[Clinical and morphological characteristics and some mechanisms of portal gastroduodenopathy in liver cirrhosis].

We have found out the clinical presentations and peculiarities of endoscopic and morphologic view of pathologies of mucous membrane of gastroduodenal zone caused by liver cirrhosis. We have examined 74 patients with liver cirrhosis of viral and nonviral etiology using the clinical, endoscopic, morphologic and immunohistochemical methods.We have found that during liver cirrhosis morphometric rates of epithelial cells of mucous coat of stomach that produce somatostatin and endothelin-1 decrease and morphometric rates of epithelial cells that produce nitrogen oxide synthase increase. We have also found out that during liver cirrhosis proliferate activity decrease and apoptosis of epithelial cell of mucous coat of stomach increase.

Altered expression of neuronal nitric oxide synthase in the duodenum longitudinal muscle-myenteric plexus of obesity induced diabetes mouse: implications on enteric neurodegeneration.

Type 2 diabetes caused by obesity shows autonomic neuropathy. Molecular mechanism involved in enteric neurodegeneration is not clear. Neuronal nitric oxide synthase (nNOS) is one of the important agents involved in gastrointestinal function. Therefore, expression of nNOS in the duodenum LM-MP of type 2 diabetes model mouse was studied. Real time RT-PCR analysis showed reduction in nNOS expression in male diabetic LM-MP compared to male control. In contrast, female diabetic LM-MP had high level of nNOS mRNA compared to female control. Western blot determination of LM-MP showed reduction in nNOS protein in male diabetic LM-MP and high level of nNOS in female diabetic LM-MP compared to their respective controls. Expression of nNOS observed by Western blot was further confirmed by nNOS immunostaining of the mouse duodenum. TUNEL staining of mouse duodenum showed apoptosis in male diabetic enteric neurons. These studies suggest that nNOS expression in LM-MP varies with gender during early stage of type 2 diabetes. In addition, reduced expression of nNOS is likely to contribute to apoptosis seen in the enteric neurons of male type 2 diabetic mice.

[Character of changes in indicators of proteinase and proteinase inhibitor activity in gastroenterological pathology in children]. / Kharakter izmenenii pokazatelei aktivnosti proteinaz i ikh ingibitorov pri gastroénterologicheskoi patologii u detei.

The aim of this study was to determine trypsin-lake proteinase activity, chymotrypsin-like proteinase activity, trypsin, alpha 1-antitrypsin and alpha 2-macroglobulin levels in blood serum at the children with gastroenterological pathology. These parameters did not chang at the children with functional disorder of stomach and duodenum. The stable balance between proteinases and inhibitors was determined only at the duration of the disease not more 5 years. The absence of normal levels these enzymes after traditional treatment was explain the necessity to continue the therapy at home with control of enzymes' levels.

[Characteristics of enzymatic function of the stomach in gastroduodenal diseases in children with regard to gastric carcinogenesis]. / Osobennosti fermentativnoi funktsii zheludka pri gastroduodenal'noi patologii u detei v aspekte gastrokantserogeneza.

The paper deals with a description of the biochemical properties of the isoforms of pepsinogen pepsin of gastric mucosa and blood serum in children suffering from duodenal ulcerative disease as well as in atrophic and subtrophic lesions of gastric mucosa. Atrophic gastritis was found to involve an inhibited biosynthesis of the Ist fraction of pepsinogen while ulcerative-erosive lesions of the gastro-duodenal area--an increased level of the 3rd isoform of pepsinogen.

[Lactate dehydrogenase isozyme profile in gastric mucosa as an early marker of possible neoplastic pathology in children with chronic gastroduodenal diseases]. / Izofermentnyi spektr laktatdegidrogenazy slizistoi obolochki zheludka kak rannii marker vozmozhnoi onkopatologii u detei s khronicheskimi gastroduodenal'nymi zabolevaniiami.

The lactate dehydrogenase (LDH) isoenzyme profile was studied in bioptic samples of gastric mucosa taken from 57 infantile patients suffering from chronic gastroduodenal pathology and 7 children with gastric functional disorders. The investigation showed LDH1 level to decrease and that of LDH5 to increase, the LDH5/LDH1 ratio increasing accordingly, in cases of erosive gastro-like gastroduodenitis and duodenal ulcers. The degree of said changes was found to correlate with the extent of morphological lesions of gastric mucosa and the most pronounced changes were recorded in cases of gastric mucosa gland atrophy. Similar changes in LDH isoenzyme profile had been identified in patients with gastric tumors. Said findings may be used in identification of groups at high risk for gastric carcinoma.

Activity of duodenal disaccharidases in relation to normal and abnormal mucosal morphology.

Endoscopic duodenal biopsy specimens from 100 predominantly adult Caucasian patients under investigation for gastrointestinal symptoms were used to establish reference ranges for lactase, sucrase, and maltase in the duodenum. Duodenal and jejunal disaccharidase values were compared and the association between disaccharidase activity and morphology in the duodenum was examined. Mean lactase activities were about 40% lower in the duodenum compared with the jejunum; maltase was reduced to a lesser extent; and sucrase activities were much the same in the two sites. Lactase deficiency was found in 24 patients of whom 14 (58%) had duodenal disease. The presence of moderate to severe duodenal lesions was associated with a significant decrease in all disaccharidase activities, while only lactase was reduced in mild lesions. Twelve patients had normal lactase activity, despite the presence of duodenal disease. It is concluded that specific reference ranges for duodenal mucosal disaccharidase activity are required as this is less than that of jejunum. Reduced duodenal disaccharidase activity is usually but not invariably associated with morphological abnormality.

Duodenal toxicity of dietary Phaseolus vulgaris lectins in the rat: an integrative assay.

It is now generally admitted that phytohemagglutinin (PHA) constitutes the main factor responsible for the dietary toxicity of raw kidney beans. In the growing rat, an impairment of growth is the unique expression of a malnutrition syndrome. The aim of this work was to precise to what extent the intestinal injuries may account for this malnutrition. PHA was administered for 9 days to growing rats at levels ranging from 0.0025 to 0.25% of food dry matter. One group of controls was fed ad libitum and other groups were restrained. In such conditions, PHA reduced the food intake when offered at a level higher than 0.04% as a linear function of the logarithm of lectin rate. Intestinal injuries were also dose-dependent: blebbing of microvilli and loss of alkaline phosphatase occurred at the smallest dose of PHA, cell loss occurred at higher doses. A compensatory hyperplasia was observed as a consequence of both intestinal injury and reduced food intake. Our main results are that, whatever may be the damages caused to the duodenal mucosa, the observed growth impairment was quasi-totally imputable to the reduction of food intake.

Intestinal phospholipase, a novel enzyme.

We evaluated phospholipase activity in the intestine of rats and other species. Phospholipase activity was assayed by a surface barostat technique or an egg yolk titration system. Mucosal activity was found only by the surface barostat technique with phosphatidylglycerol as substrate; it was not found with phosphatidylcholine as substrate in assays by either technique. In gut luminal fluid activity was found when both phosphatidylcholine and phosphatidylglycerol were used as substrate in assays by the surface barostat technique, and phosphatidylcholine as substrate yielded activity in egg yolk titration. In rats in which pancreatic juice had been diverted, mucosal and gut luminal phospholipase activity was greater than in controls, thus demonstrating that enzyme activity was not due to pancreatic phospholipase. Bacterial origin of phospholipase activity was excluded in that phospholipase activity was found in germ-free rats; gastric and salivary gland origins were excluded in that continued phospholipase activity was found in rats with gastric fistula. The physiological importance of the enzyme was established by the finding that rats with pancreatic fistula absorbed 111 mumol of phosphatidylcholine and that controls absorbed 119 mumol of a 135-mumol load. Activity was found to be three times greater in the distal than in the proximal intestine; in cryptal cells it was 10 times greater than in villus tip cells. 65% of the activity in the gut lumen was tightly bound to particulate matter. We propose that intestinal phospholipase may be important in gut bacterial control, in the digestion of vegetable matter (phosphatidylglycerol is a major phospholipid in both plants and bacteria), and in the digestion of phospholipids in the gut lumen.

A morphological and histochemical study of a drug-induced enteropathy in the Alderley Park rat.

Two experiments were devised to produce an experimental enteropathy. In Experiment I, male Alderley Park rats were dosed daily by gavage with 20 mg/kg and 60 mg/kg of an antibacterial compound ICI 17,363. Animals were killed sequentially at daily intervals up to and including Day 9 to study the development of the enteropathy. In Experiment II rats were dosed daily with 60 mg/kg of the same compound. All animals were killed on Day 5 owing to a rapid development of the enteropathic condition. The duodenum was examined histologically and histochemically. Duodenal changes included vacuolation of columnar epithelial cells and villus stunting. There were marked reductions in mitotic activity in the crypt epithelial cells from Day 7 onwards (Experiment I) and almost total loss of hydrolytic and oxidative enzyme activity. In Experiment II the changes were more severe and haemorrhage and erosion of the duodenal mucosa were observed. The development of the enteropathic lesion appears to be due largely to the antimitotic effect of the compound, although a direct toxic effect upon the intestinal mucosa cannot be ruled out.

Structural and functional abnormalities of the small intestine in infants and young children with rotavirus enteritis.

Structural and functional alterations in duodenal mucosa from 17 children with rotavirus enteritis were assessed. Structural changes were found in specimens from all patients. Patients with the most severe mucosal damage were more likely to require intravenous therapy to correct dehydration. Depression of one or more mucosal disaccharidases was found in 14 of 16 patients. Repeat duodenal biopsy three to eight weeks later in six patients showed marked improvement. The study clearly shows that rotavirus can cause a marked structural and functional lesion in the upper small intestine which is rapidly reversible.