One of the most debated biomarkers.
Ordered often, misinterpreted even more.
Let’s clear the confusion 👇
#Rheumatology #Sarcoidosis #Biomarkers @IhabFathiSulima @DrAkhilX @CelestinoGutirr
1/ 🔬 Serum ACE is produced by epithelioid cells in granulomas.
Hence, levels may be elevated in granulomatous diseases — especially sarcoidosis.
2/ 📊 When is ACE useful?
•Supporting diagnosis of sarcoidosis (not diagnostic alone)
•Monitoring disease activity (trend > absolute value)
•May fall with treatment response
3/ ⚠️ Limitations:
•Low sensitivity (40–60%)
•Low specificity — elevated in TB, leprosy, silicosis, berylliosis, histoplasmosis, even hyperthyroidism
•Normal ACE does not exclude sarcoidosis
4/ 🧪 Practical notes:
•Always correlate with clinical + imaging (esp. CXR/HRCT)
•Repeatable for follow-up but avoid over-reliance
•Genetic ACE polymorphisms can affect baseline levels
5/ ✅ Take-home:
Serum ACE is a supportive biomarker, not a stand-alone test.
Use it for trends in known sarcoidosis, not as a universal screening tool.
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A lab we all order. A deficiency we often find.
But what does it really mean in autoimmune disease?
Let’s clear the confusion 👇
#Rheumatology #VitaminD
@IhabFathiSulima @DrAkhilX @CelestinoGutirr
1/ 💡 Vitamin D is not just about bones.
It’s an immunomodulator: affects T cells, B cells, and dendritic cells.
Deficiency is linked to ↑ autoimmunity risk (RA, SLE, MS, etc.).
2/ 🔍 Testing:
•Serum 25(OH)D is the correct test (not 1,25(OH)₂D).
•Deficiency: <20 ng/mL
•Insufficiency: 20–30 ng/mL
•Sufficiency: >30 ng/mL
Tweet 1:
Serum uric acid — one of the most over-ordered and misinterpreted tests in medicine.
Here’s how to understand it in rheumatology 👇
@IhabFathiSulima @DrAkhilX @CelestinoGutirr #MedTwitter #Rheumatology
Tweet 2 (Basics):
•Uric acid = end product of purine metabolism
•Normal range: ~3.5–7 mg/dL (varies by lab/sex)
•Excreted mainly by kidneys (~70%) + gut (~30%)
Tweet 3 (Hyperuricemia ≠ Gout):
•Many people with high uric acid never develop gout
•Risk rises as uric acid >9 mg/dL
•Gout diagnosis = clinical + crystals, not just lab value
🧵 Anti-Phospholipid Antibodies (aPL) in Rheumatology:
Tweet 1:
Anti-Phospholipid Antibodies — a small blood test with big consequences.
From clots to pregnancy complications, they guide APS diagnosis and management.
Here’s what every clinician should know 👇@IhabFathiSulima @DrAkhilX @CelestinoGutirr #MedTwitter #Rheumatology
Tweet 2 (What are aPL?):
•Autoantibodies against phospholipid-binding proteins
•Main types tested:
• Lupus anticoagulant (LA)
• Anticardiolipin (aCL) IgG/IgM
• Anti-β2 glycoprotein I (β2GPI) IgG/IgM
Tweet 1:
ANCA — one antibody, many confusions.
From GPA to drug-induced vasculitis, it’s powerful when used right…
and misleading when used wrong.
Here’s a quick guide 👇
@IhabFathiSulima @DrAkhilX @CelestinoGutirr #MedTwitter #Rheumatology
🧵 HLA-B27 in Rheumatology:
Tweet 1:
“HLA-B27 — a genetic marker with a powerful reputation.
From ankylosing spondylitis to reactive arthritis, it shapes how we think about SpA.
But what does a positive result really mean? 👇”
@IhabFathiSulima @DrAkhilX @CelestinoGutirr #MedTwitter #Rheumatology
Tweet 2 (What is HLA-B27?):
•Human Leukocyte Antigen, class I molecule
•Encoded on chromosome 6
•Important in antigen presentation
•Strong association with seronegative spondyloarthritis
Tweet 3 (Prevalence):
•General population: 6–8% (varies by ethnicity)
•AS patients: >90% positive
•But: Most HLA-B27+ people never develop disease
Tweet 1:
“C3 & C4: two small proteins, big role in lupus care.
But when are they truly helpful — and when do they mislead?
A quick guide to understanding complement in rheumatology 👇”
@IhabFathiSulima #MedTwitter #Rheumatology
Tweet 2 (Basics):
•Complement = part of innate immunity.
•C3 & C4 are the most commonly measured components.
•C3 = central to both classical & alternative pathways.
•C4 = mainly reflects the classical pathway.
Tweet 3 (Why do we check them?):
•Monitoring lupus activity (esp. nephritis).
•Evidence of ongoing immune complex consumption.
•Supportive for classification in SLE.