🧵 Giant Cell Arteritis — Save a Sight in 5 Minutes
The vision loss is often permanent—and preventable.
A zero-fluff checklist: who to treat before tests, when ultrasound beats biopsy, steroid start & taper, and the traps (normal ESR/CRP, “PMR only,” jaw pain without headache).
@IhabFathiSulima @DrAkhilX @CelestinoGutirr @Janetbirdope @vascuk #MedTwitter #NEETPG
Why this matters
•GCA is the most common primary vasculitis >50 years
•~15–20% develop vision loss — often before diagnosis
•Half lose the other eye within days if untreated
•Risk drops almost to zero with prompt steroids
Red flags you must know
Treat before waiting for confirmatory tests if:
•Jaw claudication
•Vision loss/blurring
•Pale swollen optic disc on fundoscopy
•Temporal artery: tender, thick, pulseless
•Unexplained fever + ESR/CRP ↑ in patient >50
ESR & CRP are helpful but not perfect
•ESR >50 mm/hr in most — but can be normal
•CRP ↑ in ~97% — better sensitivity than ESR
•If suspicion is high → start steroids immediately
First-line tests (don’t delay steroids)
•Temporal artery ultrasound (halo sign) — sensitivity highest if done <1 week after steroid start
•Temporal artery biopsy — gold standard but can be false negative (skip lesions)
•Consider PET-CT if large-vessel GCA suspected
Steroid taper roadmap
•Maintain high dose until symptoms and labs normal (~2–4 wks)
•Gradual taper over 12–18 months
•Relapse = re-escalate to last effective dose
•Consider tocilizumab for relapsing/refractory or steroid-sparing
Common traps
•ESR normal (up to 5%) → don’t rule out
•“Only PMR symptoms” can be GCA
•Jaw claudication without headache → still GCA
•Biopsy negative ≠ no GCA (skip lesions)
Takeaway
Rule of sight in GCA:
If you think it’s GCA, start steroids now.
You can always stop them later — but you can’t give sight back.
📌 Save this — you might save a sight one day.
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🧵 C3 vs C4 — What the Pattern Really Means (in 30 seconds)
We order complements all the time.
But the pattern is the diagnosis.
Here’s the fast way to read C3/C4 without overthinking. 👇
@IhabFathiSulima @DrAkhilX @CelestinoGutirr @DurgaPrasannaM1 @SarahSchaferMD @EMJNephrology #MedTwitter #Rheumatology
1) Quick primer
•C3 = shared hub (alternative + classical).
•C4 = classical pathway marker (C1q → C4).
Pattern > any single value.
2) Both C3 ↓ and C4 ↓ → immune-complex “classical burn”
Think: active SLE, infective endocarditis, serum-sickness/drug IC, mixed cryoglobulinemia.
Next: CH50, anti-dsDNA, C1q binding/anti-C1q, blood cultures if febrile.
🧵 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
🧵 Drug Combinations That Can Kill — Interactions You Must Never Miss
We prescribe these daily.
Get the combination wrong → bleeding, rhabdomyolysis, bone marrow suppression, cardiac arrest.
Here are the 10 combinations you must always check for 👇
@DrAkhilX @IhabFathiSulima @CelestinoGutirr @Janetbirdope @DurgaPrasannaM1 @SarahSchaferMD @NeuroSjogrens #MedTwitter #RheumTwitter
1) Allopurinol or Febuxostat + Azathioprine or 6-Mercaptopurine
❌ Severe bone marrow suppression (xanthine oxidase inhibition).
✅ Avoid the combination; if unavoidable, drastically reduce azathioprine dose and monitor blood counts closely — but switching is safer.
2) Methotrexate + Trimethoprim–Sulfamethoxazole (Co-trimoxazole)
❌ Pancytopenia, mucositis, acute kidney injury.
✅ Use alternatives such as nitrofurantoin or fosfomycin for urinary tract infections.
🧵 Clues Your “Arthritis” Patient Doesn’t Actually Have RA
Not all swollen joints are rheumatoid arthritis.
Some look identical—but aren’t.
Here’s how to spot RA mimics before the label sticks forever 👇
@IhabFathiSulima @DrAkhilX @SarahSchaferMD @Janetbirdope #MedTwitter #Rheumatology
1. It’s asymmetric
RA loves symmetry.
If one side is swollen but the other is fine—think again.
2. The wrong joints are involved
RA = MCP, PIP, wrists.
If DIP joints are involved → think OA, psoriatic arthritis.
If only large joints → think reactive, viral, crystal arthritis.
🧵 When It’s Not Sepsis – Clues That It’s Actually Autoimmunity
Fever.
Tachycardia.
High CRP.
Looks like sepsis—but cultures stay negative, and antibiotics don’t work.
Let’s break down how to catch autoimmune mimicry of infection—before it’s too late. 👇
@IhabFathiSulima @DrIanWeissman @DrAkhilX @CelestinoGutirr @NeuroSjogrens @SarahSchaferMD @drkeithsiau #MedTwitter #RheumTwitter
1. The classic setup:
Patient has:
✅ Fever
✅ High CRP
✅ High neutrophils
✅ Looks toxic
But…
🧪 Cultures are negative
🧫 Antibiotics fail
🧠 Something’s not adding up
2. When you should pause:
🚩 No response to antibiotics after 48–72 hrs
🚩 Blood cultures negative
🚩 No source on imaging
🚩 Worsening cytopenias
🚩 Rising liver enzymes or ferritin
🚩 Mental status changes