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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with the human immunodeficiency virus (HIV) and the development of the acquired immunodeficiency syndrome (AIDS) is a long-term process in many individuals. The progression of HIV disease is beginning to demonstrate many commonalities with other chronic diseases. Although research has not yet shown clear-out evidence that diet can make a difference in the course of disease in HIV-infected clients, nutrition should be viewed as an important component of holistic care for HIV-infected clients because: 1) wasting and symptoms of malnutrition are common problems associated with these clients; and 2) nutrition has proven to be a beneficial component of care in other chronic conditions. This paper uses the model developed by Winett, King and Altman (1989) to review nutritional support in HIV infection from a multilevel perspective ranging from personal psychology to institutional/societal controls. The author concludes that there is a potential benefit from integrating nutritional assessment, diagnosis and education into the holistic care of HIV-infected clients at the personal, interpersonal, organizational and societal levels.
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PMID:Nutritional support in HIV infection: a multilevel analysis. 191 56

The ts1 mutant of Moloney murine leukemia virus TB causes degenerative neurologic and immunologic disease in mice, characterized by development of spongiform encephalomyelopathy resulting in hindlimb paralysis, marked thymic atrophy associated with immunodeficiency, and generalized body wasting. To investigate the pathogenesis of the thymic atrophy caused by ts1, we constructed a chimeric virus, ts1-Cas(NS), in which a major portion of the U3 region of the long terminal repeat of ts1, a T-lymphotropic and neurovirulent murine leukemia virus, was replaced by the corresponding U3 region of Cas-Br-E, a B-lymphotropic and neurovirulent murine leukemia virus. In FVB/N mice, ts1-Cas(NS) induced paralytic and wasting disease with incidence, severity, and latency similar to that induced by ts1, but it failed to cause thymic atrophy as severe as that observed in ts1-infected mice. Furthermore, thymocytes cultured from ts1-Cas(NS)-infected mice died at a much slower rate than those of ts1-infected mice. The U3 substitution in ts1-Cas(NS) specifically diminished the ability of the virus to replicate in the thymus, whereas viral replication in the spinal cord was not significantly affected; thus, neurovirulence was not changed. The correlation of reduced thymic atrophy with decreased thymic viral titers and the decreased ability of ts1-Cas(NS) to cause thymocyte death in mice suggest strongly that the marked thymic atrophy in ts1-infected mice is not an indirect effect occurring secondary to neurodegenerative and wasting disease but is a direct cytopathic effect of high-level viral replication in the thymus.
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PMID:Alteration from T- to B-cell tropism reduces thymic atrophy and cytocidal effects in thymocytes but not neurovirulence induced by ts1, a mutant of Moloney murine leukemia virus TB. 192 61

Resting energy expenditure (REE) was measured by reference to body composition in 50 malnourished patients with human immunodeficiency virus (HIV) infection and compared with that of 14 healthy subjects. Among HIV patients, 40 had acquired immune deficiency syndrome (AIDS) and 10 had AIDS-related complex (ARC). All were in stable condition and had a previous history of progressive wasting, ie, a mean body weight loss of 14.2 +/- 8.1 kg over 16.6 mo (range 2-49 ms). The mean REE was 14% higher than estimated basal energy expenditure (EBEE), according to the Harris and Benedict formula. Thirty-four patients (68%) were classified as hypermetabolic (REE greater than 110% EBEE). The best predictable variable for REE was fat-free mass (FFM), as determined by an anthropometric method (r = 0.72; P less than 0.001). The mean REE was 12% higher in HIV patients than in the control group FFM (156 +/- 19 vs 124 +/- 17 kJ.kg FFM-1.d-1). We concluded that in stable and malnourished HIV patients, the progressive wasting may be partly related to an increase in REE. The mechanism of this hypermetabolic state remains to be established.
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PMID:Resting energy expenditure is increased in stable, malnourished HIV-infected patients. 198 10

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

Nine black children aged between 3 months and 30 months of age, with human immunodeficiency virus type I (HIV-I) infection are described to draw the attention of health professionals in southern Africa to special clinical characteristics useful for recognising this problem, which has many shared features with common diseases of infancy and childhood in the Third World. The main presenting complaints were chronic cough and persistent diarrhoea and vomiting. These children frequently had diarrhoea (8 of 9 patients), mucocutaneous candidiasis (8), pneumonia (7), hepatosplenomegaly (9), significant lymphadenopathy (5) and wasting (5). All were infected by common bacteria, such as Gram-negative organisms, Mycobacterium tuberculosis and Campylobacter jejuni, or by opportunistic infections such as Candida or cytomegalovirus (CMV), or by both bacterial and opportunistic organisms. A raised total serum globulin level, anaemia, lymphopenia and a cerebrospinal fluid (CSF) pleocytosis were frequent findings. Incomplete data on parental HIV status suggest perinatal transmission. Three of the children were HIV-antigen positive. The diagnosis of full-blown acquired immunodeficiency syndrome (AIDS), using the stringent Centers for Disease Control criteria, is difficult in our situation because of limited diagnostic resources; however, using these criteria, and the clinical case definition for AIDS recommended by World Health Organisation, it is thought that probably 4 of these children could be considered as having AIDS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Some early observations on HIV infection in children at King Edward VIII Hospital, Durban. 223 85

Progressive disseminated histoplasmosis (PDH) is a relatively common infectious illness in human immunodeficiency virus (HIV)-infected patients. In Houston, Texas, (which is moderately endemic for histoplasmosis) the frequency of PDH is 5% among patients with acquired immunodeficiency syndrome (AIDS), almost as high as that of those with cryptoccal disease. In highly endemic areas, the frequency of PDH in AIDS is even greater, up to 75% in some areas. It is likely that as the HIV epidemic continues to penetrate to more remote, highly endemic areas, more and more cases of PDH will occur. It is also clear that PDH may develop in HIV-infected patients who presently live in nonendemic areas, but who previously resided in endemic areas. It is important that all physicians who care for HIV-infected patients become thoroughly familiar with the clinical manifestation of this illness. Timely diagnosis depends on a high degree of diagnostic suspicion since the illness seldom presents with primary respiratory symptoms. It is prudent to consider PDH in the differential diagnosis of any systemic, wasting, febrile illness in HIV-infected individuals, especially if currently or in the past they have resided in areas endemic for the fungus. Similarly, whenever PDH is diagnosed in any patient who is in a high-risk group for HIV infection, prompt testing for HIV should be performed.
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PMID:Progressive disseminated histoplasmosis in the acquired immunodeficiency syndrome: a model for disseminated disease. 224 9

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

Considerable progress has been made in the identification and treatment of Pneumocystis carinii pneumonia related to acquired immunodeficiency syndrome (AIDS). Prophylaxis, either primary or secondary, represents a major advance and should be used appropriately by physicians caring for patients infected with human immunodeficiency virus. Yet with success come new challenges. Centers for treatment of AIDS that aggressively use prophylaxis have seen a shift toward severe illness due to other pathogens and generalized wasting. The strategies employed in combating P carinii pneumonia are likely to be tried against other AIDS-related infections.
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PMID:The evolving challenge of Pneumocystis carinii. A deadly opportunist in AIDS. 240 75

BALB/c mice infected with ts1, a mutant of Moloney murine leukemia virus-TB, develop generalized body wasting, profound neurologic disorders, severe thymic atrophy and lymphopenia due to destruction of T lymphocytes and drastic immunodeficiency. ts1 was found not only able to infect T lymphocytes but also to impair their function. In addition, ts1 also infects and induces syncyntia formation in macrophages. The genetic determinant(s) responsible for ts1's ability to induce immunodeficiency has been localized to the env gene.
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PMID:ts1, a mutant of Moloney murine leukemia virus-TB, causes both immunodeficiency and neurologic disorders in BALB/c mice. 272 46

The human immunodeficiency virus is a member of the lentivirus subfamily of the retrovirus family. Retroviruses are RNA viruses which code for an RNA-dependent DNA polymerase (reverse transcriptase), which transcribes the RNA genome into a DNA provirus which, on integration with the host DNA, directs the synthesis of new virions. The RNA genome consists of a gag gene, which codes for the viral core proteins, a pol gene, which codes for the reverse transcriptase, an env gene, which codes for the glycoproteins of the viral envelope, and several genes (tat, rev, vif, vpr, and nef), that code for regulatory proteins. At each end of the genome are long terminal repeats, that contain regulatory elements for transcription. There are 3 subfamilies of Retroviridae (Oncovirinae, Spumavirinae, and Lentiverinae). The Lentiverinae ("slow viruses") include the bovine immunodeficiency virus (BIV), the feline immunodeficiency virus (FIV), the human immunodeficiency viruses (HIV), and the simian immunodeficiency viruses (SIV). SIV has been isolated from macaques (mac), African green monkeys (agm), sooty mangabeys (sm), and mandrills (mnd). Only SIVmac causes an AIDS-like disease in its natural host, but it is genetically closer to HIV-2 than to HIV-1. SIVsm causes an AIDS-like disease in macaques, but not in the sooty mangabey. Monkeys infected with SIV develop diarrhea, wasting, decrease in T4 lymphocytes, lymphadenopathy, development of giant cells, and encephalitis, as well as opportunistic infections. Kaposi's sarcoma, however, has not been found in SIV-infected primates. Virus is recovered from peripheral blood mononuclear cells and the brain. SIV models are useful for understanding the natural history of primate lentiviruses, for defining the pathogenesis of AIDS, and for developing vaccines. The ideal model would be one in which HIV causes AIDS, but so far only chimpanzees and gibbons have successfully been infected with HIV-1, and although virus, is recovered from peripheral blood mononuclear cells of chimpanzees within 2 weeks of infection, and 2 animals have lost antibodies to the p24 protein, none has so far developed clinical AIDS. Attempts to develop vaccines to immunize chimpanzees are continuing. Nonprimate lentiviruses include the visna virus, the feline immunodeficiency virus, and the bovine immunodeficiency virus. The visna virus infects fibroblasts by fusion of the viral envelope with the plasma membrane of the fibroblast; it infects macrophages by endocytosis. Infected macrophages regulate the production and dissemination of viral particles. The feline immunodeficiency virus infects T-lymphocytes of cats and produces oral, gastrointestinal and respiratory pathology as well as lymphadenopathy and opportunistic infections. Bovine immunodeficiency-like virus causes a generalized lymphadenopathy similar to that seen in AIDS-related complex.
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PMID:Animal models for HIV infection and AIDS: memorandum from a WHO meeting. 285 Jan 18


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