🧵 Drug vs Disease — When Side Effects Mimic the Diagnosis👇
Is it the disease—or the drug? Many “flares” are actually medication effects. Here’s a clinic-ready guide to the most common drug–disease confusions, what to check, and how to pivot fast. Save and share. #MedTwitter #RheumTwitter #FOAMed #IMTwitter #PrimaryCare #PatientSafety @IhabFathiSulima @DrAkhilX @Janetbirdope
Post 1
Big idea
Before escalating therapy, ask: could the medication be causing or unmasking the symptom? Use this checklist: timing vs start/dose change, dose–response, dechallenge/rechallenge, and alternative explanations.
Post 2
NSAIDs vs kidney/pressure
•Looks like: edema, rising creatinine, “worsening gout/OA pain”
•Could be: NSAID nephrotoxicity or hypertension
•Check: creatinine/eGFR, BP, volume status; step down NSAID, switch to topical or COX-2 cautiously; renal-safe analgesia plan.
Post 3
Steroids vs infection
•Looks like: “rheum flare” with fatigue, tachycardia
•Could be: masked infection on steroids
•Check: vitals, WBC, CRP trend (can be blunted), focal symptoms; lower steroid if safe; rule out sepsis before increasing.
Post 5
Methotrexate vs disease fatigue
•Looks like: persistent fatigue, nausea, mouth soreness “despite control”
•Could be: MTX intolerance or cytopenia
•Check: CBC, LFTs, MCV; confirm weekly dosing; optimize folate/folinic acid; consider SC MTX or switch.
Post 6
Hydroxychloroquine vs vision complaints
•Looks like: “ocular flare” or headache
•Could be: HCQ toxicity (rare early but risk accumulates)
•Check: dose by actual body weight, cumulative dose, baseline/periodic ocular exams; if visual symptoms, urgent ophthalmology.
Post 7
Allopurinol vs “gout rash”
•Looks like: flare plus rash after ULT start
•Could be: hypersensitivity (watch for fever, eosinophilia, renal involvement)
•Check: timeline to start, skin exam, labs; stop drug and escalate care if systemic features; consider HLA-B*58:01 in high-risk groups where recommended.
Post 8
Colchicine vs neuropathy/diarrhea
•Looks like: “worsening enthesitis pain” with leg weakness
•Could be: colchicine toxicity (especially with CKD or interacting CYP3A4/P-gp drugs)
•Check: CK, neuro exam, meds for interactions; dose-adjust or stop; educate on early GI signs.
Post 9
Biologics/JAKi vs infection or paradoxical inflammation
•Looks like: “psoriasis flare” on anti-TNF, “cough/fever” on therapy
•Could be: paradoxical skin disease; opportunistic infection
•Check: TB/hepatitis screening status, CRP, CXR if respiratory; dermatology/rheum plan—switch class if paradoxical.
Post 10
PPIs vs hypomagnesemia/myalgia
•Looks like: diffuse aches “not improving with DMARDs”
•Could be: electrolyte disturbance from chronic PPI
•Check: Mg2+, Ca2+, vitamin B12 if long-term; step-down strategy or alternate GI protection if appropriate.
Post 11
Statins vs myopathy vs myositis
•Looks like: “polymyalgia” or proximal weakness
•Could be: statin myopathy or rare statin-associated autoimmune myopathy
•Check: CK, pattern (pain vs weakness), temporal relation; stop statin trial, consider alternate lipid therapy; if severe weakness/high CK, evaluate for SAAM.
Post 12
ACEi/ARBs vs cough/angioedema mimicking vasculitis
•Looks like: chronic cough/airway symptoms
•Could be: ACEi cough or rare angioedema
•Check: drug list and timing; switch class; reassess before extensive vasculitis workup.
Post 13
Diagnostic pause card
Before increasing immunosuppression, run the 5 checks:
1.Timeline to med change
2.Lab signal fits drug toxicity?
3.Dechallenge feasible?
4.Interactions/organ function reviewed?
5.A single test to clarify? (e.g., CK, UA, CXR)
Post 14
What to document
•Working differential (disease activity vs adverse effect)
•Safety labs and thresholds
•Proposed dechallenge/rechallenge plan
•Patient counseling and red-flag symptoms
•Exact follow-up date/window
Post 15
Shareable takeaways
•Not every “flare” is the disease.
•Start low, go slow, review often.
•One quick lab or med switch can prevent months of overtreatment.
• • •
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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.