and safer than conventional high-dose protocols.
- name: Avacopan
  description: >-
    Oral C5a receptor inhibitor; allows glucocorticoid reduction or elimination
    during induction therapy by blocking complement-mediated neutrophil priming.
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: avacopan
      term:
        id: NCIT:C174788
        label: Avacopan
  evidence:
  - reference: PMID:36315063
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      avacopan is an effective glucocorticoid-sparing option.
    explanation: >-
      Clinical review confirms avacopan as an effective glucocorticoid-sparing
      treatment option in AAV.
  - reference: PMID:37781373
    reference_title: The involvement of NETs in ANCA-associated vasculitis.
    supports: SUPPORT
    snippet: >-
      Mechanistically, cytokines or complement factors activate and prime neutrophils
      for ANCA-binding; thus, C5a receptor blocker has garnered attention as potential
      replacement for glucocorticoids in clinical settings.
    explanation: >-
      Confirms the mechanistic rationale for avacopan as a C5a receptor blocker
      targeting complement-mediated neutrophil priming.
  target_mechanisms:
  - target: Complement Alternative Pathway Activation
epidemiology:
- name: Prevalence in Europe
  notes: >-
    European point prevalence ranges from 24 to 157 per million (2.4-15.7
    per 100,000). Higher prevalence observed in northern European countries.
  evidence:
  - reference: ORPHA:900
    reference_title: Granulomatosis with polyangiitis (Orphanet)
    supports: SUPPORT
    snippet: "1-9 / 100 000 | Europe | Point prevalence | PMID:16859601"
    explanation: Orphanet reports European point prevalence of GPA as 1-9 per 100,000.
  - reference: PMID:16859601
    reference_title: "Epidemiology of Wegener's granulomatosis: Lessons from descriptive studies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      Descriptive epidemiological studies carried out
      primarily in European countries estimate a prevalence of WG ranging from 24 to
      157 per million and annual incidence rates from 3 to 14 per million.
    explanation: >-
      European epidemiology review estimates GPA prevalence at 24-157 per million.
- name: Prevalence in the United States
  notes: >-
    US prevalence estimated at 21.8 per 100,000 in Olmsted County, Minnesota,
    substantially higher than most previous estimates worldwide.
  evidence:
  - reference: ORPHA:900
    reference_title: Granulomatosis with polyangiitis (Orphanet)
    supports: SUPPORT
    snippet: "1-9 / 100 000 | United States | Point prevalence | PMID:8546743"
    explanation: Orphanet reports US point prevalence of GPA as 1-9 per 100,000.
  - reference: PMID:28881446
    reference_title: "Epidemiology of AAV in Olmsted County, Minnesota."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The age- and sex-adjusted prevalence of GPA was 21.8 (95%CI: 12.9-30.8) per
      100,000 population
    explanation: >-
      Olmsted County study reports GPA prevalence of 21.8 per 100,000.
- name: Incidence in the United States
  notes: >-
    Annual incidence of GPA in the US is approximately 1.3 per 100,000 adults.
  evidence:
  - reference: PMID:28881446
    reference_title: "Epidemiology of AAV in Olmsted County, Minnesota."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      The age- and sex-adjusted annual incidence rate of GPA for the adult population
      was 1.3 (95%CI: 0.8-1.8) per 100,000 population.
    explanation: >-
      Olmsted County population-based study reports GPA annual incidence of
      1.3 per 100,000 adults.
- name: Incidence in Europe
  notes: >-
    Annual incidence in Europe ranges from 3 to 14 per million.
    North-South declining gradient in the Northern Hemisphere. Peak incidence
    in adulthood (40-65 years) with equal sex distribution. Over 95% Caucasian.
  evidence:
  - reference: ORPHA:900
    reference_title: Granulomatosis with polyangiitis (Orphanet)
    supports: SUPPORT
    snippet: "1-9 / 1 000 000 | Europe | Annual incidence | PMID:16859601"
    explanation: Orphanet reports European annual incidence as 1-9 per million.
  - reference: PMID:16859601
    reference_title: "Epidemiology of Wegener's granulomatosis: Lessons from descriptive studies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: >-
      annual incidence rates from 3 to 14 per million.
    explanation: European incidence rates estimated at 3-14 per million.
classifications:
  harrisons_chapter:
  - classification_value: IMMUNE_RHEUMATOLOGIC
notes: >-
  Orphanet natural history indicates onset across adolescent, childhood, adult,
  and elderly age groups. Disease course is typically relapsing-remitting; over
  50% of patients who achieve remission experience at least one relapse.
  Mortality in GPA is no longer significantly increased compared to the general
  population with modern treatment, though MPA and EGPA carry higher mortality.
references:
- reference: PMID:1739240
  title: 'Wegener granulomatosis: an analysis of 158 patients.'
  findings:
  - statement: Landmark NIH cohort establishing clinical spectrum and treatment outcomes
- reference: PMID:16859601
  title: "Epidemiology of Wegener's granulomatosis: Lessons from descriptive studies and analyses of genetic and environmental risk determinants."
  findings:
  - statement: European prevalence 24-157 per million
  - statement: Alpha-1 antitrypsin deficiency is the most consistently reported genetic risk factor
  - statement: Silica exposure is the strongest environmental risk factor
- reference: PMID:25805746
  title: Classification, epidemiology and clinical subgrouping of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.
  findings: []
- reference: PMID:28881446
  title: 'The Epidemiology of Antineutrophil Cytoplasmic Autoantibody-Associated Vasculitis in Olmsted County, Minnesota: A Twenty-Year US Population-Based Study.'
  findings:
  - statement: GPA annual incidence 1.3 per 100,000 in US
  - statement: GPA prevalence 21.8 per 100,000
  - statement: GPA mortality not significantly increased vs general population
- reference: PMID:36315063
  title: 'Diagnosing and treating ANCA-associated vasculitis: an updated review for clinical practice.'
  findings:
  - statement: Rituximab preferred for induction and maintenance
  - statement: Avacopan effective as glucocorticoid-sparing option
- reference: PMID:39257888
  title: 'Granulomatosis with polyangiitis: clinical characteristics and updates in diagnosis.'
  findings:
  - statement: GPA clinical characterization and diagnostic updates
📚

References & Deep Research

References

6
Wegener granulomatosis: an analysis of 158 patients.
1 finding
Landmark NIH cohort establishing clinical spectrum and treatment outcomes
Epidemiology of Wegener's granulomatosis: Lessons from descriptive studies and analyses of genetic and environmental risk determinants.
3 findings
European prevalence 24-157 per million
Alpha-1 antitrypsin deficiency is the most consistently reported genetic risk factor
Silica exposure is the strongest environmental risk factor
Classification, epidemiology and clinical subgrouping of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.
No top-level findings curated for this source.
The Epidemiology of Antineutrophil Cytoplasmic Autoantibody-Associated Vasculitis in Olmsted County, Minnesota: A Twenty-Year US Population-Based Study.
3 findings
GPA annual incidence 1.3 per 100,000 in US
GPA prevalence 21.8 per 100,000
GPA mortality not significantly increased vs general population
Diagnosing and treating ANCA-associated vasculitis: an updated review for clinical practice.
2 findings
Rituximab preferred for induction and maintenance
Avacopan effective as glucocorticoid-sparing option
Granulomatosis with polyangiitis: clinical characteristics and updates in diagnosis.
1 finding
GPA clinical characterization and diagnostic updates

Deep Research

2
Disorder

Disorder

  • Name: Granulomatosis with Polyangiitis
  • Category: Autoimmune
  • Existing deep-research providers: falcon
  • Existing evidence reference count in YAML: 17

Key Pathophysiology Nodes

  • ANCA-Mediated Neutrophil Activation
  • Granuloma Formation
  • Complement Alternative Pathway Activation
  • Deep research literature mapping

Citation Inventory (for evidence mapping)

  • DOI:10.1007/s00296-022-05228-8
  • DOI:10.1016/j.autrev.2025.103824
  • DOI:10.1136/rmdopen-2023-004039
  • DOI:10.2147/jir.s284768
  • DOI:10.3389/fimmu.2023.1261151
  • DOI:10.3390/ijms25105278
  • DOI:10.3390/life15050756
Falcon
Disease Characteristics Research Template
Edison Scientific Literature 43 citations 2026-05-01T07:35:04.395563

Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Characteristics Research Template

Target Disease

  • Disease Name: Granulomatosis with Polyangiitis
  • MONDO ID: (if available)
  • Category: Autoimmune

Research Objectives

Please provide a comprehensive research report on Granulomatosis with Polyangiitis covering all of the disease characteristics listed below. This report will be used to populate a disease knowledge base entry. Be thorough and cite primary literature (PMID preferred) for all claims.

For each section, suggested databases/resources are listed. These are the first places you should search for information on each topic.


1. Disease Information

Search first: OMIM, Orphanet, ICD-10/ICD-11, MeSH, PubMed

  • What is the disease? Provide a concise overview.
  • What are the key identifiers? (OMIM, Orphanet, ICD-10/ICD-11, MeSH, Mondo)
  • What are the common synonyms and alternative names?
  • Is the information derived from individual patients (e.g., EHR) or aggregated disease-level resources?

2. Etiology

  • Disease Causal Factors: What are the primary causes? (genetic, environmental, infectious, mechanistic)
  • Risk Factors:

    Search first: PubMed, Cochrane Library, UpToDate, clinical guidelines, ClinVar, ClinGen, GWAS Catalog, PheGenI, CTD, CDC, WHO, epidemiological databases

  • Genetic risk factors (causal variants, susceptibility loci, modifier genes)
  • Environmental risk factors (toxins, lifestyle, occupational exposures, age, sex, family history)
  • Protective Factors:

    Search first: PubMed, Cochrane Library, clinical trial databases, GWAS Catalog, gnomAD, WHO, CDC, nutrition databases

  • Genetic protective factors (protective variants, modifier alleles)
  • Environmental protective factors (diet, lifestyle, exposures that reduce risk)
  • Gene-Environment Interactions: How do genetic and environmental factors interact to influence disease?

    Search first: CTD, PubMed, PheGenI, GxE databases

3. Phenotypes

Search first: HPO (Human Phenotype Ontology), OMIM, Orphanet, PubMed, clinicaltrials.gov, MedDRA, SNOMED CT, DECIPHER, LOINC

For each phenotype, provide: - Phenotype type: symptoms, clinical signs, physical manifestations, behavioral changes, or laboratory abnormalities

For symptoms/signs: HPO, OMIM, Orphanet, PubMed For behavioral changes: HPO, DSM, RDoC (Research Domain Criteria), PubMed For laboratory abnormalities: LOINC, SNOMED CT, LabTests Online, PubMed - Phenotype characteristics: Search first: OMIM, Orphanet, HPO, PubMed - Age of symptom onset (neonatal, childhood, adult-onset, late-onset) - Symptom severity (mild, moderate, severe, variable) - Symptom progression (stable, progressive, episodic, fluctuating) - Frequency among affected individuals (percentage or qualitative) - Quality of life impact: Effects on daily functioning and well-being (per-phenotype when possible) Search first: EQ-5D database, SF-36, WHO QOL databases, PubMed - Suggest HPO (Human Phenotype Ontology) terms for each phenotype

4. Genetic/Molecular Information

  • Causal Genes: Gene mutations or chromosomal abnormalities responsible for disease (gene symbols, OMIM IDs)

    Search first: OMIM, ClinVar, HGMD, Ensembl, NCBI Gene

  • Pathogenic Variants:
  • Affected genes (gene symbols, HGNC IDs) > Search first: OMIM, NCBI Gene, Ensembl, HGNC, UniProt, GeneCards
  • Variant classification (pathogenic, likely pathogenic, VUS per ACMG/AMP guidelines) > Search first: ClinVar, ClinGen, ACMG/AMP guidelines, VarSome
  • Variant type/class (missense, frameshift, nonsense, splice-site, structural)
  • Allele frequency in population databases > Search first: gnomAD, 1000 Genomes, ExAC, TOPMed, dbSNP
  • Somatic vs germline origin > Search first: COSMIC (somatic), ClinVar, ICGC, TCGA
  • Functional consequences (loss of function, gain of function, dominant negative)
  • Modifier Genes: Genes that modify disease severity or expression
  • Epigenetic Information: DNA methylation, histone modifications, chromatin changes affecting disease

    Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

  • Chromosomal Abnormalities: Large-scale genetic changes (aneuploidy, translocations, inversions)

    Search first: DECIPHER, ClinVar, ECARUCA, UCSC Genome Browser

5. Environmental Information

  • Environmental Factors: Non-genetic contributing factors (toxins, radiation, pollution, occupational exposure)

    Search first: CTD (Comparative Toxicogenomics Database), TOXNET, PubMed, EPA databases

  • Lifestyle Factors: Behavioral factors (smoking, diet, exercise, alcohol consumption)

    Search first: CDC databases, WHO, PubMed, NHANES

  • Infectious Agents: If applicable, pathogens causing or triggering disease (bacteria, viruses, fungi, parasites)

    Search first: NCBI Taxonomy, ViPR, BV-BRC, MicrobeDB, GIDEON

6. Mechanism / Pathophysiology

  • Molecular Pathways: Specific signaling cascades or biochemical pathways involved (Wnt, MAPK, mTOR, PI3K-AKT, etc.)

    Search first: KEGG, Reactome, WikiPathways, PathBank, BioCyc

  • Cellular Processes: Cell-level mechanisms (apoptosis, autophagy, cell cycle dysregulation, inflammation, etc.)

    Search first: Gene Ontology (GO), Reactome, KEGG, PubMed

  • Protein Dysfunction: How protein structure or function is altered (misfolding, aggregation, loss of function, gain of function)

    Search first: UniProt, PDB (Protein Data Bank), InterPro, Pfam, AlphaFold

  • Metabolic Changes: Alterations in metabolic processes (energy metabolism, lipid metabolism, amino acid metabolism)

    Search first: KEGG, BioCyc, HMDB (Human Metabolome Database), BRENDA

  • Immune System Involvement: Role of immune response (autoimmunity, immunodeficiency, chronic inflammation)

    Search first: ImmPort, Immunome Database, IEDB, Gene Ontology

  • Tissue Damage Mechanisms: How tissues/ are injured (oxidative stress, ischemia, fibrosis, necrosis)

    Search first: PubMed, Gene Ontology, Reactome

  • Biochemical Abnormalities: Specific molecular defects (enzyme deficiencies, receptor dysfunction, ion channel defects)

    Search first: BRENDA, UniProt, KEGG, OMIM, PubMed

  • Epigenetic Changes: DNA methylation, histone modifications affecting gene expression in disease

    Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

  • Molecular Profiling (if available):
  • Transcriptomics/gene expression changes > Search first: GEO (Gene Expression Omnibus), ArrayExpress, GTEx, Human Cell Atlas, SRA
  • Proteomics findings > Search first: PRIDE, ProteomeXchange, Human Protein Atlas, STRING, BioGRID
  • Metabolomics signatures > Search first: MetaboLights, Metabolomics Workbench, HMDB, METLIN
  • Lipidomics alterations > Search first: LIPID MAPS, SwissLipids, LipidHome, Metabolomics Workbench
  • Genomic structural features > Search first: UCSC Genome Browser, Ensembl, NCBI, dbVar, DGV
  • Advanced Technologies (if applicable):
  • Single-cell analysis findings (cell-type specific mechanisms, cellular heterogeneity) > Search first: Human Cell Atlas, Single Cell Portal, GEO, CELLxGENE
  • Spatial transcriptomics findings > Search first: GEO, Spatial Research, Vizgen, 10x Genomics data
  • Multi-omics integration results > Search first: TCGA, ICGC, cBioPortal, LinkedOmics, PubMed
  • Functional genomics screens (CRISPR, RNAi) > Search first: DepMap, GenomeRNAi, PubMed, BioGRID ORCS

For each mechanism, describe: - The causal chain from initial trigger to clinical manifestation - Which mechanisms are upstream vs downstream - What cell types and biological processes are involved - Suggest GO terms for biological processes and CL terms for cell types

7. Anatomical Structures Affected

  • Organ Level:
  • Primary organs directly affected
  • Secondary organ involvement (complications, secondary effects)
  • Body systems involved (cardiovascular, nervous, digestive, respiratory, endocrine, etc.)

    Search first: Uberon, FMA (Foundational Model of Anatomy), OMIM, HPO, ICD-11, MeSH, SNOMED CT

  • Tissue and Cell Level:
  • Specific tissue types affected (epithelial, connective, muscle, nervous)
  • Specific cell populations targeted (with Cell Ontology terms)

    Search first: Uberon, Human Protein Atlas, Cell Ontology, Human Cell Atlas, CellMarker, PanglaoDB

  • Subcellular Level:
  • Cellular compartments involved (mitochondria, nucleus, ER, lysosomes) (with GO Cellular Component terms)

    Search first: Gene Ontology (Cellular Component), UniProt, Human Protein Atlas

  • Localization:
  • Specific anatomical sites (with UBERON terms) > Search first: FMA, Uberon, NeuroNames (for brain), SNOMED CT
  • Lateralization (unilateral, bilateral, asymmetric) > Search first: HPO, clinical literature, imaging databases

8. Temporal Development

  • Onset:
  • Typical age of onset (congenital, pediatric, adult, geriatric)
  • Onset pattern (acute, subacute, chronic, insidious)

    Search first: OMIM, Orphanet, HPO, PubMed

  • Progression:
  • Disease stages (early, intermediate, advanced, end-stage) > Search first: Cancer Staging Manual (AJCC), WHO classifications, PubMed
  • Progression rate (rapid, slow, variable)
  • Disease course pattern (episodic, relapsing-remitting, progressive, stable)
  • Disease duration (self-limited, chronic lifelong)

    Search first: Disease registries, longitudinal cohort databases, natural history studies, PubMed, Orphanet, OMIM

  • Patterns:
  • Remission patterns (spontaneous, treatment-induced) > Search first: Clinical trial databases, disease registries, PubMed
  • Critical periods (time windows of vulnerability or opportunity for intervention) > Search first: PubMed, developmental biology databases, clinical guidelines

9. Inheritance and Population

  • Epidemiology:
  • Prevalence (cases per 100,000 at given time)
  • Incidence (new cases per 100,000 per year)

    Search first: Orphanet, CDC, WHO, GBD (Global Burden of Disease), national registries, SEER, disease registries

  • For Genetic Etiology:
  • Inheritance pattern (AD, AR, X-linked, mitochondrial, multifactorial, polygenic) > Search first: OMIM, Orphanet, ClinVar, GTR (Genetic Testing Registry)
  • Penetrance (complete, incomplete, age-dependent) > Search first: ClinVar, OMIM, PubMed, ClinGen
  • Expressivity (variable, consistent) > Search first: OMIM, ClinVar, PubMed
  • Genetic anticipation (increasing severity in successive generations) > Search first: OMIM, PubMed (especially for repeat expansion disorders)
  • Germline mosaicism > Search first: ClinVar, OMIM, genetic counseling literature, PubMed
  • Founder effects (population-specific mutations) > Search first: gnomAD, population genetics databases, PubMed
  • Consanguinity role > Search first: OMIM, population studies, genetic counseling resources
  • Carrier frequency > Search first: gnomAD, carrier screening databases, GeneReviews, GTR
  • Population Demographics:
  • Affected populations (ethnic or demographic groups with higher prevalence) > Search first: gnomAD, 1000 Genomes, PAGE Study, PubMed, population registries
  • Geographic distribution (endemic areas, regional variation) > Search first: WHO, CDC, GBD, Orphanet, geographic epidemiology databases
  • Geographic distribution of specific variants
  • Sex ratio (male:female) > Search first: Disease registries, OMIM, PubMed, epidemiological databases
  • Age distribution of affected individuals > Search first: CDC, disease registries, SEER, Orphanet

10. Diagnostics

  • Clinical Tests:
  • Laboratory tests (blood, urine, tissue chemistry, specific enzyme assays) > Search first: LOINC, LabTests Online, PubMed
  • Biomarkers (proteins, metabolites, genetic markers, circulating biomarkers) > Search first: FDA Biomarker List, BEST (Biomarkers, EndpointS, and other Tools), PubMed
  • Imaging studies (X-ray, CT, MRI, PET, ultrasound) > Search first: RadLex, DICOM, Radiopaedia, imaging databases
  • Functional tests (pulmonary function, cardiac stress tests) > Search first: LOINC, clinical guidelines, PubMed
  • Electrophysiology (EEG, EMG, ECG, nerve conduction studies) > Search first: LOINC, clinical neurophysiology databases, PubMed
  • Biopsy findings (histopathology, immunohistochemistry) > Search first: SNOMED CT, College of American Pathologists resources, PubMed
  • Pathology findings (microscopic examination) > Search first: SNOMED CT, Digital Pathology databases, PubMed
  • Genetic Testing:

    Search first: GTR (Genetic Testing Registry), GeneReviews, ClinGen

  • Overview of recommended genetic testing approach
  • Whole genome sequencing (WGS) utility > Search first: GTR, ClinVar, GEL (Genomics England), gnomAD
  • Whole exome sequencing (WES) utility > Search first: GTR, ClinVar, OMIM, GeneMatcher
  • Gene panels (which panels, which genes) > Search first: GTR, ClinVar, laboratory-specific databases
  • Single gene testing > Search first: GTR, ClinVar, OMIM, GeneReviews
  • Chromosomal microarray (CMA) > Search first: DECIPHER, ClinVar, dbVar, ECARUCA
  • Karyotyping > Search first: Chromosome Abnormality Database, ClinVar, cytogenetics resources
  • FISH > Search first: ClinVar, cytogenetics databases, PubMed
  • Mitochondrial DNA testing > Search first: MITOMAP, MSeqDR, ClinVar, GTR
  • Repeat expansion testing > Search first: GTR, ClinVar, repeat expansion databases, PubMed
  • Omics-Based Diagnostics (if applicable):
  • RNA sequencing / transcriptomics > Search first: GEO, ArrayExpress, GTEx, RNA-seq databases
  • Proteomics > Search first: PRIDE, ProteomeXchange, FDA Biomarker database
  • Metabolomics > Search first: MetaboLights, Metabolomics Workbench, HMDB
  • Epigenomics > Search first: GEO, ENCODE, Roadmap Epigenomics, MethBase
  • Liquid biopsy > Search first: COSMIC, ClinVar, liquid biopsy databases, PubMed
  • Clinical Criteria:
  • Standardized diagnostic criteria (DSM, ICD, society guidelines) > Search first: DSM-5, ICD-11, clinical society guidelines, UpToDate
  • Differential diagnosis (other conditions to rule out, with distinguishing features) > Search first: DynaMed, UpToDate, clinical decision support systems
  • Screening:
  • Screening methods for asymptomatic individuals (newborn screening, carrier screening, cascade screening) > Search first: ACMG recommendations, CDC newborn screening, GTR

11. Outcome/Prognosis

  • Survival and Mortality:
  • Survival rate (5-year, 10-year, overall) > Search first: SEER, cancer registries, disease-specific registries, PubMed
  • Life expectancy (with and without treatment if applicable) > Search first: Orphanet, disease registries, actuarial databases, PubMed
  • Mortality rate > Search first: CDC, WHO, GBD, national mortality databases
  • Disease-specific mortality (deaths directly attributable to disease) > Search first: Disease registries, CDC Wonder, GBD, PubMed
  • Morbidity and Function:
  • Morbidity (disease-related disability and health impacts) > Search first: GBD, WHO, disability databases, PubMed
  • Disability outcomes (long-term functional impairments) > Search first: ICF (International Classification of Functioning), disability registries
  • Quality of life measures (EQ-5D, SF-36, PROMIS, disease-specific tools) > Search first: EQ-5D database, SF-36, PROMIS, PubMed
  • Disease Course:
  • Complications (secondary problems: infections, organ failure, etc.) > Search first: ICD codes, disease registries, clinical databases, PubMed
  • Recovery potential (likelihood and extent of recovery, with vs without treatment) > Search first: Natural history studies, rehabilitation databases, PubMed
  • Prediction:
  • Prognostic factors (age, disease severity, biomarkers, treatment response) > Search first: Prognostic models databases, clinical calculators, PubMed
  • Prognostic biomarkers (molecular markers predicting disease course) > Search first: FDA Biomarker database, PubMed, cancer prognostic databases

12. Treatment

  • Pharmacotherapy:
  • Pharmacological treatments (drug names, drug classes, mechanisms of action) > Search first: DrugBank, RxNorm, ATC classification, DailyMed, FDA databases
  • Pharmacogenomics (how genetic variants affect drug metabolism, efficacy, toxicity) > Search first: PharmGKB, CPIC (Clinical Pharmacogenetics), FDA Table of PGx Biomarkers
  • Advanced Therapeutics:
  • Gene therapy (viral vectors, CRISPR, gene replacement, gene editing) > Search first: ClinicalTrials.gov, FDA gene therapy database, ASGCT resources
  • Cell therapy (stem cell transplant, CAR-T, cellular therapeutics) > Search first: ClinicalTrials.gov, FDA cell therapy database, FACT standards
  • RNA-based therapies (ASOs, siRNA, mRNA therapies) > Search first: ClinicalTrials.gov, FDA approvals, PubMed
  • Targeted therapies (treatments directed at specific molecular targets) > Search first: My Cancer Genome, OncoKB, ClinicalTrials.gov, FDA approvals
  • Immunotherapies (checkpoint inhibitors, monoclonal antibodies) > Search first: Cancer Immunotherapy Database, FDA approvals, ClinicalTrials.gov
  • Surgical and Interventional:
  • Surgical interventions (types of surgery, timing, outcomes) > Search first: CPT codes, surgical registries, clinical guidelines, PubMed
  • Supportive and Rehabilitative:
  • Supportive care (symptom management, pain control, nutrition) > Search first: Clinical guidelines, Cochrane Library, PubMed
  • Rehabilitation (physical therapy, occupational therapy, speech therapy) > Search first: Rehabilitation medicine databases, clinical guidelines, PubMed
  • Experimental:
  • Experimental treatments in clinical trials (with NCT identifiers if available) > Search first: ClinicalTrials.gov, EU Clinical Trials Register, WHO ICTRP
  • Treatment Outcomes:
  • Treatment response rates > Search first: Clinical trial databases, FDA reviews, systematic reviews, PubMed
  • Side effects and adverse events > Search first: FDA Adverse Event Reporting System (FAERS), MedWatch, PubMed
  • Treatment Strategy:
  • Treatment algorithms (clinical pathways, decision trees) > Search first: Clinical practice guidelines, NCCN Guidelines, UpToDate
  • Combination therapies > Search first: ClinicalTrials.gov, treatment guidelines, PubMed
  • Personalized medicine approaches (genotype-guided treatment) > Search first: My Cancer Genome, CIViC, PharmGKB, precision medicine databases

For each treatment, suggest MAXO (Medical Action Ontology) terms where applicable.

13. Prevention

  • Prevention Levels:
  • Primary prevention (preventing disease occurrence: vaccination, risk factor modification) > Search first: CDC, WHO, USPSTF recommendations, Cochrane Library
  • Secondary prevention (early detection and treatment: screening programs, early intervention) > Search first: USPSTF, CDC screening guidelines, WHO
  • Tertiary prevention (preventing complications in those with disease) > Search first: Clinical guidelines, disease management protocols, PubMed
  • Immunization: Vaccine strategies (if applicable)

    Search first: CDC vaccine schedules, WHO immunization, FDA vaccine database

  • Screening and Early Detection:
  • Screening programs (population-based: newborn screening, cancer screening) > Search first: CDC screening programs, USPSTF, cancer screening databases
  • Genetic screening (carrier screening, preimplantation genetic diagnosis, prenatal testing) > Search first: ACMG recommendations, ACOG guidelines, GTR
  • Risk stratification (identifying high-risk individuals for targeted prevention) > Search first: Risk prediction models, clinical calculators, PubMed
  • Behavioral Interventions: Lifestyle modifications to reduce risk

    Search first: CDC, WHO, behavioral intervention databases, Cochrane Library

  • Counseling: Genetic counseling (risk assessment, family planning guidance)

    Search first: NSGC resources, ACMG guidelines, GeneReviews

  • Public Health:
  • Public health interventions (sanitation, vector control, health education) > Search first: CDC, WHO, public health databases, PubMed
  • Environmental interventions (reducing environmental risk factors) > Search first: EPA databases, WHO environmental health, PubMed
  • Prophylaxis: Preventive medications or procedures

    Search first: Clinical guidelines, FDA approvals, PubMed

14. Other Species / Natural Disease

  • Taxonomy: Species affected (with NCBI Taxon identifiers)

    Search first: NCBI Taxonomy

  • Breed: Specific breeds affected (with VBO identifiers if applicable)

    Search first: VBO (Vertebrate Breed Ontology)

  • Gene: Orthologous genes in other species (with NCBI Gene IDs)

    Search first: NCBI Gene

  • Natural Disease:
  • Naturally occurring disease in other species (companion animals, wildlife) > Search first: OMIA (Online Mendelian Inheritance in Animals), VetCompass, PubMed
  • Veterinary relevance and importance in animal health > Search first: OMIA, veterinary databases, PubMed
  • Comparative Biology:
  • Comparative pathology (similarities and differences across species) > Search first: OMIA, comparative pathology databases, PubMed
  • Evolutionary conservation of disease mechanisms > Search first: HomoloGene, OrthoMCL, Alliance of Genome Resources
  • Transmission (if applicable):
  • Zoonotic potential > Search first: CDC zoonotic diseases, WHO zoonoses, GIDEON
  • Cross-species susceptibility > Search first: NCBI Taxonomy, veterinary databases, PubMed

15. Model Organisms

  • Model Types:
  • Model organism type (mammalian, invertebrate, cellular, in vitro) > Search first: Alliance of Genome Resources, model organism databases
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  • Types available (knockout, knock-in, transgenic, conditional, humanized) > Search first: MGI, IMPC, KOMP, EuMMCR, IMSR
  • Model Characteristics:
  • Phenotype recapitulation (how well model reproduces human disease features) > Search first: Model organism databases, comparative studies, PubMed
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Citation Requirements

  • Cite primary literature (PMID preferred) for all mechanistic and clinical claims
  • Prioritize recent reviews and landmark papers
  • Include direct quotes from abstracts where possible to support key statements
  • Distinguish evidence source types: human clinical, model organism, in vitro, computational

Output Format

Structure your response as a comprehensive narrative organized by the sections above. For each section, provide: - Factual content with specific details (numbers, percentages, gene names, variant nomenclature) - Ontology term suggestions (HPO, GO, CL, UBERON, CHEBI, MAXO, MONDO) where applicable - Evidence citations with PMIDs - Direct quotes from abstracts to support key claims - Clear indication when information is not available or not applicable for this disease

This report will be used to populate a disease knowledge base entry with: - Pathophysiology descriptions with causal chains - Gene/protein annotations (HGNC, GO terms) - Phenotype associations (HP terms) with frequencies - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Treatment annotations (MAXO terms) - Evidence items with PMIDs and exact abstract quotes - Epidemiology, prognosis, diagnostic, and prevention information - Animal model descriptions with phenotype recapitulation details

Comprehensive Disease Characteristics Report: Granulomatosis with Polyangiitis (GPA)

Target disease

Granulomatosis with polyangiitis (GPA) is a rare systemic disease characterized by granulomatous inflammation of the respiratory tract and necrotizing vasculitis of small-to-medium vessels, most often associated with anti‑neutrophil cytoplasmic antibodies (ANCA) targeting proteinase‑3 (PR3). Classic organ involvement includes upper airways (ENT), lungs, and kidneys (“ELK”), although essentially any organ system can be affected. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)

Important evidence limitation (PMIDs): The full texts retrieved in this run (Frontiers in Medicine review; ACR/EULAR criteria paper excerpts; cohort studies; ClinicalTrials.gov records; genetics reviews/GWAS excerpts) did not reliably expose PubMed IDs in the available text chunks. Therefore, PMID-level citations and direct abstract quotes cannot be provided from the tool outputs; instead, this report cites the retrieved sources by DOI/URL and the internal evidence IDs shown in parentheses.


1. Disease information

1.1 Concise overview

GPA is a systemic ANCA-associated vasculitis (AAV) with necrotizing vasculitis and granulomatous inflammation, typically involving ENT tract, lungs, and kidneys. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)

1.2 Synonyms / alternative names

  • Granulomatosis with polyangiitis
  • Wegener’s granulomatosis (historical eponym referenced in genetics/GWAS literature) (xie2013associationofgranulomatosis pages 1-2)

1.3 Key identifiers (ontology and coding systems)

The current evidence set did not include machine-readable entries from OMIM, Orphanet, MeSH, ICD‑10/ICD‑11, or MONDO. Accordingly, the following fields cannot be populated from tool-grounded evidence in this run: * MONDO ID: not retrieved * OMIM / Orphanet / MeSH / ICD‑10/ICD‑11: not retrieved

1.4 Evidence sources (individual vs aggregated)

This report is derived from aggregated disease-level resources (reviews, consensus/criteria papers, cohort studies, systematic reviews) and trial registry entries rather than EHR-derived individual case series (except where retrospective cohorts use administrative claims). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2, mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2, kramer2024remissioninductiontherapies pages 1-2, NCT07176546 chunk 1)


2. Etiology

2.1 Primary causal factors (current understanding)

GPA is generally considered multifactorial, with strong immunogenetic risk and autoimmunity centered on PR3‑ANCA in many patients. The disease is strongly associated with PR3‑ANCA by serology (see Diagnostics) and with genetic loci tied to antigen presentation (HLA class II) and the PR3/alpha‑1 antitrypsin axis. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6, alberici2015geneticaspectsof pages 4-4)

2.2 Genetic risk factors (susceptibility loci)

Evidence from GWAS and genetic summaries supports a polygenic architecture with a prominent HLA class II signal:

  • HLA-DP region (HLA‑DPB1/HLA‑DPA1): A 2013 GWAS of GPA reported genome‑wide significant association at HLA‑DP (e.g., rs9277554 combined P=1.92×10−50; rs9277341 P=2.18×10−39), and the association was reported as fully accounted for by HLA‑DPB1*04. (Xie et al., 2013; https://doi.org/10.1002/art.38036) (xie2013associationofgranulomatosis pages 1-2)
  • SEMA6A: The same GWAS reported an independent non‑MHC locus near SEMA6A (rs26595) with combined P=2.09×10−8. (xie2013associationofgranulomatosis pages 1-2)
  • SERPINA1 and PRTN3: A 2015 genetics review summarizing GWAS signals reported associations for SERPINA1 (e.g., rs7151526; PR3+ subgroup OR 0.53, P=5.6×10−12) and PRTN3 (rs62132295; PR3+ subgroup OR 0.73, P=2.6×10−7). (https://doi.org/10.1093/ndt/gfu386) (alberici2015geneticaspectsof pages 4-4)
  • Replication/functional framing: A 2017 large genetic study (AAV cases and controls) reported strong HLA‑DPB1 effects (e.g., rs141530235 OR 2.99; rs1042169 OR 2.82) and described associations at SERPINA1, PTPN22, and a PRTN3 locus correlated with increased PRTN3 expression in neutrophils. (https://doi.org/10.1002/art.40034) (merkel2017identificationoffunctional pages 1-4)

Protective variants / penetrance / inheritance: No evidence in the retrieved set quantified penetrance, carrier frequency, or protective alleles specifically for GPA; the genetic evidence supports complex/polygenic susceptibility rather than Mendelian inheritance. (merkel2017identificationoffunctional pages 1-4, alberici2015geneticaspectsof pages 4-4)

2.3 Environmental and infectious risk factors; gene–environment interactions

No tool-retrieved sources in this run provided specific environmental (e.g., silica), lifestyle (e.g., smoking), or infectious triggers for GPA, nor explicit gene–environment interaction analyses. This remains an evidence gap for this report.


3. Phenotypes (clinical manifestations)

3.1 Major phenotype spectrum with frequencies (examples)

The phenotype of GPA is heterogeneous, but a recurring pattern is ENT + pulmonary + renal involvement.

ENT manifestations * ENT involvement/signs are common (reported 80–100%). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5) * Examples of reported ENT symptom frequencies: nasal crusting 75%, excessive nose‑blowing 70%, nasal obstruction 65%, epistaxis 59%; saddle‑nose deformity is described and one source reports saddle nose in 25%. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)

Pulmonary manifestations * Pulmonary involvement is frequently reported (e.g., 62–90%). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3) * Pulmonary nodules/mass lesions: 40–70%; cavitation: 20–50%. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3) * Diffuse alveolar hemorrhage (DAH): 8.8–36% in GPA. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)

Renal manifestations * Renal involvement: 70–85% during the course of disease; renal insufficiency at presentation: 11–17%; worsening GFR reported in 24.3%. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)

Ophthalmologic/orbital and oral manifestations * Ophthalmologic signs: 50–60%; orbital lesions: 5–30%. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6) * A systematic review reports ocular/orbital involvement in 16–78%, and up to 27% of patients presenting initially with ophthalmic symptoms. (moin2023ocularandorbital pages 1-2) * Oral involvement: 6–13%; “strawberry” gingival hyperplasia reported in 61.5% (in a cited subgroup context). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)

Neurologic manifestations * Peripheral nervous system involvement: 11–44%; CNS involvement: 3–11.7% (often hypertrophic pachymeningitis). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)

3.2 Onset and course

GPA can have substantial diagnostic delay: time from first symptoms to diagnosis ranged from 1 month to >3 years, and 36% of patients had symptoms for >1 year before diagnosis in one synthesis. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3, potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)

3.3 Quality of life impact (PROs)

Quantitative QoL effect sizes were not extractable from the retrieved text chunks. However, the following instruments are explicitly used as outcome measures in contemporary GPA/AAV trials focusing on steroid‑sparing approaches: * SF‑36 and EQ‑5D‑5L were used in the 2024 ADVOCATE rituximab‑subgroup analysis of avacopan. (geetha2024efficacyandsafety pages 4-5) * SNOT‑22 and AAV‑PRO are key secondary endpoints in an avacopan trial focused on ENT disease activity in GPA (NCT07176546). (NCT07176546 chunk 1)

3.4 Suggested HPO terms (non-exhaustive; to be curated)

Based on phenotypes explicitly described in the evidence set: * ENT: nasal crusting; epistaxis; chronic sinusitis; nasal septum perforation; saddle nose deformity. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5) * Pulmonary: pulmonary nodules; cavitary lung lesions; diffuse alveolar hemorrhage; hemoptysis. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3, potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5) * Renal: rapidly progressive glomerulonephritis; hematuria; proteinuria; decreased glomerular filtration rate. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6, draibe2024diagnosisandtreatment pages 2-3) * Ocular: scleritis; episcleritis; uveitis; proptosis; orbital mass. (moin2023ocularandorbital pages 1-2, draibe2024diagnosisandtreatment pages 2-3) * Neurologic: mononeuritis multiplex; cranial neuropathy; hypertrophic pachymeningitis/headache. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)


4. Genetic / molecular information

4.1 “Causal genes” vs susceptibility genes

GPA is not established as a monogenic disorder in the retrieved evidence; instead, susceptibility loci (HLA-DP, SERPINA1, PRTN3, SEMA6A, PTPN22) are repeatedly supported by GWAS and genetic syntheses. (merkel2017identificationoffunctional pages 1-4, alberici2015geneticaspectsof pages 4-4, xie2013associationofgranulomatosis pages 1-2)

4.2 ANCA serotypes and molecular targets

PR3‑ANCA is the dominant serotype in GPA, with MPO‑ANCA more characteristic of MPA (and certain pulmonary phenotypes such as ILD). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5, potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)

4.3 Mechanistic chain (current evidence-supported skeleton)

  1. Genetic predisposition (notably HLA class II DP) supports altered antigen presentation and adaptive immune recognition. (xie2013associationofgranulomatosis pages 1-2, merkel2017identificationoffunctional pages 1-4)
  2. Autoimmune effector phase characterized by PR3‑ANCA in many patients; ANCA positivity helps define phenotypes and informs classification/diagnosis. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
  3. Inflammatory vascular injury and granulomatous inflammation lead to organ manifestations in ENT tract, lungs (nodules/cavitation/DAH), and kidneys (pauci‑immune GN). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3, potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
  4. Complement pathway targeting has become clinically actionable: avacopan antagonizes C5a receptor 1 (C5AR1) and demonstrates glucocorticoid‑sparing efficacy in AAV (including GPA). (geetha2024efficacyandsafety pages 1-2, geetha2024efficacyandsafety pages 4-5)

4.4 Suggested GO (biological process) and CL (cell type) terms (evidence-aligned; to be curated)

While the retrieved sources did not provide omics-level pathway enumerations, the disease and therapies point to: * GO BP (suggestions): neutrophil activation; complement activation; adaptive immune response; antigen processing and presentation; inflammatory response; vasculature development/vasculitis-related processes. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6, geetha2024efficacyandsafety pages 1-2) * CL (suggestions): neutrophil; macrophage; T cell; B cell; endothelial cell. (merkel2017identificationoffunctional pages 1-4)

4.5 Epigenetics and multi-omics

No GPA-specific epigenomic/transcriptomic/proteomic/metabolomic results were retrieved in this run; this is an evidence gap.


5. Environmental information

No GPA-specific environmental, lifestyle, pollutant, occupational, or infectious triggers were retrieved from the current evidence set.


6. Mechanism / pathophysiology (expanded notes from retrieved evidence)

6.1 Serology-based phenotyping and diagnostic performance

ANCA specificity is clinically informative. Antigen-specific PR3/MPO assays are recommended over indirect immunofluorescence in the reviewed diagnostic updates. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)

6.2 Complement pathway as an actionable mechanism

Avacopan (TAVNEOS), a C5a receptor antagonist, is being deployed to reduce glucocorticoid exposure while maintaining disease control in AAV. ADVOCATE subgroup analyses demonstrate sustained remission and reduced steroid toxicity signals (see Treatment). (geetha2024efficacyandsafety pages 1-2, geetha2024efficacyandsafety pages 4-5)


7. Anatomical structures affected

7.1 Organ-level and system-level involvement (with suggested UBERON mapping targets)

  • Upper airway / ENT (nasal passages, paranasal sinuses, ear structures) (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)
  • Lungs (pulmonary parenchyma; alveolar capillaries in DAH; airway structures in tracheobronchial disease) (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3, potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)
  • Kidneys (glomeruli—pauci‑immune GN; renal cortex) (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6, draibe2024diagnosisandtreatment pages 2-3)
  • Eyes and orbit (scleritis/uveitis/orbital mass) (moin2023ocularandorbital pages 1-2, draibe2024diagnosisandtreatment pages 2-3)
  • Peripheral and central nervous system (mononeuritis multiplex; pachymeningitis) (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)

7.2 Tissue/cell-level and subcellular-level

The retrieved evidence supports immune and vascular pathology but did not supply histologic microanatomy beyond “granuloma/giant cells on biopsy” and “pauci‑immune glomerulonephritis.” (pyo2023comparisonofthe pages 2-4)


8. Temporal development

8.1 Onset patterns

The evidence set indicates substantial variation and frequent delay in diagnosis, with reported symptom-to-diagnosis intervals from 1 month to >3 years and 36% of patients symptomatic for >1 year pre-diagnosis. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)

8.2 Disease course

GPA is framed as chronic with relapsing-remitting features requiring close follow-up. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)


9. Inheritance and population

9.1 Epidemiology (recently summarized)

  • AAV prevalence estimate: 200–400 per million (200–400/1,000,000). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)
  • GPA annual incidence in European adults: ~7.7–15.4 per million; one Swedish study reported 15.4/million. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)
  • Pediatric GPA incidence: ~0.88–1.8 per million. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)

9.2 Population demographics

  • Peak age at diagnosis varies by cohort; one summary mentions peaks at 45–55 and 65–74 years. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)

9.3 Inheritance model

The available evidence supports complex polygenic risk rather than Mendelian inheritance. (merkel2017identificationoffunctional pages 1-4, alberici2015geneticaspectsof pages 4-4)


10. Diagnostics

10.1 Current diagnostic approach

A key practical constraint is that validated diagnostic criteria for GPA are not established; diagnosis is based on a synthesis of clinical features plus supportive laboratory testing (ANCA), imaging, and histology, acknowledging that biopsy may be infeasible and/or non‑specific. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3, potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)

10.2 ANCA testing (quantitative performance)

From the 2024 diagnostic update: * PR3‑ANCA sensitivity for GPA: 74% (MPO‑ANCA sensitivity for GPA: 11%). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6) * Specificity (PR3/MPO antigen-specific assays): mean 97% (range 93–99%). (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6) * ANCA‑seronegative proportion reported as ~8.5%. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)

10.3 Classification criteria update (2022 ACR/EULAR)

The 2022 ACR/EULAR GPA criteria are a points-based classification tool intended for research classification, not as a stand‑alone diagnostic algorithm, and require appropriate entry criteria and exclusion of mimics. (https://doi.org/10.1002/art.41986) (robson20222022americancollege pages 5-6)

Items and weights available from a 2023 summary of the criteria include: * nasal passage involvement (+3) * cartilaginous involvement (+2) * conductive/sensorineural hearing loss (+1) * PR3‑ANCA/c‑ANCA positivity (+5) * MPO‑ANCA/p‑ANCA positivity (−1) * eosinophils ≥1000/µL (−4) * granuloma/granulomatous inflammation/giant cells on biopsy (+2) * pauci‑immune glomerulonephritis (+1) * two radiology items were retained with positive weights in the summary, but the excerpt did not include the precise radiology item wording. (pyo2023comparisonofthe pages 2-4)

Threshold: classification if cumulative score ≥5 (one summary reported “>5”). (pyo2023comparisonofthe pages 2-4, robson20222022americancollege pages 5-6)

Performance: the criteria were reported (in the retrieved summary text) to have sensitivity 93% and specificity 94% in a validation set. (robson20222022americancollege pages 5-6)

Visual evidence note: A retrieved figure crop from the criteria document shows the MPA scoring table (not the GPA table) but visually confirms the ACR/EULAR points-based approach and how PR3‑ANCA/nasal involvement are used as discriminators across AAV subtypes. (robson20222022americancollege media d7729245)

10.4 Biopsy and imaging

Biopsy is “strongly recommended” but is not always feasible and may show non-specific features; imaging supports detection of pulmonary nodules/masses/cavitation and sinonasal inflammation. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2, potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3)


11. Outcomes / prognosis

11.1 Relapse and long-term outcomes (recent cohort data)

A 2024 multicenter European cohort (1999–2022; classified by 2022 criteria) reported: * Overall relapse rate: 34.6% (124/358). (kramer2024remissioninductiontherapies pages 4-5) * Relapse rate was higher in GPA than MPA: 41.3% vs 25.9% (p=0.006). (kramer2024remissioninductiontherapies pages 4-5) * Composite renal endpoint occurred in 25.4% and was more frequent in MPA than GPA (31.7% vs 21.2%, p=0.028). (kramer2024remissioninductiontherapies pages 4-5)

11.2 Kidney outcome markers in steroid-sparing complement inhibition

In the ADVOCATE rituximab subgroup analysis, urinary albumin-to-creatinine ratio (UACR) improved more with avacopan (LS mean ~−42%) versus prednisone taper (~+6%). (geetha2024efficacyandsafety pages 4-5)

Survival and disease-specific mortality: Not retrievable from current evidence set.


12. Treatment

12.1 Contemporary standard approaches (supported by evidence in this run)

Modern GPA care generally integrates: * Immunosuppression/biologics for induction and maintenance (e.g., rituximab; cyclophosphamide in some settings) * Glucocorticoid-sparing strategies * Infection prophylaxis during intensive immunosuppression (e.g., PJP prophylaxis)

The detailed regimen algorithms (dose schedules by phenotype/severity) were not fully extractable from the retrieved guideline texts in this run; however, multiple high-quality 2024 sources document evolving steroid-sparing approaches and real-world practice trends. (geetha2024efficacyandsafety pages 4-5, kramer2024remissioninductiontherapies pages 1-2)

12.2 Recent developments (2023–2024 prioritized): avacopan (C5aR1 antagonist)

Efficacy/safety in RCT subgroup analysis (2024): In the rituximab induction subgroup of ADVOCATE (NCT02994927), avacopan showed: * Sustained remission at week 52: 71.0% (avacopan) vs 56.1% (prednisone taper). (geetha2024efficacyandsafety pages 5-5) * Relapse after achieving BVAS=0 by week 52: 8.7% vs 20.2%. (geetha2024efficacyandsafety pages 4-5) * Lower cumulative prednisone-equivalent exposure weeks 0–26: mean 1417 mg vs 3265 mg. (geetha2024efficacyandsafety pages 4-5) * Serious adverse events: 34.6% vs 39.3% (as reported in trial summary text). (geetha2024efficacyandsafety pages 1-2)

Real-world implementation (2024 DAH cohort): In a single-center retrospective cohort of 15 patients with AAV presenting with diffuse alveolar hemorrhage, avacopan use was associated with most patients achieving remission during a median 17-week follow-up, but there were serious infections including one death; authors highlighted practical implementation uncertainties (timing, taper strategy, access, long-term safety). (falde2024treatmentofantineutrophil pages 1-2)

Ongoing/registered trials (real-world implementation trajectory): * ENT-focused trial: NCT07176546 (not yet recruiting; estimated 2026 start) tests avacopan vs placebo added to standard care for active ENT GPA; primary endpoint is ENT remission without relapse at week 52 with no glucocorticoid exposure in the prior 4 weeks; key secondary endpoints include SNOT‑22 and AAV‑PRO and ENT surgeries/flares. (NCT07176546 chunk 1) * ARRIA phase 4: NCT06611696 (started 2024-11-15) compares avacopan + short-term reduced-dose glucocorticoid + rituximab versus a 20-week reduced-dose glucocorticoid regimen + rituximab in new-onset GPA/MPA; primary endpoint is remission at 26 weeks (BVAS=0 and <5 mg/day prednisolone) and secondary endpoints include VDI and SF‑36 through 104 weeks. (NCT06611696 chunk 1)

12.3 Rituximab vs cyclophosphamide trends and outcomes (real-world)

In the 2024 European cohort, cyclophosphamide remained frequently used, but rituximab use increased after 2013; relapse was more common in GPA than MPA. (kramer2024remissioninductiontherapies pages 1-2, kramer2024remissioninductiontherapies pages 4-5)

12.4 Supportive care / prophylaxis: PJP prophylaxis with TMP‑SMX during rituximab

A 2023 US administrative claims cohort of rituximab-treated GPA (MarketScan 2011–2020) reported: * TMP‑SMX prophylaxis dispensed in 23% (426/1877); median persistence 141 days (IQR 83–248). (https://doi.org/10.1186/s13075-023-03114-7) (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2) * Prednisone ≥20 mg/day (vs none) strongly associated with prophylaxis (OR 3.96; 95% CI 3.0–5.2). (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2) * Female sex negatively associated with prophylaxis dispensing (OR 0.63; 95% CI 0.5–0.8). (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2) These data suggest incomplete real-world uptake of guideline-recommended prophylaxis and provide targets for quality improvement. (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2, mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 6-7)

12.5 Suggested MAXO terms (examples; to be curated)

  • Complement inhibition / C5a receptor antagonism (avacopan) (geetha2024efficacyandsafety pages 1-2)
  • B‑cell depletion therapy (rituximab) (geetha2024efficacyandsafety pages 1-2)
  • Cytotoxic immunosuppression (cyclophosphamide) (kramer2024remissioninductiontherapies pages 1-2)
  • Pneumocystis jirovecii pneumonia prophylaxis (trimethoprim‑sulfamethoxazole) (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2)

13. Prevention

Evidence in this run supports tertiary prevention via infection prophylaxis during immunosuppression (TMP‑SMX for PJP in rituximab-treated GPA), but did not yield evidence-based primary prevention strategies (e.g., vaccination schedules, exposure reduction) specific to GPA. (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2)


14. Other species / natural disease

No evidence on naturally occurring GPA in non-human species was retrieved in this run.


15. Model organisms

No evidence on specific GPA model organisms (e.g., murine PR3-ANCA models) was retrieved in this run.


Cross-cutting quantitative summary table

Domain Finding (with numbers) Population/Context Source (author/year/DOI)
A. Disease overview & organ involvement GPA is a rare systemic necrotizing vasculitis with granulomatous inflammation of the respiratory tract and small-/medium-vessel vasculitis; classically affects upper airways, lungs, and kidneys Disease overview; any organ may be affected Potentas-Policewicz & Fijolek 2024, Front Med, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)
A. Disease overview & organ involvement ENT involvement/signs: 80–100% GPA clinical phenotype Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)
A. Disease overview & organ involvement Nasal crusting 75%; excessive nose-blowing 70%; nasal obstruction 65%; epistaxis 59%; saddle nose 25% ENT manifestations in GPA Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)
A. Disease overview & organ involvement Pulmonary involvement 62–90%; pulmonary nodules/mass lesions 40–70%; cavitation 20–50% GPA pulmonary disease Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3)
A. Disease overview & organ involvement Diffuse alveolar hemorrhage (DAH) 8.8–36% GPA pulmonary capillaritis/DAH Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)
A. Disease overview & organ involvement Kidney involvement 70–85%; renal insufficiency at presentation 11–17%; worsening GFR 24.3% GPA renal disease course Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
A. Disease overview & organ involvement Ocular/orbital disease 16–78%; up to 27% present initially with ophthalmic symptoms Systematic review of ocular/orbital GPA Moin et al. 2023, doi:10.22336/rjo.2023.38 (moin2023ocularandorbital pages 1-2)
A. Disease overview & organ involvement Ophthalmologic signs 50–60%; orbital lesions 5–30% GPA extra-renal manifestations Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
A. Disease overview & organ involvement Oral involvement 6–13%; “strawberry” gingival hyperplasia 61.5% GPA oral manifestations Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
A. Disease overview & organ involvement CNS involvement 3–11.7%; PNS involvement 11–44% GPA neurologic disease Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 4-5)
B. ANCA test performance PR3-ANCA sensitivity for GPA 74% Diagnostic serology for GPA Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
B. ANCA test performance MPO-ANCA sensitivity for GPA 11% Diagnostic serology for GPA Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
B. ANCA test performance MPO-ANCA sensitivity for MPA 73%; PR3-ANCA sensitivity for MPA 7% Comparator data highlighting GPA/MPA serologic separation Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
B. ANCA test performance Specificity of PR3/MPO antigen-specific assays: mean 97% (range 93–99%) AAV serology; antigen-specific assays preferred over IIF Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
B. ANCA test performance ANCA-negative proportion about 8.5% GPA diagnostic workup Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 5-6)
B. ANCA test performance In ocular/orbital GPA case review: c-ANCA 59.2%, p-ANCA 10.8%, granulomas 47.7% 306 published ocular/orbital GPA cases Moin et al. 2023, doi:10.22336/rjo.2023.38 (moin2023ocularandorbital pages 1-2)
C. 2022 ACR/EULAR classification criteria Classification threshold: cumulative score ≥5 (one summary reported >5); intended for classification, not diagnosis Requires prior diagnosis of small-/medium-vessel vasculitis and exclusion of mimics Robson et al. 2022, Arthritis Rheumatol, doi:10.1002/art.41986; Pyo et al. 2023, doi:10.3349/ymj.2022.0435 (pyo2023comparisonofthe pages 2-4, robson20222022americancollege pages 5-6)
C. 2022 ACR/EULAR classification criteria Available weighted items: nasal passage involvement +3; cartilaginous involvement +2; hearing loss +1; PR3-ANCA/c-ANCA positivity +5; MPO-ANCA/p-ANCA positivity −1; eosinophils ≥1000/µL −4 GPA scoring items available from review/criteria summary Pyo et al. 2023, doi:10.3349/ymj.2022.0435 (pyo2023comparisonofthe pages 2-4)
C. 2022 ACR/EULAR classification criteria Additional available weighted items: granuloma/granulomatous inflammation/giant cells on biopsy +2; pauci-immune glomerulonephritis +1; 2 radiology items retained with positive weights but details truncated in excerpt Incomplete item extraction from available evidence Pyo et al. 2023, doi:10.3349/ymj.2022.0435 (pyo2023comparisonofthe pages 2-4)
C. 2022 ACR/EULAR classification criteria Validation cohort sizes: development set 578 GPA cases/652 comparators; validation set 146 GPA cases/161 comparators Original derivation/validation study Robson et al. 2022, doi:10.1002/art.41986 (from search result summary) (robson20222022americancollege pages 5-6)
C. 2022 ACR/EULAR classification criteria Performance: sensitivity 93% (95% CI 87–96), specificity 94% (95% CI 89–97) Validation set; research classification performance Robson et al. 2022, doi:10.1002/art.41986 (from search result summary) (robson20222022americancollege pages 5-6)
C. 2022 ACR/EULAR classification criteria Real-world concordance in previously diagnosed GPA: 48/65 reclassified, 73.8% concordance Korean application study comparing 2022 criteria with prior criteria Pyo et al. 2023, doi:10.3349/ymj.2022.0435 (pyo2023comparisonofthe pages 2-4)
D. Epidemiology AAV prevalence estimated at 200–400 per million Aggregated AAV epidemiology Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)
D. Epidemiology GPA annual incidence in European adults about 7.7–15.4 per million; Swedish study 15.4/million Adult epidemiology Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)
D. Epidemiology Pediatric GPA incidence about 0.88–1.8 per million Pediatric epidemiology Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)
D. Epidemiology Diagnostic delay ranged from 1 month to >3 years; 36% had symptoms >1 year before diagnosis GPA natural history/diagnostic delay Potentas-Policewicz & Fijolek 2024, doi:10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 2-3, potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)
E. Treatment developments Avacopan RTX subgroup: remission at week 26 77.6% vs 75.7%; sustained remission at week 52 71.0% vs 56.1% ADVOCATE rituximab induction subgroup; avacopan vs prednisone taper Geetha et al. 2024, Ann Rheum Dis, doi:10.1136/ard-2023-224816 (geetha2024efficacyandsafety pages 5-5, gattu2024superiorityofavacopan pages 5-6, geetha2024efficacyandsafety pages 1-2)
E. Treatment developments Avacopan RTX subgroup relapse after BVAS=0 by week 52: 8.7% vs 20.2% ADVOCATE rituximab subgroup Geetha et al. 2024, doi:10.1136/ard-2023-224816 (geetha2024efficacyandsafety pages 4-5)
E. Treatment developments Prednisone-equivalent cumulative exposure weeks 0–26: mean 1417 mg vs 3265 mg Avacopan vs prednisone taper on RTX background Geetha et al. 2024, doi:10.1136/ard-2023-224816 (geetha2024efficacyandsafety pages 4-5)
E. Treatment developments UACR change favored avacopan: about −42% vs +6%; LS mean difference −45 (95% CI −60 to −24) RTX subgroup renal response Geetha et al. 2024, doi:10.1136/ard-2023-224816 (geetha2024efficacyandsafety pages 4-5)
E. Treatment developments Serious adverse events 34.6% vs 39.3% RTX subgroup, avacopan vs prednisone taper Geetha et al. 2024, doi:10.1136/ard-2023-224816 (geetha2024efficacyandsafety pages 1-2)
E. Treatment developments Real-world DAH cohort on avacopan: n=15, median age 66, median follow-up 17 weeks; most achieved remission, but 2 serious infections including 1 death Single-center real-world adjunctive avacopan use in severe AAV with DAH Falde et al. 2024, doi:10.1002/acr2.11726 (falde2024treatmentofantineutrophil pages 1-2)
E. Treatment developments TMP-SMX prophylaxis in RTX-treated GPA: 426/1877 (23%) overall; new-user subgroup 281/919 (31%); median persistence 141 days (IQR 83–248); 42% continued ≥6 months US administrative claims cohort, 2011–2020 Mendel et al. 2023, Arthritis Res Ther, doi:10.1186/s13075-023-03114-7 (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2, mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 2-4, mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 6-7)
E. Treatment developments Factors associated with TMP-SMX dispensing: prednisone ≥20 mg/day OR 3.96 (95% CI 3.0–5.2); prednisone 1–19 mg/day OR 2.63 (1.8–3.8); methotrexate OR 1.48 (1.04–2.1); ICU hospitalization OR 1.95 (1.4–2.7); female sex OR 0.63 (0.5–0.8) RTX-treated GPA; prophylaxis targeting higher-risk patients Mendel et al. 2023, doi:10.1186/s13075-023-03114-7 (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2, mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 2-4, mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 6-7)
F. Genetics HLA-DPB1/HLA-DPA1 class II DP locus strongly associated; rs9277554 combined P=1.92×10^-50 and rs9277341 P=2.18×10^-39; signal accounted for by HLA-DPB1*04 2013 GWAS, 492 GPA cases/1506 controls with replication in 528 cases/1228 controls Xie et al. 2013, Arthritis Rheum, doi:10.1002/art.38036 (xie2013associationofgranulomatosis pages 1-2)
F. Genetics SEMA6A rs26595 reached genome-wide significance, P=2.09×10^-8 GPA GWAS non-MHC locus Xie et al. 2013, doi:10.1002/art.38036 (xie2013associationofgranulomatosis pages 1-2)
F. Genetics HLA-DP rs3117242: OR 5.39, P=3.1×10^-85 in GPA; OR 7.03, P=6.2×10^-89 in PR3+ subgroup European GWAS summary for GPA/PR3-AAV Alberici et al. 2015, NDT, doi:10.1093/ndt/gfu386 (alberici2015geneticaspectsof pages 4-4)
F. Genetics SERPINA1 rs7151526: OR 0.59, P=2.4×10^-9 in GPA+MPA; OR 0.53, P=5.6×10^-12 in PR3+ subgroup; rs28929474 OR 2.9 in PR3-ANCA+ AAV Non-HLA susceptibility locus involving alpha-1 antitrypsin pathway Alberici et al. 2015, doi:10.1093/ndt/gfu386; Dahlqvist et al. 2022, doi:10.1093/rheumatology/keab912 (alberici2015geneticaspectsof pages 4-4, merkel2017identificationoffunctional pages 1-4)
F. Genetics PRTN3 rs62132295: OR 0.78, P=2.6×10^-5 in GPA; stronger in PR3-ANCA+ subgroup OR 0.73, P=2.6×10^-7 PR3 autoantigen gene association Alberici et al. 2015, doi:10.1093/ndt/gfu386 (alberici2015geneticaspectsof pages 4-4)
F. Genetics Merkel 2017 replication/GWAS: HLA-DPB1 rs141530235 OR 2.99 and rs1042169 OR 2.82; PRTN3 locus linked to increased neutrophil PRTN3 expression; SERPINA1 and PTPN22 also significant 1986 AAV cases and 4723 controls Merkel et al. 2017, doi:10.1002/art.40034 (merkel2017identificationoffunctional pages 1-4)

Table: This table compiles key quantitative facts on granulomatosis with polyangiitis from the gathered evidence, including organ involvement, ANCA performance, classification criteria, epidemiology, treatment outcomes, and genetic associations. It is designed as a compact reference for the main numeric findings and their sources.


Key recent developments and expert-level synthesis (2023–2024 emphasis)

  1. Diagnostic modernization and phenotyping: Recent synthesis emphasizes that formal diagnostic criteria remain lacking and clinicians rely on multimodal evaluation; nevertheless, classification/phenotyping advances (especially PR3‑ANCA vs MPO‑ANCA distinction) are reshaping research cohorts and informing targeted approaches. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2, potentaspolicewicz2024granulomatosiswithpolyangiitis pages 20-22)
  2. Steroid-sparing era: Avacopan has strong 2024 evidence in rituximab-treated AAV showing improved sustained remission and reduced relapse alongside markedly reduced glucocorticoid exposure, with ongoing trials extending these concepts into organ-specific (ENT) endpoints and longer-term damage/QoL outcomes. (geetha2024efficacyandsafety pages 4-5, NCT07176546 chunk 1, NCT06611696 chunk 1)
  3. Implementation gaps in supportive care: Despite recommendations for PJP prophylaxis during AAV induction, real-world TMP‑SMX dispensing in rituximab-treated GPA was only ~23%, suggesting a measurable care gap and opportunity for improved preventive practice. (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2)

URLs and publication dates for key sources used (examples)

  • Potentas-Policewicz & Fijolek. Frontiers in Medicine (Aug 2024). https://doi.org/10.3389/fmed.2024.1369233 (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 1-2)
  • Robson et al. Arthritis & Rheumatology (Feb 2022). https://doi.org/10.1002/art.41986 (robson20222022americancollege pages 5-6)
  • Geetha et al. Annals of the Rheumatic Diseases (Feb 2024). https://doi.org/10.1136/ard-2023-224816 (geetha2024efficacyandsafety pages 1-2)
  • Mendel et al. Arthritis Research & Therapy (Jul 2023). https://doi.org/10.1186/s13075-023-03114-7 (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 1-2)
  • Xie et al. Arthritis & Rheumatism (Aug 2013). https://doi.org/10.1002/art.38036 (xie2013associationofgranulomatosis pages 1-2)
  • ClinicalTrials.gov NCT06611696 (trial record, 2024). https://clinicaltrials.gov/study/NCT06611696 (NCT06611696 chunk 1)
  • ClinicalTrials.gov NCT07176546 (trial record, 2026). https://clinicaltrials.gov/study/NCT07176546 (NCT07176546 chunk 1)

References

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  13. (draibe2024diagnosisandtreatment pages 2-3): Juliana Bordignon Draibe, Helena Marco, Meritxell Ibernon, Irene Agraz, Carola Arcal, Xoana Barros, Victoria Cabrera, Iara Da Silva, Montserrat Díaz, Xavier Fulladosa, Elena Guillén, Patricia Lescano, Laura Martínez Valenzuela, Eva Márquez, Nadia Martín, Ana Merino, Maru Navarro, Eva Rodríguez, Mª José Soler, Joan Torras, and Luís F. Quintana. Diagnosis and treatment of renal anca vasculitis: a summary of the consensus document of the catalan group for the study of glomerular diseases (glomcat). Journal of Clinical Medicine, 13:6793, Nov 2024. URL: https://doi.org/10.3390/jcm13226793, doi:10.3390/jcm13226793. This article has 2 citations.

  14. (geetha2024efficacyandsafety pages 1-2): Duvuru Geetha, Anisha Dua, Huibin Yue, Jason Springer, Carlo Salvarani, David Jayne, Peter Merkel, C. Au Peh, A. Chakera, B. Cooper, J. Kurtkoti, D. Langguth, V. Levidiotis, G. Luxton, P. Mount, D. Mudge, E. Noble, R. Phoon, A. Ritchie, J. Ryan, M. Suranyi, A. Rosenkranz, A. Kronbichler, N. Demoulin, C. Bovy, R. Hellemans, J. Hougardy, B. Sprangers, K. Wissing, C. Pagnoux, S. Barbour, S. Brachemi, S. Cournoyer, L. Girard, L. Laurin, P. Liang, D. Philibert, M. Walsh, V. Tesar, R. Becvar, P. Horak, I. Rychlik, W. Szpirt, H. Dieperink, J. Gregersen, P. Ivarsen, E. Krarup, C. Lyngsoe, C. Rigothier, J. Augusto, A. Belot, D. Chauveau, D. Cornec, N. Jourde-Chiche, M. Ficheux, A. Karras, A. Klein, F. Maurier, R. Mesbah, O. Moranne, A. Neel, T. Quemeneur, D. Saadoun, B. Terrier, P. Zaoui, M. Schaier, U. Benck, R. Bergner, M. Busch, J. Floege, F. Grundmann, H. Haller, M. Haubitz, B. Hellmich, J. Henes, B. Hohenstein, C. Hugo, C. Iking-Konert, F. Arndt, T. Kubacki, I. Kotter, P. Lamprecht, T. Lindner, J. Halbritter, H. Mehling, U. Schönermarck, N. Venhoff, V. Vielhauer, O. Witzke, I. Szombati, G. Szucs, G. Garibotto, F. Alberici, E. Brunetta, L. Dagna, S. De Vita, G. Emmi, A. Gabrielli, L. Manenti, F. Pieruzzi, D. Roccatello, C. Salvarani, M. Harigai, H. Dobashi, T. Atsumi, S. Fujimoto, N. Hagino, A. Ihata, S. Kaname, Y. Kaneko, A. Katagiri, M. Katayama, Y. Kirino, K. Kitagawa, A. Komatsuda, H. Kono, T. Kurasawa, R. Matsumura, T. Mimura, A. Morinobu, Y. Murakawa, T. Naniwa, T. Nanki, N. Ogawa, H. Oshima, K. Sada, E. Sugiyama, T. Takeuchi, H Taki, N. Tamura, T. Tsukamoto, K. Yamagata, M. Yamamura, P. van Daele, A. Rutgers, Y. Teng, R. Walker, I. Chua, M. Collins, K. Rabindranath, J. de Zoysa, M. Svensson, B. Grevbo, S. Kalstad, M. Little, M. Clarkson, E. Molloy, I. Agraz Pamplona, J. Anton, V. Barrio Lucia, S. Ciggaran, M. Cinta Cid, M. Diaz Encarnacion, X. Fulladosa Oliveras, M. Jose Soler, H. Marco Rusinol, M. Praga, L. Quintana Porras, A. Segarra, A. Bruchfeld, M. Segelmark, I. Soveri, E. Thomaidi, K. Westman, T. Neumann, M. Burnier, T. Daikeler, J. Dudler, T. Hauser, H. Seeger, B. Vogt, D. Jayne, J. Burton, R. Al Jayyousi, T. Amin, J. Andrews, L. Baines, P. Brogan, B. Dasgupta, T. Doulton, O. Flossmann, S. Griffin, J. Harper, L. Harper, D. Kidder, R. Klocke, P. Lanyon, R. Luqmani, J. McLaren, D. Makanjuola, L. McCann, A. Nandagudi, S. Selvan, E. O’Riordan, M. Patel, R. Patel, C. Pusey, R. Rajakariar, J. Robson, M. Robson, A. Salama, L. Smyth, J. Sznajd, J. Taylor, P. Merkel, A. Sreih, E. Belilos, A. Bomback, J. Carlin; Y, Chang Chen Lin, V. Derebail, S. Dragoi, A. Dua, L. Forbess, D. Geetha, P. Gipson, R. Gohh, G.T. Greenwood, S. Hugenberg, R. Jimenez, M. Kaskas, T. Kermani, A. Kivitz, C. Koening, C. Langford, G. Marder, A. Mohamed, P. Monach, N. Neyra, G. Niemer, J. Niles, R. Obi, C. Owens, D. Parks, A. Podoll, B. Rovin, R. Sam, W. Shergy, A. Silva, R. Spiera, J. Springer, C. Striebich, A. Swarup, S. Thakar, A. Tiliakos, Y. Tsai, D. Waguespack, and M. Chester Wasko. Efficacy and safety of avacopan in patients with anca-associated vasculitis receiving rituximab in a randomised trial. Annals of the Rheumatic Diseases, 83:223-232, Feb 2024. URL: https://doi.org/10.1136/ard-2023-224816, doi:10.1136/ard-2023-224816. This article has 63 citations and is from a highest quality peer-reviewed journal.

  15. (pyo2023comparisonofthe pages 2-4): Jung Yoon Pyo, Lucy Eunju Lee, Yong-Beom Park, and Sang-Won Lee. Comparison of the 2022 acr/eular classification criteria for antineutrophil cytoplasmic antibody-associated vasculitis with previous criteria. Yonsei Medical Journal, 64:11, Jan 2023. URL: https://doi.org/10.3349/ymj.2022.0435, doi:10.3349/ymj.2022.0435. This article has 95 citations and is from a peer-reviewed journal.

  16. (robson20222022americancollege pages 5-6): Joanna C. Robson, Peter C. Grayson, Cristina Ponte, Ravi Suppiah, Anthea Craven, Andrew Judge, Sara Khalid, Andrew Hutchings, Richard A. Watts, Peter A. Merkel, and Raashid A. Luqmani. 2022 american college of rheumatology/european alliance of associations for rheumatology classification criteria for granulomatosis with polyangiitis. Arthritis & Rheumatology, 74:393-399, Feb 2022. URL: https://doi.org/10.1002/art.41986, doi:10.1002/art.41986. This article has 797 citations and is from a highest quality peer-reviewed journal.

  17. (robson20222022americancollege media d7729245): Joanna C. Robson, Peter C. Grayson, Cristina Ponte, Ravi Suppiah, Anthea Craven, Andrew Judge, Sara Khalid, Andrew Hutchings, Richard A. Watts, Peter A. Merkel, and Raashid A. Luqmani. 2022 american college of rheumatology/european alliance of associations for rheumatology classification criteria for granulomatosis with polyangiitis. Arthritis & Rheumatology, 74:393-399, Feb 2022. URL: https://doi.org/10.1002/art.41986, doi:10.1002/art.41986. This article has 797 citations and is from a highest quality peer-reviewed journal.

  18. (kramer2024remissioninductiontherapies pages 4-5): Stefan Krämer, Kristian Vogt, Theresa Maria Schreibing, Martin Busch, Tobias Schmitt, Raoul Bergner, Sebastian Mosberger, Thomas Neumann, and Thomas Rauen. Remission induction therapies and long-term outcomes in granulomatosis with polyangiitis and microscopic polyangiitis: real-world data from a european cohort. Rheumatology International, Dec 2024. URL: https://doi.org/10.1007/s00296-024-05757-4, doi:10.1007/s00296-024-05757-4. This article has 10 citations and is from a peer-reviewed journal.

  19. (geetha2024efficacyandsafety pages 5-5): Duvuru Geetha, Anisha Dua, Huibin Yue, Jason Springer, Carlo Salvarani, David Jayne, Peter Merkel, C. Au Peh, A. Chakera, B. Cooper, J. Kurtkoti, D. Langguth, V. Levidiotis, G. Luxton, P. Mount, D. Mudge, E. Noble, R. Phoon, A. Ritchie, J. Ryan, M. Suranyi, A. Rosenkranz, A. Kronbichler, N. Demoulin, C. Bovy, R. Hellemans, J. Hougardy, B. Sprangers, K. Wissing, C. Pagnoux, S. Barbour, S. Brachemi, S. Cournoyer, L. Girard, L. Laurin, P. Liang, D. Philibert, M. Walsh, V. Tesar, R. Becvar, P. Horak, I. Rychlik, W. Szpirt, H. Dieperink, J. Gregersen, P. Ivarsen, E. Krarup, C. Lyngsoe, C. Rigothier, J. Augusto, A. Belot, D. Chauveau, D. Cornec, N. Jourde-Chiche, M. Ficheux, A. Karras, A. Klein, F. Maurier, R. Mesbah, O. Moranne, A. Neel, T. Quemeneur, D. Saadoun, B. Terrier, P. Zaoui, M. Schaier, U. Benck, R. Bergner, M. Busch, J. Floege, F. Grundmann, H. Haller, M. Haubitz, B. Hellmich, J. Henes, B. Hohenstein, C. Hugo, C. Iking-Konert, F. Arndt, T. Kubacki, I. Kotter, P. Lamprecht, T. Lindner, J. Halbritter, H. Mehling, U. Schönermarck, N. Venhoff, V. Vielhauer, O. Witzke, I. Szombati, G. Szucs, G. Garibotto, F. Alberici, E. Brunetta, L. Dagna, S. De Vita, G. Emmi, A. Gabrielli, L. Manenti, F. Pieruzzi, D. Roccatello, C. Salvarani, M. Harigai, H. Dobashi, T. Atsumi, S. Fujimoto, N. Hagino, A. Ihata, S. Kaname, Y. Kaneko, A. Katagiri, M. Katayama, Y. Kirino, K. Kitagawa, A. Komatsuda, H. Kono, T. Kurasawa, R. Matsumura, T. Mimura, A. Morinobu, Y. Murakawa, T. Naniwa, T. Nanki, N. Ogawa, H. Oshima, K. Sada, E. Sugiyama, T. Takeuchi, H Taki, N. Tamura, T. Tsukamoto, K. Yamagata, M. Yamamura, P. van Daele, A. Rutgers, Y. Teng, R. Walker, I. Chua, M. Collins, K. Rabindranath, J. de Zoysa, M. Svensson, B. Grevbo, S. Kalstad, M. Little, M. Clarkson, E. Molloy, I. Agraz Pamplona, J. Anton, V. Barrio Lucia, S. Ciggaran, M. Cinta Cid, M. Diaz Encarnacion, X. Fulladosa Oliveras, M. Jose Soler, H. Marco Rusinol, M. Praga, L. Quintana Porras, A. Segarra, A. Bruchfeld, M. Segelmark, I. Soveri, E. Thomaidi, K. Westman, T. Neumann, M. Burnier, T. Daikeler, J. Dudler, T. Hauser, H. Seeger, B. Vogt, D. Jayne, J. Burton, R. Al Jayyousi, T. Amin, J. Andrews, L. Baines, P. Brogan, B. Dasgupta, T. Doulton, O. Flossmann, S. Griffin, J. Harper, L. Harper, D. Kidder, R. Klocke, P. Lanyon, R. Luqmani, J. McLaren, D. Makanjuola, L. McCann, A. Nandagudi, S. Selvan, E. O’Riordan, M. Patel, R. Patel, C. Pusey, R. Rajakariar, J. Robson, M. Robson, A. Salama, L. Smyth, J. Sznajd, J. Taylor, P. Merkel, A. Sreih, E. Belilos, A. Bomback, J. Carlin; Y, Chang Chen Lin, V. Derebail, S. Dragoi, A. Dua, L. Forbess, D. Geetha, P. Gipson, R. Gohh, G.T. Greenwood, S. Hugenberg, R. Jimenez, M. Kaskas, T. Kermani, A. Kivitz, C. Koening, C. Langford, G. Marder, A. Mohamed, P. Monach, N. Neyra, G. Niemer, J. Niles, R. Obi, C. Owens, D. Parks, A. Podoll, B. Rovin, R. Sam, W. Shergy, A. Silva, R. Spiera, J. Springer, C. Striebich, A. Swarup, S. Thakar, A. Tiliakos, Y. Tsai, D. Waguespack, and M. Chester Wasko. Efficacy and safety of avacopan in patients with anca-associated vasculitis receiving rituximab in a randomised trial. Annals of the Rheumatic Diseases, 83:223-232, Feb 2024. URL: https://doi.org/10.1136/ard-2023-224816, doi:10.1136/ard-2023-224816. This article has 63 citations and is from a highest quality peer-reviewed journal.

  20. (falde2024treatmentofantineutrophil pages 1-2): Sam D. Falde, Amos Lal, Rodrigo Cartin‐Ceba, Lester E. Mertz, Fernando C. Fervenza, Ladan Zand, Matthew J. Koster, Kenneth J. Warrington, Augustine S. Lee, Nabeel Aslam, Andy Abril, and Ulrich Specks. Treatment of antineutrophil cytoplasmic antibody–associated vasculitis with diffuse alveolar hemorrhage with avacopan. ACR Open Rheumatology, 6:707-716, Jul 2024. URL: https://doi.org/10.1002/acr2.11726, doi:10.1002/acr2.11726. This article has 11 citations and is from a peer-reviewed journal.

  21. (NCT06611696 chunk 1): Shunsuke Furuta. Avacopan vs Reduced-dose Glucocorticoids in ANCA-associated Vasculitis. Chiba University. 2024. ClinicalTrials.gov Identifier: NCT06611696

  22. (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 6-7): Arielle Mendel, Hassan Behlouli, Cristiano Soares de Moura, Évelyne Vinet, Jeffrey R. Curtis, and Sasha Bernatsky. Trimethoprim-sulfamethoxazole prophylaxis during treatment of granulomatosis with polyangiitis with rituximab in the united states of america: a retrospective cohort study. Arthritis Research & Therapy, Jul 2023. URL: https://doi.org/10.1186/s13075-023-03114-7, doi:10.1186/s13075-023-03114-7. This article has 5 citations and is from a domain leading peer-reviewed journal.

  23. (gattu2024superiorityofavacopan pages 5-6): Rishma Gattu, Michelle Demory Beckler, and Marc M. Kesselman. Superiority of avacopan and mepolizumab to glucocorticoid tapering in the treatment of anti-neutrophil cytoplasmic antibody (anca)-associated vasculitis: a systematic review. Cureus, Aug 2024. URL: https://doi.org/10.7759/cureus.67161, doi:10.7759/cureus.67161. This article has 5 citations.

  24. (mendel2023trimethoprimsulfamethoxazoleprophylaxisduring pages 2-4): Arielle Mendel, Hassan Behlouli, Cristiano Soares de Moura, Évelyne Vinet, Jeffrey R. Curtis, and Sasha Bernatsky. Trimethoprim-sulfamethoxazole prophylaxis during treatment of granulomatosis with polyangiitis with rituximab in the united states of america: a retrospective cohort study. Arthritis Research & Therapy, Jul 2023. URL: https://doi.org/10.1186/s13075-023-03114-7, doi:10.1186/s13075-023-03114-7. This article has 5 citations and is from a domain leading peer-reviewed journal.

  25. (potentaspolicewicz2024granulomatosiswithpolyangiitis pages 20-22): Malgorzata Potentas-Policewicz and Justyna Fijolek. Granulomatosis with polyangiitis: clinical characteristics and updates in diagnosis. Frontiers in Medicine, Aug 2024. URL: https://doi.org/10.3389/fmed.2024.1369233, doi:10.3389/fmed.2024.1369233. This article has 49 citations.