How I Approach Patients With Elevated Serum Ferritin
An excellent article by @AmCollegeGastro with quite useful & practical points for GI Trainees. @BSGTrainees. @LiverFellow #LiverTwitter @GwentLiverUnit
journals.lww.com/ajg/Abstract/2…
👉Common Hepatology referral
❓HH/IO
⬇️ Fe = Iron Def
⬆️ Fe ≠ Iron Overload (not always)
Better used in combination with
✅History
✅TS Levels
Causes of ⬆️Fe
⬆️ Fe without IO
👉90 % cases
👉Liver (ARLD, NAFLD, Viral)
👉Inflammatory (acute,chronic, AI).
👉Metabolic-Syndrome
👉ETOH
⬆️ Fe with IO
👉Primary:Genetic
👉2ndary: ineffective erythropoiesis, frequent iron or blood transfusions.
Investigating ⬆️ Fe
👉Morning sample
👉Reactive hyperferritinemia vs IO state
( clinical evaluation, laboratory, and/or radiological investigation).
Patient history and cutoff TS value of 55% provides a high sensitivity for delineating primary from secondary IO etiologies
Genetic Testing
👉HFE ➡️ Hype 1 HH,
✅ Common form,
✅C282Y, H630, and S65C mutations
If negative and HH is still suspected
👉Non-HFE ➡️ type 2, 3, and 4 HH.
A diagnosis of secondary IO usually necessitates a hematology consultation.
Gene Testing
C282Y---> Key mutation.
👉Type I HH (C282Y/C282Y)- Most common
👉Type Ib HH (C282Y/H63D) only 0.5%–5% clinical penetrance.
‼️H63D or S65C no risk of developing clinical IO.
Role of MRI❓
✅T2W in selected patients with equivocal laboratory results .
Treatment
🙋🏻♂️Primary IO
✅phlebotomy 1st.
✅Chelation ➡️ severe heart disease/ anemia.
⬆️Fe is a predictor of hepatic fibrosis.
👉 SF goal of 50–100 μg/L.
👉Liver biopsy if Fe >1,000 μg/L.
🙋🏻♂️Secondary IO
✅Chelation.
🙋🏻♂️Reactive hyperferritinemia
✅Monitor 3 monthly.
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