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Biochemistry · Iron metabolism
Sample itemA man with long-standing rheumatoid arthritis has anaemia with low serum iron, low transferrin saturation and a raised ferritin. Which mechanism best explains the low serum iron?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
C. Interleukin-6-driven rise in hepcidin, degrading ferroportin and trapping iron in macrophages
Inflammation raises interleukin-6, which stimulates hepatic hepcidin. Hepcidin binds ferroportin and causes its degradation, so iron is not released from macrophages or absorbed from the gut. This gives anaemia of chronic disease with low serum iron but adequate stores and high ferritin.
Option by option
A. Loss of intrinsic factor impairs iron absorption
Intrinsic factor is needed for vitamin B12 absorption, not iron absorption.
B. Decreased hepcidin increases ferroportin and iron absorption
Low hepcidin would raise serum iron, as in haemochromatosis, which is the opposite of this picture.
C. Interleukin-6-driven rise in hepcidin, degrading ferroportin and trapping iron in macrophages (correct)
Correct. High hepcidin removes ferroportin, locking iron in stores and lowering serum iron.
D. Increased transferrin synthesis binds more iron
Transferrin is low or normal in chronic disease rather than raised, and transferrin synthesis does not trap iron in macrophages.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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