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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↗
PubMed1995

Molecular abnormalities of the 21-hydroxylase gene in hyperandrogenic women with an exaggerated 17-hydroxyprogesterone response to short-term adrenal stimulation.

OBJECTIVE: Our purpose was to establish the incidence of point mutations of the 21-hydroxylase gene (CYP21) in hyperandrogenic women with and without a 17-hydroxyprogesterone response to corticotropin stimulation above normal but below those levels associated with nonclassic adrenal hyperplasia. STUDY DESIGN: We studied 22 patients with hirsutism or hyperandrogenic oligoovulation: eight with an exaggerated net increase in 17-hydroxyprogesterone (i.e., change in 17-hydroxyprogesterone between 8.8 and 36 nmol/L) and 14 with a normal change in 17-hydroxyprogesterone. Large deletions of the 21-hydroxylase gene were evaluated by laser densitometry. Point mutations were detected with the polymerase chain reaction and dot blot hybridization analysis and included 30 Leu, intron-2 (G), 8 bp deletion exon-3, 172 Asn, 236-237-239 exon-6, 281 Leu, 318 stop, 339 His, 341 Trp, 356 Trp, and 453 Ser. RESULTS: Four patients with an increase in 17-hydroxyprogesterone carried a 281 Leu mutation, one patient had an intron-2 (G) mutation, and one had a complete deletion of CYP21. Only two of these patients demonstrated no obvious abnormality of CYP21. In contrast, only one of the control patients demonstrated a CYP21 abnormality, a significant difference (p < 0.001). CONCLUSIONS: These findings suggest that the majority of hyperandrogenic women with an exaggerated 17-hydroxyprogesterone response to corticotropin stimulation are heterozygotes (carriers) for inherited defects of CYP21. Whether these mutations are incidental to the androgen excess or predispose to the development of this disorder remains to be determined.

17-alpha-Hydroxyprogesterone↗
PubMed1993

17-Hydroxyprogesterone rhythms and growth velocity in congenital adrenal hyperplasia.

Six patients on steroid replacement therapy for congenital adrenal hyperplasia provided capillary blood samples collected at 0800, 1200, 1700, and 2200 h, on to filter paper for 17-hydroxyprogesterone analysis. There was a strong correlation between 17-hydroxyprogesterone day profiles and height velocity over a 4 year period of study. Steroid over-replacement, identified by significantly decreased height velocity (Standard Deviation Score [SDS] 1.92), caused suppression of 17-hydroxyprogesterone concentrations to below 10 nmol/L throughout the day. Near average height velocity (Standard Deviation Score 0.245) was accompanied by suppression of 17-hydroxyprogesterone concentrations below 40 nmol/L but with significant diurnal variation. Under-replacement with rapid height velocity and bone maturation was accompanied by non-suppression of 17-hydroxyprogesterone concentrations (i.e. > 40 nmol/L). These results suggest that serial blood spot 17-hydroxyprogesterone measurements are a convenient and helpful supplement to measurements of height velocity and bone age maturation to monitor steroid replacement therapy in congenital adrenal hyperplasia. These measurements may be useful particularly in differentiating between over-replacement and appropriate replacement, and should allow adjustments in dose before abnormal growth patterns are established.

17-alpha-Hydroxyprogesterone↗
PubMed2006

Population-based case-control teratogenic study of hydroxyprogesterone treatment during pregnancy.

Hydroxyprogesterone, a synthetic progestin, was used for the treatment of pregnant women with threatened abortion and preterm delivery. Previous studies showed some association between hydroxyprogesterone use during early pregnancy and some specific congenital abnormalities. The population-based large Hungarian data set seemed to be appropriate to check this possible association. The Hungarian Case-Control Surveillance of Congenital Abnormalities between 1980 and 1996 includes 22 843 cases with congenital abnormalities and 38 151 controls without any defect. 318 (1.4%) cases, while 433 (1.1%) controls had mothers with hydroxyprogesterone treatment during pregnancy (adjusted POR with 95% CI: 1.3, 1.1-1.5). However, there was no association between risk for any congenital abnormality group and a higher use of maternal hydroxyprogesterone treatment during the second and third month of gestation. On the other hand hydroxyprogesterone is not effective in the prevention of preterm delivery. In conclusion, there was no detectable risk for congenital abnormalities in the offspring of mothers with hydroxyprogesterone treatment during early pregnancy, however, there is no reasonable indication of this treatment during pregnancy.

17 alpha-Hydroxyprogesterone Caproate↗
PubMed1993

Inhibitory effects of 20 alpha-hydroxyprogesterone on steroid hydroxylation reactions of guinea pig adrenal microsomes.

Using guinea pig adrenal microsomes, we studied the inhibitory effects of 20 alpha-hydroxyprogesterone on steroid hydroxylation reactions catalyzed by cytochromes P-450. When 17 alpha-hydroxyprogesterone was used as a substrate, 20 alpha-hydroxyprogesterone functioned as a competitive inhibitor on the C17-C20 bond cleavage reaction of P-450(17)alpha lyase. The inhibition constant, Ki was 1.37 mumol/L. 20 alpha-hydroxyprogesterone also competitively inhibited the conversion of 17 alpha-hydroxyprogesterone to 11-deoxycortisol by the action of P-450c21. The value of Ki was 1.73 mumol/L. When progesterone was used as a substrate, 20 alpha-hydroxyprogesterone inhibited neither the 21-hydroxylation of P-450c21, the C17-C20 bond cleavage, nor 17 alpha-hydroxylation of P-450(17)alpha lyase. Based on these results, we can deduce that the production of androstenedione from progesterone by the action of P-450(17)alpha lyase proceeds through a successive monooxygenase reaction.

17-alpha-Hydroxyprogesterone↗
PubMed2006

Adequacy of saliva 17-hydroxyprogesterone determination using various collection methods.

Steroids determination in saliva offers several advantages. The collection of saliva is a noninvasive, less stressful technique than blood withdrawal and reflects the circulating unbound fractions. The suitability of saliva for 17-hydroxyprogesterone and cortisol determinations has been documented in healthy subjects as well as in diseases like Congenital Adrenal Hyperplasia and Cushing syndrome. The aim of the study was to compare the influence of different collection methods on the results of 17-hydroxyprogesterone measurement in saliva collected by different ways, using commercially available RIAs developed for plasma. 17-hydroxyprogesterone was determined in 64 healthy adult volunteers (30 males, 34 females) in serum (Group SE) and in saliva collected before meals at 8-10 p.m. by directly spitting into a plastic tube (Group SP), using a cotton swab (Group SA) and using a polyester swab Salivette (Group SB). We used a commercially available direct radioimmunoassay without separation technique. The 17-hydroxyprogesterone mean values (ng/ml) were 1.16+/-1.3 (Group SE), 0.056+/-0.046 (Group SP), 0.089+/-0.048 (Group SA) and 0.058+/-0.049 (Group SB). The detection limit was 0.010 ng/ml. The correlations between the values in serum (Group SE) and in saliva were: r=0.77, p<0.05 (Group SP); r=0.62, p<0.05 (Group SA); r=0.70, p<0.05 (Group SB). The saliva values corresponding to the serum cut-off point of 3 ng/ml upper limit of normal values were in ng/ml 0.13 (Group SP), 0.16 (Group SA) and 0.11 (Group SB). In conclusion, 17-hydroxyprogesterone determinations in saliva using commercially available RIAs primarily developed for serum, is a reliable and easy to perform procedure. The three different methods of saliva collection showed 17-hydroxyprogesterone concentrations to have good agreement.

17-alpha-Hydroxyprogesterone↗
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↗
PubMedDate not supplied

Evaluation of the basal and post-adrenocorticotrophic hormone serum concentrations of 17-hydroxyprogesterone for the diagnosis of hyperadrenocorticism in dogs.

Serum concentrations of 17-hydroxyprogesterone and cortisol were measured before and after the administration of exogenous adrenocorticotrophic hormone (ACTH) to three groups of dogs: 27 healthy dogs (group 1), 19 dogs with non-adrenal illness (group 2) and 46 dogs with hyperadrenocorticism (group 3). The median (range) post-ACTH concentrations of 17-hydroxyprogesterone were 5.0 (22.2 to 16.8), 6.9 (2.0 to 36.2) and 14.4 (1.7 to 71) nmol/litre in groups 1, 2 and 3, respectively. There were no significant differences in the basal or post-ACTH concentrations of cortisol or 17-hydroxyprogesterone between groups 1 and 2. The post-ACTH concentrations of 17-hydroxyprogesterone in group 3 were significantly (P<0.001) greater than those in groups 1 and 2 combined. The area under the receiver operating curve (ROC) for the post-ACTH concentration of cortisol (0.94) was significantly greater than that for the post-ACTH concentration of 17-hydroxyprogesterone (0.76). Using a two-graph ROC analysis, a cut-off of 8.5 nmol/litre was found to maximise both the sensitivity and specificity of the post-ACTH concentration of 17-hydroxyprogesterone for the diagnosis of hyperadrenocorticism at 71 per cent. With a cut-off of 4.5 nmol/litre the sensitivity increased to 90 per cent but the specificity decreased to 40 per cent; with a cut-off of 16.7 nmol/litre the specificity increased to 90 per cent but the sensitivity decreased to 47 per cent.

17-alpha-Hydroxyprogesterone↗
PubMed1981

Determination of serum 17 alpha-hydroxyprogesterone by liquid chromatography.

17 alpha-Hydroxyprogesterone, cortisol, and 11-deoxycortisol were extracted with methylene chloride, separated by liquid chromatography, identified by their retention times, and quantitated by monitoring the absorbance at 254 nm. The method is specific and sensitive to as little as 2.5 ng of 17 alpha-hydroxyprogesterone. Mean analytical recovery of added 17 alpha-hydroxyprogesterone was 99% (SD 11%) and the CV for the same or different assays ranged from 3.5 to 9.4%. 6 beta-Hydroxyprogesterone was used as the internal standard. Concentrations of 17 alpha-hydroxyprogesterone in serum of normal men and women were less than 2.5 micrograms/L, but women in the luteal phase of the menstrual cycle had higher values. Mean 17 alpha-hydroxyprogesterone content in serum from mixed cord blood of normal newborns was 28.1 (SD 13.8) micrograms/L. Results by this method correlated well (r = 0.97) with results by radioimmunoassay, but were somewhat higher.

Adrenal Hyperplasia, Congenital↗
PubMed2004

Impairment of male reproduction in adult rats exposed to hydroxyprogesterone caproate in utero.

Hydroxyprogesterone caproate is one of the most effective and widely used drugs for the treatment of uterine bleeding and threatened miscarriage in women. Hydroxyprogesterone caproate was administered to pregnant rats in order to assess the effect of intraperitoneal exposure to supranormal levels of hydroxyprogesterone caproate on the male reproductive potential in the first generation. The cauda epididymal sperm count and motility decreased significantly in rats exposed to hydroxyprogesterone caproate during embryonic development, when compared with control rats. The levels of serum testosterone decreased with an increase in follicle stimulating hormone and luteinizing hormone in adult rats exposed to hydroxyprogesterone caproate during the embryonic stage. It was suggested that the impairment of male reproductive performance could be mediated through the inhibition of testosterone production.

17 alpha-Hydroxyprogesterone Caproate↗
PubMed1993

Genital and nongenital teratogenesis of prenatal progestogen therapy: the effects of 17 alpha-hydroxyprogesterone caproate on embryonic and fetal development and endochondral ossification in the C57B1/6J mouse.

OBJECTIVE: The current study assesses the effects of 17 alpha-hydroxyprogesterone caproate on embryo-fetal development, with a particular focus placed on intrauterine endochondral bone development and growth. STUDY DESIGN: Primigravid C57 BI/6J mice were administered 17 alpha-hydroxyprogesterone caproate by means of subdermal pellets designed to deliver doses of 0.5, 5.0, and 50.0 mg/kg/day on gestational days 7 through 19. Assuming a dosage regimen of 250 mg per 50 kg per week in humans for the treatment of threatened spontaneous abortion, the doses used were 0.7, 7.0, and 70.0 times the human dose equivalent. The time course of exposure encompassed the period of organogenesis through the late fetal period. RESULTS: No maternal toxicity was noted throughout the course of 17 alpha-hydroxyprogesterone caproate administration. Fetal weight at term and the percentage of resorptions, dead fetuses, male fetuses, and malformations at term were not significantly affected at any evaluated dose when compared with control group values. The steroid did not exert a significant influence on any assessed parameter of endochondral bone development or growth, even at a dosage concentration that far exceeded the human therapeutic dose equivalent. As would be expected, fetal weight was directly correlated with diaphyseal length and also influenced the relationship of cartilage to osseous tissue in both the humeri and femora. There were no 17 alpha-hydroxyprogesterone caproate dose and fetal sexual phenotype interactive effects noted with regard to any developmental or bone growth parameter measured, thus discounting any sexual phenotype-related toxic or teratogenic sensitivities. CONCLUSION: The data indicate that 17 alpha-hydroxyprogesterone caproate administered at doses of up to 70 times the human dose equivalent did not induce increases in the frequency of genital and, importantly, nongenital teratogenesis in spite of exposure during the critical period of organogenesis. Additionally, the steroid did not affect limb morphogenesis or endochondral ossification.

17 alpha-Hydroxyprogesterone Caproate↗
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↗
PubMed2006

17alpha-hydroxyprogesterone caproate for the prevention of preterm delivery: A cost-effectiveness analysis.

OBJECTIVE: To evaluate whether the use of 17alpha-hydroxyprogesterone caproate for the prevention of recurrent preterm deliveries is cost-effective. METHODS: Using decision-analysis modeling, we compared the cost-effectiveness of using 17alpha-hydroxyprogesterone caproate in four subgroups: 1) Prior preterm deliveries less than 32 weeks; 2) prior preterm deliveries 32-37 weeks; 3) prior term delivery; and 4) no prior delivery. Each subgroup was compared with a "no treatment" group. Costs included those for 17alpha-hydroxyprogesterone caproate, hospital admissions, and complications from preterm deliveries. The main outcome measures include cost per quality-adjusted life-year gained and the number of preterm deliveries prevented. Secondary outcomes include neonatal complications prevented. One-way and multiway sensitivity analyses were performed. RESULTS: The use of 17alpha-hydroxyprogesterone caproate for the prevention of preterm deliveries result in cost-savings in women with prior preterm deliveries less than 32 weeks and 32-37 weeks. The sensitivity analyses revealed the model to be robust over a wide range of values for evaluated variables. CONCLUSION: Within our baseline assumptions, 17alpha-hydroxyprogesterone caproate was associated with cost-savings when used for the prevention of preterm deliveries in women with prior preterm deliveries.

17 alpha-Hydroxyprogesterone Caproate↗
PubMed1987

Production of testosterone from progesterone by rat testicular microsomes without release of the intermediates 17 alpha-hydroxyprogesterone and androstenedione.

It has been shown that during the in vitro conversion of progesterone to androstenedione, 17 alpha-hydroxyprogesterone is not an obligatory intermediate which equilibrates with freely diffusible steroids in the incubation medium. Recently a cytochrome P-450 was purified that catalyzed, in addition to hydroxylase/lyase activities, reduction of androstenedione to testosterone. In order to determine whether progesterone could be transformed to testosterone without both intermediates (17 alpha-hydroxyprogesterone and androstenedione) being equilibrated with steroids in the medium, several double-label double-substrate experiments were performed. When rat microsomes were incubated with an equimolar mixture of [14C]progesterone and 17 alpha-hydroxy[3H]progesterone, androstenedione was isolated with a 11-fold higher 14C/3H ratio than 17 alpha-hydroxyprogesterone, indicating that androstenedione could not be produced from free, diffusible 17 alpha-hydroxyprogesterone. Incubation of an equimolar mixture of 17 alpha-hydroxy[3H]progesterone and [14C]androstenedione with testicular microsomes resulted in the incorporation of 3-4-fold more 17 alpha-hydroxyprogesterone into testosterone than of androstenedione, although the latter is the immediate precursor of testosterone. In an experiment in which equimolar concentrations of [3H]progesterone and [14C]androstenedione were incubated with testicular microsomes, the large pool of progesterone inhibited competitively lyase activity, but still the label of progesterone was incorporated into testosterone to the same extent as that of androstenedione. These results indicate that testosterone can be produced by immature rat testicular microsomes from added progesterone on an organized unit without the intermediates equilibrating with the incubation medium.

17-alpha-Hydroxyprogesterone↗
PubMed1985

[Radioimmunoassay of salivary l7 alpha-hydroxyprogesterone. Values obtained in healthy subjects and in patients treated for congenital hyperplasia of the adrenal glands].

The authors describe a method for the radioimmunoassay of 17 alpha-hydroxyprogesterone in the saliva. The limit of detection is 1.96 fmole/tube. Salivary 17 alpha-hydroxyprogesterone was measured in control subjects. Values found were of 296 +/- 115 pmol/l in the male, and 251 +/- 23 pmol/l in the female during the follicular phase and 401 +/- 94 pmol/l during the luteal phase, and 115 +/- 30 pmol/l in the prepubertal child. Concentrations were much higher in the newborn and decreased during the first days of life. Variations in salivary concentrations were compared with those in plasma 17 alpha-hydroxyprogesterone during the 24-hour period and with the Synacthene stimulation test. The excellent correlation (r = 0.0969) between salivary 17 alpha-hydroxyprogesterone and plasma 17 alpha-hydroxyprogesterone in 28 patients being treated for 21 hydroxylase deficiency makes it possible to suggest salivary assay in place of plasma assay in the therapeutic follow-up of such patients.

17-alpha-Hydroxyprogesterone↗
PubMed1996

Proposed definitive methods for measurement of plasma testosterone and 17 alpha-hydroxyprogesterone.

OBJECTIVES: This report provides the results of the development and evaluation of definitive isotope dilution/mass spectrometry (ID/MS) methods for the determination of testosterone and 17 alpha-hydroxyprogesterone in human plasma at concentrations ranging from 1.4 to 37.9 nmol/L and 1.5 to 45.4 nmol/L, respectively. The internal standards were 16, 16, 17-2H-testosterone and 21,21,21, -2H-17 alpha-hydroxyprogesterone. The development of optimum extraction and derivatization procedures, and studies of storage time, temperature effects, accuracy, and precision are presented. RESULTS: The results indicate that the methods employing the TBDMS derivative of testosterone and MO-TMS derivative of 17 alpha-hydroxyprogesterone are capable of generating accurate and precise data at the inherently low concentrations given, with recovery greater than 95%. Accuracy of testosterone in the fortified steroid-free and pooled plasma by ID/MS measurement was good because the relative error ranged from +3.1% to -0.7, with a mean of 0.9% over the concentration levels of 1.4 to 37.9 nmol/L testosterone, and the imprecision ranged from 4.2% to 0.7% CV, with a mean of 1.9%. Accuracy of 17 alpha-hydroxyprogesterone in the fortified steroid-free and pooled plasma was also good, considering the inherently low concentrations. The relative error ranged from -2.1% to +1.5%, with a mean of 1.1%, and the imprecision ranged from 3.8% to 0.8% CV with a mean of 1.3% over concentration levels of 1.5 to 15.1 nmol/L. The high precision and accuracy and absence of statistically significant bias qualifies these methods as candidate definitive methods for plasma testosterone and 17 alpha-hydroxyprogesterone.

17-alpha-Hydroxyprogesterone↗
PubMed2001

Ovulation rate and litter size in gilts immunized against androstenedione and 17alpha-hydroxyprogesterone.

Two experiments were conducted to evaluate the effects of the immunization of gilts against ovarian steroids on ovulation rate and litter size. In Exp. 1, gilts (n = five gilts/treatment) at 165+/-1.6 d of age were immunized against either carrier (Control), androstenedione, or 17alpha-hydroxyprogesterone. Age at puberty and estrous cycle length averaged 208+/-5.5 (P = 0.67) and 20.3+/-2.8 d (P = 0.41), respectively, and were not affected by treatment. The androstenedione- and 17alpha-hydroxyprogesterone immunized gilts had higher (P < 0.02) ovulation rates than Controls (14.2, 14.2, and 11.4+/-0.8, respectively). Total pigs born (P = 0.66) and pigs born live (P = 0.65) for the androstenedione-treated group were not different from Controls. Gestation length was not different (P = 0.36) between any of the treatments and the Controls (115+/-0.9 d). Procedures used in Exp. 2 were similar to those in Exp. 1, except that only Control (n= 18) and 17alpha-hydroxyprogesterone (n = 16) treatments were included and only litter size at farrowing was measured. Total pigs and pigs born live were higher in the 17a-hydroxyprogesterone-treated gilts than in the Controls (12.6 vs 10.5+/-0.6, P < 0.02; and 11.4 vs 9.2+/-0.6; P < 0.01, respectively). Data from this study indicate that litter size in gilts can be increased by immunization against 17alpha-hydroxyprogesterone.

17-alpha-Hydroxyprogesterone↗
PubMed1996

Problems with salivary 17-hydroxyprogesterone determinations using the Salivette device.

After introduction of the Salivette device for saliva sampling, an increase of approximately 50 ng/l was noted normal values of salivary 17-hydroxyprogesterone in our laboratory compared with previous results obtained by collection of saliva by direct spitting. To further investigate this observation systematically, 17-hydroxyprogesterone was measured in saliva of 22 healthy adults after sampling without and with the Salivette and in 15 samples of distilled water rinsed over the cotton wool swab of the Salivette. The measurements were performed with a commercially available [125I]17-hydroxyprogesterone radioimmunoassay. All steps in assay performance were exactly the same. In both series, salivary 17-hydroxyprogesterone concentrations significantly increased by 40 ng/l (p < 0.05) with use of the Salivette. The variance of the differences covered a wide range. Our results confirmed that the use of the Salivette increased salivary 17-hydroxyprogesterone values by approximately 40 ng/l. This bias is unacceptable for the establishment of reference values, as these are in the range of 20-70 ng/l in the morning. Thus, at least with our assay, the use of the Salivette is discouraged. We speculate that the cotton wool swabs contain a material. possibly derived from the biological source of the cotton wool, which cross-reacts with the antibody in the assay or affects binding affinity.

17-alpha-Hydroxyprogesterone↗