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Sarcoidosis

1. Disease Information

2026-04-26
Falcon MONDO:0019338 Model: Edison Scientific Literature 62 citations

1. Disease Information

1.1 Definition and overview

Sarcoidosis is described as a complex multisystem immune-mediated disorder in which inflammatory cells accumulate and organize into non-caseous granulomas within affected organs (kim2024advancesincellular pages 1-5). A recent immunopathogenesis review defines it as “a granulomatous disease of unknown cause, triggered by an unidentified antigen,” with the histopathologic hallmark being “discrete, well-formed, non-necrotizing granulomas composed of epithelioid histiocytes and multinucleated giant cells surrounded by lymphocytes, plasma cells, and fibroblasts” (vagts2025immunopathogenesisofsarcoidosis pages 1-2).

1.2 Key identifiers (with availability in retrieved sources)

  • MONDO: MONDO:0019338 (Open Targets disease object) (he2025globalburdenof pages 1-2).
  • ICD-10: D86–D86.2, D86.9 (used in GBD-based epidemiologic analysis for case definition) (he2025globalburdenof pages 1-2).
  • MeSH / ICD-11 / Orphanet / OMIM (disease entry): Not directly retrievable from the current evidence set; additional database-specific queries (MeSH Browser, ICD-11, Orphanet, OMIM) would be required for authoritative IDs.

1.3 Synonyms / alternative names

The retrieved sources primarily use “sarcoidosis” and organ qualifiers (pulmonary sarcoidosis, extrapulmonary sarcoidosis, muscular sarcoidosis). Formal synonym lists were not present in the extracted texts; common clinical variants highlighted include Löfgren syndrome (acute presentation) (weeratunga2024immunemechanismsof pages 1-2, vagts2025immunopathogenesisofsarcoidosis pages 1-2).

1.4 Evidence provenance

This report synthesizes aggregated disease-level resources (reviews, meta-analyses, registry cohorts, and clinical trial registries), not individual EHR case notes, except where cohorts explicitly derive from health-system databases (e.g., Clalit) (patt2024elevatedmortalityrisk pages 1-2, patt2024elevatedmortalityrisk pages 2-3).

2. Etiology

2.1 Causal factors (current consensus)

Sarcoidosis etiology remains unknown; leading models invoke a triggering antigen in a genetically predisposed host leading to persistent immune activation and granuloma formation (vagts2025immunopathogenesisofsarcoidosis pages 1-2, papanikolaou2025phenotypesandendotypes pages 4-6).

2.2 Genetic risk factors (susceptibility/severity loci)

A 2023 integrated GWAS–eQTL approach (European and African ancestry cohorts) reported that dysregulated innate immunity and MHC-related pathways are implicated in sarcoidosis risk/severity and validated loci including NOTCH4, IL27RA, BTNL2, ANXA11, and HLA-DRB1 (doi:10.31488/ejrm.137) (casanova2023examinationofeqtl pages 1-3). This supports a polygenic architecture with strong immunogenetic involvement.

Ontology (gene) suggestions: HGNC symbols: BTNL2, ANXA11, HLA-DRB1, NOTCH4, IL27RA (casanova2023examinationofeqtl pages 1-3).
Mechanism linkage: antigen presentation / MHC class II and innate immune response pathways (casanova2023examinationofeqtl pages 1-3, papanikolaou2025phenotypesandendotypes pages 4-6).

2.3 Environmental and infectious risk factors

The retrieved mechanistic phenotype/endotype review notes infectious agents such as Mycobacterium species and Propionibacterium acnes as implicated candidates and describes innate immune sensing via TLR pathways in antigen presentation contexts (papanikolaou2025phenotypesandendotypes pages 4-6). (This reflects hypothesized triggers; causal proof is not established.)

2.4 Protective factors

A protective-factor evidence base was not directly extractable from the retrieved documents.

2.5 Gene–environment interactions

Direct GxE effect sizes were not provided in the retrieved evidence set.

3. Phenotypes (clinical manifestations)

3.1 Core clinical phenotype domain

Sarcoidosis has heterogeneous organ involvement. The lungs dominate clinical burden, with pulmonary/intrathoracic involvement reported up to ~90–95% across sources (kim2024advancesincellular pages 1-5, vagts2025immunopathogenesisofsarcoidosis pages 1-2, baratella2025ctimagingfeatures pages 1-3). Extrapulmonary involvement is common, with review-level estimates of ~30–50% (starshinova2024chronicsarcoidosisdiagnostic pages 2-3).

3.2 Example organ involvement frequencies (from retrieved sources)

From a 2024 chronic sarcoidosis review: extrapulmonary disease ~30–50%, with reported organ frequencies including cutaneous 15.9%, ocular 11.8%, and neurologic 4.6% (starshinova2024chronicsarcoidosisdiagnostic pages 2-3). Ocular complications include posterior uveitis (5–28% of ocular cases), panuveitis (up to 48%), retinal vasculitis (18%), and retinal neovascularization (1–5%) (starshinova2024chronicsarcoidosisdiagnostic pages 14-15).

3.3 Onset and course (high-level)

Löfgren syndrome is emphasized as an acute presentation that often resolves: about 80% resolution within 2 years in one review (weeratunga2024immunemechanismsof pages 1-2). Chronic/progressive disease is described in “approximately 10 to 40%” in an immunopathogenesis review excerpt (vagts2025immunopathogenesisofsarcoidosis pages 1-2).

3.4 Quality of life

Quality-of-life measures are explicitly emphasized in modern care frameworks (e.g., fatigue and health status instruments appear as key outcomes in treatment considerations) (dhanani2025immunosuppressivetherapiesin pages 3-4, dhanani2025immunosuppressivetherapiesin pages 10-12). Disease-associated fatigue is a major patient-reported concern; however, standardized QoL effect sizes were not extractable from the retrieved passages.

3.5 HPO term suggestions (non-exhaustive; mapped to retrieved phenotype domains)

(These are ontology suggestions; frequency and exact mapping should be validated against HPO definitions and organ-specific sarcoidosis cohorts.)

4. Genetic/Molecular Information

4.1 “Causal genes” vs susceptibility genes

Sarcoidosis is generally treated as complex/polygenic rather than a classic monogenic disorder. The retrieved evidence supports susceptibility and severity loci (e.g., HLA region, BTNL2, ANXA11, NOTCH4, IL27RA) rather than single-gene causality (casanova2023examinationofeqtl pages 1-3).

4.2 Pathogenic variants (status in retrieved evidence)

Specific variant nomenclature (HGVS) and ClinVar classifications were not present in extracted content; therefore, variant-level curation (pathogenic/likely pathogenic/VUS) cannot be completed from this evidence set.

4.3 Modifier genes / severity genetics

The integrated eQTL/GWAS severity analysis suggests multiple loci and pathways associated with complicated/progressive disease, emphasizing innate immunity and MHC class II involvement (casanova2023examinationofeqtl pages 1-3).

4.4 Epigenetic information

No direct methylation/histone modification datasets were extractable from the retrieved excerpts.

5. Environmental Information

The retrieved sources emphasize possible environmental/occupational and infectious triggers at a conceptual level, but do not provide a curated list of exposures with quantitative risk estimates in the available passages (papanikolaou2025phenotypesandendotypes pages 4-6).

6. Mechanism / Pathophysiology

6.1 Causal chain (trigger → granuloma → organ dysfunction)

A coherent mechanistic chain described across sources is: 1) Triggering antigen/exposure in a susceptible host →
2) Antigen presentation by macrophages/dendritic cells via MHC-II and innate sensing (e.g., TLR-related pathways) →
3) CD4+ T-cell polarization and cytokine production (classically IFN-γ; Th1/Th17/Th17.1) →
4) Macrophage differentiation into epithelioid cells and multinucleated giant cells, organizing granulomas →
5) Either resolution or persistence with tissue remodeling/fibrosis and organ impairment (lung restriction, DLCO decline), with potential extrapulmonary damage (vagts2025immunopathogenesisofsarcoidosis pages 1-2, papanikolaou2025phenotypesandendotypes pages 4-6).

6.2 Key immune pathways and cell types (with ontology suggestions)

Dominant immune phenotype: IFN-γ/Th1 with Th17/Th17.1 contributions (vagts2025immunopathogenesisofsarcoidosis pages 1-2, papanikolaou2025phenotypesandendotypes pages 4-6).

Granuloma cellular composition: macrophages/epithelioid cells/giant cells with surrounding lymphocytes; monocytes/neutrophils/fibroblasts can contribute (weeratunga2024immunemechanismsof pages 1-2, kim2024advancesincellular pages 1-5).

Ontology suggestions: * GO (biological processes): antigen processing and presentation (MHC class II), T cell activation, cytokine-mediated signaling pathway, granuloma formation, extracellular matrix organization, fibrosis. * CL (cell types): CL:0000540 (macrophage), CL:0000624 (CD4-positive, alpha-beta T cell), fibroblast, dendritic cell.

6.3 Recent developments (2023–2024 priority): single-cell / spatial / metabolic mechanisms

(a) Macrophage metabolic reprogramming and PPP (JCI 2023): A 2023 JCI study using single-cell RNA-seq in sarcoidosis reported an increase of TREM2-positive macrophages expressing ACE and lysozyme in cutaneous sarcoidosis granulomas and found macrophages to be “hypermetabolic,” particularly with activation of the pentose phosphate pathway (PPP); PPP enzyme expression (e.g., FBP1) was elevated in lesions and serum, and PPP inhibitors attenuated granuloma formation in in vitro and murine models—supporting PPP as a potential therapeutic target (doi:10.1172/jci171088) (dhanani2025immunosuppressivetherapiesin pages 10-12).

(b) Spatial transcriptomics in muscular sarcoidosis (Cells 2023): Spatial transcriptomics of two muscular sarcoidosis patients identified transcriptomic clusters spanning granuloma/perigranuloma and surrounding muscle. Granuloma regions showed immune activation (T-lymphocyte and monocyte/macrophage cytokines), while perigranuloma showed extracellular matrix and TGF-β signaling signatures. Proximity to granuloma correlated with stronger interferon/TNF/IL-1/IL-4/IL-6 response signatures and fibrotic replacement signals (doi:10.3390/cells12232747) (starshinova2024chronicsarcoidosisdiagnostic pages 26-27).

(c) High-resolution granuloma interrogation (JCI Review 2024): A 2024 JCI review highlights that “recent high-resolution studies of the granuloma in situ” using single-cell and spatial methods are clarifying plausible mechanisms in sarcoidosis and enabling comparative analysis with tuberculosis granulomas (doi:10.1172/jci175264) (weeratunga2024immunemechanismsof pages 1-2).

6.4 Imaging/biopsy advances linked to mechanism

A 2024 review of imaging and tissue-based methods emphasizes advanced approaches such as spatial transcriptomics and MALDI mass spectrometry imaging to map granuloma biochemistry and spatial organization (doi:10.1152/ajpcell.00507.2023) (kim2024advancesincellular pages 1-5).

7. Anatomical Structures Affected

7.1 Organ-level involvement

Most commonly affected: lungs and intrathoracic lymph nodes (up to ~90–95%) (kim2024advancesincellular pages 1-5, baratella2025ctimagingfeatures pages 1-3). Common extrapulmonary targets include skin, eyes, and heart, with neurologic and renal involvement less frequent but clinically high impact (kim2024advancesincellular pages 1-5, starshinova2024chronicsarcoidosisdiagnostic pages 2-3).

7.2 UBERON suggestions (non-exhaustive)

8. Temporal Development

9. Inheritance and Population

9.1 Epidemiology (incidence, prevalence, demographics)

Population ranges and geographic variation: * Reported prevalence ~4.7–64 per 100,000 and incidence ~1–35.5 per 100,000/year in a recent registry paper’s contextual epidemiology discussion (guttmannducke2025firstinsightsand pages 1-2).
Marked geographic differences: Scandinavia/UK ~64 per 100,000 and African American populations ~39 per 100,000, compared with South Korea 4.67 and Japan 3.7 per 100,000* (kim2024advancesincellular pages 1-5).

Example real-world registry demographics: * Vienna registry (2022–2023; n=199): mean age 52±13, women 57.5%; chest X-ray stage distribution 1:34.5%, 2:46%, 3:9.5%, 4:6% (guttmannducke2025firstinsightsand pages 1-2).

9.2 Genetic architecture / inheritance

Evidence supports polygenic susceptibility (HLA and non-HLA loci), rather than Mendelian inheritance, consistent with multifactorial disease (casanova2023examinationofeqtl pages 1-3).

10. Diagnostics

10.1 Diagnostic criteria (core consensus)

A 2024 review explicitly states diagnosis is based on three main criteria: (1) clinical presentation, (2) histologic detection of non-caseating granulomas in ≥1 tissue sample, and (3) exclusion of alternative granulomatous diseases (starshinova2024chronicsarcoidosisdiagnostic pages 2-3). A 2025 PET/CT meta-analysis similarly describes accepted diagnosis requiring compatible clinical picture, radiologic evidence, and histologic demonstration of non-necrotising granulomatous disease (donnelly2025metaanalysisof[18f]fdgpetct pages 1-2).

10.2 Histopathology

Granulomas are composed largely of macrophage-derived epithelioid and giant cells with surrounding lymphocytes (kim2024advancesincellular pages 1-5, starshinova2024chronicsarcoidosisdiagnostic pages 14-15).

10.3 Laboratory tests / biomarkers

Supportive biomarkers include: * Serum ACE (produced by monocytes/macrophages/epithelioid cells) reported to correlate with granuloma burden and radiologic stages II–III and may reflect activity/extrathoracic involvement (starshinova2024chronicsarcoidosisdiagnostic pages 15-17, starshinova2024chronicsarcoidosisdiagnostic pages 14-15).
Soluble IL-2 receptor (sIL-2R) as a marker of Th1 activation; may predict progression/relapse (starshinova2024chronicsarcoidosisdiagnostic pages 15-17).
 Hypercalcemia with low PTH and normal/low 25-hydroxyvitamin D can occur (starshinova2024chronicsarcoidosisdiagnostic pages 15-17, starshinova2024chronicsarcoidosisdiagnostic pages 14-15).

BAL findings may show lymphocytosis (>15%) and CD4/CD8 ≥3.5 but are not specific (starshinova2024chronicsarcoidosisdiagnostic pages 15-17).

10.4 Imaging

HRCT: preferred over CXR for sensitivity and evaluation of complications (baratella2025ctimagingfeatures pages 3-4, baratella2025ctimagingfeatures pages 1-3).
FDG-PET/CT: a 2025 meta-analysis (search through Sep 2023) reported pooled sensitivity 0.971 and specificity 0.873 for suspected pulmonary sarcoidosis; SUVmax reduction correlated with improved FVC and DLCO and may help guide immunosuppression decisions (doi:10.1007/s00330-024-10949-4) (donnelly2025metaanalysisof[18f]fdgpetct pages 1-2).

10.5 Differential diagnosis

Imaging reviews stress differentiation from tuberculosis, silicosis, malignancy, organizing pneumonia, hypersensitivity pneumonitis, etc., and emphasize integrating clinical/radiologic/pathologic evidence with exclusion of alternatives (baratella2025ctimagingfeatures pages 1-3).

11. Outcome / Prognosis

11.1 Mortality and survival (recent real-world estimates)

A 2024 population-based cohort study (Clalit Health Services; incident cases 2000–2016) reported higher mortality in sarcoidosis than controls (17.7% vs 10.6%), with adjusted all-cause mortality HR 1.79 (95% CI 1.64–1.96) and the highest hazard in the first year post-diagnosis (patt2024elevatedmortalityrisk pages 1-2). Another excerpt reports first-year multivariable HR 2.99 (95% CI 2.39–3.75), and persistent but lower hazards thereafter (patt2024elevatedmortalityrisk pages 8-9). Predictors included age at diagnosis, male sex, and comorbidity burden (patt2024elevatedmortalityrisk pages 1-2, patt2024elevatedmortalityrisk pages 8-9).

11.2 Prognostic functional markers

Imaging-focused reviews highlight functional thresholds associated with progression/response such as ≥5% decline in FVC and ≥10% decline in DLCO, and note that fibrosis extent (e.g., >20% parenchymal fibrosis on CT) correlates with worse outcomes (baratella2025ctimagingfeatures pages 3-4).

12. Treatment

12.1 Current standard pharmacotherapy (guideline-aligned approach)

A practical evidence-based review states oral glucocorticoids remain first-line for symptomatic pulmonary sarcoidosis (typical starting prednisone 20–40 mg/day) with tapering over 6–18 months guided by response; steroid-sparing agents are often required due to toxicity (doi:10.3390/jcm14196828) (dhanani2025immunosuppressivetherapiesin pages 1-3). Second-line agents include methotrexate (preferred), azathioprine, leflunomide, and mycophenolate; refractory disease options include anti-TNF agents (infliximab, adalimumab) and emerging approaches such as JAK inhibitors, rituximab, and repository corticotropin injection (RCI) (dhanani2025immunosuppressivetherapiesin pages 3-4, dhanani2025immunosuppressivetherapiesin pages 10-12).

MAXO suggestions (non-exhaustive): glucocorticoid therapy; methotrexate therapy; TNF inhibitor therapy; antifibrotic therapy; immunosuppressive therapy; JAK inhibitor therapy.

12.2 Recent developments (high-priority evidence)

Methotrexate as first-line alternative (NEJM 2025): In the PREDMETH noninferiority trial (NCT04314193), methotrexate was noninferior to prednisone for 24-week improvement in % predicted FVC (+6.11 vs +6.75 points); adverse event profiles differed (doi:10.1056/NEJMoa2501443) (kahlmann2025firstlinetreatmentof pages 1-2). This is a major development supporting steroid-minimizing strategies.

12.3 Biologics and advanced immunomodulators

Infliximab (anti-TNF): ClinicalTrials.gov record NCT00073437 describes a multicenter Phase 3 randomized, double-blind, placebo-controlled trial (n=139) assessing infliximab (3 or 5 mg/kg) with primary endpoint change in % predicted FVC at week 24, and cites associated publications including PMID 16840744 and PMID 18256069 (NCT00073437 chunk 1).
Adalimumab: NCT00311246 (progressive sarcoidosis; n=11) used adalimumab 40 mg SC weekly; primary endpoint was change in FVC from screening to week 24 (NCT00311246 chunk 2).

12.4 Antifibrotics / progressive fibrotic sarcoidosis trials

Pirfenidone: NCT03260556 is a Phase 4 randomized, triple-masked placebo-controlled trial (estimated n=60) in progressive fibrotic sarcoidosis; primary endpoint “time until clinical worsening” over two years (NCT03260556 chunk 1).
Nintedanib: NCT06479603 is recruiting and compares nintedanib vs standard of care in fibrotic sarcoidosis; the provided chunk includes fibrosis-based inclusion criteria but does not show endpoints/phase/enrollment in that excerpt (NCT06479603 chunk 2).

12.5 Efzofitimod (ATYR1923) — steroid-sparing investigational therapy

NCT03824392 is a completed early study of IV ATYR1923/efzofitimod; registry chunk cites related publications including PMID 37854715 and PMID 36356657 (NCT03824392 chunk 2). (Detailed endpoints/phase are not present in the extracted chunk.)

13. Prevention

No disease-specific primary prevention strategies were identified in the retrieved sources. Prevention in practice centers on (i) avoiding unnecessary immunosuppression in self-limited disease, (ii) monitoring and mitigating treatment complications, and (iii) addressing exposure hypotheses where relevant, but quantitative prevention evidence was not extractable from the provided texts.

14. Other Species / Natural Disease

No naturally occurring veterinary sarcoidosis analogs were identified in the retrieved evidence set.

15. Model Organisms

The PPP/macrophage study reports both in vitro giant cell and in vivo murine granuloma models in which PPP inhibitors attenuated granuloma formation, supporting tractable experimental models for granulomatous inflammation and therapeutic targeting (dhanani2025immunosuppressivetherapiesin pages 10-12). Additional organism-specific model catalogs (MGI/IMPC) were not retrieved in this run.

Expert opinions and authoritative analysis (from high-authority sources)

Key gaps and limitations of this evidence set

  • Several requested identifier systems (MeSH, ICD-11, Orphanet, OMIM disease entry) were not present in the retrieved texts and cannot be reliably asserted without dedicated database queries.
  • Variant-level (ClinVar/ACMG) pathogenic variant curation is not possible from the extracted passages.
  • Some trial details for efzofitimod Phase 3 (NCT05415137), tofacitinib trials, and the nintedanib record endpoints were not contained in the retrieved chunks; additional ClinicalTrials.gov sections would be required for full endpoint extraction.

References

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