Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

I have encountered 50 patients with clinical thrombophlebitis involving the lower extremites, with or without associated edema and pulmonary embolism, in whom longstanding self-medication with large amounts of vitamin E appeared to be a significant factor. The majority improved following cessation of vitamin E. In view of the epidemic nature of thrombophlebitis and deep vein thrombosis in the United States, the presumed innocuousness of vitamin E therapy requires reevaluation. Other clinical side effects also have been noted in patients receiving large doses of vitamin E. They include breast tenderness, elevation of blood pressure, a fatigue syndrome, myopathy, intestinal cramps, urticaria, and the possible aggravation of diabetes mellitus. The influence of concomitant metabolic, endocrine, and cardiovascular disorders on the thrombogenic potential of vitamin E is raised, and several possible mechanisms conducive to thrombophlebitis are reviewed.
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PMID:Thrombophlebitis associated with vitamin E therapy. With a commentary on other medical side effects. 43 74

The pathogenesis of the physical urticarias has not been completely defined. Indeed, different stimuli can induce similar clinical manifestations, some of which are capable of generating reactive oxygen species. In order to evaluate whether the generation of an oxidative stress response could be a common pathogenetic mechanism of the disease, we have determined the profile of a number of chemical and enzymatic antioxidants in blood samples from a group of patients with physical urticarias. Compared with controls, a systemic imbalance of the antioxidants was detected in the patient group with a decrease of both plasma vitamin E and cellular catalase and glutathione peroxidase activities along with an increase of superoxide dismutase activity. Moreover, an increase in the percentage of plasma polyunsaturated fatty acids, as a target for peroxidative damage, was also observed. These alterations may lead to an increased percentage of peroxidable compounds in skin and to the intracellular generation of reactive oxygen species and could therefore provide one possible explanation for the patients' urticarial response to stimuli. Even if the alteration of the antioxidant status is secondary to changes in cytokine or complement activation, our results suggest a common biochemical profile in patients with different forms of physical urticaria.
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PMID:Oxidative stress in physical urticarias. 1142 77