Biomedical subjects

D Shoupe

Publications and source records attributed to D Shoupe.

At least 55 records · Page 3Linked to original sources

PubMed1987

Effects of the antiprogesterone RU 486 in normal women. I. Single-dose administration in the midluteal phase.

The response to a single oral dose of the antiprogesterone RU 486 was studied in the midluteal phase in 26 normal women. Each subject received a dose between 50 and 800 mg RU 486 on days 6 to 8 after the luteinizing hormone surge and blood samples were taken over the following 48 hours. Another group of five patients received a single oral dose of 200 mg RU 486 and blood sampling was extended for 14 days. Menses were induced in all women but one within 3 days after RU 486 administration. Two distinct patient populations emerged. In nine of the subjects, there was a single bleeding episode and the treatment cycle was significantly shorter (p less than 0.05) than the following cycle. In 16 of these 25 patients a second bleeding episode occurred 19.0 +/- 0.8 days after the luteinizing hormone surge. The total treatment cycle was significantly prolonged (p less than 0.05) when compared with the following cycle. In the group with a single bleeding episode, there was a significant decline in follicle-stimulating hormone, estradiol, and progesterone over the 48-hour sampling period, but there was no change in these values in the group with two bleeding episodes. These two groups could not be separated on the basis of RU 486 dose or serum levels. After the four higher doses, there was a dose-dependent rise in serum prolactin. There were no alterations in mean cortisol values with the three lower doses, but there was a significant increase at 24 and 48 hours after the higher doses. Serum levels of RU 486 were maximal between 1 and 4 hours and the half-life of serum RU 486 was determined to be 24 hours.

Administration, Oral↗

PubMed1987

Effects of the antiprogesterone RU 486 in normal women. II. Administration in the late follicular phase.

RU 486, a synthetic steroid with antiprogesterone receptor activity, was used to investigate the importance of progesterone on gonadotropin secretory dynamics in the midcycle of the normal menstrual cycle. Six normally cycling women were followed for three consecutive cycles. During each cycle, blood samples were obtained beginning on day 10 and continued until menses. After a control cycle, 100 mg RU 486 was given orally between days 10 and 17. The patients were followed for a posttreatment cycle with no medication. When RU 486 was given before the midcycle, the luteinizing hormone surge was delayed by 15.0 +/- 2.1 days after ingestion of the last pill, resulting in cycles of 40.6 +/- 2.6 compared with 28.0 +/- 2.3 days (p less than 0.01). During RU 486 administration and at the time a normal luteinizing hormone surge was anticipated, an attenuated luteinizing hormone/follicle-stimulating hormone surge was noted that was not followed by a rise in progesterone. After the attenuated surge a normal luteinizing hormone/follicle-stimulating hormone level occurred, with a normal rise in progesterone. Estradiol levels during RU 486 administration decreased during treatment, indicating a possible direct action of RU 486 on the ovary.

Administration, Oral↗

PubMed1987

Metabolism and serum binding of RU 486 in women after various single doses.

The metabolism of RU 486 was studied in female volunteers following a single oral administration of 100, 400, 600 or 800 mg of RU 486. The serum concentrations of RU 486 were generally not affected by the dose within the range examined and they stayed at micromolar concentrations during the 48 h studied. RU 486 was metabolized extensively in a dose-dependent manner by two-step demethylation, and by hydroxylation. Serum levels of the monodemethylated metabolite always exceeded those of RU 486. The concentrations of the didemethylated and hydroxylated metabolites equalled or exceeded those of RU 486 when the ingested dose was 400 mg or more. Monodemethylation and hydroxylation were rapid high-capacity reactions, whereas didemethylation was a lower-capacity reaction. In each group of different dosage, positive correlations were found between the individual mean alpha 1-acid glycoprotein (AAG) concentrations and the peak concentration of RU 486 measured at 1-2 h, versus the plateau concentration of RU 486 measured at 6 h. The in-vitro studies showed that the specific serum transport protein of RU 486, AAG, was saturated by RU 486 concentrations exceeding 2.5 microM. In serum at 40 nM and 2.5 microM RU 486 concentrations, 2.7% and 2.4%, respectively, of [3H]RU 486 was not protein bound. Purified AAG in phosphate buffer was able to bind [3H]RU 486 in a similar manner to that of serum. Thus our results suggest that AAG regulates in part the serum concentrations of RU 486, and RU 486 exceeding the specific serum transport capacity is effectively metabolized.

Administration, Oral↗

PubMed1986

Recovery of fertility after use of the levonorgestrel 20 mcg/d or Copper T 380 Ag intrauterine device.

Following use of either the Levonorgestrel 20 mcg/day or the TCu 380 Ag IUD in a randomized comparative study, 110 women stopped contracepting to have planned pregnancies. Pregnancy rates and recovery of fertility have been assessed. Age at acceptance, duration of use, parity and intervals between last pregnancy and IUD insertion or removal were similar for both groups. Life table pregnancy rates at one year were higher than 90 per cent for both device groups; but because some women quickly changed their minds or had been at risk of pregnancy only a short time before the analysis date, only 60.9 percent had actually become pregnant. Median time to planned pregnancy was 3 months for the TCu 380 Ag group and 4 months for the Levonorgestrel 20 group. Neither duration of use nor age at insertion or age at termination affected the pregnancy rates significantly.

Adult↗

PubMed1986

Pregnancy termination with a high and medium dosage regimen of RU 486.

Sixty healthy pregnant women who wished to terminate their pregnancy and who were no more than 49 days pregnant were treated with one of three different dose regimens of a synthetic progesterone receptor blocker, RU 486. Serum cortisol was measured to determine the antiglucocorticoid effects of this compound. The high dose but shorter treatment regimen (400 mg/day RU 486 X 4 days or 200 mg/day X 4 days) was associated with a high (greater than 80%) rate of side effects, especially nausea, vomiting, weakness and heavy bleeding and a low rate of success (10%). A group of 50 subjects received the medium dose but longer treatment regimen (100 mg/day X 7 days). This group had less side effects (40-60%) and a 72.3% success rate of complete abortion. The AM cortisol values were significantly elevated in all treatment groups but higher in those receiving the high dose. These values returned to normal one week following cessation of treatment. Medium dose but longer duration (100 mg/day X 7 days) of RU 486 treatment is associated with a higher success rate and less side effects than higher dose therapy administered over a shorter period. There were no predictive indices to determine which subjects would respond successfully. The reason for the failure of the drug in 30% of the subjects on the medium dose is not known at this time.

Abortifacient Agents↗

PubMed1986

Quantitation of RU 486 in human plasma by HPLC and RIA after column chromatography.

Chromosorb column chromatography was used for separation of RU 486 from its immunologically cross-reacting metabolites prior to quantitative analysis by radioimmunoassay (RIA) or high-performance-liquid chromatography (HPLC). The results of the two assay methods were in good agreement with each other (r = 0.99, n = 29). The retention time of RU 486 in our HPLC system was 2.5 min. Plasma concentrations of RU 486 were measured by HPLC up to 48 h following single oral administration of 100, 400, 600 and 800 mg of RU 486 to female volunteers. The plasma peak concentrations (2.0-2.5 micrograms/ml) were reached within the first hour. After redistribution, the plasma concentrations of RU 486 were not significantly affected by the doses studied but remained in the same range throughout the 48 hours. The plasma half-life between 24 and 48 hours was 27 hours or more. We conclude that HPLC is valuable in studies on the metabolism and pharmacokinetics of RU 486, but a less laborious RIA method after Chromosorb column chromatography is suitable and gives reliable results in large-scale clinical studies.

Administration, Oral↗

PubMed1985

Dose-related changes in LH bioactivity with intranasal GnRH agonist administration.

In order to evaluate changes in bioactive (bio) and immunoreactive (i) LH and in FSH after intranasal administration of a GnRH agonist, two doses (125 micrograms and 250 micrograms) of nafarelin acetate were administered for 14 weeks to 7 normal women. Maximum changes in gonadotropins were observed 2-4 hours after both the first and last doses. However, the maximum acute responses of iLH, bioLH and FSH were significantly reduced after 14 weeks of treatment while no changes occurred in the bio: iLH ratio. The decrease in these acute responses were not dose-related. Serum iLH and FSH levels obtained prior to each dose (baseline) were not significantly altered by 14 weeks with either dose. However, baseline serum bioLH was significantly reduced compared to pretreatment by 14 weeks but only with the 250 micrograms dose (p less than 0.05). This level was also significantly different from the level of bioLH achieved with 125 micrograms (p less than 0.05). The bio: iLH ratio was also significantly decreased with the 250 micrograms dose. Although serum estradiol and progesterone levels suggested ovarian follicular activity and luteinization with the 125 micrograms dose, this did not occur with 250 micrograms of intranasal nafarelin. These data support a dose response effect of intranasal agonist treatment on the bioactivity of LH and also suggest the relevance of measurements of bioLH in assessing the effectiveness of agonist therapy.

Administration, Intranasal↗

PubMed1985

Ovulation inhibition with nafarelin acetate nasal administration for six months.

A group of 24 women with normal menstrual cycles were treated with nafarelin acetate administered in doses of either 125 micrograms or 250 micrograms daily intranasally for 6 months. Each subject was studied for one ovulatory control cycle, six treatment cycles, and post-treatment until the return of ovulation was documented. Once a week progesterone, estradiol, follicle stimulating hormone, and luteinizing hormone were measured in the serum. Acute hormone responses to nafarelin acetate were determined on day 1, day 98 and day 186 of treatment. Two subjects failed to complete the treatment phase. One subject using the 250 micrograms daily dose of nafarelin acetate discontinued treatment on the sixth day because of heavy uterine bleeding. One subject using the 125 micrograms daily dose of the study drug terminated treatment on day 126 because of a 21-pound weight gain. There were significantly less presumed ovulatory cycles at the higher dose (2 out of 60 cycles) than at the lower dose (10 out of 54 cycles) (p less than 0.01). On the average menstrual cycles were reestablished 28.5 +/- 8.3 (S.D.) days after discontinuing the 125 micrograms daily dose and 33.7 +/- 17.9 (S.D.) days after terminating the 250 micrograms daily dose. With the higher dose of nafarelin acetate there were significantly fewer bleeding episodes, less number of days of bleeding, and longer cycles. During the treatment phase the area under the LH curve was significantly less and the acute response of LH in the last week of treatment was significantly less with the higher dose of drug. With both doses of nafarelin acetate the acute responses of LH, FSH and estradiol were significantly greater on day 1 than on either day 98 or day 186. Side effects observed during this study included galactorrhea (2 subjects) and vasomotor symptoms (7 subjects).

Administration, Intranasal↗

PubMed1985

The effects of two doses of spironolactone on serum androgens and anagen hair in hirsute women.

Spironolactone (S) has been used successfully for the treatment of hirsutism. We evaluated whether the effects of S on serum androgens and hair growth are dose-related and whether S affects secreted androgens to the same degree as peripherally derived androgens. Two groups of 15 hirsute patients, similarly matched, received either 100 or 200 mg S daily for 3 months. Serum total testosterone (T) decreased significantly (P less than 0.05) and to a similar degree with both dosages, whereas unbound T was unaltered. Dehydroepiandrosterone sulfate was unaltered, whereas androstenedione decreased with 200 mg S (P less than 0.05). Peripherally derived serum dihydrotestosterone decreased to a similar degree with 100 and 200 mg S (P less than 0.05), whereas 5 alpha-androstane-3 alpha-17 beta-diol (3 alpha-diol) increased (P less than 0.05) similarly with both dosages. Serum 3 alpha-diol glucuronide (3 alpha-diol-G) increased with both dosages, but not significantly. Anagen hair shaft diameters decreased significantly in both groups by 19% +/- 8% and 30% +/- 4% (P less than 0.05). No correlation was found between hair growth and serum androgens. Because serum unbound T was largely unaltered by S, it is suggested that the antiandrogenic effects of S are primarily related to its peripheral effect. However, there is no good clinical marker for this effect as levels of 3 alpha-diol and 3 alpha-diol-G increase.

Adult↗

PubMed1985

Estrogen and progestin effects on urinary calcium and calciotropic hormones in surgically-induced postmenopausal women.

Seventeen surgically-induced postmenopausal (PM) women were randomized to receive either 0.625 mg of conjugated estrogens (CE) daily or 150 mg of intramuscular depomedroxyprogesterone acetate (DMPA) every 3 months. Urinary calcium/creatinine ratios were significantly higher than ratios of premenopausal controls before treatment, but were lower in all patients 2 months after both types of treatment. Compared to controls, all PM patients had similar levels of serum PTH and 25 hydroxy vitamin D before and after treatment. As a group, PM patients had lower levels of 1.25-dihydroxyvitamin D. In 5 patients who had levels which were below the normal range, 3 were treated with CE and 2 received DMPA. These patients all had significant increases in 1,25-dihydroxyvitamin D after treatment. Serum calcitonin did not change with either CE or DMPA treatment. These data suggest that, while both CE and DMPA lower calcium excretion in PM women, the mechanism(s) for the effects of hormonal treatment on bone resorption remain unsettled.

Adult↗

PubMed1985

The effects of estrogen and progestin on endogenous opioid activity in oophorectomized women.

Sex steroids may modulate the secretion of beta-endorphin (beta-EP). Naloxone (Nal), an opioid antagonist, has been used as a probe of central opioid activity. Nal-evoked responses of PRL and LH were evaluated in the midluteal (ML) and late follicular (LF) phases of ovulatory women (Pre) and compared to responses of oophorectomized women before and after the administration of conjugated estrogens (CE) and again after CE and progestin administration. In the ML and LF phases, serum LH increased significantly (P less than 0.05 and P less than 0.01, respectively) during Nal infusion for 4 h, while PRL did not change. In oophorectomized women, there were no significant changes in LH or PRL during Nal infusion. After 3 weeks of CE treatment (1.25 mg daily), LH increased during Nal infusion (P less than 0.05), as did PRL (P less than 0.01). After treatment with CE and medroxyprogesterone acetate (MPA), LH and PRL both increased (P less than 0.05 and P less than 0.01, respectively). The area under the LH curve during Nal infusion after CE and MPA treatment was greater than that after CE alone. Both of these responses were comparable to those of the LF and ML phases of Pre women. During Nal infusion, LH pulse frequency increased in the ML compared to the LF phase of the cycle and, in oophorectomized women, was greater after CE and CE with MPA treatment compared to pretreatment values (P less than 0.05). LH amplitudes during Nal infusion were highest in the ML phase and after CE and MPA treatment in oophorectomized women, and these LH amplitudes were similar. No correlation was found between peripheral plasma beta-EP and Nal-evoked LH responses. No differences were evident in plasma beta-EP levels between Pre and oophorectomized women. In conclusion, 1) endogenous opioid activity is low in oophorectomized women; 2) treatment with estrogen increases opioid activity, and the addition of a progestin increases this activity further; and 3) these data support the contention that sex steroids exert a profound influence on endogenous opioid activity.

Adult↗

PubMed1985

Prolactin response after gonadotropin-releasing hormone in the polycystic ovary syndrome.

The administration of gonadotropin-releasing hormone (GnRH) has been shown to stimulate prolactin (PRL) release under certain conditions. The authors compared PRL responses after GnRH in normoprolactinemic patients with the polycystic ovary syndrome (PCO) with those of normal ovulatory women in the follicular phase. Seven of 15 patients had a significant increase in PRL after GnRH, whereas none of the control subjects had a positive response. After 1 week of oral L-dopa, the responders no longer exhibited this positive response. Baseline PRL levels in responding patients with PCO were similar to levels in control subjects, whereas nonresponding patients with PCO had higher PRL levels. Baseline follicle-stimulating hormone (FSH)/luteinizing hormone (LH) ratios were higher in patients with a positive response. The positive PRL response after GnRH was not correlated with baseline serum LH, the LH/FSH ratio, delta maximum LH responses, serum testosterone (T), unbound T, or baseline PRL. The positive response correlated positively with serum levels of unbound estradiol (P less than 0.05) and serum unbound estradiol/unbound T ratios (P less than 0.01). These data suggest that under certain conditions a subgroup of patients with PCO may demonstrate a positive PRL response after GnRH. Dopamine, gonadotropins, and estrogen may play a role in this interaction.

Adolescent↗

PubMed1984

Priming with gonadotropin-releasing hormone restores gonadotropin secretion during first but not second trimester of pregnancy.

This study was designed to determine whether the lack of secretion of endogenous gonadotropin-releasing hormone is the etiology of the hypogonadotropic state of pregnancy. For this purpose, five pregnant women in their first trimester received a single intravenous dose of 150 micrograms of gonadotropin-releasing hormone. Another five women in the first trimester and five women in the second trimester of pregnancy received daily intramuscular injections of 500 micrograms of gonadotropin-releasing hormone for 10 consecutive days. This was followed by a single 150 micrograms gonadotropin-releasing hormone test and then a 24-hour pulsatile infusion of gonadotropin-releasing hormone of 10 micrograms/min/6 min given every hour. Baseline plasma beta-luteinizing hormone and follicle-stimulating hormone were undetectable in all women. Mean +/- SEM plasma beta-human chorionic gonadotropin was significantly higher (p less than 0.001) in the first trimester than in the second trimester, and mean plasma estradiol and prolactin were significantly increased (p less than 0.001 and 0.05, respectively) during the second trimester of pregnancy. After the 10-day treatment with gonadotropin-releasing hormone there was a significant increase (p less than 0.05) in baseline beta-luteinizing hormone and follicle-stimulating hormone only in the first-trimester pregnant women. The single as well as the pulsatile administration of gonadotropin-releasing hormone resulted in a further significant increase in both beta-luteinizing hormone and follicle-stimulating hormone. In contradistinction, women in the second trimester of pregnancy showed a blunted response to the daily and pulsatile administration of gonadotropin-releasing hormone. Since the pituitary secretion of gonadotropin was functionally restored by the administration of exogenous gonadotropin-releasing hormone, possibly there is a lack of secretion of endogenous gonadotropin-releasing hormone during the first trimester of pregnancy. An increased negative feedback produced by increasing levels of plasma estradiol might be the cause of pituitary refractoriness to gonadotropin-releasing hormone during the second trimester of pregnancy.

Female↗

PubMed1984

Evidence for altered catecholamine metabolism in polycystic ovary syndrome.

It has been hypothesized by Yen et al. that there is decreased dopaminergic control of luteinizing hormone secretion in polycystic ovary syndrome. Levels of urinary homovanillic acid, dihydroxyphenyl acetic acid, and 3-methoxy-4-hydroxyphenylglycol were measured in seven women with polycystic ovary syndrome and in six matched control subjects to reflect, in part, central dopamine and norepinephrine metabolism. In addition, gonadotropin-releasing hormone stimulation tests were carried out in women with polycystic ovary syndrome and in control subjects. In patients with polycystic ovary syndrome, serum gonadotropin levels were determined before and after gonadotropin-releasing hormone stimulation, before and after treatment with 500 mg of L-dopa for 1 week, and again before and after treatment with 400 mg of L-dopa and 100 mg of carbidopa for 1 week the following month. Urinary homovanillic acid and dihydroxyphenyl acetic acid levels were significantly lower and the level of 3-methoxy-4-hydroxyphenylglycol was significantly higher in patients with polycystic ovary syndrome (p less than 0.05). There was a significant negative correlation between levels of homovanillic acid and serum luteinizing hormone (r = -0.57, p less than 0.05) and a positive correlation between the ratio of 3-methoxy-4-hydroxyphenylglycol/homovanillic acid and luteinizing hormone (r = 0.75, p less than 0.01). After gonadotropin-releasing hormone stimulation, delta max serum luteinizing hormone was elevated in patients with polycystic ovary syndrome but decreased to control levels after treatment with L-dopa. No changes occurred in baseline levels of serum luteinizing hormone or follicle-stimulating hormone. After treatment with L-dopa-carbidopa, baseline levels of luteinizing hormone and follicle-stimulating hormone were unchanged as were responses after gonadotropin-releasing hormone stimulation. These data suggest that there may be altered catecholamine metabolism in polycystic ovary syndrome. Viewed together with previous findings by Yen et al., our data support the hypothesis that there is decreased dopaminergic control of luteinizing hormone in polycystic ovary syndrome.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1984

Central and peripheral metabolites of norepinephrine and dopamine in postmenopausal women.

Urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) sulfate and glucuronide reflect, in part, central norepinephrine activity while urinary 3-methoxy-4-hydroxymandelic (VMA) reflects peripheral norepinephrine activity. Urinary MHPG and VMA were measured, together with homovanillic acid (HVA), in 20 symptomatic and seven asymptomatic postmenopausal women and 10 premenopausal control women. Urinary HVA reflects, in part, central dopamine metabolism. After nine of the symptomatic women were treated for 2 months with 0.625 mg of conjugated estrogens, urinary catecholamine measurements were repeated. Serum estrogen levels were not different in symptomatic and asymptomatic patients. Urinary MHPG, VMA, and HVA were similar in symptomatic women before and after estrogen treatment and were not different from levels of asymptomatic postmenopausal and control subjects. The ratios of MHPG:VMA, MHPG:HVA, and VMA:HVA also were similar. While body weight and estrogen did not correlate with urinary catecholamines, there was a significant positive correlation between MHPG and age in postmenopausal subjects (r = 0.56, p less than 0.005).

Adult↗

PubMed1984

The control of bioactive luteinizing hormone secretion in women with polycystic ovary syndrome.

Serum bioactive luteinizing hormone (LH) is elevated in virtually all patients with polycystic ovary syndrome, whereas serum immunoreactive LH may not be increased. The resultant increase in the bioactive: immunoreactive LH ratio in polycystic ovary syndrome leads to the suggestion that a more biologically active form of LH may be secreted in patients with polycystic ovary syndrome. This study was designed to investigate the control of bioactive LH in polycystic ovary syndrome. Compared to matched control subjects, seven patients with polycystic ovary syndrome had higher levels of serum immunoreactive LH (24 +/- 3 mlU/ml), immunoreactive LH: follicle-stimulating hormone (FSH) ratios (4.6 +/- 0.6), bioactive LH (98 +/- 27 mlU/ml), and bioactive: immunoreactive LH ratios (4.6 +/- 0.5). Serum testosterone (64 +/- 10 ng/ml), unbound testosterone (16 +/- 3 mg/dl), and unbound estradiol (49 +/- 5 pg/ml) were also higher. In response to 150 micrograms of intravenous gonadotropin-releasing hormone, increments of both bioactive LH and immunoreactive LH were higher than those in control subjects, but the bioactive: immunoreactive LH ratio was unaltered. Although urinary homovanillic acid was lower in polycystic ovary syndrome, it did not correlate with the bioactive: immunoreactive LH ratio. Similarly, the bioactive: immunoreactive LH ratio was not altered by 1 week of L-dopa (500 mg) or after another week of L-dopa (400 mg) with carbidopa (100 mg) 1 month later. Although baseline unbound estradiol correlated with the delta maximum response of bioactive LH after gonadotropin-releasing hormone (r = 0.65, p less than 0.05), unbound estradiol did not correlate with the bioactive: immunoreactive LH ratio. However, there was a significant positive correlation between the baseline bioactive: immunoreactive LH and the increased delta maximum responses of both immunoreactive LH (r = 0.55) and bioactive LH (r = 0.58), p less than 0.05. These data suggest that, although gonadotropin-releasing hormone stimulation, dopamine, and estrogen may not selectively increase the pituitary secretion of bioactive LH, the sensitivity of the pituitary gland itself and the hyperdynamic state of gonadotropin secretion in polycystic ovary syndrome may result in the increased secretion of bioactive LH.

Adult↗

PubMed1984

Differences in the ratio of bioactive to immunoreactive serum luteinizing hormone during vasomotor flushes and hormonal therapy in postmenopausal women.

With the recognition of differences between serum bioactive (bio) and immunoreactive (i) LH concentrations in various clinical situations, we measured changes in the bio:i LH ratio in postmenopausal (PM) women in response to iv GnRH, during the vasomotor flush, and in response to both estrogen and progestin treatment. Bio LH was measured using the mouse interstitial cell assay and LER 907 as standard, with conversion to milliinternational units per ml (Second International Reference Preparation of human menopausal gonadotropin). In 22 PM women, aged 42-56 yr, serum bio LH [455 +/- 73 (+/- SE) mIU/ml] and the bio:i LH ratio (8.3 +/- 0.7) were significantly higher than in premenopausal women (25.5 +/- 5 mIU/ml and 1.5 +/- 0.2, respectively; P less than 0.002). In response to 150 micrograms iv GnRH, there was a greater rise in levels of iLH and bioLH in PM women than in premenopausal women, but there were no changes in the bio:i LH ratio after GnRH. During nine flushing episodes in three women, documented by digital temperature and iLH pulses, there was a significant increase in the bio:i LH ratio (P less than 0.001). After treatment of seven PM women for 2 months with 0.625 mg conjugated estrogens and seven other PM women with 150 mg im depomedroxyprogesterone acetate, vasomotor symptoms decreased significantly. Serum iLH did not change after treatment, but bio:i LH ratios decreased significantly, and 7 of 14 women had levels in the premenopausal range. These data suggest that bioLH and the bio:i LH ratio correlate better than iLH with symptomatology in PM women.

Adult↗

PubMed1984

The influence of androgens on insulin resistance.

Insulin resistance (IR) in polycystic ovary syndrome (PCO) has been linked to hyperandrogenism and elevated luteinizing hormone (LH) levels. Fourteen patients with idiopathic hirsutism (IH), 13 with PCO, and 6 control subjects were investigated for assessment of the effects of serum LH, peripheral tissue androgens, and sex hormone-binding globulin (SHBG) on fasting immunoreactive insulin (IRI) levels. Serum LH, dehydroepiandrosterone sulfate, dihydrotestosterone, and 3 alpha-androstanediol, SHBG, and unbound testosterone (uT) were measured. Serum testosterone (T) showed a positive correlation with IRI (P less than 0.05), and SHBG showed a negative correlation (P less than 0.02). Unbound T showed a highly significant positive correlation (P less than 0.001), whereas dehydroepiandrosterone sulfate, dihydrotestosterone, and 3 alpha-androstanediol did not correlate. Gonadotropin-releasing hormone, administered to patients with IH, raised LH levels but did not change IRI levels. Spironolactone did not affect T or IRI in patients with IH but significantly lowered T and IRI in patients with PCO. It is suggested that IR is not related to LH or peripheral androgen metabolism but highly correlated with uT and SHBG, thus coupling two important factors in IR, obesity and the androgen level.

Adult↗