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Biomedical subjects

P Falaschi

Publications and source records attributed to P Falaschi.

49 records · Page 3Linked to original sources
PubMed1980

Prolactin release in polycystic ovary.

Ten normoprolactinemic and 10 hyperprolactinemic patients, all with polycystic ovary syndrome (PCO), were subjected to prolactin (PRL) stimulatory tests with thyrotropin-releasing hormone (TRH), 200 microgram intravenously, and haloperidol (a dopamine-blocking agent), 1 mg intramuscularly. The results were compared with those of 8 women with idiopathic hyperprolactinemia and 10 normal female volunteers. Distinctive features of PCO were elevated plasma concentrations of luteinizing hormone, estrone, and testosterone in the presence of normal estradiol, whereas in idiopathic hyperprolactinemia estradiol was reduced. Both groups of patients with PCO exhibited responses to TRH and haloperidol significantly higher than the controls (P less than .001), whereas only the hyperprolactinemic PCO patients reacted with an excessive PRL discharge (P less than .001). As expected, the response to both secretagogue agents was blunted in patients with idiopathic hyperprolactinemia. The present report discusses the possible implication of estrogen and the dopaminergic system in the mechanisms leading to hyperprolactinemia and enhanced PRL release in PCO.

Estrogens↗
PubMed1978

Influence of hyperprolactinaemia due to metoclopramide on gonadal function in men.

Five clinically normal male volunteers were given metoclopramide, 10 mg t.d.s. for 6 weeks. During treatment prolactin concentrations were elevated (over 50 ng/ml) in all. LH, FSH, testosterone and cortisol concentrations were not altered. No change was observed in LH or FSH responses to LHRH testing 4 weeks after the beginning of therapy, compared with pre-treatment values. A reduction in seminal volume and total sperm count were observed in each subject. Four noticed a decrease in libido and three lost spontaneous erections. While the metoclopramide-induced hyperprolactinaemia could be the cause of the observed changes in semen and erectile activity, it is possible that this dopamine receptor blocking drug might directly affect central or peripheral mechanism of erection, the testes or accessory organs.

Adult↗
PubMedDate not supplied

Immunohistochemical localization of beta-endorphin in hyperplastic interstitial tissue of the human testis.

The immunohistochemical localization of beta-endorphin in the normal testis (two patients) and in the pathologic testis (two cases of Sertoli Cell Only Syndrome, two cases of Klinefelter Syndrome, two cases of post-orchitis tubular sclero-hialinosis) was investigated. No beta-endorphin immunostaining was detected in the normal testis, while positive beta-endorphin immunostaining has been observed in pathologic tissues. These results indicate that, as in animals, beta-endorphin is present in human Leydig cells and may play a local role in regulating male reproductive function.

Humans↗
PubMedDate not supplied

Neuroendocrinoimmunology.

Interest in neuroendocrinoimmunology has increased greatly in the last decade. The most important evidence of neuroendocrine-immune system interactions is that spleen, thymus, bone marrow and lymph nodes are innervated by neurons of the autonomic nervous system; changes in brain functions can affect different immune responses; immune and neuroendocrine cells share receptors (e.g., lymphocytes and macrophages have receptors for a vast number of hormones and neuropeptides); hormones and neuropeptides can alter the functional activity of immune system cells; several hormones and neuropeptides can be synthesized by leukocytes; cytokines produced by leukocytes are able to modulate neuroendocrine system activity, behaviour, sleep and thermoregulation. The recent literature on neuroendocrinoimmunology has laid the physiopathological groundwork for a new clinical approach which perceives and treats the patient as a psychic and somatic whole.

Autonomic Nervous System↗
PubMedDate not supplied

Hormonal and metabolic effects of transdermal estradiol/progestagen administration in postmenopausal women.

OBJECTIVE: To evaluate the effects on hormonal and metabolic variables and bone density of a transdermal system delivering estrogen and progestagen. DESIGN: Twenty-one patients were included in the study and randomly assigned to the following treatments: group A was treated with transdermal 17 beta-estradiol, 50 micrograms/day (Estraderm TTS 50), from the first to the fourteenth day of the cycle and with a transdermal combination of 17 beta-estradiol (50 micrograms/day) and norethisterone acetate (NETA) 250 micrograms/day during the following 14 days; group B was treated with Estraderm TTS 50 from the first to the twenty-eighth day, adding oral medroxyprogesterone acetate (MPA), 10 mg/day, during the final 14 days. DHEAS, testosterone, SHBG, prolactin, gonadotropins, and estrogens were measured in basal conditions and after 6 months' therapy. In the same schedule, lipid patterns (total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides), phosphocalcium variables (osteocalcin, calcitonin, parathormone), and bone mineral density were also studied. RESULTS: Both treatments were efficient in reducing menopausal symptoms. An increase of DHEAS (P < .05) and a decrease of FSH and LH (P < .02, < .01, respectively) were observed in group B. No significant modifications in lipid and lipoprotein metabolism were shown in either group after 6 months. The calcium-regulating hormone osteocalcin (BCG) decreased significantly (P < .05) only in group A; calcitonin, parathormone, and bone density were unchanged after treatment. CONCLUSION: Transdermal administration of estrogen plus progestagen reduces menopausal symptoms, but does not induce changes in metabolic variables and hormonal levels (androgens and prolactin).

Absorptiometry, Photon↗