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)

The author discusses problems on the mechanisms of formation of immunodeficiency state in pulmonary diseases. It is suggested that T-cell deficit revealed in pulmonary pathology is caused by several factors (intoxication, mediators of allergic-reactions immune complexes, C-reactive protein, hormones, endorphin-like substances etc.), the removal of which furthers normalization of the immune system. Data are reported on the possible variants of secondary immunodeficiency states and the main regularities for immunocorrection are discussed.
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PMID:[Immunodeficiency states in lung diseases and the possible ways for their correction]. 141 90

A protein profile has been monitored during human immunodeficiency virus (HIV) infection. The investigation concerned 60 patients suffering from acquired immunodeficiency syndrome (AIDS), 24 asymptomatic HIV-antibody seropositive subjects and 22 healthy HIV-antibody seronegative, individuals voluntary blood donors. Data show that retinol-binding protein, thyroxin-binding prealbumin and beta 2-microglobulin are already modified in HIV infection (p less than 0.05) whereas the other protein alteration becomes apparent during AIDS. These studies demonstrate that severe, but progressive malnutrition occurs in patients with AIDS. On the other hand nutritional abnormalities can be shown to have a deleterious effect upon the disease course as revealed by increasing alpha-1-acid glycoprotein and C-reactive protein levels for 60 to 70% of patients.
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PMID:[Inflammatory reaction markers and nutritional markers in HIV infection]. 177 13

A survey conducted in rural southern African black subjects indicated that dietary iron overload remains a major health problem. A full blood count, erythrocyte sedimentation rate, serum concentrations of iron, total iron-binding capacity, ferritin, C-reactive protein (CRP), gamma-glutamyltransferase (GGT) and serological screening for hepatitis B and human immunodeficiency virus (HIV) infections were carried out in 370 subjects (214 inpatients and 156 ambulatory Mozambican refugees). The fact that the geometric mean (SD range) serum ferritin concentration was much higher in the male hospital patients than in subjects living in the community [1,581 micrograms/l (421-5,944 micrograms/l) and 448 micrograms/l (103-1,945 micrograms/l) respectively] suggested that dietary iron overload was not the only factor raising the serum ferritin concentration. The major additional factor appeared to be inflammation, since the geometric mean (SD range) serum CRP was significantly higher in male hospital patients [21 mg/l (8-53 mg/l)] than in subjects in the community [3 mg/l (1-5 mg)]. Alcohol ingestion, as judged by history and by serum GGT concentrations, was also associated with significantly raised serum ferritin concentrations. This finding was ascribed to the fact that traditional brews are not only associated with alcohol-induced hepatic damage but are also a very rich source of highly bio-available iron. The role of iron overload in the genesis of the raised serum ferritin concentrations are confirmed in the diagnostic liver biopsy study. The majority of biopsies showed heavy siderosis, with varying degrees of hepatic damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary iron overload in southern African rural blacks. 197 6

The lymphokine interleukin-2 (IL-2) has been shown to enhance natural cell-mediated cytotoxicity, the generation of cytolytic T lymphocytes, and several other aspects of cellular immune function. The gene coding for human IL-2 has been cloned, and recombinant IL-2 will be available for clinical trials in patients with neoplastic, infectious, and immunodeficiency diseases. The present investigation was undertaken to determine if IL-2 was similar to interleukin-1 (IL-1) in its ability to induce fever and the acute-phase response. These studies were based on recent work with recombinant human interferon (IFN)-alpha, which is intrinsically pyrogenic and capable of producing fever by inducing the synthesis of prostaglandin E2 (PGE2). The prospect that IL-2 might exert similar physiologic effects is of critical concern since elevated temperature, PGE2, and acute-phase reactants may profoundly inhibit natural cell-mediated cytotoxicity. Our studies have shown that recombinant human IL-2 is not intrinsically pyrogenic in rabbits at doses as high as 10,000 units/kg when administered by a single intravenous injection. In contrast to IL-1, IL-2 does not stimulate cultured hypothalamus cells to synthesize PGE2, and, furthermore, IL-2 does not elevate serum C-reactive protein levels. These results predict that the administration of IL-2 to patients in doses that stimulate cellular immune function will not induce fever and other toxic side effects frequently seen in individuals receiving IFN.
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PMID:Dissimilarities between purified human interleukin-1 and recombinant human interleukin-2 in the induction of fever, brain prostaglandin, and acute-phase protein synthesis. 387 45

Complement activity in normal human serum was rapidly depleted by the addition of monosodium urate crystals (MSUC), while the same MSUC preparation had little effect on complement activity in 4 of 8 sera from patients with common variable immunodeficiency (CVID). The degree of complement depletion in the CVID sera correlated with their C-reactive protein (CRP) concentrations but not with their concentrations of IgG. MSUC-induced complement depletion in the 4 poorly reactive sera was partially restored by addition of CRP or by normalizing the IgG concentration, but not by addition of IgM or IgA. It is proposed that CRP, an acute phase protein, may play a role in the pathogenesis of gouty arthritis attacks occurring in some patients following surgery or acute physical illness.
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PMID:Effect of IgG and C-reactive protein on complement depletion by monosodium urate crystals. 688 65

Increased interleukin-6 (IL-6) production and expression by malignant cells of the IL-6 receptor has been evidenced in a subgroup of non-Hodgkin's lymphomas, suggesting that this cytokine plays a role in lymphoma growth and in B clinical symptoms. In this study, the effect of the administration of an anti-IL-6 monoclonal antibody (MoAb) was analyzed in 11 patients seropositive for human immunodeficiency virus-1 and suffering from an immunoblastic or a polymorphic large-cell lymphoma. The antibody (BE-8, 10 to 40 mg/day) was administered for 21 days. Neutralization of in vivo IL-6 effect was assessed by monitoring C-reactive protein levels in the serum. In 5 patients, the lymphoma progressed during treatment. Among them were the 2 patients in whom endogenous IL-6 effect was not neutralized. Five patients experienced a stabilization, and 1 a partial remission. This effect on lymphoma growth lasted for 8 to 28 weeks. The anti-IL-6 MoAb had a clear effect on lymphoma-associated fever and cachexia. The mean body weight increase was 1.4 +/- 0.5 kg between day 1 and day 21, and reached 12 kg in 120 days in 1 patient who received three courses of treatment. Side effects were a consistent but moderate thrombocytopenia, and an occasional and moderate decrease of neutrophil counts. Immunization against the MoAb was observed in only 2 patients. These results indicate that in some cases of lymphomas growth of malignant cells may be partially IL-6-dependent and that neutralizing endogenous effect of IL-6 completely abrogates B clinical symptoms.
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PMID:Administration of an anti-interleukin-6 monoclonal antibody to patients with acquired immunodeficiency syndrome and lymphoma: effect on lymphoma growth and on B clinical symptoms. 791 67

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

Highly specialized, state-of-the-art diagnostic tests are available for identifying congenital and acquired immune defects. These methods should only be resorted to when less complicated means have created suspicion of an immune defect. The case history, including the family history, represents the core of the diagnostic procedure. Initially, only simple clinical investigations are indicated. These should enable the physician to exclude or delimit a defect in the immune system which then can be defined more closely by specific tests. Screening includes clinical chemistry (erythrocyte sedimentation rate, total serum protein, serum electrophoresis, C-reactive protein, blood count including differential blood count, ferritin, urine analysis, and a quantitative assay of the immunoglobulins A, G and M), bacteriological, serological, and radiological investigations, and finally skin tests with recall antigens. Thereby, it is usually possible to reliably detect primary B cell defects with humoral antibody deficiency syndromes. Lymphocyte subset counts, immunoelectrophoresis, and bone marrow biopsy are necessary for the differential diagnosis, or for the confirmation, of malignant lymphatic proliferation, especially in adults. IgG subclass defects as well as granulocyte dysfunction and complement defects must be excluded in patients who are susceptible to bacterial infection despite normal immunoglobulin concentrations. In suspected cases of primary or secondary (HIV, cytomegalovirus, Epstein-Barr virus) T cell defects, lymphocyte subset counts and, where applicable, T cell function tests are indicated. The majority of secondary immunodeficiency syndromes, in which the primary disease is known, do not currently require specialized diagnosis. Nevertheless, monitoring of the lymphocyte subsets in HIV-positive patients has already become standard practice in health care (for evaluating the prognosis and deciding on the therapy).
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PMID:[Laboratory diagnosis of immune deficiency]. 849 52

In vitro experiments have suggested that interleukin (IL)-6 may contribute to human immunodeficiency virus (HIV) burden and to immunological abnormalities in HIV-infected patients. We had the opportunity to directly address this question in vivo through the virological and immunological monitoring of HIV-infected patients treated with an anti-IL-6 monoclonal antibody (mAb) for a lymphoma (ANRS 018 trial). Sixteen courses of anti-IL-6 mAb administration, performed in 11 patients, were studied. All patients were at a late stage of HIV infection. The HIV load and the immunological status were determined at the initiation of each course and at its end, 21 days later. The mAb induced no significant change of HIV load, as evaluated by p24 antigenemia, plasma viremia, and quantification of circulating HIV RNA by reverse transcriptase-polymerase chain reaction and branched DNA techniques. The anti-IL-6 mAb also did not affect CD4+, CD8+, and CD19+ circulating cell counts, nor the serum concentrations of sIL-2R and of sCD8. In contrast, the mAb completely abrogated acute-phase reaction, as demonstrated by the normalization of C-reactive protein and fibrinogen circulating levels (p = 0.013 and p = 0.008, respectively). It increased serum albumin concentration. The latter effect was restricted to patients with a spontaneously low albuminemia (p = 0.01). It decreased B-lymphocyte hyperactivity, as reflected by decreased IgG and IgA serum levels (p = 0.008 and p < 0.001, respectively), and by a decreased production of IgG in vitro (p = 0.017). In contrast, the IgM hyperproduction was not affected by the mAb. Therefore, increased IL-6 production in HIV-infected patients at a late stage of the infection may not stimulate HIV replication in vivo, but it may represent a key mechanism contributing to the metabolic and immunological dysbalance of the disease.
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PMID:In vivo role of IL-6 on the viral load and on immunological abnormalities of HIV-infected patients. 852 34

Wasted mice bear the spontaneous autosomal recessive mutation wst/wst; this genotype is associated with weight loss beginning at 21 days of age, neurologic dysfunction, immunodeficiency at mucosal sites, and increased sensitivity to the killing effects of ionizing radiation. The pathology underlying the disease symptoms is unknown. Experiments reported here were designed to examine thermoregulation and liver expression of specific cytokines in wasted mice and in littermate and parental controls. Our experiments found that wasted mice begin to show a drop in body temperature at 21-23 days following birth, continuing until death at the age of 28 days. Concomitant with that, livers from wasted mice expressed increased amounts of mRNAs specific for cytokines IL-6 and IL-1, the acute phase reactant C-reactive protein, c-jun, and apoptosis-associated Rp-8 when compared to littermate and parental control animals. Levels of beta-transforming growth factor, c-fos, proliferating cell nuclear antigen, and ornithine amino transferase transcripts were the same in livers from wasted mice and controls. These results suggest a relationship between an acute phase reactant response in wasted mice and temperature dysregulation.
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PMID:Dysregulation of temperature and liver cytokine gene expression in immunodeficient wasted mice. 861 95


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