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At least 19 recordsLinked to original sources
PubMed1979

Interrelationships of circulating maternal steroid concentrations in third trimester pregnancies. III. Effect of intravenous cortisol infusion on maternal concentrations of estriol, 16 alpha-hydroxyprogesterone, 17 alpha-hydroxyprogesterone, progesterone, 20 alpha-dihydroprogesterone, delta 5-pregnenolone, delta5-pregnenolone sulfate, dehydroepiandrosterone sulfate, and cortisol.

The effect of a large dose (1000 mg) of iv cortisol-hemisuccinate on circulating steroid concentrations in five women, 28--34 weeks, gestational age, is reported. Maternal concentrations of estriol, 16 alpha-hydroxyprogesterone, 17 alpha-hydroxyprogesterone, progesterone, 20 alpha-dihydroprogesterone, delta 5-pregnenolone, delta 5-pregnenolone sulfate, dehydroepiandrosterone sulfate, and cortisol were measured by RIA before and at 8 and 12 h after iv cortisol infusions at 0 and 8 h. Data were evaluated by repeated measure analysis of variance. Estriol and 17 alpha-hydroxyprogesterone suppressed initially (P less than 0.05) and suppressed further with retreatment and increased treatment time (P less than 0.05). Dehydroepiandrosterone sulfate and progesterone suppressed initially (P less than 0.05) but did not suppress further with retreatment and increased treatment time (P greater than 0.05). delta 5-Pregnenolone and delta5-pregnenolone sulfate increased initially (P less than 0.05) but did not increase further (P greater than 0.05). Concentrations of 16 alpha-hydroxyprogesterone and 20 alpha-dihydroprogesterone were unchanged by cortisol infusion initially (P greater than 0.1) and with retreatment and increased treatment time (P greater than 0.1).

20-alpha-Dihydroprogesterone↗
PubMed1975

Inhibition of 17,20(17-hydroxyprogesterone)-lyase by progesterone.

14C-17-hydroxyprogesterone was incubated with 7000 times g times 20 min supernatants of rat testis homogenates in the presence of various concentrations of 3H-progesterone, both under conditions where metabolism would take place and where it would be prevented. When metabolism was prevented, the ratio of progesterone to 17-hydroxyprogesterone in the microsomal fraction was 3 times that which was added to the incubation medium. Progesterone competitively inhibited 17,20-lyase action on added 17-hydroxyprogesterone but not on 17-hydroxyprogesterone formed from the added progesterone. The rate of formation of 17-hydroxyprogesterone from progesterone, however, was inhibited by added 17-hydroxyprogesterone. The results indicate that there is no free exchange of an intermediate between progesterone and androstenedione with the soluble fraction, either inside or outside the microsomal vesicle. The limited exchange with 17-hydroxyprogesterone in solution probably represents exchange with an enzyme-bound intermediate.

Animals↗
PubMed1978

In vitro effect of 16alpha-hydroxyprogesterone on the enzyme activities related to androgen production in human testes.

Progesterone was converted in vitro to 16alpha- and 17alpha-hydroxyprogesterones in the presence of NADPH by the testicular microsomal fraction (precipitate at 10 000 x g-105 000 x g) obtained from patients with prostatic carcinoma. 16alpha-Hydroxyprogesterone was not metabolized by either the microsomal or the cytosol fractions, and accumulated in the incubation medium. 16alpha-Hydroxyprogesterone competitively inhibited the activity of the C-17-C-20 lyase in the testicular microsomal fraction with an estimated inhibitor constant of 72 micron. Moreover, the 16alpha-hydroxyprogesterone non-competitively inhibited the activity of the 20alpha-hydroxysteroid dehydrogenase in the testicular cytosol fraction and had an estimated inhibitor constant of 52.9 micron. Other testicular enzymes related to steroid metabolism, such as delta5-3beta-hydroxysteroid dehydrogenase coupled with the delta4-delta5 isomerase, 16alpha-hydroxylase, 17alpha-hydroxylase, and 17beta-hydroxysteroid dehydrogenase were not influenced in vitro by 16alpha-hydroxyprogesterone at the concentration of 0.1 mM. From these findings, it is concluded that 16alpha-hydroxyprogesterone inhibit specifically the cleavage of the side-chain of 17alpha-hydroxypregnenes in the course of androgen formation from pregnenolone in vitro.

Androgens↗
PubMed1992

Ketoconazole inhibition of the bifunctional cytochrome P450c17 does not affect androgen formation from the endogenous lyase substrate. The catalytic site remains refractory in the course of intermediary hydroxyprogesterone processing.

The inhibition of the bifunctional steroidogenic cytochrome P450c17 (CYP17: steroid-17 alpha-hydroxylase/steroid-17,20-lyase) by the imidazole-type fungicide, [(+/-)-cis-1-acetyl-4-[4-[[2-(2,4-dichlorophenyl)-2-(1H-imidazol-1-yl- methyl)-1,3-dioxolan-4-yl]methoxy]phenyl]piperazine) (ketoconazole), was investigated with the aim of differentiating between effects on androgen formation from exogenously added and endogenously produced 17 alpha-hydroxyprogesterone. Using microsomal membranes from rat testis, turnover of progesterone by P450c17 was competitively inhibited by ketoconazole with KI = 0.40 microM. Ketoconazole did not affect the linear relationship between the ratio of productive events (corresponding to androgen formation rates) versus abortive events (corresponding to 17 alpha-hydroxyprogesterone formation rates) and the sum of catalytic events. This was an indication that this inhibitor did not interfere with intermediate processing by P450c17. Androgen formation from exogenous but not from endogenous 17 alpha-hydroxyprogesterone was competitively inhibited by ketoconazole. The simultaneous conversion of 1 microM each of [3H]progesterone and 17 alpha-hydroxy[14C]progesterone was also reduced by ketoconazole. Calculation of 3H/14C ratios in the 17 alpha-hydroxyprogesterone and androgen fractions revealed that the endogenous 17 alpha-hydroxyprogesterone pool was metabolized to androgens at rates 6.4, 11.6, 17.6 and 21.2-fold faster than the exogenous pool in the presence of 0.5, 1, 2 and 4 microM ketoconazole, respectively; this value was only 4.0 in controls. It is concluded that ketoconazole inhibits turnover of steroid ligands only when they approach the P450c17 active site in a substrate-state and that inhibition of androgen formation from progesterone is due to inhibition of the first catalytic step only. A model is described in which the P450c17 active site is refractory towards ketoconazole when the intermediary steroid is retained and being processed at that site.

17-alpha-Hydroxyprogesterone↗
PubMed1976

In vivo and in vitro studies of 15alpha-hydroxyprogesterone in the human placenta.

Studies were conducted to determine the fate of 15alpha-hydroxyprogesterone in human placental tissue. Tritiated 15alpha-hydroxyprogesterone was perfused through normal human placentas in situ at the time of Cesarean section and incubated with a 10,000x g microsomal supernate of the placenta in vitro. In both systems the substrate, but no additional metabolites were identified. These findings indicate that 15alpha-hydroxyprogesterone is not metabolized during its passage in the human term placenta, and suggests that because of its fetal origin clinical measurements of 15alpha-hydroxyprogesterone may provide a valuable index to the status of fetal viability.

Crystallization↗
PubMed1979

Radioimmunoassay of 17 alpha-hydroxyprogesterone in saliva, parotid fluid, and plasma of congenital adrenal hyperplasia patients.

We report a radioimmunoassay sensitive enough to determine 17 alpha-hydroxyprogesterone concentrations in 200 microliter of parotid fluid or mixed whole saliva. Because the correlation of concentrations in matched samples of parotid fluid and saliva was excellent (r = 0.98), we exclusively used saliva, which is easier to collect, in later studies. The assay is specific; saliva samples assayed with and without thin-layer chromatographic purification showed no significant difference. The assay is also precise, and has a lower limit of sensitivity of 4 pg per assay tube. In 14 patients having congenital adrenal hyperplasia from a C21-hydroxylase enzyme deficiency, all of whom were receiving cortisol replacement therapy, the range in 17 alpha-hydroxyprogesterone concentrations observed in saliva (67-26,300 pmol/L) was about 20-fold that seen in 32 healthy children (90-1520 pmol/L). The close correlation (r = 0.91) between 17 alpha-hydroxyprogesterone concentrations in matched samples of saliva and plasma from these patients indicates that determination of steroids in saliva could well replace determination in plasma. This concept is supported by 17 alpha-hydroxyprogesterone concentrations monitored throughout 24 h from one patient and following stimulation with synthetic corticotropin in another patient.

Adolescent↗
PubMed1975

Early diagnosis of congenital adrenal hyperplasia by measurement of 17-hydroxyprogesterone.

Plasma 17-hydroxyprogesterone was measured by a simple radioimmunoassay technique in six infants, aged 3 days to 3 months, with congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Hormonal levels in this group were compared to those of twenty normal newborns and to those found in sixty samples of umbilical vein blood from normal deliveries. Plasma 17-hydroxyprogesterone concentrations were markedly elevated in all congenital adrenal hyperplasia infants (range 544.7-1837 nmol/l, normal 3.03-19.06) at a time when urinary studies in some of these were either not diagnostic or inconclusive. In one infant whose cord blood was analysed, the level was also greatly raised. The data suggest that early definitive diagnosis of congenital adrenal hyperplasia can be established by measurement of plasma 17-hydroxyprogesterone.

Adrenal Glands↗
PubMed1975

Role of 11 beta-hydroxyprogesterone in biosynthesis of corticosterone from progesterone in guinea pig adrenals.

Slices of male guinea pig adrenals were incubated with trace amount of 3-H7 alpha-progesterone and the percentage of incorporation of 3-H into various steroids at various intervals was measured. It was found that 3-H accumulates predominately in 11 beta-hydroxyprogesterone as compared to DOC. This indicates that, in guinea pig adrenals, 11 beta-hydroxyprogesterone plays a dominant role in a formation of corticosterone from progesterone. The observed sequence of changes in progesterone label accumulation in 17-hydroxycompounds indicates they pathway of cortisol synthesis through the intermediate formation of 17-hydroxyprogesterone and 11-deoxycortisol.

Adrenal Glands↗
PubMed1975

[Simultaneous study of plasma gonadotropins, estrogens, progesterone and 17-hydroxyprogesterone during the ovulatory cycle].

Plasma levels of gonadotrophins, estrone, estradiol, 17-hydroxyprogesterone and progesterone were studied throughout an ovulatory cycle in 11 normal women. For each of these hormones, the initiation of a secretory cycle occured at a different time: on the 10th day after mid-cycle surge for gonadotrophins, on the 3 rd day of menses for estradiol and somewhat later for estrone, on the 8th day of cycle for 17-hydroxyprogesterone and on the day of the LH surge for progesterone. Mean plasma levels and range were reported for every studied hormone. The mid-cycle surges of LH and FSH were found always coincident, after which their concentration decreased simultaneously; during the late follicular phase the increasing LH curve intersected the decreasing FSH curve. A peak of estradiol occured in every subject except one on the day before the mid-cycle surge of LH; a peak of plasma estrone occured either on the day of the LH peak or on the day before. For these two hormones the luteal phase range is always below the peak level. A peak of 17-hydroxyprogesterone occured in every subject on the same day than the mid-cycle LH peak, but the plasma level increased during the luteal phase up to higher levels. Progesterone concentration increased on the day of the LH surge, indicating the initiation of luteinization prior to ovulation.

Adult↗
PubMed1992

Estradiol, progesterone, 17-hydroxyprogesterone, androstenedione and CA125 in patients with ovarian carcinoma.

Estradiol, progesterone, 17-hydroxyprogesterone, androstenedione and CA125 were assayed in 25 women (12 oophorectomized before entering the study) with ovarian carcinoma. The data from patients were ordered according to the presence or absence of the gonads. The patients with ovaries (Group A) showed significantly higher levels of estradiol (p less than 0.01), progesterone (p less than 0.01) and 17-hydroxyprogesterone (p less than 0.01) than controls. This difference was not observed between oophorectomized patients (Group B) and controls. CA125 levels were significantly higher in patients that in controls (p less than 0.001) irrespective of the ovarian status of the patients. Eleven patients were followed during chemotherapy. Significant reductions of estradiol (p less than 0.01) and CA125 (p less than 0.001) levels after three courses of chemotherapy were observed. These data confirm that women with ovarian carcinoma produce an abnormal amount of steroids. Nevertheless, a marked difference between patients with and without ovaries was observed, suggesting that reported data might be biased by the presence of gonadal tissue. Thus the clinical application of steroids as tumor markers in unselected patients is limited.

17-alpha-Hydroxyprogesterone↗
PubMed1976

Experimental studies on the positive feedback effect of progesterone, 17 alpha-hydroxyprogesterone and 20 alpha-dihydroprogesterone on the pituitary release of LH and FSH in the human female. The estrogen priming of the progesterone feedback on pituitary gonadotropins in the eugonadal woman.

Administration of progesterone eugonadal women during the midfollicular phase of the menstrual cycle failed to induce a positive feedback effect on the serum concentrations of LH and FSH. The levels of estradiol in serum decreased following the injection of progesterone without a parallel change in LH and FSH concentrations indicating a direct ovarian effect of the exogenous progesterone. In the late follicular phase of the cycle, when preovulatory levels of estradiol were present in serum, or under a ethinyl estradiol treatment progesterone was able to induce an LH discharge indicating the requirement of an estradiol priming of the positive feedback of progesterone in eugonadal women. In order to establish the time required for a sufficient estrogen priming with preovulatory levels of estradiol in serum 3 mg of estradiol-benzoate were administered i.m. 1, 12 and 24 h prior to the administration of 30 mg of microcristalline progesterone in the midfollicular phase of the menstrual cycle, when progesterone alone did not cause an LH surge. Only when estradiol-benzoate was injected 24 h prior to the progesterone administration an LH surge reproducible in time course and magnitude occurred. Administration of estradiol-benzoate alone under these conditions did not cause an LH surge within the elapse of time after the injection when the progesterone induced LH surge occurred. Thus, these experiments demonstrate that a defined estrogen priming is required for the positive feedback effect of progesterone on the gonadotropin release in eugonadal women. Furthermore, progesterone levels in serum of about only 1--2 ng/ml were required for the induction of an LH surge indicating that under physiological conditions progesterone may have an supplementory effect on the primarily estradiol induced LH midcycle peak. 17-hydroxyprogesterone administered during the mid follicular phase of the menstrual cycle and under pretreatment with ethinyl estradiol failed to induce a positive feedback effect on the serum concentrations of LH and FSH, indicating that this steroid does not play a regulatory role on the midcycle LH release in women. 20alpha-dihydroprogesterone administered under the same experimental conditions as 17-hydroxyprogesterone seems to be able to induce an LH surge in serum provided there is an adequate estrogen priming.

20-alpha-Dihydroprogesterone↗
PubMed1976

Diurnal testosterone and 17alpha-hydroxyprogesterone in peripheral plasma of young post-pubertal bulls. A study by frequent sampling.

Testerone and 17alpha-hydroxyprogesterone were measured in the peripheral plasma of 6 young post-pubertal bulls of 1 year of age, by separate radioimmunoassays. Samples were collected every hour for 25 h at the beginning of each of four seasons. On a separate occasion blood samples were collected from one bull every 10 min for 2 h. As a result of the study, testosterone and 17alpha-hydroxyprogesterone appeared to be secreted episodically. These two steroid peaks showed good correlation. Each 24 h period showed its own characteristic pattern of pulsatile changes. Episodic secretion seems to be progressive rather than rapid and short lived. No real circadian rhythm was observed but at about 10.00 a.m. a trough in these steroid secretions occurred. This was followed by an increase in peripheral plasma concentration. These troughs occurred at all seasons after the morning feed and while semen was being collected in the performance test station.

Animals↗
PubMed1977

Treatment of benign prostatic hyperplasia with hydroxyprogesterone-caproate: placebo-controlled study.

A placebo-controlled study with progesterone compound, 17-alpha-hydroxyprogesterone 17-n-caproate (Primostat), in 39 patients with benign enlargement of the prostate is reported. Statistical analysis of the results showed no evidence of significant improvement in patients receiving hydroxyprogesterone-caproate. No evidence of an effect as compared with the placebo was found when the residual urine, prostatic size, and histologic and ultrastructural changes of the removed prostatic gland in 6 of the patients, and in the luteinizing hormone, follicle-stimulating hormone, and estrogen urine levels in 21 patients were examined. Subjective effects, when carefully analyzed, provided some beneficial evidence, however not substantiated, when the patients' mode of voiding was carefully watched. The reported beneficial subjective improvement might be attributed to the enhancement of the beta-adrenergic response by the progesterone compound of the adrenergic receptors in the posterior urethra and bladder, presumably causing relaxation of its smooth muscle. The problems associated with the choice and measurement of parameters to be used in this type of investigation are discussed, and the absolute necessity of proper controls, statistical analysis, and close follow-up of the patients is pointed out.

Aged↗
PubMed1992

Incidental adrenal nodules: association with exaggerated 17-hydroxyprogesterone response to adrenocorticotropic hormone.

The etiology of incidentally discovered, nonfunctional adrenal nodules was evaluated by using the 17-hydroxyprogesterone (17-OHP) response to synthetic adrenocorticotrophin (cosyntropin) (ACTH) administration. Patients who were discovered to have adrenal nodules and age-matched volunteers were studied. A total of 12 patients with adrenal nodules and 10 control subjects were studied. None of the patients with adrenal nodules had any evidence of hormonal hypersecretion consistent with pheochromocytoma, Cushing's syndrome or hyperaldosteronism. All subjects had serum 17-OHP and cortisol responses measured at baseline and at 30 and 60 min following the intravenous administration of 250 micrograms of ACTH. Baseline 17-OHP levels in patients with adrenal nodules were not significantly different from those of the normal controls (adrenal nodules 17-OHP: 75 +/- 13 vs control 68 +/- 11 ng/dl). After stimulation with ACTH, both 30 min and 60 min 17-OHP levels in patients with adrenal nodules (322 +/- 47 and 361 +/- 54 ng/dl, respectively) were significantly elevated over the responses seen with the controls (169 +/- 29 ng/dl at 30 min, p < 0.015, and 158 +/- 20 ng/dl at 60 min, p < 0.004). Baseline and post-ACTH serum cortisol levels were similar in both groups. Out of these twelve patients with adrenal nodules, nine were reevaluated twelve months later. In this group the basal 17-OHP remained comparable to normal levels (72 +/- 8.4 ng/dl) whereas the post-ACTH levels still remained exaggerated (30 and 60 min values 327 +/- 37 and 373 +/- 39 ng/dl).(ABSTRACT TRUNCATED AT 250 WORDS)

17-alpha-Hydroxyprogesterone↗
PubMed1991

Serum 17 alpha-hydroxyprogesterone in infants and children as measured by a direct radioimmunoassay kit.

A direct 17 alpha-hydroxyprogesterone (17-OHP) radioimmunoassay kit was used for the assay of samples from 219 infants and children. The kit was used according to the manufacturer's protocol on unextracted serum or plasma and also on reconstituted material extracted from the serum with propanol-heptane. The extraction protocol recovers approximately 88% of 17-OHP. Patients were grouped as infants 3-90 days (96 subjects) or older children, adolescents and young adults 91 days-20 years (123 subjects). 17-OHP results by the direct and extraction protocols correlated but the slopes of the regression lines (0.43 and 0.63) differed in the two groups, indicating that only about 49% of the immunoreactive material measured by the kit in the infants was 17-OHP whereas the corresponding percentage was 72% in the older children. Despite this nonspecificity, the present antibody is much more specific for 17-OHP in the presence of neonatal plasma steroids than that used previously. Reference values were obtained for the two groups using the method with and without an extraction step. 17-OHP values on four untreated patients with CAH were clearly elevated at the time of diagnosis. It is recommended that when the kit is used with neonatal and infant samples, an extraction step should be incorporated to enhance specificity.

17-alpha-Hydroxyprogesterone↗
PubMed1992

The effect of 17 alpha-hydroxyprogesterone caproate/oestradiol valerate on the development and outcome of early pregnancies following in vitro fertilization and embryo transfer: a prospective and randomized controlled trial.

A prospective and randomized study was performed to investigate the effect of supportive hormones on the development and outcome of early pregnancies following in vitro fertilization and embryo transfer. Immediately after pregnancies were confirmed endocrinologically on day 15 after oocyte collection, 17 alpha-hydroxyprogesterone caproate and oestradiol valerate (PC/EV) was administered to half of the patients in a randomly controlled trial. One group received supportive treatment until the twelfth week of gestation, whereas the other group received no treatment at all. Both groups were followed up by measurements of serum levels of human chorionic gonadotrophin (HCG), oestradiol and progesterone every three days until day 35, when a first ultrasound examination was carried out to confirm fetal vitality. Subsequently, pregnancies were monitored sonographically at regular intervals. In cases of miscarriage, dilatation and curettage was performed and histology analysed. A total of 120 pregnant patients entered the study: 55 of them received hormone treatment and 65 patients were controls. Within the treatment group 48 (89%) clinically ongoing pregnancies were observed, five (9%) miscarriages occurred after the seventh week of gestation and one preclinical pregnancy was noted. In the control group, 38 (59%) ongoing pregnancies were observed, nine (14%) miscarriages occurred and 17 (27%) preclinical pregnancies were recorded. Two ectopic pregnancies, one in each group, were excluded from evaluation. A significantly higher percentage of pregnancies were intact at 7 weeks of gestation after treatment with PC/EV (p less than or equal to 0.01).

17 alpha-Hydroxyprogesterone Caproate↗