Dissociated responses of plasma testosterone and estradiol to human chorionic gonadotropin in adult men.

Plasma testosterone (T), dihydrotestosterone (DHT) and estradiol (E2) were determined by radioimmunoassay in 10 normal males receiving hCG im 5000 IU on days 1, 2 and 3. The mean increase of plasma steroid on days 2, 3 and 1, respectively, was: 1.42, 1.79 and 1.87 times for T; 1.17, 1.56 and 1.49 times for DHT; 4.04, 3.29 and 2.33 times for E2. While T was still significantly increasing from day 2 to day 4, E2 significantly decreased. A positive correlation (P less than 0.01) was found between the basal T and the E2 peak after hCG, suggesting a release of E2 from a storage compartment in the testis. No significant change of either steroid was detected 4 h after the first hCG injection. In 6 cases of primary male hypogonadism, the mean basal values of T to hCG was defective, despite considerable individual variations. In 14 males with gonadotropin deficiency, basal values of T and E2 were very low; the T response to hCG ranged from undetectable to dramatic, and was correlated with the degree and duration of previous exposure to gonadotropin; and impaired response of E2 in all cases porvides a better estimate of the actual gonadotropin deficiency.

Hormonal changes induced by bromocriptine (CB-154) at the early stage of treatment.

Fifteen female patients with amenorrhea and hyperprolactinemia were studied 1 to 3 times daily during the first 4 days of treatment with bromocriptine (2.5 mg b.i.d). Normal PRL levels were reached within one day in 12 while the mean value for the whole group showed no further significant decrease. Estradiol, LH and FSH levels did not vary significantly at this stage even in those 10 patients who subsequently resumed menstruation.

Reversible gonadotropin deficiency in male Cushing's disease.

Twelve adult males with documented active Cushing's disease were studied. Mean plasma testosterone (T) was significantly decreased: 1.8 +/- 0.3 (SEM) ng/ml (N=6.8 +/- 0.5); gonadotropin measurements in 8 patients, in basal conditions and under LH-RH iv, showed a significant decrease in both FSH and LH. A further study of 11 patients in remission of Cushing's disease indicated a significant increase in plasma T and gonadotropins up to the normal range. One patient with an initial low T value had a normalized T while in remission, then a dramatic decrease when the disease relapsed. We conclude: a hypogonadotropic hypogonadism is found in male Cushing's disease; it disappears as early as hypercortisolism is suppressed. Some possible mechanisms are discussed.

Urogenital manifestations of Wegener granulomatosis.

We report 8 patients with Wegener granulomatosis (WG) who suffered from symptomatic urogenital involvement including acute urinary retention related to prostatitis, orchitis, ureteral stenosis, bladder pseudotumor, and penile ulceration. Urogenital manifestations occurred as an isolated manifestation of WG in 4 patients, at the onset of the disease in 1 patient, and as the only symptom of relapse in 3. Data used to distinguish specific WG involvement from infection or cyclophosphamide urothelial toxicity are discussed. Four patients needed a surgical procedure consisting of suprapubic cystostomy for acute urinary retention, bilateral ureteral double J stents for bilateral ureteral stenosis, and prostate transurethral resection. Urogenital symptoms promptly resolved with medical therapy. High-dose corticosteroids and immunosuppressive drugs should be used as first-line therapy to avoid unnecessary surgery.

Monthly intravenous pulse cyclophosphamide therapy in Wegener's granulomatosis.

OBJECTIVE: To study the long term effects of monthly intravenous cyclophosphamide therapy in Wegener's granulomatosis. METHODS: Fourteen consecutive patients with active Wegener's granulomatos treated with a first-line combination of high-dose prednisone and monthly intravenous pulse cyclophosphamide were retrospectively studied. RESULTS: One patient died from septicemia complicating severe leukopenia after the first pulse. At 8 months after instituting intravenous pulse cyclophosphamide therapy, failure was observed in 6 other patients. Between month 16 and 18, 2 other patients relapsed when the time between 2 pulses was lengthened. Five patients developed cyclophosphamide-related side-effects: infection (n = 2), amenorrhea (n = 1), alopecia (n = 2) and vomiting (n = 2). Except for one fatal infection, no major side-effect of intravenous cyclophosphamide therapy was observed. At the end of the study, all patients were off intravenous cyclophosphamide therapy with more than 6 months of followup. The 6 responders were in remission on low-dose prednisone or without treatment. CONCLUSION: A combination of high-dose prednisone and intravenous cyclophosphamide may achieve long-term remission in 42% of patients with Wegener's granulomatosis. Responders to intravenous cyclophosphamide therapy had less extensive disease than non-responders.

[Influence of gonadotropins on inhibin secretion]. / Influence des gonadotrophines sur la sécrétion d'inhibine.

Inhibin is produced by Sertoli cells in the male and by granulosa cells in the female. Follicular-stimulating hormone acts directly to stimulate production whereas luteinizing hormone exerts an indirect effect by stimulating production of androgens which themselves activate synthesis and release of inhibin. Prolactin has no effect on inhibin. These interpretations, derived from numerous in vivo and in vitro studies, explain why inhibin is not secreted in the hypophysectomized animal. Interruption of spermatogenesis by ligature of deferens canals, by experimental cryptorchidism in the rat, and in human primary azoospermias, provokes a reduction in production of inhibin and an increased secretion of FSH. The second must be the consequence of the first. Restoration of normal spermatogenesis results in normal production of inhibin. Biochemical mechanisms linking spermatogenesis and inhibin production are still unknown.

[Endocrine, paracrine and autocrine mechanisms involved in follicular development]. / Mécanismes endocriniens, paracrines et autocrines du développement folliculaire.

Development of a single follicle during the menstrual cycle is under control of hormones stimulating follicular maturation, ovulation and luteogenesis. Several factors intervene locally to avoid other follicles developing at the same time as the dominant follicle. These other follicles remain quiescent or go on to atresia. Atresia results from the action of several endocrine, paracrine and autocrine mechanisms which synergistically inhibit aromatase activity. The subsequent lack of oestrogens reduces granulosa cell multiplication. The oocyte will not become fertilizable before the preovulatory peak of LH, after the resumption of meiosis and after reaching the metaphase of the second meiotic division. Several factors are involved in this inhibition of spontaneous resumption of meiosis: cyclic nucleotides, sex steroids, somatostatin, oocyte maturation inhibitor(s) (OMI). Ovulation is related to breakdown of connective tissue synthesized by granulosa cells under the influence of FSH. Connective tissue lysis is dependent on proteolytic enzymes which are released and activated by FSH, LH and relaxin. A paracrine control could be involved in ovulation: LH induces the production of prostaglandin and relaxin by theca cells which, in turn, stimulate collagenase and proteoglycanase secretion by granulosa cells.

[Antiandrogenic effect of spirolactones: different mechanisms of action (author's transl)]. / Effets anti-androgéniques des spirolactones: différents modes d'action

The spirolactones decrease the plasma testosterone levels in men. They also inhibit the specific dihydrotestosterone binding to rat prostate, and have no effect on 5 alpha-reductase. The spirolactones are antiandrogenic drugs, acting at several levels.

[Action of luteinizing hormone-releasing hormone (LH-RH) on gonadotropin secretion in normal subjects]. / Action de l'hormone hypothalamique libérant l'hormone lutéinisante (LH-RH) sur les gonadotrophines chez le sujet normal

PIP: Gonadotropin release after synthetic LH-RH injection was studied under a variety of experimental conditions. In male subjects, LH-RH (25 mcg) induces release of LH and FSH before and during puberty, but only of LH in adults. Larger doses of LH-RH do induce FSH release, with LH release proportional to LH-RH dose; FSH release is smaller than LH release and follows it. In prepuberal females, LH-RH induces a large release of FSH and a weak release of LH. In puberty, LH response becomes greater than FSH. In eugonadal women, FSH and LH responses are more marked during luteal phase than during preovulatory phase. Nonsequential hormonal contraceptives inhibit FSH and LH response to 50 mcg of LH-RH, but not to 100 mcg. In postmenopausal women, LH increases after 25 mcg of LH-RH; 200 mcg ethinyl estradiol for 5 days permits an increase of both gonadotropins. These results suggest that gonadotropin response to LH-RH depends on endocrine equilibrium and gonadal steroids which may modify the synthesis and/or release of pituitary gonadotropins. On the basis of selective LH response to small doses of LH-RH, ti is speculated that an FSH releasing factor may exist.^ieng

[Indications and results of pituitary radiotherapy after microsurgery in acromegaly. 15 cases]. / Indications et résultats de la radiothérapie hypophysaire après microchirurgie dans l'acromégalie. Quinze cas.

The present treatment of acromegaly consists of selective adenomectomy followed, when unsuccessful, by pituitary gland irradiation. Fifteen acromegalic patients were evaluated after adenomectomy, then radiotherapy. Growth hormone assays were performed after carbohydrate load and administration of thyroid stimulating hormone. Somatomedins were measured by radiocompetition using the vector protein. Cure was obtained with adenomectomy alone in 3 of the 15 patients (mean follow-up 39 months). The remaining 12 patients were all cured by subsequent irradiation at the cost of pituitary insufficiency in one-third of them. Post-surgical cure of acromegaly can only be asserted from range of strict criteria. The best indicators of persisting activity are high levels of growth hormone and/or somatomedins. A solitary somatotropic dysregulation does not necessarily herald a relapse.

[Evaluation of the hypothalamo-hypopituitary axis after long-term inhalation corticotherapy for nasal polyposis]. / Evaluation de l'axe hypothalamo-hypophysaire après corticothérapie inhalée de longue durée pour polypose naso-sinusienne.

OBJECTIVE: To assess the hypothalamic-pituitary-adrenal (HPA) axis after long-term intranasal corticosteroid treatment in nasal polyposis. PATIENTS AND METHODS: A short synacthen test was performed in 24 patients who received the highest dose of inhaled beclomethasone among a population of 392 patients treated for nasal polyposis with inhaled corticosteroid therapy and short-term oral corticosteroids. RESULTS: Mean yearly dose of oral prednisone administered in short-term treatment was 371 mg/year. The amount of short-term oral prednisone decreased during the treatment. Mean daily dose of inhaled beclomethasone was 2861 micrograms/day, decreasing during treatment. Morning plasma cortisol was normal in all patients before and after stimulation (163 +/- 44 and 1 +/- 60 micrograms/ml respectively). Nolomethasone dose and plasma cortisol level before or after stimulation. DISCUSSION: The high dose of inhaled beclomethasone used to treat nasal polyposis does not affect the HPA axis. Some authors in the literature contest the validity of short synacthen test to detect HPA axis suppression. This test does however detect severe impairments of the HPA axis in outpatients.