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)

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

The gastrointestinal tract is a major target of the human immunodeficiency virus. Many AIDS patients have weight loss and/or diarrhea. Parenteral nutrition can be used to treat malnutrition associated with malabsorption. We reviewed retrospectively the clinical course of 22 patients with AIDS and weight loss greater than 10% who received home parenteral nutrition (HPN) for 56.2 patient-months. Mean weight loss was 21.4%, mean duration of HPN 2.55 months, mean age 37.4 years. Fifteen patients gained weight, six stabilized and two continued to lose weight. Nine patients returned to previous activity. Five died. The rates of catheter-related sepsis, complications, and metabolic disturbances were 0.12, 0.25, and 0.12/100 catheter days, respectively, results identical to those reported in other patient populations where HPN is commonly applied. We found that HPN induced weight gain and clinical improvement in most patients without higher risks of sepsis than in patients with malignancies.
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PMID:Risks and benefits of home parenteral nutrition in the acquired immunodeficiency syndrome. 190 Nov 11

Because gastrointestinal dysfunction is a major problem in children with human immunodeficiency virus (HIV) infection, we utilized breath hydrogen measurements to determine the relationship between disaccharide malabsorption and gastrointestinal dysfunction in HIV-infected children. We found a strong association between lactose intolerance and persistent diarrheal disease in this population (p less than 0.007, Mann-Whitney U test). We also found evidence of sucrose malabsorption and persistent diarrheal disease in three of the children. Extensive microbiologic evaluations failed to reveal an etiologic agent related to the occurrence of gastrointestinal symptoms. Our findings indicate that disaccharide intolerance is a common occurrence in HIV-infected children with persistent diarrheal disease. Careful attention to dietary intake may be required to ameliorate clinical symptoms and to maintain adequate nutrition.
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PMID:Gastrointestinal dysfunction and disaccharide intolerance in children infected with human immunodeficiency virus. 199 74

Chronic diarrhea and malabsorption accompanied by simultaneous infection with the protozoa Giardia lamblia and Cryptosporidium occurred in a 22-year-old homosexual man with antibody to human immunodeficiency virus (HIV). Small bowel biopsy demonstrated total villous atrophy and marked mononuclear infiltration in the lamina propria simulating celiac disease. Treatment with metronidazole resulted in resolution of diarrhea, clearance of parasites, and marked improvement in small bowel histology. Although diarrhea and malabsorption in immunocompromised patients with cryptosporidiosis are regarded as ominous, our patient remained disease free for the next 3 years. Thus, infection with Cryptosporidium in patients with HIV does not always lead to intractable diarrhea or death.
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PMID:Cryptosporidium infection in acquired immunodeficiency syndrome: not always a poor prognosis. 200 56

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

Malnutrition is a frequent problem in persons infected with the human immunodeficiency virus. The origin of malnutrition in patients with AIDS may be multifactorial. The primary mechanisms include disorders of food intake, alterations in intermediary metabolism, and nutrient malabsorption. Attention to the problems of malnutrition in patients with AIDS is of paramount importance because the timing of death in these patients may be more closely related to degree of body cell mass depletion than to any specific underlying infection. Nutritional support can improve nutritional status in selected patients, and repletion of body cell mass may be associated with functional improvement. Early assessment, attention to nutritional requirements, and prompt intervention can minimize wasting and replete body cell mass. This article examines the evidence for malnutrition in patients with AIDS, reviews the studies of nutritional support, and presents an approach to the management of malnutrition in AIDS.
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PMID:Malnutrition in patients with AIDS. 212 39

The class II major histocompatibility complex antigen deficiency syndrome is a rare immunodeficiency disease associated with defective expression of the class II antigens encoded for by the major histocompatibility complex. Clinically, this syndrome is manifest as a combined immunodeficiency presenting early in life, and affected individuals are susceptible to a variety of severe and/or opportunistic infections. Chronic, severe diarrhea and malabsorption are also characteristically found, and death is common within the first few years of life. Although the precise molecular lesions responsible for the failure of membrane antigen expression in this syndrome have not yet been identified, the pathogenetic mechanisms involve regulatory defects in the transcription of structural genes encoding for class II antigens. The absence of class II MHC antigens results in profound abnormalities in lymphocyte function and differentiation. Of central importance is the defective MHC-restricted interactions between CD4+ "helper" T lymphocytes and the various types of antigen-presenting cells found in the skin and elsewhere. The absence of class II MHC antigens also appears to alter the ability of affected B cells to be activated by a variety of membrane-mediated stimuli, and it profoundly disrupts both the intrathymic development and post-thymic differentiation of immunoregulatory T cells. This "experiment of nature" thus demonstrates the critical role of class II MHC antigens in the proper development and function of the immune system.
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PMID:The class II major histocompatibility complex antigen deficiency syndrome: consequences of absent class II major histocompatibility antigens for lymphocyte differentiation and function. 219 Oct 47

Even in the absence of anorexia and malabsorption, weight loss is frequently observed in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC). To investigate whether increased resting energy expenditure (REE) might be responsible for this weight loss, indirect calorimetry was performed in 18 human immunodeficiency virus (HIV)-infected men free of clinically active opportunistic infections for at least 2 months. Patients with AIDS (n = 11) or ARC (n = 7) had 9% higher rates of REE when compared with 11 healthy volunteers (P less than .05) with similar food intake and of the same body composition. The results obtained from patients with AIDS or ARC were identical. As no differences were found between patients and controls in plasma concentrations of catecholamines, thyroid hormones, cortisol, or tumor necrosis factor, except for lower concentrations of norepinephrine in the patients (mean +/- SD, 233 +/- 111 v 367 +/- 125 ng/L, patients v controls, P less than .01), this hypermetabolism is not explained by higher levels of these catabolic hormones. The results indicate that even in the absence of acute concomitant infections, increased REE may contribute to the weight loss in patients with AIDS or ARC.
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PMID:Increased resting energy expenditure in human immunodeficiency virus-infected men. 223 80

Relationships between nutrition and infection are generally complex, bidirectional, and not perfectly worked out. Healthy people can adapt to simple decreases in intake or increases in expenditure. However, the imposition of infection with associated cytokines may impair such adaptations, resulting in wasting of lean tissue. In human immunodeficiency virus (HIV) infection, nutritional abnormalities are common. Lean body mass depletion is associated temporally with death in a subset of acquired immune deficiency syndrome (AIDS) patients. Weakness, fatigue, and anorexia are important symptomatic complaints affecting quality of life. Pathophysiologic mechanisms remain speculative, although there is reason to suspect four theoretic factors: decreased intake, malabsorption, hypermetabolism, and altered metabolism. More than one disturbance may be necessary for clinical wasting to develop; ie, a primary abnormality plus a failure of homeostatic adaptation. Excess cytokine production also may be involved, but this is uncertain. Therapeutics remain empiric in the absence of known mechanisms. Current options are restricted to diet adjustments or supplements, treatment of underlying diseases (where possible), and rarely, parenteral alimentation. Promising investigational possibilities include an appetite stimulant (megestrol acetate) and therapies to oppose cytokine production or actions, but definitive beneficial effects on nutritional status, subjective performance, disease activity, or survival have not yet been demonstrated. Advances in clinical therapeutics await an improved understanding of pathophysiologic mechanisms and carefully designed clinical trials testing proposed interventions.
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PMID:Current approach to the treatment of human immunodeficiency virus-associated weight loss: pathophysiologic considerations and emerging management strategies. 225 24


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