Lesion topography in two cases of nifedipine-related pemphigus.

Similar lesion topography which resembled an inverted fir tree in two patients with nifedipine-related pemphigus vulgaris is described. The possible relation of the lesion pattern to the offending drug is discussed.

Pemphigus and pemphigoid-like effects of nifedipine on in vitro cultured normal human skin explants.

BACKGROUND: A variety of drugs have been implicated in the onset and exacerbation of pemphigus and bullous pemphigoid. The demonstration of biochemical acantholysis in skin explants to various drugs in the absence of autoantibodies, in which the tested drugs evoke a biochemical reaction that leads to desmosomal function loss, may be a valuable adjunct to patient management by confirming the suspicion of drug-related pemphigus or bullous pemphigoid. OBJECTIVE: To determine whether a skin explant model might serve as a possible in vitro correlate of drug-induced pemphigus and pemphigoid-like effects related to the calcium channel blocker nifedipine. METHODS: Normal human breast skin obtained from nonpemphigus and nonpemphigoid patients undergoing mastectomy was cultured with nifedipine at final concentrations of 2, 4, and 8 mM. The drug effect on skin explants evidenced by morphologic changes was evaluated by microscopy by three observers. RESULTS: Five out of seven explants cultured with nifedipine at concentrations ranging from 2 to 8 mM exhibited obvious morphologic changes of two types: intraepithelial (or pemphigus-type) splittings and subepithelial (or pemphigoid-type) splittings. Two explants showed no acantholysis and no subepithelial splittings. Control cultures without polyethylene glycol 200 (PEG) showed no changes. Skin control samples cultured in medium supplemented with 10% PEG displayed vacuolar degeneration throughout the entire epidermis, but no sign of cell-cell dyshesion or dermo-epidermal detachment. CONCLUSIONS: A type of skin susceptibility to nifedipine may be genetically determined, with some nifedipine-treated patients developing an acantholytic reaction and others a subepidermal bullous eruption.

Recognition of pemphigus antigens in drug-induced pemphigus vulgaris and pemphigus foliaceus.

BACKGROUND: The clinical appearance and biologic behavior of drug-induced pemphigus depend on the type of inducing drug. OBJECTIVE: Our purpose was to investigate patients with drug-induced pemphigus vulgaris and pemphigus foliaceus antigens and compare results of studies to detect antibody reactivity in sera of these patients with the serology of patients with idiopathic pemphigus. METHODS: Ten patients with drug-induced pemphigus were studied. Antibody reactivity was determined against the pemphigus vulgaris antigen, desmoglein 3, and against desmoglein 1. RESULTS: The patient with pemphigus foliaceus and low levels of autoantibodies precipitated neither antigen. One patient with pemphigus vulgaris and high levels of antibody also failed to precipitate any specific antigen. Sera from eight patients with drug-induced pemphigus vulgaris had circulating autoantibodies directed to either the pemphigus vulgaris or pemphigus foliaceus antigen. Low levels of antibody in two of these eight patients precipitated only the pemphigus foliaceus antigen. High levels of antibody in five of the eight patients precipitated the pemphigus vulgaris antigen; two of these also reacted with the pemphigus foliaceus antigen. CONCLUSION: The autoantibody response was similar in both spontaneous and drug-related disease. A similar molecular mechanism in the two types of pemphigus is suggested.

Paraneoplastic subacute cutaneous lupus erythematosus: report of a case associated with cancer of the lung.

A case of subacute cutaneous lupus erythematosus (SCLE) associated with lung carcinoma is presented. A review of the literature revealed only 5 other cases of SCLE associated with internal malignancy. The tumor in the described case most probably developed before the appearance of the eruption. Cancer chemotherapy was followed by shrinkage of tumor mass and regression of the skin lesions. The sequence of these events corresponds to the definition of paraneoplastic dermatoses.

Diclofenac: a new trigger of pemphigus vulgaris?

Many drugs have been shown to induce pemphigus, including thiol and nonthiol drugs. We present a case of pemphigus vulgaris where a nonsteroidal anti-inflammatory medication, diclofenac in suppositories and topical gel preparations, is suspected of having triggered the disease. The temporal relationship between drug and outbreak of disease together with the positive migration inhibition factor test to diclofenac point to the possible involvement of this drug in triggering pemphigus vulgaris.

Penicillamine-induced bullous dermatoses.

The successful therapeutic use of D-penicillamine (DPA) has been hindered by its many adverse effects. Autoimmune bullous syndromes are among the less common adverse DPA reactions; they are not dose dependent and appear late in the treatment of diseases of altered immunity, most often rheumatoid arthritis. The majority of the DPA-induced bullous syndromes belong to the pemphigus spectrum, usually pemphigus foliaceus or erythematosus, have a lower prevalence of demonstrable tissue-fixed or circulating antibodies than spontaneously occurring pemphigus, display abnormal direct immunofluorescent patterns, and have a generally favorable prognosis. However, many cases do exhibit a full-blown chronic disease, unaffected by DPA withdrawal. DPA-induced cicatricial pemphigoid is a severe disease of both mucous and cutaneous involvement with a prognosis similar to the spontaneous disease. Cases of DPA-induced epidermolysis bullosa acquisita and DPA-induced bullous pemphigoid were not sufficiently substantiated by immunofluorescence or immunoprecipitation criteria.