Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Increased release of tumour necrosis factor is thought to contribute to human-immunodeficiency-virus-associated wasting syndrome. Elevated serum concentrations of tumour necrosis factor have, however, mainly been found during acute opportunistic infections and were not correlated with the degree of wasting. This finding may be explained by the paracrine release and the rapid inactivation of tumour necrosis factor. Serum levels of the two recently detected soluble tumour necrosis factor receptor proteins (p55 and p75) are assumed to reflect tumour necrosis factor release. 2. Serum levels of soluble tumour necrosis factor receptors 55 and 75 were measured by an enzyme-linked immunological and biological binding assay in 45 human-immunodeficiency-virus-infected patients and seven healthy control subjects. Patients were followed up for survival. Serum albumin, prealbumin, total iron-binding capacity (transferrin) and C-reactive protein concentrations were measured using standard laboratory methods. Body composition was determined by bioelectrical impedance analysis. 3. Serum concentrations of soluble tumour necrosis factor receptor 55 and 75 were both significantly increased in human-immunodeficiency-virus-infected patients as compared with the health control subjects (P < 0.05); soluble tumour necrosis factor receptor concentrations were even more increased in patients with elevated C-reactive protein levels (> or = 5mg/l) as compared with those with normal C-reactive protein levels (< 5mg/l; P < 0.0001 and P < 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tumour necrosis factor receptor levels are linked to the acute-phase response and malnutrition in human-immunodeficiency-virus-infected patients. 816 42

A landmark paper on autopsies of representative samples of HIV-1 and/or HIV-2-infected patients in Abidjan, Cote d'Ivoire, found disseminated tuberculosis (TB) as the chief cause of morbidity (wasting syndrome) and mortality. Another important finding was the high prevalence of cerebral toxoplasmosis in contrast to somewhat lower figures for East African AIDS patients. The authors argue that few HIV-infected patients in Africa survive long enough to develop the state of immunodeficiency that allows for the development of Pneumocystis carinii pneumonia. This is disputable, since Pneumocystis carinii pneumonia in industrialized countries is an early opportunistic event and was by far the most important AIDS-indicator diagnosis before the introduction of prophylaxis. Moreover, as judged by their CD4+ cell counts, the autopsied patients had a fairly advanced level of immunosuppression. 50% of the patients admitted to the medical wards in Abidjan were HIV-seropositive; in some East-African cities this figure nears 80%, with bed occupancy rates of nearly 200%. The authors point out that over 50% of the deaths were caused by potentially preventable infections. A recent study in Haiti has shown that a 12-month course of daily isoniazid effectively decreases the incidence of TB and delays the onset of HIV-related disease in symptom-free HIV-infected individuals. In another study in Zambia, daily isoniazid treatment of HIV-1-infected individuals without signs of active TB led to reduced mortality rates. Cotrimoxazole (trimethoprim-sulphamethoxazole) has been an effective prophylaxis against cerebral toxoplasmosis. Cotrimoxazole is also active against Pneumocystis carinii. Prophylaxis with a combination of these drugs in African HIV-infected patients may significantly increase survival. Based on the above studies, the Steering Committee on Clinical Research and Drug Development of the Global Programme on AIDS has given priority to studies on combined chemoprophylaxis with isoniazid and cotrimoxazole in African HIV-infected patients.
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PMID:HIV-related morbidity and mortality in sub-Saharan Africa: opportunities for prevention. 790 50

To better understand the clinical manifestations of human immunodeficiency virus (HIV) infection in women in Louisiana, we conducted a retrospective review of the records of HIV-infected women who presented to the largest HIV outpatient clinic in Louisiana as well as to a tertiary care university hospital in New Orleans between January 1987 and December 1991. A total of 224 women were evaluated. Gynecologic examinations revealed that 17.5% had cervical intraepithelial neoplasia and that 35% had evidence of candidal vulvovaginitis or colonization. The following conditions were diagnosed among indicated percentages of patients: syphilis, 22.2%; Neisseria gonorrhoeae infection, 7.2%; Chlamydia trachomatis infection, 12.3%; pelvic inflammatory disease, 5.3%; trichomonal vulvovaginitis, 26.9%; genital ulcers due to herpes simplex virus, 16.5%; and clinically evident genital human papillomavirus infections, 16.5%. Both trichomonal vulvovaginitis and syphilis were more common among intravenous drug users. A total of 82 opportunistic processes were observed in 55 women. Pneumocystis carinii pneumonia was the most frequent complication of AIDS, followed by candidal esophagitis and wasting syndrome. Over 85% of women had received a diagnosis of AIDS before death. Gynecologic diseases occurred often in this population; the frequency of AIDS-defining events was similar to that reported previously in the literature.
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PMID:Clinical manifestations of infection with the human immunodeficiency virus in women in Louisiana. 839 61

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

Vacuolization of duodenal enterocytes was found by light microscopic examination in five patients meeting the Centers for Disease Control criteria for the acquired immunodeficiency wasting syndrome. Four of these patients had chronic diarrhea and malabsorption as documented by an abnormal D-xylose test, whereas one patient had no diarrhea or malabsorption. Enterocyte vacuolization was patchy in distribution, although affected cells were most notable on villous tips. Staining with period acid-Schiff, acid-fast bacilli, periodic acid-Schiff following diastase treatment, Congo red, and alcian blue were negative, suggesting that vacuolization is due to lipid accumulation. Immunoperoxidase staining for the human immunodeficiency virus envelope protein gp41 was positive in lamina propria mononuclear cells in all five patients. The authors hypothesize that lipid accumulation represents an enterocyte response to injury, possibly by an indirect effect of the human immunodeficiency virus.
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PMID:Focal enterocyte vacuolization. A new microscopic finding in the acquired immune deficiency wasting syndrome. 842 11

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

The increased levels of tumor necrosis factor-alpha (TNF-alpha) seen in patients with acquired immune deficiency syndrome (AIDS) may contribute to the AIDS-related wasting syndrome. TNF also induces expression of human immunodeficiency virus (HIV) through activation of the transcription factor NF-kappa B, which binds to the viral long terminal repeat (LTR). Because TNF can decrease the antiretroviral activity of zidovudine (AZT) in vitro, pentoxifylline (PTX) may increase the efficacy of AZT. PTX decreases HIV replication in acutely infected cells and inhibits gene expression controlled by the HIV-1 LTR. The antiretroviral activity of PTX is associated with decreased binding of NF-kappa B to its recognition sequences. Therefore, PTX may inhibit HIV expression indirectly by diminishing TNF production and directly, by decreasing activity of NF-kappa B. PTX, and an inhibitor of the viral transactivator TAT, Ro24-7429, may inhibit HIV gene expression in a cooperative fashion. The first clinical study of PTX in AIDS patients was conducted by us through the AIDS Clinical Trial Group of the National Institutes of Health. AIDS patients on antiretroviral therapy received PTX 400 or 800 mg three times daily for 8 weeks. TNF assays included TNF mRNA levels in peripheral blood mononuclear cells (PBMCs) and inducible TNF protein levels in the supernatant of PBMCs cultured in the presence of 0.1 microgram/ml lipopolysaccharide (LPS). The median change in TNF mRNA was a 30% decrease. There was a median and significant 40% decrease in the production of inducible TNF protein. HIV load decreased in 10 patients and increased in four patients, but did not change in the group as a whole. Others have extended our initial observations in HIV-infected patients. In a placebo-controlled trial, TNF production by unstimulated PBMCs decreased by 52% in the PTX arm and increased by 7.2% in the placebo arm. In a study comparing AZT, PTX, or a combination of the two, viral load after treatment was ninefold above baseline in the AZT or PTX alone arm, compared to only twofold in the combination arm. In a quality of life trial, PTX was associated with improvement in depression, anger, and social and cognitive function: a placebo effect, however, was not ruled out. PTX 400 mg three times daily is safe and well tolerated. PTX decreases PBMC TNF expression in HIV-infected patients, measured as protein in culture supernatant or as mRNA, and may decrease viral replication. Further studies of HIV-infected persons are needed to ascertain the benefit of PTX as an adjunct either to inhibitors of reverse transcriptase (e.g., AZT) or of transcription (e.g., TAT inhibitor).
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PMID:Pentoxifylline for the treatment of HIV infection and its complications. 869 54

Microsporidian infections are increasingly recognized as an important cause of morbidity for persons infected with the human immunodeficiency virus. Encephalitozoon (formerly Septata) intestinalis is a recently described microsporidian that causes intestinal and disseminated infections in severely immunocompromised patients with acquired immunodeficiency syndrome. Several studies suggest that albendazole is an effective therapy for E intestinalis infection. However, relapses of symptoms and reappearance of microsporidian spores in diagnostic specimens have been reported following treatment in some cases. Because these results are based on examination of feces or cytologic specimens with an inherent sampling bias, it would be ideal to have autopsy data on the complete tissue evaluation of major organ systems of patients who had antemortem E intestinalis infection treated with albendazole. This report describes an acquired immunodeficiency syndrome patient with diarrhea and wasting syndrome associated with E intestinalis infection. Treatment with albendazole produced relief of his clinical symptoms and eliminated microsporidian spores in his feces. Following his death from other causes, an autopsy was performed. Comprehensive microscopic examination of all major organs revealed no evidence of residual microsporidian infection, suggesting parasitologic cure of E intestinalis with albendazole. The postmortem finding of complete clearance of microsporidia from body tissues is significant for future albendazole treatment of patients infected with E intestinalis and provides strong support for the value of the autopsy in evaluating the therapeutic efficacy of antimicrobials in emerging infections.
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PMID:Autopsy verification of Encephalitozoon intestinalis (microsporidiosis) eradication following albendazole therapy. 871 99

We report 17 patients seropositive for the human immunodeficiency virus, with muscle tissue involvement in different stages of the disease. Some patients are treated with azidothymidine (AZT). Others have no opportunistic infections. In all cases, there are some muscular symptoms such as progressive symetric and proximal muscular weakness with myalgias, elevated serum muscle enzymes, abnormal electromyogramma and very often a peripheral neuropathy. The muscle biopsy reveals the following features: rarely a focal muscular opportunistic infection in advanced stage of the disease is observed; a polymyositis is quite often the first clinical manifestation of the disease; a myopathy with mitochondrial involvement is observed in some of the AZT treated patients; some cachectic, under nourrished, bedridden patients present a type II muscle fiber atrophy. We conclude that a muscle biopsy could help us in our therapeutic planning directing us to a corticotherapy in the polymyositis, mitochondriopathies and wasting syndrome. Interruption alone of AZT or associated with a treatment by carnitine could allow remission of the muscular pathology.
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PMID:[Muscular involvement in the course of AIDS. Anatomo-clinical study of 17 cases]. 872 Aug 38


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