Vitamins and minerals: iron overload in thalassaemia intermedia: practice question

A Biochemistry question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Biochemistry · Vitamins and minerals: iron overload in thalassaemia intermedia

Sample item

A 12-year-old with untreated non-transfusion-dependent beta-thalassaemia intermedia develops progressive iron overload and a raised ferritin. Which mechanism is mainly responsible?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

B. Ineffective erythropoiesis suppresses hepcidin, so gut iron absorption rises

Expanded, ineffective erythropoiesis releases erythroferrone and other signals that suppress hepatic hepcidin. Low hepcidin keeps ferroportin active, so duodenal absorption and macrophage release of iron increase, causing overload even without transfusions. Chelation is guided by liver iron and ferritin.

Option by option

  • A. Raised hepcidin traps iron in macrophages, which then release it excessively

    High hepcidin would trap iron in macrophages and cause anaemia of chronic disease, not overload.

  • B. Ineffective erythropoiesis suppresses hepcidin, so gut iron absorption rises (correct)

    Correct. Suppressed hepcidin increases intestinal iron absorption and release from stores.

  • C. Loss of ferroportin in duodenal enterocytes blocks iron export to the plasma

    Losing ferroportin would block absorption and prevent iron overload.

  • D. Reduced transferrin synthesis leaves unbound iron free to enter tissues

    Transferrin synthesis is not the cause; saturation is high but because iron input is excessive.

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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Questions about this Biochemistry question

What is the answer to this Biochemistry question?

The best answer is B, Ineffective erythropoiesis suppresses hepcidin, so gut iron absorption rises. Expanded, ineffective erythropoiesis releases erythroferrone and other signals that suppress hepatic hepcidin.

Why is "Raised hepcidin traps iron in macrophages, which then release it exce…" not the answer?

High hepcidin would trap iron in macrophages and cause anaemia of chronic disease, not overload.

Why is "Loss of ferroportin in duodenal enterocytes blocks iron export to the…" not the answer?

Losing ferroportin would block absorption and prevent iron overload.

Why is "Reduced transferrin synthesis leaves unbound iron free to enter tissu…" not the answer?

Transferrin synthesis is not the cause; saturation is high but because iron input is excessive.

What concept does this question test?

It tests Vitamins and minerals: iron overload in thalassaemia intermedia in Biochemistry. Low hepcidin keeps ferroportin active, so duodenal absorption and macrophage release of iron increase, causing overload even without transfusions. Chelation is guided by liver iron and ferritin.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Vitamins and minerals: iron overload in thalassaemia intermedia?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.