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

Random fecal alpha-1-antitrypsin concentration was measured in children with various gastrointestinal diseases and in normal subjects. One hundred fifteen subjects were evaluated: controls (39); chronic inflammatory bowel disease (20); chronic diarrhea (18); acute gastroenteritis (17); allergic gastroenteropathy (5); chronic pancreatic exocrine insufficiency (4); acute gastrointestinal bleeding (4); nonspecific colitis (4); celiac disease (3); and intestinal lymphangiectasia (1). Mean fecal-alpha-1-antitrypsin for the controls was 0.98 mg/g lyophilized stool. All children with celiac disease, allergic gastroenteropathy, lymphangiectasia, nonspecific colitis, acute gastrointestinal bleeding, and 19 of 20 patients with active chronic inflammatory bowel disease had fecal alpha-1-antitrypsin concentrations greater than 2.6 mg/g stool (mean of the controls + 2 SD). These disorders have all been previously documented to cause protein-losing enteropathy by 51Cr-labeled albumin excretion tests. The other study patients had normal fecal alpha-1-antitrypsin excretion when compared with controls. Serial fecal antitrypsin concentrations paralleled disease activity and clinical response to therapy. The results suggest that random fecal antitrypsin concentration is a valuable screening test for mucosal disorders associated with abnormal transmucosal serum protein loss.
 ...
PMID:Random fecal alpha-1-antitrypsin concentration in children with gastrointestinal disease. 697 Jul 2

Pharmaceutical agents are often given inappropriate precedence in the treatment of gastrointestinal tract diseases. Nutrients have marked influences on the gastrointestinal tract and manipulation of the diet provides clinicians with a powerful therapeutic strategy to be used alone or concurrently with drug therapy. During acute gastroenteritis a change from the animal's regular food to a diet containing novel protein sources minimizes the likelihood of acquired food allergies to the staple protein components of the diet. "Feeding through" diarrhea, a method used in human infants, has limited applicability in dogs and cats. The ideal diet for chronic small bowel-type diarrhea is highly digestible, gluten-free, hypoallergenic, isosmolar, low in fat and low in lactose. Dietary protein requirements increase in protein-losing enteropathy. Dietary fat is kept to a minimum during gastrointestinal dysfunction because malabsorbed fatty acids and bile acids cause secretory diarrhea. In diseases of the small bowel, it is traditional to use low fiber diets. This recommendation needs revision because the binding and gelling properties of fiber are of potential benefit in the treatment of small bowel diarrhea. High fiber diets are useful in most large bowel diseases. The specific fiber type used markedly influences the clinical result.
 ...
PMID:Nutritional management of gastrointestinal tract diseases of dogs and cats. 799 63

Intestinal biopsy in a boy with gastroenteritis-induced protein-losing enteropathy (PLE) showed loss of heparan sulfate (HS) and syndecan-1 core protein from the basolateral surface of the enterocytes, which improved after PLE subsided. Isoelectric focusing analysis of serum transferrin indicated a congenital disorder of glycosylation (CDG) and subsequent analysis showed three point mutations in the ALG6 gene encoding an alpha1,3-glucosyltransferase needed for the addition of the first glucose to the dolichol-linked oligosaccharide. The maternal mutation, C998T, causing an A333V substitution, has been shown to cause CDG-Ic, whereas the two paternal mutations, T391C (Y131H) and C924A (S308R) have not previously been reported. The mutations were tested for their ability to rescue faulty N:-linked glycosylation of carboxypeptidase Y in an ALG6-deficient Saccharomyces cerevisiae strain. Normal human ALG6 rescues glycosylation and A333V partially rescues, whereas the combined paternal mutations (Y131H and S308R) are ineffective. Underglycosylation resulting from each of these mutations is much more severe in rapidly dividing yeast. Similarly, incomplete protein glycosylation in the patient is most severe in rapidly dividing enterocytes during gastroenteritis-induced stress. Incomplete N:-linked glycosylation of an HS core protein and/or other biosynthetic enzymes may explain the selective localized loss of HS and PLE.
 ...
PMID:Reduced heparan sulfate accumulation in enterocytes contributes to protein-losing enteropathy in a congenital disorder of glycosylation. 1110 64

Infant small-bowel intussusceptions, most of the time idiopathic, may exceptionally reveal a severe digestive disease. We report the case of a 4-month-old infant who presented multiple and simultaneous ileal intussusceptions associated with severe acute gastroenteritis. Initially, the infant showed a protein-losing enteropathy with a clear alteration of the general state of health and undocumented fever, resistant to broad-spectrum antibiotic therapy. Skin and splenic nodules associated with hepatosplenomegaly and pancytopenia set in progressively. The etiologic evaluation led to the diagnosis of a Mycobacterium bovis BCG infection related to severe combined immune deficiency. The treatment consisted in anti-tuberculosis quadruple therapy in association with immunoglobin supplementation. Secondarily, the patient underwent gene therapy in a clinical trial. An early BCG vaccine in the first weeks of life, before the outbreak of infection revealing the immune deficiency, is a risk factor in triggering a disseminated BCG infection in immunodepressed infants. This clinical case is the first reported of severe combined immune deficiency revealed by small-bowel intussusceptions related to a disseminated BCG infection.
...
PMID:[Recurrent small-bowel intussusceptions revealing a disseminated BCG infection related to severe combined immunodeficiency]. 2496 83