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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since human immunodeficiency virus (HIV) is known to lead to modifications of immune function and interrelationships among malnutrition, anergy and drug addiction have been shown, the aim of this work was to assess the nutritional status of 36 male heroin addicts under a period of detoxication (3 months). They were divided into two groups: (1) HIV negative (n = 20) and (2) HIV positive (n = 16); heights, weights and serum albumin concentration were measured and immune function was tested, using delayed hypersensitivity skin tests containing 7 antigens. No significant differences in anthropometric measurements were found between both groups, but anthropometric improvement was shown in every patient after the detoxication period. Serum albumin, often used as a classical index of malnutrition, remained within the normal values in both groups. The whole response to skin tests was depressed in both groups and no significant differences were shown between them. Therefore, these results might suggest that in spite of the apparent anthropometric recovery and the normal values of albumin, a subclinical malnutrition was indicated by the depressed immune function, which was more noticeable in the HIV-positive group.
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PMID:Nutritional status assessment of HIV-positive drug addicts. 238 76

Severe protein-calorie malnutrition is common in patients with AIDS and could contribute to the progressive deterioration characteristic of that disease. Selenium deficiency could also have a negative impact on immune function and other organ functions vital for recovery from infectious diseases. Therefore, to assess any role for selenium in AIDS we determined plasma and erythrocyte selenium levels and glutathione peroxidase activity in 13 patients with AIDS compared to 8 patients with AIDS-related complex (ARC) and 14 healthy controls. Plasma selenium levels were significantly reduced in AIDS patients compared to controls (p less than .0001) and to ARC (p less than .02). Erythrocyte selenium levels in both AIDS and ARC were also reduced compared to controls (p less than .02), but not to each other. Glutathione peroxidase activity in AIDS was 28.9 +/- 1.4 U/g Hb vs 38.4 +/- 6.9 in ARC (p = NS) and 52.3 +/- 1.7 in controls (p less than .0001 vs AIDS; p less than .02 vs ARC). When all groups were combined, there were significant correlations between total lymphocyte count and both plasma selenium (r = .53; p less than .002) and erythrocyte glutathione peroxidase activity (r = .65; p less than .0001). In addition, strong correlations were noted between plasma selenium and serum albumin (r = .68; p less than .0001), plasma selenium and glutathione peroxidase (r = .77; p less than .0001), and glutathione peroxidase and hematocrit (r = .66; p less than .0001). In AIDS or ARC, no correlations between selenium with disease duration or weight loss were present. We conclude that, in comparison to normals, patients manifesting infection with human immunodeficiency virus have evidence of selenium deficiency as determined by diminished plasma and erythrocyte levels and glutathione peroxidase activity. These abnormalities are most marked in patients with AIDS, but are also present in patients with AIDS-related complex. Selenium deficiency has important implications for the progression and pathogenesis of clinical disease in AIDS.
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PMID:Abnormalities of blood selenium and glutathione peroxidase activity in patients with acquired immunodeficiency syndrome and aids-related complex. 248 15

Review of animal and human studies concerning the impact of iron deficiency on immune function in vivo indicates that in many instances there is no firm consensus of opinion as to the relationship between iron status and immunity. One major problem with almost all human studies is that other micro- and macronutrient deficiencies are inadequately controlled for and thus it is often unclear as to whether reported abnormalities of immune function can be attributed specifically to iron deficiency. Even when abnormalities of immune function have been detected it is often uncertain as to the biological and clinical relevance that these may have for the host. Within these restraints the available studies suggest that iron deficiency may at least contribute to impaired T lymphocyte function as judged by DTH responses in skin and impaired mitogen-induced proliferation. As in protein energy malnutrition, humoral immunity is largely spared in humans, the balance of evidence suggesting that immunoglobulin production and function is normal, as are serum concentrations of complement. The only other abnormality of non-specific immunity which has been reported consistently to be abnormal is that of reduced bactericidal activity of polymorphonuclear leucocytes. The clinical relevance of these abnormalities remains to be established. There is, however, no evidence to suggest that individuals with iron deficiency suffer the devastating infective complications of the well defined immunodeficiency syndromes either congenital or acquired. It seems likely therefore that despite the fundamental importance of iron in maintaining the integrity of immune function, humans can tolerate the extremes of deficiency and excess and survive in a relatively healthy state.
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PMID:Iron and immunity. 248 83

Eleven infants with protracted diarrhea were treated with modular diet and short-term parenteral nutrition. Mean age at admission was 3.7 months with males predominating. Enteropathogenic E. coli, classic serotypes, were isolated from 7 patients and rotavirus from one. A child with combined, severe immunodeficiency died. Milk protein intolerance was diagnosed in another patient. Balance studies and peroral biopsies were performed. Malnutrition was more frequent and hospital stay was longer in those infants who developed nosocomial infections. Even though this treatment shortened the duration of the hospitalization, the negative nutritional impact persisted: Weight/Age (NCHS) decreased from 84% to 61%, with rapid recovery after discharge. Fecal lactic acid excretion was increased on admission to 1,296 mg x day and disaccharidase activity was decreased. The modular diet decreased both fecal volume and lactic acid excretion.
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PMID:[Modular diet and parenteral support in persistent diarrhea]. 251 64

The pertinent clinical data and histologic features of the testes in 57 autopsied acquired immunodeficiency syndrome (AIDS) patients were analyzed and compared with those of 55 age-matched control patients without AIDS. The testes of the AIDS patients showed a significantly lower degree of spermatogenesis (determined by a testicular score count), as well as more prominent thickening of the basement membrane and interstitial fibrosis when compared with the controls. While the precise cause of testicular atrophy in AIDS patients remains to be determined, the chronicity of the disease, prolonged fever, malnutrition, testicular infection, and chemotherapy are all contributing factors. Since the vast majority of the studied AIDS patients were homosexual and most control patients were heterosexual, the observed testicular changes can be ascribed to AIDS and/or homosexuality. Because of a high prevalence of sexually transmitted diseases, antisperm antibodies, and possible zinc deficiency and endocrine disorders, homosexual men appear predisposed to tubular atrophy. Conversely, AIDS-related factors, such as a direct toxic effect of the human immunodeficiency virus on germinal epithelium or as yet undetermined endocrine imbalances might exert a detrimental effect on the testis independent of homosexuality.
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PMID:Testicular atrophy in AIDS: a study of 57 autopsy cases. 254 50

AIDS is an acquired immunodeficiency syndrome defined by a severe depletion of T cells and over 20 conventional degenerative and neoplastic diseases. In the U.S. and Europe, AIDS correlates to 95% with risk factors, such as about 8 years of promiscuous male homosexuality, intravenous drug use, or hemophilia. Since AIDS also correlates with antibody to a retrovirus, confirmed in about 40% of American cases, it has been hypothesized that this virus causes AIDS by killing T cells. Consequently, the virus was termed human immunodeficiency virus (HIV), and antibody to HIV became part of the definition of AIDS. The hypothesis that HIV causes AIDS is examined in terms of Koch's postulates and epidemiological, biochemical, genetic, and evolutionary conditions of viral pathology. HIV does not fulfill Koch's postulates: (i) free virus is not detectable in most cases of AIDS; (ii) virus can only be isolated by reactivating virus in vitro from a few latently infected lymphocytes among millions of uninfected ones; (iii) pure HIV does not cause AIDS upon experimental infection of chimpanzees or accidental infection of healthy humans. Further, HIV violates classical conditions of viral pathology. (i) Epidemiological surveys indicate that the annual incidence of AIDS among antibody-positive persons varies from nearly 0 to over 10%, depending critically on nonviral risk factors. (ii) HIV is expressed in less than or equal to 1 of every 10(4) T cells it supposedly kills in AIDS, whereas about 5% of all T cells are regenerated during the 2 days it takes the virus to infect a cell. (iii) If HIV were the cause of AIDS, it would be the first virus to cause a disease only after the onset of antiviral immunity, as detected by a positive "AIDS test." (iv) AIDS follows the onset of antiviral immunity only after long and unpredictable asymptomatic intervals averaging 8 years, although HIV replicates within 1 to 2 days and induces immunity within 1 to 2 months. (v) HIV supposedly causes AIDS by killing T cells, although retroviruses can only replicate in viable cells. In fact, infected T cells grown in culture continue to divide. (vi) HIV is isogenic with all other retroviruses and does not express a late, AIDS-specific gene. (vii) If HIV were to cause AIDS, it would have a paradoxical, country-specific pathology, causing over 90% Pneumocystis pneumonia and Kaposi sarcoma in the U.S. but over 90% slim disease, fever, and diarrhea in Africa.(viii) It is highly improbable that within the last few years two viruses (HIV-1 and HIV-2) that are only 40% sequence-related would have evolved that could both cause the newly defined syndrome AIDS. Also, viruses are improbable that kill their only natural host with efficiencies of 50-100%, as is claimed for HIVs. It is concluded that HIV is not sufficient for AIDS and that it may not even be necessary for AIDS because its activity is just as low in symptomatic carriers as in asymptomatic carriers. The correlation between antibody to HIV and AIDS does not prove causation, because otherwise indistinguishable diseases are now set apart only on the basis of this antibody. I propose that AIDS is not a contagious syndrome caused by one conventional virus or microbe. No such virus or microbe would require almost a decade to cause primary disease, nor could it cause the diverse collection of AIDS diseases. Neither would its host range be as selective as that of AIDS, nor could it survive if it were as inefficiently transmitted as AIDS. Since AIDS is defined by new combinations of conventional diseases, it may be caused by new combinations of conventional pathogens, including acute viral or microbial infections and chronic drug use and malnutrition. The long and unpredictable intervals between infection with HIV and AIDS would then reflect the thresholds for these pathogenic factors to cause AIDS diseases, instead of an unlikely mechanism of HIV pathogenesis.
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PMID:Human immunodeficiency virus and acquired immunodeficiency syndrome: correlation but not causation. 264 42

The literature is briefly summarized as to how several nutrients affect immune function, susceptibility to infection, and cancer susceptibility or progression. Nutritional deficiencies can impair immunity and so influence susceptibility to infectious agents, including ones that are common and relatively virulent in acquired immune deficiency syndrome (AIDS) patients. A variety of nutrients affect several of the immune functions that are defective in human immunodeficiency virus (HIV)-infected individuals. For example, beta-carotene increased the number of CD4+ cells; vitamin E decreased the number of CD8+ cells and increased the CD4+/CD8+ ratio; vitamin D decreased the CD4+/CD8+ ratio; and iron increased the number of peripheral lymphocytes in humans receiving supplementation. Furthermore, nutritional deficiencies can influence gastrointestinal function, while infectious diseases can influence nutrient requirements by altering the efficiency of absorption and the rate of tissue metabolism. Malnutrition, depressed serum zinc levels, and intestinal nutrient malabsorption have been found in AIDS patients. The above findings suggest that dietary manipulations might diminish the immune defects in HIV infection and enhance resistance to opportunistic infections. However, dietary alterations in immune defects are generally not well quantified and may be small relative to the magnitude of the defects observed in AIDS patients. Because conflicting or adverse effects have been reported for some nutrients, recommendations for dietary supplementation in HIV-infected individuals are premature and possibly hazardous. Further studies are much needed to relate dietary nutrient intakes to clinical outcomes.
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PMID:The potential role of nutritional factors in the induction of immunologic abnormalities in HIV-positive homosexual men. 265 89

The authors pointed out that contamination may be exogenous, as a result of invasive diagnostic techniques, patient preparation, surgery, catheter insertion and wound dressing, or endogenous, especially in patients with specific risk factors (age, metabolic disorder, malnutrition, immunodeficiency) and aspecific risk factors (anesthesia, blood transfusion, surgery). Pharmacologic prophylaxis of infection may be unspecific (artificial nutrients, anticoagulants, immunomodulators) or specific (antibiotics). Prophylaxis is indicated in clean-contaminated and contaminated surgery; antibiotic chemoprophylaxis is also indicated in risk patients and permanent prosthesis surgery. The authors emphasized that antibiotics are no substitution for careful surgery.
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PMID:Short-term antimicrobial prophylaxis in surgery. The state of the art. 273 12

The growth of 22 boys with hemophilia, infection with human immunodeficiency virus (HIV), and lymphadenopathy, but not overt acquired immunodeficiency syndrome (AIDS) was evaluated. Three patients were found to have significant growth failure for 3-4 years with the onset after HIV infection. Extensive endocrine evaluation revealed that two of the three had neurodysregulation of growth hormone release with hyposomatomedinemia. None had classical growth hormone deficiency, thyroid deficiency, or evidence of malnutrition/malabsorption or other systemic illness. It appears that growth failure is not rare in boys with hemophilia and HIV infection and that this might be due to a direct effect on the physiologic secretion of growth hormone.
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PMID:Growth failure in boys with hemophilia and HIV infection. 278 55

Antilymphocytic monoclonal antibodies of HKO and OKT series were used to study surface antigens of peripheral blood and lymph node lymphocytes in 13 untreated patients with Hodgkin's disease. The purpose of the study was to identify the pathogenetic mechanism underlying the development of immunodeficiency in the early disease stages. The data obtained have demonstrated that the deficiency of T lymphocytes in the peripheral blood was connected with that of mature T cells in the lymph nodes revealed with the use of differential antigens complex. Deficiency of immunologically differentiated T lymphocytes in the lymph nodes combined with high counts of the cells whose membranes carry Ia-like antigen point to the immunologically unfavourable course of the disease.
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PMID:[Pathogenesis of immunologic deficiency in the initial stage of lymphogranulomatosis in children]. 278 85


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