Fixed drug eruption and epididymitis due to antipyrine.
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Nicolau's syndrome, also called embolica cutis medicamentosa, is characterized by well- circumscribed livedoid dermatitis with aseptic necrosis after intramuscular injection. We report the case of a 45-year-old woman with severe necrosis of the thigh several days after a routine intramuscular injection of hydroxyzine who was transferred to and treated at our Regional Burn Center. Although there has been one case report and numerous voluntarily reported instances of intramuscular hydroxyzine-induced necrosis to the Food and Drug Administration Spontaneous Reporting System, this phenomenon is rare.
Nicolau Syndrome, also known as livedo-like dermatitis (LLD) or embolia cutis medicamentosa (ECM) is an infrequent complication following intramuscular and intra-articular injection of various drugs. This rare entity is characterized by severe pain and erythematous-ecchymotic reticular lesions at the injection site, which in many cases lead to necrotic ulcers and scarring. We report three cases of Nicolau Syndrome following injection of diclofenac, penicillin G, and cyanocobalamin.
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Deterioration of acne vulgaris or eruption of an acneiform exanthema could be established during treatment with vitamin B6 and/or vitamin B12 in 14 patients. Females were by far the more frequently affected. The appearance of skin symptoms, even outside the age groups typically affected by acne vulgaris is characteristic. The clinical appearance of acneiform exanthema occurring during treatment with vitamin B6 or B12 consists of loosely disseminated small papules or papulopustules on the face (especially on the forehead and chin), on the upper parts of the back and chest and spreading to the upper arm. The pathogensis of the change is not yet certain. The acneiform rash generally fades within a short time after vitamin B6 or vitamin B12 treatment has been stopped.
The pathogenesis of local skin necroses after intramuscular injection of various drugs such as phenylbutazone (Embolia cutis medicamentosa, Nicolau's syndrome) is not clear. In an attempt to simulate this clinical feature experiments were performed on the rabbit ear lobe. A 20% phenylbutazone solution was injected paraarterial, intraarterial and paraarterial after perforation of the vessel. The drug produced a violent inflammation with all kinds of application. The local inflammation induced by paraarterial injection resulted in a fine scarring. Both other kinds of application produced necroses or even perforations. The histological examinations in these cases revealed massive destructions of the inner arterial wall. In control-experiments necroses or perforations were nerve observed. From these data the following conclusions on the etiology of Nicolau's syndrome can be drawn: Phenylbutazone injected into the vascular or perivascular tissue causes an obligatory inflammation. After lesion of an artery complete destruction of the vessel followed by necrosis of the skin may occur. It seems obvious that this secondary effect can not completely be avoided.