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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Direct radioimmunoassay are described for the measurement of each of three specific estrogen glucosiduronates: estrone glucosiduronate, 17 beta-estradiol-17-glucosiduronate and estriol-16 alpha-glucosiduronate in urine. Each assay utilizes a specific antiserum prepared by complexing the carboxylic acid group of the appropriate glucosiduronate to the epsilon-amino group of lysine in bovine serum albumin or bovine thyroglobulin. The antisera showed little or no cross reactivity toward other estrogens that might be present in significant amounts in urine. These antisera were used for the direct assay of the conjugates in urine from normal men and nonpregnant women without prior extraction or chromatography. The values were similar to those obtained after extraction, chromatographic purification on DEAE-Sephadex and subsequent immunoassay; The following mean values +/- SE (microgram/g creatinine) were obtained: estrone glucosiduronate, male 10.1 +/- 0.6, follicular phase female 17.3+/- 1.6, luteal phase female 31.8 +/- 2.5; 17 beta-estradiol-17-glucosiduronate, male 1.7 +/- 0.3, follicular phase female 2.4 +/- 0.1, luteal phase female 4.2 +/- 0.4; estriol-16 alpha-glucosiduronate, male 1.8 +/- 0.2, follicular phase female 4.7 +/- 0.9, luteal phase female 10.0 +/- 1.6.
Steroids 1978 Mar
PMID:Direct radioimmunoassay of specific urinary estrogen glucosiduronates in normal men and nonpregnant women. 20 99

Intravenous infusions of 14C-testosterone (Te) either alone or in combination with 3H-estradiol (E2) were given to five normal male subjects, twelve male patients on haemodialysis (HD) treatment and to one patient with a very restricted renal function. The elimination of radioactivity was measured in urine, HD fluid and faeces. Urinary excretion diminished with renal function. It was negligible at a creatinine clearance of less than one ml per minute. A quarter of both isotopes was eliminated by six HD treatments within three weeks. No difference was found in this respect between nephrectomized patients and those who were still in possession of their kidneys. The main excretion occurred in the stools. E2 metabolites, and to a lesser extent Te metabolites, appeared in the faeces within 24 hours, which might be explained by biliary excretion only. More 3H (E2 metabolites) than 14C (Te metabolites) was found in the faeces; more 14C than 3H found in HD fluid.
Steroids 1975 Oct
PMID:The excretion of metabolites of testosterone and of estradiol in male patients with chronic renal failure. 120 65

This article describes concepts of drug treatment for patients with severe renal failure (creatinine clearance less than 10 ml/min), especially in intensive care. These subjects often develop multiorgan failure and require special considerations: 1. Not only should the maintenance dose of digoxin be reduced to 0.05-0.1 mg/day, but the loading or digitalizing dose should also be diminished to 0.4-0.6 mg. 2. Penicillins, cephalosporins, quinolones, and other antibiotics with a high therapeutic ratio can be given as recommended by the manufacturer or reference lists according to renal insufficiency. 3. For drugs with a low therapeutic index, such as aminoglycosides, vancomycin, flucytosine, some antiarrhythmic agents, cardiac glycosides, and theophylline, therapeutic drug monitoring is mandatory. 4. Steroids, insulin, atropine, catecholamines, anticoagulants, thrombolytic agents, antihypertensive drugs, and organic nitrates can be given according to their effect. However, nitroprusside should be discontinued after 2 days because its metabolites may be toxic. 5. The dose of H2-receptor antagonists used for the control of gastric acidity and the treatment of peptic ulcers should be reduced to 20-50% of the normal. The administration of aluminum, magnesium, and bismuth compounds should be avoided. 6. Loop diuretics (e.g., furosemide) can be effective at increased doses in patients with chronic renal failure and fluid overload, particularly when used in combination with a thiazide in refractory edema. Thiazides alone are useless, and potassium-sparing diuretics are contraindicated. 7. Colloid-containing solutions should be infused cautiously at a maximal rate of 2 x 500 ml/week only when the plasma volume is contracted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal failure--concepts for drug therapy in intensive care]. 181 28

Between January 1, 1984 and October 1, 1988, 36 cadaveric kidney transplantations were performed in 60 to 66 years' old patients (mean: 62.4 years). Induction immunosuppression consisted of rabbit antithymocyte globulins for 10 days or 33B3.1, an anti RIL2 monoclonal antibody (n = 6), with azathioprine and corticosteroids (less than 1 mg/kg/day). Cyclosporin A (CSA) was given on day 10 in doses of 8 mg/kg/day. Steroids were withdrawn on day 45. Actuarial patient and graft survivals were 66 per cent and 80.5 per cent respectively at 1 and 2 years. Mean +/- SD serum creatinine level was 178 +/- 77 mumol/l at one year. The mean CSA dose adjusted to total blood CSA levels was 4.75 +/- 1.7 mg/kg. Five patients died in the first quarter, 2 of opportunistic infections, 2 of cardiovascular disease and 1 of gastric haemorrhage. The prevalence of rejection episodes during the first 3 months was lower than in the general population (22 per cent vs 27 per cent); all were reversible with bolus injections of corticosteroids. These results indicate that kidney transplantation can successfully be performed in elderly patients with a low rejection rate and an excellent long-term graft survival. However, the mortality was higher than in younger recipients.
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PMID:[Kidney transplantation after 60 years of age. Survival of patients and functional results]. 213 14

Thyroid dysfunction in humans is known to alter the excretory pattern of estrogen metabolites, suggesting that thyroid hormone directly influences the oxidative metabolism of estradiol. We examined the extent to which a brief period of hyperthyroidism specifically affected estradiol hydroxylation at C-2 and C-16 alpha, the two primary and competing sites of estrogen oxidation, using an in vivo radiometric assay in healthy male volunteers. Hydroxylation at C-2 was increased by a 2-week course of thyroxine (4.3 micrograms/kg/d) from 29.9% +/- 2.6% to 35.9% +/- 3.1% (P = 0.04), while 16 alpha-hydroxylation was unchanged (10.3% +/- 0.8% versus 9.3% +/- 0.5%). The greater extent of oxidation at C-2 was evidenced by a twofold increase in the urinary excretion of 2-hydroxyestrone (2.88 +/- 0.32 versus 5.30 +/- 0.85 micrograms/g creatinine), while the excreted products of 16 alpha-hydroxylation were unchanged. At the same time, significant reductions in total cholesterol (173.8 +/- 7.9 versus 139.4 +/- 8.9 mg/dl), low-density lipoprotein cholesterol (110.0 +/- 5.3 versus 83.8 +/- 7.7 mg/dl), and apolipoprotein B (68.2 +/- 3.3 versus 53.1 +/- 3.6 mg/dl) were observed. Serum levels of estrone, estradiol, sex hormone-binding globulin, high-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, triglycerides, and apolipoprotein A-I were not significantly affected. This study adds to the growing evidence that catechol estrogen production in humans is more readily regulated than 16 alpha-hydroxylation, which is relatively refractory to treatment.
Steroids 1990 Jan
PMID:Effects of exogenous thyroxine on C-2 and C-16 alpha hydroxylations of estradiol in humans. 230 54

A 57-year-old male with mild impairment of renal function secondary to diabetic glomerulosclerosis developed acute renal failure (creatinine 32.4 mg/dl) associated with a generalized desquamative skin rash and peripheral eosinophilia shortly after initiation of antihypertensive therapy with captopril. An acute interstitial nephritis was demonstrated on renal biopsy, and improvement was temporally related to initiation of therapy with prednisone. A review of the literature revealed 5 similar cases in whom acute deterioration of renal function occurred following initiation of captopril and in whom there were features of a hypersensitivity reaction, including skin rash, fever, eosinophilia, azotemia, eosinophiluria, and a Coombs-positive hemolytic anemia. Renal biopsy, where available, revealed an acute interstitial nephritis. Observations from these cases suggest that, of the angiotensin-converting enzyme inhibitors, this syndrome appears to be specific for captopril, begins within the 1st month of therapy, is not dose-dependent, and generally resolves on cessation of therapy. Steroids may hasten recovery, but sufficient data are not available to confirm their efficacy.
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PMID:Captopril-associated acute interstitial nephritis. 252 7

The measurement of urinary estradiol-17-sulfate concentration by direct radioimmunoassay was established. The urinary estradiol-17-sulfate levels measured by the radioimmunoassay correlated well with those determined by high-performance liquid chromatography equipped with electrochemical detector. Estradiol-17-sulfate concentrations in early morning urine of six healthy adult men was 8.2 +/- 2.0 ng/mL, or 5.7 +/- 1.8 ng/mg creatinine. The urinary levels in women throughout the menstrual cycle showed a characteristic three-peak excretion pattern: the first and the second peaks appeared just after and three days before the urinary LH peak, and the third peak appeared a few days before menstruation.
Steroids
PMID:Determination of estradiol-17-sulfate in human urine by a direct radioimmunoassay: urinary levels throughout the menstrual cycle. 285 67

A nonsteroid antiinflammatory agent (Ibuprofen) was used in a controlled randomized study to determine its ability to replace steroids in the prophylaxis of cadaveric kidney rejection. Thirty-three cadaver kidney recipients were randomly assigned either to a control group (16 patients) receiving azathioprine, high doses of prednisolone, and antithymocyte globulin (ATGAM) for three months, or to an experimental group (17 patients) receiving azathioprine and ATGAM according to the same protocol, ibuprofen instead of steroids. The frequency of rejection was higher in the experimental group (2.18 episodes per patient) than in the control group (1.44 episodes per patient). Nevertheless, in the experimental group 5 patients had no early rejection episode, 60% of early rejections were totally reversible without steroids, and 3 patients never received steroids at all during the first year and had normal renal function and biopsies. Steroids had to be introduced in the treatment of 14 patients, but after an average period of 32.5 days after surgery OKT3+ cell level was higher in the experimental group than in the control group, but similar to the OKT3+ cell level of patients receiving conventional therapy without ATGAM. Whatever the type of treatment, an increase in the OKT4+/OKT8+ ratio was associated in most cases with increased serum creatinine values. Conversely, a decreased OKT4+/OKT8+ ratio associated with renal failure was found in cases showing biological evidence of cytomegalovirus infection.
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PMID:Nonsteroid antiinflammatory agents as a substitute treatment for steroids in ATGAM-treated cadaver kidney recipients. 642 Sep 59

Because of the high rate of spontaneous remission, treatment of membranous nephropathy with prednisolone and chlorambucil is still controversial. The aim of this study was to give this therapy only to those patients at risk of developing renal insufficiency and to test the efficacy of a low-dose therapeutic regimen. Seventeen patients with more than 10 g protein excretion per day (mean 16.9) and/or a deterioration in renal function (mean serum creatinine, 162 mumol/l) were included. Serum total protein, serum lipids, proteinuria, serum creatinine, and blood pressure were measured, along with the diuretic and antihypertensive medication. The observation time before the start of treatment was 27 +/- 27 months. Steroids were given during months 1, 3, and 5 (methylprednisolone 3 x 500 mg intravenously) prednisolone 0.5 mg/kgBW daily per os for 1 week, then tapered by 0.1 mg/kg BW/week for 1 month). Chlorambucil was given during months 2, 4, and 6 at a dose of 0.12 mg/kgBW daily. At the end of treatment proteinuria had significantly decreased (mean of all patients, 7.8 +/- 1.4 g/d) in all patients. Six months after the end of treatment proteinuria was significantly lower than at baseline in 14 of 17 patients. Hypoproteinemia and hyperlipidemia had improved; diuretic and antihypertensive medication were reduced. Elevated serum creatinine decreased in 7 of 9 patients (pretreatment, 227 +/- 39 mumol/l; 6 months, 176 +/- 28 mumol/l). Nonresponders with respect to serum creatinine responded with respect to proteinuria. Regarding adverse effects, two patients complained of dyspepsia while taking steroids; during chlorambucil treatment two patients experienced nausea and lack of appetite, and one developed leukopenia (1600/microliters).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low-dose prednisolone/chlorambucil therapy in patients with severe membranous glomerulonephritis. 804 74

A commercial 125I radioimmunoassay designed for the quantification of dehydroepiandrosterone sulfate (DHEAS) in blood samples was tested for its direct applicability to 24-hour urine samples from children and adults. Average recoveries in parallelism and spiking experiments were found to be near 100%. Intra- and inter-assay coefficients of variation were below 10%. Urinary DHEAS concentrations determined directly by the radioimmunoassay (x) differed only slightly from corresponding radioimmunoassay values (y) obtained after C18 reversed-phase extraction and LH-20 chromatography (y = 0.85x + 0.12; r = 0.99). Cross-reactivity data from related steroids suggested only a small contribution to the DHEAS titer by other steroids. In 8-year-old children compared to preadrenarchal children (4 years old) a clearly increased median daily urinary DHEAS output could be observed both for absolute excretion data (0.163 versus 0.05 mumol/d, P < 0.01) and for excretion values related to body surface area (0.181 versus 0.071 mumol/d/1.73 m2, P < 0.05). However, this "onset of adrenarche" was no longer statistically significant when urinary creatinine was taken as adjustment parameter for renal androgen sulfate output. After correction with the individual body surface area, rises of urinary DHEAS from childhood to adulthood were nearly in the order of the literature data on age-corresponding serum increases of DHEAS. In conclusion, the direct radioimmunological quantification of DHEAS in 24-hour urine samples with subsequent correction for individual body surface area appears to present a physiologically meaningful way to assess the adrenal gland's secretory activity for this androgen sulfate.
Steroids 1994 Jan
PMID:Measurement of urinary androgen sulfates without previous hydrolysis: a tool to investigate adrenarche. Validation of a commercial radioimmunoassay for dehydroepiandrosterone sulfate. 814 May 96


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