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PubMed1999

Longitudinal measurements of 17alpha-hydroxyprogesterone in premature infants during the first three months of life.

AIMS: To determine normal concentrations of 17alpha-hydroxyprogesterone (17OHP) for premature infants. METHODS: 17OHP was measured in 66 consecutive premature infants once a week during the first month, and once every two weeks thereafter, until the age of 3 months. The 17OHP values in 100 full term healthy neonates on the third day of life served as controls. Blood was sampled on filter paper using a neonatal radioimmunoassay kit. Findings were correlated with gestational age, birthweight, mode of delivery, Apgar scores, presence of respiratory distress syndrome and intake of maternal steroids. RESULTS: Mean 17OHP was raised at 7 days of age (138.9, 46.3, 53.3, 29.9 nmol/l, respectively, for infants whose gestational age was under 29 weeks, 29 to 30 weeks, 31 to 32 weeks, and 33 weeks and above). It fell sharply in the first two weeks after which it gradually decreased further, reaching 32.7, 23.6, 16.9, and 13.0 nmol/l, respectively, by the age of 90 days. The mean (SEM) 17OHP concentration in full term infants on day 3 of life was 17.8 (8.9) nmol/l. These values were independent of the presence and severity of respiratory distress syndrome and of prenatal maternal steroids. CONCLUSIONS: The increased 17OHP concentrations found at birth fell to those found in term infants during the first three months of life in infants over 31 weeks of gestation. Postconceptional age is the most important factor determining 17OHP concentration.

17-alpha-Hydroxyprogesterone↗

PubMed2004

Exaggerated 17-hydroxyprogesterone response to intravenous infusions of recombinant human LH in women with polycystic ovary syndrome.

Studies using pharmacological gonadotropin stimulation suggest that ovarian steroidogenesis is abnormal in the polycystic ovary syndrome (PCOS). We assessed ovarian steroid secretion in response to near-physiological gonadotropin stimuli in 12 ovulatory controls and 7 women with PCOS. A gonadotropin-releasing hormone-receptor antagonist (ganirelix, 2 mg sc) was given to block endogenous LH secretion, followed by dexamethasone (0.75 mg orally) to suppress adrenal androgen secretion. After ganirelix injection (12 h), intravenous infusions of recombinant human LH (0, 10, 30, 100, and 300 IU; each over 8 min) were administered at 4-h intervals in a pseudorandomized (highest dose last) manner. Plasma LH, 17-hydroxyprogesterone (17-OHP), androstenedione, and testosterone were measured concurrently. LH dose-steroid response relationships (mean sex-steroid concentration vs. mean LH concentration over 4 h postinfusion) were examined for each subject. Linear regression of 17-OHP on LH yielded a higher (mean +/- SE) slope in PCOS (0.028 +/- 0.010 vs. 0.005 +/- 0.005, P < 0.05), whereas extrapolated 17-OHP at zero LH was similar. The slopes of other regressions did not differ from zero in either PCOS or controls. We conclude that near-physiological LH stimulation drives heightened 17-OHP secretion in patients with PCOS, suggesting abnormalities of early steps of ovarian steroidogenesis. With the exception of 17-OHP response in PCOS, no acute LH dose-ovarian steroid responses were observed in controls or PCOS. Defining the precise mechanistic basis of heightened precursor responsiveness to LH in PCOS will require further clinical investigation.

17-alpha-Hydroxyprogesterone↗

PubMed1999

Luteal phase support with 17alpha-hydroxyprogesterone versus unsupported cycles in in vitro fertilization: a comparative randomized study.

This study was designed to determine the efficacy of 17alpha-hydroxyprogesterone caproate (17-OHPc) for luteal phase support in in vitro fertilization (IVF). For this purpose, a total of 86 IVF patients undergoing embryo transfer were randomly allocated to two groups as follows: (1) group A, including 43 patients who received the support of luteal phase through the intramuscular administration of 17-OHPc at a dosage of 341 mg every 3 days, and (2) group B, including 43 patients who received the intramuscular administration of a saline solution as placebo every 3 days. In both groups, the treatment was started within 24 h after embryo transfer until beta-HCG evaluation. In case of positive beta-HCG, it was extended until 12 weeks. Efficacy was assessed using the pregnancy rates, which was, per transfer, statistically significantly higher in group A than in group B (32.5 vs. 18.3% respectively). On the basis of our results, we emphasize the use of 17-OHPc for luteal phase support after IVF and embryo transfer.

17-alpha-Hydroxyprogesterone↗

PubMed2000

Cortisol and 17-hydroxyprogesterone levels in saliva of healthy neonates: normative data and relation to body mass index, arterial cord blood ph and time of sampling after birth.

The measurement of cortisol and 17-hydroxyprogesterone (17-OHP) in saliva has become a reliable tool for both the scientist and the clinician for studying adrenal cortical function in the adult and the older child. We have now established in parallel normative data for salivary cortisol and 17-OHP levels in healthy neonates. We have asked whether or not there is a circadian rhythm of cortisol and 17-OHP saliva levels in neonates. Furthermore, we have asked whether salivary hormone levels correlated with auxologic and clinical data and time of sampling. Cortisol and 17-OHP levels in saliva samples from 119 healthy neonates (55 girls, 64 boys) were measured using in-house time-resolved fluorescent immunoassays. Saliva samples were obtained using a saliva collecting tube three times a day on the first or second day of life. Gender and gestational age did not influence salivary cortisol and 17-OHP levels. No significant circadian rhythm of salivary hormone levels was detected in this group of newborns. However, body mass index, arterial cord blood pH and time of saliva sampling significantly influenced salivary hormone levels. In conclusion, measurement of cortisol and 17-OHP in saliva is feasible in healthy neonates. The existence of normative data forms the basis for future studies on pathophysiologic states in the newborn period.

17-alpha-Hydroxyprogesterone↗

PubMed1979

Association of tritium-labelled estradiol, progesterone and 17 alpha-hydroxyprogesterone with the proteins of the serum and cerebrospinal fluid in the rhesus monkey.

The electrophoretic profiles of the proteins in the serum and cerebrospinal fluid (CSF) of the rhesus monkey were studied by polyacrylamide gel electrophoresis. The association of tritium labelled estradiol (3H-E), progesterone (3H-P) and 17 alpha-hydroxyprogesterone (3H-17OHP) with these proteins was studied under in vitro and in vivo conditions. The CSF was found to contain, besides albumin, at least 4 globulins with similar electrophoretic mobilities as those found in the serum. The electrophoretic mobilities of these globulins were Ralb 0.4, 0.6, 0.8 and 0.9. The electrophoretic profiles of the monkey serum and CSF proteins were found to be similar to those described for human serum and CSF. 3H-E and 3H-P were respectively associated with serum globulins of Ralb 0.4 and 0.8 both in the in vitro and in vivo studies. The respective Ralb of these 2 globulins were similar to the testosterone-estradiol binding globulin and cortisol binding globulin in human serum. 3H-17OHP was found to be associated with several globulins under both in vitro and in vivo conditions. In marked contrast to the in vitro studies, radioactive products were found to be associated with albumin in vivo. It is presumed that these products may be steroidal conjugates derived from the systemic metabolism of the administered steroids. No radioactivity was associated with the CSF protein after in vitro incubation with any of the three 3H-steroids. In the in vivo studies, however, radioactivity was associated with such of the CSF proteins that were similar to those found in the serum and with which the administered steroids were associated.

Animals↗

PubMed1975

Radioimmunoassay of 17-hydroxyprogesterone in serum with or without thin-layer chromatographic purification.

A radioimmunoassay for the measurement of 17-hydroxyprogesterone (17-OHP) is described. The antigen 11-desoxycortisol-21-hemisuccinate-bovine serum albumin has been used to produce two antisera of different antibody populations in the same animal. The thin-layer chromatographic system described can be used to separate all the cross-reacting steroids investigated from 17-OHP. A simplified method is also presented using preliminary solvent extraction only. The mean 17-OHP levels measured, using this method, were, for normal men, 0.86 +/- 0.19 ng/ml (SD), for normal females 0.30 +/- 0.19 ng/ml in the follicular phase and 1.72 +/- 0.18 ng/ml in the luteal phase of the menstrual cycle, and 0.45 +/- 0.17 ng/ml in normal postmenopausal women.

Chromatography, Thin Layer↗

PubMed1980

Plasma progesterone, 17-hydroxyprogesterone, androstenedione and testosterone in prepubertal, pubertal and adult subjects with congenital virilizing adrenal hyperplasia as indicators of adrenal suppression.

To determine whether a single morning plasma level of 17-hydroxyprogesterone (17OH-P), androstenedione, testosterone and progesterone reflected the degree of control of 21-hydroxylase congenital virilizing adrenal hyperplasia (CVAH) as indicated by 24-hour urinary 17-ketosteroid and pregnanetriol excretion, 142 simultaneous 24-hour urine and morning blood collections were made from 65 patients with CVAH. Patients were grouped into five categories on the basis of age, skeletal age, and sex. Paired blood and urinary data were analyzed. The results suggest that androstenedione is the most reliable indicator for all patient categories. Testosterone is an excellent indicator for children of both sexes and for adolescent and adult females. Levels of 17OH-P are difficult to interpret, as they can be several fold higher than the normal values when adrenal suppression appears adequate on the basis of urinary data. In general, progesterone is a poor indicator.

17-Ketosteroids↗

PubMed1997

Longitudinal study of plasma cortisol and 17-hydroxyprogesterone in very-low-birth-weight infants during the first 16 weeks of life.

There are few published data on plasma cortisol and 17-hydroxyprogesterone (17-OHP) in very-low-birth-weight (VLBW) infants beyond the 1st week of life. We therefore measured plasma cortisol and 17-OHP longitudinally in 26 infants (median birth weight 930 g, median gestational age 28 weeks) from 1 to 16 postnatal weeks to document normative values. We also examined the effect of clinical state on plasma cortisol and 17-OHP levels. Median plasma cortisol decreased with postnatal age from 1 to 8 weeks (110 vs. 60 nmol/l; p = 0.0007) and with postconceptional age from 25 to 36 weeks (104 vs. 47 nmol/l; p = 0.002). Median plasma 17-OHP decreased with postnatal age from 1 to 16 weeks (17.0 vs. 7.1 nmol/l; p < 0.0005) and also with postconceptional age from 25 to 42 weeks (21.1 vs. 7.1 nmol/l; p < 0.0005). Plasma cortisol was not influenced by the clinical state. Median plasma 17-OHP was significantly higher for 'unwell' versus 'well' infants at 5-8 weeks postnatal age (23.0 vs. 12.5 nmol/l; p = 0.012) but not at other postnatal age intervals. These data provide information on adrenocortical function in VLBW infants during the first 4 months of life.

17-alpha-Hydroxyprogesterone↗

PubMed1969

Plasma progesterone and 17-hydroxyprogesterone in normal men and children with congenital adrenal hyperplasia.

Plasma 17-hydroxyprogesterone (17-OHP) concentrations in normal men averaged 0.094 mug/100 ml. Studies using suppressive doses of androgens and glucocorticoids showed that 90% of the 17-OHP originated from the Leydig cell. The 17-OHP production rate was 1.8 mg/24 hr. Plasma 17-OHP has a marked circadian variation, the 8 p.m. values being only 40% of the 8 a.m. values. Plasma luteinizing hormone measured in the same samples did not vary. The adrenal cortex has the capacity to synthesize and secrete 17-OHP and progesterone since adrenocorticotrophic hormone (ACTH) caused a fourfold increase in these plasma steroids. In children with congenital adrenal hyperplasia, plasma 17-OHP levels were 50-200 times those of normal men and plasma progesterone was increased 6- to 10-fold over normal men.

Adolescent↗

PubMed1980

Plasma levels of aldosterone, corticosterone, 11-deoxycorticosterone, progesterone, 17-hydroxyprogesterone, cortisol, and cortisone during infancy and childhood.

Plasma aldosterone (A), corticosterone (B), deoxycorticosterone (DOC), progesterone (P), 17-hydroxyprogesterone (17-OHP), cortisol (F), and cortisone (E) were measured simultaneously by specific radioimmunoassays in small plasma samples obtained from 174 normal infants and children between 2 hr and 15 yr of age. The significantly elevated neonatal mean levels (ng/ml) of 2.5 (A), 4.1 (DOC), 53.0 (P), and 6.6 (17-OHP) dropped significantly during infancy reaching prepubertal levels between 3 months and 3 yr of age, with a transient, significant DOC increase between 1--7 yr. The glucocorticoids F andB declined significantly from means of 68 and 4.4 to 11.4 and 0.28 ng/ml, respectively, during the first weeks of life, then increased significantly reaching adult levels between 1--3 yr of age. Mean E fell progressively from 74 ng/ml after birth to 10 ng/ml during 1--5 yr (P less than 0.0001), then slightly increased to adult levels. After age 7 yr, P and 17-OHP, in contrast to the other steroids, rose significantly in both boys and girls relative to pubertal development. The observed changes are thought to be due to (1) adaptation of the adrenal neocortex to extrauterine life after disruption of the fetoplacental unit, (2) a physiologic lack of corticosteroid binding globulin (CBG) during infancy due to maturation of hepatic CBG biosynthesis, (3) the functional immaturity of the infant kidney compensated by an increased activity of the renin-angiotensin-aldosterone system, and (4) gradually increasing gonadal secretion of progestins during puberty.

Adolescent↗

PubMed1998

Development of a highly sensitive nonisotopic immunoassay for the determination of salivary 17-hydroxyprogesterone: reference ranges throughout childhood and adolescence.

A sensitive nonisotopic immunoassay for the determination of 17-hydroxyprogesterone (17-OHP) levels in saliva was developed. The new time-resolved fluorometric immunoassay employs a specific polyclonal anti-17-OHP antiserum immobilized onto microtiter plates, a 17-OHP-biotin conjugate as a tracer, and streptavidin-europium a as secondary probe. The lower detection limit of the assay is 23.6 pmol/L (mean -3 s of a 22-fold zero determination) corresponding to 0.39 pg/well. The coefficients of intraassay variation are 8.8, 5.3, and 8.3% at the respective concentrations of 90.9, 454.5, and 1363.5 pmol/L. The coefficients of interassay variation are 8.8, 5.3, and 8.3% at the respective concentrations. Saliva was collected in commercially available devices. Reference ranges were established using 394 saliva samples from 132 healthy children, adolescents, and adults. Morning, midday, and evening levels of 17-OHP levels in saliva varied significantly in all age groups with morning levels being higher than midday and evening levels. Saliva samples (n = 57) were also obtained from 18 children with congenital adrenal hyperplasia (CAH). Salivary 17-OHP levels in the limited number of CAH patients studied ranged from 121 to 106,050 pmol/L. In conclusion 1) a new, sensitive nonisotopic immunoassay for measurement of 17-OHP in saliva has been developed; 2) reference ranges for healthy children, adolescents, and adults have been established; 3) there is a circadian pattern of 17-OHP levels in saliva at all ages; and 4) measurement of 17-OHP in saliva should be further evaluated over a longer period of time as a potentially reliable and powerful technique to monitor metabolic control in patients with CAH. As 17-OHP levels in saliva are stable for > 10 wk at 4 degrees C, the technique is ideally suited for outpatient sampling.

17-alpha-Hydroxyprogesterone↗

PubMed2004

Effect of single and multiple courses of prenatal corticosteroids on 17-hydroxyprogesterone levels: implication for neonatal screening of congenital adrenal hyperplasia.

Measurement of 17-hydroxyprogesterone (17-OHP) from filter-paper blood is widely used to screen for congenital adrenal hyperplasia (CAH). However, in pregnancies with an expected preterm delivery, prenatal treatment with steroids to induce pulmonary maturation could suppress the fetal adrenals and interfere with this screening. In 160 infants who were born between 25 and 35 wk of gestation, we measured 17-OHP in filter-paper blood at 72-96 h and compared the values between those who had not received antenatal steroids (n=50) and those who had (n=110). A single course of steroids was two 12-mg injections of betamethasone given within a 24-h interval: 30 infants received a half single course, 45 received a full single course, and 35 received multiple courses. Results are expressed as medians (25th percentile; 75th percentile). Blood 17-OHP differed significantly among groups: 23.7 (14.2; 30.7) nmol/L, 26.1 (15.0; 50.1) nmol/L, 20.1 (13.8; 29.1) nmol/L, and 14.9 (9.5; 26.2) nmol/L (for, respectively, no steroid, half a single course, a full single course, and multiple courses; p <0.05, multiple comparisons with the Kruskal-Wallis test). However, only infants who were treated with multiple antenatal courses of steroids had lower blood 17-OHP than those who were untreated (p <0.05 with the Mann-Whitney U test). In multiple regression analysis, steroid treatment and intrauterine growth retardation were significant negative predictors of blood 17-OHP, whereas respiratory distress syndrome was a significant positive predictor (multiple R=0.50, p <0.001). Multiple courses of steroids in preterm infants decrease 17-OHP values by approximately 30% in filter-paper blood, thus raising the risk of false-negative results in screening programs for CAH.

17-alpha-Hydroxyprogesterone↗

PubMed1995

11 alpha- and 11 beta-hydroxyprogesterone, potent inhibitors of 11 beta-hydroxysteroid dehydrogenase (isoforms 1 and 2), confer marked mineralocorticoid activity on corticosterone in the ADX rat.

The effects of 11 alpha- and 11 beta-hydroxyprogesterone (11 alpha-OHP, 11 beta-OHP), on the activity of the glucocorticoid inactivating enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) were studied. 11 alpha-OHP and 11 beta-OHP were potent inhibitors of both 11 beta-HSD1 in rat liver microsomes and 11 beta-HSD2 in lysates of JEG-3 cells, a human choriocarcinoma cell line. In addition, both progesterone metabolites were markedly potent in conferring mineralocorticoid activity upon B in the adrenalectomized rat. These results provide insight into the structural properties required of inhibitors of 11 beta-HSD activity and indicate a possible role for endogenous 11 beta-HSD inhibitors in the regulation of glucocorticoid-induced Na+ retention.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed1996

11 beta-Hydroxysteroid dehydrogenase type 2 complementary deoxyribonucleic acid stably transfected into Chinese hamster ovary cells: specific inhibition by 11 alpha-hydroxyprogesterone.

The 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta HSD-2) enzyme is thought to confer aldosterone specificity upon mineralocorticoid target tissues by protecting the mineralocorticoid receptor from binding by the more abundant glucocorticoids, corticosterone and cortisol. We have developed a Chinese hamster ovary cell line stably transfected with a plasmid containing the rat 11 beta HSD-2 complementary DNA. This cell line has expressed the enzyme consistently for many generations. The 11 beta HSD-2 was located primarily in the microsomes, but significant amounts also existed in the nuclei and mitochondria. The enzymatic reaction was unidirectional, oxidative, and inhibited by the product, 11-dehydrocorticosterone, with an IC50 of approximately 200 nM. The K(m) for corticosterone was 9.6 +/- 3.1 nM, and that for NAD+ was approximately 8 microM. The enzyme did not convert dexamethasone to 11-dehydrodexamethasone. Tunicamycin, an N-glycosylation inhibitor, had no effect on enzyme activity. 11 alpha-Hydroxyprogesterone (11 alpha OH-P) was an order of magnitude more potent a competitive inhibitor of the 11 beta HSD-2 than was glycyrrhetinic acid (GA) (approximate IC50 = 0.9 vs. 15 nM). 11 beta OH-P, progesterone, and GA were almost equipotent (IC50 = 10 and 6 nM, respectively), and 5 alpha-pregnandione and 5 beta-pregnandione were less potent (IC50 = 100 and 500 nM, respectively) inhibitors of the enzyme. When the inhibitory activities were examined with intact transfected cells, 11 alpha OH-P was more potent than GA (IC50 = 5 and 150 nM, respectively). 11 alpha OH-P was not metabolized by 11 beta HSD-2. We were unable to demonstrate the presence of 11 alpha OH-P in human urine. In conclusion, a cell line stably transfected with the rat 11 beta HSD-2 was created, and the enzyme kinetics, including inhibition, were characterized. 11 alpha OH-P was found to be a potent relatively specific inhibitor of the 11 beta HSD-2 enzyme. Its potential importance is that it is the most specific inhibitor of the 11 beta HSD-2 so far encountered and would aid in the study of the physiological importance of the isoenzyme.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed2004

Significantly higher adrenocorticotropin-stimulated cortisol and 17-hydroxyprogesterone levels in 337 consecutive, premenopausal, caucasian, hirsute patients compared with healthy controls.

OBJECTIVE: To investigate whether elevated ACTH-stimulated 17-hydroxyprogesterone (17OHP) levels are caused by CYP21 genetic defects or by a general adrenal hyperresponsiveness in hirsute patients. METHODS: A total of 337 hirsute patients were evaluated by Ferriman-Gallwey score, serum testosterone, ACTH-stimulated 17OHP, and cortisol during the follicular phase. A cutoff value of 16 nmol/liter for maximum ACTH-stimulated 17OHP (M17OHP) responses was defined as the upper limit of the 95% confidence interval (CI) for the 97.5 percentile in 42 female controls. All patients were offered total screening of the CYP21 gene, and 252 healthy, premenopausal women with regular menses underwent genetic screening. RESULTS: Patients were divided into idiopathic hirsutism (IH) (n = 180) and polycystic ovary syndrome (PCOS) (n = 157) groups. M17OHP levels were significantly higher in IH [geometric mean value (nmol/liter +/- 2 sd) 12.2 (4.6-32.3)] and PCOS [11.9 (5.3-27.2)] compared with controls [8.5 (5.1-14.2)] (P < 0.001). A similar percentage of IH and PCOS patients had elevated M17OHP (20.5 vs. 20.8%, not significant), and these also had significantly higher 30-min cortisol levels compared with controls (P < 0.05). The prevalence of CYP21 mutations in patients was 8.6% compared with 6.3% in controls (P = 0.38). Ten of 19 carriers had M17OHP levels below the cutoff limit. CONCLUSION: The significantly higher ACTH-stimulated levels of cortisol and 17OHP in hirsute patients indicated adrenal hyperresponsiveness in IH and PCOS. CYP21-carrier status could not explain the observed high prevalence of abnormal ACTH-stimulated 17OHP levels in the hirsute population.

17-alpha-Hydroxyprogesterone↗

PubMed2005

Cutoff levels of 17-alpha-hydroxyprogesterone in neonatal screening for congenital adrenal hyperplasia should be based on gestational age rather than on birth weight.

OBJECTIVE: In newborn screening programs for congenital adrenal hyperplasia, 17-alpha-hydroxyprogesterone (17OHP) cutoff levels are based on birth weight (BW) or on gestational age (GA). We investigated which approach would result in the greatest specificity and sensitivity. STUDY DESIGN: For the determination of 17OHP, a neonatal 17OHP assay was used in filter paper blood of 9492 newborns. The relationships between 17OHP and BW and between 17OHP and GA were studied by regression analysis. Reference curves with a specificity of 99.95% were constructed with the method that summarizes the distribution by three smoothed curves representing the skewness (L curve), the median (M curve), and the coefficient of variation (S curve). Median cutoff levels for BW and for GA according to the 99.95% reference curves were calculated. RESULTS: Regression analysis showed that GA is a better predictor of 17OHP than BW (R(2) was 50.6 vs. 35.8%, respectively). At a specificity of 99.95%, the calculated median 17OHP cutoff level was lower for GA [12.6 microg/liter (38 nmol/liter)] than for BW [17.6 microg/liter (54 nmol/liter)], thus leading to a greater sensitivity. CONCLUSION: This study demonstrates that GA is a better predictor of 17OHP in newborns and will result in greater specificity than BW despite the fact that the determination of GA might be less reliable than BW.

17-alpha-Hydroxyprogesterone↗

PubMed2006

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.

INTRODUCTION: 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 somewhat underestimated. MATERIALS AND METHODS: In 133 patients (89 females/44 males; 10 d-20.9 yr) with alleged classic 21OHD and five (three females/two males; 7.3-21 yr) with documented 11betaOHD, we measured serum 21-deoxycortisol (21DF), 17-hydroxyprogesterone (17OHP), and 11-deoxycortisol (S), 48 h after glucocorticoid withdrawal. We also studied 20 sex- and age-matched control subjects. Serum steroid levels were determined by RIA after HPLC purification. OBJECTIVES: The objectives of this study were to: 1) quantify 21DF in patients with congenital adrenal hyperplasia, 2) correlate hormonal with clinical data, and 3) identify possible misdiagnosed patients with 11betaOHD among those with 21OHD. RESULTS: In 21OHD, 17OHP (217-100,472 ng/dl) and 21DF (<39-14,105 ng/dl) were mostly elevated and positively correlated (r = 0.7202; P < 0.001). Except for higher 17OHP in pubertal patients, 17OHP and 21DF values were similar according to sex, disease severity, or prevailing glucocorticoid dose. One additional patient with 11betaOHD was detected (1%) and also one with apparent combined 11beta- and 21OHD. S levels were elevated in 11betaOHD and normal but significantly higher in 21OHD than in controls. CONCLUSION: To recognize patients with 21- and/or 11betaOHD, we recommend evaluation of 17OHP or 21DF and S. Also, 21DF may be useful to follow up pubertal patients with 21OHD. Because 1% of patients with alleged 21OHD may have 11betaOHD, its frequency seems underestimated, as per our experience in a Brazilian population.

17-alpha-Hydroxyprogesterone↗

PubMed1975

A nonchromatographic radioimmunoassay for 17alpha-hydroxyprogesterone.

A radioimmunoassay is described for the measurement of 17alpha-hydroxyprogesterone in human plasma. We have employed the principle of "immunologic purification." 17-OHP and related steroids are bound to an excess of antiserum. Steroids with a low affinity for the antibody are extracted by ether. The 17-OHP is subsequently freed from antibody by acid hydrolysis and this extract is assayed by radioimmunoassay.

Adult↗