Vesiculobullous disorders: IVIG in refractory pemphigus: practice question

A Dermatology 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.

Try it

Dermatology · Vesiculobullous disorders: IVIG in refractory pemphigus

Sample item

A patient with extensive pemphigus vulgaris develops recurrent sepsis on immunosuppressants. Intravenous immunoglobulin is added. What is the proposed mechanism of its benefit?

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

The answer and the reasoning

C. Saturation of the neonatal Fc receptor, hastening catabolism of autoantibodies

High-dose IVIG saturates the neonatal Fc receptor that normally recycles IgG, so pathogenic autoantibodies are degraded faster. It also has immunomodulatory effects. It is useful when conventional immunosuppression is contraindicated or has failed.

Option by option

  • A. Calcineurin inhibition in T cells

    Calcineurin inhibition is the mechanism of ciclosporin and tacrolimus.

  • B. Depletion of CD20 B cells

    CD20 depletion is the mechanism of rituximab.

  • C. Saturation of the neonatal Fc receptor, hastening catabolism of autoantibodies (correct)

    Correct. FcRn saturation increases clearance of pathogenic IgG.

  • D. Inhibition of dihydrofolate reductase

    Dihydrofolate reductase inhibition is the mechanism of methotrexate.

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.

More Dermatology questions

Questions about this Dermatology question

What is the answer to this Dermatology question?

The best answer is C, Saturation of the neonatal Fc receptor, hastening catabolism of autoantibodies. High-dose IVIG saturates the neonatal Fc receptor that normally recycles IgG, so pathogenic autoantibodies are degraded faster.

Why is "Calcineurin inhibition in T cells" not the answer?

Calcineurin inhibition is the mechanism of ciclosporin and tacrolimus.

Why is "Depletion of CD20 B cells" not the answer?

CD20 depletion is the mechanism of rituximab.

Why is "Inhibition of dihydrofolate reductase" not the answer?

Dihydrofolate reductase inhibition is the mechanism of methotrexate.

What concept does this question test?

It tests Vesiculobullous disorders: IVIG in refractory pemphigus in Dermatology. It also has immunomodulatory effects. It is useful when conventional immunosuppression is contraindicated or has failed.

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 Vesiculobullous disorders: IVIG in refractory pemphigus?

Learn each condition by its primary lesion, site and signature sign. Then use the flashcards and the other Dermatology 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.