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)

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

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

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

Sixty percent of HIV-infected children malabsorbed carbohydrate (lactose or D-xylose). Surprisingly, however, carbohydrate malabsorption was not predictive of growth failure. Although HIV infection, in the absence of detectable enteric infection, may result in small intestinal injury, additional factors may also be responsible for growth failure in HIV-infected children.
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PMID:Is malabsorption an important cause of growth failure in HIV-infected children? 177 Oct 35

Case management strategies for the nutritional support of patients infected with the human immunodeficiency virus (HIV) are evolving as the disease becomes less rapidly fatal and more chronic. Nutritional status changes in advanced HIV infection are similar in many respects to protein-calorie malnutrition. Current clinical effort and research focuses on the beneficial effects of preserving lean body mass and keeping asymptomatic patients in good nutritional status by preventing micronutrient deficiencies and by treating preexisting nutritional problems rather than attempting to intervene late in the disease's course, after secondary malnutrition has already developed. Nutrition support and intervention trials only late in the disease process have not been promising in reversing weight loss once it has occurred. Special diets, such as lactose- or gluten-free diets, may be helpful in some cases as asymptomatic treatment of some opportunistic infections, and such measures may slow additional losses. However, secretory diarrhea, which often seems to be inherent to the disease itself, is not ameliorated by such measures. Current research is focusing on the potential role of glutamine in slowing malabsorption and on combinations of diet and drug treatments. Asymptomatic patients are now the focus of concern. Preserving good nutritional status by attention to preventing weight loss and loss of lean body mass and assuring food safety are primary. Symptomatic patients require specific assistance depending on the presence of opportunistic infections and the drugs required. Specific nutrition support measures depend on whether or not the gut is functional.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nutrition support of HIV+ patients. 185 4

A prospective study of 60 consecutively admitted patients with HIV infection was performed to document the prevalence, etiology and manifestations of low serum vitamin B-12 in such patients. Low serum B-12 levels were found in 10 patients (16.7%). In 6, vitamin B-12 absorption was impaired and hog intrinsic factor addition did not improve it. Patients with low vitamin B-12 levels showed lower hemoglobin, leukocytes, lymphocytes, CD4 lymphocytes and CD4/CD8 lymphocyte ratio than HIV patients with physiological serum vitamin B-12 levels. However, bone marrow megaloblastosis was found in only 3 low vitamin B-12 patients and the deoxyuridine suppression test was pathological in only 1 case. In 7 patients, parenteral treatment was begun with variable response despite serum vitamin B-12 correction. In conclusion, low serum vitamin B-12 is often found in HIV-infected patients and it could be related to malabsorption, but clear megaloblastic abnormalities and treatment response could not be demonstrated. A decreased concentration of the serum binders due to disturbances in the leukocytes and related immunocompetent cell may play an additional role.
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PMID:Vitamin B-12 abnormalities in HIV-infected patients. 186 15

The nutritional needs of children with human immunodeficiency virus infection are poorly understood. Twenty-eight children with vertically transmitted human immunodeficiency virus infection were evaluated for carbohydrate malabsorption using lactose hydrogen breath tests and d-xylose absorption studies. Lactose malabsorption was a common finding in human immunodeficiency virus-infected children and occurred in 8 of 20 patients who had no identifiable enteric pathogen. Lactose malabsorption occurred at an earlier age in human immunodeficiency virus-infected children than in an age-matched group of 45 symptomatic control children (P = 0.02). However, lactose malabsorption was not associated with higher rates of diarrhea or growth failure. Abnormalities in d-xylose absorption were not significantly associated with either diarrhea or growth failure. However, 39% of d-xylose studies (9 of 23) showed abnormal results and were significantly associated with enteric infections (P = 0.004). Abnormalities in small-bowel morphology were found in 4 of 9 children with growth failure, 3 of whom had an enteric infection and low d-xylose absorption. Lactose hydrogen breath testing and d-xylose testing showed carbohydrate malabsorption in 61% of children (17 of 28). This study demonstrates that human immunodeficiency virus-infected children are at risk for malabsorptive disorders, which are not always related to clinical symptoms. We speculate that human immunodeficiency virus may be directly involved in the development of lactose malabsorption. Carbohydrate malabsorption in human immunodeficiency virus-infected children may not be the only factor responsible for growth failure.
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PMID:Malnutrition and carbohydrate malabsorption in children with vertically transmitted human immunodeficiency virus 1 infection. 201 74

Intestinal malabsorption is a recognized cause of malnutrition in patients infected with human immunodeficiency virus. However, the relationships among human immunodeficiency virus infection, morphological changes in the intestine, and development of intestinal malabsorption are not well established. Nine patients infected with human immunodeficiency virus underwent tests of intestinal absorption and jejunal biopsies for morphometric measurements, enzyme assays, and virus detection by in situ hybridization. Steatorrhea and low lactase activities were found in more than 85% of the patients. All biopsy specimens were abnormal with reversal of the ratio of villus length to crypt depth in seven and enlarged enterocyte nuclear size in nine. Human immunodeficiency virus was detected in five jejunal biopsy specimens, within villus enterocytes of one patient who had the most severe malabsorption of the group and in four other biopsy specimens in mononuclear infiltrating cells of the lamina propria. These results suggest that human immunodeficiency virus infection of the small intestinal mucosa is an early event that is associated with altered enterocyte differentiation and function.
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PMID:Human immunodeficiency virus infection of enterocytes and mononuclear cells in human jejunal mucosa. 201 58

Until now, recommendations for nutrition therapy of HIV-infected subjects can only be regarded as preliminary, because of the lack of scientific results regarding the interactions between HIV-infection and nutrition. HIV-infected patients have a high risk to become malnourished during the course of the disease, as a consequence of multiple pathogenetic factors--similar to the nutritional problems of tumor patients. At the moment, the following procedure is recommended in order to treat or prevent HIV-associated malnutrition: The nutritional status and history should be assessed in each HIV-positive subject as early as possible. Independent of the actual nutritional status, each patient should obtain a nutrition education. A continuous nutrition therapy becomes necessary in the case of evident or imminent malnutrition. Nutrients should be applied by oral access as long as possible. But especially for patients with opportunistic infections of the GI-tract accompanied by malabsorption, total parenteral nutrition may be the only effective way of nutrition.
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PMID:[Malnutrition--a clinically relevant problem in HIV-1 infection?]. 211 23

Gastrointestinal symptoms and malabsorption are frequent in HIV-infected patients even in the absence of opportunistic infections. In earlier studies we found indications that the gastrointestinal mucosa itself may be affected by HIV. Since there is evidence that the mucosal structure is influenced by changes in the gut-associated lymphoid tissue, we have investigated mucosal structure and immune cells in HIV-infected patients. Sixty patients (3 f, 57 m; age 21-61, median 37 years; 11 at CDC stage II or III, 49 at stage IV) with gastrointestinal complaints undergoing upper endoscopy were examined for enteric pathogens. Duodenal biopsies were labelled by immunohistology for HIV antigen p24 and for lymphocyte surface markers; mucosal architecture was studied by three-dimensional morphometry. Biopsies from HIV seronegative patients without abnormal findings served as controls. In 29 patients an enteric pathogen was identified. In 22 patients HIV-infected mononuclear cells were detected in the lamina propria. In the lamina propria CD25+ cells were decreased, CD3+ and CD8+ cells were increased in HIV-infected patients compared with controls, while the numbers of CD4+, Leu8+, and HML-1+ cells, and of macrophages were not different. Patients at stage IV had decreased numbers of CD4+ T cells compared with patients at stage II or III. Villus surface area was reduced in HIV-infected patients compared with controls. Crypt depth was increased in patients with intestinal infection compared with controls while numbers of mitotic figures were normal. Patients without intestinal infection and patients with mucosal HIV-infected cells had decreased numbers of mitotic figures and normal crypt depth compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mucosal atrophy is associated with loss of activated T cells in the duodenal mucosa of human immunodeficiency virus (HIV)-infected patients. 226 63


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