Biomedical subjects

E Carmina

Publications and source records attributed to E Carmina.

At least 55 records · Page 3Linked to original sources

PubMed1994

Physiological estrogen replacement may enhance the effectiveness of the gonadotropin-releasing hormone agonist in the treatment of hirsutism.

GnRH agonists (GnRH-A) have been used for the treatment of hirsutism in women with ovarian hyperandrogenism. However, significant side-effects, including vasomotor symptoms and bone loss, have prevented the long term use of this therapy. In this study, we evaluated the effects of low dose (physiological) estrogen replacement on the side-effects and clinical and hormonal parameters of 22 hirsute women with ovarian hyperandrogenism when treated with a long-acting GnRH-A, Decapeptyl. Ten patients with Ferriman-Gallwey (FG) scores averaging 13.4 +/- 1.5 were randomly assigned to be treated with Decapeptyl alone (3.75 mg, im, every 28 days for 6 months), and 12 other patients with FG scores averaging 13.3 +/- 1 received Decapeptyl with estrogen (conjugated equine estrogens, 0.625 mg) for 21 days and medroxyprogesterone acetate (10 mg) for 10 days (days 12-21). After 6 months, LH was suppressed in both groups, whereas FSH was significantly reduced only in the group receiving GnRH-A with estrogen (2.5 +/- 4 vs. 4.8 +/- 0.6 IU/L; P < 0.01). Serum androgen levels were reduced in both groups, although the reduction of testosterone and unbound testosterone was greater in the group receiving hormonal replacement [1.73 +/- 0.3 vs. 2.57 +/- 0.4 nmol/L for testosterone (P < 0.05); 8.3 +/- 1 vs. 14.6 +/- 2.8 pmol/L for unbound testosterone (P < 0.05)]. The reduction in hirsutism scores was greater with hormonal replacement (FG scores, -4.1 +/- 0.3 vs. -2.5 +/- 0.3; P < 0.05), whereas the polycystic appearance of ovaries by ultrasound was decreased in both groups. Amenorrhea and vasomotor symptoms were observed only with GnRH-A alone. Serum osteocalcin rose significantly with GnRH-A alone, reflecting a change in bone turnover (0.49 +/- 0.05 to 0.64 +/- 0.09 nmol/L; P < 0.05), but was unchanged with hormonal replacement. Patients receiving hormonal replacement had treatment extended to 1 yr. A further improvement of hirsutism, with scores dropping into the normal range (4.9 +/- 0.7), as well as a normalization of ovarian morphology were evident at this time. In conclusion, low dose (physiological) estrogen replacement may enhance the effects of GnRH-A treatment, while preventing most of the side-effects encountered with GnRH-A alone. This may allow more prolonged treatment, which is necessary for hirsutism.

Adolescent↗

PubMed1993

Evidence for increased androsterone metabolism in some normoandrogenic women with acne.

Increased androgen production from the ovary, adrenal or locally in skin has been implicated in the pathogenesis of acne. Recent data have provided evidence that androsterone (Ao) metabolism is exaggerated in acne and serum metabolites of Ao differentiate between acne and hirsutism in hyperandrogenic women. Here we have extended these studies to normoandrogenic women who have moderate to severe acne. We measured serum ovarian and adrenal androgens as well as the glucuronide and sulfate metabolites of Ao and 3 alpha-androstanediol which reflect, in part, peripheral androgen action. In a group of 15 well-selected normoandrogenic patients with acne, both serum Ao glucuronide (G) and Ao were elevated (P < 0.01; P < 0.05). The ratios of Ao G to androgen precursors of both ovarian and adrenal origin were elevated as was the ratio of Ao G/Ao (P < 0.05). These data suggest that increased Ao metabolism is a specific abnormality found in both normoandrogenic and hyperandrogenic women with acne. Our findings also provide a rationale for antiandrogen therapy at least in some normoandrogenic women with acne.

Acne Vulgaris↗

PubMed1992

Does ethnicity influence the prevalence of adrenal hyperandrogenism and insulin resistance in polycystic ovary syndrome?

OBJECTIVE: Our purpose was to determine the prevalence of adrenal hyperandrogenism and insulin resistance in patients with hyperandrogenic chronic anovulation, also called polycystic ovary syndrome, living in the United States, Italy, and Japan. STUDY DESIGN: Seventy-five women with polycystic ovary syndrome, 25 each from the United States, Italy, and Japan, and 10 ovulatory controls were studied. Hirsutism, obesity, and the presence of cystic ovaries were assessed, as were blood levels for estrogen, luteinizing hormone, testosterone, adrenal androgens, and insulin. All patients received an insulin tolerance test to assess insulin resistance. RESULTS: Women from Japan were less obese (p < 0.05) and did not have hirsutism, although the percentage of cystic ovaries (68% to 80%) was comparable. Serum luteinizing hormone, testosterone, and estradiol were similar, but levels of 3 alpha-androstanediol glucuronide, which was elevated in women from the United States and Italy, was normal in women from Japan. The adrenal androgens, dehydroepiandrosterone sulfate and 11 beta-hydroxyandrostenedione were elevated in 48% to 64% of the patients and by a similar percentage in the three groups. Fasting insulin was elevated in all groups, but was significantly higher in women from the United States and Italy compared with women from Japan (p < 0.05). However, insulin resistance as assessed by dissociation constant of insulin tolerance test values was significantly elevated but similar in the three groups and occurred in 68% to 76% of patients. CONCLUSION: In polycystic ovary syndrome, although obesity and hirsutism vary according to dietary, genetic, and environmental factors, the prevalence of adrenal androgen excess and insulin resistance appear to be fairly uniform. These results suggest that these factors may be involved in the pathophysiologic features of the disorder.

Adrenal Gland Diseases↗

PubMed1992

Increased circulating levels of immunoreactive beta-endorphin in polycystic ovary syndrome is not caused by increased pituitary secretion.

OBJECTIVE: Our purpose was to investigate the source and role of elevated levels of immunoreactive beta-endorphin in polycystic ovary syndrome. We wished to determine whether immunoreactive beta-endorphin secretion in patients with polycystic ovary syndrome is influenced by body weight and whether the pituitary release of immunoreactive beta-endorphin with corticotropin-releasing hormone is related to luteinizing hormone levels or adrenal androgen secretion. STUDY DESIGN: Eighteen patients with polycystic ovary syndrome and 10 ovulatory controls were studied. Each subject received 1 microgram/kg intravenous corticotropin-releasing hormone and an oral glucose tolerance test on alternate days. Levels of plasma immunoreactive beta-endorphin, corticotropin, luteinizing hormone, cortisol, adrenal androgens, and insulin were measured. RESULTS: Although immunoreactive beta-endorphin levels were elevated in patients with polycystic ovary syndrome (p < 0.01), incremental responses after corticotropin-releasing hormone were similar to controls and were not influenced by body weight. Serum luteinizing hormone levels were not affected by corticotropin-releasing hormone and did not correlate with immunoreactive beta-endorphin levels. Adrenal androgen responses after corticotropin-releasing hormone were increased in patients with polycystic ovary syndrome (p < 0.01) but were not correlated with immunoreactive beta-endorphin secretion. After oral glucose was given, elevated fasting insulin levels increased significantly in patients with polycystic ovary syndrome (p < 0.01), as did immunoreactive beta-endorphin levels (p < 0.05). The increases in insulin and immunoreactive beta-endorphin levels were correlated (p < 0.05). CONCLUSIONS: Pituitary secretion of immunoreactive beta-endorphin is normal in patients with polycystic ovary syndrome, and pancreatic secretion appears to be increased. Corticotropin-releasing hormone does not influence luteinizing hormone levels, and adrenal androgen sensitivity is not influenced by immunoreactive beta-endorphin secretion.

Adult↗

PubMed1992

The ratio of androstenedione:11 beta-hydroxyandrostenedione is an important marker of adrenal androgen excess in women.

OBJECTIVE: To determine if the ratio of serum androstenedione (A):11 beta-hydroxyandrostenedione (OHA) would be helpful in differentiating adrenal from ovarian hyperandrogenism. DESIGN/SETTING: Prospective study of outpatients being evaluated for hyperandrogenism. PATIENTS/PARTICIPANTS: Normal women (n = 27), those with hyperandrogenic chronic anovulation (n = 25), and 7 with adult onset of congenital adrenal hyperplasia (CAH) because of 21-hydroxylase deficiency. INTERVENTIONS: Fasting serum between 8:00 A.M. and 9:00 A.M. Patients with hyperandrogenic chronic anovulation and CAH received dexamethasone (DEX) 2 mg for 7 days. MAIN OUTCOME MEASURES: Serum testosterone (T), unbound T, dehydroepiandrosterone sulfate (DHEAS), A, and 11 beta-OHA by radioimmunoassay. RESULTS: Serum 11 beta-OHA and DHEAS were elevated in 52% and 40% of patients with hyperandrogenic chronic anovulation and in 7 of 7 and 1 of 7 patients with CAH. The ratio of A:11 beta-OHA was significantly higher (P less than 0.05) in hyperandrogenic chronic anovulation and significantly lower (P less than 0.05) in CAH compared with controls. Serum A:11 beta-OHA correlated with T (r = 0.58, P less than 0.05). The ratios of A:11 beta-OHA were similar and significantly lower in CAH and hyperandrogenic chronic anovulation patients who were DEX sensitive compared with those who were not DEX sensitive. The ratio correlated with the percentage suppression of T, unbound T, and A after DEX (P less than 0.01). There were no differences with measurements of DHEAS and 11 beta-OHA. Using the mean ratio of controls (1.3) as a cutoff value, the sensitivity of the A:11 beta-OHA in detecting adrenal hyperandrogenism, as assessed by DEX sensitivity, was 100%, the specificity was 84%, and the predictive value was 67%. CONCLUSIONS: The ratio of A:11 beta-OHA appears to be an excellent marker for identifying patients with adrenal hyperandrogenism and CAH.

Adolescent↗

PubMed1992

Cutaneous application of an androstenedione gel as an in vivo test of 5 alpha-reductase activity in women.

OBJECTIVE: Assessment of an in vivo test for 5 alpha-reductase activity using serum markers, 5 alpha-androstane-3 alpha,17 beta-diol glucuronide and androsterone glucuronide, after the cutaneous application of androstenedione (A). DESIGN: An A gel was applied for 6 days to the skin of normal women, male volunteers, and hirsute and nonhirsute patients with polycystic ovarian syndrome (PCOS). Blood samples were obtained at baseline and on day 6 of the A gel application. Blood samples were assayed for A, 5 alpha-androstane-3 alpha,17 beta-diol glucuronide, and androsterone glucuronide. In three hirsute women, the protocol was followed before and after receiving an oral contraceptive (OC) and spironolactone 200 mg/d for 3 months. SETTING: The study was performed in the outpatient clinic of the Division of Reproductive Endocrinology and Infertility, Women's Hospital of the Los Angeles County and University of Southern California Medical Center in Los Angeles, California. PATIENTS, PARTICIPANTS: A total of eight nonhirsute patients with PCOS, seven hirsute patients with PCOS, and six male volunteers were enrolled in the study. Five normal women served as a control group. MAIN OUTCOME MEASURE: Serum A increased after 6 days by a similar magnitude in all groups. Serum androsterone glucuronide showed a significant increase from baseline only in the hirsute group (P < 0.03), whereas the increase in 5 alpha-androstane-3 alpha,17 beta-diol glucuronide was not statistically significant. RESULTS: The ratio of the increases in serum androsterone glucuronide over serum A was significantly higher in the hirsute group (P < 0.02). In the three hirsute patients who were placed on an OC and spironolactone, serum 5 alpha-androstane-3 alpha,17 beta-diol glucuronide and androsterone glucuronide decreased after 3 months and did not increase with application of the gel for another 6 days. CONCLUSION: The cutaneous application of A provides a useful assessment of in vivo 5 alpha-reductase activity. However, because we found that A absorption varied considerably (30% to 62%), we suggest that this in vivo test may not provide more information than baseline determinations of 5 alpha-androstane-3 alpha,17 beta-diol glucuronide and androsterone glucuronide. It may, however, be useful as a parameter for assessing the effectiveness of various treatment regimens for hirsutism.

Administration, Cutaneous↗

PubMed1991

Is 11 beta-hydroxyandrostenedione a better marker of adrenal androgen excess than dehydroepiandrosterone sulfate?

To determine whether the adrenal androgen 11 beta-hydroxyandrostenedione is a more sensitive and specific marker than dehydroepiandrosterone sulfate, we compared these serum androgens in 81 women with anovulatory hyperandrogenism before treatment, after corticotropin and corticotropin-releasing-factor stimulation, and after short- and long-term dexamethasone suppression. Of all subjects, 65% and 57% had elevated levels of 11 beta-hydroxyandrostenedione (greater than 2.0 ng/ml) and dehydroepiandrosterone sulfate (greater than 2.8 micrograms/ml), respectively. However, 11 beta-hydroxyandrostenedione and dehydroepiandrosterone sulfate levels did not correlate in either the women with hyperandrogenism (r = 0.12) or the 26 normal women (r = 0.29). After 0.25 mg corticotropin was administered intravenously (n = 16), 11 beta-hydroxyandrostenedione increased by 157% +/- 53% (mean +/- SEM), whereas dehydroepiandrosterone sulfate, androstenedione, dehydroepiandrosterone, and cortisol increased by 6% +/- 2%, 46% +/- 10%, 416% +/- 80%, and 2326% +/- 371%, respectively. After intravenous administration of 100 micrograms corticotropin-releasing factor to eight patients, the percent change from baseline level to peak was 148% +/- 26%, 24% +/- 5%, 61% +/- 15%, 117% +/- 15%, and 116% +/- 18% for 11 beta-hydroxyandrostenedione, dehydroepiandrosterone sulfate, androstenedione, dehydroepiandrosterone, and cortisol, respectively. After 2 mg dexamethasone for 3 days (n = 10), 11 beta-hydroxyandrostenedione, dehydroepiandrosterone sulfate, androstenedione, and testosterone were suppressed by 95% +/- 2%, 74% +/- 3%, 51% +/- 9%, and 32% +/- 9%, respectively. Suppression with 0.5 mg dexamethasone for 3 months lowered 11 beta-hydroxyandrostenedione and dehydroepiandrosterone sulfate levels equally by 50% +/- 14% and 62% +/- 12%, respectively. 11 beta-Hydroxyandrostenedione is a useful marker of adrenal androgen secretion with a calculated sensitivity and specificity greater than that of dehydroepiandrosterone sulfate. The greater sensitivity of 11 beta-hydroxyandrostenedione over dehydroepiandrosterone sulfate to adrenal stimulation and suppression suggests its unique diagnostic use.

Adolescent↗

PubMed1991

Is the inappropriate gonadotropin secretion of patients with polycystic ovary syndrome similar to that of patients with adult-onset congenital adrenal hyperplasia?

OBJECTIVE: To assess gonadotropin alterations in adult-onset congenital adrenal hyperplasia (CAH) and to compare these findings with those of patients with polycystic ovary syndrome (PCOS) in an effort to better understand the pathophysiology of these abnormalities. DESIGN: Prospective study of 9 newly diagnosed patients with CAH, 10 with PCOS, and 10 ovulatory controls. INTERVENTIONS: Baseline measurements of serum androgens, progestins, estradiol (E2), estrone (E1), unbound E2, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Serum LH and FSH were measured after intravenous gonadotropin-releasing hormone (GnRH) and in 15-minute blood samples for 6 hours to determine LH pulsatility. RESULTS: Serum androgens were elevated but comparable in the two patient groups. Serum LH was also elevated (P less than 0.05) but was higher in PCOS than CAH. Serum LH:FSH ratios were similar as were the responses to GnRH. Serum E1 was elevated only in PCOS, but unbound E2 was elevated to the same degree in both PCOS and CAH (P less than 0.05). Patients with PCOS had a decreased LH interpulse interval compared with controls and CAH (P less than 0.05), but LH pulse amplitude was increased in both PCOS and CAH (P less than 0.05). Serum E2 and unbound E2 correlated significantly with LH (P less than 0.05), LH responses to GnRH as well as to LH pulse amplitude in CAH (P less than 0.05). The LH interpulse interval did not correlate with estrogen in any group. None of the LH parameters correlated with serum progestin levels in CAH. CONCLUSIONS: The gonadotropin abnormalities of CAH appear to be intermediate between those of controls and PCOS. Although elevated estrogen may explain these abnormalities in CAH, additional factors may be operative in PCOS.

Adolescent↗

PubMed1991

Serum androsterone conjugates differentiate between acne and hirsutism in hyperandrogenic women.

OBJECTIVE: To determine if among hyperandrogenic women acne may be differentiated from hirsutism by markers of peripheral androgen metabolism. DESIGN: Prospective outpatient study of 36 hyperandrogenic women and controls divided into groups based on the presence or absence of significant hirsutism and the presence or absence of moderate to severe acne. Serum levels of adrenal and ovarian derived androgens were elevated but similar in all patient groups. INTERVENTIONS: Measurement of serum androgens including metabolites of 5 alpha-reductase activity: 3 alpha-androstanediol glucuronide and sulfate and androsterone (A) glucuronide and sulfate. RESULTS: 3 alpha-androstanediol glucuronide and sulfate were elevated in all groups (P less than 0.05) and could differentiate between hirsute and nonhirsute patients but were similar in patients with and without acne. Serum A glucuronide and sulfate were only significantly elevated in patients with acne (P less than 0.01) and were higher than levels in controls and hirsute patients without acne. Ratios of precursor androgens to A glucuronide and sulfate were significantly higher in patients with acne compared with patients without acne (P less than 0.05). CONCLUSIONS: Altered peripheral metabolism in acne may favor the formation of A conjugates, which may help differentiate acne from hirsutism among hyperandrogenic women.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗

PubMed1991

Peripheral androgen blockade versus glandular androgen suppression in the treatment of hirsutism.

Hirsutism in women is often explained on the basis of abnormal peripheral androgen metabolism. To determine whether serum markers of ovarian, adrenal, or peripheral androgen production may be helpful determinants in the treatment of hirsutism and to compare the efficacy of treatment with dexamethasone or spironolactone, 20 hyperandrogenic hirsute patients were treated for up to 2 years. Eleven women who were selected on the basis of sensitivity to dexamethasone were treated with a daily dose of 0.37 mg dexamethasone and had androgen levels suppressed into the normal range. Although significant (P less than .05), Ferriman-Gallwey scores decreased only by 20%: 14.2 +/- 0.5 to 11.4 +/- 0.6. Nine other women received spironolactone 100 mg/day for 1 year and did not have significant changes in serum androgens, but had a significant (P less than .01) 47% reduction in the Ferriman-Gallwey score (15.2 +/- 0.8 to 8 +/- 0.8). Thus, with either treatment, the reduction in Ferriman-Gallwey scores did not correlate with the change in androgen levels. The patients treated with dexamethasone for 1 year then received spironolactone 100 mg/day together with dexamethasone for an additional year. Serum androgen levels did not change further, but the Ferriman-Gallwey scores decreased significantly (P less than .01) from 11.4 +/- 0.6 to 3.74 +/- 0.7 (-61%). These data suggest that serum androgens are not helpful in assessing response to the treatment of hirsutism and that despite normal androgen levels, only modest clinical improvement may be expected with dexamethasone treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Pituitary-adrenal responses to corticotropin-releasing factor in late onset 21-hydroxylase deficiency.

Intravenous corticotropin-releasing factor (CRF) and adrenocorticotropin hormone (ACTH) were administered in patients with adult onset 21-hydroxylase deficiency to compare their diagnostic capability as well as to investigate hypothalamic-pituitary-adrenal function in this disorder. Responses of 17-hydroxyprogesterone, which were markedly elevated compared with controls, were identical with CRF and ACTH. However, intravenous ACTH resulted in higher androstenedione levels in comparison to CRF. Adrenocorticotropin hormone also resulted in decreased cortisol responses, confirming a defect in steroidogenesis, a finding that was not evident with CRF. Plasma ACTH responses to CRF were similar in patients and controls. We conclude that CRF may be as useful as ACTH as a diagnostic test for adult onset 21-hydroxylase deficiency, and that because normal levels of plasma ACTH were evoked by CRF in 21-hydroxylase deficiency, lower doses of exogenous ACTH may be sufficient for making this diagnosis. Although no obvious hypothalamic-pituitary dysfunction could be demonstrated in our patients with 21-hydroxylase deficiency by using CRF, our data confirm the adrenal sensitivity of patients with adult onset 21-hydroxylase deficiency.

17-alpha-Hydroxyprogesterone↗

PubMed1990

Ovine corticotropin-releasing factor and dexamethasone responses in hyperandrogenic women.

Eighteen hyperandrogenic, hirsute women received ovine corticotropin-releasing factor (CRF; 1 microgram/kg) as well as a dexamethasone (DEX) suppression test. Nine of the 18 hirsute women exhibited increased DEX sensitivity. Plasma adrenocorticotropic hormone (ACTH) responses after ovine CRF were significantly lower in the DEX-sensitive subgroup, but serum androstenedione was higher. Baseline serum androgen levels could not predict DEX responses. A significant negative correlation existed between the suppression of androgens after DEX and the increase in ACTH after ovine CRF. The suppression of androgen correlated with the ratio of the increase in androgen to the increase in ACTH after ovine CRF. We conclude that DEX sensitivity occurs frequently and cannot be predicted by levels of serum androgens. Blunted ACTH responses to ovine CRF may reflect enhanced adrenal sensitivity and altered feedback control.

Adolescent↗

PubMed1990

Pituitary-adrenal responses to ovine corticotropin-releasing factor in polycystic ovary syndrome and in other hyperandrogenic patients.

This study was carried out to further characterize the pituitary-adrenal androgen responses of hyperandrogenic patients with 'classic' polycystic ovary syndrome (PCO) and others who were less distinctive and have been called 'PCO-like'. PCO-like patients differed from PCO only in that serum luteinizing hormone (LH) levels were normal and anovulation was not consistent. Ovine corticotropin-releasing factor (CRF) resulted in normal responses of adrenocorticotropic hormone and cortisol in the two groups when compared to controls, while androstenedione (delta 4A) and dehydroepiandrosterone (DHEA) responses were significantly elevated. There were no differences in the responses of PCO and PCO-like patients. Although basal DHEA levels correlated with DHEA responses of CRF, basal levels of DHEA sulfate (S) could not be used to predict CRF responses. These data further confirm that there is heightened adrenal androgen activity in PCO whether the patients are 'classic' or PCO-like. Serum DHEA-S does not appear to be a good marker for this adrenal hyperactivity and might in turn also be under the control of other factors.

Adolescent↗

PubMed1988

Prevalence of late-onset 11 beta-hydroxylase deficiency in hirsute patients.

Serum levels of 11-deoxycortisol were determined in 182 hirsute women. Three patients presented high basal 11-deoxycortisol levels and an exaggerated response of this steroid to ACTH stimulation. A fourth patient had normal basal 11-deoxycortisol but was hyperresponsive to ACTH stimulation. Therefore diagnosis of late-onset 11 beta-hydroxylase deficiency was made in 4 out of 182 hirsute women with a prevalence of 2.2% in the group studied. In these patients, clinical findings and other hormonal patterns were not different from those of other women suffering from hirsutism.

Adolescent↗

PubMed1986

Increased DHEAs levels in PCO syndrome: evidence for the existence of two subgroups of patients.

In 49 patients affected by PCO syndrome the serum levels of dehydroepiandrosterone-sulphate (DHEAs) were determined and correlated with the clinical presentation and the endocrine pattern. Twenty-three patients (47%) had high DHEAs levels (h-DHEAs patients). They presented a milder clinical presentation (low incidence of amenorrhea) than PCO patients with normal DHEAs levels (n-DHEAs patients). In h-DHEAs patients the finding of a normal DHEAs response to ACTH and of slightly increased 170HP serum levels suggested that the elevation of serum DHEAs was not due to an adrenal enzymatic deficiency but to a tonic hyperstimulation of the adrenals. Two subgroups of h-DHEAs patients were identified: in the first subgroup, PRL and estrone levels were increased and probably explained the DHEAs hypersecretion; in the second subgroup, the endocrine pattern was very similar to that observed in n-DHEAs patients and a clear explanation for DHEAs increase was not found, although the possibility of an exaggerated secretion of some pituitary hormones with adrenal androgen stimulating activity must be considered.

Adolescent↗

PubMed1984

The endocrine pattern of late onset adrenal hyperplasia (21-hydroxylase deficiency).

We describe 5 adult women with severe hirsutism due to late onset 21-hydroxylase deficiency. Diagnosis was performed on the finding of high serum 17-hydroxyprogesterone (17OHP) levels with a marked hyperresponse to an ACTH test. The endocrine study showed in most patients a gonadotropin behavior similar to that observed in classical polycystic ovary (PCO) syndrome. Prolactin levels were slightly increased in basal conditions and presented an exaggerated response to TRH stimulation.

17-alpha-Hydroxyprogesterone↗

PubMed1984

Prolactin secretion in polycystic ovary syndrome (PCO): correlation with the steroid pattern.

To evaluate the prevalence of hyperprolactinaemia in PCO patients and its possible correlation with a steroid pattern, we studied prolactin secretion (basal and after TRH stimulation) in 40 women affected by typical PCO. LH, FSH, testosterone, oestradiol, oestrone, DHEA-s and 17-OHP serum levels were also evaluated. Twenty-one patients had prolactin (Prl) values in the normal range both in baseline conditions and after TRH stimulation; 10 patients had normal basal values of Prl but an exaggerated response to TRH stimulation; 9 patients had high Prl basal values and an exaggerated response to TRH. The presence of hyperprolactinaemia was associated with increased serum levels of oestrone (P less than 0.01), DHEA-s (P less than 0.01) and 17-OHP (P less than 0.05). In conclusion, hyperprolactinaemia is as relatively frequent condition which affects almost half the patients suffering from PCO and is probably related to an increase of serum oestrogens, mostly oestrone. Moreover, in patients with PCO and hyperprolactinaemia, the production of some other steroids is also affected.

17-alpha-Hydroxyprogesterone↗

PubMed1983

Hypothalamic-pituitary-thyroid axis in acromegaly.

To evaluate the hypothalamic-pituitary-thyroid axis in acromegaly, total and free thyroid hormones and TSH response to TRH were determined in 36 acromegalic patients. In 10 patients, rT3 and thyroxine binding globulin (TBG) were also assayed by radioimmunoassay. In 15 patients the TSH response to TRH was also studied after medical or surgical therapy of the acromegaly. In 34 patients total thyroid hormones were in the normal range whereas two patients had low serum levels of free thyroid hormones. Thirty-two of the acromegalic patients were euthyroid. However, only 43.7% of the euthyroid patients had a normal TSH response to TRH. Nine patients had a reduced TSH rise after TRH, whereas in 4 patients the response was exaggerated and 5 delayed. In all patients studied rT3 and TBG were in the normal range. After medical or surgical therapy of the acromegaly we observed improvement or normalization of the TSH response to TRH. In conclusion, the TSH response to TRH is frequently altered in acromegaly, whereas thyroid function is generally normal. Hypothalamic effects of GH hyperproduction may explain the alterations of TSH secretion in many cases in view of the normalization of TSH secretion after therapy of acromegaly.

Acromegaly↗