Aravind Palraj Profile picture
Aug 22, 2025 16 tweets 6 min read Read on X
🧵 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 @JanetbirdopeImage
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. Image
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. Image
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. Image
Post 4
Steroids vs diabetes/mood/sleep
•Looks like: “new inflammatory pain, poor sleep, anxiety”
•Could be: steroid-induced hyperglycemia, insomnia, mood change
•Check: fasting/random glucose, sleep/mood screen; morning dosing, taper where possible, brief sleep aids, consider steroid-sparing plan.Image
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. Image
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. Image
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.Image
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.Image
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.Image
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. Image
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.Image
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. Image
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) Image
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 Image
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. Image

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More from @Rheumat_Aravind

Jan 8
Tweet 1 🧵

Thrombocytopenia is encountered daily in the ER, ICU, and wards - yet it often triggers panic, shotgun testing, or delayed diagnosis.

A simple, bedside framework can clarify most cases within minutes.

Here’s a practical approach to thrombocytopenia in Internal Medicine 🧵

#InternalMedicine #Hematology @DrAkhilX @IhabFathiSulima #MedTwitter #ClinicalReasoningImage
Tweet 2 – First Rule

First rule:
Confirm it is real thrombocytopenia.

Always exclude:
• EDTA-related platelet clumping
• Pseudothrombocytopenia on analyzer

👉 Check the peripheral smear before anything else.

#Diagnostics #LabMedicine #PatientSafety Image
Tweet 3 – The Core Framework

Almost all causes of thrombocytopenia fall into three buckets:

1️⃣ Destruction
2️⃣ Reduced production
3️⃣ Sequestration

If you identify the bucket, the diagnosis becomes straightforward.

#ClinicalFramework #MedEd #Hematology Image
Read 12 tweets
Dec 27, 2025
🧵 Modern Gout Management - Evidence-Based Thread

Tweet 1

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. 🧵

#MedEd #Gout #Rheumatology #InternalMedicine @DrAkhilX @IhabFathiSulimaImage
Tweet 2 - The Diet Myth

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.Image
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 clearanceImage
Read 11 tweets
Dec 26, 2025
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 #MedicalEducationImage
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 #PrimaryCareImage
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.

#LabMedicine #RheumTwitter #MedTwitterImage
Read 12 tweets
Nov 17, 2025
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.

@DrAkhilX @IhabFathiSulima #MedTwitter #ozempic #mounjaro #weightloss #diabetesImage
1️⃣ Mechanism
Ozempic = GLP-1 agonist only
Mounjaro = Dual GLP-1 + GIP agonist
Dual agonism → stronger metabolic effect. Image
2️⃣ Weight loss
Ozempic: 10–15%
Mounjaro: 22%+ (SURMOUNT-3/4)
Mounjaro consistently produces greater and sustained loss. Image
Read 11 tweets
Nov 6, 2025
🧵 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 #AutoimmunityImage
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.
Read 8 tweets
Oct 26, 2025
🧵“100 Named Clinical Signs — Hutchison’s Clinical Methods (25th Edition)”

AI detects patterns.
Hutchison detected patients.

Here are 100 named clinical signs that still shape bedside diagnosis —
signs that live in the wards, not in the algorithms.

The lost language of observation begins below 👇
@DrAkhilX @IhabFathiSulima @drkeithsiau @ArunInamadar @nirmalregency #MedTwitterImage
General and Systemic Signs

1️⃣ The body speaks before the lab does.

From Murphy’s to Nikolsky’s — every sign here was discovered by listening to the patient, not the monitor.

The skin, breath, and reflex still tell the truth first. Image
Cardiovascular Signs

2️⃣ The pulse has poetry.

Corrigan, Quincke, de Musset — names that still echo with each beat.

You don’t need an echo when your fingers already know. Image
Read 12 tweets

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