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

Gastrointestinal (GI) infections are frequent in AIDS patients. The frequency and type of opportunistic GI infections are exactly the same in homosexuals and heterosexuals. Diarrhoea is the usual sign of GI infection, and its mechanism seems to combine a secretory component and a malabsorption. Although a number of pathogens can be isolated, in many cases the diarrhoea cannot be explained by an infection or a lesion. The hypothesis of a primary HIV infection in the epithelium of the small bowel and colon has not been confirmed by immunofluorescence and molecular hybridization. The HIV virus has been found in the GI mucosa, but it was probably carried by the immune cells in general circulation (CD4 lymphocytes and macrophages) which subsequently colonize the chorion of the mucosa.
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PMID:[Diarrhea in AIDS. Group AIDS GIT]. 131 17

This 54-year-old Korean coal miner suffered from continuous watery diarrhea and weight loss after corticosteroid treatment (beta-methasone, 4 mg daily for 1 week) due to hip-bone fracture in January 1991. Except for the short therapy of steroid, no other histories were contributory. The malabsorption syndrome was aggravated while the case was treated under the impression of amebiasis or intestinal tuberculosis. AIDS antibody test by EIA was negative and quantitative analysis of serum immunoglobulins was in normal ranges. Nine months after the onset of symptoms, the case was diagnosed as malabsorption syndrome caused by complexed and aggravated infection by Strongyloides stercoralis, Isospora and cytomegalovirus in the small intestine, which were proved by stool examination and duodenal biopsy. His clinical course became worse even after high-dosed and prolonged albendazole treatment for strongyloidiasis with supportive fluid therapy. The patient was discharged in hopeless status in November, 1991 and died after one week at home.
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PMID:[A case of fatal malabsorption syndrome caused by strongyloidiasis complicated with isosporiasis and human cytomegalovirus infection]. 131 69

AIDS-associated gastric secretory failure has been characterized by decreased secretion of acid, pepsin, and gastric juice volume. To determine whether decreased intrinsic factor secretion and vitamin B12 malabsorption occur in this entity, we performed prospective measurements of maximal acid output, intrinsic factor output, vitamin B12 absorption, serum vitamin B12, and holotranscobalamin II in 10 consecutive AIDS patients. Four of 10 patients had low maximal acid output, i.e., < or = 1.5 mEq/h (control = 12.8 +/- 9.0, range 2.5-25 mEq/h). Four patients had low intrinsic factor output, i.e., < or = 1.1 microgram/h (control = 8.2 +/- 6.9, range 3.1-19.4 micrograms/h). One patient with low intrinsic factor output had low serum vitamin B12 and a Schilling test consistent with pernicious anemia. A second patient with very low intrinsic factor output (0.16 micrograms/h) had low parts I and II Schilling tests; malabsorption most likely resulted from both low intrinsic factor secretion and ileal disease. One of three vitamin B12 malabsorbing patients, with normal serum vitamin B12, had low holotranscobalamin II, 25 pg/ml (control holotranscobalamin II = 76 +/- 44, range 44-152 pg/ml). Maximal acid output and intrinsic factor output did not correlate in AIDS (r = 0.36, p = 0.30) in contrast to the expected correlation in controls (r = 0.91, p = 0.03). We conclude that low intrinsic factor secretion is common in AIDS and contributes to vitamin B12 malabsorption. Decreased parietal cell secretion of intrinsic factor and acid may occur independently in human immunodeficiency virus-associated gastric secretory failure. Low holotranscobalamin II, an early manifestation of vitamin B12 malabsorption, results in decreased delivery to vitamin B12-dependent tissues prior to depletion of serum vitamin B12. Regular supplementation with vitamin B12 may therefore be warranted in patients with advanced HIV infection.
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PMID:Decreased intrinsic factor secretion in AIDS: relation to parietal cell acid secretory capacity and vitamin B12 malabsorption. 144 41

Involuntary weight loss or wasting indicative of severe protein energy malnutrition is a frequent complication of acquired immune deficiency syndrome (AIDS). Malnutrition, with its associated adverse effects on immunocompetence, may contribute to the progression of AIDS itself. Since death from wasting is ultimately related to the magnitude of tissue depletion, restoration of body cell mass may enhance survival. The mechanism of weight loss in AIDS has not been clearly elucidated. The etiology is likely to be multifactorial, the result of interactions between decreased caloric intake, malabsorption, and alterations in energy expenditure secondary to hormonal and/or metabolic abnormalities. Although weight loss is occasionally reversible with treatment of underlying infections and/or easily identifiable and reversible causes, the majority of patients are not this fortunate. Enteral and parenteral nutrition, which are expensive, cumbersome, and potentially morbid, have been suggested by some as therapeutic options. Megestrol acetate, a synthetic, orally active progestational agent, has been reported to stimulate appetite and weight gain. Data regarding the use of megestrol acetate for the treatment of cachexia related to human immunodeficiency virus (HIV) infection demonstrate convincingly its effectiveness in treating many patients with HIV-related anorexia and cachexia.
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PMID:HIV-related cachexia: potential mechanisms and treatment. 146 29

Two appetite stimulants, megestrol acetate and cyproheptadine were administered in a randomized trial to 14 patients who had no evidence of opportunistic infection or malabsorption but were wasted (had lost more than 5 kg body weight) as a result of human immunodeficiency virus (HIV) infection. Energy intakes were calculated from a 7 day weighed dietary record. Mean energy intakes per kilogramme body weight were similar in both treatment groups (greater than 34 kcal/kg) and were higher than that in well British males. Energy intakes increased by just over 500 kcal during both treatments, but fell to pretreatment levels after therapy. Patients in both treatment groups gained a moderate amount of weight. Megestrol acetate was associated with impotence in 4 patients. Insufficient calorie intake alone is not a common cause of wasting associated with HIV and the role of appetite stimulants is likely to be limited.
Int J STD AIDS
PMID:Megestrol acetate vs cyproheptadine in the treatment of weight loss associated with HIV infection. 150 60

Diarrhoea is defined as the frequent passage of loose or watery stools. Most patients can easily recognise and accurately define acute diarrhoea as an abrupt change in their bowel habits. Chronic or recurrent diarrhoea is more difficult for the patient to define, since it may mean malabsorption, tenesmus or true diarrhoea. Serious disorders not to be missed include neoplasia, AIDS, various serious infections such as amoebiasis, and inflammatory bowel disease.
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PMID:Diarrhoea. 152 Jan 38

Studies of body composition in acquired immunodeficiency syndrome (AIDS) patients demonstrated body cell mass depletion out of proportion to losses of body weight or fat. The timing of death from wasting was related to the extent rather than the specific cause. However, some patients remain stable for indefinite periods, indicating that wasting is not a constant phenomenon. The development of malnutrition is multifactorial and includes disorders of food intake, nutrient absorption and intermediary metabolism. Nutritional repletion has been demonstrated in several studies. The effect of treating infections that promote wasting was shown in a study of ganciclovir therapy for cytomegalovirus colitis, in which untreated patients underwent progressive wasting whereas treated patients repleted body mass. Total parenteral nutrition had a variable effect upon body composition, with repletion occurring in patients with eating disorders or malabsorption syndromes and progressive depletion occurring in patients with serious systemic infections. Enteral nutrition also can replete body mass in AIDS patients without severe malabsorption. Pharmacologic stimulation of appetite also may lead to weight gain. The results of these studies indicate that nutritional support can improve nutritional status in properly selected AIDS patients.
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PMID:Nutritional effects and support in the patient with acquired immunodeficiency syndrome. 154 39

Many parasitic opportunistic infections occur in AIDS patients. In a young female drug abuser, HIV-positive at the IV stage, a microsporidian was detected and identified in urine by cell culture in fibroblast monolayers (MRC-5) and formally recognized by electron microscopy. This parasite has been involved in hepatitis, myositis and malabsorption syndromes in AIDS patients. Its diagnosis is difficult and this is the first time that its replication has been reported in human diploid cells in vitro.
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PMID:Isolation and replication in human fibroblast cells (MRC-5) of a microsporidian from an AIDS patient. 161 29

The significance of the human immunodeficiency virus (HIV) in the small intestinal lamina propria in patients with the acquired immune deficiency syndrome or conditions related to that syndrome who have chronic diarrhea and malabsorption is unclear. To investigate this issue, upper endoscopy (after a 12- to 16-hour fast) with duodenal biopsy and aspirate was performed in 20 HIV-infected seropositive homosexual men referred for diarrhea of more than 8 weeks duration (Group 2) and in 9 HIV-infected homosexual men referred for dysphagia or dyspepsia with no symptoms of malabsorption (Group 1). All biopsy specimens were examined by light microscopy and immunochemical staining with monoclonal antibody against HIV glycoprotein gp41. Electron microscopy was performed in 18 patients in Group 2 and in all patients in Group 1. Immunogold electron microscopy was used as a confirmatory test for identified HIV particles. In addition, D-xylose absorption was measured in all patients after a 25-g dose of D-xylose with measurement of serum D-xylose concentration 1 hour after the dose and measurement of 5-hour urinary D-xylose excretion. Mean serum D-xylose was 35.4 +/- 4.5 mg/dL in Group 1 and 15.8 +/- 2.3 mg/dL in Group 2 (P less than 0.001), whereas mean urine D-xylose was 5.5 +/- 0.6 g in Group 1 and 2.0 +/- 0.4 g in Group 2 (P less than 0.001). Immunoperoxidase for gp41 was positive in 5 (56%) patients in Group 1 and in 12 (60%) patients in Group 2. Lamina propria HIV viral particles were identified by electron microscopy in both patient groups. Viral particles were seen within and adjacent to the cytoplasm of mononuclear cells and were not present in enterocytes or neuroendocrine cells. There were no significant differences in serum or urine D-xylose tests between patients with and without lamina propria HIV. In addition, lipid accumulation in intercellular spaces near the basolateral membrane of adjacent enterocytes was seen in 33% of patients with chronic diarrhea. These findings suggest that lamina propria HIV is not a direct cause of enteropathy in HIV-infected patients and that lymphatic obstruction may be one pathophysiologic mechanism producing this malabsorptive state.
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PMID:Histopathologic findings of duodenal biopsy specimens in HIV-infected patients with and without diarrhea and malabsorption. 141 28

The pathologic changes associated with human cryptosporidiosis have not been well characterized. In this report, 15 cases of cryptosporidiosis in acquired immunodeficiency syndrome patients are described. Organisms were found in autopsy tissue specimens in 13 cases, and only in antemortem stool samples in two. Gastrointestinal/hepatobiliary distribution of organisms was as follows: small intestine (13 cases), extrahepatic bile ducts (eight), intrahepatic bile ducts (seven), large intestine (six), pancreas (five), stomach (three), and esophagus (one). At all sites, infection was usually associated with nonspecific reactive epithelial changes, architectural abnormalities such as villous flattening in the small intestine, and interstitial edema with mixed inflammatory cell infiltrates. Presence of organisms and associated mucosal injury were patchy and of variable severity in the intestine. In the biliary tract, injury was commonly diffuse and severe. Pancreatic duct injury was generally mild and often limited to hyperplastic squamous metaplasia. In late-stage acquired immunodeficiency syndrome patients with cryptosporidiosis, widespread infection in the gastrointestinal and biliary systems by this coccidian was more common and severe than previously suggested. Although the mechanisms have yet to be determined, infection usually is accompanied by pathologic changes that may be causally related to pathophysiologic abnormalities, such as diarrhea and malabsorption, and may account for other clinical manifestations of pancreatitis, cholangitis, and obstructive cholestasis.
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PMID:Cryptosporidiosis in the acquired immunodeficiency syndrome: a study of 15 autopsy cases. 174 28


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