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Biomedical subjects

E Vicari

Publications and source records attributed to E Vicari.

At least 73 records · Page 4Linked to original sources
PubMed1987

Dynamics of plasma gonadotropin and sex steroid release in polycystic ovarian disease after pituitary-ovarian inhibition with an analog of gonadotropin-releasing hormone.

To assess the dynamics of the suppression and recovery of plasma gonadotropins and sex steroids during and after inhibition of pituitary-ovarian function by a long-acting agonist GnRH-analog (GnRH-A), eight patients with polycystic ovarian disease were treated with 12 micrograms/kg X day GnRH-A for 56 consecutive days. In response to GnRH-A, these patients had a sharp and pronounced decline of their initially elevated immunoreactive LH and bioactive LH (bioLH) levels. Plasma immunoreactive FSH levels declined more rapidly than did bioLH, but the FSH decline was less sustained. Plasma testosterone, androstenedione, and estrone (E1) levels also declined during GnRH-A administration. The pattern of plasma androgen decrease resembled that of bioLH. There was a positive correlation between bioLH and the two androgens (r = 0.85; P less than 0.05, by Spearman's rank correlation, for both hormones). Cessation of GnRH-A administration was followed by prompt progressive increases in gonadotropin and androgen concentrations to pretreatment values. FSH recovered faster than bioLH. BioLH plasma concentrations reached pretreatment values by day 28. The recovery of plasma androstenedione and testosterone levels correlated positively with that of bioLH. Although plasma E1 levels were higher during the recovery period than during treatment, they never reached the concentrations found during the basal period, whereas estradiol concentrations were slightly but not significantly higher than those in the basal period. As a consequence, the E1 to estradiol ratio, very high in the basal period, approximated unity during recovery. These data indicate that hyperandrogenism in polycystic ovarian disease is gonadotropin dependent and accompanied by a relative abundance of LH bioactivity basally and during GnRH-A administration. Thus, the relative increase in bioLH secretion appears to be independent of the rate of gonadotropin secretion and the circulating sex steroid concentrations.

Adolescent↗
PubMed1986

Effect of gonadotrophin-releasing hormone analogue (GnRH-A) administration on serum gonadotrophin and steroid levels in patients with polycystic ovarian disease.

A gonadotrophin-releasing hormone (GnRH) analogue, D-Ser[TBU]LRH-EA10, (GnRH-A), at a dose of 200 micrograms was given daily for 2 months to 6 women with polycystic ovarian disease (PCO). Prior to therapy the patients presented elevated LH, testosterone (T), oestrone (E1) and dihydrotestosterone (DHT) in the circulation. In response to GnRH-A, these subjects exhibited a marked decrease in circulating T, DHT and androstenedione (A) levels as measured 24 h after GnRH-A injection, by 4 weeks and onwards (P less than 0.05). After 2 weeks of daily administration, the serum LH profile, evaluated by sampling at 2, 4, 7 and 24 h after injection of GnRH-A, was not different from baseline, whereas after 4, 6 and 8 weeks the levels were significantly lower (*P less than 0.01). The profile of serum T levels was unmodified at the second week, but significantly decreased thereafter (*P less than 0.01). At the end of treatment, the E1 concentrations, elevated in pre-injection condition, were markedly decreased. These data demonstrate that in PCO subjects, GnRH-A significantly lowered the elevated levels of androgens commonly found in these patients. The close correlation observed between reduced serum LH and androgen concentrations suggests that pituitary desensitization could be responsible for the reduction in androgen levels, and may be evidence for a gonadotrophin dependence of the elevated concentrations of T in these patients.

Adult↗
PubMed1986

Failure of GnRH analogue to inhibit serum concentrations of testosterone and 17 alpha-hydroxyprogesterone in hCG-substituted hypogonadotropic hypogonadism.

Gonadotropin-releasing hormone analogues (GnRH-A) induce inhibition of testicular function and reduction of serum testosterone (T) in man, but the mechanism involved is still debatable. To elucidate it we studied six patients with hypogonadotropic hypogonadism (HH) in chronic substitution with hCG for correction of androgen deficiency symptoms, and evaluated the effect of addition of GnRH-A to the hCG therapy on plasma levels of T and 17 alpha-hydroxyprogesterone (17 OHP). All patients were treated with 1000 U of hCG in every 3rd day for 24 weeks. After 8 weeks of this regimen, GnRH-A, Buserelin (D-Ser-TBU-EA-LHRH), 200 micrograms per day sc, was added and given for 8 weeks. After cessation of analogue administration patients were followed for 8 further weeks. The levels of the two steroids did not differ markedly in the pre- and post-GnRH-A period. GnRH-A given for two months did not lower T or 17 OHP levels as in eugonadal men after similar treatment. The median T concentrations during GnRH-A tended to be increased, with plasma values higher (P less than 0.025) than the peak values observed during hCG alone. Since administration of Buserelin did not inhibit hCG-sustained steroid levels in these HH patients, it is conceivable that GnRH-A may have lacked a direct inhibitory gonadal effect in such experimental conditions.

17-alpha-Hydroxyprogesterone↗
PubMed1986

Enhancing detection of gonococcus in ejaculates of adult males using sperm dilution.

Specific cultures were used to detect growth of Neisseria Gonorrhoeae (NG) in 90 ejaculates of partners of childless marriages. Although no gonococcal growth was observed in undiluted semen, 9 out of 68 subjects with silent infection presented growth of NG in seminal plasma after dilution 1:2 with saline. It is concluded that semen dilution increases the chances of detection of NG in semen samples of asymptomatic gonococci carriers.

Adult↗
PubMed1985

The prolactin-secreting system in relation to aging.

It is known that an increase in serum PRL can be responsible in men of impotence. The frequent sexual disturbances that are present in aging have suggested that in this age the PRL levels may be increased. Some authors have found elevated levels of PRL and an alteration in PRL response to pharmacological stimuli in elderly subjects. Other authors suggest that this increase of serum PRL in aging may be develop for determinating prostatic disease. In the present study we not have found differences in serum PRL between adult men, elderly subjects and prostatic subjects, while the responses to pharmacological stimuli observed in prostatic patients was higher than that of old age subjects. This finding is suggestive of an alteration in PRL-secreting system operating in aging.

Aged↗
PubMed1984

hCG-induced maturation of the seminiferous epithelium in hypogonadotropic men.

The effect of long-term hCG administration on sperm output was evaluated in a study in 3 hypogonadal patients with a selective deficiency of gonadotrophins (LH and FSH). The diagnosis of complete hypogonadotropic hypogonadism was based on clinical and hormonal findings as well as testicular histology. Pubertal maturation took place gradually during hCG therapy. 2 out 3 patients, who were azoospermic before treatment, had spermatozoa in their ejaculate after 12 and 24 months of therapy respectively. These effects on spermatogenesis were reversed after hCG withdrawal for 4 months and the patients again became azoospermic. This azoospermia was not reversed by testosterone (T) replacement therapy, or by addition of HMG to T. In vitro, the crude hCG preparation stimulated cAMP accumulation in rat Sertoli cell cultures indicating that this hCG preparation possesses an 'FSH-like' action. The present findings indicate that hCG therapy alone can induce and maintain spermatogenesis in some patients with complete hypogonadotropic hypogonadism.

Adolescent↗
PubMed1984

Kinetics of steroid responsiveness to hCG during chronic inhibition of testicular function by GnRH analogue.

The effect of daily injections of D-Ser-(TBU)6-LRH-EA10 (GnRH analogue (GnRH-A) 100 micrograms sc) on serum testosterone (T), 17 alpha-hydroxyprogesterone (17OHP) and oestradiol-17 beta (E2) was studied in 4 men. During GnRH-A therapy T, 17OHP and E2 were markedly decreased by the end of the second month. Continuous long-term administration of GnRh-A inhibited testicular function. To test whether the biosynthetic pathway was affected by the regimen, a bolus of 2000 U hCG was given to each subject after 10 months of therapy. Evaluation of the kinetics of steroid responsiveness showed a significant release of T in response to the trophic stimulus, with little or no elevation of serum 17OHP and E2. The response seen in these treated men appeared similar to that found in hypogonadotrophic men and prepubertal boys.

17-alpha-Hydroxyprogesterone↗
PubMed1983

Down-regulation of prolactin secretion in men during continuous thyrotropin-releasing hormone infusion: evidence for induction of pituitary desensitization by continuous TRH administration.

TRH was administered as a 5-h constant rate iv infusion (5 micrograms/min) to seven healthy adult men. Serum samples were collected at regular intervals for measurement of PRL, TSH, and T3. Serum levels of PRL during TRH infusion increased sharply to maximum level by 40 min, and then, despite continued TRH stimulation, PRL levels declined gradually to a plateau value after 100 min. No further rise in serum PRL was observed when a bolus of 200 micrograms TRH was administered to three subjects after 240 min of infusion. Conversely, an iv bolus of sulpiride (25 mg), a dopaminergic antagonist, given to four subjects after 240 min, brought about a marked increase in serum PRL values above the plateau level. These results are consistent with the interpretation that down-regulation in PRL secretion which follows the initial peak of response most likely represents pituitary desensitization to TRH. During the infusion serum TSH increases in two phases. A first phase of secretion was observed by 40 min followed by a plateau, with a second phase of increase occurring between 80-180 min.

Adolescent↗
PubMed1982

Hydrotestolactone lowers serum oestradiol and PRL levels in normal men: evidence of a role of oestradiol in prl secretion.

The effect on serum PRL levels of lowering serum oestradiol (E2) concentration by short-term administration of an aromatase activity inhibitor, hydrotestolactone (HT), was studied in six healthy male subjects. After HT administration serum E2 levels decreased from 68 +/- 5.8 to 26 +/- 2.5 pmol/l (mean +/- SE, P less than 0.05). These E2 changes were accompanied by a significant decrease in mean 2-h PRL levels from 11.2 +/- 2.1 to 6.5 +/- 1.6 ng/ml mean +/- SE, P less than 0.05). The evaluation of individual percentage change from basal concentrations showed a varying decrease in all subjects. These findings suggest that under physiological conditions E2 may be one of the factors which control blood PRL concentrations in men.

Adult↗
PubMed1982

Testicular responsiveness to chronic human chorionic gonadotropin administration in hypogonadotropic hypogonadism.

Steroidogenic responsiveness to long term hCG administration (1500 U three times a week for 23 months) was characterized in 8 males with hypogonadotropic hypogonadism (HH). During hCG treatment, testosterone (T), which was in the prepuberal range under basal conditions, rose considerably to the upper end of the normal range and remained at that level during the 23 months of observation. A 2.5-fold increase was observed in serum levels of 17 beta-estradiol (E2) an increment less than seen with T. The increment in 17 alpha-hydroxyprogesterone was also lower than that in T throughout the study; thus, the 17 alpha-hydroxyprogesterone to T ratio, despite continuous hCG administration, remained low. Serum androstenedione was slightly increased during hCG therapy. No significant changes were observed in serum levels of dehydroepiandrosterone. These data indicate that continuous long term hCG administration stimulated T levels in HH, with a relatively small change in E2. The kinetics of the T and E2 responses to 2000 U hCG, evaluated after 23 months of therapy, indicated that the testicular response was markedly reduced. No increment in T levels was observed at 24 h; the maximal response occurred at 48 h. This pattern of T response supports the idea that partial testicular desensitization occurs in HH patients receiving chronic treatment with hCG.

Adolescent↗
PubMed1982

Dynamics of Prl release in galactorrhoeic normoprolactinaemic women.

Prl responsiveness to TRH and sulpiride was evaluated in 14 galactorrhoeic normoprolactinaemic women. Radiological signs of sellar alteration were present in 6 of these patients. Pituitary responses to TRH did not differ from those obtained in a group of 16 healthy women. Serum Prl levels after sulpiride were higher in the patients than in the controls (P less than 0.01). The delta max response was 256 +/- 16 SE vs 158 +/- 10.6 ng/ml in the control group (P less than 0.01). The mean integrated area after sulpiride was also greater 20738 +/- 1263 SE ng/ml/2 h vs 13 188 +/- 408) (P less than 0.01). The markedly enhanced Prl response to sulpiride in our patients with galactorrhoea could be due to a functional disorder of the hypothalamic-pituitary axis or to a lactotrope hyperplasia.

Adult↗
PubMed1981

Some critical considerations on the use of the nomifensine test in the hyperprolactinaemic syndrome.

Nomifensine has recently been proposed as a dynamic test to discriminate tumoral from functional hyperprolactinaemia. In the present study, this test was performed in 9 subjects with radiological signs of sellar alteration and in 6 with no signs of pituitary lesion. Adopting the criterion reported in the previous study, the test was considered positive in 2 subjects of the first group and in 2 subjects of the second group. Therefore, our study indicates that the ability of this test to discriminate subjects with tumorous or non-tumorous hyperprolactinaemia still appears debatable.

Adenoma↗
PubMed1981

Direct evidence in men for a role of endogenous oestrogens on gonadotrophin release.

In six healthy subjects serum oestradiol was selectively decreased by administering an aromatase activity inhibitor, hydrotestolactone (HT). After HT administration serum oestradiol (Oe2) decreased from 18.7 +/- 2.3 (SEM) to 6.7 +/- 0.6 pg/ml whereas testosterone (T) and dihydrotestosterone (DHT) blood levels were not modified. These oestradiol changes were associated with a significant increase in serum LH and FSH concentrations (P less than 0.001). The administration of tamoxifen, an oestrogen antagonist, to 5 subjects caused a sharp increase in LH and FSH levels (P less than 0.001). Oe2 was unchanged after the treatment with tamoxifen, whereas T levels were significantly higher. The sum of these data suggests that oestradiol under physiological conditions plays a specific role in the feedback mechanism of gonadotrophin release.

Adolescent↗
PubMed1981

Dynamic evaluation of prolactin secretion with sulpiride and thyrotrophin releasing hormone in amenorrhoeic and normally menstruating women.

Sulpiride and TRH were used to evaluate the dynamics of prolactin (Prl) release in normoprolactinaemic, amenorrhoeic and normally menstruating women. The two tests were performed in a randomomized order with an interval of 2-3 days. In the normal women the first test was carried out between days 2 and 4 of their cycle. Basal values during the two tests were not statistically different (9.6 +/- 1.2 SE vs. 10.7 +/- 1.4 ng/ml in amenorrhoeic women with sulpiride and 11.3 +/- 1.4 vs. 12.4 +/- 1.7 in amenorrhoeic women during the TRH test). The two tests were performed while the subjects of the two groups had identical serum oestrogen concentrations. The Prl response following TRH administration was similar in both groups (delta max mean 49.5 +/- 12.5 SE and 49.4+/- 8.5 SE in normal and amenorrhoeic women, respectively). In contast, when release by sulpiride administration was studied the normal women had greater Prl release (delta max mean 169.9 +/- 18.2 SE) than amenorrhoeic women (delta max mean 99.8 +/- 9.4). Either the different oestrogen status (lower in amenorrhoeic women than in menstruating women) or the hypothalamic pituitary dysfunction likely to be responsible for the amenorrhoea in our patients, may explain the lower Prl release observed after sulpiride in subjects with amenorrhoea.

Adolescent↗
PubMed1979

Effect of cyproterone acetate acutely administered on the pituitary-testicular axis.

The effect of cyproterone acetate (CA) on the pituitary-testicular axis was studied in 6 healthy men. A dose of 300 mg of CA was administered orally in the early morning, after 3 h blood samples were collected using a multiple sample technique. Testosterone (T) levels were decreased by CA in all subjects (p 0.01), LH in all (p less than 0.01) but one whereas 17-hydroxyprogesterone did not show any significant variation. In vitro, using an equilibrium dialysis, CA displaced T from plasma-binding proteins in males at 37 degrees C. The role of testosterone-binding globulin on the effects of CA on the pituitary-testicular axis remains to be clarified.

Adolescent↗
PubMed1979

Effect of androgens on prolactin (PRL) release in humans.

In order to evaluate whether androgens were able to affect PRL release, testosterone and dihydrotestosterone were injected intramuscularly in male and female subjects. PRL blood levels were not modified by testosterone either in healthy males or in amenorrhoeic women, and PRL release in males proved unaffected by dihydrotestosterone at the dose used.

Adolescent↗