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

Human protein-energy malnutrition and zinc deficiency have common clinical features. These were related to the plasma zinc concentrations in 42 severely malnourished children. A low plasma zinc concentration was strongly associated with nutritional edema but not with the degree of edema or the plasma albumin concentration. In the absence of edema, there were significant relationships between plasma zinc concentrations and stunting, skin ulceration, and wasting. Infection was not necessarily associated with a lower zinc concentration. From these data it can be predicted that a malnourished child with edema, skin ulceration, stunting, or severe wasting, will have a low plasma zinc concentration.
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PMID:Plasma zinc and the clinical features of malnutrition. 11 39

Infection with the human immunodeficiency virus type 1 (HIV-1) results in a variety of pathological changes culminating in the acquired immune deficiency syndrome (AIDS). While most of these changes can readily be accounted for either by direct effects of HIV-1 on the immune system or by indirect effects of secondary infectious agents as a result of faulty immune surveillance, the direct cause for a number of disease states, including some neuropathies, myopathies, nephropathy, thrombocytopenia, wasting syndromes and increased incidence of cancers (primarily lymphoma) has remained an enigma. We have recently shown that the HIV-1 protease, a viral encoded enzyme necessary for virus maturation and infectivity, can cleave a variety of host cell cytoskeletal proteins in vitro. Potential substrates for the HIV-1 protease are found in all of the cell types affected in these unexplained diseases. Recent proposals suggest that elements of the cytoskeleton may play an important role in the regulation of large scale genetic regulation. We propose that some of the degenerative changes associated with infection by HIV-1 are a direct consequence of cleavage of host cell cytoskeletal proteins, which in turn may be responsible for the increased incidence of cancer in HIV-1 infected individuals as a result of the perturbation of the regulation of gene expression by cytoskeletal components.
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PMID:Potential role of the viral protease in human immunodeficiency virus type 1 associated pathogenesis. 158 3

Chronic diarrhea accompanied by weight loss is a common and often debilitating problem associated with human immunodeficiency virus (HIV) infection. Enterocytozoon bieneusi, a newly identified species of the phylum of protozoa, Microspora, has been reported associated with chronic diarrhea and wasting in 11 acquired immunodeficiency syndrome (AIDS) patients in the United States, Europe, and Africa. Diagnosis has been based solely on the ultrastructural identification of this small, intracellular parasite in bowel biopsies. Seventy-one small bowel biopsies from 67 homosexual AIDS and AIDS-related complex patients with chronic diarrhea and with no pathogens identified by light microscopy on paraffin sections, were embedded in plastic and studied by light and transmission electron microscopy. Enterocytozoon bieneusi microsporidiosis was diagnosed by electron microscopy in 20 (22 biopsies) of the patients. More jejunal biopsies (16 of 36) were positive than duodenal biopsies (six of 35). Parasites and spores were clearly visible at the light microscopic level in the semi-thin plastic sections from 17 and 21 of the biopsies, respectively. In retrospect, parasites could be identified by light microscopy in standard hematoxylin and eosin-stained paraffin sections. Infection was confined to enterocytes covering the villi, especially the tips, and was associated with villous atrophy and cell degeneration, necrosis, and sloughing. Release of spores into the bowel lumen was evident. Colorectal biopsies from two of the patients with small bowel microsporidiosis were negative for microsporidia. Enterocytozoon bieneusi infection of the small bowel may be an important cause of diarrhea in HIV-infected persons.
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PMID:Intestinal microsporidiosis as a cause of diarrhea in human immunodeficiency virus-infected patients: a report of 20 cases. 169 61

Infection of several mouse strains with Trypanosoma cruzi stimulates high levels of T and B lymphocyte activities which persist during the chronic phase and is followed by specific immunosuppression and severe autoimmune pathology. Infected BALB.Xid mice carrying an X-linked mutation and lacking CD5 B cells, display poor B cell responses to T. cruzi infection, accompanied by low levels of specific and non-specific immunoglobulins in the serum. However, these animals control parasitemia, do not show the wasting observed in BALB/c mice, and develop almost no pathology early in the chronic phase. The infection of (BALB.Xid female x BALB/c male) F1 animals shows that immunodefective males behave like Xid animals in contrast to females which respond as normal BALB/c mice. These results indicate that the Xid locus controls lymphocyte responses, parasite clearance and pathology in experimental Chagas' disease.
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PMID:Xid immunodeficiency imparts increased parasite clearance and resistance to pathology in experimental Chagas' disease. 191 32

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

Infection-triggered, life-threatening salt-loss and hyperkalaemia developed in two male infants with wasting, inappropriately low plasma aldosterone concentrations and elevated plasma renin activity. The presumptive diagnosis of a defective terminal step in aldosterone biosynthesis was made by the presence of large amounts of 11-dehydrotetrahydrocorticosterone and its 18-hydroxylated metabolite (18-OH-THA), free 18-hydroxycorticosterone (18-OH-B) and 18-hydroxytetrahydrocorticosterone in the urine of both patients. The diagnosis of corticosterone methyl oxidase type II (CMO II) deficiency was confirmed by an elevated urinary 18-OH-THA to tetrahydroaldosterone ratio in one boy and by an elevated plasma 18-OH-B to aldosterone ratio in the other boy. Unknown steroids responsible for the salt-loss were not identified. Sodium supplementation but not short-term high dose oral 9 alpha-fluorcortisol (FF) normalized the hyponatraemia in one patient, in whom sodium (Na+)/potassium (K+) co-transport was decreased. Both patients eventually received long-term FF treatment to prevent impairment of longitudinal growth caused by chronic salt-loss. The diagnosis of CMO II deficiency should always be confirmed by elevated precursor-product ratios in urine or plasma, using radioimmunoassays with prior chromatographic separation. Metabolic studies as the short-term response of serum Na+ to high dose FF may not be helpful in differentiating aldosterone biosynthetic defects from end-organ resistance to mineralocorticoids.
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PMID:Severe hypoaldosteronism due to corticosterone methyl oxidase type II deficiency in two boys: metabolic and gas chromatography-mass spectrometry studies. 204 81

A prospective study on health and mortality of children under 7 years of age was conducted in rural parts of PDR Yemen during 1982-84. Altogether, 2071 children and 976 mothers were followed for 1 year and visited twice. The infant mortality rate (IMR), child mortality rate and under-5 mortality rate were 86, 11 and 129 per 1000, respectively. Sixty per cent of all deaths occurred during infancy. Diarrhoea commonly preceded death during infancy, and symptoms of measles during the 2nd year of life. The mothers of the deceased children were younger than the average rural mother (P less than 0.05) and more often primiparae, whereas illiteracy rates and median income did not differ from families which had not experienced death of a child. The risk of dying within 1 year was three times greater for wasted children in general, but 24 times greater for 1-2-year-olds. No increased risk was found for stunted children at any age. The prevalence of bottle feeding up to 18 months of age was high, and exclusive breastfeeding below 6 months of age was rare in the villages with the highest IMR (P less than 0.05). Infections seemed to be the trigger factor for death, but wasting predisposed to death at least after infancy.
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PMID:Mortality among children in rural areas of the People's Democratic Republic of Yemen. 247 5

Although many viral infections have on occasion been associated with hemorrhagic complications, infection with any of several RNA viruses regularly results in vascular involvement and the syndrome called viral hemorrhagic fever (VHF). In spite of clinically useful similarities among various VHFs, there are significant differences in their pathogenesis and clinical evolution; these are often related to characteristics of their viral taxon. Infection with Rift Valley fever (RVF) virus, a phlebovirus, appears to be regulated by interferon and terminated by neutralizing antibody. In contrast, Lassa fever (LF) virus, an arenavirus, is resistant to interferon, and LF is terminated by cellular immune effector mechanisms. The lytic virus-cell interaction typical of RVF virus suggests its major effects occur by direct, virus-induced cellular necrosis, particularly in the liver. In the primate RVF model, disseminated intravascular coagulation (DIC) may be important. LF virus--characteristically noncytopathic--may exert its effects through induction of mediator secretion from infected macrophages. DIC does not appear to be a central pathogenetic mechanism in LF. Pichinde virus, which is not pathogenic for humans, provides an alternate model for study of LF. Infected guinea pigs do not show histologic lesions that could explain their body wasting, cardiovascular deterioration, and pulmonary edema. In the heart, for example, loss of tissue mass, protein, and contractile function proceed without direct viral involvement or myocarditis. Sulfidopeptide leukotrienes have been implicated as one relevant soluble mediator participating in the disease state.
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PMID:Pathogenesis of viral hemorrhagic fevers: Rift Valley fever and Lassa fever contrasted. 266 11

During the first nine months of 1987, the bacteriological and virological tests as well as the indirect fluorescence test to Legionella pneumophila were performed in 40 children with bronchopneumonia (one- or both-sided) or pleuropneumonia and in 10 children with protracted bronchitis. In a 15 month old boy we have proved (by titer dynamics) the infection with Legionella pneumophila serotype 5, and in a 15 month old girl and in a 16 month old boy serotype 1. The infection was sporadic and the possible source of infection was unknown. The course of the disease was not wasting and the infection was accompanied with fever. The patients had an increased sedimentation rate of red cells and leukocytosis. All the other laboratory findings were within normal limits. In seven children seropositiveness 1:256 to Legionella pneumophila serotype 1, and in two children an increased titer to adenovirus was proved. The high titer to Legionella pneumophila in those seven children indicates an early contact with the causal agent. The patients were successfully treated with cefuroxim, which is not the drug of choice. Infection due to Legionella pneumophila in children does not exhibit a clinical or laboratory characteristic features that differ from those of the other respiratory diseases in children. It means that Legionnaires' disease in children with intact immunity is not the wasting illness. We stress the importance of using serologic examination to Legionella pneumophila as a routine procedure in the aetiological diagnosis of respiratory diseases in children.
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PMID:[Legionnaires' disease in children]. 279 76

Studies of rabies virus in several animal models consistently showed hypothalamic infection, hypophyseal infection, dramatic growth impairment (in the form of failure to thrive), wasting syndrome, and immune depletion. Rabies virus infection was studied through routine monoclonal antinucleocapsid antibody immunofluorescence and through a peroxidase-antiperoxidase immunoperoxidase method. The latter was modified to detect the in situ production of growth hormone by uninfected and rabies virus-infected adeno-a-pituicytes (with confirmation of the results both in vivo and in vitro). Infection with rabies virus made the specialized pituicytes produce less growth hormone. Growth before rabies virus infection and its reduction due to infection were investigated in a linear regression model. The fit was statistically significant (P less than .05) in all species studied: mouse, rat, rabbit, cow, and cat. Immune depression was studied in terms of alterations in the immunotopography of the thymus and also the specific T- and B-cell homing areas of the spleen (although spleen data are not presented here). On the basis of these results and a thorough review of wasting syndromes encountered in other diseases, a primary failure to thrive and an ensuing wasting syndrome were described and characterized for rabies, and their origin was assigned to a dysfunction of the hypophyseal/hypothalamic/thymic axis associated with at least (but not necessarily only) one of the centrally controlled growth hormones.
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PMID:Failure to thrive, wasting syndrome, and immunodeficiency in rabies: a hypophyseal/hypothalamic/thymic axis effect of rabies virus. 320 86


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