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)

A 35-year-old male uremic patient developed the classical presentation of Reiter's syndrome after 3 years of regular hemodialysis. He had painful swelling of the left knee, sacroilitis, urethritis, balanitis, painless oral ulcers, acute uveitis and positive HLA-B27. Disease activity persisted and was aggravated although immune function studies showed depressed cellular immunity. The clinical course of this patient seemed to contradict our belief that activity of immunologically mediated disease will abate after uremia, but it concurred with the report that Reiter's activity was unchanged in AIDS despite the significant immunodeficiency of AIDS patients.
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PMID:Reiter's syndrome in uremia: report of a case. 276 18

The high prevalence of human immunodeficiency virus (HIV-1) infection in populations at risk in Miami prompted a seroepidemiologic study of both HIV-1 and the human T-cell leukemia virus type I (HTLV-I), a closely related virus, in our patients receiving chronic hemodialysis. One hundred twenty-nine patients undergoing hemodialysis in 1986 and 1987 were tested for antibody against both viral antigens by EIA (Abbott Laboratories, Abbott Park, IL). Seroreactive samples for HIV-1 and/or HTLV-I were confirmed by Western blot and, for HTLV-I, by viral cultures. Thirty patients (23.2%) were positive for retroviral infection (22 for HIV-1 alone, four for HTLV-I alone, and four for both HIV-1 and HTLV-I). The most important risk factor was intravenous drug use, followed by blood transfusion. Patients with HIV-1 had lower T4-T8 ratios and higher mortality than those with HTLV-I infection alone. It was concluded that HTLV-I, as well as HIV-1, infection is endemic in chronic dialysis centers in Miami. The clinical consequences of HTLV-I infection in relatively immunocompromised patients with chronic uremia who are undergoing chronic hemodialysis remains to be established.
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PMID:Human immunodeficiency virus and human T-cell leukemia virus type I in patients undergoing maintenance hemodialysis in Miami. 278 17

Uremic patients are at high risk of hepatitis B virus (HBV) infection and, despite the availability and efficacy of hepatitis B vaccine, a high rate of non responders has been reported. Forty uremic patients undergoing maintenance hemodialysis who failed to produce any measurable anti-HBs antibody response after 4 administrations of 5 micrograms of Hevac B Pasteur vaccine were admitted to a randomized controlled clinical trial. Group A (14 patients) received 3 doses of 5 micrograms s.c. each of vaccine at monthly intervals and 12 doses of 50 mg s.c. of thymopentin on alternate days between the first and the second vaccination. Group B (11 patients) received 3 doses of 5 micrograms s.c. each of vaccine at monthly intervals. Group C (15 patients) received 3 doses of 10 micrograms s.c. each of vaccine at monthly intervals. Immunization rates were 86% in group A (on both 1-month and 6-month checks), 36% on the 1-month and 27% on the 6-month check in group B, 53% on the 1-month and 47% on the 6-month check in group C. Anti-HBs antibody titers were similar in group A and C but notably lower in group B. Thymopentin seems as useful therapeutical tool for non responder patients. As it promotes T cell maturation and responsiveness, which are impaired in uremia, it could play a major part in the management of uremic immunodeficiency.
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PMID:Controlled trial of thymopentin in hemodialysis patients who fail to respond to hepatitis B vaccination. 306 61

Zinc deficiency is a common nutritional problem observed both in human and in animal populations that has profound effects on host defense mechanisms. Using the young adult mouse as a model, it has been demonstrated that a moderate period of suboptimal zinc causes thymic atrophy, lymphopenia, and alterations in the proportions of the various subsets of lymphocytes and mononuclear phagocytes. As a result, antibody-mediated responses to both T cell-dependent and T cell independent antigens are significantly reduced. Cytolytic T cell responses, natural killer (NK) cell activity, and delayed-type hypersensitivity (DTH) reactions are also depressed. Suboptimal zinc during in utero development of mice causes persistent states of immunodeficiency in the offspring that can even be transferred to subsequent generations. In regard to human immunological consequences of zinc deficiency, patients with the genetic disorder of zinc absorption, acrodermatitis enteropathica, also exhibit atrophic thymuses, lymphopenia, anergic DTH responses, and reduced NK cell activity. Patients suffering from sickle cell anemia or uremia with associated deficiencies in zinc exhibit similar immune deficiencies. An additional outcome of these studies has been shown to be an essential cofactor for thymulin, one of the thymic hormones. Furthermore, addition of zinc salts to culture can polyclonally activate lymphocytes as well as augment responses to mitogens in adjuvant-like manner.
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PMID:Interrelationships between zinc and immune function. 348 44

Assays for suppressor cells were used to investigate the immunological status of uraemic patients (39) and transplant patients (66), and results were compared with those for normal controls (52). The functional assays were depletion of suppressor activity by preincubation (suppressor index) and the concanavalin-A-inducible suppressor assay and, in the uraemic patients, T gamma, T mu, and T0 cells were enumerated. The results of these assays were discordant, supporting previous suggestions that they measure different suppressor cell populations. The level of concanavalin-A-inducible suppressor cell activity was significantly below normal in both uraemic and transplant patients. The number of T mu cells in uraemia was significantly reduced. The findings do not support the possibility that suppressor cells are involved in the immunodeficiency of uraemia or the maintenance of renal transplants. Moreover, it could be suggested that uraemic toxaemia depresses both helper and suppressor modalities with the net effect being a 'pan-deficiency' of immune function.
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PMID:Suppressor cells in stable dialysis and transplant patients. 621 27

We have studied purine metabolism in mononuclear and polymorphonuclear cells from uraemic patients using microradiochemical enzyme assays and high-pressure liquid chromatography. In mononuclear cell lysates the mean activities of adenosine deaminase (EC 3.5.4.4) and 5'-nucleotidase (EC 3.1.3.5) were significantly diminished. The activities of adenylate kinase (EC 2.7.4.3), purine nucleoside phosphorylase (EC 2.4.2.1), adenine phosphoribosyltransferase (EC 2.4.2.7), and hypoxanthine phosphoribosyltransferase (EC 2.4.2.8) were not significantly different in the two groups. The activities of adenosine deaminase and adenine phosphoribosyltransferase were reduced in the polymorphonuclear cell lysates. No clear differences emerged in the concentration of adenine nucleotides in the mononuclear cells. The significance of these changes, which are less marked than those in erythrocytes, is discussed with reference to the immunodeficiency associated with uraemia.
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PMID:Activities of enzymes involved in purine metabolism and some related adenine nucleotide concentrations of leucocytes in renal failure. 629 37

Isogeneic BN rats were made uremic by subtotal renal resections. After different periods of uremia the possibility of an immunodeficiency was evaluated by (WF X BN) F1----BN heterotopic heart transplantations. A prolongation of transplant survival was found that was not related to the duration of uremia. In some rats the uremia was reversed by isogeneic BN----BN kidney transplantation before cardiac grafting. An immediate reversal of the immunodeficiency occurred. Thus an immunosuppressive effect by uremia can be documented, and to some extent quantitated, by heterotopic heart transplantation between rats of different isogeneic strains.
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PMID:The immunosuppressive effect of experimentally induced uremia. 638 19

To evaluate cellular immunity in uremia, we studied 235 uremic patients (178 on regular hemodialysis and 57 on medical treatment). E-rosettes were significantly lower (p less than 0.01) in all patients. The active E-rosettes test was found less significant to study T lymphocyte markers. The kind of correlations made with primary disease, small molecule levels, rehabilitation, suggests that cell-mediated immunodeficiency in uremia is a premature phenomenon and scarcely influenced by adequate hemodialysis treatment.
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PMID:[Rosette E and active rosette E tests in the evaluation of cell-mediated immunity in uremic patients]. 710 4

The trial entered 41 patients with chronic renal failure. Group I (15 patients) received conventional therapy involving infusion detoxication, antibiotics, immunostimulators, anabolic agents. 26 patients of group II in addition to standard therapeutic measures underwent plasmapheresis. The effect was assessed by immunological and renal function parameters. Group I patients have benefited from conventional treatment, but signs of immunodeficiency remained: B-lymphocyte, IgG and IgA levels were lowered and elevated, respectively. Patients of group II improved clinically, got rid of uremia and immunodeficiency.
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PMID:[The correction of the immune disorders in patients with chronic pyelonephritis and chronic kidney failure]. 753 80

Patients with end-stage renal disease present an immunodeficiency that paradoxically coexists with activation of most immunocompetent cells, and the roles of chronic uremia and maintenance dialysis are poorly understood. We determined circulating levels of IL-1 beta and IL-1Ra, TNF-alpha and its soluble receptors (TNF-sR55 and TNF-sR75), and activation markers of T cells (soluble CD25), B cells (soluble CD23), and monocytes (neopterin) in a large cohort of undialyzed patients at various stages of chronic renal failure and in dialyzed patients on maintenance hemodialysis or chronic peritoneal dialysis. The progression of uremia was associated with a gradual increase in soluble CD25, CD23, and especially neopterin levels. Although IL-1 beta could not be detected, IL-1Ra levels were significantly increased from the earliest stage of renal failure. Plasma levels of TNF-alpha, TNF-sR55, and TNF-sR75 progressed with the severity of renal failure and correlated with soluble CD25, CD23, and neopterin levels, whereas IL-1Ra levels correlated exclusively with TNF-sR55 levels. Compared with undialyzed patients, levels of IL-1 beta were higher in patients on maintenance hemodialysis, whereas those of IL-1Ra were lower and decreased further at the end of dialysis sessions. In contrast, both TNF-sR55 and TNF-sR75 levels were significantly higher than in undialyzed patients and increased further at the end of dialysis sessions in the absence of an increase of TNF-alpha. Such an imbalance between cytokines and their inhibitors may play a pivotal role in the multifaceted process of immune dysfunction.
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PMID:Balance between IL-1 beta, TNF-alpha, and their specific inhibitors in chronic renal failure and maintenance dialysis. Relationships with activation markers of T cells, B cells, and monocytes. 781 91


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