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Query: UMLS:C0024523 (malabsorption)
7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The biliary bile acid composition was determined for patients with cystic fibrosis and associated liver disease before and after the administration of ursodeoxycholic acid (10 to 15 mg/kg body wt/day). Bile acids were analyzed by fast atom bombardment ionization-mass spectrometry, high performance liquid chromatography and gas chromatography-mass spectrometry after individual bile acids were separated according to their mode of conjugation using the lipophilic anion exchanger, diethylaminohydroxypropyl Sephadex LH-20. More than 50 individual bile acids were identified in the bile of cystic fibrosis patients and these acids were predominantly secreted as glycine and taurine conjugates. Small proportions (less than 8% of the total) of unconjugated and sulfate conjugates were present. Of interest was the identification of two side-chain-elongated (C25) bile acids, homocholic and homochenodeoxycholic acids. After ursodeoxycholic acid was administered, duodenal bile became enriched with the conjugated species of ursodeoxycholic acid (accounting for 11.9% to 32.5% of the total biliary bile acids), but to a lesser extent than reported previously for patients with other liver diseases or gallstones who received comparable doses of ursodeoxycholic acid, and this presumably occurs because of bile acid malabsorption that is a feature of cystic fibrosis. The mean glycine/taurine ratio increased from 2.4 before ursodeoxycholic acid administration to 5 after ursodeoxycholic acid administration even though these patients also received taurine. Despite the relatively low enrichment of the bile by ursodeoxycholic acid, biochemical indices of liver function all improved in these patients after ursodeoxycholic acid administration.
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PMID:Comprehensive study of the biliary bile acid composition of patients with cystic fibrosis and associated liver disease before and after UDCA administration. 239 Oct 71

A 54 years old white woman and a 38 years old white man with short-bowel disease are reported. Both of them were submitted to surgical procedures for urinary oxalate calculi. They presented malabsorption syndrome with steatorrhea and severe malnutrition. The patients received parenteral nutrition. The woman had also cholelithiasis and acute pancreatitis. The clinical and laboratory data are presented and the pathophysiology of short-bowel disease with emphasis on bile salts depletion, the effect of bile salts on colon oxalate absorption, and intestinal loss of water is commented. The management of short-bowel disease and the use of cholesteramine and the supplementary diet is discussed.
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PMID:[Physiopathology of the short bowel: apropos of 2 cases]. 263 97

The pathogenesis of malabsorption has been studied in 70 patients who presented over the age of 65 years and who were referred to a special investigative unit. Often more than one cause was apparent. Fourteen patients had pancreatic insufficiency, most of whom had no history of pain, alcoholism or gallstones. Twenty-three patients had the postgastrectomy syndrome or small-bowel diverticulosis or both. There were eight coeliacs aged 65-72 years at diagnosis. Fifteen patients had an anatomically normal small bowel; eight of these were over 80 years old, and 10 had vitamin B12 deficiency of whom five had confirmed pernicious anaemia. Enterobacterial overgrowth was a feature of all diagnostic groups except pancreatic and coeliac disease. Vitamin B12 deficiency may be an effect of malabsorption, but can also be a cause through impairment of enterocyte function. The association of pernicious anaemia and B12 deficiency with otherwise unexplained malabsorption and bacterial overgrowth suggests that gastric atrophy is a major causal factor in this syndrome, combined in some cases with a 'vicious circle' of B12 malabsorption and deficiency.
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PMID:Causes of malabsorption in the elderly. 309 95

Common variable hypogammaglobulinemia (immunodeficiency), a disorder characterized by late-onset immunoglobulin deficiency and lack of humoral immunity, has a variable association with bronchiectasis, cholelithiasis, nodular lymphoid hyperplasia, gastrointestinal neoplasia, megaloblastic anemia, and malabsorption. The patient described in this report had all of the above except neoplasia. In addition, he had calcium oxalate renal stones probably secondary to his malabsorption. The first case demonstrating the beneficial effect of home hyperalimentation in patients with severe malabsorption refractory to other treatments is described. Home hyperalimentation overnight allows the patient freedom for daily activities while also being more cost-effective than in-hospital parenteral nutrition.
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PMID:Home hyperalimentation for common variable hypogammaglobulinemia with malabsorption secondary to intestinal nodular lymphoid hyperplasia. 311 40

For determination of the factors that regulate biliary cholesterol secretion and the lithogenity of bile in ileal dysfunction, plasma and biliary lipids and fecal excretion of bile acids were studied in 29 patients who had undergone ileal resection. Seven patients with ileal resection had normal bile acid excretion (less than 10 mg/kg/day), and 22 had various degrees of bile acid malabsorption. None of the patients had gallstones when examined with abdominal sonography. LDL cholesterol levels were decreased in bile acid malabsorption and demonstrated a positive correlation with the molar percentage of biliary cholesterol. Biliary cholesterol (mol percent) was inversely correlated with fecal bile acid excretion. This finding suggests that biliary cholesterol secretion decreases with increasing loss of bile acids to feces in ileal dysfunction, leading to an actual decrease in the lithogenic index and to hyposaturation of cholesterol in bile. The reduction in biliary cholesterol, regarded as protecting the gallbladder mucosa against the detergent properties of bile acids, may play an important role in the pathogenesis of increased gallstone formation in ileal dysfunction.
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PMID:Biliary cholesterol and lithogeneity of bile in patients after ileal resection. 329 Nov 68

Cholestyramine, colestipol, clofibrate, gemfibrozil, nicotinic acid (niacin), probucol, neomycin, and dextrothyroxine are the most commonly used drugs in the treatment of hyperlipoproteinaemic disorders. While adverse reaction data are available for all of them, definitive data regarding the frequency and severity of potential adverse effects from well-controlled trials using large numbers of patients (greater than 1000) are available only for cholestyramine, clofibrate, nicotinic acid and dextrothyroxine. In adult patients treated with cholestyramine, gastrointestinal complaints, especially constipation, abdominal pain and unpalatability are most frequently observed. Continued administration along with dietary manipulation (e.g. addition of dietary fibre) and/or stool softeners results in diminished complaints during long term therapy. Large doses of cholestyramine (greater than 32 g/day) may be associated with malabsorption of fat-soluble vitamins. Most significantly, osteomalacia and, on rare occasions, haemorrhagic diathesis are reported with cholestyramine impairment of vitamin D and vitamin K absorption, respectively. Paediatric patients have been reported to experience hyperchloraemic metabolic acidosis or gastrointestinal obstruction. Concurrent administration of acidic drugs may result in their reduced bioavailability. Serious adverse reactions to clofibrate will probably limit its role in the future. Of particular concern are ventricular arrhythmias, induction of cholelithiasis and cholecystitis, and the potential for promoting gastrointestinal malignancy which far outweigh the reported benefits in preventing new or recurrent myocardial infarction, cardiovascular death and overall death. Patients with renal disease are particularly prone to myositis, secondary to alterations in protein binding and impaired renal excretion of clofibrate. Drug interactions with coumarin anticoagulants and sulphonylurea compounds may produce bleeding episodes and hypoglycaemia, respectively. Nicotinic acid produces frequent adverse effects, but they are usually not serious, tend to decrease with time, and can be managed easily. Dermal and gastrointestinal reactions are most common. Truncal and facial flushing are reported in 90 to 100% of treated patients in large clinical trials. Significant elevations of liver enzymes, serum glucose, and serum uric acid are occasionally seen with nicotinic acid therapy. Liver enzyme elevations are more common in patients given large dosage increases over short periods of time, and in patients treated with sustained release formulations.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adverse effects of hypolipidaemic drugs. 354 4

In a consecutive series of 107 patients operated on for Crohn's disease involving the distal ileum, the overall incidence of gallstones was 17% and of renal stones 12%. Whereas the frequency of gallstone disease was 9% in patients with minor resections, patients with more than 100 cm diseased or resected small bowel had a frequency of 35%. The probability of gallstone development in both sexes was calculated to be approximately 50% after 20 years of distal ileopathy. The frequency of renal stone disease in patients with minor resection was comparable to that of a population in Sweden but was significantly commoner in patients with resection of more than 100 cm (28%), provided they were not colectomized. The high frequency of stone disease after resection of distal ileum is attributed to metabolic disturbances due to steatorrhea and bile salt malabsorption.
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PMID:Cholelithiasis and urolithiasis in Crohn's disease. 357 31

Recycling of bile acids through the enterohepatic cycle is very efficacious. Bile acids contribute to bile formation and, by forming micelles, participate in lipid solubilization and absorption. The small fraction which escapes in the feces, is synthesized daily by the liver to compensate for losses. In CF, bile acid malabsorption has been documented; these large losses are accompanied by an interruption in the enterohepatic circulation with concomitant reduction in bile acid pool and disturbances in biliary composition. The various intraluminal factors implicated in bile acid malabsorption include: unhydrolysed triglycerides and phospholipids, precipitation of bile acids in acidic duodenal content, adsorption to residues and modification of colonic microflora. A defect in bile acid ileal uptake has also been advocated. These disturbances in bile acid metabolism associated with CF might lead to aggravation of diarrhea and steatorrhea, cholelithiasis and perhaps liver disease.
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PMID:Bile acid metabolism in children with cystic fibrosis. 390 28

Lipid composition of fasting duodenal bile was studied in 56 patients with nonoperated Crohn's disease, 21 normals matched for age and sex, 13 patients with cholesterol cholelithiasis, and 9 patients with ileal resections. Crohn's patients had a significantly higher mean saturation index, calculated according to Thomas (0.84 +/- 0.51) when compared to normal (0.63 +/- 0.25). Patients with ileocolonic Crohn's disease and patients with severe bile acid malabsorption, particularly, showed an increased incidence of cholesterol saturated bile. Saturation in patients with nonoperated Crohn's disease was not increased to the levels found in patients with ileal resection or cholesterol gallstones. Bile acid composition of gallbladder bile was characterized by a significant decrease of the deoxycholate fractions in patients with Crohn's ileocolitis and colitis as well as in ileal resected patients. These qualitative changes of bile acid composition may influence cholesterol solubility. It is concluded that patients with nonoperated Crohn's disease may have an increased risk of developing cholesterol gallstones.
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PMID:Biliary lipid composition in patients with nonoperated Crohn's disease. 394 Aug 21

Ileal disease or resection causes bile salt malabsorption and a reduction in the bile salt content of bile. Since cholesterol solubility requires adequate bile salt concentrations, depletion of the bile salt content of bile might, therefore, jeopardize cholesterol solubility and predispose to cholesterol gallstone formation. To study this, we examined biliary lipid composition in 10 patients with ileal dysfunction and in 25 healthy controls. Biliary lipid composition, as analysed in cholecystokinin-stimulated, bile-rich duodenal fluid, was shown to be representative of gallbladder bile and reproducible on repeat duodenal intubation. Nine of the 10 patients with ileal dysfunction had an abnormal, supersaturated bile in which the limits of cholesterol solubility were exceeded, and while nine of 25 control subjects also had an unstable bile, the mean bile composition in the ileal dysfunction group was significantly different from the control population. These studies provide a physicochemical explanation for the clinical observation that patients with ileal dysfunction have an increased incidence of gallstones.
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PMID:Lithogenic bile in patients with ileal dysfunction. 504 Aug 30


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