Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Benzoate-metabolizing capacity was studied in control subjects and in liver disease patients after intra-venous loading of 15 mg benzoate per kg of body weight. In the 7 control subjects, the mean level (+/- SEM) of Cmax for serum benzoate was 104.1 +/- 6.8 micrograms/ml, AUC was 2.57 +/- 0.32 mg.min/ml, MRT was 21.5 +/- 1.5 min and T1/2 was 15.5 +/- 1.3 min. For serum hippurate, on the other hand, Tmax was 27.9 +/- 6.0 min, Cmax was 33.4 +/- 2.1 micrograms/ml, AUC was 1.96 +/- 0.13 mg.min/ml, MRT was 39.6 +/- 2.9 min and T1/2 was 30.7 +/- 2.4 min. In 12 patients with chronic hepatitis, Cmax, AUC, MRT and T1/2 for benzoate and Tmax, MRT and T1/2 for hippurate remained at control levels, but Cmax and AUC for hippurate were slightly decreased compared to controls. However, in 18 patients with liver cirrhosis, Cmax and AUC for benzoate were in the control range but MRT and T1/2 were significantly delayed (p less than 0.01 for both). Moreover, the MRT value was increased in proportion to the severity of liver disease (p less than 0.01). AUC for hippurate was not changed to any extent, and Tmax, MRT and T1/2 were slightly delayed, while Cmax was significantly reduced. AUC, MRT and T1/2 for benzoate and Tmax, MRT and T1/2 for hippurate showed significant correlation with serum albumin levels, prothrombin time and indocyanine green clearance rate. These results suggest that benzoate-metabolizing capacity, especially as indicated by the MRT value for serum benzoate, appears to be a better index than the indocyanine green clearance rate for determining hepatic functional reserve in chronic liver disease.
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PMID:Clinical significance of benzoate-metabolizing capacity in patients with chronic liver disease: pharmacokinetic analysis. 151 61

A highly sensitive radioimmunossay for arginine8-vasopressin (argipressin; INN) measurement was developed using Amberlite XAD 2 resin columns to extract arginine8-vasopressin from acidified human plasma. Arginine8-vasopressin was determined by a rapid radioimmunoassay method (2 x 20 h) using a specific antibody and 125I-labelled antigen. The bound fraction was separated by adsorption of the free fraction onto bovine serum albumin-coated charcoal; this resulted in low unspecific binding of less than 2%. Recovery experiments in the physiological range resulted in a mean (+/- SEM) recovery of 88 +/- 3%. The radioimmunoassay consistently yielded a detection limit of 0.3 ng/l (ED90) and a mean 50% binding intercept (ED50) of 3.5 ng/l. Arginine8-vasopressin immunoreactivity was characterized by reverse-phase high performance liquid chromatography, which confirmed the specificity of the assay. Serial plasma dilution curves paralleled the standard curve. The intra- and inter-assay variations were 9.4% and 15%, respectively. Arginine8-vasopressin concentrations in healthy subjects were determined in normal hydration status (2.2 +/- 0.3 ng/l; n = 11), as well as during suppression by water immersion (1.5 +/- 0.2 ng/l; n = 11) or by water loading (1.6 +/- 0.2 ng/l; n = 8). Thus, this assay allows for a sensitive, accurate and rapid quantification of plasma arginine8-vasopressin concentrations.
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PMID:A highly sensitive and rapid radioimmunoassay for the determination of arginine8-vasopressin. 152 54

Acute, usually reversible, renal failure has been observed in patients with normal or minimally altered glomeruli on renal biopsy. This review aims to examine the clinical features of acute renal failure in these patients and to evaluate factors that may contribute to the reduction in glomerular filtration rate (GFR). In an analysis of 79 cases affecting 75 patients reported in the English literature since 1966, with acute renal failure associated with minimal change disease or mild histopathological changes in glomeruli, the average age was 58 +/- 2 years (mean +/- 5 SEM), urine protein excretion 11.6 +/- 0.6 g/d, and serum albumin level 19 +/- 1 g/L (1.9 +/- 0.1 g/dL). Acute renal failure was documented an average of 29 +/- 5 days after onset of nephrotic syndrome, and persisted for 7 weeks in 62 episodes in the 58 patients in whom recovery of renal function occurred. Fourteen patients died of uremia or required chronic dialysis, and 3 were lost to follow-up. Although plasma volume depletion was sometimes cited as the cause of renal failure, objective signs of hypovolemia were not documented and most patients did not improve after treatment designed to correct volume deficits. In contrast, histopathological changes consistent with acute tubular necrosis (ATN) were observed in at least 60% of cases. Since the pathogenesis of acute renal failure in minimal change nephrotic syndrome is unknown, we evaluated hemodynamic determinants of GFR in patients with minimal change disease with normal or near-normal renal function, and in relevant animal models, to obtain insights into the effect of nephrotic syndrome on GFR. Although acute renal failure is uncommon, GFR is reduced concurrently with nephrotic syndrome in approximately 30% of children and adults. Absolute and effective blood volume and renal plasma flow are relatively well preserved. However, clinical and experimental observations suggest that the glomerular ultrafiltration coefficient may be reduced by as much as 50%. These findings, together with renal biopsy changes in cases with acute renal failure, suggest that severe reductions in GFR in some patients with minimal change nephrotic syndrome may result from an interaction between acute ischemic tissue injury and preexisting intrinsic renal abnormalities.
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PMID:Reversible renal failure in the nephrotic syndrome. 155 65

Human albumin infusions are frequently administered to patients with nephrotic syndrome. We reviewed the clinical course of 27 patients with minimal change nephrotic syndrome (MCNS) in which 16 patients were treated with human albumin (group A) and 11 were not (group B). The percent of body weight gain, serum total protein, serum albumin, urine protein excretion and renal function were equivalent in both groups as was the initial dose of corticosteroid and amount of dietary protein intake. The period from the start of corticosteroid therapy to complete remission for group A (73.4 +/- 19.2 days, mean +/- SEM) was significantly longer than that for group B (17.1 +/- 3.6), (p less than 0.05). 10 patients of group B (10/11 = 90.9%) showed complete remission within 20 days from the start of corticosteroid therapy, but more than 20 days were needed for 9 cases (9/16 = 56.3%) of group A. Moreover, significant correlations were observed between the period required for remission and the duration of albumin administration (p less than 0.01) or the total volume of albumin infused (p less than 0.01). Proportion of relapsers within 2 years after discharge was also higher in group A (68.8%) than in group B (9.1%), (p less than 0.01). In conclusion, administration of albumin may delay the response to corticosteroid therapy and induce more frequent relapses after remission, possibly due to more severe glomerular epithelial changes induced by albumin infusion in addition to preexisting glomerular epithelial changes from the MCNS.
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PMID:Aggravation of minimal change nephrotic syndrome by administration of human albumin. 156 13

Nineteen patients undergoing elective gastrointestinal surgery were randomised to receive recombination human growth hormone (n = 9) or placebo (n = 10) for the first five postoperative days. All received epidural analgesia and total parenteral nutrition during the same period (energy supply 125% of basal metabolic rate, mean nitrogen (+/- SEM) 5.7 (+/- 0.1) g/m2). Nitrogen and potassium retention was induced in the growth hormone group compared with the placebo group (cumulative nitrogen balance 4.1 (+/- 1.1) g/m2 in the growth hormone group and -3.1 (+/- 1.8) g/m2 in the placebo group, p less than 0.01; cumulative potassium balance 80.8 (+/- 4.7) mmol/m2 in the growth hormone group and 43.1 (+/- 11.4) mmol/m2 in the placebo group, p less than 0.01). In the growth hormone group, serum glucose concentrations increased each evening and mean serum albumin concentrations were reduced throughout the period; the morning pulse rates were decreased, and the patients gained weight compared with the placebo group.
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PMID:Nitrogen retention caused by growth hormone in patients undergoing gastrointestinal surgery with epidural analgesia and parenteral nutrition. 167 77

The toxicity due to interleukin-2 (IL-2) strongly resembles the clinical picture seen during septic shock. In septic shock activation of polymorphonuclear neutrophils (PMN) and the complement system contribute significantly to the pathophysiology of the condition. We therefore investigated whether similar events contributed to the toxicity observed with IL-2. Four patients received seven cycles of escalating dose IL-2 (18.0 to 72.0 X 10(6) IU m-2 day-1) and 16 were treated with 20 cycles of fixed dose IL-2 (12.0 or 18.0 X 10(6) IU m-2 day-1). Toxicity, as judged by hypotension (P = less than 0.005) and capillary leakage (fall in serum albumin 18.2 vs 4.0 gm l-1; P = less than 0.0005 and weight gain 4.0 vs 1.2 kg; P = less than 0.025) were worse with the esc. dose protocol. PMN became activated following IL-2 with mean peak elastase/alpha 1-antitrypsin (E alpha 1 A) and lactoferrin values of 212 (SEM = 37) and 534 (SEM = 92) ng ml-1 respectively occurring 6 h after the IL-2. Peak values for the esc. dose IL-2 group being generally higher than 500 ng ml-1. Activation of the complement cascade was evidenced by a dose dependent elevation of peak C3a values (fixed dose 9.1 (SEM = 0.6); esc. dose 25.7 (SEM = 6.33); P = less than 0.005) on day 5 of IL-2. There was a significant correlation between C3a levels and the degree of hypotention during the first 24 h after IL-2 (r = 0.91) and parameters of capillary leakage such as weight gain and fall in serum albumin (r = 0.71). These data suggest that activation of PMN initiates endothelial cell damage which subsequently leads to activation of the complement cascade. This latter system then contributes to the haemodynamic changes and capillary leakage seen in IL-2 treated patients.
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PMID:The activation of polymorphonuclear neutrophils and the complement system during immunotherapy with recombinant interleukin-2. 173 48

The effects of concurrent administration of albumin with total parenteral nutrition were studied in 12 premature newborns (birth weight 1.26 +/- 0.1 kg [mean +/- SEM] and gestational age 30 +/- 0.8 weeks [mean +/- SEM]) compared with a control group of 12 premature newborns (birth weight 1.17 +/- 0.2 kg and gestational age 29 +/- 0.1 weeks) who received total parenteral nutrition. All newborns had a plasma albumin level below 3 g/dL and were in cardiorespiratory distress requiring assisted ventilation. Albumin supplementation of total parenteral nutrition resulted in a sustained increase in serum albumin concentration as well as increased mean arterial blood pressures in the study group. Slow albumin infusion had no observed effect on the severity of respiratory distress. Study group infants regained birth weight earlier than control group infants. These data suggest that the concurrent administration of albumin may be clinically beneficial in critically ill newborn infants.
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PMID:Concurrent administration of albumin with total parenteral nutrition in sick newborn infants. 173 19

This study compares the nutritional status and dietary intake of 14 tubefed nursing home patients with pressure sores (age: 70 +/- 5 years, mean +/- SEM) to 12 tubefed patient-controls without sores (age: 60 +/- 7 years). Patients tended to have higher calorie intake (32 +/- 3 kcal/kg) than patient-controls (26 +/- 2 kcal/kg, p = 0.11). Protein intake was significantly higher in patients (1.4 +/- 0.2 g/kg) than patient-controls (0.9 +/- 0.1 g of protein per kg, p less than 0.05). Despite increased calorie and protein intake, biochemical measures of nutritional status were worse in the patients. Serum albumin was lower in patients (33 +/- 1 g/L) than in patient-controls (37 +/- 1 g/L, p less than 0.05) as was level of hemoglobin (patients: 117 +/- 5; patient-controls: 132 +/- 5 g/L, p less than 0.05). Patients with stage IV (severe) sores had lower serum cholesterol levels (3.46 +/- 0.31 mmol/L, n = 5) than patients with stage II/III (milder) sores (4.58 +/- 0.23 mmol/L, n = 9, p less than 0.05). Plasma zinc was low in both patients (11.2 +/- 0.6 mumol/L) and patient-controls (11.5 +/- 0.7 mumol/L, p = NS). Pressure sore surface area was positively correlated with calorie intake per kilogram of body weight (r = +0.59, p less than 0.04) and negatively correlated with body mass index (r = -0.70, p less than 0.03), hemoglobin (r = -0.55, p less than 0.07) and serum cholesterol (r = -0.57, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malnutrition in tubefed nursing home patients with pressure sores. 176 57

We developed a simple and sensitive radioimmunoassay (RIA) for adenosine. The RIA is based on the double antibody method with adenosine 2', 3'-0-disuccinyl-3-[125I]-iodotyrosine methyl ester (diSc-adenosine-[125I]-TME) as a tracer. Anti-adenosine antiserum for the RIA was raised in rabbits immunized with diSc-adenosine conjugated to human serum albumin (diSc-adenosine-HSA). All samples and standards were succinylated prior to assay. The present immunoassay allows detection of 6.25-400 pmol/ml of adenosine in sample. Values obtained by the RIA and by a HPLC analysis showed a high correlation with correlation coefficient of 0.997. In order to determine adenosine in plasmas, blood cells must be separated in the presence of 6 mM EDTA, 0.006% dipyridamole (Dip) and 23 microM 2'-deoxycoformycin (dCF) at 2 degrees C. Adenosine in plasma could be accurately determined by the proposed method even without any pretreatments by deproteinizing. The adenosine levels with or without EDTA-treated normal human plasmas determined were 26.2 +/- 7.26 and 100 +/- 3.62 pmol/ml (mean +/- SEM), respectively.
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PMID:A simple and sensitive radioimmunoassay for adenosine. 180 86

The effects of angiotensin converting enzyme inhibitors (ACEI) on proteinuria, renal function, and serum proteins were evaluated in six children with steroid-resistant nephrotic syndrome and proteinuria of 3-15 g/24 h (277 +/- 47 mg/m2 per hour). Following ACEI, proteinuria decreased from 7,408 +/- 2,385 (mean +/- SEM) to 3,746 +/- 1,395 mg/24 h (P less than 0.05). Creatinine clearance was 87.8 +/- 22.6 before and 96.4 +/- 23.6 ml/min per 1.73 m2 after ACEI. In two patients, inulin and para-aminohippuric acid clearances were normal before and after ACEI, together with parallel reductions of urine protein of 50% and 46%. Clearance of total protein was reduced by 56% following ACEI, compared with reduction in the clearance of gamma globulin by 58% and albumin by 39.5%. No significant change was seen in blood pressure, serum albumin, or total protein following ACEI. After ACEI, diuretic doses were able to be reduced or eliminated in three patients. Reduction of proteinuria was sustained during a followup period of 11-20 months in three patients. ACEI may be of benefit in the clinical management of children with steroid-resistant nephrotic syndromes, allowing reduction in diuretic requirements.
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PMID:Angiotensin converting enzyme inhibitors for reduction of proteinuria in children with steroid-resistant nephrotic syndrome. 191 Nov 44


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