Induced pemphigus.
The reports of induced pemphigus have multiplied over the last 10 years. Several heterogeneous factors, such as drugs (penicillamine, pyritinol, captopril, rifampicin, etc.), physical agents (burns, UV, and ionizing radiation) and viruses, can play an inducing role. Usually, the disease is preceded by prodromal, non-specific lesions. The full-blown stage shows features of pemphigus foliaceus, erythematosus or herpetiformis. Histologically, acantholytic splits mostly occur at the highest malpighian layers. Intercellular antibodies and frequently concomitant other auto-antibodies are found in the serum, the titre of the former usually being low and unrelated to the severity or course of the disease. The biological progress is variable and ranges from rapidly and definitively healing cases (induced pemphigus proper) to others which, in spite of the elimination of the inducing factor, self perpetuate just like true pemphigus (triggered pemphigus). Pathogenic hypotheses are based on the act that some inducing factors can alter the antigen distribution on keratinocyte membranes and/or interfere with immune surveillance by impairing T-suppressor cells.
D000906:Antibodies / Q000032:analysis; D000941:Antigens / Q000276:immunology; D001323:Autoantibodies / Q000276:immunology; D002056:Burns / Q000150:complications; D006801:Humans; D009369:Neoplasms / Q000150:complications; D010392:Pemphigus / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D010396:Penicillamine / Q000009:adverse effects; D014466:Ultraviolet Rays / Q000009:adverse effects; D014780:Viruses / Q000472:pathogenicity
D000906:Antibodies; D000941:Antigens; D001323:Autoantibodies; D010396:Penicillamine