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)

Tissue wasting often occurs during human immunodeficiency virus infection and acquired immune deficiency syndrome. While weight-loss in the human immunodeficiency virus-infected individual can be seen as an isolated symptom, catabolism during acquired immune deficiency syndrome is usually associated with complications such as diarrhea, malabsorption, fever and secondary infection. Glutamine is an amino acid central to many important metabolic pathways and recent findings suggest that glutamine depletion may explain the progression of tissue wasting during human immunodeficiency virus infection.
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PMID:Glutamine deficiency as a cause of human immunodeficiency virus wasting. 867 62

Children with human immunodeficiency virus (HIV) infection have a higher prevalence of intestinal malabsorption. Anemia is also a common feature in these children. The aims of this work were (a) to establish the prevalence of iron deficiency in HIV-infected children, (b) to test the hypothesis that iron deficiency is related to intestinal malabsorption, (c) to see whether it may contribute to anemia, and (d) to evaluate the sensitivity of oral iron load in the investigation of intestinal function. To accomplish these goals, 71 HIV-infected symptomatic children were enrolled. Iron serum values were determined before and after oral load with ferrous sulfate. The correlation between basal and post-load iron levels was evaluated by linear regression. Xylose level after oral load, fecal fat, and fecal alpha 1-antitrypsin concentration were also determined. Iron deficiency was detected in 48% of patients, and it was significantly associated with intestinal iron malabsorption. Sugar malabsorption, steatorrhea, and fecal protein loss were detected in 26, 36, and 17% of patients, respectively. Low hemoglobin levels were detected in 66% of patients. The majority of children with iron deficiency also had anemia. Preliminary data showed that oral iron administration was sufficient for raising hemoglobin in children with normal iron absorption, whereas parenteral administration was required in those with iron malabsorption. We conclude that (a) iron deficiency is a major feature of pediatric HIV infection, (b) it is related to intestinal malabsorption, and (c) it contributes to anemia. Finally, oral iron load is a sensitive test for investigating intestinal function.
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PMID:Iron deficiency and intestinal malabsorption in HIV disease. 873 98

Infants and young children with HIV infection commonly suffer from gastrointestinal manifestations of their disease. Many HIV infected children have evidence of persistent diarrhoea, malabsorption, malnutrition or growth failure. The aetiology and pathogenesis of gastrointestinal dysfunction in HIV infected children have not been well defined. We performed immunocytochemical analyses on intestinal tissue from 19 HIV-infected children with gastrointestinal dysfunction or growth failure. None of these 19 children had microbial pathogens identified in faecal samples using standard microbiological methods. Intestinal tissues were obtained from the children by biopsy and were examined for antigens from Pneumocystis carinii, cytomegalovirus (CMV) and herpes simplex virus (HSV) using the avidin-biotin-complex immunohistochemical technique and monoclonal or monospecific antibodies. We detected at least one of these pathogens in samples from eight (42%) of 19 HIV infected children. P. carinii was the most prevalent pathogen, found in five of the eight HIV infected children. All of the children with intestinal pneumocystis infection were receiving prophylaxis directed at the prevention of pulmonary disease with this organism and none of them were undergoing active pulmonary infection. We also identified CMV antigens in intestinal tissues from four children and HSV antigens in intestinal tissues from one child. Two children were infected with more than one pathogen. On the other hand, none of these pathogens were found in the tissues obtained from 10 HIV-uninfected patients who had intestinal tissues obtained for chronic non-infectious diarrheal and inflammatory diseases (P < 0.01, Fisher's exact test). Our findings indicate that some children with HIV infection and gastrointestinal dysfunction may be infected with opportunistic pathogens despite negative analyses employing standard microbiological methods. Our study also indicates that HIV infected children can undergo intestinal infection with P. carinii despite the administration of standard immunoprophylactic regimens directed at the prevention of infection with this organism.
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PMID:Enteric pathogens associated with gastrointestinal dysfunction in children with HIV infection. 873 89

Multiple infectious causes of diarrhea are known in patients with HIV/AIDS. Maldigestion and malabsorption have been reported in patients with HIV/AIDS and may be independent of infectious etiologies. Among ambulatory patients with HIV/AIDS, we examined the prevalence of fat malabsorption (steatorrhea). Sixty-one patients with unexplained diarrhea (defined as > 2 stools/d) and/or weight loss despite adequate caloric intake (and without clinical evidence of chronic pancreatitis) were evaluated in our outpatient Gastroenterology-Nutrition Clinic between March 1, 1993, and July 1994. Patients were instructed by a dietitian to follow a > or = 100 g/d fat diet for 24 h before submitting a stool sample for qualitative (or quantitative) fecal fat determination. Forty-five patients, 32 with ongoing diarrhea and 13 without diarrhea, submitted stool samples. Twenty-two of 45 patients (49%) had qualitative or quantitative steatorrhea, 16/32 with diarrhea (50%) and 6/13 patients without diarrhea (46%). Thirty of 32 patients with diarrhea had had extensive microbiologic and/or endoscopic evaluations. Only 9 patients had a detectable intestinal pathogen, 5 patients had cytomegalovirus (4 treated), 4 patients had cryptosporidia (3 treated), and 1 patient had microsporidia. Steatorrhea, as determined by abnormal qualitative fecal fat, is detectable in nearly 50% of patients with HIV/AIDS. Fat malabsorption appears to be a primary defect in these patients independent of detectable pathogens. Assessment of fat malabsorption should be considered in patients with unexplained weight loss or diarrhea before extensive evaluation for opportunistic infections.
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PMID:Steatorrhea: a common manifestation in patients with HIV/AIDS. 887 43

Failure to downregulate resting energy expenditure (REE) as an adaption to anorexia or malabsorption is often stated as the major cause of weight loss in individuals with AIDS. In a prospective study, REE was compared with weight changes in HIV-infected patients. The impact of altered body composition on REE was reassessed by critical review of the literature. Patients were 65 male HIV-infected patients, 28 with recent weight loss (WL), and 37 who were weight stable (WS); 50/65 patients had AIDS, and 29/65 had acute infections; 29 male healthy persons served as controls. Indirect calorimetry, prospective intake protocol, and bioelectrical impedance analysis were performed. Absolute REE was lower in WL patients than in controls (1459 +/- 309 versus 1711 +/- 151 kcal/d, p < 0.001) and in WS patients (1625 +/- 402 kcal/d, p < 0.05). REE/kg body cell mass (BCM) was higher in WL and WS than in controls (both p < 0.01) due to lower BCM in both patient groups (p < 0.001). REE (%Harris-Benedict) was not different among the three groups. Weight changes around the measurement were not correlated to REE (r2 = 0.0008, p = 0.82). REE was independent of diarrhea, acute infection, fever, or caloric intake. REE had a stronger correlation to body weight and to Harris-Benedict's prediction than to fat-free mass or BCM. REE explains < 1% of weight changes. Many patients can downregulate REE as an adaption to anorexia and/or malabsorption. Higher REE/kg BCM does not signify hypermetabolism at the cellular level but can be explained by the maintenance of energy-consuming visceral tissue within the BCM during BCM loss.
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PMID:Resting energy expenditure, weight loss, and altered body composition in HIV infection. 887 75

Microsporidia are emerging as opportunistic pathogens in patients with AIDS. Enterocytozoon bieneusi and Encephalitozoon (Septata) intestinalis have been implicated in enteric infections in AIDS patients with chronic diarrhea, a wasting syndrome, and malabsorption. We used the polymerase chain reaction (PCR) and primers that amplify the conserved regions of the small-subunit rRNA (SSU-rRNA) gene of E. bieneusi and E. intestinalis in tissue specimens from HIV-infected patients with and without diarrhea to examine the association between microsporidia and diarrhea in patients with AIDS. Tissue specimens were obtained from 68 patients with AIDS and diarrhea (mean CD4 lymphocyte count, 21/mm3) and 43 AIDS patients without diarrhea (mean CD4 lymphocyte count, 60/mm3). By means of PCR with use of the SSU-rRNA primers specific for E. bieneusi and E. intestinalis, we found that 44% of patients with diarrhea were infected with microsporidia, whereas only 2.3% of the patients without diarrhea were infected with microsporidia (P < .001). There was a clear association between the presence of microsporidia and diarrhea. In addition, the SSU-rRNA primers proved to be sensitive and specific when used in this clinical setting.
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PMID:Prevalence of microsporidiosis due to Enterocytozoon bieneusi and Encephalitozoon (Septata) intestinalis among patients with AIDS-related diarrhea: determination by polymerase chain reaction to the microsporidian small-subunit rRNA gene. 892 93

Since its introduction in 1987, zidovudine monotherapy has been the treatment of choice for patients with HIV infection. Unfortunately it has been established that the beneficial effects of zidovudine are not sustained due to the development of resistant viral strains. This has led to the strategy of combination therapy, and in 1995 treatment with zidovudine plus didanosine, or zidovudine plus zalcitabine, was demonstrated to be more effective than zidovudine monotherapy in preventing disease progression and reducing mortality in patients with HIV disease. Recent work demonstrates an even greater antiviral effect from triple therapy with 2 nucleosides, zidovudine plus zalcitabine with the addition of saquinavir, a new protease inhibitor drug. The HIV protease enzyme is responsible for the post-translational processing of gag and gag-pol polyprotein precursors, and its inhibition by drugs such as saquinavir, ritonavir, indinavir and VX-478 results in the production of non-infectious virions. As resistance may also develop to the protease inhibitors they may be used in combination, and future strategies may well include quadruple therapy with 2 nucleoside analogues plus 2 protease inhibitors. Administration of protease inhibitors alone or in combination with other drugs does raise a number of important pharmacokinetic issues for patients with HIV disease. Some protease inhibitors (e.g. saquinavir) have kinetic profiles characterised by reduced absorption and a high first pass effect, resulting in poor bioavailability which may be improved by administrating with food. Physiological factors including achlorhydria, malabsorption and hepatic dysfunction may influence the bioavailability of protease inhibitors in HIV disease. Protease inhibitors are very highly bound to plasma proteins (> 98%), predominantly to alpha 1-acid glycoprotein. This may influence their antiviral activity in vitro and may also predispose to plasma protein displacement interactions. Such interactions are usually only of clinical relevance if the metabolism of the displaced drug is also inhibited. This is precisely the situation likely to pertain to the protease inhibitors, as ritonavir may displace other protease inhibitor drugs, such as saquinavir, from plasma proteins and inhibit their metabolism. Protease inhibitors are extensively metabolised by the cytochrome P450 (CYP) enzymes present in the liver and small intestine. In vitro studies suggest that the most influential CYP isoenzyme involved in the metabolism of the protease inhibitors is CYP3A, with the isoforms CYP2C9 and CYP2D6 also contributing. Ritonavir has an elimination half-life (t1/2 beta) of 3 hours, indinavir 2 hours and saquinavir between 7 and 12 hours. Renal elimination is not significant, with less than 5% of ritonavir and saquinavir excreted in the unchanged form. As patients with HIV disease are likely to be taking multiple prolonged drug regimens this may lead to drug interactions as a result of enzyme induction or inhibition. Recognised enzyme inducers of CYP3A, which are likely to be prescribed for patients with HIV disease, include rifampicin (rifampin) [treatment of pulmonary tuberculosis], rifabutin (treatment and prophylaxis of Mycobacterium avium complex), phenobarbital (phenobarbitone), phenytoin and carbamazepine (treatment of seizures secondary to cerebral toxoplasmosis or cerebral lymphoma). These drugs may reduce the plasma concentrations of the protease inhibitors and reduce their antiviral efficacy. If coadministered drugs are substrates for a common CYP enzyme, the elimination of one or both drugs may be impaired. Drugs which are metabolised by CYP3A and are likely to be used in the treatment of patients with HIV disease include the azole antifungals, macrolide antibiotics and dapsone; therefore, protease inhibitors may interact with these drugs. (ABSTRACT TRUNCATED)
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PMID:Protease inhibitors in patients with HIV disease. Clinically important pharmacokinetic considerations. 908 59

We measured plasma levels of all the antioxidant-micronutrients in subjects with HIV infection and controls. Plasma levels of all the carotenoids, including lutein, cryptoxanthin, lycopene, alpha-carotene and beta-carotene as well as vitamins A, C and E and cholesterol were assayed in 35 subjects with HIV infection and 38 controls. We found a significant depletion of all the carotenoids (P < 0.001) and vitamin C (P < 0.01) and cholesterol (P < 0.001) but not vitamins A or E in HIV-infected subjects. Further analysis of the HIV-infected subjects revealed that plasma levels of 4 of the groups of carotenoids and cholesterol were correlated with CD4 count but that beta-carotene and vitamins A, C and E were not. These results are reviewed in the light of the published literature and we conclude that these abnormalities of antioxidant-micronutrients are likely to reflect a metabolic phenomenon associated with HIV infection. However, an additional contribution to these deficiencies from malabsorption later in HIV disease cannot be ruled out.
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PMID:Antioxidant-micronutrients and HIV infection. 911 64

Interactions between undernutrition, infection, and growth and development are complex, and are reviewed in this article, giving particular emphasis on the importance of diarrheal infection in this process. The effects of diet, nutrition and infection on the nutritional status of a child can vary according to the disease ecology, the age of the child, patterns of feeding and types of food consumed. There are two possible ways in which this relationship can begin; one in which poor nutritional status leads to impaired immunocompetence and reduced resistance to infection, and the other in which exposure to infectious disease can lead to appetite loss and anorexia, malabsorption, and elevated metabolism of energy and other nutrients. Once started, the interactions between these two major environmental stressors becomes increasingly complex, with the nature of the disease ecology influencing the balance of immunoparesis and adaptive immunity and its effect on subsequent disease experience. Furthermore, the disease ecology influences the type and extent of associated physiological phenomena including anorexia, fever, and malabsorption, all of which have an impact on nutritional status. Of disease categories, diarrhea has particularly potent effects in this relationship. The predicted impact of HIV infection among newborn infants is the earlier onset of the undernutrition-infection cycle, as low CD4+ T lymphocyte counts soon after birth are likely to predispose such infants to earlier opportunistic infection.
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PMID:Transdisciplinarity in the study of undernutrition-infection interactions. 922 95

A documented association exists between nutritional status and immunologic function, development, and outcome of infectious processes, and treatment-related toxicity and vital organ function. In persons with AIDS, nutritional deficits precipitate a cycle that results in a downward spiral of weight lost, malabsorption, diarrhea, anorexia, body image disturbance, and increased risk for morbidity and mortality. This article presents an overview of the malnutrition in HIV/AIDS patients. It critiques the current Centers for Disease Control's definitions of wasting syndrome, describes the incidence of weight loss, delineates the implications of untreated malnutrition, and traces the etiology of weight loss and contributing factors. This article serves as an introduction to HIV/AIDS related malnutrition. A subsequent article will review nursing implications and clinical management programs.
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PMID:Malnutrition associated with HIV/AIDS. Part One: Definition and scope, epidemiology, and pathophysiology. 924 67


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