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Fixed drug eruption, a common finding in Lagos, was observed among patients being treated with two heavily promoted drugs: a pyrazolone analgesic and a benzodiazepine. Offending drugs should be considered in general classes rather than as individual compounds.
Twenty-one patients with fixed drug eruption were studied with the lymphocyte transformation test. In no patient was there blast transformation when the responsible drug (1:10,000 dilution) was added to the lymphocyte culture. The addition to the lymphocyte culture of 0.4 ml of autologous serum, taken at the acme of the clinical reaction, produced blast transformation of the lymphocytes, and when the responsible drug (1:10,000 dilution) was added to this system, blast transformation increased by several times. The addition of the responsible drug to autologous serum obtained during clinical remission produced a minimal or negative response. These findings suggest that during fixed drug eruptions a blast transforming factor appears temporarily in the serum and increases its activity in the presence of the responsible drug. This factor spontaneously diminishes or disappears a few days after clinical exacerbation.
Although any drug may cause any dermatitis, it is possible to categorize a relatively few types of dermatitis and a relatively small number of drugs in such a way as to afford a practical approach to a sometimes confusing problem. These problems are generally clinical ones not requiring laboratory work and an experienced clinician will probably be able to manage most of these cases without extensive consultations.
A case of bullous fixed drug eruption involving upper lip, tongue and foot, presumably due to erythromycin, is reported. It is perhaps the first report of erythromycin to be very likely the cause of fixed drug eruption.
A fixed drug eruption due to paracetamol is reported. Over 10,000,000 prescriptions (EC10) for paracetamol are issued annually and rashes occurring as possible adverse reactions to this drug are reported fairly frequently to the Committee on Safety of Medicines (Committee on Safety of Medicines-personal communication). These include urticaria, angioneurotic oedema, purpura, morbilliform and scarlatiniform rashes, erythema nodosum, eczema, alopecia and nail changes but in many of these cases the cause-effect relationship is unproven. One strongly suspected case (Savin, 1970) was reported from St John's Hospital. This was a patient who developed a fixed drug rash after taking a chlormezanone-paracetamol combination. However, no other reports of a fixed drug rash which was proved to be due to parcetamol have been found.
We observed 11 cases of fixed drug eruption to tetracyclines. Two cases were in a mother and her adult son, and two patients experienced fading of their lesions while continuing to take 1 g of the drug per day. Several patients were cross-reactive to different salts.
Fifty-five patients with fixed drug eruption were investigated to determine the drug(s) causing the reaction. History, classic clinical features of well circumscribed erythema, edema and violaceous pigmentation, and the recurrence of the eruptions on the same sites on readministering drug were used as diagnostic criteria. This was confirmed by a provocative test. Sulfonamides and analgesics either alone or in combination were the most common causes of reaction.
The serum globulins IgG, IgA and IgM were studied in the serum of 47 patients with fixed drug eruption due to identified drugs. The diagnosis was established by using as a test the readministration of the responsible drug and the consequent appearance of the eruption. IgM was found in normal amounts in the acute phase and after the remission of the eruption, whereas IgG and IgA were found increased during the acute phase of the eruption though after the remission, levels returned to normal.
Drug eruption was diagnosed in a 4-year-old German Shepherd Dog being treated with sulfonamides for vertebral osteomyelitis due to infection with Nocardia spp. The eruption was characterized by generalized, pruritic, eczematous dermatitis. Diagnosis was based on a history of repeated exposure to sulfonamides, skin biopsy findingd, and clinical recovery on cessation of sulfonamide therapy.
A 29-year-old woman developed a pulsating, fixed drug eruption following a year's course of both oral and parenteral administration of tetracycline for pharyngitis. Patch testing of tetracycline powder under occlusion at the site confirmed the diagnosis.
Electron microscopic studies have been carried out on three cases of fixed drug eruption, with particular regard to the dyskeratotic cells. The authors have tried to show the sequence of events leading from a normal basal keratinocyte to a dyskeratotic body. Ribosomes were first increased in number; then the tonofibrillar system looked thicker, cytoplasmic organelles degenerated and numerous melanosomes appeared. Many dyskeratotic bodies were later found in epidermal macrophages and in the intercellular space. Several intra-cytoplasmic desmosomes were found in the dyskeratotic cells and their evolution is discussed. The increased number of melanosomes seen in the dyskeratotic bodies could be due to injury to epidermal lysosomal catabolism or it could be due to an apparent increase in melanosome numbers, within cells whose volume has been reduced.
Azapropazone is a new, powerful, antiinflammatory analgesic. Initial trails have confirmed its efficacy as an antirheumatic agent, with a low incidence of adverse reactions. Recently the authors have seen two patients, each of whom developed a distinctive but clinically dissimilar, bizarre, bullous eruption after taking this drug. A brief account of these cases has been published elsewhere (1).
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