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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acquired immunodeficiency syndrome and (human immunodeficiency virus) infection loom as our major public health priorities for at least the next two decades. Despite the recent exciting early development of vaccines and newer drug therapies, we are all faced with a reservoir of almost one-quarter million cases in the United States and several times that worldwide. Since the vast majority of HIV-infected patients develop AIDS, which is a chronic progressive disease that produces gastrointestinal dysfunction and wasting, development of rational strategies for nutritional support of these patients should also be a high priority.
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PMID:Toward rational nutritional support of the human immunodeficiency virus-infected patient. 190 46

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

Gastrointestinal dysfunction is a serious problem in many children infected with human immunodeficiency virus (HIV), the etiology of which has not been clearly defined. Quantitative nucleic acid amplification was used to study the correlation between shedding of HIV nucleic acids and gastrointestinal symptoms in HIV-infected infants and children. Many with HIV infection and persistent diarrheal disease shed HIV nucleic acids in their feces, as did an HIV-infected patient without apparent diarrheal disease. HIV nucleic acids were not found in feces of non-HIV-infected individuals. Intestinal infection with HIV appears to be important in the pathophysiology of gastrointestinal dysfunction in infants and children with HIV infection. Furthermore, the fecal shedding of HIV may play a role in HIV transmission in environments prone to high levels of fecal-oral contamination.
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PMID:Persistent diarrhea and fecal shedding of retroviral nucleic acids in children infected with human immunodeficiency virus. 205 18

AIDS-related gastrointestinal disease is common, presenting a challenge to all nutritional support clinicians. Patients frequently suffer from weight loss, diarrhea, malabsorption, and cachexia. Many factors complicate the course of AIDS-related gastrointestinal disease, including decreased food intake (resulting from fatigue and malaise), increased metabolic demand and nutritional requirements, and identifiable gastrointestinal pathology. Gastrointestinal pathology is well-documented, and in approximately 50% of persons with AIDS-related gastrointestinal disease, a causative agent can be identified. In general, treatment of AIDS-related gastrointestinal disease is not always curative. Much of the chronic gastrointestinal dysfunction is caused by recurring opportunistic pathogens that are resistant to chemotherapy. Often, patient care and long-term management can focus only on fluid and electrolyte balance, nutritional support, and symptom control. Even clinically stable patients have been diagnosed as chronically malnourished and, for reasons that remain unclear, are prone to rapid nutritional deterioration during disease exacerbations. Published reports of nutritional assessment and intervention in persons with AIDS are now appearing in the literature. However, the eventual mortality associated with AIDS still results in a hesitancy on the part of many clinicians to prescribe aggressive nutritional support, especially parenteral nutrition. Who to treat and at what stage of illness becomes the question. As new agents, such as AZT, are prescribed on a more frequent basis for persons with AIDS, the use of nutritional support as adjunctive therapy early in the course of disease becomes an issue. Although improving nutrition has not been shown to reverse any of the cellular immunodeficiency caused by HIV infection, quality of life may be improved. In specific cases, nutritional support, whether through diet counseling, food programs, or intervention with enteral or parenteral nutrition, appears to improve strength and endurance, thus enhancing quality of life.
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PMID:Gastrointestinal manifestations of the acquired immunodeficiency syndrome. 249 50

Parenteral nutrition is a part of the nutritional support regimen of patients with AIDS-associated wasting syndrome and gastrointestinal dysfunction. The cholesterol (CHOL) level in human immunodeficiency virus (HIV) membrane is very high, and recent lipid formulations with high phospholipid (PL) content have demonstrated the ability to trap CHOL from endogenous sources, modifying the composition of cell membranes. We administered lipid-based home parenteral nutrition for 3 mo to malnourished AIDS patients. The patients were randomly divided into two groups: 23 received the regular 20% fat emulsion formulation, and 27 received a 2% formulation enriched 10-fold with PLs but containing the same amount of triglycerides. All patients gained weight and improved their activity level. Those receiving the high-PL composition showed increased serum CHOL concentrations (from 147 to 241 mg/dL; P < 0.01), but no increase was seen in the number of CD4 cells or improvement in immune function. HIV infectivity was not modified. Patients receiving regular PLs had significantly decreased (P < 0.02) IgA concentrations (from 776 to 300 mg/dL) and improved mitogen response to phytohemagglutinin and to concanavalin A. This formula, too, had no effect on HIV infectivity. We conclude that standard parenteral nutritional influences the nutritional and immune status of malnourished AIDS patients. A PL-enriched parenteral formulation can trap CHOL, but it does not affect the immune profile or HIV infectivity in patients with advanced disease.
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PMID:Home parenteral lipids in AIDS: a three-month study. 910 87

Enteropathogenic Escherichia coli (EPEC) was recognized as a common opportunistic pathogen of simian immunodeficiency virus-infected rhesus macaques (Macaca mulatta) with AIDS. Retrospective analysis revealed that 27 of 96 (28.1%) animals with AIDS had features of EPEC infection, and EPEC was the most frequent pathogen of the gastrointestinal tract identified morphologically. In 7.3% of animals dying with AIDS, EPEC represented the sole opportunistic agent of the gastrointestinal tract at death. In 20.8% of cases, it was seen in combination with one or more gastrointestinal pathogens, including Cryptosporidium parvum, Enterocytozoon bieneusi, Mycobacterium avium, Entamoeba histolytica, Balantidium coli, Strongyloides stercoralis, cytomegalovirus, and adenovirus. Clinically, infection was associated with persistent diarrhea and wasting and was more frequent in animals that died at under 1 year of age (P < 0.001, Fisher exact test). The organism was associated with the characteristic attaching and effacing lesion in colonic tissue sections and produced a focal adherence pattern on a HEp-2 assay but was negative for Shiga toxin production as assessed by PCR and a HeLa cell cytotoxicity assay. A 2.6-kb fragment encompassing the intimin gene was amplified and sequenced and revealed 99.2% identity to sequences obtained from human isolates (GenBank AF116899) corresponding to the epsilon intimin subtype. Further investigations with rhesus macaques may offer opportunities to study the impact of EPEC on AIDS pathogenesis and gastrointestinal dysfunction.
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PMID:Identification of enteropathogenic Escherichia coli in simian immunodeficiency virus-infected infant and adult rhesus macaques. 1123 Apr 13

Gastrointestinal disease and inflammation are common sequelae of human and simian immunodeficiency virus (SIV) infection. Nevertheless, the molecular mechanisms that lead to gastrointestinal dysfunction remain unclear. We investigated regulation of the interleukin (IL)-6-JAK-STAT3 pathway in jejunum and colon, collected at necropsy, from 10 SIV-infected macaques with diarrhea (group 1), 10 non-SIV-infected macaques with diarrhea (group 2), and 7 control uninfected macaques (group 3). All group 1 and 2 macaques had chronic diarrhea, wasting, and colitis, but group 1 animals had more frequent and severe lesions in the jejunum. A significant increase in IL-6 and SOCS-3 gene expression along with constitutive STAT3 activation was observed in the colon of all group 1 and 2 macaques and in the jejunum of only group 1 macaques compared to controls. Further, in colon, histopathology severity scores correlated significantly with IL-6 (groups 1 and 2) and SOCS-3 (group 2) gene expression. In jejunum, a similar correlation was observed only in group 1 animals. Phosphorylated STAT3 (p-STAT3) was localized to lymphocytes (CD3+) and macrophages (CD68+), with fewer CD3+ lymphocytes expressing p-STAT3 in group 1 macaques. Despite high SOCS-3 expression, STAT3 remained constitutively active, providing a possible explanation for persistent intestinal inflammation and immune activation that may favor viral replication and disease pro-gression.
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PMID:Gastrointestinal disease in simian immunodeficiency virus-infected rhesus macaques is characterized by proinflammatory dysregulation of the interleukin-6-Janus kinase/signal transducer and activator of transcription3 pathway. 1805 58