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)

Mucormycosis is an infection caused by fungi in the Mucorales order, of which the most relevant family is Mucoraceae, which includes the Rhizopus, Mucor and Absidia genera. It is a severe infection which involves diabetic patients with ketoacidotic decompensation and immunosuppressed patients. We report here five cases (four with rhino-cerebral forms) attended at our hospital in the last ten years. Three patients had diabetes, one was infected with the human immunodeficiency virus, and the other was on a programme of peritoneal dialysis due to renal failure. The most relevant clinical manifestation was the presence of the necrotic lesion in three of the four patients with rhinocerebral involvement (two in the palate, one in the nasal mucosa). Two patients died as a result of the direct infection a few days after diagnosis. In summary, mucormycosis is an infection with a low prevalence but still maintaining a high mortality rate. An early diagnosis is essential and thereby a high index of clinical suspicion is required in patients with predisposing factors.
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PMID:[Mucormycosis: a classical infection with a high mortality rate. Report of 5 cases]. 1144 2

HIV-associated nephropathy (HIVAN) is the most common cause of renal failure in patients infected with type 1 human immunodeficiency virus (HIV-1). The renal prognosis for HIVAN is poor and is typically associated with rapid progression to renal death. We report a patient with biopsy-proven HIVAN who was successfully treated with corticosteroids and review the currently available evidence supporting the specific treatments of this condition. A 34-year-old African-American male with a 2-year history of uncomplicated HIV disease developed progressive azotemia despite treatment with highly active antiretroviral therapy (HAART). He was treated with an uncomplicated 4-month course of prednisone, which improved his serum creatinine from 2.9 to 1.9 mg/dl and decreased his degree of proteinuria from 8 to 2.1 g/day. Two years post-steroid treatment his renal function remains stable. Increasing evidence supports that both ACE inhibitors and HAART are effective in preventing and in some cases of reversing HIVAN induced renal failure. In selected patients who progress despite these measures, a limited course of corticosteroid may achieve long-standing disease remissions. In general, with adequate supervision, corticosteroid therapy appears to be well tolerated and has an acceptable side effect profile. Although persuasive in view of the abysmal natural history of HIVAN, the currently available studies are subject to major methodological limitations. Appropriate randomized controlled trials are urgently required in order to further examine the efficacy, optimal timing, and potential side effects of these treatments.
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PMID:Treatment of HIV-associated nephropathy. 1148 63

This research profiles nursing home residents who have human immunodeficiency virus (HIV) and anemia at the time of admission, utilizing the minimum data set (MDS). In addition, this article compares residents with HIV and anemia to other nursing home residents with HIV. These resident profiles include sociodemographic characteristics, health status measures, and special treatments and procedures received. This study analyzed 1,281 admission assessments for HIV residents with anemia and 3,832 admission assessments for other residents with HIV in the MDS between June 22, 1998 and January 17, 2000. A significantly greater percentage of HIV residents with anemia were female (38.6%) compared to other residents with HIV (27.9% female). Almost two-thirds of HIV residents with anemia and three-quarters of other residents with HIV received Medicaid coverage at the time of their admission to the nursing home. Approximately 3 of every 4 residents with HIV and anemia and other residents with HIV were from racial/ethnic minority groups. Significantly greater percentages of residents with HIV and anemia also had dementia, depression, pneumonia, hepatitis, renal failure, anxiety disorder, and cancer than other residents with HIV. These analyses demonstrate that at the time of admission to the nursing home, those residents with HIV and anemia were significantly more likely to have other diseases, infections, and health care conditions than other residents with HIV. In addition, HIV residents with anemia were significantly more likely to receive special treatments and procedures in the nursing home than other residents with HIV.
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PMID:Nursing home residents with HIV and anemia. 1148 64

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

Human immunodeficiency virus-associated nephropathy (HIVAN) is a distinct clinico-pathological syndrome that occurs almost exclusively in black patients with an AIDS defining diagnosis. It is characterized by rapidly progressive renal failure with a severe nephrotic syndrome. The renal biopsy typically shows a collapsing glomerular sclerosis and variable tubulo-interstitial nephritis. The pathogenesis most likely involves infection of renal tubular and epithelial cells with HIV. The use of ACE-inhibitors and steroids may slow down the progression to end-stage renal failure. With the introduction of highly active anti-retroviral therapy, HIVAN may now be treated effectively although clinical data are so far limited to case-reports.
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PMID:Diagnosis and treatment of HIV-associated nephropathy. 1158 26

Viral hepatitis and human immunodeficiency virus (HIV) infection are important causes of mortality and morbidity in patients treated by haemodialysis (HD). Both are further promoted by the characteristic immunological dysfunction that develops in renal failure and interferes with the patient's ability to eliminate these viruses. The hepatotropic viruses A through G remain the causative agents in 60 to 80% of hepatitis. But, as far as HD is concerned, hepatitis B virus (HBV) and hepatitis C virus (HCV) are the two most important organisms responsible for almost all the patients' morbidity. In HD, both patients as well as staff are at a high risk of acquiring hepatitis B infection. The prevalence of HBV in the dialysis population in India is reported to range between 3.4% and 42%. The acute course of the infection is often anicteric and peak transaminase concentration is significantly less than in patients with normal renal function. Up to 60% of dialysis patients with HBV infection develop chronic hepatitis with persistence of hepatitis B surface antigen (HBsAg) and infectivity. The risk of transmission of HBV infection due to blood from one patient to another is mostly because of inadequate precautions taken by the dialysis staff. Combined therapy with interferon (6-10 million units) three times a week and lamivudine (100-300 mg/day) would be more effective in controlling viral replication. The most important modality for prevention of HBV infection is induction of immunity by hepatitis B vaccination. Administration of 40 microg doses at months 0, 1, 2 and 6 is the most rapid immunogenic schedule. The prevalence of HCV in HD patients ranges from 6% in the United Kingdom to 60% in Poland and Eastern Europe, 8-36% in North America. HD patients in different parts of India exhibit high anti-HCV positivity (12.1%, 45.2%, 33.3% and 41.9%) in various studies. The incidence and prevalence of HCV infection among patients on dialysis in developed countries are steadily declining because of (i) reduction in post-transfusion HCV infection, (ii) infection control measures to prevent nosocomial infection. Among HD patients with HCV infection, serum alanine aminotransferase (ALT, SGPT) levels are elevated in only 4 to 67% patients who are positive for anti-HCV, in only 12 to 31% patients with HCV RNA and only in one-third of those with biopsy proven hepatitis. Number of blood transfusion, duration of HD treatment, and mode of dialysis are important risk factors. Patient to patient transmission of HCV occurs in HD units by needle stick injury, breakdown in standard infection control practices, physical proximity to an infected patient, dialysis machines, dialysis membranes and HD ultrafiltrate and reprocessing of dialyser. The prevalence of HIV infection in dialysis populations varies according to different countries and geographic areas, 0% and 13% in 1990 and 1995 respectively. There was no evidence of transmission within the centre transmission, from patient to patient or patient to staff. Antiretroviral therapy is the corner-stone of the HIV infection in end stage renal disease (ESRD). Most commonly, zidovudine (AZT) has been used in these patients. Currently recommended dose of 200 mg three times a day is probably safe in these patients.
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PMID:Hepatitis and HIV infection during haemodialysis. 1166 25

The purpose of this study was to review the preclinical and clinical literature relevant to the efficacy and safety of anabolic androgen steroid therapy for palliative treatment of severe weight loss associated with chronic diseases. Data sources were published literature identified from the Medline database from January 1966 to December 2000, bibliographic references, and textbooks. Reports from preclinical and clinical trials were selected. Study designs and results were extracted from trial reports. Statistical evaluation or meta-analysis of combined results was not attempted. Androgenic anabolic steroids (AAS) are widely prescribed for the treatment of male hypogonadism; however, they may play a significant role in the treatment of other conditions as well, such as cachexia associated with human immunodeficiency virus, cancer, burns, renal and hepatic failure, and anemia associated with leukemia or kidney failure. A review of the anabolic effects of androgens and their efficacy in the treatment of these conditions is provided. In addition, the numerous and sometimes serious side effects that have been known to occur with androgen use are reviewed. Although the threat of various side effects is present, AAS therapy appears to have a favorable anabolic effect on patients with chronic diseases and muscle catabolism. We recommend that AAS can be used for the treatment of patients with acquired immunodeficiency syndrome wasting and in severely catabolic patients with severe burns. Preliminary data in renal failure-associated wasting are also positive. Advantages and disadvantages should be weighed carefully when comparing AAS therapy to other weight-gaining measures. Although a conservative approach to the use of AAS in patients with chronic diseases is still recommended, the utility of AAS therapy in the attenuation of severe weight loss associated with disease states such as cancer, postoperative recovery, and wasting due to pulmonary and hepatic disease should be more thoroughly investigated.
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PMID:Clinical review 138: Anabolic-androgenic steroid therapy in the treatment of chronic diseases. 1170 61

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

This article reports the case of a 33-year-old woman with common variable immunodeficiency (CVI) who developed renal failure 17 years after diagnosis and initiation of treatment with monthly IVIG. A renal biopsy revealed mesangial and paramesangial immune complex deposition and interstitial granulomatous infiltration. Renal function improved with oral corticosteroids, but did not return to normal. Decreasing the dose of IVIG had no effect on renal function. Immune dysfunction can be associated with both granulomatous disease and immune complex glomerulonephritis, or the latter may be related to chronic infection or immunoglobulin use. This is the first report of concomitant glomerular-tubulointerstitial lesions in this immunodeficiency syndrome. Renal function should be closely followed in patients with CVI.
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PMID:A unique renal lesion in common variable immunodeficiency. 1183 5

Collapsing glomerulopathy (CG), an aggressive variant of focal segmental glomerular sclerosis, is a renal disease with severe proteinuria and rapidly progressive renal failure. The pathogenesis of CG is unknown. It strongly resembles human immunodeficiency virus (HIV)-associated nephropathy, but the patients are HIV negative. The characteristic glomerular lesion is capillary loop collapse with prominent podocytes filling Bowman's space. Interestingly, these glomerular changes are usually associated with severe tubulointerstitial injury, including tubular epithelial degenerative changes, microcystic dilation of several tubules, and interstitial inflammatory cell infiltrate. Recently, it became evident that the morphologic pattern of CG may appear not only in native kidneys, but also de novo in renal allografts, and that the pattern of CG in renal transplants is not always associated with severe proteinuria. Studies describing CG in renal allografts are all based on biopsies. We report 3 allograft nephrectomy specimens that showed a zonal distribution of the characteristic collapsing glomerular changes with associated tubulointerstitial injury. All 3 kidneys had obliterative vascular changes. One nephrectomy specimen had chronic obliterative transplant arteriopathy, 1 had acute vascular rejection, and 1 had thrombotic microangiopathy. None of the patients had severe proteinuria. Our cases suggest that the morphologic pattern of CG in renal allografts may not represent the same disease process as CG in native kidneys and provide further evidence that collapsing glomerular changes do not define the disease entity of CG, but rather represent a pattern of renal injury. Among other factors, hemodynamic disturbance may play a role in the development of the pattern of CG in renal allografts.
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PMID:Zonal distribution of glomerular collapse in renal allografts: possible role of vascular changes. 1205 80


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