PubMed Health⌕ Search

Biomedical subjects

A Lanzone

Publications and source records attributed to A Lanzone.

At least 127 records · Page 7Linked to original sources

Human growth hormone enhances progesterone production by human luteal cells in vitro. II. Evidence of a distinct effect on two luteal cell types.

OBJECTIVE: To examine the differential effect of human GH (hGH) on basal and hCG-stimulated production by cultured small and large human luteal cells. DESIGN: Distinct cultures of small and large luteal cells from early and midluteal phase. SETTING: All corpora lutea were obtained from the Obstetrics and Gynecology Department of the Catholic University, a public care center in Rome, Italy. PATIENTS, PARTICIPANTS: Ten nonpregnant women between 31 and 43 years of age underwent surgery for various nonendocrine disorders such as leiomyomatosis. INTERVENTIONS: Corpora lutea were obtained at the time of hysterectomy. MAIN OUTCOME MEASURES: Small and large luteal cells were incubated with or without hCG and/or hGH at different concentrations. RESULTS: Human GH neither at 250 nor at 500 micrograms/L increased basal P production by small luteal cells, whereas from 1,000 micrograms/L, P concentration in media was significantly increased. The concomitant treatment with ineffective doses of hCG (30 and 60 IU/L) and hGH (250 and 500 micrograms/L) enhanced P production to that obtained with the highest doses of hGH (1,000 micrograms/L or more) or hCG (125 to 250 IU/L) alone. Human GH addition did not change the amount of P release by large luteal cells at any concentration. CONCLUSIONS: These results indicate a distinct and differential effect of hGH on in vitro luteal steroidogenesis by the two luteal cell types.

Adult↗

Indomethacin in vivo inhibits the enhancement of the progesterone secretion in response to gonadotrophin-releasing hormone by human corpus luteum.

Different prostaglandins (PG) seem to have luteolytic or luteotrophic function in relation to the phases of life of the human corpus luteum and in-vitro studies demonstrate a luteotrophic function of PGE2, PGI2, PGD2. The present study evaluated the effect of an inhibitor of prostaglandin synthesis on the hypophyseal and luteal responses to gonadotrophin-releasing hormone (GnRH) in women during the mid-luteal phase. Twenty normal menstruating women participated in the study. Two different protocols were applied. After monitored ovulation (day 0), eight patients were treated with indomethacin for 7 days and 12 untreated patients served as controls. To evaluate luteal progesterone production, blood samples were taken every 15 min for 2 h basally and after a bolus of GnRH (25 micrograms i.v.); eight control patients were also treated with indomethacin for one day, and the endocrine study was repeated. The long-term administration of indomethacin significantly reduced basal as well as luteinizing hormone (LH)-stimulated progesterone production by the corpus luteum in respect to controls. Short-term administration failed to influence basal progesterone production, but abolished its secretory response to LH. A luteotrophic role for prostaglandins in human luteal function is suggested.

Adult↗

Evaluation of ovarian and adrenal sources of androgens in women with polycystic ovary syndrome. Dexamethasone and GnRH-agonist administration.

Ovarian and adrenal production of androgens was evaluated in 18 patients with polycystic ovary syndrome (PCOS) by administering a combination of short-term dexamethasone (DEX) and long-term gonadotropin-releasing hormone agonist (GnRH-A). At day 6 of the cycle, blood samples were collected at 7 A.M. (basal) and 11 P.M. At midnight, 2 mg DEX was given orally, and blood samples were collected at 7 A.M. the following day (DEX1). Blood samples were obtained for 6 weeks at the same time after administration of a potent GnRH-A (400 micrograms/day given subcutaneously). Eight normal subjects served as controls. The amounts of androgens and 17-hydroxyprogesterone (17-OHP) suppressed by using DEX (adrenal-source suppression) and GnRH-A (ovarian-source suppression) were greater in PCOS patients than in controls. We differentiated PCOS patients as having a normal or an exaggerated response to DEX or GnRH-A administration; threshold values were considered average +2SD of the suppressed androgen amounts of controls. Three patients had an exaggerated response to GnRH-A treatment for androstenedione, testosterone and 17-OHP, while DEX inhibition was similar to controls. The remaining 15 patients had an exaggerated response to DEX for all three androgens; seven also had an exaggerated response to GnRH-A. Thus, the combination of GnRH-A and DEX permitted us to selectively study and identify adrenal and ovarian sources of hyperandrogenemia.

Adrenal Glands↗

Long-term naltrexone treatment reduces the exaggerated insulin secretion in patients with polycystic ovary disease.

OBJECTIVE: To evaluate the involvement of endogenous opiates in the pathophysiology of the hyperinsulinism in patients affected by polycystic ovary disease by administering naloxone and naltrexone. We also studied the hormonal status following long-term opioid antagonist administration. METHODS: Twenty-one women affected by polycystic ovary disease participated in the study. An oral glucose tolerance test (GTT) was performed at baseline and repeated after short-term naloxone infusion and after 6 weeks of naltrexone administration. Plasma glucose and insulin levels were evaluated in all samples. Gonadotropins, sex hormone-binding globulin, and androgen levels were determined initially and after the naltrexone treatment. RESULTS: None of the patients showed any alteration of glucose tolerance. Based on the insulin response to the GTT, the patients were classified as normo- or hyperinsulinemic. Opioid antagonist administration significantly reduced the insulin response to the GTT in hyperinsulinemic patients, without affecting their glycemic levels. In normoinsulinemic patients, glucose plasma levels were increased whereas insulin levels were not modified by the treatments. Gonadotropin and androgen plasma concentrations were not modified after naltrexone administration. CONCLUSIONS: This work supports a role for the endogenous opiates in the regulation of exaggerated insulin secretion in patients with polycystic ovary disease. The reduction of insulin secretion failed to demonstrate any hormonal modification in such hyperandrogenized patients.

Adult↗

Human growth hormone enhances progesterone production by human luteal cells in vitro: evidence of a synergistic effect with human chorionic gonadotropin.

OBJECTIVE: To examine the possible direct effect of human growth hormone (hGH) on basal and human chorionic gonadodotropin (hCG)-stimulated progesterone (P) production by cultured human luteal cells. DESIGN: Cultures of human luteal cells from early and midluteal phase. SETTING: All corpora lutea were obtained from the Obstetrics and Gynecology Department of the Catholic University, a public care center. PATIENTS, PARTICIPANTS: Twelve nonpregnant women between 35 and 47 years of age underwent surgery for various nonendocrine disorders such as leiomyomatosis. INTERVENTIONS: Corpora lutea were obtained at the time of hysterectomy. MAIN OUTCOME MEASURE: Luteal cells were incubated with or without hCG and/or hGH at different concentrations. RESULTS: Human growth hormone neither at 250 nor at 500 ng/mL increased basal P production, whereas from 1,000 ng/mL P concentration in media was significantly increased (P less than 0.05). The concomitant treatment with uneffective doses of hCG (6 and 12 ng/mL) and hGH (250 and 500 ng/mL) enhanced P production similarly to that obtained with the highest doses of hGH (1,000 ng/mL or more) or hCG (25 to 50 ng/mL) alone. CONCLUSIONS: These results indicate a direct effect of hGH on the luteal steroidogenesis in vitro.

Adult↗

Differential androgen response to adrenocorticotropic hormone stimulation in polycystic ovarian syndrome: relationship with insulin secretion.

OBJECTIVE: To investigate the relationship between insulin and adrenal androgens in patients with polycystic ovarian disease (PCOD). DESIGN: Patients with PCOD and a group of volunteers who attended the department during a period of 6 months were studied. SETTING: Department of Gynaecology and Obstetrics, Università Cattolica del Sacro Cuore, Roma, Italy. PARTICIPANTS: Healthy women with ovulatory cycles (hospital personnel, n = 8) and women affected by PCOD (n = 32) were studied on day 5 to 6 of their follicular phase. INTERVENTIONS: All women had an oral glucose tolerance test (OGTT) (75 g) on day 5 to 6 of the cycle. Then plasma samples were collected at 7.00 A.M.; at 11.00 P.M., 2 mg of dexamethasone (DEX) were orally administered with blood samples collected the day after at 7.00 A.M. (effect of DEX). Then adenocorticotropic hormone (ACTH, Synacten; Ciba-Geigy, Varese, Italy) 250 micrograms was injected intravenously (IV) and samples collected 60 minutes later (effect of ACTH). MAIN OUTCOME MEASURES: Plasma glucose and insulin concentration were assayed on OGTT samples collected at time 0, 30, 60, 90, 120, 180, and 240 minutes after glucose ingestion. Data are expressed as area under the curve. Cortisol, 17 alpha-hydroxyprogesterone (17-OHP), testosterone (T), androstenedione (A), and dehydroepiandrosterone sulphate (DHEAS) plasma levels were evaluated on the samples collected before and after DEX or ACTH administration. Data are expressed as absolute concentrations and percent increase in respect to values before the treatment. RESULTS: According to the OGTT response, 21 patients were classified as hyperinsulinemic and 11 as normoinsulinemic. The ideal body weight was greater in hyperinsulinemic patients. No differences in baseline hormone levels were found between the two groups. Only sex hormone binding globulin levels were significantly greater in normoinsulinemic patients (P less than 0.05). Also, the plasma concentration of all steroids after DEX were similar in both groups. Intravenous injection of ACTH significantly increased plasma androgens levels. Cortisol, DHEAS, and T enhancement did not differ in normoinsulinemic and hyperinsulinemic patients, whereas significantly greater A (P less than 0.01) and 17-OHP (P less than 0.05) plasma concentrations were observed after ACTH injection in hyperinsulinemic when compared with normoinsulinemic PCOD subjects. Control group after IV ACTH showed an increase of A and 17-OHP similar to those found in normoinsulinemic PCOD group. CONCLUSIONS: These data suggest that insulin could be involved in the androgen production by adrenal gland and it could influence the responsiveness of adrenal to its trophic hormones.

17-alpha-Hydroxyprogesterone↗

Multiple serum marker assay in the diagnosis of endometriosis.

Serum levels of CA-125, CA-15-3 and TAG-72 were measured in 81 patients with endometriosis, diagnosed by laparoscopy, and staged according to the Revised American Fertility Society, and in 31 control subjects. The values of CA-125 and CA-15-3 were also determined in peritoneal fluid. The aim of the present study was to evaluate the clinical usefulness of these various markers in the diagnosis of endometriosis by using them either by themselves or combined. High serum levels of CA-125 were found in 43 of 81 patients with endometriosis (53%) and in five of 38 control subjects (13%). The values of serum CA-125 progressively increased in relation to the severity of the disease. High serum values of CA-15-3 and TAG-72 were also found in patients with endometriosis, but with a similar incidence also in control patients. High CA-125 and CA-15-3 values in peritoneal fluid were found in all patients investigated. These results suggest that measurement of serum CA-15-3 and TAG-72 in addition to CA-125, does not provide any advantage for the diagnosis of endometriosis.

Adult↗

Ovulation induction with human menopausal gonadotropin versus follicle-stimulating hormone after pituitary suppression by gonadotropin releasing hormone agonist in polycystic ovary disease. A cross-over study.

Ten patients with polycystic ovary disease (PCOD) had ovulation induction after pituitary suppression by gonadotropin releasing hormone agonist (GnRHa) with GnRHa plus pure follicle-stimulating hormone (FSH) or plus human menopausal gonadotropin (hMG). Duration of the stimulation period and gonadotropin doses were superimposable. A multifollicular response was observed in both treatments. Bioassay and radioimmunoassay of luteinizing hormone, androstanedione and testosterone plasma levels were higher in hMG cycles compared to FSH-treated cycles. No differences was found in FSH and estradiol (E2) plasma concentrations, whereas in hMG-treated cycles the E2/number of follicles and E2/ovarian volume ratios were greater than in the FSH-treated cycles. Clinical results in terms of percentages of ovulation and pregnancies were the same in the two protocols. We conclude that the presence of luteinizing hormone in induction of ovulation in patients with PCOD does not seem to influence follicular recruitment and development, but it may have a role in the enhancement of steroid production.

Adult↗

Low-dose aspirin and vascular response in pregnant patients sensitive to angiotensin II.

The angiotensin sensitivity test was performed in 25 high risk pregnant women before and after administration of low-dose aspirin (100 mg/day for 7 days). After aspirin administration there was a significant decrease in AII sensitivity in sensitive patients with no change in nonsensitive patients. Low-dose aspirin favorably affects sensitivity to AII in sensitive patients, thus indicating a reduced vascular reactivity as a consequence of this regimen.

Angiotensin II↗

Effect of opiate receptor blockade on the insulin response to oral glucose load in polycystic ovarian disease.

In order to test the hypothesis that endogenous opiates are at least partially responsible for hyperinsulinaemia in patients with polycystic ovarian disease (PCOD), the effect of naloxone (an opiate receptor blocker) on the insulin response to oral glucose load (OGTT) was studied in 20 women with PCOD and 17 control subjects at days 5-8 of their follicular phase. After fasting overnight for 10-12 h, each woman received an i.v. bolus injection (2 mg) of naloxone or an equal volume of saline infusion followed by a constant infusion of naloxone or saline solution at a rate of 8 ml/h (1 mg/h of naloxone) for 5 h. OGTT (75 g) was performed 1 h after the bolus injection. The naloxone study was performed 48 h after the saline study. Naloxone did not modify the insulin response to OGTT in either group. When the data were related to the insulin response, in PCOD hyperinsulinaemic patients, naloxone significantly reduced (P less than 0.02) the insulin response to OGTT without any change in glycaemic response curves. In control and PCOD normoinsulinaemic patients, naloxone did not change significantly either the glycaemia or the insulin levels after OGTT. No change of gonadotrophin and steroid secretion was found in any patient receiving naloxone. In conclusion, endogenous opiates may play a significant role in hyperinsulinaemia in PCOD.

Adolescent↗

Assessment of the adrenal-ovarian contribution by short-term dexamethasone and ACTH tests in hyperandrogenized patients.

Fifty-four hyperandrogenized women were studied to evaluate the importance of the adrenal or ovarian contribution to androgen secretion. Forty-six had the polycystic ovarian (PCOD) syndrome. Eight normal women represented a control group. The endocrine study was performed during the follicular phase. The plasma samples were collected at 7.00 am (A1) and at 11.00 pm (A3). Dexamethasone 2 mg was administered orally at 11.30 pm and blood samples were collected the day after, at 7.00 am (B). The adrenocorticotropic hormone (ACTH) was injected, 250 micrograms i.v. and samples were collected after 60 min. Cortisol dehydroepiandrosterone-sulfate (DHEAS), androstenedione, testosterone and 17-hydroxyprogesterone (17OHP) were measured. The hyperandrogenized patients had A1 androgen levels higher than the controls (p less than 0.01). 17OHP and androstenedione A3 values showed a cortisol-related decrease. After dexamethasone, androgen levels, since DHEAS, were normalized in all patients. We found that baseline androgen levels and circadian and dexamethasone-inhibited amounts were strongly correlated (p less than 0.01). The ACTH test revealed five cases of enzymatic adrenal deficiencies. Moreover, the amplitude of the response of 17OHP and androstenedione to ACTH is predictable in relation to both circadian and dexamethasone-inhibited amounts (p less than 0.01). In conclusion, our study confirms and makes quantifiable the importance of the adrenal contribution to androgen secretion in hyperandrogenized patients. The ACTH test is important for detecting the presence of mild enzymatic adrenal defects.

Adolescent↗

Serum CA-125 levels in the diagnosis and management of endometriosis.

The value of CA-125 for the diagnosis and management of endometriosis (EN) was investigated by assaying the marker in the serum and peritoneal fluid (PF) from patients with the disease in comparison with control subjects. Of women who underwent 270 consecutive laparoscopies, 81 with various stages of EN (18 stage I, 13 stage II, 35 stage III and 15 stage IV) and 38 with normal pelvic findings were studied. CA-125 serum values increased progressively in relation to the severity of the disease. The levels in stages III and IV EN were significantly higher (P less than .01) than in stages I and II or control patients. The latter two groups did not differ from each other. High CA-125 PF values were found in all the patients investigated. Twenty-two patients with EN were treated with a gonadotropin releasing hormone agonist for six months before second-look laparoscopy or laparotomy. CA-125 values decreased significantly after one month of medical treatment and remained unchanged during the course of therapy. No significant relationship was found in the outcome after therapy.

Adult↗

Serum CA-125 levels do not depend on ovarian steroidogenesis.

To investigate the relationship between CA-125 production and ovarian steroidogenesis, serum CA-125 levels were evaluated in patients with normal pelvis in different ovarian endocrine situations: (1) during the menstrual cycle, (2) during stimulatory treatment with gonadotropin for the induction of ovulation, and (3) during suppression treatment with gonadotropin-releasing hormone agonists. In spite of the spontaneous or the markedly induced variations of estradiol (E2) or ovarian volume, CA-125 levels remained unvaried in all patients. Moreover, CA-125 serum levels did not correlate with the increasing values of the plasma E2 or ovarian volume. In conclusion, steroidogenetic activity of the ovary is unlikely to affect CA-125 production.

Adult↗

Insulin secretion in polycystic ovarian disease: effect of ovarian suppression by GnRH agonist.

Nine obese and ten non-obese women with polycystic ovarian disease (PCO), and seven obese and eight non-obese normal women, had an oral glucose tolerance test (OGTT) before and after treatment with GnRH agonist (buserelin 400 micrograms/day s.c. for 8 weeks) in order to investigate the effect of ovarian suppression on their insulinaemic secretion. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), oestradiol (E2), androstenedione (A), testosterone (T), DHEAS, cortisol and insulin (I) were measured at time 0 of OGTT; in all samples of OGTT, E2, T, A and I were also assayed. PCO patients showed higher basal androgen levels than control patients. All subjects showed a normal glycaemic response to OGTT. The mean fasting and areas under the curve (ISA) of plasma I were significantly greater in the obese PCO women than in non-obese PCO, the normal obese and non-obese women. All PCO patients showed significantly higher fasting I and ISA values in respect to all control patients. Hyperinsulinaemic responses were 89% in PCO obese, 30% in non-obese PCO and 29% in obese control patients. After buserelin treatment, these values did not change significantly in respect to pretreatment in all groups, in spite of a significant decrease of androgen secretion. During OGTT, no variations of steroid plasma concentrations were seen in both normal or hyperinsulinaemic PCO patients. The data of this study show that hyperandrogenism, hyperinsulinism and obesity were associated with different modalities in PCO patients and that a marked decrease of androgen secretion did not restore a normal insulinaemic response to OGTT, suggesting that hyperandrogenism does not produce hyperinsulinism.

Adult↗

Gonadotrophin releasing hormone agonist (buserelin) in the treatment of endometriosis: changes in the extent of the disease and in CA 125 serum levels after 6-month therapy.

Twenty-two women with endometriosis were treated with the luteinizing hormone-releasing hormone (LHRH) agonist buserelin for 6 months. At second-look laparoscopy the mean score of endometriosis had decreased from 23.1 (SD 17.0) to 17.2 (SD 20.2) (P less than 0.05). CA 125 serum levels decreased from 38.4 (SD 32.2) U/ml at diagnosis to 15.5 (SD 7.0) at second look (P less than 0.005). CA 125 levels correlated at diagnosis with total score of endometriosis (P less than 0.05) and with active score of endometriosis (P less than 0.05), but not with the adhesion score. CA 125 levels were not correlated with endometriosis scores at second look laparoscopy, thus suggesting that mechanisms other than the change in the extent of the disease may be involved in the CA 125 decrease during therapy. CA 125 levels may therefore not be a reliable indicator for monitoring the efficacy of LHRH agonist treatment of endometriosis.

Adult↗

Growth hormone and somatomedin-C secretion in patients with polycystic ovarian disease. Their relationships with hyperinsulinism and hyperandrogenism.

Nineteen women with polycystic ovarian disease (PCO; 9 obese) and 15 normal ovulatory women (7 obese) were studied at their follicular phase. All patients had an oral glucose tolerance test (OGTT) before and after treatment with gonadotropin-releasing hormone (GnRH) agonist (Buserelin 400 micrograms/die s.c. for 8 weeks) to investigate the relationship between ovarian steroidogenesis and insulin and growth hormone (GH) and insulin-like growth factor (SmC) secretion. Luteinizing hormone, follicle-stimulating, estradiol, androstenedione, testosterone, dehydroepiandrosterone sulfate, cortisol, insulin, GH and SmC were measured basally at the time of OGTT. PCO patients showed higher androgen basal levels than control patients. All subjects showed a normal glycemic response to OGTT. The mean fasting level and area under the curve of plasma insulin were also significantly greater in PCO than in control patients (p less than 0.05), while GH and SmC plasma concentrations did not differ between the groups. Despite a considerable decrease in androgens and the similar levels in both PCO and control women, buserelin treatment did not determine any significant changes of insulin and GH-SmC secretion. GH and SmC did not correlate with ideal body weight (IBW), insulin or androgens, whereas insulin correlated with both testosterone and androstenedione levels (p less than 0.05) and with IBW (p less than 0.01); after the buserelin regimen only IBW remained related to plasma insulin (p less than 0.01). In conclusion results of this study confirm that hyperinsulinism is a characteristic picture of PCO and is related in an unclear way with hyperandrogenism and obesity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Importance of echographic and endocrine monitoring for the assessment of ovulation by follicle stimulating hormone in polycystic ovarian disease.

Sixteen patients with polycystic ovarian disease (PCOD) were treated for 39 cycles with pure follicle-stimulating hormone (FSH) for the induction of ovulation. At ovulation time human chorionic gonadotropin (hCG) was administered. Twenty-one cycles were ovulatory. Twenty-three were classified as normostimulated (N): six pregnancies and three abortions were observed. In the remaining eight hyperstimulated (H) cycles there were four full-term pregnancies. Dosage and length of treatment were greater in patients with excess body weight (P less than 0.01). H cycles were characterized in respect to N cycles by: (1) higher baseline values of 17-hydroxy progesterone (17-OHP) plasma levels and LH/FSH ratios; (2) higher plasma concentrations and rate of increase of 17-OHP periovulatory levels. E2 plasma levels did not permit a clear differentiation between H and N cycles, and it was not useful for the timely recognition of hyperstimulation. Our data show that a slight controlled degree of ovarian hyperstimulation is beneficial to pregnancy rate and outcome.

17-alpha-Hydroxyprogesterone↗