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Biomedical subjects

I Mastrogiacomo

Publications and source records attributed to I Mastrogiacomo.

13 recordsLinked to original sources
PubMed1990

Gonadotropin decrease induced by prolonged exercise at about 55% of the VO2max in different phases of the menstrual cycle.

In order to evaluate the influence of physical exercise on the hypothalamic-pituitary-ovarian axis, we studied ten women in the early follicular phase (EFP), twelve in the late follicular phase (LEP) and nine in the luteal phase (LP). The test consisted of a 90-minute physical exercise on a motor driven treadmill at 55-60% of VO2max. Blood samples were taken before, during and after the test. Prolactin and cortisol did not increase in any phase. Estradiol showed a significant increase in LFP (from 361.5 +/- 110.6 to 472.7 +/- 138.9 pmol/L) and in LP (from 457.2 +/- 94.6 to 555.3 +/- 96.9 pmol/L) but not in EFP. Progesterone levels increased significantly only in LP (from 28.2 +/- 6.7 to 33.5 +/- 6.7 mmol/L): Luteinizing hormone (LH) levels decreased significantly in all phases: from 13.7 +/- 2.0 to 10.5 +/- 1.1 IU/L in EFP; from 14.6 +/- 2.1 to 11.5 +/- 1.9 IU/L in LFP and from 7.5 +/- 1.3 to 5.7 +/- 1.0 IU/L in LP, while follicle stimulating hormone (FSH) levels decreased only in LFP (from 8.1 +/- 0.5 to 6.7 +/- 0.6 IU/L). Our exercise protocol (prolonged, continuous and moderate) was able to cause a decrease in gonadotropins levels, and this phenomenon is not due to changes in the other tested hormones.

Adult↗
PubMed1989

Sex hormones and sex hormone binding globulin in males with compensated and decompensated cirrhosis of the liver.

The present work investigates the sex hormone profiles in 50 male patients with liver cirrhosis of different etiology according to the degree of liver dysfunction. The only hormonal impairment in well-compensated cirrhotics (group A) was an increase in mean serum concentrations of estrone, androstenedione, and sex hormone binding globulin. In decompensated cirrhotic patients with ascites (group B), low mean levels of total and free testosterone were found along with normal gonadotropins mean levels. Estrone and androstenedione levels were still elevated, whereas sex hormone binding globulin levels were not different from controls. In decompensated cirrhotics patients with encephalopathy (group C), total and free testosterone mean levels were lower than in group B, and LH mean levels were elevated; estrone levels were markedly high, but androstenedione levels were subnormal; sex hormone binding globulin concentrations were again not different from controls. The few patients with high prolactin levels belonged primarily to this group. Estradiol mean levels were not significantly elevated in any of the groups. It is concluded that the various hormonal patterns of gonadal failure and of the impairment of steroid metabolism and transport, observed in cirrhosis, can be attributed to the degree of liver dysfunction.

Adult↗
PubMed1989

Childhood's enuresis in the history of women with hyperprolactinemic amenorrhea.

Hyperprolactinemia, or elevated levels of prolactin in blood, is a normal physiologic post-partum response in lactating women. Non-lactating women with hyperprolactinemia often present during the reproductive years since they may have amenorrhea, galactorrhea, or both. Hypersecretion of prolactin is most commonly due to pituitary adenomas. Women with hyperprolactinemic amenorrhea are often quite anxious, depressed and hostile. It has been hypothesized that these psychological symptoms might antecede the onset of hyperprolactinemia and that hyperprolactinemia may be associated with early developmental problems and may be psychogenic in origin. Twenty patients with hyperprolactinemic amenorrhea and twenty-one normoprolactinemic patients with amenorrhea had an interview covering psychiatric history in order to establish whether they had ever met DSM-III criteria for functional nocturnal enuresis at one time during their childhood. While seven out of twenty (35%) patients with hyperprolactinemic amenorrhea were found to have had functional enuresis during their childhood, only two out of twenty-one (9.5%) normoprolactinemic amenorrheic women reported having had functional enuresis. The difference between the two groups was statistically significant (chi-squared: 3.88; p less than 0.05). We postulate that early stress and developmental problems may present in children as psychological distress and functional enuresis and in women as psychological symptoms (e.g., anxiety and depression) and hyperprolactinemic amenorrhea.

Adult↗
PubMed1988

Hyperprolactinemia and psychological distress in women undergoing chronic hemodialysis.

In order to investigate the possible relationship of hyperprolactinemia to psychological distress in patients undergoing chronic hemodialysis, 19 uremic women were evaluated by a semistructured interview and administered the Kellner Symptom Questionnaire. Group A (10 uremic women with hyperprolactinemia) did not differ significantly in anxiety, depression, somatization and hostility from group B (9 normoprolactinemic uremic women). Both groups rated themselves more depressed and hostile than a normal control group of 10 women, and hyperprolactinemic patients were also significantly more anxious than the normal controls.

Anxiety Disorders↗
PubMed1988

Male hypogonadism of uremic patients on hemodialysis.

Primary hypogonadism occurring among uremic men on hemodialysis has been widely investigated, yet few data are available concerning the general pattern of steroidogenesis. In 161 hemodialysis patients and in 83 healthy subjects, serum levels of gonadotropins (LH and FSH), prolactin (PRL), testosterone (T), androstenedione (A), estrone (E1), estradiol (E2), and dehydroepiandrosterone-sulphate (DHEA-S) were assessed through RIA methods. Mean +/- SD hormone levels were: LH 45.6 +/- 41.1 mIU/ml, FSH 16.3 +/- 16 mIU/ml, PRL 42.4 +/- 69.1 ng/ml, A 0.83 +/- 0.27 ng/ml, E1 64.3 +/- 31.7 pg/ml, all higher than controls; T 289 +/- 125 ng/100 ml, E2 11.8 +/- 3 pg/ml, and DHEA-S 1.4 +/- 1.4 micrograms/ml, all lower than controls. The A/T and E1/E2 ratios were also higher than controls and showed a good positive linear correlation (r = 0.40; p less than 0.001) between each other. The uremic damage acts at the testis level, impairing the activity of the enzyme 17-beta-hydroxysteroid-dehydrogenase (17-OHSD), even if a derangement of the peripheral interconversion between steroids cannot be excluded.

Adult↗
PubMedDate not supplied

Testicular function and prolactin responsiveness to TRH and cimetidine after renal transplantation.

The hypothalamic-pituitary-testicular axis and the regulation of prolactin secretion were investigated in eleven male renal transplant recipients. Mean serum levels of testosterone and estrone were normal, whereas those of androstenedione and estradiol were low. Mean basal luteinizing hormone (LH) levels were slightly elevated, but the peak responses to 50 micrograms i.v. gonadotropin-releasing hormone (GnRH) were not dissimilar from controls. Both basal and GnRH-stimulated follicle-stimulating hormone (FSH) levels were elevated (p less than 0.02-0.05) and also positively correlated with the time spent on hemodialysis (p less than 0.005-0.002). Basal prolactin (PRL) levels were normal, in all subjects. Nine out of 11 patients had a normal PRL response to Thyrotropin-releasing Hormone (TRH). However only six out of 11 had a normal response to 200 mg i.v. Cimetidine (Cim). Three subjects normally responding to TRH failed to respond to Cim. Uremic primary hypogonadism is not fully reversed by renal transplantation: a slight defect in the pituitary LH release may persist and the impairment of the tubular testicular function is left unchanged. While uremic hyperprolactinemia is corrected, the responsiveness to PRL-stimulating agents, particularly Cim, is not restored to normal, reflecting a derangement at the pituitary as well as the hypothalamic level.

Adult↗
PubMedDate not supplied

Achievement of spermatogenesis and genital tract maturation in hypogonadotropic hypogonadic subjects during long term treatment with gonadotropins or LHRH.

15 subjects with Hypogonadotropic Hypogonadism (HH) were treated with either gonadotropins (13 cases) or pulsatile subcutaneous Luteinizing Hormone Releasing Hormone (LHRH) (2 cases) for up to 42 months, to study the effects of therapy step by step. The following results were obtained: (A) In postpubertal HH (5 cases = Group A), therapy brought about onset of spermatogenesis within 3 months and its normalization within 6 months. In HH of prepubertal onset (10 cases = Group B), spermatogenesis started within 9 to 21 months and became normal in only 3 cases after at least 18 months. The best sperm counts were obtained in Group A in the third month of treatment (41.75 +/- 43.68 mil./ml) and in Group B in the 36th month (14.87 +/- 17.06 mil./ml). Sperm motility was normal in the majority of the cases in Group A from the beginning but did not become normal in Group B. (B) Seminal fructose and zinc were normal from the beginning of therapy in 66% of the cases in both groups. Zinc became normal in 100% within 3 months in Group A, in Group B within 18. Carnitine was normal in 50% of cases in both groups, contemporaneous with sperm appearance. Transferrin was normal in Group A after appearance of spermatozoa, but in Group B never became normal. (C) We hypothesize that the recovery of fertility passes through the following stages: (1) Functional recovery of Leydig cells, followed by seminal vesicles and prostate. (2) Recovery of epididymal function, which probably implies beginning of the tubular function. Recovery of Sertoli cell function occurs with more difficulty.

Adult↗
PubMedDate not supplied

[Treatment of male hypogonadotropic hypogonadism].

Males affected by hypogonadotropic hypogonadism can be treated with androgen replacement therapy, if they do not wish fertility. In order to limit or avoid androgen toxicity on the liver, it is possible to use testosterone undecanoate (which is absorbed in the gut by lymphatic system) at the dose of 160-240 mg/die or testosterone esters administered intramuscolarly at the dose of 250 mg/month. Estradiol and DHT derived from testosterone catabolism can be in excess therefore they can be provoke toxic phenomena, even if slight, such as gynecomastia or prostatic diseases. If patients wish fertility, they must be treated with gonadotropins or pulsatile LHRH. Therapeutic effects are very different depending on the different origin of the hypogonadism. In postpubertal onset hypogonadotropic hypogonadism, the response is constant and rapid; sperm count normalization can be reached within 6 months with the only hCG. Prepubertal onset hypogonadotropic hypogonadal men need hu-FSH too and longer treatment (18-24 months); sperm count normalization can be reached in less than half case. Nevertheless fertility can be reached even in oligozoospermic stage. Negative prognostic factors are: pan-hypopituitarism, cryptorchidism, how old are the patients at the beginning of the treatment and small testis volume. It is not yet clear if pulsatile LHRH therapy is profitable in terms of therapeutic results.

Gonadotropins↗
PubMedDate not supplied

[Pulsatile treatment with gonadotropin-releasing hormone (GnRH)].

The different ways of administration condition the frequency of the pulsatile GnRH, because of the different rate of depot. High frequencies (60-90/min) can be reached only with the intravenous route which is suitable for ovulation induction: ovulation is reached in 73-92% of women affected by hypothalamic amenorrhoea and in 41-51% of women affected by polycystic ovarian syndrome (previously suppressed with buserelin); overstimulation risk is lesser than during therapy with gonadotropins. Subcutaneous route is suitable for puberty induction which needs long-term treatment (18-24 months); the results are generally good, except in hypopituitaric patients. Intranasally route needs frequencies greater than 150-180 min: low frequencies administration (3 times/day) is sufficient to treat cryptorchidism and to reach good results (30-70%); moreover intranasally route can be useful to maintain the results reached with long term therapy with LHRH or gonadotropins.

Gonadotropin-Releasing Hormone↗