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

Food intake, appetite and a variety of feelings were measured pre- and post-operatively in obese patients undergoing jejuno-ileal bypass surgery. Decreased food intake correlated closely with the amount of weight loss at both 4 and 30 months after surgery. Malabsorption correlated with weight loss at 4 months but not 30 months post-operatively. The cause of the decreased food intake is unknown and cannot be completely explained by either depression, nausea, malabsorption, liver disease, an attempt to avert diarrhoea, or decreased appetite.
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PMID:Reduced caloric intake following small bowel bypass surgery: a systematic study of possible causes. 42 87

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Results relative to long term treatment with Colestipol (a new resin sequestering bile acids) in 23 subjects with familial hypercholesterolemia, 12 with Type II A, 8 with Type II B and 3 homozygotes are reported. The patients had previously undergone treatment with clofibrate together with a hypocholesterolemic diet. After six weeks with placebo, the patients were given 15 g/die active drug for a period of 12 months and a double dose (30 g/die) for a successive period of 4 months. During the experimental trial the same hypocholesterolemic, isocaloric diet which had been followed during the previous hypolipidemic treatment was maintained. In the entire group taken as a whole, the total mean decrease was --56,9 +/- 15 mg/dl (P less than 0,01) after 12 months of 15 g/die Colestipol and --62,8 +/- 13 mg/dl (P less than 0,01) during the following 4 months with 30 g/die Colestipol. The difference between the two periods of treatment (15 g and 30 g/die) is not statistically significant. During the active drug treatment a slight but not statistically significant triglyceride increase was observed. The increase was most marked in the Type II B patients: the triglyceride variations in this group could be partly caused by slight variations in mean body weight. Starting from a mean basal value of 3,9 +/- 0,2 mg/dl, serum uric acid showed a significant increase which was maintained throughout the entire period of treatment, reaching a peak of 5,6 +/- 0,3 mg/dl (P less than 0,001) at the twelfth month. During the experimental trial no significant modifications were observed in the hematological routine analysis and liver functional tests, no malabsorption syndrome and no signs of toxicity were seen. Most frequent side effects were constipation, nausea, metheorism which, with the exception of four cases, which were withdrawn from the study, were reported as being transitory and mild. In conclusion, since Colestipol treatment significantly lowers cholesterol levels in patients with familial hypercholesterolemia and does not manifest any toxicity or serious side effects, it can be used effectively in the long term treatment of this disease which is characterized by an elevated frequency of cardiovascular complications.
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PMID:[Long term treatment of familial hypercholesterolemia with Colestipol, a new anionic exchange resin (author's transl)]. 114 65

Results related to long term treatment with Colestipol (a new resin sequestering bile acids) in 23 subjects with familial hypercholesterolaemia, 12 with Type IIA, 8 with Type IIB and 3 homozygotes are reported. Patients were given 15 g/day active drug for a period of 12 months and a double dose (30 g/day) for a successive period of 4 months along with a low cholesterol, low saturated fat, polyunsaturated fat-rich diet. Mean cholesterol decrease was --42 +/- 18 mg/dl (P less than 0.05) after 12 months of 15 g/day Colestipol and --69 +/- 17 mg/dl (P less than 0.01) after the following 4 months of 30 g/day Colestipol. The difference between the two periods of treatment (15 g and 30 g/day was not statistically significant. A slight but not significant increase in triglyceride levels was observed. Serum uric acid showed a significant increase throughout the entire period of treatment. No malabsorption syndrome or signs of toxicity were seen. Most frequent side effects were constipation, nausea, and metheorism which, with the exception of 4 cases which were withdrawn from the study, were reported as being transitory and mild.
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PMID:Long-term effects of colestipol (U-26,597 A) on plasma lipids in familial type II hyperbetalipoproteinaemia. 120 Nov 45

A 58 year old Chinese male, one week after arriving in Canada from Hong Kong, presented with acute abdominal pain and diarrhoea which was rapidly followed by Escherichia coli infection causing septicaemia and meningitis. His past history revealed bronchial asthma for 15 years treated with steroids. At laparotomy, 7 days after the onset of symptoms, he was found to have extensive haemorrhagic infarction of the small bowel and right colon. Examination of the fibrosed mesenteric vessels revealed numerous filariform larvae of Strongyloides stercoralis, within the walls, and in all layers of bowel wall. The role of the parasite in the production of obliterative arteritis in this fatal case of haemorrhagic enteropathy is discussed. Clinical strongyloidiasis, in uncomplicated cases, varies from mild to severe with gastroenteritis, nausea, colicky abdominal pain, electrolyte imbalance and symptoms of malabsorption syndrome (MARCIAL-ROJAS, 1971). In malnourished individuals and patients with debilitating infections, either newly acquired or asymptomatic latent infection with S. stercoralis can assume severe dimensions (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). Similarly, in patients on steroid (CRUZ et al., 1966; WILLIS and MWOKOLO, 1966; NEEFE et al., 1973) and immunosuppressive therapy for lymphomatous diseases or deficient in immune response (ROGERS and NELSON, 1966; RIVERA et al., 1970), systemic strongyloidiasis is often fatal. The increased frequency of auto-infection in such patients with a breached immune barrier is, however, unclear. Further complications of this infection due to severe enterocolitis result in sepsis, bacteraemia and meningitis (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). This paper presents a fatal case of S. stercoralis infection which illustrates an uncommon if not unique, mechanism in its production of haemorrhagic enteropathy leading to sepsis and death.
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PMID:Fatal bowel infarction and sepsis: an unusual complication of systemic strongyloidiasis. 122 84

Acarbose, an alpha-glucosidase inhibitor, delays absorption of carbohydrate in the gut, thereby lowering postprandial glucose levels. Safety data on this drug have been gathered in a series of studies on animals and in extensive clinical trials in humans. Although an initial long term feeding study in rats showed an excess of renal tumours at very high dosages of acarbose (up to 300 mg/kg bodyweight daily), further evaluation with similar studies in rats, hamsters, and dogs indicated that the problem was related to carbohydrate malabsorption. With adequate glucose intake and in gavage studies, no difference in tumour incidence between placebo- and acarbose-treated groups was seen. From 1976 to 1989, safety data on acarbose were obtained in approximately 8800 patients in 2 separate groups of clinical trials, the Bayer International Clinical Data Pool and the American phase III trials. Almost all adverse experiences, as reported by 56 to 76% of patients on acarbose vs 32 to 37% of patients on placebo, were related to the digestive system and included diarrhoea, flatulence, bloating and nausea. Most symptoms were of mild to moderate intensity and tended to improve with time. In the American trials a small but significant increase in liver transaminases was seen, 3.8% in acarbose-treated patients vs 0.9% in controls together with a 1% increase in anaemia in the acarbose group. Overall, acarbose was well tolerated and the adverse experience profile was clinically acceptable.
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PMID:Safety profile of acarbose, an alpha-glucosidase inhibitor. 128 May 77

A 50-year-old woman with a typical history of chronic idiopathic intestinal pseudo-obstruction was admitted to hospital because of an acute episode of abdominal cramps, nausea, and vomiting. The diagnosis of chronic idiopathic intestinal pseudo-obstruction had been established in this patient who had malnutrition and extreme weight loss as a result of severe malabsorption syndrome. The abdominal roentgenogram showed a typical hypotonic intestine with an enlarged stomach and distended intestinal loops with the radiological signs of an ileus. In addition to former episodes, there was also a transient aerobilia. The patient had not undergone biliary surgery or endoscopic sphincterotomy. To investigate the cause of the findings, endoscopic retrograde cholangiopancreatography and endoscopic manometry of the sphincter of Oddi were performed. The endoscopy showed the stomach and duodenum with a wide and dilated lumen and no spontaneous motility. Endoscopic manometry of the biliary tract and the sphincter of Oddi showed several abnormalities compared with a group of normal volunteers or patients who were examined via biliary manometry for other reasons. There was a low basal pressure (3.5 mm Hg) in the sphincter of Oddi together with low-amplitude phasic contractions (25-30 mm Hg), but the contraction frequency was in the normal range. Further investigations of the motility of the gastrointestinal tract in this patient showed diffuse esophageal spasms and a markedly delayed gastric emptying. The findings of biliary manometry in this patient suggest involvement of the sphincter of Oddi and the biliary system in chronic idiopathic pseudo-obstruction.
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PMID:Aerobilia and hypomotility of the sphincter of Oddi in a patient with chronic intestinal pseudo-obstruction. 129 27

Since his birth, we have been monitoring a 12-year-old boy suffering from selective severe magnesium malabsorption. Our essential problem is to prepare a form of galena with acceptable taste, tolerated by the digestive tract and well absorbed; also, the carrier compound must not cause short- or long-term side effects. An additional factor is the steadily increasing need for magnesium from 1 mmol/kg.d at 1 year to 14 mmol/kg.d at present age (345 mg/kg.d). The galena forms currently on sale were, with the exception of lactate and pyrollidone carboxylate, immediately rejected since they contain insufficient Mg2+. Following short trials resulting in diarrhoea, the other two preparations were also rejected. We then constituted - and also abandoned - our own galena compounds: aspartate (bitterness), aspartate + glycerophosphate (GLP) (bitterness), glutamate + GLP ('Chinese restaurant syndrome' and fear of the long term toxic effect of the glutamate), gluconate (excessive volume: 11/1 proportion with Mg2+). A recent test featuring GLP of Mg 40 g + cocoa butter 40 g + cocoa 10 g, brought about vomiting and diarrhoea, and was not adequately absorbed. The best tolerated formula is: Mg GLP 21.33 g; saccharose 6 g; aspartam 1 g; gelatin 0.5 g; citric acid, conserving agent, fruity aroma; water: qs 100 g. Such composition yields a caramel cream absorbed in five small portions, at a daily quantity of 375 g (80 g GLP Mg, 10 g Mg2+). Vitamin B6, which promotes intestinal absorption of magnesium, must be given separately in tablet form at a dose of 1 g/d, since it causes nausea if it is included in the Mg preparation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Severe selective magnesium malabsorption: tests of tolerance of oral magnesium supplements. 213 77

A 25-year-old man, who was admitted for evaluation of arthralgia and fever of 2-weeks duration, complained of a 10 kg weight loss during the previous weeks. Systemic lupus erythematosus (SLE) was diagnosed on the basis of leukopenia, LE cells, antinuclear antibodies, antibodies to double-stranded DNA, and arthritis, Malabsorption was diagnosed because of the finding of hypoalbuminemia, fat droplets in the feces, a pathological D-xylose test, and an appropriate X-ray image. Approximately half the patients with SLE develop minor expressions of gastrointestinal tract involvement, such as nausea, vomiting, and diarrhea. Major manifestations, such as intestinal obstruction or perforation, ascites, peritonitis and pancreatitis have been reported with varying frequency. Despite the frequent association of SLE with gastrointestinal manifestations, malabsorption, as in this case, has rarely been reported.
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PMID:[Malabsorption in systemic lupus erythematosus]. 235 16

We describe a patient with systemic lupus erythematosus (SLE) and overlapping syndrome who had repeated gastrointestinal (GI) symptoms such as nausea, vomiting and malabsorption. With a subacute process, she developed paralytic ileus and contracted bladder, and died of perforation of the ileum. When 13 reported cases with lupus cystitis were reviewed, an extremely strong correlation between GI and urinary tract symptoms was observed, indicating the presence of a unique subgroup of SLE.
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PMID:Lupus cystitis and performation of the small bowel in a patient with systemic lupus erythematosus and overlapping syndrome. 268 79


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