🧵 💡 “Sjögren’s Syndrome: Why Do So Many Trials Fail?”
From hydroxychloroquine to rituximab to belimumab — let’s walk through the key trials that shaped (and shook) pSS treatment.👇
#Sjögrens #RheumTwitter #MedTwitter @DurgaPrasannaM1 @IhabFathiSulima @NeuroSjogrens @SjogrensOrg @SjogrensCa @SarahSchaferMD @elisa_comer @SjogrensForum
1️⃣ JOQUER Trial – The HCQ Wake-Up Call
💊 Hydroxychloroquine — once used for fatigue, arthralgia, dryness.
🧪 JOQUER (NEJM 2014) showed:
❌ No significant benefit over placebo.
✅ Some trends for low-inflammatory patients.
Lesson? HCQ ≠ miracle drug in pSS.
2️⃣ TEARS Trial – The Rituximab Reality Check
🧬 B-cell targeting made sense.
💉 Rituximab = logical next step.
👨🔬 TEARS trial (2013):
❌ No big win on fatigue or dryness
🟡 But systemic benefit signals emerged
Lesson? Choose patients wisely.
3️⃣ TRACTISS Trial – Double Down on RTX
🇬🇧 UK-based TRACTISS (2017) repeated the test.
💉 Again, no major relief for dryness
✅ Trends toward benefit in systemic features.
👀 Takeaway: RTX may help outside the glands.
4️⃣ BELISS Trial – Enter Belimumab
🔵 Belimumab (anti-BAFF) — aimed at B-cell overdrive.
Gout is the most common inflammatory arthritis, yet nearly 80% of patients are suboptimally managed, leading to preventable flares, tophi, and joint damage.
Forget the old myths of “kings and diet.”
Here is the modern, evidence-based approach to gout management, aligned with ACR guidelines, for the busy clinician. 🧵
MYTH: Gout is purely a “lifestyle disease” fixed by diet.
FACT: Diet typically alters serum urate by ~1 mg/dL at most.
Gout is primarily a genetically determined disorder of renal urate under-excretion.
You cannot “diet away” established gout. Medication is usually required.
Tweet 3 - The Goal (Treat-to-Target)
The goal of therapy isn’t just stopping flares - it’s dissolving monosodium urate crystals.
That requires a Treat-to-Target strategy:
• Target serum urate < 6.0 mg/dL for all gout patients
• If tophi are present: < 5.0 mg/dL for faster crystal clearance
The Clinical Approach to a Positive Antinuclear Antibody (ANA):
A positive ANA is one of the most common consults in Internal Medicine, yet it is widely misunderstood.
Positive ANA ≠ Lupus.
It causes significant patient anxiety and unnecessary referrals.
Here is the evidence-based approach to interpreting a positive ANA for the busy clinician. 🧵
#MedEd #Rheumatology #MedTwitter @DrAkhilX @IhabFathiSulima #InternalMedicine #Lupus #MedicalEducation
First, understand the pre-test probability.
ANA is not a screening test for fatigue or nonspecific pain.
Why? Up to 20–30% of the healthy population has a positive ANA at 1:40 titer. Even at 1:160, ~5% of healthy individuals are positive.
#Diagnostics #ClinicalPearls #PrimaryCare
The Titer is the key to specificity.
• 1:40 to 1:80: Low positive. Low clinical significance in isolation.
• 1:160: Intermediate.
• ≥ 1:320: High positive. Higher specificity for autoimmune disease, but still requires clinical correlation.
Treat the patient, not the number.
Ozempic vs Mounjaro — the REAL 2025 comparison.
🧵Thread🔥👇
Everyone is talking about weight-loss drugs. But the REAL showdown is Ozempic vs Mounjaro — and the winner is clear.
Ozempic and Mounjaro should be prescribed ONLY after medical assessment — never self-started.
🧵 5 Lab Traps That Delay Lupus Diagnosis (with one example)
I’ve seen lupus hide behind “normal” labs more times than I can count.
Here are 5 lab traps that delay the diagnosis — with one real case that’ll stick with you. 🧵👇
@DrAkhilX @IhabFathiSulima @DrNikhilMD @Janetbirdope @DurgaPrasannaM1 #MedTwitter #RheumTwitter #Autoimmunity
1️⃣ “ANA is negative, so it’s not lupus.”
Wrong.
Early SLE can have low-titer or even transiently negative ANA.
🧠 If your gut says lupus, repeat it after a few weeks.
2️⃣ “CRP is high, so it must be infection.”
Not always.
Lupus flares often have normal CRP.
High CRP just means: check if there’s serositis, arthritis… or yes, infection.