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)

Ten patients were identified at Jackson Memorial hospital/University of Miami Hospitals and Clinics with enteric coccidial infection due to Cryptosporidium spp. or Isospora belli. All had the acquired immunodeficiency syndrome as manifested by Kaposi's sarcoma or multiple opportunistic infections, or both. They presented with profuse diarrhea associated with weakness, anorexia, and weight loss. Routine examinations of stools for eggs and parasites as performed by the hospital laboratory were negative in all patients. Sugar flotation and modified acid fast techniques were used in the Tropical Disease Laboratory to identify oocysts of Cryptosporidium spp. in stools of seven patients. Malabsorption, characterized by a low 5-hour D-xylose and positive fecal fat, was observed in 6/6 of these patients. In three other patients Isospora belli oocysts were identified in stool specimens or via a duodenal string test. Spiramycin was the only drug found to be effective in treating patients with cryptosporidiosis. Patients with Isospora belli responded to a prolonged course of trimethoprim-sulfamethoxazole.
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PMID:Enteric coccidiosis among patients with the acquired immunodeficiency syndrome. 633 48

To explore the effect of the acquired immunodeficiency syndrome on gastrointestinal structure and absorption, the cases of 12 homosexual men with the syndrome and 11 homosexual controls were studied. Seven patients had diarrhea with weight loss. Bacterial or parasitic infections were not detected. All patients were malnourished; had significantly fewer T-lymphocyte helper and suppressor cells; and had significantly lower body weights, midarm circumferences, serum albumin concentrations, and iron binding capacities than homosexual controls. D-Xylose malabsorption and steatorrhea were present in patients, especially those with diarrhea. Jejunal and rectal biopsy samples were histologically abnormal in all patients with diarrhea. Jejunal abnormalities included partial villus atrophy with crypt hyperplasia and increased numbers of intraepithelial lymphocytes. Rectal abnormalities included intranuclear viral inclusions, mast cell infiltration in the lamina propria, and focal cell degeneration near the crypt base. The histologic findings suggest that a specific pathologic process occurs in the lamina propria of the small intestine and colon in some patients with the syndrome.
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PMID:Enteropathy associated with the acquired immunodeficiency syndrome. 647 31

Two homosexual Danish men with the acquired immunodeficiency syndrome (AIDS) contracted cryptosporidium enterocolitis. One patient died in another opportunistic infection, the other developed severe chronic enterocolitis with malabsorption. The cryptosporidia escape detection on routine stool examination, but are easily demonstrated by a modified Ziehl-Neelsen stain. It is suggested that this procedure should be applied when persons from AIDS high risk groups or patients with other forms of immunological incompetence develop prolonged diarrhoea.
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PMID:Cryptosporidium enterocolitis in homosexual men with AIDS. 654 55

Chronic diarrhea and weight loss are common in patients with AIDS. We report on an AIDS patient with chronic diarrhea, steatorrhea, and marked weight loss. A 75SeHCAT test demonstrated that the diarrhea was mainly due to bile acid malabsorption. Therapy with cholestyramine dramatically reduced bowel movements and led to significant reversal of weight loss.
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PMID:HIV-enteropathy and bile acid malabsorption: response to cholestyramine. 748 23

Cryptosporidium parvum is a coccidian parasite originally described a century ago and, until recently, not considered to be a human pathogen. It has a complex life cycle, including both sexual and asexual reproduction, an auto-infectious cycle, and the ability to complete its development within a single host. The transmission form is a robust, environmentally resistant oocyst, excreted in the stool, which can exist for long periods of time in the environment. Because animals, in particular domesticated livestock, are its primary host, human infection is usually zoonotic. Oocysts often find their way into water supplies, and it resists chlorination and is incompletely filtered from processed drinking water supplies, even when filtration is working optimally. Transmission via ingestion of fecally contaminated swimming pool water, food, fomites, and sexual activities facilitating fecal-oral inoculation have been demonstrated. The major target of C. parvum in the host is the intestinal epithelial cell, resulting in diarrhea, sometimes profuse and persistent, although it may also infect other organs such as the gall bladder and lungs. Pathogenesis involves attachment, probably via a sporozoite lectin, invasion, probably involving apical organelles, replication within a parasitophorous vacuole with the host cell membrane, causing cellular dysfunction. Diagnosis is generally made by visualization of the oocyst form in stool by staining methods, the best of which appears to be auramine and fluorescence microscopy. Those at greatest risk are immunocompromised adults and children, especially those with AIDS, children in day care, travelers to endemic regions, dairy or cattle farm workers of their families or contacts, household contacts of cases or carriers, and possibly owners of infected dogs or cats or their neighbors. There is no specific therapy available, however in the immunocompetent host the illness is self-limited, lasting from a few days to 3 weeks, and long term carriage is uncommon. In the immunocompromised host, infection is prolonged, sometimes asymptomatic, but may result in chronic debilitating diarrhea with dehydration, malabsorption and wasting. Public health measures to reduce contamination of water supplies and vigilant surveillance will reduce the risk to populations. Reducing behaviors favoring fecal-oral transmission, such as certain sexual activities, and scrupulous hygiene in the day care setting would also reduce the likelihood of transmission but not eliminate it. Given our lack of knowledge about Cryptosporidium biology and pathogenesis, high priority should be given to research designed to increase our understanding of the organism and improve the chance of developing useful therapeutic or preventative drugs or strategies.
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PMID:Cryptosporidia--who is at risk? 777 Jul 51

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.
AIDS Res Hum Retroviruses 1994 Aug
PMID:Wasting syndrome: nutritional support in HIV infection. 781 45

AIDS patients may have achlorhydria, a condition that could result in drug malabsorption, especially of antifungals. The effect of a reduction in the production of gastric acid on the pharmacokinetics of the antimycotic fluconazole after a single 100 mg dose was investigated in a randomized two-way crossover study with 12 healthy volunteers. Gastric acid production was reduced by pretreatment with 20 mg omeprazole/day over a period of 7 days; pH and gastric emptying times were measured by a radiotelemetering pH capsule. Omeprazole pretreatment significantly raised the median gastric pH (from pH 1.1 to pH 4.7, p < 0.0001), but had no significant influence on gastric emptying time of the pH capsule (median = 4.3 vs 4.9 hours). The pharmacokinetics of fluconazole were unchanged; plasma parameters were Cmax = 2.04 micrograms/ml, tmax = 4.08 h and AUC = 98.91 h micrograms/ml after the omeprazole treatment, compared to 2.06 microliters/ml, 3.92 hours and 97.29 h micrograms/ml, respectively. The median bioavailability ratio of fluconazole before and after omeprazole treatment was 1.00. It is inferred that there is no interference of omeprazole with the plasma pharmacokinetics of fluconazole. The findings suggest that changes in gastric pH, as in patients with AIDS or those being treated with anti-ulcer drugs, should not influence the pharmacokinetics of fluconazole.
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PMID:The influence of gastric pH on the pharmacokinetics of fluconazole: the effect of omeprazole. 782 Mar 33

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

Clinical observation suggests that the natural history of intestinal cryptosporidiosis in patients with acquired immunodeficiency syndrome varies greatly. The relation between clinical, small-bowel functional, and nutritional status and the intestinal distribution of the organism was studied in 41 patients who had acquired immunodeficiency syndrome and cryptosporidiosis and who had undergone both proximal small-bowel and colonic biopsies. Two patterns of enteric cryptosporidiosis were identified: severe clinical disease with malabsorption in patients with cryptosporidia in proximal small-bowel biopsy specimens (61% of cases) and less severe clinical disease in patients with cryptosporidia only in the colon or stool (39% of cases). Patients with cryptosporidia in proximal small-bowel biopsy specimens had small-bowel crypt hyperplastic villous atrophy, lamina propria inflammatory infiltrates, poorer D-xylose absorption, greater weight loss, and shorter survival and more often needed intravenous hydration or hyperalimentation. Patients with cryptosporidia in the small-bowel villi only had less severe disease than those with cryptosporidia in the small-bowel crypts. In conclusion, the anatomic distribution of intestinal cryptosporidia in patients with acquired immunodeficiency syndrome varies, and this variation may explain differences in clinical course. Cryptosporidial infection of the proximal small bowel correlates with mucosal injury, malabsorption, dehydration, weight loss, and shortened survival.
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PMID:Variation in the enteric distribution of cryptosporidia in acquired immunodeficiency syndrome. 794 97

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


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