🧵 Procalcitonin (PCT) –
Tweet 1:
Procalcitonin- once just a peptide in calcitonin synthesis, now a powerful biomarker in infection & sepsis care. But when should we trust it, and when not? 🧵@IhabFathiSulima @DrAkhilX @CelestinoGutirr #MedTwitter #Rheumatology #ID
Tweet 2 (Basics):
🔹 What is Procalcitonin?
•Precursor of calcitonin, normally produced in thyroid C-cells.
•During bacterial infection, PCT is released from multiple tissues in response to endotoxins & cytokines (IL-1β, TNF-α).
•Viral infections usually suppress PCT.
Tweet 3 (Why important?):
✨ PCT rises early (within 6–12 hrs) in systemic bacterial infection → helps clinicians:
•Differentiate bacterial vs viral infections
•Assess sepsis severity
•Guide antibiotic decisions
Tweet 4 (Interpretation):
📊 Levels & meaning (general guide):
•<0.1 ng/mL → Normal
•0.1–0.25 → Low likelihood of bacterial infection
•0.25–0.5 → Possible bacterial infection
•0.5 → Suggestive of bacterial infection/sepsis
(Higher = more severe infection)
Tweet 5 (Pros):
✅ Advantages of PCT:
•Rises earlier than CRP in sepsis
•Falls rapidly with infection control → good for monitoring
•Useful in ICU, pneumonia, sepsis management
•Helps reduce unnecessary antibiotics
Tweet 6 (Cons & pitfalls):
⚠️ Limitations:
•Can rise in non-infectious inflammation (major surgery, trauma, burns, CKD)
•May not rise in localized infections (e.g., abscess)
•Viral infections may keep it low despite illness
•Should never replace clinical judgment
Tweet 7 (Special note for Rheumatology):
💡 In autoimmune & rheumatic diseases, PCT helps:
•Distinguish flare vs infection in patients on immunosuppressants
•Guide safe antibiotic use
But beware → high-dose steroids & biologics may blunt inflammatory markers.
Tweet 8 (Take-home):
Procalcitonin = 🧪 helpful tool, not a magic bullet.
Best used with clinical exam + other labs (CRP, cultures, imaging).
👉 It guides antibiotics, but doesn’t write the prescription for you.
#MedEd #Procalcitonin #Sepsis
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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.