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Biomedical subjects

H G Bohnet

Publications and source records attributed to H G Bohnet.

At least 55 records · Page 3Linked to original sources
PubMed1981

Changes of prolactin secretion following long-term danazol application.

Patients (n = 10) with endometriosis or fibrocystic mammary disease were treated with an oral dose of 4 x 200 mg danazol for 6 months. Prolactin and gonadotropin secretion was evaluated before, and in some of them during 1, 3, and 6 months of therapy, as well as 4 weeks after discontinuation of the steroid. Prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol, and progesterone were measured before a bolus of 10 mg metoclopramide and 25 micrograms LH-releasing hormone (LH-RH) had been given. The serum concentrations of prolactin and LH were estimated 25 minutes and those of FSH 45 minutes thereafter. Basal and stimulated serum prolactin levels, measured during the luteal phase of the control cycle preceding danazol application, decreased continuously, reaching serum concentrations seen during the early follicular phase of the cycle. This was paralleled by a decrease of estradiol and a lack of progesterone secretion. While basal and LH-RH-stimulated LH was practically unchanged, basal and stimulated FSH showed a significant increase. Within 4 weeks of discontinuation of the drug all hormonal parameters were similar to pretreatment values. The data presented may explain the beneficial effect of the drug on fibrocystic mammary disease, i.e., by the decrease of serum and pituitary prolactin. The selective increase of FSH secretion is unclear but may reflect the lack of negative feedback mechanisms of follicular inhibin.

Danazol↗
PubMed1981

Intermittent stimulation with LH-RH in postmenopausal hypergonadotropism.

Ten postmenopausal women received 8 consecutive (1 hour interval) i.v. bolus injections of either 25 or 500 micrograms of LH-RH. Gonadotropin release was monitored before and during LH-RH stimulation. After the first LH-RH bolus a dose-dependent LH release was seen. All consecutive LH-RH boli elicited similar LH responses resulting in pulse-type LH release. Throughout the whole stimulation period the pituitary gland remained highly responsive to LH-RH, FSH release was uncharacteristic. It is concluded that during postmenopause LH-RH is hyper-secreted. Thus the pituitary gland remains responsive to repeated injections of even supraphysiological LH-RH doses.

Estrogens, Conjugated (USP)↗
PubMed1980

[Luteal insufficiency as a prolactin-related disorder of the menstrual cycle].

Infertile women exhibiting a short luteal phase in 3 consecutive menstrual cycles as judged from basal body temperature recordings underwent a prolactin (PRL) stimulation test with metoclopramide (MTCL) on day 22 of the 4th cycle. While serum progesterone (P) concentrations were decreased (less than 35 nmol/l), PRL was increased only in about two thirds of the women. When compared to normally ovulating women, 3 groups could be segregated: in group I basal (less 500 mU/l) as well as MTCL stimulated PRL (less 8000 mU/l) was normal; in group II-patients only basal PRL levels were elevated; in group III baseline levels of serum PRL were at the borderline, but PRL release after MTCL stimulation was exaggerated. Correlation of sleep induced PRL peaks, observed during the night preceding the MTCL test, with maximal MTCL stimulated PRL showed a positive relation (r = 0.7, p less than 0.05) in group I- and III-patients as well as in normal volunteers. Suppression of PRL release by bromocriptin (2.5 mg bid) from the day following the MTCL test resulted in significantly reduced basal as well stimulated serum PRL on day 22 of the treatment cycle. Luteal P secretion was normalized in group II- and III-patients only. The data presented indicate that some of the patients with luteal phase defects react to various stimuli with an exaggerated PRL release, while others exhibit permanently increased serum PRL levels. Inappropriate luteal P secretions is not only caused by PRL elevations, but also by other pathophysiological mechanisms. This is underlined by the fact that bromocriptin treatment resulted in normalization of luteal P output only, when PRL was elevated.

Amenorrhea↗
PubMed1980

[Diagnosis and therapy of amenorrhea (author's transl)].

The most simple testing of the hypothalamus-hypophysis unit can be carried out with ovulation releasers such as antiestrogens; these simultaneously provide a therapeutical effect. In case of failure, dynamic functional tests are to be carried out two weeks after the attempted ovulation release in order to determine the hypophyseal reserves in gonadotropin (LH-RH) and prolactin. This point in time corresponds to the expected luteinic phase. Lack of estrogens, hyperprolactinemia and disorders of the gonadotropic partial functions can be assessed simultaneously with this method. Gestagen-testing can then evaluate estrogen activity in the specific organ and exclude organic disorders. At present, we have nearly reached the point of enacting a causal therapy for functional sterility.

Adult↗
PubMed1980

Determination and properties of proteohormone receptors in malignant gynecological tumors with special reference to lactogen receptors in human breast cancer.

Proteohormone receptors have been demonstrated in gynecological malignancies, but more sensitive methods for measurement of such receptors are required and should be a matter of intensive research. The clinical response of hormone-dependent tumors to endocrine therapy has not yet been correlated with the occurrence of proteo-hormone receptors in neoplastic tissue from gynecological patients and such studies are required.

Breast Neoplasms↗
PubMed1980

Epimestrol in treatment of inadequate luteal progesterone secretion.

Seventeen infertile normoprolactinemic women with luteal phase defects were treated with epimestrol. In ten patients, normalization of the impaired luteal phase was achieved. Under epimestrol treatment, periovulatory estradiol concentrations (1077.3 +/- 121.5 pmoles/liter versus 612.7 +/- 64.2 pmoles/liter; mean +/- SEM; P < 0.01) and cervical scores (10.8 +/- 0.3 versus 7.9 +/- 0.38; mean +/- SEM; P < 0.01) were improved, and luteal progesterone (60.0 +/- 9.1 nmoles/liter versus 19.98 +/- 3.14 nmoles/liter; mean +/- SEM; P < 0.001) and estradiol secretioon (813.1 +/- 101.1 pmoles/liter versus 581.9 +/- 73.7 pmoles/liter; mean +/- SEM; P < 0.05) were significantly increased in those women with normalization of the luteal phase as compared with the seven patients in whom epimesterol was without effect. Prolactin levels were elevated in all patients after epimestrol therapy (P < 0.05). Basal LH levels and LH-RH stimulated levels improved following administration of epimestrol (P < 0.01) in the 10 women with normal luteal phases. FSH levels were not significantly affected. Two patients became pregnant. No side effects were noted.

Adult↗
PubMed1980

[Epimestrol in the treatment of normoprolactinemic corpus-lutem deficiency (author's transl)].

The treatment of normoprolactinemic corpus-luteum deficiency with epimestrol is reported. This is a frequent cause of infertility. The clinical and hormonal parameters for the diagnosis and follow-up evaluation of the treatment are described. In the present series 10 of 17 patients with primary infertility and normoprolactinemic corpus-luteum deficiency showed a normalization of the luteal phase. Two pregnancies occured following one cycle of treatment with epimestrol at 5 mg. daily from day 3 to day 12 of the cycle. Epimestrol shows no anti-estrogenic properties in contra-distinction to other ovulation stimulating drugs. The quality of the cervical secretion is therefore not impaired by epimestrol. Side effects or ovarian cysts were not observed.

Adult↗
PubMed1980

LH-RH therapy in functional amenorrhea based on clinical subclassification.

The diagnostic approach to functional amenorrhea comprising a gestagen test, an LH-RH test, and the response to clomiphene as well as the recording of endogenous LH episodes allows a subclassification of the patients with regard to different therapeutic approaches. According to the degree of endogenous LH-RH deficiency, which is reflected by this diagnostic workup, a therapy with clomiphene alone, LH-RH combined with clomiphene, or LH-RH alone is effective. To avoid paradoxical effects any LH-RH substitution has to meet physiological conditions. Thus pulsatile and low-dose LH-RH administration of varied duration proved able to prime the hypothalamo-pituitary unit for either clomiphene or gonadal feedback signals resulting in ovulation and corpus luteum formation.

Amenorrhea↗
PubMed1980

Gonadotropin release after administration of LH-RH during early follicular phase.

On day 7 of the menstrual cycle 15 ovulatory women received 8 bolus injections of 25 microgram, 100 microgram, or 500 microgram of LH-RH at hourly intervals. With increasing LH-RH doses total LH release increased significantly (P less than 0.05) whereas total FSH release did not differ among the groups. A biphasic release pattern independent of the LH-RH dose administered was obtained for both. After the first three LH-RH injections a stepwise augmentation of gonadotropin release followed by a rapid decline of LH and a more moderate decrease of FSH release were observed. The increase of pituitary sensitivity after repeated LH-RH stimulation may be explained by a self potentiating effect of LH-RH on its own secretion. The decrease in pituitary sensitivity observed with continuing LH-RH stimulation may be due to a refractory effect on the pituitary receptors.

Estradiol↗
PubMed1979

[Gonadoblastoma and overgrowing dysgerminoma in Turner mosaicism [45, XO/46, Xi (Xq)] (author's transl)].

It is well established that the Y-chromosome is associated with germ cell tumor development. There is a considerable tumour risk in XY- and XY/XO-gonadal dysgenesis. In the absence of Y-chromosome germ cell tumours are extremely rare. The history of a patient with 45 XO/46 Xi (Xq)-karyotype is presented, who had a gonadoblastoma with overgrowing dysgerminoma. According to basal body temperature recordings, this patient ovulated up to the age of 22 years. After this cyclical ovarian function was exhausted; histologically no primordial follicles could be detected. Gonadotropin as well as prolactin binding sites in the tumours could not be demonstrated, suggesting hormone independency and complete malignant transformation of the tumor. In general the clinician should be aware of a possible germ cell tumour development in the absence of a Y-chromosome. However as far as the clinical management of patients with dysgenetic gonads is concerned, prophylactic gonadectomy is only indicated in the presence of a Y-chromosome.

Adult↗
PubMed1979

Suppression of prolactin secretion by lisuride throughout the menstrual cycle and in hyperprolactinaemic menstrual disorders.

Normally menstruating volunteers as well as patients with hyperprolactinaemic menstrual disorders were treated with lisuride hydrogen maleate (200 micrograms b.i.d.), an ergoline derivative with dopaminergic properties. Within 3 h after an oral dose of 200 micrograms lisuride, PRL levels decreased significantly in all subjects to a plateau which lasted up to 3 h. Thereafter a gradual increase of serum PRL was noted. In the normally menstruating volunteers lisuride treatment did not result in any significant change of gonadotrophin or of sex steroid secretion, while both, basal as well as metoclopramide (MTCL) stimulated PRL release were significantly diminished. The inhibition of PRL secretion in patients with short luteal phases resulted in an increase of luteal progesterone output. In both treated groups ovulation occurred 1 to 5 days earlier in cycles on lisuride than in control cycles. LF-RH/MTCL tests performed in the patient bearing a pituitary prolactinoma before and after lisuride treatment revealed a continuous increase of pituitary LH pools, while PRL secretion decreased under lisuride therapy. Subsequently ovulation and menstruation occurred. The data presented demonstrate that lisuride is a potent inhibitor of PRL secretion and has proven its clinical usefulness for treatment of hyperprolactinaemic menstrual disorders. Application of lisuride resulted in an increase of luteal progesterone secretion in previously demonstrated corpus luteum insufficiency as well as in restoration of normal cyclical feedback mechanisms in tumorous hyperprolactinaemic anovulation. The MTCL-PRL stimulation test is suitable to monitor PRL suppression during lisuride treatment, while LH-RH testing reveals the effectiveness of lisuride by demonstrating an increase of pituitary gonadotrophin pools.

Adenoma↗