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

Patients with acquired immunodeficiency syndrome (AIDS) often suffer from weight loss manifested by a loss of body cell mass (BCM). The causes of human immunodeficiency virus (HIV)-associated wasting may include anorexia, malabsorption, and a variety of altered metabolic states. Malabsorption and diarrhea may result from gastrointestinal tract opportunistic infections or from direct effects of HIV on the gastrointestinal tract. Infection with HIV may produce metabolic derangements that alter nutrient utilization, resulting in loss of BCM. Nutritional assessment of the patient with AIDS should include an evaluation of BCM and physical and psychosocial functioning. Antiretroviral therapy and eradication of opportunistic infections do not always reverse wasting. Treatment should include nutritional counseling. Total parenteral nutrition is sometimes of benefit, particularly in patients with damaged gastrointestinal tracts. Dronabinol and megestrol acetate may promote weight gain; however, dronabinol may have adverse effects, and most of the gain with megestrol acetate is in fat rather than BCM. If gonadal dysfunction is present, testosterone replacement therapy should be included in the treatment plan. Some studies suggest that oral anabolic steroids may improve muscle strength and body composition. In randomized, placebo-controlled trials, mammalian-derived human growth hormone (rhGH[m]) has produced sustained weight and BCM gains in AIDS patients. If a patient continues to lose BCM after the above factors have been addressed and corrected, a 12-week course of rhGH[m] is indicated. Halting the progression of HIV-associated wasting may improve survival, enhance physical and social functioning, and enrich quality of life.
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PMID:Treatment guidelines for HIV-associated wasting. 1076 94

Infection with human immunodeficiency virus (HIV) is associated with marked disturbance of metabolism affecting the metabolism of carbohydrates, fats and proteins. In the first decade of clinical experience of HIV, the primary clinical manifestation of such disturbed metabolism was wasting. Such wasting was often severe and contributed significantly to the morbidity and mortality of AIDS. Mechanistic studies demonstrated that in addition to the effects of altered intermediary metabolism, reduced food intake played a major role in the causation of AIDS-related wasting. More recently, potent anti-retroviral drugs have dramatically changed the clinical consequences of HIV infection. Wasting has become far less frequent among infected patients and occurs in only a small percentage of subjects on effective anti-retroviral therapy. However, a new constellation of metabolic syndromes has become apparent characterized by altered body fat distribution ('lipodystrophy'), lactic acidosis and evidence of mitochondrial dysfunction. The mechanistic basis for such syndromes is currently unclear, but is the subject of ongoing research.
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PMID:Metabolic syndromes in human immunodeficiency virus infection. 1140 60

This article tests the hypothesis that the presence of gastrointestinal parasites in Colombian boys is negatively associated with anthropometric characteristics, physical work capacity, blood hemoglobin (Hb) levels, and nutritional status. Anthropometric, Hb, &Vdot;O(2) max, and parasite load data were collected on 1,016 boys in Cali, Colombia. The boys were classified as lower socioeconomic class (SEC) from either urban or rural environments, and upper SEC from an urban environment. Sixty-three percent of the boys were infected with gastrointestinal parasites and, of the infected boys, 80-95% had light parasite loads. Parasites found included Necator americanus, Ascaris lumbricoides, Entamoeba histolytica, Trichuris trichiura, Giardia spp., and Enterobius vermicularis. Infected boys had significantly lower weight, stature, weight-for-height (among 6-9-year-old boys), Hb levels, and &Vdot;O(2) max (ANCOVA, controlling for age and SEC). In terms of nutritional status, infected boys were 1.47 times more likely to be classified as iron deficient than noninfected boys (chi-square, P < 0.001), and 1.61 times more likely to be classified as stunted (P < 0.001). Infection was not associated with wasting in any SEC group. In conclusion, light to moderate gastrointestinal parasite loads were associated with significantly lower weight, stature, weight-for-height (in 6-9-year-old boys), Hb levels, and &Vdot;O(2) max, and a significantly higher frequency of IDA and stunting. These data suggest that comprehensive analyses of the nutritional status of populations in regions endemic for parasitic infection should include testing for the presence of infection. Am. J. Hum. Biol. 11:763-771, 1999. Copyright 1999 Wiley-Liss, Inc.
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PMID:Gastrointestinal parasitic infection, anthropometrics, nutritional status, and physical work capacity in Colombian boys. 1153 92

Infection with the human immunodeficiency virus (HIV) is often associated with the acquired immunodeficiency syndrome (AIDS), and wasting is one of the defining clinical features of AIDS. Muscular weakness due to myopathy may develop at any stage of HIV infection. We report two illustrative cases of HIV-associated myopathies. One was due to inflammatory myosits most likely directly related to the HIV infection, and the other was most likely the result of mitochondrial damage due to zidovudine, a nucleoside analogue commonly used in treating HIV infection. Biopsies from both patients showed alterations of myofiber structures, of varying severity, culminating in necrosis, lipid droplets, and lymphoplasmocytic inflammatory response. The zidovudine-treated patient also showed distinctive mitochondrial changes, predominantly enlargement, variation in shape and size, and disorganization of the cristae. These two types of HIV-associated inflammatory myopathies are reviewed, along with other HIV-associated myopathies, including HIV wasting syndrome, nemaline rod myopathy, pyomyositis, rhabdomyolysis, cardiomyopathy, and other miscellaneous myopathies associated with HIV infection.
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PMID:AIDS-related myopathy. 1181 Apr 29

Infection with pathogens often leads to loss of body weight, but the cause of weight loss during infection is poorly understood. We used the infection of mice with lymphocytic choriomeningitis virus (LCMV) as a model to study how pathogens induce weight loss. If LCMV is introduced into the CNS of CTL-deficient mice, the immune response against the virus leads to a severe weight loss called wasting disease. We planned to determine what components of this antiviral immune response mediate wasting disease. By adoptive transfer, we show that CD4 T cells activated by LCMV infection are sufficient to cause wasting disease. We examined the role of cytokines in LCMV-induced wasting disease using mice lacking specific cytokines or cytokine receptors. Results of adoptive transfer experiments suggest that TNF-alpha is not involved in LCMV-induced wasting disease and show that IFN-gamma contributes to the disease. Consistent with a role for IFN-gamma in wasting, we find that IFN-gamma is necessary for LCMV-specific CD4 T cell responses in the CNS, most likely because it is required to induce MHC class II expression. Our data also indicate that IL-1 is required for LCMV-induced wasting and that IL-6 contributes to the wasting disease. Additionally, our results identify alpha-melanocyte-stimulating hormone as a potential mediator of the disease. Overall, this work defines the critical role of virus-primed CD4 T cells and of proinflammatory cytokines in the pathogenesis of wasting disease induced by LCMV infection.
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PMID:The role of proinflammatory cytokines in wasting disease during lymphocytic choriomeningitis virus infection. 1207 63

Microsporidia are ubiquitous spore-forming parasites that are important worldwide pathogens in the HIV/AIDS pandemic. They are also increasingly being seen in HIV(-) individuals. Infection has been documented in almost every tissue and organ in the body and in a broad spectrum of cell types, including epithelial, mesenchymal, and neural. Microsporidia elicit a wide range of pathology, e.g., inflammation and cell death, and symptoms, e.g., shortness of breath, sinusitis, and diarrhea with wasting. Untreated, microsporidiosis has been documented as a cause of death.
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PMID:Diagnostic pathology of microsporidiosis. 1277 4

Infections with subspecies of the protozoan parasite Trypanosoma brucei cause important wasting diseases in Africa (nagana in cattle and sleeping sickness in humans). These diseases were little known until the end of the nineteenth century when serious epidemics of nagana were reported and raised concern among the colonial powers. The early history of sleeping sickness revolves around the discovery of the causative organism, its mode of transmission,and its life cycle in the tsetse fly. The history continues into the twentieth century with the discovery of how the parasites evade the immune response, frustrating the development of a vaccine; the failure to develop cheap and effective drugs; and the development of alternative approaches to control the tsetse fly vector.
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PMID:History of sleeping sickness (African trypanosomiasis). 1514 78

In 1986, a new progressive neurological condition similar to scrapie of sheep and goats was recognised in cattle in the United Kingdom (UK), and was named bovine spongiform encephalopathy (BSE). There is an ongoing discussion whether BSE should be classified as infectious, contagious, or zoonotic, and if it fits the definition of a production disease. The objective of this work is to briefly describe the main characteristics of transmissible spongiform encephalopathies (TSE), to review the epidemiology of BSE, and to address the question of how to classify BSE. TSEs are characterised as chronic wasting diseases with spongiform vacuolation and the accumulation of infectious prion protein (PrP(Sc)) in the central nervous system. TSE infectivity is very difficult to inactivate. Cattle BSE most likely originated from sheep scrapie, although this will remain to be an issue for debate. The disease can be transmitted from cattle to a range of species, and has resulted in smaller TSE epidemics in domestic cats, zoo cats and zoo ruminants, and in humans. Transmission in the field occurred through feed containing ruminant-derived protein, and measures to prevent the recycling of infectivity have proven effective to reduce the number of new infections. Mandatory reporting of clinical suspects combined with targeted screening of risk populations is needed to assess the BSE status of a country. Infection studies and the transmissibility to other species classify BSE as infectious and zoonotic. Absence of excretion of the agent, and therefore of horizontal transmission, categorise BSE as non-contagious. However, BSE is a multifactorial infectious disease that is dependent on management factors (mainly feeding), and therefore fits into the broader definition of production diseases.
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PMID:Bovine spongiform encephalopathy (BSE)--infectious, contagious, zoonotic or production disease? 1525 78

Infection with the human immunodeficiency virus (HIV) and the development of acquired immunodeficiency syndrome (AIDS) have had a significant impact on domestic and global health, social, political, and economic outcomes. Prevention and treatment efforts to control HIV infection are more demanding than in previous decades. Achieving food and nutrition security, and managing nutrition-related complications of HIV infection and the multiple aspects of disease initiated by or surrounding HIV infection, referred to as HIV disease, remain challenges for patients and for those involved with HIV/AIDS prevention, care, and treatment efforts. Confounding clinical issues include medication interactions, coinfection with other infections and diseases, wasting, lipodystrophy, and others. Dietetics professionals, other health care professionals, and people infected with HIV will need to understand and address multiple complex aspects of HIV infection and treatment to improve survival, body functions, and overall quality of life. Individualized nutrition care plans will be an essential feature of the medical management of persons with HIV infection and AIDS.
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PMID:Position of the American Dietetic Association and Dietitians of Canada: nutrition intervention in the care of persons with human immunodeficiency virus infection. 1535 61

The present study compared the nutritional status of schoolchildren from recently settled, ethnic minority tribespeople with those from a Persian village in southern Iran. Height and weight were measured and blood was collected from school children at three time points over 1.5 years. Supplemental Fe was provided to children with low Hb after the first screening. Twenty-one per cent of the children were wasted, 57 % were stunted and 23 % were anaemic. No statistically significant difference in the prevalence of wasting, stunting and anaemia was found between gender or ethnic groups. Children over the age of 12 years had a higher prevalence of wasting than children aged below 12 years. In a sub-sample of forty-one children the average BMI-for-age decreased. Fe supplementation increased Hb levels to normal in most children, but did not increase Fe level in a few children. Dietary deficiency of micronutrients, especially Zn and Fe, probably accounts for the high prevalence of stunting and anaemia in these children. Infection with Helicobacter pylori is another possible explanation for the Fe-deficiency anaemia. Further investigation is in progress to determine the cause(s) of the observed deficiencies.
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PMID:Nutritional status of schoolchildren in rural Iran. 1617 10


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