Vasculitis is a shapeshifter.
It never walks into clinic saying, “Hello, I am vasculitis.”
Instead, it hides behind everyday symptoms.
Here are the common masks it wears 👇
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1. Just a rash?
Palpable purpura on the legs may look like “allergy.”
But when it’s non-blanching, raised, and painful → small-vessel vasculitis should be suspected.
2. Just sinusitis?
Recurrent sinusitis, ear infections, or epistaxis might be ENT’s problem.
But add hematuria or lung shadows, and GPA (Granulomatosis with polyangiitis) enters the picture.
3. Just asthma?
Late-onset, steroid-dependent asthma with eosinophilia may not be “just asthma.”
It could be EGPA (Eosinophilic granulomatosis with polyangiitis).
4. Just neuropathy?
Sudden foot drop or wrist drop without trauma often signals vasculitic neuropathy (mononeuritis multiplex).
5. Just kidney disease?
Rapidly progressive renal failure with RBC casts in urine = a red flag for ANCA-associated vasculitis.
6. Just stroke in the young?
Infarcts in multiple territories or with systemic features → think primary angiitis of CNS or systemic vasculitis.
💡 Clinical pearl:
Vasculitis rarely appears in isolation.
It leaves a trail across multiple systems — skin, lungs, kidneys, nerves.
The key is to connect the dots before irreversible damage.
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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. 🧵
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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.
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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.