allopurinol and Erythema

Topics: Allopurinol; Ampicillin; Antibody Formation; Cross Reactions; Cytomegalovirus Infections; Drug Contamination; Drug Eruptions; Drug Synergism; Erythema; Humans; Immunity, Cellular; Infectious Mononucleosis; Leukemia, Lymphoid; Lymphocytes; Lymphoma, Large B-Cell, Diffuse; Urticaria

A 58-year-old woman was admitted for heart failure and concern for cardiogenic shock. The patient had been recently placed on colchicine and allopurinol, 4 months and 3 weeks, respectively, prior to admission. Upon admission, she had a cutaneous eruption that had started abruptly several days after allopurinol initiation. It included multiple erythematous papules with scant scale on the forearms and numerous erythematous papules on the legs. Because of the varied morphologic presentation, biopsies from both the thigh and forearm were performed for a suspected drug reaction. The specimen from the thigh showed a superficial-dermal, band-like lymphocytic infiltrate with dyskeratosis and numerous intraepidermal mitotic figures predominantly in metaphase. In addition, there were neutrophils with leukocytoclasia. The specimen from the forearm showed superficial perivascular lymphocytic inflammation and intraepidermal dyskeratosis with mitotic figures similar to the thigh biopsy specimen but without a dermal neutrophilic infiltrate. An unusual drug eruption with features of colchicine toxicity was favored. Colchicine toxicity is not a commonly encountered clinical scenario and cutaneous findings have only rarely been described. Herein we report an exceedingly rare case of an unusual drug reaction with "colchicine figures" (i.e., ring-shaped mitotic figures arrested in metaphase) consistent with colchicine toxicity.

Topics: Allopurinol; Colchicine; Drug Eruptions; Erythema; Exanthema; Female; Humans; Middle Aged

Topics: Aged; Aged, 80 and over; Allopurinol; Asian People; Case-Control Studies; Drug-Related Side Effects and Adverse Reactions; Erythema; Female; Gout Suppressants; HLA-B Antigens; Humans; Japan; Male; Odds Ratio; Pharmacogenetics; Stevens-Johnson Syndrome

In this study we attempted to demonstrate whether endothelial cell nitric oxide synthase (eNOS) and xanthine oxidase (XO) could be activated to release nitric oxide (NO) and peroxynitrite (ONOO-) following exposure to ultraviolet B (UVB) radiation and to define whether this light-induced response could be involved in the pathogenesis of sunburn erythema and inflammation. Treatment of human endothelial cells with UVB (290-320 nm) radiation (up to 100 mJ/cm2) resulted in an increase of both NO and ONOO- release that was inhibited by NG-monomethyl-L-arginine (L-NMMA). Treatment of cell cytosol with various doses of UVB radiation (up to 20 mJ/cm2) resulted in a threefold increase of XO activity that was inhibited (approximately 90% by oxypurinol. In reconstitution experiments, when purified eNOS was added to purified XO, an almost fourfold increase in ONOO- production at 20 mj/cm2 UVB radiation was observed. UVB radiation (100 mg/cm2) decreased cell membrane fluidity, indicating changes in the physicochemical characteristics of the membranes. In in vivo experiments, when human volunteers were subjected to UVB light, a protection factor (PF) of 3.90 +/- 0.85 was calculated when an emulsified cream formulation containing nitro-L-arginine (L-NA; 2%) and L-NMMA (2%) was applied to their skin. The present studies indicate that UVB radiation acts as a potent stimulator of eNOS and XO in human endothelial cells. The cytotoxic effects of NO and ONOO- may be the main factors in the integrated response of the skin leading to vasodilatation, the first key event of erythema production and the inflammation process.

Topics: Cells, Cultured; Dermatitis; Endothelium, Vascular; Enzyme Activation; Erythema; Humans; Nitrates; Nitric Oxide; Nitric Oxide Synthase; Sunburn; Ultraviolet Rays; Umbilical Veins; Xanthine Oxidase

The effect of vitamin E on the modulation of keratinocytes was studied in rats. A 1% lauroylsarcosine (LS) ointment caused skin erythema with keratinocyte-damage. A 30% vitamin E ointment markedly alleviated this erythema and protected keratinocytes from cell damage. Vitamin E (100 micrograms/ml) was also effective on LS (7.5 micrograms/ml)-induced proliferative reduction of cultured keratinocytes. On the other hand, ointment containing superoxide dismutase (SOD) (99,000 U/g) decreased the LS-induced erythema, suggesting that superoxide anion (O2-) produced from keratinocytes play an important role in the skin irritation. Indeed, LS induced O2- production from cultured keratinocytes. The O2- was significantly reduced by vitamin E and SOD, although vitamin E had no effects on O2- production in a xanthine-xanthine oxidase system, unlike the effect observed with SOD. These results indicate that vitamin E is an inhibitor of keratinocyte-modulation.

Topics: Animals; Cell Division; Cells, Cultured; Detergents; Dose-Response Relationship, Drug; Epidermal Cells; Epidermis; Erythema; Keratinocytes; Male; Ointments; Rats; Rats, Wistar; Sarcosine; Skin Tests; Superoxide Dismutase; Superoxides; Vinblastine; Vitamin E; Xanthine; Xanthine Oxidase; Xanthines

Topics: Animals; Erythema; Female; Guinea Pigs; Hypoxanthine; Hypoxanthines; Oxygen; Superoxide Dismutase; Time Factors; Xanthine Oxidase