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PubMed1975

Puberty in boys: correlation of plasma levels of gonadotropins (LH, FSH), androgens (testosterone, androstenedione, dehydroepiandrosterone and its sulfate), estrogens (estrone and estradiol) and progestins (progesterone and 17-hydroxyprogesterone).

Mean serum concentration dehydroepiandrosterone (DHA), DHA sulfate (DHAS), progesterone (P), 17-hydroxyprogesterone (17-OH-P), estrone (E1), estradiol (E2), and androstenedione (A) were compared from 43 boys followed longitudinally for as long as 4 yr during puberty. These data were also compared with serum levels of LH, FSH, and testosterone. Elevation is recognized early in puberty for DHAS, late in puberty for P and A, and gradually throughout puberty for E1, 17-OH-P, and DHA. When compared by age, the same general pattern is apparent with adult levels of E1 reached at age 12, DHAS and E2 by 13, and DHA, P, 17-OH-P, and A not until after age 15. Significant elevations of DHA occurred with the onset of pubic hair and voice change; elevations of DHAS occurred with the onset of genital and axillary hair growth; and testosterone increased with the onset of genital and pubic hair growth and voice change.

Adolescent↗

PubMed1977

Twenty-four hour integrated concentrations of progesterone, 17-hydroxyprogesterone and cortisol in normal male subjects.

The 24 h integrated concentrations of progesterone, 17-hydroxyprogesterone (17-OHP) and cortisol were determined in 5 male subjects ranging in age from 25 to 36 years. Using a nonthrombogenic catheter and a constant withdrawal pump, blood was collected for a period of 24 h in 30 min aliquots. All five subjects had similar 24 h integrated concentrations of cortisol (9.2 +/- 5.4). One subject had elevated 24 h integrated concentrations of progesterone (55.2 +/- 18.7) and 17-OHP (352 +/- 122) when compared to the mean integrated concentrations (progesterone: 24.9 +/- 4.7; 17-OHP: 109 +/- 33) of the 4 other subjects. The 30 min integrated concentrations showed a diurnal variation for both 17-OHP and cortisol but not for progesterone. The best correlation between cortisol and 17-OHP occurred when the concentration of 17-OHP 90 or 120 min earlier. No significant correlation occurred between cortisol and progesterone.

Adult↗

PubMed1977

Studies on human sexual development. V. Concentrations of testosterone, 17-hydroxyprogesterone and progesterone in human amniotic fluid throughout gestation.

Concentrations of unconjugated testosterone, 17-hydroxyprogesterone (170HP) and progesterone were measured by radioimmunoassay in amniotic fluid (AF) specimens from normal pregnancies of 9-40 weeks gestation. In two-thirds of samples from pregnancies with male fetuses. AF testosterone exceeded the upper limit found in female samples, with minimal overlap in the 12-18 week period of gestation. Although AF testosterone levels associated with male and female fetuses were both significantly lower toward term, the sex-difference persisted. Between 9-19 weeks gestation, fetal sex was also found to influence AF 170HP, a steroid thought to be predominantly of placental and fetal adrenal origin; in this case, female levels exceeded male. Awareness of the influence of sex and gestation upon AF concentrations of these steroids is an important prerequisite for their application to the prenatal diagnosis of endocrine disease (e.g., congenital adrenal hyperplasia). There was no sex difference in AF progesterone concentrations at 12-18 weeks gestation. The median progesterone concentration at 34-40 weeks was higher with female fetuses, but this difference may be related to a difference in gestational age between AF samples obtained from male and female fetuses.

Amniotic Fluid↗

PubMed1977

Plasma 17alpha-hydroxyprogesterone in spironolactone-treated hypertensives.

When measured by a specific radio-assay method which excludes drug interference, plasma 17alpha-hydroxyprogesterone levels were found to be similar in spironolactone treated hypertensives, in untreated hypertensives, and in normotensive volunteers. No in vivo evidence for a significant inhibitory effect of spironolactone on adrenal 11beta, 17alpha and 21 hydroxylases was uncovered.

Humans↗

PubMed1978

Basal and human chorionic gonadotropin-stimulated 17 alpha-hydroxyprogesterone and testosterone levels in Klinefelter's syndrome.

In nine patients with Klinefelter's syndrome, mean basal plasma levels of testosterone (302 +/- 145 ng/100 ml) and its major precursor, 17 alpha-hydroxyprogesterone (17-OHP; 86 +/- 46 ng/100 ml), were significantly lower (P less than 0.01 to less 0.05) than in eight eugonadal men (605 +/- 180 and 136 +/- 39 ng/100 ml, respectively). The ratio of 17-OHP to testosterone, however, was comparable in both groups (0.29 +/- 0.09 vs. 0.24 +/- 0.08; P less than 0.10). In the Klinefelter patients, basal plasma testosterone and 17-OHP levels were positively correlated (rs = 0.87). Administration of hCG for 3 days raised plasma testosterone and 17-OHP levels in both groups. In the Klinefelter patients, the plasma 17-OHP rise exceeded the testosterone increment, leading to a statistically significant increase (0.48 +/- 0.19) of the 17-OHP to testosterone ratio, whereas this ratio remained virtually unchanged in the control subjects (0.20 +/- 0.06). Together, these findings indicate that in the basal state testicular steroidogenesis is globally attenuated, whereas short term hCG stimulation shows that the later steps in the biosynthesis of testosterone may be rate limiting in Klinefelter's syndrome.

Adolescent↗

PubMed1980

Dissociated responses of plasma testosterone and 17-hydroxyprogesterone to single or repeated human chorionic gonadotropin administration in normal men.

After both single (1500 IU) and daily repeated (1500 IU daily for 3 days) im administration of hCG, peak values of 17-hydroxyprogesterone (17OHP) were achieved 24 h after the single or first injection, whereas plasma testosterone (T) levels reached their maximum 48 h later. After the peak value of 17-OHP at 24 h, both steroids ran dissociated courses with the T levels rising and the 17-OHP levels falling. In both the single and repeated hCG experiments, the initial rise of 17-OHP was more pronounced than that of T, leading to a steep temporary increase of the 17-OHP to T ratio in the first 24 h. Repeated hCG administration for 3 days to the same subjects elicited T responses at 48 and 72 h quantitatively similar to those produced by single hCG loading, although the 17-OHP response appeared slightly higher in the multiple dose experiment. The data indicate that exogenous gonadotropins may influence testicular steroidogenesis not only quantitatively, but also qualitatively, possibly by altering enzyme activities.

Adult↗

PubMed1980

Tamoxifen suppresses gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men.

Intramuscular administration of 1500 IU hCG daily for 3 days induced a transient accumulation of 17 alpha-hydroxyprogesterone (17 OHP) relative to testosterone (T) in normal men, reaching its maximum 24 h after the first injection (17 OHP to T ratio, 1.7 +/- 0.3 times baseline; P < 0.01). Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone). These data indirectly suggest that, in man, the hCG-induced steroidogenic lesion might be mediated through its estrogen-stimulating effect.

Adult↗

PubMed1981

Concentrations of aldosterone, corticosterone, 11-deoxycorticosterone, progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, cortisol, and cortisone determined simultaneously in human amniotic fluid throughout gestation.

Corticosteroids (CS) are essential for fetal organ maturation; yet, knowledge of endogeneous CS and precursor levels throughout fetal life is limited. Therefore, unconjugated aldosterone (Aldo), corticosterone (B), 11-deoxycorticosterone (DOC), progesterone (P), 17 alpha-hydroxyprogesterone (17-OHP), 11-deoxycortisol (S), cortisol (F), and cortisone (E) were simultaneously determined by RIA after automated Sephadex LH-20 chromatography in 70 control samples of amniotic fluid (AF) obtained at all gestational ages between 14-42 weeks. Levels of the progestins P and 17-OHP slowly increased from means (+/- SE) of 14.7 +/- 2.8 and 1.63 +/- 0.21 ng/ml, respectively, in early gestation to maximum levels of 32.4 +/- 3.5 and 3.80 +/- 0.74 ng/ml at 36-38 weeks (P less than 0.005), then dropped significantly (P less than 0.01) to 19.2 +/- 2.2 and 1.58 +/- 0.22 ng/ml at term. All CS levels except E rose very markedly by 3- to 12-fold (P less than 0.0001) from the weeks 14-16 (DOC, 0.44 +/- 0.08; B, 1.49 +/- 0.23; Aldo, 0.043 +/- 0.012; S, 0.51 +/- 0.10; F, 5.96 +/- 0.93 ng/ml) until the 36-38th weeks (DOC, 3.50 +/- 0.66; B, 4.60 +/- 0.78; Aldo, 0.530 +/- 0.109; S, 6.00 +/- 0.75; F, 60.8 +/- 8.9 ng/ml). Term levels were significantly reduced (P less than 0.01) in the less active CS DOC (0.51 +/- 0.07 ng/ml), B (2.35 +/- 0.35 ng/ml), and S (1.14 +/- 0.14 ng/ml), whereas those of the biologically most potent CS Aldo and F declined less markedly (0.272 +/- 0.053 and 23.0 +/- 0.75 ng/ml, respectively, at 39-42 weeks). Levels of the inactive glucocorticoid E rose from 8.83 +/- 1.08 ng/ml at 14-16 weeks to 16.8 +/- 2.6 ng/ml at 31-35 weeks (P less than 0.01), then remained rather constant around 11.5 ng/ml until term. It is concluded that after the 25th week, large amounts of biologically active CS are available in AF which probably directly induce the final epithelial maturation of fetal lungs and intestinal tract.

Adrenal Cortex Hormones↗

PubMed1996

Ovarian 17-hydroxyprogesterone hyperresponsiveness to gonadotropin-releasing hormone (GnRH) agonist challenge in women with polycystic ovary syndrome is not mediated by luteinizing hormone hypersecretion: evidence from GnRH agonist and human chorionic gonadotropin stimulation testing.

Women with polycystic ovary syndrome (PCOS: hyperandrogenism and oligomenorrhea) have been shown to have exaggerated ovarian 17-hydroxyprogesterone (17-OHP) responses after GnRH agonist stimulation, suggestive of disordered ovarian cytochrome P450c17 alpha activity. However, most hyperandrogenic women also have an exaggerated LH response to both native GnRH and GnRH agonists. To assess whether the known LH hyperresponsiveness in PCOS patients mediates their exaggerated 17-OHP response to GnRH agonist challenge or whether the 17-OHP response can be duplicated by direct stimulation of the ovary with a fixed amount of hCG, 25 PCOS women [age, 20.6 +/- 1.1 yr; body mass index (BMI), 24.9 +/- 1.3 kg/m2] and 5 controls (age, 29.4 +/- 2.3 yr; BMI, 29.2 +/- 3.0) underwent both GnRH agonist (leuprolide acetate) and hCG testing. In addition, 23 normal women (age, 26.5 +/- 1.5 yr; BMI, 27.2 +/- 1.7 kg/m2) underwent hCG testing, and 21 other normal women (age, 19.3 +/- 0.5 yr; BMI, 23.0 +/- 0.8 kg/m2) underwent leuprolide acetate challenge. Blood was sampled before and 24 h after (the previously determined time of the peak response) leuprolide acetate (500 micrograms, sc) and hCG (5000 IU, im) stimulation tests. The tests were administered during the early follicular phase in women who were ovulatory and in randomized order in the subjects receiving both stimuli. Peak serum 17-OHP levels did not differ between leuprolide acetate or hCG stimulation in PCOS patients or controls when measured at 24 h (324.9 +/- 41.9 vs. 360.4 +/- 54.0 in PCOS; 183.2 +/- 19.6 vs. 141.2 +/- 11 ng/dL in controls). Peak 17-OHP levels after hCG challenge and GnRH agonist stimulation were highly correlated (r = 0.82; P < 0.001) in the subjects receiving both stimuli. Although leuprolide acetate elicited a higher estradiol (E2) response than hCG in all subjects, serum E2 levels increased significantly after hCG treatment in both patients and controls (P < 0.001 and P < 0.0001). The small, but significant, increase in serum E2 after hCG stimulation suggests that a rigid two-cell model of ovarian steroidogenesis may be an oversimplification of in vivo physiology. Our results suggest that exaggerated 17-OHP responses to GnRH agonist stimulation in hyperandrogenic women are not mediated by the known hyperresponsiveness of LH in these patients, but are due to increased ovarian androgen sensitivity to LH stimulation.

17-alpha-Hydroxyprogesterone↗

PubMed2002

Variable ACTH-stimulated 17-hydroxyprogesterone values in 21-hydroxylase deficiency carriers are not related to the different CYP21 gene mutations.

The currently used cutoff level for ACTH-stimulated 17- hydroxyprogesterone (17OHP) for the diagnosis of the nonclassical (NC) form of 21-hydroxylase deficiency (21OHD), established before molecular studies, is based on the mean + 2 SD of 17OHP levels of obligate heterozygotes. However, carriers of CYP21 mutations present variable ACTH-stimulated 17OHP levels, ranging from normal values up to 30 nmol/liter. The aim of this study was to determine whether ACTH-stimulated 17OHP levels in obligate carriers for 21OHD would be correlated with the impairment of the enzyme activity caused by these mutations, which would affect the 17OHP cutoff level for the diagnosis of the NC form. Fifty-nine parents of patients with the classical and NC forms of 21OHD had their DNA screened for the mutations found in the index case and were divided into three mutation groups according to the impairment of enzyme activity (A = 0%, B = 3%, and C > 20%). All parents carried mutations in one allele (29 of group A, 9 of group B, and 21 of group C). Blood samples were collected at baseline condition and 60 min after ACTH (250 microg i.v.) to measure 17OHP levels. The levels among groups A, B, and C were compared using the Kruskall Wallis test. ACTH-stimulated 17OHP levels identified 39% of the carriers (9 in group A, 2 in group B and 12 in group C). The mean +/- SD basal 17OHP levels in groups A, B, and C were: 2.94 +/- 1.89, 1.77 +/- 0.81 and 3.90 +/- 2.43 nmol/liter, respectively (P > 0.05) and for ACTH-stimulated levels were 12.6 +/- 7.2, 13.2 +/- 12.9 and 16.8 +/- 7.8 nmol/liter, respectively (P > 0.05). Two carriers presented ACTH-stimulated 17OHP levels between 30 and 45 nmol/liter and their entire CYP21 sequencing revealed only one mutation in heterozygous state indicating that the current cutoff level might overestimate the diagnosis of the NC form. We conclude that the variable ACTH-stimulated 17-OHP levels in carriers are not related to CYP21 gene mutations with different impairment of enzyme activity.

17-alpha-Hydroxyprogesterone↗

PubMed2004

Limitations of 17-hydroxyprogesterone in investigating neonatal hyponatraemia.

Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is a possible cause of hyponatraemia in the neonate. Elevated 17-hydroxyprogesterone (17-OHP) is considered diagnostic of the condition, although there have been reports of anomalous high concentrations, up to 110 nmol/L, in premature, sick infants subsequently shown to have normal adrenocortical function. We describe a case of a 6-week-old girl with a chest infection and hyponatraemia whose plasma 17-OHP concentration was 300 nmol/L, well within the range associated with 21-hydroxylase deficiency. However, there was no genital ambiguity and plasma cortisol was also significantly elevated, raising the possibility of generalized adrenal hyperstimulation rather than CAH. The patient was treated with antibiotic and saline infusions but no steroids. CAH was subsequently excluded by normal 17-OHP and cortisol responses to Synacthen stimulation. In sickness, an increased plasma 17-OHP concentration may not be synonymous with 21-hydroxylase deficiency, even when grossly raised. Simultaneous measurement of plasma cortisol could aid interpretation and avoid potential misdiagnosis, especially in male infants.

17-alpha-Hydroxyprogesterone↗

PubMed2002

Twenty-four hour 17-hydroxyprogesterone response to adrenocorticotropine in adrenal incidentalomas: augmented response after adrenalectomy in two patients.

The current study aimed to investigate the midterm (24 hour) response of 17-hydroxyprogesterone (17-OHP) and dehydroepiandrosterone sulphate (DHEA-S) to synthetic high-dose adrenocorticotropin (ACTH) in adrenal incidentalomas (Al). Seventeen patients with Al and 40 age- and sex-matched controls received synthetic ACTH (tetracosactide, 1000 microg, IM). Plasma, 17-OHP and DHEA-S were collected in basal conditions and after 1, 4, 6, 8 and 24 hours. (HPA) axis was also evaluated using circadian serum cortisol, urinary free cortisol and over-night 2 mg dexamethasone suppression. Basal plasma 17-OHP levels did not differ among the groups. However, the increment in plasma 17-OHP in patients both in terms of peak [13.76 +/- 2.52, 4.77 +/- 0.30ng/ml, mean +/- S.E.M, p < 0.001] and area under the curve [190 +/- 46, 96.75 +/- 32 ng/ml/h, p < 0.001] were significantly higher than that of the controls. Stimulated 17OH-P levels never reached 9.1 ng/ml in controls. Sixty-five (11/17) % of the patients were found to have exaggerated response. Three of the patients were found to have subclinical Cushing's syndrome and interestingly, two augmented their 17-OHP response to ACTH after unilateral adrenalectomy and normalisation of their HPA axis. Basal DHEA-S levels of the patients were significantly lower [99.21 +/- 45, 230.18 +/- 34 microg/dl, p < 0.01] and stayed persistently lower than that of the controls. Evidence of a heterozygous 21 hydroxylase deficiency, as indicated by the exaggerated 17-OHP response to ACTH, has been widely reported in Al patients. However, to our knowledge to date there is no report on augmented 17-OHP response to ACTH after adrenalectomy. Possible reasons for the augmentation were discussed.

17-alpha-Hydroxyprogesterone↗

PubMed2004

Adrenocorticotropic hormone and 17-hydroxyprogesterone levels during high-dose glucocorticoid supplement for the management of clitoroplasty of CYP21A2 deficiency.

ACTH and 17-hydroxyprogesterone (17OHP) levels during clitoro- and labinoplasty for CYP21A2 deficiency have not been reported. In this study, we measured these levels during surgery. Intensive glucocorticoid supplement (IGS Tx; intravenous bolus injection of daily dose (14.6 to 22.2 mg/m(2)) of hydrocortisone followed by continuous infusion of three times the daily dose for 24 hours) was done to eight patients for surgery. ACTH and 17OHP levels were generally suppressed during operation by this protocol, but mid-surgical elevations of ACTH and 17OHP levels were observed in four out of the eight. In another three patients than the eight as described, oral dexamethasone pretreatment (1 mg/m(2)) was administered for two days before surgery in addition to IGS Tx. ACTH and 17OHP levels were completely suppressed throughout operation, indicating that this kind of additional pretreatment is more effective approach.

17-alpha-Hydroxyprogesterone↗

PubMed1976

The simultaneous assay of progesterone, 17-hydroxyprogesterone, and deoxycorticosterone in human plasma by competitive protein binding.

A method is described for the simultaneous measurement of prosterone (P), 17-hydroxyprogesterone (17-OHP) and deoxycorticosterone (DOC) in plasma by competitive protein-binding assay. After extraction, these steroids were purified by Sephadex LH-20 columns. The methods described here is sensitive enough to detect the above-mentioned steroids in as little as 5 ml of plasma under physiological conditions. The mean physiological plasma level (ng/100 ml) of P, 17-OHP and DOC are 18.2+/-1.6 (SE), 136.5+/-11.7, and 8.6+/-1.0 in men, 14.7+/-1.7, 61,2+/-3.6 and 6.0+/-1.2 in women in the follicular phase, and 645.0+/-108.1, 155.2+/-16.9, and 7.5+/-1.2, in the luteal phase of the menstrual cycle. By this method and others, the responses of plasma levels of 7 adrenal steroids (P, 17-OH, doc, corticosterone, deoxycortisol, cortisol and aldosterone) to ACTH infusion (25U i.v. over 8 hours) were investigated in healthy men. The increase of DOC was more pronounced than that of the other steroids.

Adult↗

PubMed1979

Plasma levels of 16 alpha-hydroxypregnenolone, 16 alpha-hydroxyprogesterone and 16 alpha-hydroxydehydroepiandrosterone in the fetus and neonates.

Simultaneous determination of unconjugated 16 alpha-hydroxypregnenolone (16 alphaOH-Preg), 16 alpha-hydroxyprogesterone (16 alphaOH-Prog) and 16 alpha-hydroxydehydroepiandrosterone (16 alphaOH-DHEA) in fetal and neonatal plasma was performed utilizing a newly developed radioimmunoassay. In all neonates, the three 16 alpha-hydroxysteroid levels were consistently higher in umbilical cord plasma than in the maternal peripheral circulation. 16 alpha-OH-Preg in the umbilical arterial plasma increased from 11.2 +/- 3.1 at 24 weeks to 29.7 +/- 12.0 ng/ml at term, 16 alphaOH-Prog from 15.5 +/- 3.2 to 34.3 +/- 11.0 ng/ml and 16 alphaOH-DHEA from 5.1 +/- 1.2 to 5.9 +/- 1.0 ng/ml. In the anencephalic neonates, only 16 alphaOH-Preg showed an increase pattern under ACTH priming. 16 alpha-OH-Preg levels for normal full term neonates remain relatively constant at the first 24 hr and show a slight decrease at 3 days post partum. In small full term neonates, 16 alphaOH-Preg levels in umbilical arterial plasma are considerably higher than in normal neonates and remain at roughly equivalent levels for the first 5 days post partum. 16 alphaOH-Prog and 16 alphaOH-DHEA levels in umbilical arterial plasma in normal and small full term neonates are almost equal and both groups show a rapid decrease during the first 24 hr. Comparison with findings of the three 16 alpha-hydroxysteroids in fetal and neonatal plasma is discussed.

17-alpha-Hydroxypregnenolone↗

PubMed2004

Comparison of three commercial assays for the measurement of 17alpha-hydroxyprogesterone (17alpha-OHPR): limitations of the quality control system.

The measurement of 17alpha-hydroxyprogesterone (17alpha-OHPR) is of value for the diagnosis and management of congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency. In the central laboratory from 2000 to 2002, we observed, using the assay from the manufacturer DSL, an elevation of the moving average of 17alpha-OHPR concentrations and a number of adrenocorticotropic hormone (ACTH) stimulation tests despite the lack of any changes to the internal and external quality control, of which the criteria were continuously fulfilled. We studied a population of n=49 patients for the measurement of 17alpha-OHPR, with and without extraction, to evaluate the quality of different commercially available radioimmunoassays. The internal and external quality controls were successful in determining 17alpha-OHPR. An excellent measurement and correlation of 17alpha-OHPR was expressed with the assay from the manufacturer IBL without extraction and from the manufacturer DSL with extraction. The quantitative determination of 17alpha-OHPR requires adequate specificity and accuracy of the 17alpha-OHPR radioimmunoassays. The results show that internal and external quality control systems are not sufficient to resolve analytical problems described in this study.

17-alpha-Hydroxyprogesterone↗

PubMed2006

Newborn screening levels of 17-hydroxyprogesterone in very low birth weight infants and the relationship to chronic lung disease.

OBJECTIVES: 17-Hydroxyprogesterone (17-OHP), an intermediary hormone in cortisol synthesis, has been shown to be elevated in premature infants. However, the relationship between levels of 17-OHP with chronic lung disease (CLD) have not been extensively explored. The objective of this study was to determine whether there is an association between CLD and levels of 17-OHP in a population of very low birth weight infants. STUDY DESIGN: Cohort study of very low birth weight infants cared for at a single level 3 NICU during a 3-year period from July 2001-July 2004, n=435. Infants had a minimum of one screen for 17-OHP. 17-OHP was measured on the 5th day of life and at 2-4 weeks of life as part of the State of Delaware Newborn Screening Program. Statistical analysis included chi-squared, Pearson correlation, and logistic regression. RESULTS: Levels of 17-OHP were higher at the time of the 1st screen compared to the 2nd screen (42.2 +/- 36.7 vs 23.5 +/- 32.3 ng/ml, respectively, p = 0.01). After controlling for potential confounding variables, gestational age and prenatal steroids were independently associated with 17-OHP. However, logistic regression analysis showed no association between a 1 log increase in levels of 17-OHP with the outcomes of CLD (odds ratio 1.7, 95% CI 0.7-3.8), or death and/or CLD (odds ratio 2.1, 95% CI 0.9-4.8). CONCLUSIONS: In our population of very low birth weight infants elevated levels of 17-OHP were not associated with the development of CLD.

17-alpha-Hydroxyprogesterone↗

PubMed1976

Plasma aldosterone concentrations related to 17alpha-hydroxyprogesterone in congenital adrenal hyperplasia.

Plasma aldosterone and 17alpha-hydroxyprogesterone (17-OHP) concentrations were measured in 35 patients with congenital adrenal hyperplasia resulting from 21-hydroxylase deficiency. Ten patients had never been treated and among them were 4 salt-losing infants. Both aldosterone and 17-OHP were high in the 6 untreated non salt-losers. The values ranged respectively from 110 to 376 pg/ml and from 150 to 292 ng/ml. Results were variable in the 4 salt-losers. Three out of 5 untreated non salt-losers who were submitted to a low sodium diet, responded by doubling their aldosterone levels. When plasma 17-OHP concentrations were less than 30 ng/ml, the mean aldosterone level in the treated non salt-losers (n=6) was 15.3 pg/ml +/- 4.3 (SE). This value was not different from the mean level found in the control children (n=7), 18.8 pg/ml +/- 3.2. In the treated salt-losers (n=9), the measured aldosterone levels were less than or equal to 10 pg/ml 7 times out of 9. When the treated patients exhibited plasma 17-OHP concentrations greater than 30 ng/ml, the salt-losers (n=11) were distinguished from the non salt-losers (n=8) in that they showed as significantly lower aldosterone mean level, 24.6 pg/ml +/- 4.3 against 69 pg/ml +/- 13.4 found in the non salt-losers. The salt-losers displayed no aldosterone increases to synthetic ACTH stimulation under treatment or at the withdrawal of treatment, while positive aldosterone responses were often observed in the non salt-losers. In the latter group, studied under different conditions (with and without therapy, on low sodium diet, after ACTH test) a significant correlation was found between aldosterone and 17-OHP levels expressed in log. values, (n=38, r=0.80, P less than 0.001). The relationship could also be established with the values obtained from all the salt-losers, but it was less significant, (n=35, r=0.46, P less than 0.02).

Adolescent↗