Biomedical subjects
Publications and source records attributed to J Lysy.
A 19-year-old man without apparent predisposing factors was found to have chronic pancreatitis and 6 months later developed ulcerative colitis. Is there a real association between pancreatitis and inflammatory bowel disease? We discuss previous reports.
The effect of duodenal ulcer healing induced by omeprazole on gastroduodenal generation of eicosanoids, platelet-activating factor (PAF), pepsinogen A, and gastrin was evaluated. Sixty patients with endoscopically proven duodenal ulcer were randomized to receive 20 mg omperazole once daily or 300 mg ranitidine at bedtime for 2 weeks. Patients whose ulcers did not heal were treated for an additional 2 weeks. Endoscopic biopsy specimens and serum samples were obtained before and after treatment. There was no significant difference in the healing rate between the two treatment modalities. At 2 weeks healing rates were 60% and 56% in the omperazole and ranitidine groups, respectively, whereas at 4 weeks the respective healing rates were 96% and 86%. Ulcer healing induced by omeprazole and ranitidine was not accompanied by significant changes in mucosal leukotriene B4 or C4 generation. Mucosal PAF significantly decreased in patients treated with omeprazole for 4 weeks. In omperazole-treated patients there was a trend towards increase in mucosal prostaglandin E2 generation which was significant in the fundus after 4 weeks of treatment. After 2 weeks of omeprazole treatment, serum gastrin and pepsinogen A levels almost doubled when compared with their pretreatment levels. In conclusion, duodenal ulcer healing with 20 mg omeprazole daily is not superior to healing rates with 300 mg ranitidine at bedtime after both 2 and 4 weeks of treatment. In omeprazole-treated subjects ulcer healing was accompanied by a significant decrease in mucosal PAF generation and increased levels of serum gastrin and pepsinogen A.
The seasonal pattern of community-based acute bleeding from the upper gastrointestinal (UGI) tract was studied prospectively in 1988-1991. Out of 3343 emergency admissions to the Departments of General Surgery, 321 (9.6%) were due to acute UGI bleeding. There was a significant monthly variation in the total number of admissions, as well as in the number of admissions due to acute UGI bleeding (p < 0.0001). However, there was no correlation between the two. Significant seasonal fluctuations were noted both in the absolute number of admissions due to acute UGI bleeding and in the percentage of UGI bleeding admissions of the total number of admissions to the Departments of General Surgery (p = 0.0002). During summer (July through September), the incidence declined significantly to a nadir of 5.5% of total number of admissions in July. The seasonal fluctuation correlated closely with the incidence of duodenal ulcer, but not with that of gastric ulcer. The seasonal pattern was consistent both in patients who had used aspirin or other nonsteroidal anti-inflammatory drugs as well as in those who had not.
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The clinical characteristics and endoscopic appearance of inflammatory bowel disease (IBD) may be very similar to those of amebic colitis. Physicians, especially in areas in which amebiasis is endemic, are familiar with this difficulty. Moreover, in individual cases, it may even be impossible to distinguish between the two conditions, since stool specimens, bowel biopsies, and serological studies may be negative for Entamoeba histolytica, even in the presence of invasive amebic colitis. Invasive amebiasis may rarely be superimposed on IBD, which further complicates the issue. We report here a young patient with a 7-yr history of Crohn's colitis proven histologically who developed invasive amebic colitis during steroid and 6-mercaptopurine treatment for active disease. Stool specimens, mucosal biopsies, and serological studies were negative for E. histolytica, and the diagnosis was established on pathological examination of a surgically resected bowel. Anti-amebic therapy should be considered in endemic areas in cases of persistent IBD.
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In the present study we evaluated the role of endogenous glucocorticoids in the biosynthesis of prostaglandins (PG) in cortical brain tissue of the rat. Experiments were carried out under basal conditions and in response to insulin-induced hypoglycemia and 2-deoxyglucose (2-DG) induced-cytoglucopenia. In intact rats, following hypoglycemia and cytoglucopenia, the production of brain PG was decreased. These two stress stimuli also activated adrenocortical secretory responses, as manifested by an increase in circulating ACTH and corticosterone. Bilateral adrenalectomy did not modify the brain production of PG under basal conditions. In contrast, in adrenal-ectomized rats, the biosynthesis of brain cortical PG was markedly increased in response to insulin and 2-DG. These results suggest that adrenal hormones may be involved in the modulation of cortical PG production under stressful conditions.
We describe a patient with a highly unusual appearance of pyoderma gangrenosum. The pyoderma was located on the auricular region and preceded other manifestations of inflammatory bowel disease by 11 years. There was no correlation between the course of the pyoderma and the clinical activity of the associated bowel disease. Mycotic superinfections masked and delayed the diagnosis in our patient for several years. Only when typical pyoderma gangrenosum lesions developed on the legs at the site of trauma and responded dramatically to systemic corticosteroids was the correct diagnosis established. Pyoderma gangrenosum with secondary fungal infection was thus distinguished from deep ulcerated skin fungal infection simulating pyoderma.
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Glucocorticoid hormones are known to inhibit the production of prostaglandins in many cell types and tissues. The effect of these hormones on the biosynthesis of brain tissue is not yet clear. In the present study we investigated the effect of dexamethasone on the release of prostaglandin E2 (PGE2), thromboxane B2 (TXB2), and 6-keto-PGF1 alpha from various brain areas of male rats. Slices from cortex, hippocampus, hypothalamus, and striatum taken from rats pretreated with dexamethasone 4 mg/kg body weight or vehicle, 18 h and 2 h prior to killing, were incubated in Krebs-Ringer-bicarbonate for 1 h. The accumulation of PGs in the medium was determined by radioimmunoassay. Pretreatment with dexamethasone significantly reduced the release of all PGs from the cortex by 40-50%. In the striatum and hippocampus only TXB2 was reduced by approximately 40%. In the hypothalamus the effect of dexamethasone was not significant. When slices of the same brain areas from intact rats were incubated for 1 h in the presence of 40 microM dexamethasone, only the release of PGE2 from the cortex was reduced (by 30%). These results suggest that glucocorticoids can inhibit PG synthesis in brain tissue, and that the cortex is the most sensitive area to the inhibitory effect of the hormone.
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A rare case of pulmonary pneumatoceles complicating the course of Proteus pneumonia in an adult is described. The pneumatoceles which appeared early in the course of the pneumonia resolved completely without complications. A brief review of the literature regarding formation of cavities in Proteus pneumonia is given.
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A rare case of solitary CNS chloroma in a patient with chronic granulocytic leukemia (CGL) is described. This appears to be the first reported case of intracranial chloroma in CGL without systemic blastic crisis.
With a single exception among 11 strains, each strain of Y. enterocolitica representing one of the six O-groups possesses, as judged by the sugar composition of its lipopolysaccharides, a particular chemotype. All 14 of the strains examined possessed glucosamine, KDO, two heptoses and glucose. In the most complicated chemotype 10 sugars were demonstrable. Of three Y. enterocolitica strains not included in the 6 O-groups, two had the same chemotype as the representatives of the O-groups IV and VI. Details can be seen in the two tables.