Vesiculobullous disorders: desmoglein compensation theory: 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: desmoglein compensation theory

Sample item

A patient has painful oral erosions for months without skin blisters. Serum contains autoantibodies against desmoglein 3 only. Which explanation best accounts for the absence of skin lesions?

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

The answer and the reasoning

C. Desmoglein 1 in the skin compensates for the loss of desmoglein 3

In the desmoglein compensation theory, mucosa expresses mainly desmoglein 3, so anti-Dsg3 antibodies cause mucosal-dominant pemphigus vulgaris. In skin, abundant desmoglein 1 can compensate, and blistering appears only when anti-Dsg1 antibodies are also present.

Option by option

  • A. Desmoglein 3 is absent from the skin

    Dsg3 is present in the lower epidermis, so its absence does not explain sparing.

  • B. Skin keratinocytes do not express any desmogleins

    Keratinocytes express several desmogleins, with Dsg1 predominant in the upper epidermis.

  • C. Desmoglein 1 in the skin compensates for the loss of desmoglein 3 (correct)

    Correct. Skin has enough Dsg1 to maintain adhesion, so isolated anti-Dsg3 spares it.

  • D. The antibodies cannot bind to cutaneous keratinocytes

    The antibodies do bind to skin, but the skin has Dsg1 to compensate.

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, Desmoglein 1 in the skin compensates for the loss of desmoglein 3. In the desmoglein compensation theory, mucosa expresses mainly desmoglein 3, so anti-Dsg3 antibodies cause mucosal-dominant pemphigus vulgaris.

Why is "Desmoglein 3 is absent from the skin" not the answer?

Dsg3 is present in the lower epidermis, so its absence does not explain sparing.

Why is "Skin keratinocytes do not express any desmogleins" not the answer?

Keratinocytes express several desmogleins, with Dsg1 predominant in the upper epidermis.

Why is "The antibodies cannot bind to cutaneous keratinocytes" not the answer?

The antibodies do bind to skin, but the skin has Dsg1 to compensate.

What concept does this question test?

It tests Vesiculobullous disorders: desmoglein compensation theory in Dermatology. In skin, abundant desmoglein 1 can compensate, and blistering appears only when anti-Dsg1 antibodies are also present.

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: desmoglein compensation theory?

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.