🧵 CK Can Lie — Catching Myositis When Creatine Kinase Is Normal
Myalgia + weakness.
CK is normal.
Everyone relaxes.
That’s how dangerous myositis gets missed. Let’s fix it. 👇
@IhabFathiSulima @DrAkhilX @CelestinoGutirr #MedTwitter
1) First principle
Normal CK ≠ no muscle disease. CK reflects muscle necrosis, not strength. Patchy disease, low muscle mass, or perimysial-predominant injury can keep CK normal.
2) When CK is often normal (or only mildly ↑)
•Dermatomyositis (esp. MDA5 phenotype)
•Steroid myopathy (treatment complication, not inflammation)
•Inclusion body myositis (>50 yrs; finger flexors/quads)
•Early/patchy disease, chronic burnt-out myositis
3) Red flags that trump a normal CK
•True proximal weakness (chair rise, comb hair, neck flexors)
•Dysphagia/aspiration, nasal speech, weak cough
•Dyspnea or rapid desaturation (think RP-ILD)
•Pathognomonic rashes: heliotrope, Gottron papules, mechanic’s hands
•Dark urine (heme-positive, no RBCs)
4) What to order next (CK normal but you’re worried)
•Aldolase, LDH, AST/ALT, GGT
•AST/ALT high with normal GGT → likely muscle source
•Urine dip: heme + / RBC − → myoglobinuria
•Ferritin (very high with MDA5/RP-ILD or MAS)
•If breathless: CXR/HRCT ± PFTs
5) Pattern pearls
•CK normal + Aldolase high → perimysial process (think dermatomyositis, overlap)
•AST ≫ ALT, GGT normal → muscle, not liver
•LDH high supports muscle injury but is nonspecific
6) Don’t confuse with steroid myopathy
•Timing: weeks after starting/high-dose steroids
•Painless proximal weakness, CK normal
•Plan: taper steroids, add physio, use steroid-sparing agent for underlying rheum disease.
7) Statin story (two different beasts)
•Simple statin myalgia: CK normal or mild ↑; resolves on stopping
•Immune-mediated necrotizing myopathy (anti-HMGCR): very high CK, weakness persists after stopping → needs immunosuppression
8) Inclusion body myositis (don’t overtreat like PMR/RA)
•Men >50, finger-flexor and quadriceps weakness, falls, CK normal–mild
•Poor steroid response; think biopsy, rehab, assist devices.
9) The lethal miss: MDA5-Dermatomyositis with RP-ILD
•Minimal/normal CK, sky-high ferritin, hand ulcers or palmar papules
•Rapidly progressive ILD → treat early (high-dose steroids + calcineurin inhibitor ± cyclophosphamide/rituximab; center-specific)
10) 30-second algorithm
Weakness ± myalgia + CK normal →
→ Check aldolase, AST/ALT, LDH, GGT, urine heme
→ Look for DM rash / IBM pattern / steroid exposure / ILD signs
→ If positive: myositis panel (MDA5, TIF1-γ, NXP2, SAE1, HMGCR, SRP, Jo-1, etc), EMG/MRI, and early rheum/pulm referral.
📌 Takeaway
CK can lie. Muscles don’t.
If your exam and the story say “myositis,” keep digging even with a normal CK.
If this thread prevents one missed myositis or RP-ILD, share it. Someone will thank you later. 🔁
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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. 🧵
#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.