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Aortitis

1. Disease Information

2026-05-05
Falcon MONDO:0006656 Model: Edison Scientific Literature 45 citations

1. Disease Information

1.1 Overview / definition

Aortitis is explicitly defined as “inflammation of the aorta”. (staniforth2024aortitisincreasesthe pages 1-2)

Clinically, it is best conceptualized as a syndrome with divergent causes and management imperatives (e.g., immunosuppression for inflammatory aortitis vs antimicrobials ± surgery for infectious aortitis). (arcilla2025thegreatvasculitis pages 7-9, staniforth2024aortitisincreasesthe pages 1-2)

1.2 Key identifiers (requested: OMIM/Orphanet/ICD/MeSH/MONDO)

1.3 Evidence sources

The information here is derived from aggregated disease-level resources (systematic reviews, narrative reviews, cohort studies) and case-based reviews; several sources are surgical-cohort based (histology from aortic resections) and thus reflect a selected population (patients undergoing major aortic surgery). (staniforth2024aortitisincreasesthe pages 1-2, bosch2023imagingindiagnosis pages 1-2, arcilla2025thegreatvasculitis pages 7-9)

2. Etiology

2.1 Major causal categories

  1. Noninfectious (immune-mediated) aortitis
  2. Large-vessel vasculitis: Giant cell arteritis (GCA), Takayasu arteritis (TAK), and variable-vessel vasculitis such as Behçet disease can involve the aorta/major branches. (popescu2024imaginginlarge pages 4-5)
  3. Clinically isolated aortitis (CIA): defined as aortitis without systemic vasculitis or other inflammatory conditions, often detected on histology after aortic surgery. (staniforth2024aortitisincreasesthe pages 1-2)

  4. IgG4-related periaortitis/aortitis is a distinct fibro-inflammatory entity (review evidence retrieved is 2025). (wang2025unravelingthecomplexity pages 6-7)

  5. Infectious aortitis

  6. Pathogens include Salmonella, Staphylococcus aureus, Streptococcus spp., Enterococcus, Haemophilus influenzae, Mycobacterium tuberculosis, Treponema pallidum, fungi, and others; infection can seed damaged aortic wall (e.g., atherosclerosis) with pseudoaneurysm formation and high rupture risk. (arcilla2025thegreatvasculitis pages 7-9, arcilla2025thegreatvasculitis pages 6-7)

  7. Drug-induced aortitis

  8. G-CSF–induced aortitis has been characterized through systematic case aggregation, particularly in chemotherapy settings. (zhao2024literaturereviewanalysis pages 1-2, zhao2024literaturereviewanalysis pages 5-7)

2.2 Risk factors

2.3 Protective factors

A bicuspid aortic valve was associated with lower likelihood of histologic aortitis in a surgical cohort (association, not necessarily causal protection). (staniforth2024aortitisincreasesthe pages 6-8)

2.4 Gene–environment interactions

Direct gene–environment interaction studies specific to “aortitis” were not retrieved. However, TAK genetic susceptibility (e.g., MLX variant; HLA associations) plausibly interacts with inflammatory triggers; infectious mimics can also induce autoantibodies and confound immune phenotyping. (tamura2018singlenucleotidepolymorphismof pages 6-7, arcilla2025thegreatvasculitis pages 7-9)

3. Phenotypes (with HPO suggestions)

Aortitis phenotypes vary by etiology and vascular territory involved. A curated phenotype-to-HPO mapping table is provided below.

Table (click to expand)
Phenotype (plain) HPO term(s) suggestion Evidence details (including onset/course, frequencies, quantitative lab values) Major etiologies/subtypes where seen Key citations (pqac ids)
Constitutional symptoms / malaise / fatigue / weight loss HP:0012378 Fatigue; HP:0004305 Malaise; HP:0001824 Weight loss Aortitis often presents nonspecifically with fatigue, feeling generally ill, and weight loss; GCA usually has gradual onset over weeks to months; TAK has a prodromal constitutional phase; IgG4-related PAO/PA also includes fatigue/weight loss/malaise; Behçet often relapsing-remitting General aortitis, GCA, TAK, IgG4-related aortitis, Behçet disease (staniforth2024aortitisincreasesthe pages 1-2, popescu2024imaginginlarge pages 4-5, wang2025unravelingthecomplexity pages 6-7)
Fever HP:0001945 Fever Fever is common in GCA and TAK constitutional phases; in G-CSF-induced aortitis, 68/72 (96%) were symptomatic, commonly with fever; mean temperatures around 38.6°C; infectious aortitis also commonly presents with systemic inflammatory illness GCA, TAK, G-CSF-induced aortitis, infectious aortitis (popescu2024imaginginlarge pages 4-5, zhao2024literaturereviewanalysis pages 5-7, arcilla2025thegreatvasculitis pages 7-9)
Pain (chest, back, abdominal, neck, sore throat) HP:0100749 Chest pain; HP:0002027 Abdominal pain; HP:0003418 Back pain; HP:0003202 Cervical pain G-CSF-induced aortitis commonly caused fever plus pain (chest, back, abdominal, neck, sore throat); IgG4-related PAO/PA commonly causes abdominal or back pain; thoracic involvement may cause chest pain and dyspnea G-CSF-induced aortitis, IgG4-related aortitis/periaortitis (zhao2024literaturereviewanalysis pages 5-7, wang2025unravelingthecomplexity pages 6-7)
Polymyalgia-type proximal stiffness HP:0002829 Arthralgia; HP:0003326 Myalgia Noninfectious aortitis may include polymyalgic symptoms with proximal shoulder/pelvic girdle stiffness; polymyalgia rheumatica co-occurs in 40–60% of GCA Noninfectious aortitis, especially GCA-associated aortitis (staniforth2024aortitisincreasesthe pages 1-2, popescu2024imaginginlarge pages 4-5)
Headache HP:0002315 Headache GCA cranial phenotype includes headache; onset usually gradual over weeks to months, though ~20% may be abrupt GCA-associated aortitis/large-vessel GCA (popescu2024imaginginlarge pages 4-5)
Jaw or tongue claudication HP:0200044 Jaw claudication Characteristic cranial ischemic symptom in GCA; occurs with chewing and supports cranial involvement in patients who may also have aortitis/large-vessel disease GCA-associated aortitis (popescu2024imaginginlarge pages 4-5)
Visual loss / ischemic optic neuropathy HP:0000572 Visual loss; HP:0000648 Optic atrophy (suggestive downstream term if chronic) In GCA, vascular occlusion can cause cranial ischemia and ischemic optic neuropathy; vision loss is typically painless and irreversible; ischemic optic neuropathy reported in ~14% in imaging review context GCA-associated aortitis/large-vessel GCA (popescu2024imaginginlarge pages 4-5)
Limb claudication / arm or leg claudication HP:0004936 Intermittent claudication Aortic or main-branch involvement in GCA can cause limb claudication; TAK vascular phase includes arm or leg claudication; IgG4 iliac/femoral disease can also cause claudication GCA, TAK, IgG4-related aortitis (popescu2024imaginginlarge pages 4-5, chan2025strokeaorticregurgitation pages 2-4, wang2025unravelingthecomplexity pages 6-7)
Pulseless vascular phase / pulse deficits HP:0031808 Abnormality of peripheral pulse TAK classically progresses from a constitutional “pre-pulseless” phase to a “pulseless” vascular phase with stenotic lesions in >90% TAK-associated aortitis (popescu2024imaginginlarge pages 4-5)
Hypertension HP:0000822 Hypertension Common in TAK (30–90%); IgG4-related renal artery involvement can also cause hypertension TAK, IgG4-related aortitis (popescu2024imaginginlarge pages 4-5, wang2025unravelingthecomplexity pages 6-7)
Stroke / transient ischemic attack HP:0001297 Stroke; HP:0002326 Transient ischemic attack TIAs/strokes occur in 2–7% of GCA and 10–20% of TAK; aortitis cohorts also report increased stroke risk during follow-up GCA, TAK, general aortitis complications (popescu2024imaginginlarge pages 4-5, staniforth2024aortitisincreasesthe pages 8-9)
Mucocutaneous ulcers HP:0000197 Oral ulcer; HP:0000135 Genital ulcer Behçet disease phenotype includes oral and genital ulcers with frequent relapses/remissions and potential large-vessel aortitis/aneurysm/thrombosis Behçet disease-associated aortitis (popescu2024imaginginlarge pages 4-5)
Uveitis / ocular inflammation HP:0000554 Uveitis Behçet disease includes uveitis as a key systemic phenotype accompanying possible large-vessel complications Behçet disease-associated aortitis (popescu2024imaginginlarge pages 4-5)
Thrombosis / occlusion HP:0004930 Venous thrombosis; HP:0012393 Arterial thrombosis; HP:0004417 Vascular occlusion Behçet large-vessel involvement may include thrombosis and occlusion; aortitis overall can cause stenosis/occlusion; infectious aortitis can present with pseudoaneurysm and occlusive thrombus Behçet disease, infectious aortitis, general aortitis (popescu2024imaginginlarge pages 4-5, staniforth2024aortitisincreasesthe pages 1-2, arcilla2025thegreatvasculitis pages 7-9)
Elevated CRP / ESR / inflammatory markers HP:0011227 Elevated C-reactive protein level; HP:0003565 Increased erythrocyte sedimentation rate Aortitis workup commonly shows high inflammatory markers; G-CSF-induced cases had CRP means ~26.06 ± 15.39 mg/dL (filgrastim), 24.81 ± 9.65 mg/dL (pegfilgrastim), 10.45 ± 9.91 mg/dL (lenograstim); giant cell aortitis case had CRP 82 mg/L and ESR 140 mm/h General aortitis, G-CSF-induced aortitis, giant cell aortitis case, IgG4-related aortitis (staniforth2024aortitisincreasesthe pages 1-2, zhao2024literaturereviewanalysis pages 5-7, chan2025strokeaorticregurgitation pages 2-4, wang2025unravelingthecomplexity pages 6-7)
Leukocytosis HP:0001974 Leukocytosis Reported as a common laboratory abnormality in infectious/inflammatory aortitis differential workup Infectious aortitis and mimics (arcilla2025thegreatvasculitis pages 7-9)
Thrombocytosis HP:0001873 Thrombocytosis Mild-to-moderate thrombocytosis reported in infectious/inflammatory aortitis differential workup Infectious aortitis and mimics (arcilla2025thegreatvasculitis pages 7-9)
Normocytic/normochromic anemia HP:0001877 Abnormality of erythrocytes; HP:0001892 Normocytic anemia Normochromic/normocytic anemia described among laboratory abnormalities in infectious/inflammatory aortitis evaluation Infectious aortitis and mimics (arcilla2025thegreatvasculitis pages 7-9)
Hypoalbuminemia HP:0003073 Hypoalbuminemia Reported among laboratory abnormalities in infectious/inflammatory aortitis differential workup Infectious aortitis and mimics (arcilla2025thegreatvasculitis pages 7-9)
Polyclonal hypergammaglobulinemia HP:0003237 Hypergammaglobulinemia Reported in inflammatory/infectious aortitis differential workup Infectious/inflammatory aortitis (arcilla2025thegreatvasculitis pages 7-9)
Aortic aneurysm HP:0002617 Aortic aneurysm A major downstream complication across aortitis subtypes. In surgical cohort, re-operations for new aneurysm formation were increased (14% with aortitis vs 3.8% without); GCA CT study reported >20% (12/54) developing aneurysm after 4–10 years; Behçet and infectious aortitis also associated with aneurysms General aortitis, GCA, Behçet, infectious aortitis, IgG4-related aortitis (staniforth2024aortitisincreasesthe pages 4-6, popescu2024imaginginlarge pages 7-9, popescu2024imaginginlarge pages 4-5, arcilla2025thegreatvasculitis pages 7-9, wang2025unravelingthecomplexity pages 6-7)
Aortic dissection HP:0002647 Aortic dissection Aortitis may present as dissection; G-CSF-induced review documented dissections among complications; giant cell aortitis case involved aneurysmal/root pathology; infectious/IgG4-related disease can also progress to dissection General aortitis, G-CSF-induced, giant cell aortitis, IgG4-related aortitis (staniforth2024aortitisincreasesthe pages 1-2, zhao2024literaturereviewanalysis pages 5-7, chan2025strokeaorticregurgitation pages 2-4, wang2025unravelingthecomplexity pages 6-7)
Stenosis / arterial narrowing / occlusion HP:0005290 Arterial stenosis; HP:0004417 Vascular occlusion Aortitis can cause wall thickening, loss of elasticity, stenosis, and occlusion; TAK has stenotic lesions in >90%; CTA shows luminal stenosis/narrowing General aortitis, TAK, infectious aortitis (staniforth2024aortitisincreasesthe pages 1-2, popescu2024imaginginlarge pages 4-5, popescu2024imaginginlarge pages 5-7)
Aortic regurgitation HP:0001659 Aortic valve regurgitation Case report of giant cell aortitis described severe aortic regurgitation with aortic root aneurysm and destructive transmural inflammation; MLX variant study in TAK linked severity with aortic regurgitation morbidity Giant cell aortitis case, Takayasu arteritis (chan2025strokeaorticregurgitation pages 2-4)
Dyspnea / compressive thoracic symptoms HP:0002094 Dyspnea Thoracic IgG4-related lesions may cause chest pain, dyspnea, and mediastinal compression; may reflect advanced local disease IgG4-related aortitis/periaortitis (wang2025unravelingthecomplexity pages 6-7)
Abdominal angina / bowel ischemia HP:0031106 Intestinal ischemia; HP:0002574 Abdominal pain Mesenteric involvement in IgG4-related disease may cause abdominal angina or bowel ischemia IgG4-related aortitis/periaortitis (wang2025unravelingthecomplexity pages 6-7)
Renal ischemia / hydronephrosis / renal injury HP:0000105 Renal insufficiency; HP:0000126 Hydronephrosis IgG4-related renal artery/periaortic involvement can cause ischemic nephropathy, post-obstructive hydronephrosis, and potentially permanent renal injury IgG4-related aortitis/periaortitis (wang2025unravelingthecomplexity pages 6-7)

Table: This table summarizes key clinical, laboratory, and complication phenotypes reported for aortitis across major etiologic subtypes, with suggested HPO mappings. It is useful for disease knowledge-base curation because it links observed features to onset/course details, frequencies where available, and source-backed evidence.

Key phenotype highlights with quantitative data (when available): - GCA: gradual onset over weeks–months (≈20% abrupt), cranial/constitutional symptoms; polymyalgia rheumatica in 40–60%; TIAs/strokes 2–7%; aortic/major branch involvement 27%. (popescu2024imaginginlarge pages 4-5) - TAK: constitutional phase → pulseless vascular phase; stenotic lesions >90%; aneurysms ≈25%; hypertension 30–90%; stroke/TIA 10–20%. (popescu2024imaginginlarge pages 4-5) - Behçet: large vascular involvement up to 40%; mortality ≈4%; frequent relapsing course. (popescu2024imaginginlarge pages 4-5) - G-CSF–induced aortitis: symptomatic in 96% (68/72); fever and pain common; CRP markedly elevated; blood cultures uniformly negative in the compiled case series. (zhao2024literaturereviewanalysis pages 5-7)

Quality-of-life measures (EQ-5D/SF-36/PROMIS) were not reported in the retrieved texts; QoL impact is inferred from chronicity/relapse and major vascular complications rather than quantified. (popescu2024imaginginlarge pages 4-5, staniforth2024aortitisincreasesthe pages 8-9)

4. Genetic / Molecular Information

4.1 Genetic susceptibility (human)

4.2 Mechanistic pathways and causal chains

  • TAK MLX-Q139R → inflammasome axis (primary research): MLX-Q139R increases MondoA–MLX activity, upregulates TXNIP, and promotes NLRP3 inflammasome activation with increased IL-1β, oxidative stress, and impaired autophagy (mTOR axis), supporting a causal chain from genotype to macrophage-driven vascular inflammation. (tamura2018singlenucleotidepolymorphismof pages 6-7, tamura2018singlenucleotidepolymorphismof pages 2-3)
  • GCA vascular immunopathology (review evidence retrieved is 2026): initiation includes activation of arterial-wall dendritic cells, T cell invasion enabled by monocyte-derived MMP-9, NETs, macrophage polarization, and tertiary lymphoid organ signals (CXCL13/BAFF/APRIL/LT-β), implicating innate and adaptive immune circuits and stromal remodeling. (muratore2026treatmentstrategiesin pages 29-33)

4.3 Suggested GO biological processes and CL cell types

(These are suggested ontology mappings based on mechanisms described in retrieved sources.) - GO terms (suggested): inflammatory response; granulomatous inflammatory response; leukocyte migration; cytokine-mediated signaling pathway; inflammasome complex assembly; autophagy; extracellular matrix organization; angiogenesis/neovascularization. (popescu2024imaginginlarge pages 4-5, tamura2018singlenucleotidepolymorphismof pages 6-7, muratore2026treatmentstrategiesin pages 29-33) - CL terms (suggested): macrophage / monocyte-derived macrophage; CD4-positive T cell; CD8-positive T cell; dendritic cell (arterial wall); neutrophil; B cell; vascular endothelial cell; vascular smooth muscle cell; fibroblast. (tamura2018singlenucleotidepolymorphismof pages 6-7, muratore2026treatmentstrategiesin pages 29-33)

5. Environmental Information

5.1 Infectious agents

Infectious aortitis pathogens frequently cited include Salmonella, Staphylococcus aureus, Streptococcus spp., Enterococcus, Haemophilus influenzae, Mycobacterium tuberculosis, Treponema pallidum, fungi, and others. (arcilla2025thegreatvasculitis pages 7-9, arcilla2025thegreatvasculitis pages 6-7)

5.2 Drug exposure

G-CSF exposure (notably pegfilgrastim) is associated with rare aortitis, most commonly presenting within days after dosing in the compiled case series (agent-dependent mean onset times). (zhao2024literaturereviewanalysis pages 5-7)

Lifestyle/environmental risks (e.g., smoking) were associated with surgical-cohort aortitis risk. (staniforth2024aortitisincreasesthe pages 6-8)

6. Mechanism / Pathophysiology

6.1 Upstream-to-downstream causal chain (integrated)

Aortitis pathophysiology can be summarized as: 1. Trigger/etiology (autoimmune LVV, infection, drug-induced immune activation) → 2. Aortic wall inflammation (granulomatous inflammation in GCA/TAK; neutrophil-predominant infiltration in infection; IgG4+ lymphoplasmacytic infiltration with storiform fibrosis in IgG4-RD) → 3. Structural remodeling (intimal hyperplasia, neovascularization, fibrosis; medial degradation) → 4. Clinical consequences: aneurysm, dissection, stenosis/occlusion, ischemia, stroke, valve involvement (aortic regurgitation), rupture. (popescu2024imaginginlarge pages 4-5, arcilla2025thegreatvasculitis pages 7-9, wang2025unravelingthecomplexity pages 6-7, staniforth2024aortitisincreasesthe pages 1-2)

6.2 Tissue damage mechanisms

7. Anatomical Structures Affected

7.1 Organ/system level

7.2 Suggested UBERON terms (not exhaustive; suggestions)

8. Temporal Development

9. Inheritance and Population

9.1 Epidemiology (selected quantitative data from retrieved sources)

9.2 Population/sex patterns

10. Diagnostics

10.1 Laboratory evaluation (common elements)

10.2 Imaging: current standards and performance

EULAR 2023 evidence base (systematic review/meta-analysis) for GCA imaging: - Ultrasound, MRI, and FDG-PET have “good performance” for GCA diagnosis; in low risk-of-bias studies, ultrasound sensitivity/specificity 88% / 96% and pooled LR+ 20.07, LR− 0.13. (bosch2023imagingindiagnosis pages 3-4) - Ultrasound assessing both cranial and extracranial arteries improves sensitivity (93% vs 80%) with similar specificity. (bosch2023imagingindiagnosis pages 1-2) - FDG-PET pooled sensitivity/specificity reported as 76% / 95% (context: GCA imaging studies in the SLR). (bosch2023imagingindiagnosis pages 1-2)

Practical CTA/MRI/PET criteria from narrative imaging review (2024): - Active inflammation suggested by wall thickening >2 mm (aorta) and >1 mm (branch vessels) on CTA/MRI. (popescu2024imaginginlarge pages 7-9) - Arterial wall enhancement defined as >20 HU increase compared to unenhanced CT. (popescu2024imaginginlarge pages 7-9) - PET positivity criterion: segmental FDG uptake ≥ liver. (popescu2024imaginginlarge pages 7-9)

FDG-PET/CT in clinical practice (2023 review): - For cranial artery involvement (when performed before/≤72h after glucocorticoids), sensitivity 82–92% and specificity 85–100% reported. (nassarmadji202318fluorodeoxyglucosepositronemission pages 1-2)

10.3 Histopathology

10.4 Differential diagnosis

A key diagnostic principle is to exclude infection and malignancy before immunosuppression; infectious aortitis can induce autoantibodies (ANCA/MPO/PR3), mimicking primary vasculitis. (arcilla2025thegreatvasculitis pages 6-7, arcilla2025thegreatvasculitis pages 7-9)

11. Outcome / Prognosis

  • Surgical cohort outcomes: aortitis increased re-operation risk; re-operation rate was roughly doubled (17.5% vs 9.4%). (staniforth2024aortitisincreasesthe pages 1-2)
  • Long-term complications: vascular stenosis, stroke risk, and new aneurysm formation are emphasized, with cited studies reporting 58% 5-year vascular complication rates in a French series and new aneurysm development in CIA cohorts (as cited in the surgical paper). (staniforth2024aortitisincreasesthe pages 8-9)
  • Infectious aortitis: high mortality noted for thoracic infectious aortitis (reported up to 30–50% in a case-based review). (arcilla2025thegreatvasculitis pages 1-3)

12. Treatment

12.1 Noninfectious/CIA and LVV-associated aortitis

  • Center practice regimen (CIA/noninfectious): prednisolone 0.75–1 mg/kg plus methotrexate 20–25 mg/week; refractory cases may use pulsed IV cyclophosphamide 15 mg/kg; tocilizumab 162 mg SC weekly used for relapsing/refractory disease after failure of two conventional strategies. (staniforth2024aortitisincreasesthe pages 8-9)

  • Tocilizumab real-world effectiveness (extracranial GCA/LV-GCA and TAK; 2025 observational): at 12 months, remission 74.5% (LV-GCA) and 76.9% (TAK); imaging-complete resolution only 18.9% and 21.1%, respectively; severe infections led to discontinuation in 4 LV-GCA and 3 TAK patients. (lasateja2025tocilizumabinextracranial pages 1-2)

  • GC + TCZ RCT benchmark (GiACTA; summarized in 2024 trial protocol): sustained remission at 52 weeks 56%/53% (weekly/q2w TCZ) vs 14%/18% (GC alone). (kreis2024themeteoriticstrial pages 1-2)

12.2 Infectious aortitis

  • Early empiric broad-spectrum antibiotics covering Gram-positive cocci and Gram-negative rods; ampicillin/cephalosporins suggested empirically for Salmonella; prolonged therapy often required (≥6–8 weeks), especially with endovascular repair; surgery/endovascular (TEVAR/EVAR) indicated for rapid expansion/large aneurysm but with infection-related complication risk. (arcilla2025thegreatvasculitis pages 7-9)

12.3 MAXO term suggestions (examples)

13. Prevention

Evidence retrieved is limited. Practical prevention/mitigation approaches include: - Secondary prevention of complications via long-term surveillance imaging (annual CT aortogram ≥5 years in one center protocol) and cardiovascular risk modification measures (statins, beta-blockers, ACE inhibitors, antithrombotics) used in clinical practice. (staniforth2024aortitisincreasesthe pages 8-9) - For biologic therapy: TB screening (PPD/QuantiFERON, chest X-ray) and isoniazid prophylaxis for latent infection before biologics in one multicenter observational practice description. (lasateja2025tocilizumabinextracranial pages 2-4)

14. Other Species / Natural Disease

No retrieved evidence in this run addressed naturally occurring aortitis across non-human species or zoonotic considerations.

15. Model Organisms

No direct “aortitis model organism” papers were retrieved in this run. Mechanistic TAK genetics work used immune cell systems and vascular cells (e.g., PBMC-derived macrophages; human aortic smooth muscle cells) supporting in vitro mechanistic modeling. (tamura2018singlenucleotidepolymorphismof pages 6-7)

Recent developments (priority 2023–2024)

  1. Imaging evidence synthesis informing EULAR 2023 update: pooled diagnostic performance metrics for ultrasound/MRI/FDG-PET in GCA and evidence supporting inclusion of extracranial (axillary) ultrasound to increase sensitivity. (Aug 2023; https://doi.org/10.1136/rmdopen-2023-003379) (bosch2023imagingindiagnosis pages 1-2, bosch2023imagingindiagnosis pages 3-4)
  2. High-sampling surgical cohort redefining CIA prevalence and postoperative risk: histology-sampled prevalence 10.6% with 75% CIA; higher re-operation risk and identified risk associations (age, female sex, smoking, inflammatory disease). (Dec 2024; https://doi.org/10.3390/jcdd11120405) (staniforth2024aortitisincreasesthe pages 1-2, staniforth2024aortitisincreasesthe pages 6-8, staniforth2024aortitisincreasesthe media bd38afdc)
  3. Drug-induced aortitis (G-CSF) systematic case synthesis: 72-case dataset describing demographics, lesion distribution, complication rate (~4.2%), and recurrence on rechallenge, emphasizing diagnostic vigilance. (Dec 2024; https://doi.org/10.3389/fphar.2024.1487501) (zhao2024literaturereviewanalysis pages 1-2, zhao2024literaturereviewanalysis pages 5-7)

Key quantitative summary table (etiology/risk statistics)

Table (click to expand)
Category Typical patient profile Key statistics Diagnostic clues (labs/imaging) Notes/quotes Key citations
Noninfectious: overall surgically identified aortitis / clinically isolated aortitis (CIA) Often older adults; more common in women; associated with smoking and prior inflammatory disease; many cases asymptomatic until aneurysm/dissection surgery In a major aortic surgery cohort, histology-confirmed aortitis prevalence was 10.6% (57/537); 75% of aortitis cases were CIA; CIA prevalence 8.0% (43/537); re-operation 17.5% vs 9.4% in non-aortitis; multivariable associations: age OR 1.03, female sex OR 4.10, current smoking OR 3.43, prior inflammatory disease OR 9.01; bicuspid aortic valve associated with lower odds OR 0.34 Elevated inflammatory markers; PET-CT to map inflammation; intra-operative histology is essential; annual CT aortogram suggested in follow-up “Aortitis, defined as inflammation of the aorta”; “75% were clinically isolated” (staniforth2024aortitisincreasesthe pages 1-2, staniforth2024aortitisincreasesthe pages 6-8, staniforth2024aortitisincreasesthe media bd38afdc)
Noninfectious: giant cell arteritis (GCA)-associated aortitis Usually adults >50 years; Northern European populations higher incidence; can coexist with PMR; risk factors for aneurysmal complications include male sex, smoking, hypertension, hyperlipidemia/coronary disease GCA incidence about 44/100,000 persons >50 in Northern Europe; aorta or major branch involvement in about 27% of GCA; in large-vessel GCA, aortic involvement 45–65%; thoracic aortic aneurysm/dissection incidence reported 8.2–33%; meta-analysis suggests ~3-fold increased TAA risk; one cohort found 3.1% TAA among 2,344 GCA patients; >20% (12/54) developed aortic aneurysm after 4–10 years in one CT study CTA/MRA/PET-CT/US; CTA/MRI wall-thickness thresholds suggesting active disease: >2 mm aorta, >1 mm branch vessels; PET uptake may identify higher-risk patients for future aneurysm “a granulomatous vasculitis”; “Imaging is essential”; “The literature review disclosed an increased incidence and relative risk of TAA among patients with GCA” (popescu2024imaginginlarge pages 4-5, strachan2025thoracicaorticaneurysm pages 2-4, popescu2024imaginginlarge pages 7-9, popescu2024imaginginlarge pages 1-2)
Noninfectious: Takayasu arteritis (TAK)-associated aortitis Typically younger individuals; often women; systemic large-vessel vasculitis affecting aorta and branches Annual incidence 0.4–3.4 per 1,000,000; TAK is “the primary cause of aortitis in younger individuals”; aorta/major branches involved in about 65%; coronary arteries 44%; pulmonary arteries 63%; stenotic lesions in >90%; aneurysms in about 25%; hypertension 30–90%; stroke/TIA 10–20% MRI first-line in suspected TAK; CTA shows circumferential wall thickening in active disease, later stenosis/occlusion; PET-CT can complement luminal imaging by showing active inflammation “characterized by variable degrees of inflammation... of all arterial layers (panarteritis)” (popescu2024imaginginlarge pages 4-5, popescu2024imaginginlarge pages 7-9, popescu2024imaginginlarge pages 1-2)
Noninfectious: Behçet disease-associated aortitis/large-vessel vasculitis Often younger to middle-aged adults; autoinflammatory/systemic vasculitis phenotype; HLA-B51 association noted in review Up to 40% may experience large vascular complications; mortality around 4% CTA/MRA/PET-CT/US depending territory; evaluate aneurysm, thrombosis, arterial wall inflammation “mainly considered an auto-inflammatory systemic vasculitis” (popescu2024imaginginlarge pages 4-5)
Noninfectious: drug-induced aortitis (G-CSF-associated) Predominantly older women receiving chemotherapy; especially breast cancer; also reported in healthy stem-cell donors; majority reported from Asian populations Review of 72 patients: 58 female/14 male (80.6% female), mean age 61.83 ± 10.30 years; pegfilgrastim implicated most often (63.4%); lesion distribution: aortic arch 36.11%, abdominal aorta 26.39%, thoracic aorta 22.22%; 4/72 asymptomatic; complications in 3/72 (~4.2%) including dissection/aneurysm; recurrence after rechallenge reported Typically fever/pain with elevated CRP and negative blood cultures; CT most often identifies aortic arch/branch involvement “Most patients had a good prognosis, but 3 cases developed complications”; “G-CSF-induced aortitis was also found in 4 asymptomatic patients” (zhao2024literaturereviewanalysis pages 1-2, zhao2024literaturereviewanalysis pages 5-7, zhao2024literaturereviewanalysis pages 7-8, zhao2024literaturereviewanalysis pages 2-3)
Infectious aortitis: overall bacterial/fungal/mycobacterial/spirochetal Often patients with atherosclerosis, damaged vessel wall, immunosuppression, infection, trauma, congenital abnormalities, or malignancy; may present with aneurysm, pseudoaneurysm, or sepsis-like syndrome Thoracic aortitis mortality reported 30–50%; blood cultures positive in only 50–82%; mycotic aneurysms account for 0.6–2% of all aortic aneurysms in Western populations; infectious aortitis more often abdominal (56% in cited series) Labs: leukocytosis, thrombocytosis, normocytic anemia, elevated inflammatory markers/CRP (often >100 mg/L in cited review); imaging: CTA/MRA/PET-CT/US; infected aneurysm clues include saccular morphology, peri-aortic edema/fat stranding, wall thickening, loss of contour, gas in wall “Differentiating between infectious and inflammatory cases is crucial”; “blood cultures (positive in only 50% to 82%) are recommended” (arcilla2025thegreatvasculitis pages 7-9, arcilla2025thegreatvasculitis pages 1-3, arcilla2025thegreatvasculitis pages 6-7)
Infectious aortitis: common pathogens / microbiology Bacterial predominance; consider bacteremia/endovascular seeding via vasa vasorum or damaged wall Gram-positive organisms about 44% in one review; Gram-negative rods 33%; intracellular/fastidious organisms 43%; Cox review notes Gram-positive bacteria account for about 60% of thoracic infections; common pathogens include Staphylococcus aureus, Streptococcus spp., Enterococcus, Salmonella, Haemophilus influenzae, Mycobacterium tuberculosis, Treponema pallidum, fungi Obtain repeated blood cultures, tissue culture/PCR/serologies; histology often shows neutrophilic infiltration; CTA/PET-CT used to define extent and plan intervention “Gram positive bacteria such as Staphylococcus, Enterococcus and Streptococcus accounting for approximately 60% of the infections” (arcilla2025thegreatvasculitis pages 7-9, arcilla2025thegreatvasculitis pages 6-7)
Infectious aortitis: management-relevant clues Patients may initially mimic primary vasculitis; wrong early immunosuppression can be harmful No large comparative trials; prolonged antibiotics typically at least 6–8 weeks with TEVAR/EVAR/open repair depending anatomy and infection control Broad-spectrum bactericidal therapy first; defer steroids/biologics until infection excluded; CTA gives high-resolution 3D anatomy, PET may help distinguish infection/inflammation and occult extent “Steroids and biological therapy were held until comprehensive investigations were completed”; “optimal approach must be decided on a case-by-case basis” (arcilla2025thegreatvasculitis pages 7-9, arcilla2025thegreatvasculitis pages 6-7)

Table: This table summarizes major noninfectious and infectious aortitis categories, highlighting patient profiles, quantitative epidemiology, diagnostic clues, and brief source-supported notes from the current evidence set. It is designed as a compact reference for comparing causes of aortitis and the numbers most relevant to diagnosis and risk stratification.

Real-world implementations / workflows

  • Surgical pathology workflow: routine intra-operative aortic sampling can uncover aortitis/CIA otherwise missed, changing follow-up intensity and rheumatology referral patterns. (staniforth2024aortitisincreasesthe pages 1-2)
  • Clinical imaging workflow: many centers increasingly integrate FDG-PET with CTA/MRA/US for LVV/aortitis assessment; reimbursement changes (CMS 2021) and guideline incorporation have accelerated PET use in some health systems. (ahlman2023advancedmolecularimaging pages 1-2)
  • Long-term monitoring: annual CT aortogram surveillance for at least 5 years after diagnosis is used in at least one specialized center pathway for CIA/noninfectious aortitis. (staniforth2024aortitisincreasesthe pages 8-9)

Items requested but not fully retrievable in this run

  • MONDO/Orphanet/ICD-10/ICD-11/MeSH identifiers: not present in retrieved full texts. (staniforth2024aortitisincreasesthe pages 9-11, staniforth2024aortitisincreasesthe pages 2-4)
  • PMIDs preferred: Several retrieved items are identified by DOI within text extracts but PMIDs were not consistently present in the extracted evidence snippets; therefore, DOI-based URLs are provided where available.
  • Model organism literature and cross-species natural disease: not retrieved.

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