Monday, 16 February 2026

Vexas s. Med

 A




VEXAS Syndrome



VEXAS = Vacuoles, E1 enzyme, X-linked, Autoinflammatory, Somatic


A severe adult-onset autoinflammatory disorder caused by acquired (somatic) mutations in the UBA1 gene in hematopoietic stem cells.


First described in 2020 by researchers at the National Institutes of Health.





1. Cause & Pathophysiology



  • Somatic mutation in UBA1 (ubiquitin-activating enzyme E1)
  • Mutation occurs in bone marrow stem cells (not inherited)
  • X-linked → predominantly affects men
  • Leads to:
    • Dysregulated innate immunity
    • Excess inflammatory cytokine production
    • Bone marrow dysfunction
    • Cytoplasmic vacuoles in myeloid precursors






2. Who Gets It?



  • Typically men >50 years
  • Rare in women (usually with X monosomy or mosaicism)
  • Often previously diagnosed with:
    • Relapsing polychondritis
    • Vasculitis
    • Myelodysplastic syndrome (MDS)






3. Clinical Features




Systemic



  • Recurrent fevers
  • Weight loss
  • Severe fatigue




Skin



  • Neutrophilic dermatoses
  • Vasculitic rashes




Cartilage



  • Ear/nasal chondritis (mimics relapsing polychondritis)




Pulmonary



  • Infiltrates
  • Pleural effusions




Hematologic



  • Macrocytic anaemia
  • Thrombocytopenia
  • Myelodysplastic syndrome
  • High CRP/ESR




Thrombosis



  • Increased risk of venous thromboembolism






4. When to Suspect VEXAS



Consider in an older male with:


  • Steroid-dependent systemic inflammation
  • Macrocytic anaemia
  • Elevated inflammatory markers
  • Relapsing chondritis or unexplained vasculitis
  • Bone marrow showing vacuoles in myeloid/erythroid precursors






5. Diagnosis




Step 1 – Lab Clues



  • Persistent CRP elevation
  • Macrocytosis (↑ MCV)
  • Cytopenias




Step 2 – Bone Marrow



  • Cytoplasmic vacuoles in myeloid precursors




Step 3 – Confirmatory Test



  • Genetic testing showing somatic UBA1 mutation



Diagnosis is molecular.





6. Treatment



No standardized cure; management is evolving.



1️⃣ Corticosteroids



  • Often highly responsive
  • Many become steroid-dependent




2️⃣ Steroid-Sparing Agents



  • Limited efficacy:
    • Methotrexate
    • Azathioprine
    • Mycophenolate




3️⃣ Biologics



  • IL-6 inhibitors (e.g., Tocilizumab)
  • JAK inhibitors (e.g., Ruxolitinib)
    • Increasing evidence of benefit




4️⃣ Hematologic Management



  • Treat MDS if present
  • Transfusions as needed




5️⃣ Allogeneic Stem Cell Transplant



  • Potentially curative
  • Consider in severe disease
  • High-risk procedure






7. Prognosis



  • Chronic, relapsing course
  • Significant morbidity
  • Mortality often related to:
    • Infection
    • Thromboembolism
    • Progressive bone marrow failure






8. Key Clinical Pearls



  • Think VEXAS in older men with unexplained inflammatory disease + macrocytosis
  • Steroid dependence is a major clue
  • It bridges rheumatology + hematology
  • Increasingly recognized as underdiagnosed





If you’d like, I can also provide:


  • A diagnostic algorithm
  • A comparison table: VEXAS vs relapsing polychondritis vs MDS
  • Exam-style revision notes
  • A hematology board-level summary


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