Sulpiride stimulation of prolactin secretion in adolescents with gynecomastia: relation to the circulating levels of estradiol (original) (raw)
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Role of Testosterone and Dihydrotestosterone in Spontaneous Gynecomastia of Adolescents
Systems Biology in Reproductive Medicine, 1992
To test a possible hormonal mechanism of gynecomastia at puberty, a group of pubertal spontaneous gynecomastia (PSG) and healthy young volunteers (HYV), Tanner's stage 11-V, were studied. Peripheral blood samples were obtained for measuring follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), testosterone (T), dihydrotestosterone (DHT), estradiol (E-2) and estrone (E-I). No difference was established in steroids in pituitary hormonal concentration when both groups were compared on a sexual stage-matched control basis, except for T 2 SD in 519 subjects of PSG and DHT 2 SD in all of PSG. The T:DHT ratio varied from 5.0 to 15.4 in PSG and from 0.42 to 2.224 in HYV. Whether spontaneous gynecomastia might exist in an enzimatic blockade of Sa-reductase and whether a decrease in the T:DHT ratio might favor the estrogen action for the progression of breast enlargement deserve further analysis.
Journal of andrology
To elucidate the effects of sulpiride-induced (300 mg daily) long-term (64 days) hyperprolactinemia on basal and hCG-stimulated plasma testosterone (T), hCG was given to five normal men five times at 2-week intervals (before sulpiride administration and at 2, 4, 6 and 8 weeks). Mean integrated hCG responses of plasma T did not change significantly as compared with baseline. However, mean (+/- SEM) basal plasma levels of T decreased significantly (P less than 0.05) from 1011 +/- 148 ng/dl to 852 +/- 13 at 2 weeks, 520 +/- 53 at 4 weeks, 572 +/- 137 at 6 weeks and 554 +/- 140 at 8 weeks. These results suggest that sulpiride-induced hyperprolactinemia (73.8 ng/ml, the average of mean values obtained at 2, 4, 6 and 8 weeks) for 64 days does not suppress secretion of T in response to hCG in spite of a decrease in basal plasma T concentrations. It is unlikely that the low concentrations of plasma T are due to direct effects of hyperprolactinemia on the testis.
Effect of normal aging on the prolactin response to graded doses of sulpiride and to arginine
Progress in Neuro-Psychopharmacology and Biological Psychiatry, 1985
Effect of normal aging on the prolactin response to graded doses of sulpiride and to arginine. Prog. Neuro-Psychopharmacol. & Biol. Psychiat. 1985, 2 (5/6): 633-637. 1. 2. 3. 4. 5. 6. The prolactin (PRL) response to placebo, sulpiride (2.5, 5, 10 and 20 mg im) and arginine HCl infusion (0.33G/kg) was examined in young (18-25 yrs) and old (65-75 yrs) normal men. Analysis of variance for the sulpiride data showed no significant dose x age group interaction or dose x age group x period interaction. There was, however, a significant age group x period interaction (p < 0.05). PRL concentrations were significantly lower in the old subjects (N=9) 'compared with the young (N=9) 15 min after 2.5, 5, or 10 mg but not significantly after 20 mg sulpiride or at any other time interval. The areas under the concentration-time curves and the mean individual peak PRL concentrations were not significantly different between the two groups. The pattern of findings suggests a delayed absorption of sulpiride in the elderly rather than a change in pituitary dopamine (DA) receptor sensitivity to account for the lower PRL concentrations at 15 min. Differences in magnitude of the PRL response between the four doses of sulpiride were small and results suggest that the 2.5 mg dose is close to that required to saturate DA receptors on the lactotrophe and that the 10 and 20 mg doses are sufficient to completely block pituitary DA receptors. There was no significant age effect on arginine-induced PRL secretion (N=ll in each group) These results suggest that (a) the PRL secretory reserve is unchanged in normal aging (b) the mechanism subserving arginine-induced PRL secretion is unaffected by age (c) studies using a lower dose range of sulpiride combined with measurements of serum sulpiride levels are required to evaluate any age effect on lactotrophe DA receptor sensitivity.
Clinical and Biochemical Phenotype of Adolescent Males with Gynecomastia
Journal of Clinical Research in Pediatric Endocrinology, 2019
Objective: Gynecomastia is defined as benign proliferation of male breast glandular tissue. Its prevalence during puberty stands at 50-60% and this condition is common also in neonatal and elderly males. It develops mainly due to the disequilibrium between estrogen and androgen activity in breast tissue, where estradiol binds to estrogen receptor and stimulates ductal and glandular cells. The aim of this work was to find a relationship between the sex hormones alterations and the natural history (evolution) of gynecomastia. Furthermore, the work tries to indicate the importance of checking the E2/TTE ratio. Materials and Methods: Participants in this study were 93 male patients aged 9 to 18 (mean age 13.8 ± 2.6) referred to an outpatient clinic between January 2011 and February 2016 with breast enlargement. Results: In 63 of 93 boys the gynecomastia was confirmed and 28 of them were follow-up (median of 3 months). None of all observed boys have reduced the size of breast during the observation and there was no correlation between BMI Z-Score and size of breast (p>0.05). Breast enlargement progressed in 9 boys (32.1%). We have observed a positive correlation between E2/TTE Ratio and Tanner B stage (r=0.47; p=0.034). Conclusions: The E2/TTE ratio may be a helpful tool in diagnosing gynecomastia. Altered E2/TTE ratio might be responsible for part of cases described previously as idiopathic. Additionally, weight loss does not imply reduction of breast size in boys, nonetheless it should be the first step before further treatment of prolonged gynecomastia.
Andrology, 2016
Pubertal gynecomastia is a common condition observed in up to 65% of adolescent males. It is usually idiopathic and tends to regress within 1-2 years. In this descriptive cross-sectional study, we investigated 25 adolescent males with prominent (>B3) and/or persistent (>2 years) pubertal gynecomastia (P/PPG) to determine whether a hormonal/genetic defect might underline this condition. Endocrine investigation revealed the absence of hormonal disturbance for 18 boys (72%). Three patients presented Klinefelter syndrome and three a partial androgen insensitivity syndrome (PAIS) as a result of p.Ala646Asp and p.Ala45Gly mutations of the androgen receptor gene. The last patient showed a 17a-hydroxylase/17,20-lyase deficiency as a result of a compound heterozygous mutation of the CYP17A1 gene leading to p.Pro35Thr(P35T) and p.Arg239Stop(R239X) in the P450c17 protein. Enzymatic activity was analyzed: the mutant protein bearing the premature stop codon R239X showed a complete loss of 17a-hydroxylase and 17,20-lyase activity. The mutant P35T seemed to retain 15-20% of 17a-hydroxylase and about 8-10% of 17,20-lyase activity. This work demonstrates that P/PPG had an endocrine/genetic cause in 28% of our cases. PAIS may be expressed only by isolated gynecomastia as well as by 17a-hydroxylase/17,20-lyase deficiency. Isolated P/PPG is not always a 'physiological' condition and should thus be investigated through adequate endocrine and genetic investigations, even though larger studies are needed to better determine the real prevalence of genetic defects in such patients.
Human Prolactin: Measurement in Plasma by In Vitro Bioassay
Journal of Clinical Investigation, 1971
tracted human plasma by a sensitive and specific in vitro bioassay. Secretory activity of breast tissue fragments from mid-pregnant mice, incubated in organ culture with human plasma, serves as the histologic end point. Sensitivity is 5 ng/ml (0.14 mU/ml) or somewhat better for ovine prolactin, and approximately 0.42 mU/ml for prolactin activity of human plasma at the dilutions used in the assay. Human growth hormone as it circulates in blood, like the material extracted from pituitary glands, is strongly lactogenic. Antisera to human growth hormone are capable of completely neutralizing the prolactin effect of large amounts (600 ng/ml) of human growth hormone added to the system. Plasma prolactin activity is less than 0.42 mU/ml in normal men and women. Of 26 patients with nonpuerperal galactorrhea, 14 had elevated prolactin activities ranging from 0.42 to 3.5 mU/ml. Growth hormone levels by radioimmunoassay were far too low, in general, to account for the observed prolactin activity. All of 14 nursing mothers, 1-30 days post partum, had elevated prolactin activity with a mean of 2.29 and a total range of 0.56-4.5 mU/mi. Growth hormone was in the low normal range in all of these subjects. Seven patients on psychoactive drugs of the phenothiazine series similarly had elevated prolactin activity with low growth hormone. Antiserum to human growth hormone, when preincubated with plasma samples from each of these three groups of subjects, produced no significant inhibition of prolactin activity. In two acromegalic patients with markedly elevated growth hormone levels, antiserum to growth hormone produced complete inhibition of prolactin activity in one and partial inhibition in the other. These studies indicate that human growth hormone and human prolactin This work was presented in part at the Annual Meeting of the American Federation for Clinical Research, Atlantic City, N. J., May 1970 (1).
Journal of Endocrinology, 1982
The effect of daily injections of sulpiride was compared with that of a single injection of the drug in male rats which had been treated with oestradiol diundecenoate for various periods of time. We studied the effect of the different treatments on weight of the pituitary gland, concentration of prolactin and incorporation of [3H]thymidine into DNA in the pituitary gland and on serum levels of prolactin. Administration of the oestrogen produced a marked increase in the synthesis of DNA at day 7. The stimulation diminished at day 21 and was not significant at day 45. The maximum increase in the concentration of prolactin in serum and pituitary glands was observed during the first 7 days (approximately 400 and 150% respectively) and in the weight of the anterior pituitary gland after 21 days of treatment (approximately 107%). A single injection of sulpiride markedly stimulated the release of prolactin and the synthesis of DNA at day 7. Both these effects diminished at day 21 and disappeared by day 45. Daily injections of sulpiride also produced similar changes in the release of prolactin and in the replication of DNA. The growth of the anterior pituitary gland was greater in this group than in the rats which had been treated with oestradiol diundecenoate only. After the end of treatment with oestrogen and sulpiride the pituitary weight and the concentration of prolactin in the anterior pituitary gland diminished together with levels of prolactin and oestrogen in serum. There was a good correlation between weight of the gland and serum levels of prolactin. The results further support the idea of a mechanism which controls the proliferation of lactotrophs in which the release of the hormone is accompanied by an increase in pituitary DNA synthesis.