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)

Concomitant immune deficiency and activation of immuno-competent cells, together with a disequilibrium between inflammation-inducing cytokines and their specific natural inhibitors is the basis of our current understanding of immune system dysregulation in patients with chronic uraemia. These anomalies may even be accentuated by dialysis. Clinically, bacterial infections, viral hepatitis and amyloidosis all play important roles. Humoral factors include abnormal immunoglobulin response to specific antibodies and complement activation. The response of T lymphocytes, long sought as the origin of the immunodeficiency associated with chronic uraemia, is also significantly decreased in these patients. The decreased antibody responses to specific stimuli may be related to B cell dysfunction. Monocyte and polymorphonuclear cell reactions are also perturbed. A deficiency in natural killer cells is observed although the mechanisms involved and the consequences are still debated. The factors determining the anomalies leading to immune system dysregulation in chronic uraemia and dialysis and their relationship with the reduction in active nephron mass as well as their metabolic and/or endocrine consequences remain to be fully described. A better understanding of the mechanisms involved should lead to new strategies for immuno-intervention in patients with chronic renal failure and help in optimizing haemodialysis.
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PMID:[Dysregulation of the immune system in chronic uremic and hemodialysed patients]. 789 21

A 46-year-old woman who noticed tightness of the skin in September, 1993, was admitted to a local hospital due to hypertension, congestive heart failure and renal dysfunction on the 2nd of November. After admission, renal function deteriorated progressively. A diagnosis of scleroderma renal crisis (SRC) was suspected from her skin biopsy and clinical course. She was referred to our hospital for further evaluation and maintenance of hemodialysis. Her blood pressure was kept normal by anti-hypertensive drugs including cilazapril. Acute interstitial pneumonia, microangiopathic hemolytic anemia and thrombocytopenia appeared during her clinical course. Corticosteroid therapy was effective for acute interstitial pneumonia, but in-effective for thrombocytopenia. Plasma exchange was not effective for thrombocytopenia, which was successfully treated with intravenous gamma-globulin therapy. She died of cytomegaloviral encephalitis, which might have resulted from immunodeficiency caused by prolonged corticosteroid therapy and uremia. Complications other than SRC might have appeared during the clinical course based on the immune disorder of progressive systemic sclerosis itself. In order to improve the prognosis of patients with SRC such complications should be detected promptly and treated correctly.
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PMID:[A case of scleroderma renal crisis with acute interstitial pneumonia, microangiopathic hemolytic anemia and refractory thrombocytopenia]. 796 79

Animal and human studies suggest that vitamin B6 deficiency affects both humoral and cell-mediated immune responses. Lymphocyte differentiation and maturation are altered by deficiency, delayed-type hypersensitivity responses are reduced, and antibody production may be indirectly impaired. Although repletion of the vitamin restores these functions, megadoses do not produce benefits beyond those observed with moderate supplementation. Additional human studies indicate that vitamin B6 status may influence tumor growth and disease processes. Deficiency of the vitamin has been associated with immunological changes observed in the elderly, persons infected with human immunodeficiency virus (HIV), and those with uremia or rheumatoid arthritis. Future research efforts should focus on establishing the mechanism underlying the effects of vitamin B6 on immunity and should attempt to establish safe intake levels that optimize immune response.
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PMID:Vitamin B6 and immune competence. 830 91

Minimizing the risk for infection to laboratory staff from a contaminated blood sample is a major safety goal in the clinical laboratory. One dangerous pathogen, the human immunodeficiency virus (HIV), can be deactivated by heating sera at 56 degrees C for 30 minutes. The authors previously reported that if serum was subjected to those conditions, the concentrations of the nine most commonly monitored drugs were not altered, whereas phenytoin and carbamazepine concentrations were reduced slightly. Monitoring free phenytoin, free valproic acid, and free carbamazepine concentrations is strongly recommended for patients with uremia, liver disease, and hypoalbuminemia. Because drug protein binding can be affected by temperature, the authors investigated the effect on free drug concentrations of sera heated to levels necessary for deactivation of the HIV virus. They measured total and free drug concentrations in serum pools prepared from patients receiving phenytoin, valproic acid, and carbamazepine. Serum pools were heated at 56 degrees C for 30 minutes and then brought to room temperature. The total and free drug concentrations were measured immediately after heating and then at 20- and 45-minute intervals. The concentrations of free phenytoin and free valproic acid were significantly higher after heat treatment. However, after equilibration of sera at room temperature for 20 minutes, the free concentrations of phenytoin were comparable to preheating values, although total phenytoin concentrations (Serum Separator Tubes) were reduced slightly. In contrast, free valproic acid concentrations did not return to the original levels even after 45 minutes. Free carbamazepine concentrations did not change even immediately after heating. However, total carbamazepine concentrations were reduced slightly when sera were heated in serum separator tubes (SST Tubes).
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PMID:Effect of heating human sera at a temperature necessary to deactivate human immunodeficiency virus on measurement of free phenytoin, free valproic acid, and free carbamazepine concentrations. 1044 96

Patients with chronic renal failure show an immunodeficiency characterized by frequent infectious complications and a low response to vaccinations. This is paralleled in vitro by a low T-cell proliferation on mitogenic stimuli because of an impaired costimulation by accessory cells. Furthermore, alterations of the cytokine profile are correlated with impaired immune function. The immune system is influenced by both uremia and renal replacement therapy. To evaluate the influence of hemodialysis on immune parameters, we studied patients before and after the initiation of chronic hemodialysis therapy. Fourteen patients with end-stage renal failure were tested before dialysis initiation and during the first 6 weeks of hemodialysis treatment. We determined the in vitro T-cell proliferation, as well as plasma levels of interleukin-6 (IL-6) and the release of IL-6 and IL-10 into culture supernatant poststimulation with lipopolysaccharide. After 6 weeks of intermittent hemodialysis, in vitro T-cell proliferation on stimulation improved significantly (stimulation index, 21.6 +/- 18.5 versus 58.1 +/- 45.5; P < 0.01). This improvement occurred regardless of whether synthetic dialyzers or cellulosic membranes were used for the initiation of dialysis. Plasma IL-6 levels, as well as IL-6 and IL-10 secretion, did not change during the study period. In patients with end-stage renal disease, the initiation of hemodialysis led to a significant improvement of in vitro T-cell proliferation. This effect may have a role for an improvement of immune function in vivo. The expected normalization of IL-6 and IL-10 production may be masked by cytokine induction through hemodialysis membranes.
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PMID:Initiation of hemodialysis treatment leads to improvement of T-cell activation in patients with end-stage renal disease. 1073 80

Reactive oxygen species, formed in various biochemical reactions, are normally scavenged by antioxidants. Glutathione in its reduced form (GSH) is the most powerful intracellular antioxidant, and the ratio of reduced to oxidised glutathione (GSH:GSSG) serves as a representative marker of the antioxidative capacity of the cell. Several clinical conditions are associated with reduced GSH levels which as a consequence can result in a lowered cellular redox potential. GSH and the redox potential of the cell are components of the cell signaling system influencing the translocation of the transcription factor NF kappa B which regulates the synthesis of cytokines and adhesion molecules. Therefore, one possibility to protect cells from damage caused by reactive oxygen species is to restore the intracellular glutathione levels. Cellular GSH concentration can be influenced by exogenous administration of GSH (as intravenous infusion or as aerosol), of glutathione esters or of GSH precursors such as glutamine or cysteine (in form of N-acetyl-L-cysteine, alpha-lipoic acid). The modulation of GSH metabolism might present a useful adjuvant therapy in many pathologies such as intoxication, diabetes, uremia, sepsis, inflammatory lung processes, coronary disease, cancer and immunodeficiency states.
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PMID:Therapeutic potential of glutathione. 1100 22

Patients with chronic renal failure suffer from defective host defenses which are directly the result of the renal impairment, in addition to those dependent on the primary illness leading to the renal failure. The mechanisms underlying the defective responses in phagocytic cells, lymphocytes and antigen processing are likely due to either failure to adequately eliminate suppressive compounds by the defective kidneys or to improper metabolic processing of the factors by the damaged renal parynchema. That some of the defects are reversed by transplantation and not dialysis suggests that renal parenchymal metabolic activities may be involved, although it is also possible that functioning glomerular cells are capable of filtering substances that membranes are not currently capable of eliminating. The current strategy for dealing with the immunodeficiency appears to be totally based on developing means to circumvent the defective function. The other approach, correction of the impaired function, cannot be even considered until the mechanisms underlying the defective function of the cells involved in defenses are better delineated. It seems possible that one or a few compounds are pivotal in altering the function of all the affected cell lines, since, with only a small amount of effort, it is possible to relate the dysfunction to abnormal cell membrane functions in phagocytic cells, dendritic cells and lymphocytes. Until the biochemical basis of the dysfunction of all the cell types affected are better defined, such exercises cannot be translated into better management of patients with chronic renal failure. Proper function of host defenses requires that appropriate cells can properly respond to threats to host viability. For the cells of the immune system (phagocytes and lymphocytes) this means that their response to regulatory molecules be appropriate, that their mobility be normal, that their adherence to substrates be preserved, and that they can generate the appropriate response to the challenge. For neutrophils, for example, it is necessary that they recognize and mobilize appropriately to chemotactic stimuli, that they be able to adhere to and migrate through endothelial lining, that their phagocytic activity be sufficient, and that they can kill and degrade endocytosed particles and generate appropriate secretions. Similar lists of requirements for good function can be generated for any cell type in the immune defense system. Uremia, as well as currently available treatments for uremia, directly or indirectly alters the function of all phases of appropriate immune cell function. Defective host responses in uremia have been recognized for decades and there has been considerable effort in the past decade to better define the extent and mechanisms of impaired defenses. Despite the multitude of major defects in humoral, cellular, and inflammatory processes, uremic patients who are cared for today, although they remain at higher risk of serious infectious complications, can and do maintain a good quality of life, with most remaining free of major infections for years and decades.
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PMID:Immunologic defects and vaccination in patients with chronic renal failure. 1157 Jan 43

ABSTRACT. End-stage renal failure (ESRF) and chronic hemodialysis (HD) induce a state of immunodeficiency that involves T cell-mediated responses. A decreased T cell number combined with a reduced T cell lifespan and an increased T cell activation might play a role in the immune impairment associated with ESRF and chronic HD. Increased T cell activation associated with immunodeficiency suggests that activated T cells may be driven to apoptosis. To test this hypothesis, CD3+ T cell activation (CD69) and apoptosis (annexin V, CD95 (Fas), and DNA fragmentation) were analyzed in a case control study after blood draw sampling (ex vivo), in culture conditions, and after phytohemagglutinin or anti-CD3 stimulation. Ex vivo evaluation of T cells showed an increased number of activated CD69+ T cells in chronic HD patients (142 +/- 5 cells/mm3) compared with patients with ESRF (115 +/- 2 cells/mm3, P = 0.04) and controls (74 +/- 2 cells/mm3, P = 0.0006). These data were confirmed in culture conditions and after stimulation. Similarly, annexin V and CD95 (Fas)-positive T cells were more numerous in both patient groups than in controls, irrespective of the experimental conditions (P < or = 0.005 for both markers), and their percentage was always significantly higher in chronic HD patients than in patients with ESRF. The amount of DNA fragmentation was also significantly higher in the cultured resting T cells of chronic HD patients (37 +/- 3%) than in those of patients with ESRF (25 +/- 3%) and controls (20 +/- 2%) (P = 0.01). Percentage of cultured resting T cells expressing both CD69 and annexin V markers was higher in chronic HD patients (17 +/- 4%) than in patients with ESRF (10 +/- 4%) and controls (6 +/- 2%), (P = 0.005). After stimulation (phytohemagglutinin or anti-CD3), CD69+ T cell apoptosis increased by 2.4-fold in chronic HD patients compared with 1.8-fold in patients with ESRF and only 1.2-fold in controls (P = 0.001). T cells from chronic HD patients and patients with ESRF thus showed an aberrant state of early activation that contrasted with an increased proportion of annexin V and CD95 (Fas)-positive T cells engaged in apoptosis, as confirmed by DNA fragmentation. Increased susceptibility to early activated T cell apoptosis is not only associated with uremia, but is also enhanced by HD procedure. This may account for the T lymphopenia, progressive immunodeficiency, and increased infection risk seen in these patients.
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PMID:Early T cell activation correlates with expression of apoptosis markers in patients with end-stage renal disease. 1175 39

Pruritus is a common manifestation of dermatologic diseases, including xerotic eczema, atopic dermatitis, and allergic contact dermatitis. Effective treatment of pruritus can prevent scratch-induced complications such as lichen simplex chronicus and impetigo. Patients, particularly elderly adults, with severe pruritus that does not respond to conservative therapy should be evaluated for an underlying systemic disease. Causes of systemic pruritus include uremia, cholestasis, polycythemia vera, Hodgkin's lymphoma, hyperthyroidism, and human immunodeficiency virus (HIV) infection. Skin scraping, biopsy, or culture may be indicated if skin lesions are present. Diagnostic testing is directed by the clinical evaluation and may include a complete blood count and measurement of thyroid-stimulating hormone, serum bilirubin, alkaline phosphatase, serum creatinine, and blood urea nitrogen levels. Chest radiography and testing for HIV infection may be indicated in some patients. Management of nonspecific pruritus is directed mostly at preventing xerosis. Management of disease-specific pruritus has been established for certain systemic conditions, including uremia and cholestasis.
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PMID:Pruritus. 1452 1

The conventional approach for management of retroperitoneal fibrosis (RF), an inflammatory process of retroperitoneal fibro-adipose tissue, leading to the compression and obstruction of the ureters and other adjacent organs is ureterolysis with omental wrapping, and an effective alternative to surgery is immunosupressive medication such as oral corticosteroids. Sairei-to (TJ-114) is a traditional herbal medicine used for the treatment of RF in Japan. It has both anti-inflammatory and anti-allergic effects. Here we report two cases of RF successfully treated with Sairei-to. One case was idiopathic and the other was caused by artificial graft-induced vasculitis. Both cases were treated with Sairei-to following the decompression of uremia by precutaneous nephrostomy or indwelling ureteral stents. There was hardly any ureteral obstruction three months after the administration of Sairei-to. They have been doing well for 12 and 26 months. Sairei-to rarely causes side effects such as immunodeficiency, gastro-duodenal ulcer and osteoporosis that often accompany long-term administration of corticosteroids. Sairei-to is a safe and effective medicine for the treatment of RF. We therefore recommend Sairei-to as an alternative for corticosteroid therapy.
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PMID:The efficiency of Sairei-to for retroperitoneal fibrosis: two case reports. 1691 May 87


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