Protective effect of a cysteine prodrug and antioxidant,L-2-oxothiazolidine-4-carboxylate,against ethanol-induced gastric lesions in rats

Earlier studies have suggested an important role of glutathione (GSH) in cytoprotection against free radicals induced oxidative damage. This study reports gastroprotective effects of a cysteine precursor, L-2-oxothiazolidine-4-carboxylate (OTC), in experimental models of gastric secretion and ulceration. Acid secretion studies (volume and acidity) were undertaken in pylorus-ligated rats whereas the gastric lesions were induced by ethanol. Different groups of animals were treated with OTC (0, 100, 200 and 400 mg/kg). The levels of gastric wall mucus, nonprotein sulfhydryls (NP-SH) and myeloperoxidase (MPO) were measured in the glandular stomach of rats following ethanol-induced gastric lesions. Both medium and high doses of OTC significantly reduced the volume and acidity of gastric secretion in pylorus-ligated rats. Pretreatment with OTC significantly and dose-dependently attenuated the formation of ethanol-induced gastric lesion. OTC significantly protected the gastric mucosa against ethanol-induced depletion of gastric wall mucus, NP-SH and MPO. The gastroprotective effects of OTC may be attributed to its ability to inhibit neutrophils activity and replenish GSH demand.     

Kawasaki disease in an infant after administration of hexavalent vaccine

Kawasaki disease is a vascular disorder of unknown etiology that affects children. Kawasaki disease mainly involves medium-sized blood vessels and may cause cardiovascular complications, particularly coronary artery aneurysms. Concern has been raised against various types of vaccines becoming potential risk factors for Kawasaki disease. Here, we describe a case of a 4-month-old Saudi infant who presented with incomplete Kawasaki disease a few hours after receiving his hexavalent vaccine and there was a significant dilatation of all coronary arteries. Although a relationship between vaccinations and Kawasaki disease has been suggested, there is no strong evidence of an increased risk or causal association. This possibility of adverse effects is rare but should be observed and further investigated.     

Effects of a change in the pattern of insulin delivery on carbohydrate tolerance in diabetic and nondiabetic humans in the presence of differing degrees of insulin resistance.

While it is well established that people with non-insulin dependent diabetes mellitus have defects in both insulin secretion and action, the relative contribution of each to glucose intolerance is not known. Therefore, nondiabetic (lean and obese) and non-insulin dependent diabetes mellitus subjects were studied on two occasions. On each occasion, insulin secretion was inhibited with somatostatin and glucose was infused in a pattern and amount that mimicked the systemic delivery rate normally observed after ingestion of 50 g of glucose. Insulin also was infused so as to mimic postprandial insulin profiles observed in separate groups of diabetic and nondiabetic subjects after food ingestion. Glucose turnover was measured using the isotope dilution method. A delayed pattern of insulin delivery (i.e., a "diabetic" insulin profile) led to higher (P < 0.05) glucose concentrations in all groups; however, the effects were transient, resulting in only a modest increase in the integrated glycemic responses. An isolated defect in insulin action had little effect on peak glucose concentration; however, it prolonged the duration of hyperglycemia, leading to a 2.5-4.2-fold increase (P < 0.05) in the integrated glycemic response. A combined defect in the pattern of insulin secretion and action was additive rather than synergistic. Both defects caused hyperglycemia by altering suppression of endogenous glucose release and stimulation of glucose disposal. Whereas obese diabetic and nondiabetic subjects had comparable defects in glucose clearance, non-insulin dependent diabetes mellitus subjects also had defects in hepatic insulin action. Thus, abnormalities in the pattern of insulin secretion and action alone or in combination impair glucose tolerance. An isolated defect in insulin action has a more pronounced and prolonged effect than does an isolated change in the pattern of insulin secretion. Hepatic and extrahepatic insulin resistance results in marked and sustained hyperglycemia.     

Unusual causes of calf swelling--2. Rhabdomyolysis mimicking deep vein thrombosis

A 55 year old woman with pain and swelling of the leg was heparinized on the basis of a clinically diagnosed ilio-femoral deep vein thrombosis (DVT). Subsequent investigation showed her to have extensive rhabdomyolysis of the leg. Rhabdomyolysis can mimic the appearance of deep vein thrombosis and this case further illustrates the importance of venography in the assessment of the swollen leg.     

Polycystic ovaries: do these represent a specific endocrinopathy?

Serum pituitary gonadotrophins, oestradiol, testosterone and insulin pulse patterns were examined at 15-min intervals for 6 h in 40 women with a previous diagnosis of polycystic ovarian disease (PCO) based on clinical, endocrinological and ultrasound data. Age, duration of symptoms, body mass index (BMI) and ovarian volume showed no correlation with the 6-h mean value of any hormone and testosterone blood levels did not correlate with those of insulin. Some patients had high and others low LH pulse pattern components, and few had an inverted LH:FSH ratio. Morphological polycystic ovarian changes may be a reflection of various rather than a single pattern of gonadotrophin secretion.     

Treatment of hypercalcaemia in thyrotoxicosis with aminohydroxypropylidene diphosphonate

Two patients had symptomatic hypercalcaemia accompanying thyrotoxicosis, despite initial treatment with volume repletion, beta blockade and antithyroid drugs. They were further managed with intravenous infusions of aminohydroxypropylidene diphosphonate resulting in rapid normalization of the serum calcium, with relief of symptoms. Aminohydroxypropylidene diphosphonate effectively suppressed the increased bone resorption of thyrotoxicosis without any undesirable adverse effects.