Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cow's milk allergy (CMA) is multifaceted disease representing systemic, skin or gastrointestinal reactions to cow's milk (CM) protein. This article shortly reviews the intestinal form of CMA (ICMA). According us the child is allergic to CM when the immunologic reaction to CM is associated with clinical symptoms. The incidence of CMA is 1.3-1.9% in general, but the ICMA only 0.6 pro mille among the children less than six months of age. The majority of infants shows symptoms within a month of starting CM feeding. The majority of children with CMA have gastrointestinal symptoms. Manx of these infants has additionally dermatological symptoms and some respiratory symptoms. The mode of onset is often acute diarrhoea and vomiting, as in acute gastroenteritis. Laboratory findings indicate iron deficiency anemia in 20-70%. Half to two thirds of infants with chronic diarrhoea have moderate to severe steatorrhoea. The morphologic lesion in the gastrointestinal tract in ICMA is widespread, often being present from stomach to rectum. Jejunal lesion is most severe in the proximal part of the intestine and nowadays most patients have only partial villous atrophy or slight changes of the villi. Both the epithelium and the lamina propria of the jejunum are infiltrated with inflammatory cells. The morphology of the small intestine speaks for a strong immune reaction which leads increased destruction of surface epithelial cells. We recommend elimination of CM proteins to the age of 1.5 to 2 years. Most patients tolerate CM by the age of 2 years without symptoms. Prolonged breast-feeding and avoidance of early contact with CM are important in reducing the severity and frequency of CMA.
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PMID:Intestinal cow's milk allergy. 404 93

The name juvenile tropical pancreatitis syndrome (JTPS) is proposed for a disease which affects young people of both sexes in certain parts of the tropics and which is characterised by abdominal pain, diabetes, steatorrhoea, and pancreatic calcification. The condition seems to start with blockage of the pancreatic ducts by laminated secretions or inspissated mucus plugs which later calcify. Chronic pancreatitis follows. The hypothesis is that plugs are the result of pancreatic stasis due to prolonged lack of food in the stomach and/or gastroenteritis and dehydration. Most plugs are probably dislodged during convalescence when protein-containing foods are eaten and stimulate vigorous flow of pancreatic juice. The sluggish pancreatic flow produced by very-low-protein diets may not dislodge plugs. Repeated infection and anorexia can enlarge the plugs which ultimately calcify. JTPS therefore occurs in Third-World areas with a high rate of childhood infections, and where low-protein staples are taken. Cereal staples seem to reduce the incidence of JTPS in endemic areas because of their protein content.
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PMID:Pathogenesis of juvenile tropical pancreatitis syndrome. 610 87

Steatorrhoea was a significant feature in an outbreak of rotavirus gastroenteritis which affected adults and infants in hospital. Fat globules or fatty acid crystals were obvious by light microscopy (LM) in faeces from 14 of 25 patients examined. Ten of the fatty stools and two of the remainder were very pale. By electron microscopy (EM) a rotavirus was seen in 11 of the 14 fatty faeces and in only two of 11 specimens without visible fat. In a further study of pale or fatty faeces 20 such specimens sent for laboratory examination from patients not involved in the hospital outbreak were compared microbiologically with a similar number which were neither pale nor fatty. Viruses were found by EM in 11 (55%) of the pale or fatty stools; eight rotaviruses, two astroviruses and an uncultivable adenovirus were seen; one further patient had acute jaundice. In contrast, no viruses were seen by EM in the twenty specimens which were normally pigmented and without evident fat. Steatorrhoea was significantly associated with rotavirus infection of the alimentary tract which usually presented as a fatty enteritis. We conclude that rotaviruses certainly, and other viruses possibly, can impede both the digestion of fat and the pigmentation of the faeces. Inspection and LM of faeces are easy. In acute enteritis a fatty or pale stool is an indication for virological examination.
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PMID:Virus diarrhoea associated with pale fatty faeces. 627 Feb 9

23 patients with gastroenteritis and 9 with severe malabsorption syndrome related to giardiasis were investigated in a semi-prospective fashion as follows: (1) conjugated bile acid levels measured in duodenal aspirate (thin layer chromatography) in 6 patients with steatorrhea. (2) intraepithelial lymphocytes count (results expressed as the number of intraepithelial lymphocytes per 100 epithelial cells) in small intestinal biopsies from the 32 patients, 11 of which had immunoglobulin deficiency (9 IgA deficiency). The results indicate that there is no decrease in the percentage of conjugated bile acids (mean percentage 90%; normal = 80); a significantly increased percentage of intra-epithelial lymphocytes is documented in giardiasis (11.1% +/- 6.7), versus 2.3% +/- 0.5 in acute gastroenteritis (9 patients) and 6.3 +/- 0.5 in chronic diarrheas (6 patients) (p less than 0,001). This percentage, however, is significantly lower than in untreated coeliac sprue (23 patients) (12.17 +/- 11.6) (p less than 0,01). Conversely a high intraepithelial lymphocyte count does not correlate with the degree of intestinal villous atrophy (3 patients had severe and 6 partial villous atrophy) (r = 0.170). IgA deficiency should be suspected in patients with giardiasis presenting with intestinal villous atrophy (5 patients). Steatorrhea in our patients does not appear related to bile acid deconjugation. To explain enterotoxicity in giardiasis, more than a direct effect of the ventral disk of the parasite on intestinal mucosa, one should incriminate the host immune cell mediated response as shown by lymphocytic infiltration of the epithelium on small bowel biopsies.
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PMID:[Enteropathogenic mechanisms involved in giardiasis in children (author's transl)]. 710 70

Chylomicron retention disease (CMRD), also known as Anderson's disease, is an autosomal recessive condition with a genetic mutation in the secretion associated Ras related GTPase 1B (SAR1B) gene, a protein coding gene. CMRD classically manifests as steatorrhea, vomiting, failure to thrive or abdominal bloating shortly after birth or in childhood. Here, we report a rare case of a 50-day-old male infant who was, at first, overseen as a case of acute gastroenteritis with sepsis owing to the non-specific symptoms i.e. multiple episodes of loose stools with a low-grade fever and failure to thrive, and was managed accordingly. However, the symptoms did not resolve; moreover, the clinical condition deteriorated. Later, lipid profile, clinical presentation and pathological features led to a presumptive diagnosis of CMRD. Our patient showed significant improvement when treated with a trial of medium- and short-chain fatty acids. We conclude that, in resource-restricted countries, a therapeutic trial with the dietary changes is essential to not only prevent the devastating complication but also support the diagnosis.
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PMID:Chylomicron Retention Disease in A Male Infant: A Rare Case from Pakistan. 3225 23