[Effect of protein synthesis inhibitors on the activity of enzymes - cholestasis indicators - in experimental mechanical jaundice (author's transl)].
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Biomedical subjects
Publications and source records attributed to A Kryszewski.
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BACKGROUND/AIMS: Combined BT-A (botulinum toxin A) therapy and local application of nitrates can be more effective than BT-A alone for chronic anal fissure treatment, but so far the optimal dose of BT-A is not known. The aim of our study was to learn if BT-A doses higher than those used so far could change the outcome of fissure treatment. METHODOLOGY: We enrolled 14 consecutive patients suffering from idiopathic chronic anal fissure who did not respond to previous local treatment of nitric oxide donor and subsequent BT-A therapy (25 U of Botox). They were offered a local nitroglycerin treatment. In failure cases patients received the greater doses of BT-A (50 U of Botox). RESULTS: In all 11 patients with chronic anal fissure who applied nitroglycerin after BT-A injection, an effect on the internal anal sphincter relaxation was observed but fissure healing after topical nitroglycerin occurred only in 1 case. Of 13 patients with chronic anal fissure who received 50 U of BT-A no healing was reported in 6 cases. One male from this group received a greater dose (100 U of Botox) and then the fissure healed. CONCLUSIONS: The effect of topical nitrates on internal anal sphincter relaxation after botulinum toxin injection is not the last line for nonsurgical treatment of chronic anal fissure. Always we ought to consider using the next greater dose of BT-A before surgical treatment.
The reported studies were carried out on 22 persons, 15 anaesthetists and 7 anaesthetic nurses with a history of long-term exposure to halothane in low concentrations. The activity of gamma-glutamyl-transpeptidase (GGTP) and aminotransferases, the level of bilirubin and thymol turbidity test were determined. No significant abnormalities were found in the mean values of these determinations. In some cases a rise in alkaline phosphatase activity and in two cases a rise of GGTP were found. The results are not suggesting the presence of hepatocellular damage in this group.
Haemorrhage from oesophageal varices is one of the most common reason of death of patients with liver cirrhosis. The possibility of treatment and prevention of the haemorrhage by endoscopic sclerotherapy (ES) has become one of the achievements of contemporary medicine. Nevertheless there are some complications described after this procedure, the most severe being the pulmonary embolia. In our study we analyzed the pulmonary circulation by perfusion scintigraphy after ES. Among twelve patients treated by ES we found two cases of disturbed pulmonary perfusion. We did not find clinical or gasometric changes in these patients. We suggest there should be done pulmonary perfusion monitoring after ES.
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Seven cases of adult patients with gluten enteropathy (1 male and 6 female patients, including 1 patient with Duhring's disease) are presented. These patients suffered from diarrhoea lasting for 1-10 years prior to the diagnosis of gluten enteropathy. Transient diarrhoea was noted in one female patient in her childhood. Blood calcium levels were lowered in all patients and were accompanied by tetany in five and osteomalacia in two patients. One patient's sister is suffering from mucoviscidosis. Earlier, coeliac disease was not diagnosed in any patient. Previous diagnoses included enteritis, hypoparathyroidism or neuro- and myopathies of unknown etiology. The authors suggest that the difficulties in diagnosing gluten enteropathies in adults are due to the lack of biopsy capsules, low acquaintance of physicians with this disease, and indications to small intestine biopsy.
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Three cases of hypogammaglobulinemia are described. In all cases the first symptoms of disease manifesting as pneumonia were preceded by diarrhea. In gastric biopsy there was atrophic gastritis with lack of plasmocytes. All patients demonstrated gastric achylia and symptoms of malabsorption syndrome. The causes of gastrointestinal changes, most probably infections, with simultaneous defective mucosal barrier are discussed.