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Induced pemphigus

V Ruocco, M Pisani

    Archives of Dermatological Research
    |January 1, 1982
    PubMed
    Summary
    This summary is machine-generated.

    Induced pemphigus, often triggered by drugs, radiation, or viruses, presents varied clinical courses. Some cases resolve upon removing the trigger, while others persist like true pemphigus.

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    Area of Science:

    • Dermatology
    • Immunology

    Background:

    • Reports of induced pemphigus have increased significantly in the past decade.
    • Various factors including drugs (e.g., penicillamine, captopril), physical agents (burns, UV, radiation), and viruses can induce pemphigus.
    • The disease often begins with non-specific prodromal lesions before manifesting full-blown symptoms.

    Purpose of the Study:

    • To review the clinical and pathological features of induced pemphigus.
    • To discuss the variable biological progression and pathogenic hypotheses of induced pemphigus.

    Main Methods:

    • Review of clinical reports and histological findings in induced pemphigus.
    • Analysis of serological markers, including intercellular antibodies and other auto-antibodies.
    • Examination of pathogenic mechanisms involving antigen distribution and immune surveillance.

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    Main Results:

    • Induced pemphigus can mimic pemphigus foliaceus, erythematosus, or herpetiformis.
    • Histologically, acantholytic splits are typically found in the upper malpighian layers.
    • Low titers of intercellular antibodies are common, often unrelated to disease severity or progression.

    Conclusions:

    • Induced pemphigus exhibits diverse clinical outcomes, ranging from complete healing after trigger removal to self-perpetuating disease resembling true pemphigus.
    • Pathogenic theories suggest that inducing factors may alter keratinocyte membrane antigen distribution or impair T-suppressor cell function.
    • Understanding these mechanisms is crucial for managing and potentially preventing induced pemphigus.