Antiinflammatory effects of oxatomide.

There is increasing evidence that histamine may have wider proinflammatory and immunomodulatory activities than previously reported. It may influence several functions of lymphocytes, monocytes, basophils and macrophages, modulating the release of inflammatory mediators and cytokines. These observations have aroused interest in the pharmacology and clinical applications of histamine H1 receptor antagonists and have led to the identification of novel antiinflammatory properties for this class of drugs. Oxatomide, initially characterized as an H1 antagonist, inhibits the secretion of several mediators of inflammation from human basophils and mast cells. In vitro oxatomide inhibits the release of both preformed (histamine and tryptase) and de novo synthesized mediators (leukotriene C4 and prostaglandin D2). The inhibitory effect is not restricted to basophils and mast cells but is also evident on other inflammatory cells such as the neutrophils. In this cell, oxatomide inhibits arachidonic acid mobilization, and leukotriene B4 and platelet-activating factor synthesis, presumably by reducing the activity of cytosolic phospholipase A2. These observations extend the pharmacological activities of oxatomide beyond H1 receptor antagonism and suggest that this drug influences a variety of biochemical events in human inflammatory cells. These antiinflammatory activities help to explain its beneficial effect in various allergic and inflammatory disorders, including urticaria, allergic rhinitis and bronchial asthma.

Giardiasis as a cause of hypokalemic myopathy in congenital immunodeficiency.

Hypokalemic myopathy may occur in several infections. We report a case of severe and transient myopathy secondary to hypokalemia induced by chronic intestinal infection with Giardia lamblia in a patient with common variable hypogammaglobulinemia. Hypokalemic myopathy is documented by serum enzymes, electromyography (reduction in the number of voluntarily activated motor unit action potentials and an increase in polyphasic motor unit action potentials, and pathological changes (hematoxylin-eosin, ATPase staining). The case reported involves hypokalemic myopathy induced by giardiasis in a patient with primary immunodeficiency; the histopathological changes observed in a skin/muscle biopsy from this patient are described for the first time.

Effect of experimental infarct on the mortality rate in alloxan-diabetic rats.

The authors report the wide mortality observed in alloxan diabetic rats infarcted with large doses of isoproterenol. The experimental data are in line with the results of clinical studies testifying that the diabetic disease involves the cardiovascular system and affects the prognosis of myocardial infarct. These experiences do not permit to define the direct mechanism(s) responsible for the high mortality in diabetic infarcted rats over controls (diabetic not infarcted); however these results give rise to a discussion on the following topics: 1. The damage of intramural coronary vessels as a cause of depressed cardiac contractility in diabetic rats. 2. The role of reduced plasmatic levels of insulin in depressing myocardial performance in alloxan diabetic rats. 3. The hyperglycaemia-provoking effect of isoproterenol as a contributing factor in the death of diabetic rats. 4. The possible direct action of diabetogenic doses of alloxan on the myocardium.