Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The primary hematologic abnormalities in 2 adult horses with chronic weight loss were hypoalbuminemia and hyperglobulinemia. One horse was anemic, had subclinical disseminated intravascular coagulation, and prolonged plasma sulfobromophthalein half-life. Small-intestinal dysfunction with malabsorption was indicated by abnormal D-xylose absorption test results. Clinicopathologic and pathologic findings were consistent with a diagnosis of malabsorption and protein-losing enteropathy, attributable to lymphocytic and plasmacytic infiltration of the intestine.
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PMID:Lymphocytic-plasmacytic enteritis in two horses. 236 25

Copper deficiency developed in a five-month-old prematurely born infant with an abdominal wall closure defect and a small bowel fistula under long-term parenteral nutrition. The first manifestations were typical bone changes including diffuse osteoporosis, delayed bone age, widened cupped metaphyses with beaks and a fracture, subperiosteal hematomas and ossifications in the shafts of long bones, and a diaphyseal fracture. Other findings that confirmed the diagnosis included edema of the limbs with pseudoparalysis, neurologic abnormalities, anemia, leukoneutropenia, and very low serum levels of copper and ceruloplasmin. Following initiation of copper supplementation, clinical, hematological and biological disorders resolved within a few days and roentgenologic bone abnormalities within four months. Copper deficiency develops only in the presence of specific risk factors, that are often combined in a single patient: inadequate stores due to prematurity, excessive loss due to chronic diarrhea, exudative enteropathy, a proximal stoma, or a biliodigestive fistula; and inadequate intake due to malabsorption or long-term exclusive parenteral nutrition (EPN). Appropriate copper supplementation is needed in all these high risk situations. Early, continuous copper supplementation is required for young children under EPN. Serum copper assays should be included among the periodically monitored biochemical parameters.
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PMID:[Nutritional copper deficiency. Apropos of a case]. 250 Aug 84

The development of peptide-based enteral formulas is a significant milestone in the advancement of nutritional care of the nutritionally compromised patient. Although previously limited to specific gastrointestinal mucosal diseases, the use of peptide-based formulas has been extremely useful in the critically ill patient with impaired gastrointestinal absorption associated with hypoalbuminemia resulting from hypermetabolic states. Based on previous animal studies, several investigators have noted improved nitrogen absorption, greater nitrogen utilization, higher branched chain amino acid levels, and increased insulin secretion with the use of peptide-based formulas compared with intact protein or free amino acid diets. Recent studies have indicated an improved gastrointestinal tolerance with peptide-based diets, with the rate of absorption and the degree of tolerance dependent on the presence of small molecular weight peptides. In addition, we have found that the critically ill patient suffering from severe hypoalbuminemia frequently develops a protein-losing enteropathy, which can be attenuated by the use of a peptide-based formula. Thus, peptide-based formula may attenuate albumin turnover in the intestine and thus be efficacious in patients with a protein-losing enteropathy from a variety of etiologies (table 2). We therefore recommend that enteral support with a peptide-based diet is safe and extremely useful in the catabolic, critically ill patient or in patients with significant gastrointestinal malabsorption associated with a protein-losing enteropathy. Tolerance of these formulas is dependent on the catabolic state of the patient, with more catabolic patients needing higher concentrations of nitrogen in the form of peptides and/or supplemental parenteral branched chain amino acids.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A reappraisal of the peptide-based enteral formulas: clinical applications. 251 72

Diarrhoea is a frequent symptom in ulcerative colitis (UC) and Crohn's disease (CD) which it often reveals. Its clinical features, course, physiopathology and treatment are different in these two diseases. UC is accompanied by an imperative, blood-stained, diurnal and often noctural diarrhoea the intensity of which fluctuates with the course of the disease, usually regressing under medical treatment but capable of becoming severe. This diarrhoea is due to several physiopathological mechanisms such as loss of colonic absorption function, exudative enteropathy and disorders of motility. Contrary to the lesions of UC, those of CD involve the whole digestive tract; they are multisegmental, ileal, colonic, ileocolonic or diffuse. Diarrhoea takes different forms depending on the site and evolutive stage of the lesions: malabsorption of bile salts and/or fatty acids in ileal lesions or after surgical resections, bacterial proliferation above stenoses, intestinal shunts due to internal fistulae, reduced absorbing area, exudative enteropathy and motor disorders in colonic lesions. In UC, treatment of the diarrhoea is that of exacerbations: systemic or topical corticosteroids or 5-aminosalicylic acid. In CD, side by side whit the maintenance treatment of the disease with anti-inflammatory drugs, the symptomatic treatments of diarrhoea play an important role and must be tailored to the responsible physiopathological mechanisms; some patients need artificial feeding.
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PMID:[Diarrhea in intestinal inflammatory diseases]. 260 92

A new family syndrome is described that affected three of seven siblings and another patient who had been abandoned at birth but came from the same area of France. All four patients were young women with a very peculiar phenotype, poikiloderma and greying of the hair, and idiopathic non-arteriosclerotic cerebral calcifications. Pathological studies demonstrated small-vessel hyalinosis due to basal membrane thickening, mainly in the digestive tract, kidneys and calcified areas of the brain. The clinical and biological expressions of these vascular changes varied. Peripheral retinal ischemic syndrome and chorioretinal scars were found in the ocular fundi of three patients. Malabsorption and protein-losing enteropathy was the main problem in all four, and was the cause of one patient's death. A subarachnoid hemorrhage due to a right sylvian aneurysm also occurred in two of the three sisters and was lethal for one. Nephropathy with renal failure and systemic hypertension is the major problem of the two surviving patients.
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PMID:Retinal and choroidal ischemic syndrome, digestive tract and renal small vessel hyalinosis, intracerebral calcifications and phenotypic abnormalities: a new family syndrome. 277

A 20-year-old woman is presented who had eosinophilic gastroenteritis of the muscularis and serosal type which involved the terminal ileum. The diagnosis was initially acute appendicitis, but clues to the correct diagnosis included the presence of malabsorption, protein-losing enteropathy, abdominal pain and ascites, and especially a history of recurrent bouts. Peripheral eosinophilia is found in most cases and biopsy, or a peritoneal tap when ascites is present, may demonstrate a predominantly eosinophilic infiltration. Radiographic findings include a rigid, open ileocecal valve. There is rapid response to corticosteroid therapy, but long term follow-up is required because the disease may run a chronic, relapsing course.
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PMID:[Eosinophilic gastroenteritis]. 280 53

A 24-year-old man with agammaglobulinemia developed a form of chronic inflammatory bowel disease over the past 18 years characterized by recurrent diarrhea, malabsorption, and protein-losing enteropathy. In the most recent admission he presented with abdominal cramps and active intestinal bleeding. Radiologic studies showed distal ileal irregularities and strictures that led to two distal intestinal and ileocecal resections. The gross pathologic appearance of these specimens was consistent with regional enteritis. Microscopically, healing ulcers, mucosal irregularities, and a prominent lymphocytic infiltrate without plasma cells or granulomas were observed. Immunocytochemical studies revealed a prominent T-helper cell and a modest T-suppressor/cytotoxic lymphocyte population in the lamina propria. Early and late B-cell differentiation markers were not detected in any of the cells. The immunocytologic findings suggest that T-helper lymphocytes proliferated without inhibition to stimulate non-existent B cells. The study confirms the occurrence of a regional enteropathy-like lesion in the total absence of B-cell function.
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PMID:Regional enteritis-like enteropathy in a patient with agammaglobulinemia: histologic and immunocytologic studies. 296 59

We studied the effects of oral taurine supplementation on bile acids conjugation and duodenal bile salt concentrations in infants. Seventeen infants receiving enteral artificial nutrition were investigated. At the beginning of the study they were 6 to 14 weeks old, in good nutritional state, without malabsorption, protein-losing enteropathy and liver or infectious diseases. After at least 8 days of a stable, taurine-free regimen the infants received oral taurine supplementation (36-45 micromol/kg.24 h) for 8 days. Bile acids were measured before and after each supplementation period in bile samples obtained by duodenal tubing, using enzymatic methods and colorimetry. According to the initial plasma taurine levels before supplementation, the infants were divided into two groups: I) plasma taurine levels less than 60 mumol/l (mean 47 +/-5 mumol/l, n = 8); II) plasma taurine levels greater than 70 mumol/l (mean 77 +/- 2 mumol/l, = 9). After 8 days of taurine supplementation a significant increase of plasma and urinary taurine (P less than 0.01),total duodenal bile salt concentrations (P less than 0.05), total duodenal tauroconjugates (P less than 0.05),taurocholate (P less than 0.01), taurochenodeoxycholate (P less than 0.05), and glycocholate (P less than 0.01), duodenal concentrations, and a significant decrease of the glycoconjugate/tauroconjugate ratio (P less than 0.05), were observed, but only in group I. in group II infants we only noted a significant increase of urinary taurine (P less than 0.01), and of duodenal total tauroconjugates (P less than 0.05). This study shows that the biliary effects of an oral taurine supplementation depends on taurine status and that in taurine-depleted infants intakes of exogenous taurine higher than 45 mumol/kg. 24 h are perhaps necessary for optimal bile salt effects.
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PMID:[Influence of oral taurine supplementation on the intraduodenal concentration and conjugation of bile acids in full-term newborn infants]. 297 13

A new familial syndrome that affected 3 of 7 siblings is described. All 3 patients were young women with a very peculiar phenotype, poikilodermia and hair greying, and idiopathic nonarteriosclerotic cerebral calcifications. Pathological studies demonstrated a marked and progressive hyalinosis involving capillaries and often arterioles and small veins of the digestive tract, kidneys, and calcified areas of the brain. Using electron microscopy, we found that the hyalin substance in the intestinal capillaries consisted of several concentric layers of basal membrane-like deposits within a finely granular fluffy material. Huge deposits of this material were present in the subepithelial and mesangial spaces of the kidneys. Endothelial cells and, in the kidneys, mesangial cells were markedly abnormal, and a true mesangiolysis pattern was present in 2 patients. The clinical and biologic expression of these vascular changes was variable. Diarrhea, rectal bleeding, malabsorption, and protein-losing enteropathy were the main and lethal clinical problems in the proband. Hypertension appeared in the early stage of a second pregnancy in 1 sister, and mild proteinuria was found in all 3 affected patients. Peripheral retinal ischemic syndrome and chorioretinal scars were found in the ocular fundi of both affected sisters of the proband. A subarachnoid hemorrhage, due to a right sylvian aneurism, also occurred in both sisters and was lethal in 1 sister. None of the known causes of distal vessel hyalinosis could be ascertained.
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PMID:Digestive tract and renal small vessel hyalinosis, idiopathic nonarteriosclerotic intracerebral calcifications, retinal ischemic syndrome, and phenotypic abnormalities. A new familial syndrome. 348 63

A 35 year old woman with primary hypogammaglobulinaemia developed intestinal villous atrophy, a severe malabsorption syndrome, osteomalacia and protein-losing enteropathy. The syndrome did not respond to treatment with antibiotics, vitamins, or gluten free diet. Regular intravenous administration of a native immunoglobulin preparation induced continuous elevation of IgG serum levels above 240 mg/dl. This led to rapid, complete and persistent normalisation of all clinical symptoms and pathologic findings. Additional therapy was not required. Side effects of the treatment that has now been maintained for 48 months were not observed.
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PMID:[Severe malabsorption syndrome and exudative enteropathy in hypogammaglobulinemia: complete involution with intravenous immunoglobulin substitution]. 406 Aug 18


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