Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

Friend leukemia complex (FLC) is known to induce immunosuppression but the use of FLC in studies of immune cells function is disadvantageous since the immunosuppression always is accompanied by an acute erythroleukemia. To obtain immunosuppressive variants of FLC with reduced leukemogenic potential, we isolated T-helper cells from FLC infected mice, and passed lysates of the cells to recipient uninfected mice. A group of these mice developed a condition distinct from the disease induced by FLC. A viral stock prepared from these mice, designated Fd-MIV for friend derived murine immunodeficiency virus, induced a profound suppression of the primary antibody response without acute transformation in adult NMRI mice. Terminally a wasting disease with weight loss, atrophy of the thymus and lymph nodes and renal disease was observed in some mice. Analysis of viral DNA and RNA from infected NIH 3T3 cells showed that Fd-MIV contained at least two viral components, a 8.4 kb friend murine leukemia virus (F-MuLV) and a 7.4 kb mink cell focus (MCF)/xenotropic virus related genome. The 7.4 kb genome was not detected in Fd-MIV infected, immunocompromised mice indicating that the 8.4 kb genome might be responsible for the disease.
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PMID:A low oncogenic variant of Friend murine leukemia virus with strong immunosuppressive properties. 834 77

Five specific pathogen free cats were inoculated with feline immunodeficiency virus (FIV) isolated in Japan to observe changes toward development of acquired immunodeficiency syndrome (AIDS)-like disease. All inoculated cats had lymphadenopathy and mild respiratory disease shortly after inoculation. Following the initial acute phase lasting for more than 40 weeks, the clinical signs gradually diminished in three animals, and the asymptomatic carrier (AC) stage was observed at 45 (1 cat) and 70 (2 cats) weeks postinoculation (p.i.). Two of the three cats developed respiratory signs and diarrhea at 105 or 106 weeks p.i. One cat died at 121 weeks p.i. with severe wasting, with necropsy findings consistent with AIDS-related complex (ARC). The others were surviving at 150 weeks p.i. with mild clinical signs or asymptomatic. Another group of two cats developed more severe illness without the AC phase. One died at 48 weeks p.i. with the ARC illness. The other cat developed marked emaciation with diarrhea at 75 weeks p.i., and died at 100 weeks p.i. with a histologic diagnosis suggestive of terminal immunodeficiency. Histologically, the lymph nodes showed serial changes toward the terminal illness, from follicular hyperplasia at the acute phase to the lymphoid depletion at the ARC and AIDS-like terminal stages. The FIV antigen was demonstrated in the lymph nodes. The virus was isolated from peripheral blood mononuclear cells of all the inoculated animals. These data demonstrated possible etiologic association of FIV with development of AIDS-like disorders in the cat.
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PMID:Pathologic features of acquired immunodeficiency-like syndrome in cats experimentally infected with feline immunodeficiency virus. 839 25

Body wasting, characterized by disproportionate loss of body cell mass, is a feature of many chronic diseases, including infection with the human immunodeficiency virus (HIV). Therapies that merely increase energy intake do not consistently restore body cell mass in patients with the wasting syndrome. Because treatment with GH has induced nitrogen (N) retention in catabolic patients after surgery, burns, cancer, and hypocaloric feeding, we designed this study to determine whether GH could also produce an anabolic response in persons with HIV-associated weight loss. Six HIV-positive (HIV+) men with an average weight loss of 19% and six healthy weight-stable controls (HIV-) were hospitalized on a metabolic ward, where they consumed a constant metabolic diet during successive 5-day precontrol, 7-day baseline, and 7-day treatment [recombinant human GH (rhGH), 0.1 mg/kg.day] periods. The effects of rhGH on body weight, N and electrolyte excretion, energy expenditure, substrate oxidation, and integrated lipid and carbohydrate metabolism were assessed. Body weight increased promptly and progressively during treatment (2.0 +/- 0.3 and 1.6 +/- 0.2 kg in HIV+ and HIV-, respectively). Urinary N excretion decreased by 288 +/- 17 and 287 +/- 42 mmol/day in HIV+ and HIV-, respectively. Resting energy expenditure increased by 7.5% in both groups. Protein oxidation decreased, whereas lipid oxidation increased significantly. Glucose flux increased, and modest increases in fasting plasma triglyceride, glucose, and insulin levels were observed. Thus, short term rhGH treatment increased both protein anabolism and protein-sparing lipid oxidation, effects that should increase body cell mass if sustained during chronic therapy.
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PMID:Anabolic effects of recombinant human growth hormone in patients with wasting associated with human immunodeficiency virus infection. 840 71

Survival analysis was performed for AIDS cases diagnosed in Washington state from 1982 through 1989 and reported through October 31, 1991. No difference in survival time among diagnosis years 1987, 1988, and 1989 (p = 0.29) was found. Since September 1987, survival time was longest for cases with human immunodeficiency virus (HIV) wasting syndrome and HIV encephalopathy. Adjusted risk for death was significantly lower for these cases relative to all other cases (relative risk, 0.5; 95% confidence interval, 0.4-0.6). Explanations for the absence of continuing increase in survival time between 1987 and 1989 include changes in the frequency and timing of anti-HIV therapy. Longer survival time among cases diagnosed with HIV wasting or HIV encephalopathy is likely due to diagnosis earlier in the course of HIV disease. These results emphasize how changes over time in the definition of AIDS and evolving therapeutic standards may affect assessment of survival time when using surveillance data.
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PMID:Survival after AIDS diagnosis in Washington State: trends through 1989 and effect of the case definition change of 1987. 841 Jun 72

Resting energy expenditure (REE) and body composition were investigated in 60 clinically stable patients with human immunodeficiency virus (HIV) infection varying with respect to immune impairment. REEs differed significantly from predicted values (> or < 10% of the Harris-Benedict [HB] equation) in 40% of patients. Seven percent of patients showed markedly increased REE (> +20% of HB prediction), whereas REE was decreased in 13% (< -10%). Increased REE was found during all clinical stages of the disease (Walter Reed [WR] 2 through 6) and was not strictly associated with the degree of immune impairment, presence of diarrhea or Kaposi's sarcoma, nutritional state, or anamnestic wasting. Twenty-seven patients were evaluated for a mean period of 319 days; 11 lost more than 5% of their initial body weight during the observation period. Weight-losing patients were normometabolic before but showed a significantly increased REE (+7% of predicted values or +8% when compared with previous measurements) during weight loss. The degree of deviation from estimated REE was strongly associated with the degree of weight loss. We summarize that increased REE is not a constant feature of HIV infection. It is not associated with clinical and laboratory parameters of immune deficiency, but may occur during weight loss. Thus increased REE represents an inadequate adaptation to malnutrition and contributes to wasting.
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PMID:Resting energy expenditure and weight loss in human immunodeficiency virus-infected patients. 841 72

We measured de novo lipogenesis in human immunodeficiency virus (HIV) infected men using a newly developed stable isotope method. HIV-infected subjects with a history of weight loss (n = 17, mean weight loss 14.9 +/- 3.2 kg), asymptomatic HIV-seropositive subjects with normal CD4 T-cell counts (n = 7) and healthy HIV seronegative controls (n = 11) were studied. Hepatic lipogenesis was determined by infusion of [2-13C]-acetate, using the recently described xenobiotic probe technique with mass isotopomer analysis. Hepatic acetyl-coenzyme A enrichment was measured by high performance liquid chromatography/mass spectrometry of secreted sulfamethoxazole-acetate, with measurement of incorporation into very low density lipoprotein-fatty acids by gas chromatography-mass spectrometry. Circulating tumor necrosis factor (TNF), interleukin-1 (IL-1), interferon alpha (IFN alpha), insulin, and triglycerides were measured concurrently, and 7-day weighed food records were performed. De novo hepatic lipogenesis was increased 3- to 4-fold in HIV-infected subjects with weight loss compared to normal controls (P < 0.05 for palmitate and stearate in both overnight-fasted and fed states), and was also significantly increased in asymptomatic HIV seropositive subjects. Circulating TNF and IL-1 were not measurable in any subject (detection limit 2 pg/ml for IL-1 and 20 pg/ml for TNF). Serum IFN alpha was measurable in 11 out of 17 subjects with wasting and correlated significantly with de novo lipogenesis in overnight-fasted but not fed states. Serum IFN alpha was unmeasurable in asymptomatic HIV-infected subjects despite elevated lipogenic rates. Serum triglyceride concentrations were elevated in subjects with weight loss (2.09 +/- 0.28 mmol/L) and asymptomatic HIV-positives (1.34 +/- 0.34 mmol/L) in comparison to controls (0.67 +/- 0.08 mmol/L), and correlated with lipogenesis. Food intake correlated inversely with lipogenesis in the overnight-fasted state. We conclude that HIV infection is characterized by abnormal fat anabolism. This applies to subjects with reduced lean body mass and to asymptomatic HIV-positive subjects with normal T-cell counts. The former observation may have implications for the pathophysiology and treatment of the wasting syndrome. The latter observation is consistent with activation of the immune response and a state of viral nonlatency in early HIV disease.
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PMID:Increased de novo hepatic lipogenesis in human immunodeficiency virus infection. 844 11

Excessive weight loss due to protein calorie malnutrition (PCM) is a significant problem in Nigerian children. This syndrome may be difficult to differentiate from the wasting disease caused by human immunodeficiency virus type 1 (HIV-1) infection. We studied 70 children admitted to the Baptist Medical Center in Ogbomosho, Nigeria in 1990 with PCM for prevalence of antibodies to HIV-1 and HIV-2. The cohort was from low-risk mothers and had a median age of 25 months (range, 4 months-9 years) with a weight deficit of at least 20% of the theoretical weight for age. Two sera were positive for anti-HIV-1 by both ELISA and Western blot (WB). A high prevalence of samples negative for HIV-1 antibody by ELISA were repeatedly reactive (11%, 8/70) or indeterminate (46%, 32/70) by WB. None of the sera was positive for antibody to HIV-2. There was no correlation of ELISA positivity or extent of WB banding with successful recovery from malnutrition. These results indicate a relatively low but significant prevalence of HIV-1 infection in Nigerian children with PCM. The high prevalence of indeterminate reactions in WB assays for HIV-1 suggests that other procedures may be necessary for confirmatory diagnosis of HIV-1 infection in this African population.
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PMID:Seroprevalence of HIV-1 and HIV-2 infection among children diagnosed with protein-calorie malnutrition in Nigeria. 847 80

A 35-year-old homosexual man developed a composite nodal Kaposi's sarcoma and peripheral T-cell lymphoma that were associated with a peripheral blood CD4-positive lymphocyte count of only 43/mm3. The patient subsequently developed Pneumocystis carinii pneumonitis and eventually died due to disseminated Cryptococcus neoformans. Numerous premortem tests for the presence of human immunodeficiency virus (HIV) types 1 and 2 were negative by the enzyme-linked immunosorbent assay, Western blot, viral isolation, and polymerase chain reaction techniques. Postmortem evaluations for HIV-1, HIV-2, human T-cell lymphotropic virus (HTLV)-I, and HTLV-II also were negative by polymerase chain reaction, immunofluorescence assays, and viral isolation. A systemic infection by Mycoplasma fermentans, however, was documented by immunohistochemistry and polymerase chain reaction in premortem and postmortem tissues. This recently recognized human pathogen has produced systemic infections in patients with the acquired immunodeficiency syndrome (AIDS) and in previously healthy non-AIDS patients who characteristically have a fulminant flu-like illness. Additionally, M fermentans has enhanced the cytopathic effect of HIV in in vitro studies and has produced fatal wasting illnesses with terminal lymphopenia in inoculated adult silvered leaf monkeys. This report is the first description of an association between M fermentans infection and an AIDS-like illness in an HIV-negative individual. The etiology of the severe immunosuppression in this patient and the associated role of M fermentans remain to be determined by further investigations.
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PMID:Acquired immunodeficiency syndrome-like illness associated with systemic Mycoplasma fermentans infection in a human immunodeficiency virus-negative homosexual man. 849 93

Gastrointestinal dysfunction and wasting are frequent complications of human immunodeficiency virus (HIV) infection. Nutrient malabsorption, decreased digestive enzymes and HIV transcripts have been documented in jejunal mucosa of HIV-infected patients; however, the pathogenesis of this enteropathy is not understood. Rhesus macaques infected with simian immunodeficiency virus (SIV) also exhibit diarrhea and weight loss; therefore, we investigated the use of this animal model to study HIV-associated intestinal abnormalities. A retrospective study of intestinal tissues from 15 SIV-infected macaques was performed to determine the cellular targets of the virus and examine the effect of SIV infection on jejunal mucosal morphology and function. Pathological and morphological changes included inflammatory infiltrates, villus blunting, and crypt hyperplasia. SIV-infected cells were detected by in situ hybridization in stomach, duodenum, jejunum, ileum, cecum, and colon. Using combined immunohistochemistry and in situ hybridization, the cellular targets were identified as T lymphocytes and macrophages. The jejunum of SIV-infected animals had depressed digestive enzyme activities and abnormal morphometry, suggestive of a maturational defect in proliferating epithelial cells. Our results suggest that SIV infection of mononuclear inflammatory cells in intestinal mucosa may alter development and function of absorptive epithelial cells and lead to jejunal dysfunction.
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PMID:Simian immunodeficiency virus infection of the gastrointestinal tract of rhesus macaques. Functional, pathological, and morphological changes. 850 46

Tumor necrosis factor alpha (TNF-alpha), a cytokine produced during the host defense against infection, is associated with fevers, weakness, and progressive weight loss. Thalidomide inhibits the synthesis of TNF-alpha both in vitro and in vivo and may have clinical usefulness. We therefore initiated a pilot study of thalidomide treatment in patients with human immunodeficiency virus type 1 (HIV-1)-associated wasting with or without concomitant infection with tuberculosis. Thirty-nine patients were randomly allocated to treatment with either thalidomide or placebo in a double-blind manner for 21 days. Thirty-two patients completed the study. In patients with concomitant HIV-1 and tuberculosis infections, thalidomide therapy was associated with a reduction in both plasma TNF-alpha levels and HIV-1 levels. No significant reduction in either TNF-alpha or HIV- 1 levels was observed in patients with HIV-1 infection only. During the study period, patients receiving thalidomide treatment (n=16) showed a significant weight gain (mean +/- SEM: 6.5 +/- 1.2%; p<0.02) relative to placebo-treated patients (n=16). Patients with simultaneous HIV-1 and tuberculosis infections experienced a higher mean weight gain during thalidomide treatment than the group of patients with HIV-1 infection only. The results of this pilot study suggest that thalidomide may have a clinical role in enhancing weight gain and possibly reducing TNF-alpha and HIV-1 levels in patients with HIV-1 and concomitant mycobacterial infections.
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PMID:The effect of thalidomide on the pathogenesis of human immunodeficiency virus type 1 and M. tuberculosis infection. 860 61


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