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)

The growth of 22 boys with hemophilia, infection with human immunodeficiency virus (HIV), and lymphadenopathy, but not overt acquired immunodeficiency syndrome (AIDS) was evaluated. Three patients were found to have significant growth failure for 3-4 years with the onset after HIV infection. Extensive endocrine evaluation revealed that two of the three had neurodysregulation of growth hormone release with hyposomatomedinemia. None had classical growth hormone deficiency, thyroid deficiency, or evidence of malnutrition/malabsorption or other systemic illness. It appears that growth failure is not rare in boys with hemophilia and HIV infection and that this might be due to a direct effect on the physiologic secretion of growth hormone.
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PMID:Growth failure in boys with hemophilia and HIV infection. 278 55

Diarrhoea and weight loss are common features of human immunodeficiency virus (HIV) disease. The mechanism of diarrhoea occurring in the absence of known enteropathogens is currently unknown. We have measured fat absorption, using the 14C triolein breath test, and quantitatively assessed jejunal villous architecture in 20 male homosexuals at various clinical stages of HIV disease. Enteropathogens were not detected in any subject at the time of jejunal biopsy in stool or jejunal mucosa. Partial villous atrophy was the sole histological abnormality and was detected at any clinical stage of HIV disease. The 14C triolein breath test quantitatively correlated with the degree of jejunal villous atrophy. In addition subjective presence of diarrhoea was related to the detection of fat malabsorption. Thus diarrhoeal disease in HIV infected patients in the absence of enteropathogens may be due to jejunal enteropathy and may be present at early clinical stages of HIV disease.
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PMID:Jejunal mucosal architecture and fat absorption in male homosexuals infected with human immunodeficiency virus. 327 81

Involuntary bodyweight loss is a frequent manifestation of HIV infection and ultimately affects the majority of patients. Because it portends a poor prognosis and adversely affects quality of life, nutritional intervention has an important role in the care of all HIV-infected persons. The mechanism of HIV-related bodyweight loss is multifactorial and includes complex interactions between decreased caloric intake, malabsorption and metabolic and/or hormonal abnormalities. Treatment of reversible and identifiable causes of bodyweight loss such as opportunistic infections and adverse effects of therapy are essential for the maintenance of bodyweight. For patients with anorexia of unclear aetiology, there are effective appetite stimulants available. Enteral and parenteral alimentation are under evaluation for their role in maintenance and/or repletion of bodyweight for patients with HIV infection.
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PMID:Management of HIV-related bodyweight loss. 752 Aug 57

Malnutrition and wasting are common in patients with HIV infection. Nutritional needs vary with the stage of HIV disease. Severe weight loss is associated with increased mortality in patients with AIDS and is multifactorial in development. Possible causes of weight loss include decreased food intake due to oral or GI pathology or anorexia, nutrient malabsorption, and systemic infections. Severe malabsorption is limited to patients with advanced HIV disease with CD4+ cell counts < 100 and usually < 50 cells/microliters. The spectrum of GI pathogens continues to broaden. For hypermetabolic patients, evaluation for systemic infection followed by effective antiinfective treatment is critical. For nonhypermetabolic patients, a variety of metabolic and endocrinological abnormalities may be present. It is important to recognize that micronutrient deficiencies often accompany macronutrient deficits. Providing appropriate nutritional support to patients with AIDS is fundamental to optimal medical care. Overall indications for nutritional support in a patient with AIDS are the same as in any other chronic disease. Nutritional repletion is well documented, and there are a variety of approaches to achieving appropriate intake, including volitional (megestrol or dronabinol therapy) and nonvolitional (feeding tubes and total parenteral nutrition). Parenteral nutrition should not be undertaken without preset limits. The value of nutritional pharmacology with supraphysiological doses of micronutrients has not been established.
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PMID:Wasting syndrome: nutritional support in HIV infection. 781 45

Children with HIV infection have an unusual susceptibility to bacterial infection, related to several immune abnormalities. Selection of initial antibiotic therapy must be individualized in these children. Patients with community-acquired disease are most likely to have infection by polysaccharide-encapsulated bacterial organism, most commonly Streptococcus pneumoniae and less frequently by Haemophilus influenzae type b. If it is possible to treat the patients at home, the use of amoxicillin-clavulanic acid might be appropriate. Other authors propose management with parenteral ceftriaxone because of the better compliance and the malabsorption. In hospitalized patients, concern for Gram-negative enteric pathogens other than polysaccharide-encapsulated organisms requires initial therapy with a third-generation cephalosporine in combination with an aminoglycoside. Trimethoprim-sulfamethizole is the most common drug used in HIV-infected children because it is recommended for the initial therapy and for prophylaxis of pneumocystis carinii pneumonia, which occurs in as many as 42% of these children.
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PMID:The use of antibiotics in the treatment and prevention of infection in HIV-infected children. 783 66

The immune system is impaired by either malnutrition or human immunodeficiency virus infection. When these occur together, their compounding effects promote altered metabolism, inadequate intake, and malabsorption, which further impair immune function and contribute to human immunodeficiency virus wasting. Careful dietary management can help meet nutritional needs without further compromising the immune status of the person living with acquired immune deficiency syndrome.
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PMID:AIDS and malnutrition: dual assaults on the body. 786 Mar 43

Deficiency of vitamin B12 is commonly reported in HIV-infected patients. We measured vitamin B12 levels in 36 HIV-infected patients with chronic diarrhea (> 3 stools/day for six weeks or more). Eight patients had an identifiable cause of diarrhea. Vitamin B12 levels were low in 39%. Sixteen of these patients were selected to undergo further testing, eight patients with low levels of vitamin B12 and eight with normal B12 levels. These 16 patients had both a stage II Schilling test and measurement of multiple serum D-xylose concentrations performed after both oral and intravenous doses of D-xylose. Integrated areas under the curves (AUC) for D-xylose concentration versus time were calculated for intravenous and oral doses, and D-xylose bioavailability was determined. Stage II Schilling tests were abnormal in 11 patients, (69%). D-Xylose bioavailability correlated closely with vitamin B12 absorption (r = 0.648, P < 0.01). Comparisons of mean values for CD4 count, serum albumin, Karnovsky score, six-month weight loss, 1-hr serum D-xylose levels and MCV failed to reveal a significant difference between those with and without abnormal serum vitamin B12 levels. These data indicate that below-normal levels of vitamin B12 are highly prevalent in HIV-infected patients with chronic diarrhea. Malabsorption of vitamin B12 occurs in the setting of an enteropathic process effecting both the proximal and distal small bowel. Since no risk factors for vitamin B12 deficiency could be identified, screening for vitamin B12 deficiency in HIV-infected patients with chronic diarrhea is strongly recommended.
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PMID:Malabsorption and deficiency of vitamin B12 in HIV-infected patients with chronic diarrhea. 792 36

Human intestinal lamina propria T cells have a low expression of the CD45RA antigen and a high expression of the CD45RO antigen. This phenotype is characteristic for memory T cells. In addition, T cells in the effector compartment of the mucosa bear surface antigens that are very rarely found in other sites of the immune system. Intestinal T cells also express functional IL-2 receptors, and IL-2 receptor alpha-chain mRNA, and are able to synthesize high amounts of IL-2. However, other markers of memory T cells, as CD29, are not expressed in high density in the lamina propria, indicating that lamina propria T cells differ from "classical" memory T cells. This is supported by functional studies in nonhuman primates infected rectally with Chlamydia trachomatis that show that lamina propria T cells do not proliferate after stimulation with antigen but rather provide helper function for immunoglobulin synthesis. These findings indicate a specific state of differentiation of lamina propria T cells that is adapted to the specific requirements in the gut. In inflammatory bowel disease (IBD) and in celiac disease, an increase in the number of CD25-positive activated T cells is found in involved mucosa. It has been shown that mucosal T-cell activation induces epithelial cell damage and mucosal transformation. Thus, a T cell-mediated damage may contribute to the pathogenesis of IBD. HIV-infected patients have a decreased number of CD4-positive T cells in the intestinal lamina propria. The number of CD25-positive activated T cells is also significantly decreased in the intestine compared to controls. Correlating with the presence of HIV-infected mononuclear cells in the mucosa, mucosal atrophy with hyporegeneration and enterocyte dysmaturation is observed. HIV might thus cause impairment and depletion of activated regulatory T cells in the intestinal lamina propria, which could lead not only to a breakdown of the mucosal immune barrier, resulting in a variety of opportunistic infections, but also to malabsorption, due to mucosal atrophy or enterocyte dysfunction. These findings indicate a close relationship between mucosal T cells and enterocyte proliferation and maturation.
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PMID:Cell differentiation and proliferation in the gastrointestinal tract with respect to the local immune system. 797 5

Wasting may not be an inevitable consequence of HIV infection but may be a consequence of multiple nutritional insults that are additive without periods of replenishment in between. Protein energy malnutrition in AIDS patients may be consequential to underlying illness and concomitant to death as a result of that illness or may hasten a patient's demise, that is, starvation with fatal loss of body cell mass. Mortality is closely related to weight loss. Malnutrition may be a result of decreased intake, malabsorption, altered metabolism, or any combination of the three. Nutritional strategies to prevent PEM include appetite stimulation, early nutritional supplementation with oral supplements, and the diagnosis and treatment of malabsorption and underlying infections. More aggressive measures such as gastrostomy or jejunostomy tube placement and total parenteral feedings are still being evaluated. Nutritional supplementation to enhance the immune system or manipulate metabolism may be adjunctive to the above strategies. Early intervention and attention to nutritional status may have long-term benefits to patients with this disease.
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PMID:Nutritional aspects of HIV infection. 808 74

Gastrointestinal pathogens are of three varieties, those that can, and often do, take the life of the host, those that infect transiently and rarely are life-threatening, and those (parasites) that establish a relatively prolonged residence or colonization of the host's alimentary tract. In the case of the second form, if infections are recurrent, both catabolic effects during the episode and failure to digest foods and/or absorb nutrients results. Similarly, catabolic wastage through activation of the acute phase response, and interference with the host's acquisition of nutrients by maldigestion, malabsorption, intestinal losses and competition with the parasite burden can impair growth and nutrition with helminthic infections. Growth and nutrition with respect to all of the macronutrients and virtually all of the micronutrients have been documented to be adversely affected by gastrointestinal pathogens. For its burgeoning importance as a worldwide health problem, both with the HIV virus as a direct intestinal pathogen and with the opportunistic gut infections occurring in the immunocompromised host, AIDS represents the emerging context of the impairment of nutritional status by intestinal pathogens.
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PMID:Pathways to the impairment of human nutritional status by gastrointestinal pathogens. 811 84


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