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)

Postprandial serum bile acids (expressed as integrated bile acid response [IR]) after a standardized test meal were compared with 75SeHCAT retention, measured in a whole body counter, in healthy controls (n = 20), in 44 patients with ileal disease or resection and in 23 patients with colitis without ileal involvement. In the controls the IR after 180 min was 736 +/- 186 mumol x min x 1(-1) (mean +/- standard deviation), the 75SeHCAT retention 31 +/- 9%. 80% of the patients with ileal disease or resection had a decreased 75SeHCAT retention, indicating bile acid malabsorption, but only 59% had a diminished IR. One of the 23 patients with colitis and radiologically normal ileum had a decreased 75SeHCAT retention but a normal IR, reflecting a dysfunction of the morphologically normal ileum. The characteristics of the two tests are: 75SeHCAT retention test: sensitivity 80%, specificity 98%, accuracy 89%; postprandial serum bile acids: sensitivity 64%, specificity 74%, accuracy 69%. With respect to chronic inflammatory bowel disease the positive predictive value of the 75SeHCAT retention test is 1.0%, for postprandial serum bile acids 0.1%, whereas the negative predictive values amount to 99% for both tests. Thus 75SeHCAT retention is more reliable in detecting bile acid malabsorption than the determination of postprandial serum bile acids, although both tests are not usefull for screening the population for ileal disease.
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PMID:[Postprandial serum bile acid level and 75SeHCAT retention in diagnosis of bile acid malabsorption syndrome. A comparative study]. 846 95

The article describes two female patients with severe diarrhoea. Both patients were suspected of having an organic diarrhoea syndrome and underwent extensive investigations. No specific diagnoses such as inflammatory bowel disease, pancreatic cholera, malabsorption and surreptitous ingestion of laxatives could be established. Histologic examination of biopsy specimens from apparently normal colon revealed microscopic changes characteristic of "microscopic colitis" in one of the patients, and of collagenous colitis in the other. The authors discuss similarities between these two microscopic abnormalities in colonic mucosa and their close association with chronic watery diarrhoea.
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PMID:["Microscopic colitis" and collagenous colitis. Unusual explanation of diarrhea of unknown origin]. 848 Feb 90

Fermentation, the process whereby anaerobic bacteria break down carbohydrates to short-chain (C2-C6) fatty acids (SCFAs), is an important function of the large bowel. SCFAs constitute approximately two-thirds of the colonic anion concentration (70-130 mmol/l), mainly as acetate, propionate, and butyrate. Gastroenterologists have, in spite of these facts, addressed this scientific field surprisingly late, in contrast to veterinarians, for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades. Interest in the effects of SCFA production on the human organism has been growing rapidly in the last 10 years, because gastrointestinal functions and beneficial effects are associated with these acids. SCFAs are of major importance in the understanding of the physiological function of dietary fibre and their possible role for colonic neoplasia. SCFA production and absorption are closely related to the nourishment of the colonic mucosa and sodium and water absorption, and mechanisms of diarrhoea. Patients with severe malabsorption compensate by the fermentation of otherwise osmotic active saccharides to SCFAs, which are readily absorbed and used as energy fuels in the organism. SCFA production from dietary carbohydrates is a mechanism whereby considerable amounts of calories can be salvaged in short-bowel patients with remaining colonic function if dietary treatment is adjusted. SCFA enemas are a new and promising treatment modality for patients with ulcerative colitis. The effect has been attributed to the oxidation of SCFAs in the colonocytes. An impressive number of papers have described the effects of butyrate on various cell functions, the significance of which is still unknown. Up until now, attention has been related especially to cancer prophylaxis and treatment. Diminished production of SCFAs appears to be involved in antibiotic-associated diarrhoea, diversion colitis, and possibly in pouchitis. The interaction between bacterial fermentation, ammonia metabolism, and bacterial growth and protein synthesis appears to be the main mechanism of action of lactulose treatment in hepatic coma. Pathological and extremely high rates of saccharide fermentation explain the severe deterioration in patients with D-lactate acidosis. Hence, this scientific field has come late to clinical working gastroenterologists, but as work is progressing the production of SCFAs in the large bowel becomes involved in several well-known intestinal disorders.
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PMID:Short-chain fatty acids in the human colon: relation to gastrointestinal health and disease. 872 86

Review of the medical records of 43 patients with common variable immunodeficiency (CVID) and 23 patients with X-linked agammaglobulinemia (XLAG) revealed a high incidence of chronic gastrointestinal complaints, most commonly diarrhea. Thirty-eight biopsies, four small-bowel resection specimens, and one autopsy from 10 patients with CVID and one patient with XLAG showed a wide range of abnormalities. A pattern resembling acute graft-versus-host disease, with apoptotic bodies and lymphocytes in crypts, was seen in the stomach (four patients), small bowel (three patients), and colon (three patients). Small-bowel specimens from three CVID patients with malabsorption showed mild to severe villous atrophy. Three CVID patients had Giardia in biopsies. Two cases of small bowel lymphoma associated with nodular lymphoid hyperplasia were identified in CVID patients. One patient's small bowel contained foamy histiocytes in the lamina propria, resembling Whipple's disease or chronic granulomatous disease, with numerous apoptotic bodies in crypts. Ultrastructurally, the histiocytes contained cellular debris. The patient with XLAG had recurrent fissuring necrosis of small bowel resembling Crohn's disease; a patient with CVID had colitis with features similar to ulcerative colitis. Poorly formed granulomas were seen in the stomach (one CVID patient) and the colon (two CVID patients). Lymphocyte populations were dominated by T cells; B cells were scarce except in lymphoid follicles in CVID patients with nodular lymphoid hyperplasia. Patients with CVID and XLAG manifest a spectrum of abnormalities in the gastrointestinal tract, with patterns superficially resembling graft-versus-host disease, inflammatory bowel disease, and Whipple's disease, but often lacking some of the diagnostic features of the diseases. Many of the CVID patients with chronic gastrointestinal complaints (62%) also had evidence of autoimmune phenomena, suggesting that in some patients the inflammatory process in the gastrointestinal tract has an autoimmune component.
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PMID:Gastrointestinal pathology in patients with common variable immunodeficiency and X-linked agammaglobulinemia. 882 31

A 54-year-old female presented with a pulmonary infection that resolved completely with antibiotic treatment. Peripheral blood films showed features characteristic of splenic hypofunction, and radiolabelling studies confirmed an absence of splenic reticulo-endothelial cell activity, which is typical of functional asplenia. The patient had a remote history of watery diarrhea but no clinical and laboratory features of malabsorption. Extensive upper and lower gastrointestinal tract biopsy studies revealed histopathological features of collagenous colitis without gastric or small intestinal inflammatory changes or epithelial lymphocytosis. Hyposplenism has been associated with different gastrointestinal disorders, particularly celiac disease. This is the first report of functional asplenia and microscopic collagenous colitis.
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PMID:Functional asplenia and microscopic (collagenous) colitis. 911 86

Three cases of apparent primary villous atrophy of the terminal ileum in women with chronic diarrhoea are reported. Eight cases have previously been reported in the literature. Clinical characteristics are the presence of severe chronic secretory diarrhoea with episodes of hypokalaemia combined with signs of ileal malabsorption and/or efficacy of cholestyramine. Diagnosis is based on ileoscopy and histology. An association with microscopic colitis was present in the three patients and in four cases in the literature. The pathogenesis of primary ileal villous atrophy remains unknown and may involve dysimmunity. Its association with microscopic colitis may indicate a common pathogenesis or support the hypothesis that the faecal stream or bile salts play a role in the pathogenesis of microscopic colitis.
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PMID:Primary ileal villous atrophy is often associated with microscopic colitis. 939 Dec 60

A case report of a young patient (born in 1980) with a 2-year history of chronic ulcerative proctocolitis was described. Checking colonoscopy 6 months from the beginning of disease showed multiple and even confluent polypoid lesions in transverse gut starting from hepatic flexure in addition to diffuse inflammatory rectosigmoideal changes. Biopsy found only colic mucosa without any tumorous structures. Five months later the patient's state got worse accompanied instantly by vomiting, weight loss and malabsorption symptoms. A duodenocolic fistula was supposed according to gastroduodenoscopy and biopsy. Because of progressive suffering of the patient colectomy with ileoduodenoanastomosis and ileosigmoidoanastomosis was performed. Polypous lesions were observed from the blind gut up to descendent colon and a transversoduodenal fistula was proved. The removed part of gut was completely changed into a dense network of elongated polypous lesions. In microscopy, bigger polyps showed an inner stromal part often with bands of smooth muscle cells covered by nearly normal gut mucosa. Smaller polyps were formed by hypertrophic gut mucosa only. At the base of polyps, a stagnation of gut contents was found as well as ulcerous defects of various depth. Macroscopy and microscopy of polypoid lesions formed by non-neoplastic gut mucosa were those of so called bizzare ("giant") inflammatory polyposis of the gut. Up to now the patient's clinical picture and local finding in the stump of resected gut have been typical for chronic ulcerous colitis and polypous lesions were not revealed by checking investigations.
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PMID:[A bizarre inflammatory polyposis of the colon in chronic ulcerative proctocolitis]. 962 28

In the rapidly increasing elderly population, diarrhoea as a result of drug therapy is an important consideration. The elderly consume a disproportionately large number of drugs for multiple acute and chronic diseases. Drugs can compromise both immune and nonimmune responses. Aging decreases the quality and proportion of T cells which in turn reduces the production of secretory IgA, the primary immune response of the gut. Acid production in the stomach decreases with increasing age and this compromise its vital 'self-sterilising' function, thus increasing the risk of diarrhoea due to viral, bacterial and protozoal pathogens. Other nonimmune defence mechanisms include the motility of the small intestine and the host-protective commensal bacteria of the colon. Drug induced hypomotility may result in bacterial overgrowth, deconjugation of bile salts and diarrhoea. Less commonly, diarrhoea may occur due to hypermotility because of a cholinergic-like syndrome. In the colon the host-protective commensal bacteria provide a powerful defence against pathogens. Disruption of this commensal population by antibiotic therapy may result in Clostridium difficile supra-infection which causes diarrhoea through toxin production. This is especially important in the elderly patient on chemotherapy for malignancy and those with multiple diseases. The organism responds to vancomycin, metronidazole and bacitracin. Metronidazole is the suggested drug of choice, with vancomycin reserved for relapses. Drugs also cause diarrhoea by interfering with normal physiological processes. Drugs impair fluid absorption by activating adenylate cyclase within the small intestinal enterocyte which increases the level of cyclic AMP. This causes active secretion of Cl- and HCO3-, passive efflux of Na+, K+ and water and inhibition of Na+ and Cl- into the enterocyte. Examples of these drugs (secretagogues) are bisacodyl, misoprostol and chenodeoxycholic acid (used to dissolve cholesterol gallstones). Drugs may also affect a second mechanism that regulates water and electrolyte transport, the Na+, K+ exchange pump. The energy for this pump is provided by the ATPase mediated breakdown of ATP. ATPase may be inhibited by digoxin, auranofin, colchicine and olsalazine. A number of drugs cause osmotic diarrhoea including antacids containing magnesium trisilicate or hydroxide. Lactulose is being used increasingly in compensated liver disease to increase protein tolerance and prevent hepatic encephalopathy. Sorbitol, an osmotic laxative agent also used in some liquid pharmaceutical preparations, induces diarrhoea by virtue of its osmotic potential. Another mechanism by which drugs cause diarrhoea is by mucosal damage of the small and large bowel. In the small intestine mucosal damage causes diarrhoea and fat malabsorption, as may occur with neomycin and colchicine. In the colon, for example, gold salts and penicillamine cause colitis of varying severity. Though the causes of diarrhoea are diverse, a drug-associated aetiology should always be considered and actively sought and addressed to prevent the complications of dehydration, electrolyte imbalance and undernutrition.
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PMID:Mechanisms of drug-induced diarrhoea in the elderly. 978 28

Trace elements constitute important prosthetic groups in a number of antioxidant enzymes which neutralize free radicals generated during inflammatory conditions such as colitis. However, the status of trace elements in colitis remains to be found. In the present study the concentrations of zinc, copper, manganese and selenium in the colon, liver and serum of rats with acetic acid (HAc)- or trinitrobenzenesulfonic acid (TNBS)-induced colitis were measured using atomic absorption spectrophotometer. Myeloperoxidase and glutathione peroxidase activities were measured spectrophotometrically. Our results show that the selenium concentration was significantly decreased by 33 and 37.5% in the colon and 69 and 78% in liver by HAc and TNBS treatment, respectively. Similarly the zinc concentration in the colon was decreased by 21 and 28% by HAc- and TNBS-induced colitis as compared to the controls, but manganese and copper, remained unaltered. The serum concentrations of copper, zinc and selenium also remained unaltered during colitis. The weight of HAc-treated rats did not decrease while there was a significant weight loss in the TNBS-treated rats. Myeloperoxidase activity was increased, whereas glutathione peroxidase activity was significantly decreased in the colon inflamed by HAc or TNBS as compared to the controls. These findings suggest that colitis induces a reduction in the tissue levels of trace elements which is independent of the way colitis is induced. Our findings of a reduction in Se and glutathione peroxidase activity together suggest that the reduction in the trace element concentrations is not due to dietary factors or malabsorption. The decrease may severely affect the antioxidant potential of the colon and therefore is a putative factor for the progression of disease.
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PMID:Colitis-induced changes in the level of trace elements in rat colon and other tissues. 981 22

We sought to determine, in a piglet model, whether severe sugar malabsorption causes colonic injury or inflammation. Twenty-four piglets were randomized to receive either control formula (CON) or CON supplemented with lactulose (LAC) (N = 12 each group). After seven days, inflammation, apoptosis, and crypt cell proliferation were assessed in the proximal colon (cecum). Lactulose feeding caused persistent diarrhea. In both groups, breath H2 concentration was low, suggesting no increased fermentation in the LAC group. Weight gain/volume formula intake was identical in the CON and LAC groups (0.09+/-0.13 and 0.09+/-0.11 g/ml) respectively. Injury to the colon did not occur, but inflammation of the colon (scale 0-5) was greater in LAC (score of 1.5+/-1.38) than in CON (0.42+/-0.79; P<0.05). Cell proliferation at the basal 40% of the crypt was 92% increased in CON (labeling index 22.8+/-9.9 vs. 11.9+/-2.8; P<0.05). We conclude that persistent feeding during severe sugar malabsorption permits weight gain but may cause colitis.
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PMID:Lactulose feeding in piglets: a model for persistent diarrhea and colitis induced by severe sugar malabsorption. 1048 35


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