UMLS:C0019693 - FACTA Search

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Query: UMLS:C0019693 (HIV)
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Cryptococcosis, particularly cryptococcal meningitis (CM), has become an increasing problem globally in the AIDS era. In the present investigation we have made an effort for the first time to study Indian cases (100) both HIV-positive (23 cases, male, mostly Indian professional blood donors, PBDs') confirmed by an ELISA test and Western Blot but asymptomatic for CM and HIV-negative (77:49 male and 28 female) asymptomatic or symptomatic. These subjects were patients from the Lucknow hospitals admitted during the period between February, 1991 to February, 1994, for suspected cryptococcosis or CM. Of those cases, 10% were positive for cryptococcosis or CM. Meningoencephalitis was the dominant clinical manifestation in four (HIV-negative) cases of CM. CT scanning of the head of those cases revealed a noncommunicating hydrocephalus due to aqueductal stenosis (in 2 cases) and a communicating hydrocephalus with granuloma (by MRI) in another case. The latex agglutination test (LAT) of the sera was positive for Cryptococcus antigen in 6 (26%) of the (HIV-positive) patients and 4 (5%), of the HIV-negative cases. In the cases of CM, there was a lower antigen titre in CSF than in the pronase-treated sera. The LAT was found to be useful in diagnosis of cryptococcosis, especially in asymptomatic cases. The CSF of CM-positive cases revealed low levels of glucose, reduced cell count and high proteins. Among the HIV-negative cases, the onset of meningitis in 4 cases was preceded by the presence of encapsulated budding yeast cells in CSF India ink smear, or cryptococci in a direct urine smear in one case. The CSF culture of 3 cases was positive for mucoid Cryptococcus neoformans, showing brown colour effect (BCE) on Staib agar (syn. Guizotia abyssinica creatinine agar, bird seed agar). The isolated yeast strains were identified as C. neoformans var. neoformans by physiological tests. The pathogenicity test of strains revealed virulence to BALB/c mice evidenced by a high mortality of mice and significantly (p < 0.05) high CN burden (> 4-5 mean log(10) cfu), in the brain followed by other visceral organs (lung, liver, spleen, kidney and heart). The in-vitro susceptibility (MIC mu gmL(-1)) of strains.
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PMID:Cryptococcosis associated with HIV negative Indian patients and HIV positive Indian blood donors. 886 75

A review of all native kidney biopsies at our center from 1974 to 1993 identified 43 cases of idiopathic focal segmental glomerulosclerosis (FSGS) with predominantly collapsing features and lacking evidence of HIV-1 infection or intravenous drug use. No case was identified before 1979 and the incidence of this entity has progressively increased over the past two decades. Compared to 50 age-matched controls of idiopathic FSGS with typical perihilar scars, the group of idiopathic collapsing FSGS displayed black racial predominance, a higher serum creatinine and more severe features of nephrotic syndrome at biopsy. Morphologic features of visceral epithelial cell hypertrophy and hyperplasia, tubular microcysts, tubular epithelial degenerative and regenerative features and interstitial edema were more prevalent and severe in collapsing FSGS. Median time to ESRD was rapid in collapsing FSGS versus controls (13.0 months vs. 62.5 months, P < 0.05). Correlates of progression to ESRD included a higher initial serum creatinine and failure to undergo remission of proteinuria. Both glomerulosclerosis and certain features of tubular damage were independent predictors of the level of renal function at time of biopsy, but not of the rate of progression of renal insufficiency. Although three patients had partial or complete spontaneous remissions, none of 26 patients treated with steroids alone responded. Idiopathic collapsing FSGS is a variant of FSGS with increasing incidence, distinct clinicopathologic features, black racial predominance, a rapidly progressive course and relative steroid resistance.
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PMID:Idiopathic collapsing focal segmental glomerulosclerosis: a clinicopathologic study. 891 44

The acquired immunodeficiency syndrome (AIDS) wasting syndrome (AWS) is a devastating complication of human immunodeficiency virus infection characterized by a disproportionate decrease in lean body mass. The pathogenesis of the AWS is unknown, but recent data suggest that endogenous secretion of the potent anabolic hormone, testosterone; is decreased in 30-50% of men with AIDS. However, it is unknown whether decreased androgen levels are associated with decreased lean body mass and/or functional decreases in muscle strength and aerobic capacity in hypogonadal men with the AWS. In addition, testosterone is known to have stimulatory effects on GH secretion, and the loss of these effects on the GH-insulin-like growth factor I (IGF-I) axis may be an additional mechanism of decreased lean body mass in this population. Twenty hypogonadal subjects (free-testosterone < 12 pg/mL) with weight loss > 10% of preillness weight or absolute weight < 90% ideal body weight (IBW) were enrolled in the study. None of the subjects were receiving Megace. Lean body mass and fat-free mass were determined by potassium-40 isotope analysis (40K) and dual-energy x-ray absorptiometry, respectively, and analyzed with respect to gonadal function by linear regression analysis. Muscle mass was determined by urinary creatinine excretion, and exercise functional capacity was assessed by a 6-min walk test, a sit-to-stand test, and a timed get-up-and-go test. Results also were compared with gonadal function by regression analysis. IGF-I and mean overnight GH levels, determined from frequent sampling (q20 min from 2000-0800 h), were compared with results obtained from age- and sex-matched normal controls. Subjects were 26-58 yr of age (39 +/- 7 yr, mean +/- SD) with a CD4 cell count of 150 +/- 186 cells/mm3. Serum levels of FSH were elevated in 30% of the subjects. Muscle mass was significantly reduced, compared with expected mass for height (23.3 +/- 5.5 vs. 29.3 +/- 1.7 kg, P = 0.0001) and was decreased disproportionately to weight (77% of expected value for muscle mass vs. 93% of expected value for weight). Free-testosterone levels were correlated with total body potassium (R = 0.45, P < 0.05) and muscle mass (R = 0.45, P < 0.05). Total-testosterone levels were correlated with exercise functional capacity (R = 0.64, P = 0.01 for the sit-to-stand test and R = 0.53, P < 0.05 for the 6-min walk test). Mean GH levels were significantly increased (3.03 +/- 1.76 vs. 0.90 +/- 0.37 ng/mL, P < 0.001) and IGF-I levels decreased (167 +/- 66 vs. 225 +/- 69 ng/mL, P < 0.01), compared with age- and sex-matched eugonadal controls. GH levels were inversely correlated with caloric intake (R = -0.60, P = 0.02) and percent fat mass by dual-energy x-ray absorptiometry (R = 0.58, P = 0.02). Six additional hypogonadal subjects receiving Megace for AIDS wasting were analyzed separately. Nutritional status and parameters of body composition were compared in the Megace and non-Megace-treated subjects. No significant differences in caloric intake, lean body mass, fat mass, or muscle mass were demonstrated. These data demonstrate that changes in body composition, including loss of lean body and muscle mass, and deterioration in exercise functional capacity are highly correlated with androgen levels in hypogonadal men with the AWS. Furthermore, our data demonstrate significantly increased GH levels and decreased IGF-I in association with low weight in this population. These data suggest that androgen deficiency combined with classical GH resistance may contribute to the critical loss of lean body and muscle mass in hypogonadal men with the AWS. These data are the first to link muscle and lean body wasting with progressive gonadal dysfunction among the large percentage of men with AIDS wasting who are hypogonadal. This demonstrates the need for additional studies to determine the efficacy of gonadal steroid replacement to increase lean body mass in this population.
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PMID:Loss of lean body and muscle mass correlates with androgen levels in hypogonadal men with acquired immunodeficiency syndrome and wasting. 892 60

Magnesium (Mg) deficiency, commonly diagnosed as hypomagnesemia based upon low serum Mg concentrations, is a frequent electrolyte abnormality in critically ill patients. Intravenous replacement therapy is empiric and serum Mg concentrations have traditionally been used as guidelines for measuring efficacy. Recent studies have shown that the Mg content of mononuclear blood cells (MBCs) may provide a better index for Mg status than serum concentrations. The purpose of this study was to evaluate the effects of intravenous Mg replacement therapy on MBC Mg content and serum Mg concentrations in critically ill hypomagnesemic patients. Adult patients admitted to the trauma intensive-care unit (ICU) with serum Mg concentration < or = 0.6 mmol/L (< or = 1.5 mg/dL) were considered for study entry. Patients with severe renal disease (Scr > 133 mumol/L), pregnancy, or those who were seropositive for HIV were excluded. Ten patients with moderate (> 0.4-0.6 mmol/L [> 1.0-1.5 mg/dL]) and severe (< or = 0.4 mmol/L [< or = 1.0 mg/dL]) hypomagnesemia received 0.5 and 0.75 mmol/kg of intravenous MgSO4, respectively, over 24 h. MBC Mg content and serum concentrations of magnesium, phosphorus, calcium, sodium, potassium, blood urea nitrogen, creatinine, glucose, and albumin were measured at baseline (0 h), end of infusion (24 h), 36 h, and 48 h. Data were analyzed using ANOVA with repeated measures and a P value < 0.05 was considered significant. Serum Mg concentrations increased significantly from baseline to 48 h (0.5 +/- 0.1 to 0.8 +/- 0.2 mmol/L, P < 0.001). MBC Mg content did not change significantly within the study period (2.6 +/- 1.0 to 3.0 +/- 1.3 fmol/cell, P > 0.7). The doses of MgSO4 (0.5-0.75 mmol/kg) used in this study increased serum Mg concentrations, but did not result in a statistically significant change of MBC Mg content in this group of trauma ICU patients.
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PMID:Mononuclear blood cell magnesium content and serum magnesium concentration in critically ill hypomagnesemic patients after replacement therapy. 917 93

We report the case of a patient with acquired immunodeficiency syndrome (AIDS) who developed nephrotic syndrome and progressive renal failure mimicking human immunodeficiency virus (HIV)-associated focal segmental glomerulosclerosis (FSGS) who required initiation of hemodialysis and was found on renal biopsy to have membranous nephropathy. Hepatitis B and C serologies were negative. Although she required hemodialysis, she was treated with prednisone and experienced a progressive decline in her serum creatinine from 10.1 mg/dL to 1.9 mg/dL, which permitted the discontinuation of hemodialysis. After she abruptly discontinued prednisone, her creatinine level increased to 4.8 mg/dL, and she experienced marked worsening of her nephrotic syndrome. Resumption of prednisone resulted in normalization of serum creatinine and reduction in urine protein excretion. No adverse effects of prednisone occurred during this time. She remains off of hemodialysis for 1 year with a serum creatinine level of 1.0 mg/dL and urine protein excretion of 0.4 g/d. Although most patients with HIV infection, nephrotic-range proteinuria, and renal failure have FSGS, a minority may have membranous nephropathy. Although typically not a steroid-responsive lesion in the setting of advanced renal failure, membranous nephropathy may be a highly steroid-responsive lesion in the HIV-infected patient, and treatment may help avert the need for dialysis in a patient population that generally has a poor outcome on dialysis.
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PMID:AIDS-associated membranous nephropathy with advanced renal failure: response to prednisone. 921 10

Angiotensin-converting enzyme inhibition (ACEI) delays progression of diabetic and nondiabetic renal disease. This study examined the effect of fosinopril, 10 mg by mouth daily, in HIV-associated nephropathy (HIV-AN). Twenty patients with HIV-AN were studied. Of 11 patients with non-nephrotic-range proteinuria, 7 received treatment and 4 did not. Average baseline creatinine (mg/dl) for treated and nontreated patients was 1.3 +/- 0.24 and 1.0 +/- 0.25, respectively (P = 0.07). At 24 wk, creatinine of treated and nontreated patients was 1.5 +/- 0.34 and 4.9 +/- 2.4 (P = 0.006). Average baseline 24-h urine protein excretion (g/d) for treated and nontreated patients was 1.6 +/- 0.68 and 0.78 +/- 0.39, respectively (P = 0.02). At 24 wk, 24-h protein excretion of treated and non-treated patients was 1.25 +/- 0.86 and 8.5 +/- 1.4 (P = 0.006). Of nine patients with nephrotic-range proteinuria, five were treated and four were not. Average baseline creatinine for treated and nontreated patients was 1.7 +/- 0.46 and 1.9 +/- 0.42, respectively (P = 0.4). At 12 wk, creatinine for treated and nontreated patients was 2.0 +/- 1.0 and 9.2 +/- 2.0 (P = 0.02). The baseline 24-h protein excretion for treated and nontreated patients was 5.4 +/- 1.6 and 5.2 +/- 0.97 (P = 0.9). At 12 wk, 24-h protein excretion for treated and nontreated was 2.8 +/- 1.0 and 10.5 +/- 3.5 (P = 0.008). These preliminary data suggest that treatment with ACEI may stabilize serum creatinine and 24-h protein excretion for up to 24 wk in patients with non-nephrotic-range proteinuria and for up to 12 wk in patients with nephrotic-range proteinuria when initial serum creatinine is < or = 2.0 mg/dl. Furthermore, the renin-angiotensin system may play a role in HIV-AN, and early treatment with ACEI may be beneficial in HIV-AN.
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PMID:Effect of angiotensin-converting enzyme inhibition in HIV-associated nephropathy. 921 64

Thrombotic thrombocytopenic purpura (TTP) is a syndrome characterised by the clinical pentad of microangiopathic haemolytic anaemia (MAHA), thrombocytopenia, renal failure, fluctuating neurologic signs, and fever. The aetiology of TTP is unknown, but associations with various underlying diseases, infections and drugs have been identified. One of these associations is with HIV infection. We describe the clinical picture, the laboratory results and the response to plasma therapy of two cases of HIV-associated TTP. In both patients, a longitudinal semiquantitative assessment of the numbers of schistocytes in blood was made, which correlated well with the more traditional parameters of disease activity. Since 1987, at least 49 patients with HIV-associated TTP have been reported. A case-analysis of the 38 patients who were described in sufficient detail and a review of the literature in the setting of HIV infection is presented. The most important conclusions from these combined data are: (1) TTP usually seems to occur in patients with a CD4+ lymphocyte count < 250 x 10(6).l(-1); (2) more than 50% of the patients present with TTP soon after or during an infectious or malignant disease; (3) plasma exchange is the therapy of choice, still resulting in mortality of 22%; (4) higher initial platelet count and creatinine level are correlated with an adverse outcome.
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PMID:HIV-related thrombotic thrombocytopenic purpura: report of 2 cases and a review of the literature. 936 Apr 10

The occurrence of alterations was verified in some parameters of the asymptomatic individuals' renal function infected by the virus of the human immunodeficiency (HIV). Forty seven individuals were studied, taking place renal functional tests, as: creatinine clearance, clearance of free water, clearance osmolar, reabsorption tubular proximal and distal of sodium and potassium and urinary pH. The results revealed significant differences (p < 0.05) in the urinary pH, larger in the group with HIV (6.36 +/- 0.41), that in the controls (6.02 +/- 0.41); in the clearance of free water, that indicated reabsorption of larger water in the group with HIV (1.00 +/- 0.64 ml/min) and in the clearance osmolar, that was 2.00 +/- 0.83 ml/min in the group with HIV and 1.57 +/- 0.48 ml/min. The remaining of the indicators of renal function was not shown statistically different between an and other group. It was ended that those differences are significant, in spite of the absolute values they be inside of the normality, because could be associated to late evolutionary alterations of the disease, such as the increase of the frequency of infections of the urinary treatment and the dilution hyponatremia. More studies are necessary for if they confirm those hypotheses.
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PMID:[Renal function aspects in carriers of the human immunodeficiency virus]. 960 36

A prospective semi-longitudinal study was undertaken to determine if urinary neopterin was a predictor for survival in HIV-positive patients. One hundred and one HIV-positive subjects attending a department of genitourinary medicine over a 41-month period were included. Survival data were analysed 6 months after the end of recruitment. Ninety-two subjects were followed up for a minimum of 6 months. Survival figures at 1 and 2 years were 93% (SE 3%) and 79% (SE 5%). There was an inverse relationship between urinary neopterin excretion and 1 and 2-year survival. Two-year survival fell from 70% (SE 6%) for neopterin levels > or = 300 mmol/mol creatinine to 25% (SE 9%) for levels > or = 700 mmol/mol creatinine (P < 0.001). Urinary neopterin may be a useful non-invasive technique in predicting survival in HIV-positive patients.
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PMID:Urinary neopterin as a prognostic index of survival time in HIV-1 infection. 967 Dec 45

Transgenic mice (T26) bearing the envelope, regulatory, and accessory genes of HIV- I develop renal disease resembling human HIV-associated nephropathy (HIVAN). Effects of vehicle (VEH) and the angiotensin-converting enzyme inhibitor captopril (CAP) were examined in wild-type (WT) or T26 mice treated from 7 to 100 d of age. Mortality was lower in CAP T26 mice (30 mg/kg: 8%; 100 mg/kg: 12%) than VEH T26 mice (52%). The urinary protein/creatinine ratio was increased in VEH T26 mice (19.5+/-7.60) versus WT mice (6.1+/-0.83), but not in low-dose (7.3+/-0.94) or high-dose (8.2+/-1.02) CAP T26 mice. Blood urea nitrogen was higher in VEH T26 mice (52+/-16.2 mg/dl) than VEH WT mice (24+/-0.8). Blood urea nitrogen was also elevated in CAP WT (high dose: 43+/-2.1 mg/dl) and T26 mice (high dose: 42+/-2.4 mg/dl). Glomerular injury was higher in VEH T26 mice (6.8+/-0.58) than VEH WT mice (0.2+/-0.08) or CAP T26 mice (low dose: 1.1+/-0.17; high dose: 0.7+/-0.13). Tubulointerstitial injury was also greater in VEH T26 mice (1.1+/-0.10) than VEH WT mice (0.2+/-0.08) or CAP T26 mice (low dose: 0.4+/-0.10; high dose: 0.3+/-0.10). These data validate recent nonrandomized studies of captopril in HIV-infected patients, and suggest that an angiotensin-converting enzyme substrate is an important mediator in HIVAN. A randomized placebo-controlled trial of captopril in HIVAN may be warranted.
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PMID:Captopril prevents nephropathy in HIV-transgenic mice. 969 66

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