D-062

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关键词:'D-062'

显示 1-27 共 27 条结果关于 "D-062" 范围论文

Cortisol, aldosterone, cortisol precursor, androgen and endogenous ACTH concentrations in dogs with pituitary-dependant hyperadrenocorticism treated with trilostane.

N S Sieber-Ruckstuhl et al.

Domestic animal endocrinology, 31(1), 63-75 (2005-10-20)

Trilostane is thought to be a competitive inhibitor of the 3beta-hydroxysteroid dehydrogenase (3beta-HSD), an essential enzyme system for the synthesis of cortisol, aldosterone and androstenedione. Due to its reliable clinical efficacy, trilostane is increasingly used to treat dogs with pituitary-dependant

Hirsutism and acne in women: coordinated radioimmunoassays for eight relevant plasma steroids.

J Fiet et al.

Clinical chemistry, 40(12), 2296-2305 (1994-12-01)

We developed and validated a coordinated set of RIAs for the following eight steroids in single small aliquots (< or = 1 mL) of plasma: androstenedione, dehydroepiandrosterone, 11-deoxycortisol, 21-deoxycortisol (21-DF), 11 beta-hydroxyandrostenedione, 17 alpha-hydroxypregnenolone (17-Hpreg), 17 alpha-hydroxyprogesterone, and testosterone. Samples

Radioimmunoassay of three deoxycorticoids in human plasma following HPLC separation.

M Hill et al.

Steroids, 60(9), 615-620 (1995-09-01)

A radioimmunoassay of three deoxycorticoids, namely 11 beta,17 alpha-dihydroxy-4-pregnene-3,20-dione (21-deoxycortisol), 17 alpha,21-dihydroxy-4-pregnene-3,20-dione (11-deoxycortisol), and 21-hydroxy-4-pregnene-3,20-dione (11-deoxycorticosterone) which are important for differential diagnosis of congenital adrenal disorders, is described and evaluated. Antisera against 3-(O-carboxymethyl)oximes conjugated to bovine serum albumin were raised

21-hydroxylase deficiency transiently mimicking combined 21- and 11beta-hydroxylase deficiency.

Vânia Tonetto-Fernandes et al.

Journal of pediatric endocrinology & metabolism : JPEM, 21(5), 487-494 (2008-07-29)

21-Hydroxylase deficiency (21OHD) is the commonest form of congenital adrenal hyperplasia, while 11betaOHD represents 5% of cases. Although both result from mutations in distinct genes, cases of 'apparent' combined 21OHD and 11betaOHD (AC21,11OHD) have been occasionally reported. A 6 year-old

Surface-activated chemical ionization ion trap mass spectrometry in the analysis of 21-deoxycortisol in blood.

Simone Cristoni et al.

Rapid communications in mass spectrometry : RCM, 18(12), 1392-1396 (2004-06-03)

Menstrual disturbance and hypersecretion of progesterone in women with congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

D J Holmes-Walker et al.

Clinical endocrinology, 43(3), 291-296 (1995-09-01)

While menstrual disturbance is often quoted as a feature of congenital adrenal hyperplasia (CAH), little is known about the mechanism of this symptom. We set out to determine the relationship between menstrual pattern and biochemical characteristics of women with CAH

The application of a new highly-sensitive radioimmunoassay for plasma 21-deoxycortisol to the detection of steroid-21-hydroxylase deficiency.

J Fiet et al.

Annals of clinical biochemistry, 31 ( Pt 1), 56-64 (1994-01-01)

21-deoxycortisol (21-DF) is a steroid of strictly adrenal origin formed by the 11-hydroxylation of 17-hydroxyprogesterone. This metabolic pathway is minor in normal subjects, in whom basal plasma concentrations range from 0.03 to 0.63 nmol/L and from 0.865 to 1.50 nmol/L

Newborn screening for congenital adrenal hyperplasia: additional steroid profile using liquid chromatography-tandem mass spectrometry.

N Janzen et al.

The Journal of clinical endocrinology and metabolism, 92(7), 2581-2589 (2007-04-26)

Neonatal screening programs for congenital adrenal hyperplasia (21-CAH) using an immunoassay for 17alpha-hydroxyprogesterone (17-OHP) generate a high rate of positive results attributable to physiological reasons and to cross-reactions with steroids other than 17alpha-OHP, especially in preterm neonates and in critically

Premature pubarche in Mediterranean girls: high prevalence of heterozygous CYP21 mutation carriers.

Françoise Paris et al.

Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology, 26(5), 319-324 (2010-01-12)

This study investigated the prevalence and consequences of heterozygous CYP21A2 mutations in premature pubarche (PP) girls. We investigated 36 French Mediterranean girls with isolated PP. We performed synacthen testing with 17OHP and 21-deoxycortisol evaluation, along with molecular analysis of the

Two novel mutations in splice donor sites of CYP11B1 in congenital adrenal hyperplasia due to 11beta-hydroxylase deficiency.

O Chabre et al.

Endocrine research, 26(4), 797-801 (2001-02-24)

We present an in vivo and in vitro study of congenital adrenal hyperplasia in a patient with 11beta-hydroxylase deficiency. Genetic analysis showed two new base substitutions of CYP11B1, a conservative transition at the last base of exon 5, and a

[21-Deoxycortisol].

Y Okatani

Nihon rinsho. Japanese journal of clinical medicine, 53 Su Pt 2, 444-447 (1995-03-01)

Exhaustive screening of the 21-hydroxylase gene in a population of hyperandrogenic women.

H Blanché et al.

Human genetics, 101(1), 56-60 (1998-01-07)

21-hydroxylase (21-OH) deficiency accounts for the vast majority of nonclassic (NC) forms of congenital adrenal hyperplasia (CAH), and is associated with symptoms detectable either in childhood (precocious puberty) or sometimes only later in adulthood (hirsutism, acne, amenorrhea). While the severe

Analysis of 21-deoxycortisol, a marker of congenital adrenal hyperplasia, in blood by atmospheric pressure chemical ionization and electrospray ionization using multiple reaction monitoring.

Simone Cristoni et al.

Rapid communications in mass spectrometry : RCM, 18(1), 77-82 (2003-12-23)

Congenital adrenal hyperplasia (CAH) is an autosomal recessive disorder mainly caused by 21-hydroxylase deficit (21-OHD). Deletions or mutations of the CYP21 gene induce the impairment of glucocorticoid and mineralcorticoid synthesis. 17-Hydroxyprogesterone (17-OHP) is the hormonal marker in patients, but not

Evaluation of cortisol precursors for the diagnosis of pituitary-dependent hypercortisolism in dogs.

N S Sieber-Ruckstuhl et al.

The Veterinary record, 162(21), 673-678 (2008-05-27)

The serum concentrations of cortisol, 17alpha-hydroxypregnenolone, 17alpha-hydroxyprogesterone, 21-deoxycortisol and 11-deoxycortisol were measured in 19 healthy dogs, 15 dogs with pituitary-dependent hypercortisolism (pdh) and eight dogs with other diseases before and one hour after an injection of synthetic adrenocorticotrophic hormone (acth).

Neonatal screening: identification of children with 11β-hydroxylase deficiency by second-tier testing.

Nils Janzen et al.

Hormone research in paediatrics, 77(3), 195-199 (2012-04-18)

21-Hydroxylase deficiency (21-OHD) is the target disease of newborn screening for congenital adrenal hyperplasia (CAH). We describe the additional detection of patients suffering from 11β-hydroxylase deficiency (11-OHD) by second-tier testing. Over a period of 5 years, screening for CAH was

Zona fasciculata 21-hydroxysteroids and precursor-to-product ratios in 21-hydroxylase deficiency: further characterization of classic and non-classic patients and heterozygote carriers.

F A Costa-Barbosa et al.

Journal of endocrinological investigation, 34(8), 587-592 (2010-10-07)

Although much is known about the increased levels of the 21-hydroxylase substrates 17-hydroxyprogesterone (17OHP) and 21-deoxycortisol (21DF) - the biochemical markers of all forms of 21-hydroxylase deficiency (21OHD), only limited information is available on the zona fasciculata (ZF) products distal

[11-deoxycortisol and 21-deoxycortisol].

Y Okatani et al.

Nihon rinsho. Japanese journal of clinical medicine, 57 Suppl, 129-133 (2000-04-25)

Evaluation of 21-deoxycortisol as a marker for the detection of heterozygous carriers of 21-hydroxylase deficiency.

A Milewicz et al.

Endokrynologia Polska, 44(2), 187-193 (1993-01-01)

The study was aimed at evaluation of usefulness of determination of blood serum 21-deoxycortisol concentration for the detection of heterozygous carriers of incomplete block of 21-hydroxylase synthesis leading to adrenal hyperplasia. An earlier observation of the authors that the determination

Apparent activities of 21-hydroxylase, 17alpha-hydroxylase and 17,20-lyase are impaired in adrenal incidentalomas.

J L Sadoul et al.

European journal of endocrinology, 141(3), 238-245 (1999-09-04)

An increased response of 17-hydroxyprogesterone to ACTH stimulation has been observed in adrenal incidentaloma and linked to an impairment of either 21-hydroxylase or of 11beta-hydroxylase activity. To analyse this question further, we investigated the steroidogenic pathways in a series of

Diagnosis of adrenal cortical dysfunction by liquid chromatography-tandem mass spectrometry.

P C Kao et al.

Annals of clinical and laboratory science, 31(2), 199-204 (2001-05-08)

Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to measure 6 metabolic compounds of the adrenocorticosteroid pathway simultaneously on residual specimens from patients who had previously been previously diagnosed, on the basis of immunoassays, as having congenital adrenal hyperplasia (CAH), 11

Diagnosing Cushing's syndrome.

A A Ismail et al.

Annals of clinical biochemistry, 35 ( Pt 2), 324-325 (1998-04-21)

Superior discriminating value of ACTH-stimulated serum 21-deoxycortisol in identifying heterozygote carriers for 21-hydroxylase deficiency.

Flávia A Costa-Barbosa et al.

Clinical endocrinology, 73(6), 700-706 (2010-09-18)

Congenital adrenal hyperplasia caused by classic 21-hydroxylase deficiency (21OHD) is an autosomal recessive disorder with a high prevalence of asymptomatic heterozygote carriers (HTZ) in the general population, making case detection desirable by routine methodology. HTZ for classic and nonclassic (NC)

Serum 21-Deoxycortisol, 17-Hydroxyprogesterone, and 11-deoxycortisol in classic congenital adrenal hyperplasia: clinical and hormonal correlations and identification of patients with 11beta-hydroxylase deficiency among a large group with alleged 21-hydroxylase deficiency.

Vania Tonetto-Fernandes et al.

The Journal of clinical endocrinology and metabolism, 91(6), 2179-2184 (2006-03-23)

21-Hydroxylase deficiency (21OHD) is the most common cause of congenital adrenal hyperplasia, followed in frequency by 11beta-hydroxylase deficiency (11betaOHD). Although the relative frequency of 11betaOHD is reported as between 3 and 5% of the cases, these numbers may have been

Plasma 21-deoxycortisol: comparison of a time-resolved fluoroimmunoassay using a biotinylated tracer with a radioimmunossay using (125)iodine.

J Fiet et al.

The Journal of steroid biochemistry and molecular biology, 72(1-2), 55-60 (2000-03-25)

Plasma 21-deoxycortisol (21DF) is an excellent marker of 21-hydroxylase deficiency. Currently, it is the only marker able to detect heterozygous carriers with 21-hydroxylase deficiency after ACTH stimulation. We have already developed radioimmunoassays for 21DF using first tritiated, then 125I-21DF which

Late diagnosis of congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

K Müssig et al.

Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association, 114(4), 208-214 (2006-05-18)

Congenital adrenal hyperplasia results from 21-hydroxylase deficiency in more than ninety percent of cases. The classical form of 21-hydroxylase deficiency presents in the neonatal period with virilization or adrenal insufficiency, with or without concurrent salt wasting. We report on a

Association between the insertion/deletion polymorphism of the angiotensin I-converting enzyme gene and risk for psoriasis in a Chinese population in Taiwan.

Y-C Chang et al.

The British journal of dermatology, 156(4), 642-645 (2007-02-01)

Genetic factors play an important role in susceptibility for psoriasis. The angiotensin I-converting enzyme (ACE) is expressed by keratinocytes. Administration of ACE inhibitors may induce or exacerbate psoriasis in clinical practice. Thus, ACE gene variants may contribute to the genetic

Host genetic background at CCR5 chemokine receptor and vitamin D receptor loci and human immunodeficiency virus (HIV) type 1 disease progression among HIV-seropositive injection drug users.

Y Barber et al.

The Journal of infectious diseases, 184(10), 1279-1288 (2001-10-27)

The effect of polymorphisms on genes encoding the CCR5 chemokine receptor and vitamin D receptor (VDR) in human immunodeficiency virus (HIV) type 1 disease progression was analyzed in a cohort of 185 HIV-seropositive injection drug users. Results confirmed a lack

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