menotropins and Hypopituitarism

Most women with panhypopituitarism will undergo successful ovulation induction with gonadotropin therapy. Few proven treatment options exist for those who respond poorly to such therapy. A poor response may indicate diminished ovarian reserve, or reflect a deficiency of other key components for ovarian function.. A 31-year-old female with panhypopituitarism and a poor response to gonadotropin therapy took growth hormone (GH) replacement for 4 months prior to restarting gonadotropins. When the serum level of insulin-like growth factor-I normalized, she began ovulation induction with gonadotropins with transdermal estradiol. After 63 days of gonadotropin therapy, she had a leading follicle of 18 mm, followed by follicles of 16.5 mm and 15.5 mm. The serum estradiol was 796 pg/ml, and human chorionic gonadotropin was administered. The patient conceived with timed intercourse. A prior attempt at ovulation induction with gonadotropins alone failed to produce follicular development.. Prolonged gonadotropin treatment may be necessary to achieve ovulation and avoid the misdiagnosis of ovarian failure. Co-treatment with GH and estrogen may improve the follicular response in a poor responder with panhypopituitarism.

Topics: Adult; Estradiol; Female; Follicle Stimulating Hormone; Human Growth Hormone; Humans; Hypopituitarism; Insulin-Like Growth Factor I; Live Birth; Menotropins; Ovarian Follicle; Ovulation Induction; Pregnancy; Ultrasonography

A case of Sheehan's syndrome presented with secondary amenorrhea and was put on L-thyroxine, prednisolone and cyclical estrogen and progestin. Ovulation induction with gonadotrophins and intrauterine insemination with husband's semen resulted in a twin pregnancy. Antepartum course was complicated by bronchial asthma, gestational diabetes and pregnancy-induced hypertension. Cesarian section was done at 34 weeks gestation for preterm rupture of membranes and breech presentation. Both babies and their mother were doing well at 6 months of follow-up.

Topics: Adult; Amenorrhea; Asthma; Breech Presentation; Cesarean Section; Diabetes, Gestational; Female; Fertility Agents, Female; Fetal Membranes, Premature Rupture; Humans; Hypertension; Hypopituitarism; Menotropins; Ovulation Induction; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Twins

There are many methods that can be used to induce ovulation when there is a fault in ovulation in patients who have normal prolactin levels. These are: Bringing the weight to a normal level. Giving Clomiphene. Giving Tamoxifen. Giving cyclofenil and bromocriptine, which really have no more effect than giving a placebo. Giving gonadotrophins in a classical way. This is very useful where there is hypogonadic amenorrhoea but much less useful when the failure of ovulation occurs with normal gonadic function. It is accompanied by a risk of multiple pregnancies and of hyperstimulation, which should be monitored by ultrasound very strictly so that it cannot become too serious. The use of purified FSH which theoretically should be more adequate, at least in cases where the gonadic function is normal in spite of failure of ovulation. Pulsatile administration of LHRH, which in cases of hypothalamic amenorrhoea carries less total risk than giving gonadotrophins. Finally, wedge resection of the ovaries which is reversed for polycystic ovaries that are larger than normal in size, and allied methods. The first choice for hypogonadic hypothalamic amenorrhoea would seem to be the LHRH pump; and for failure of ovulation with normal gonadic function Clomiphene or Tamoxifen. When anti-oestrogens fail to correct these latter cases one can choose according to the case between gonadotrophins, choosing if possible pure FSH, and/or wedge resection. In the last resort in these cases the LHRH pump can be used. The frequent failure of these methods show that perhaps it is possible to create a hypogonadotrophic hypogonadism by giving agonists for a long time or antagonists to LHRH in such a way that a second attempt can be made to induce ovulation using gonadotrophins in better conditions of efficacy and safety.

Topics: Amenorrhea; Anovulation; Clomiphene; Cyclofenil; Epimestrol; Female; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Humans; Hypogonadism; Hypopituitarism; Hypothalamic Diseases; Menotropins; Obesity; Ovary; Ovulation Induction; Tamoxifen; Thinness

Do patients with congenital combined pituitary hormone deficiency (CCPHD) have different responses to gonadotrophin-induced spermatogenesis compared with those with idiopathic hypogonadotropic hypogonadism (IHH)?. CCPHD patients have a better response to gonadotrophin therapy than IHH patients.. Gonadotrophins are effective in inducing spermatogenesis in patients with hypogonadotropic hypogonadism.. This retrospective cohort study included 75 patients, 53 of whom had IHH and 22 CCPHD. They were diagnosed, treated and followed up between January 2008 and December 2013.. Combined gonadotrophin therapy, consisting of human chorionic gonadotrophin and human menopausal gonadotrophin, was administered for 24 months. The success rate of spermatogenesis (≥1 sperm in ejaculate), serum total testosterone level, testicle size and sperm concentration during the treatment, as well as the first time sperm were detected in the ejaculate, were compared between the two diagnostic groups. All patients were treated in Peking Union Medical College Hospital.. Spermatogenesis was successfully induced in 85% of IHH patients and 100% of CCPHD patients after 24-month combined gonadotrophin treatment (P = 0.03). In comparison with IHH, CCPHD patients had larger mean testicle sizes during the gonadotrophin treatment at 6, 12, 18 and 24 months (all P < 0.05). The initial time for sperm appearance in IHH group (n = 45) and CCPHD group (n = 22) was 13.2 ± 5.9 versus 10.4 ± 3.8 months (P = 0.045). Generally, CCPHD patients had higher sperm counts [median (quartiles)] than IHH patients during the treatment, but the difference was only statistically significant at 12 months of treatment, 3.3 (1.8, 12.0) versus 1.0 (0.0, 4.6) million/ml, P = 0.001. There was a higher level of serum total testosterone [mean (SD)] in the CCPHD group than the IHH group (676 ± 245 versus 555 ± 209 ng/dl, P = 0.035).. First, the inherent nature of a retrospective designed study was a main shortcoming. Secondly, pathological gene mutations in IHH and CCPHD patients should be further investigated. Clarification of the underlying mechanisms between cryptorchidism and mutated genes may provide more information for the divergent therapeutic responses between two groups. Only a minority of patients were actively seeking to have children so information about fertility is limited.. CCPHD patients had a lower incidence of cryptorchidism and a better response to gonadotrophin therapy than IHH patients, reflecting multiple defects on the different levels of reproduction axis in IHH. Furthermore, growth hormone is not indispensable for spermatogenesis in CCPHD patients.. The study was supported by Natural Science Foundation of China (No: 81100416). None of the authors has any conflicts of interest to declare.

Topics: Adolescent; Adult; Cell Count; Chorionic Gonadotropin; Cryptorchidism; Follow-Up Studies; Humans; Hypogonadism; Hypopituitarism; Male; Menotropins; Outcome Assessment, Health Care; Reproductive Control Agents; Retrospective Studies; Sperm Count; Spermatogenesis; Testis; Testosterone; Young Adult

Topics: Anovulation; Body Mass Index; Exercise; Feeding and Eating Disorders; Female; Gonadotropin-Releasing Hormone; Gonadotropins; Humans; Hypogonadism; Hypopituitarism; Hypothalamic Diseases; Infertility, Female; Menotropins; Ovulation Induction; Polycystic Ovary Syndrome; World Health Organization

To report a successful pregnancy in a woman with panhypopituitarism who received 3 months of pretreatment with growth hormone (GH) before ovulation induction. Prior attempts at ovulation induction had failed for this patient.. Case report.. Department of Endocrinology.. A 32-year-old woman with panhypopituitarism and secondary infertility.. GH (1 IU/day) alone for 3 months; during the next cycle, 1 IU/day of GH; 3 ampules of hMG per day during days 1-21; 1 ampule of hCG on day 21. GH was discontinued on day 35 when a pregnancy test was positive.. Pregnancy and delivery.. Pregnancy and birth of a normal child after a single ovulation stimulation using GH and gonadotropins.. This case report suggests interest in a new protocol for follicular stimulation in women with hypopituitarism who are responding poorly to gonadotropin therapy.

Topics: Adult; Chorionic Gonadotropin; Drug Therapy, Combination; Female; Human Growth Hormone; Humans; Hypopituitarism; Infant, Newborn; Infertility, Female; Labor, Obstetric; Male; Menotropins; Pregnancy

A 17-year-old male diagnosed as having Cat Eye Syndrome (CES) with hypogonadotropic hypogonadism showed short stature and no development of secondary sex characteristics. Exogeneous gonadotropin replacement therapy combining human chorionic gonadotropin (hCG) and human menopausal gonadotropin (hMG) was started. As a result, the short stature and androgen deficiency were relieved. The critical region of CES was tetrasomy of 22 pter-->q11. Abnormalities of other chromosomes which cause hypogonadotropic hypogonadism may exist, thus further investigation is needed.

Topics: Abnormalities, Multiple; Adolescent; Anus, Imperforate; Chorionic Gonadotropin; Chromosomes, Human, Pair 22; Dwarfism, Pituitary; Humans; Hypogonadism; Hypopituitarism; Male; Menotropins; Pituitary Hormones; Puberty, Delayed; Syndrome; Testosterone; Trisomy

Several authors have suggested that growth hormone may augment ovarian responses to follicle stimulating hormone in women (Homburg et al., Clin. Endocrinol., 29, 1988; Ibrahim et al., Fertil. Steril., 55, 1991), and that this effect may be mediated by insulin-like growth factor I (IGF-I) (Davoren and Hsueh, Endocrinology, 118, 1986). Menashe et al. (Hum. Reprod., 6, 1991) reported spontaneous pregnancies in women with a deficiency in growth hormone receptors and, consequently, low serum concentrations of IGF-I. In this report, we present the case of a patient with a rare syndrome first described by Oliver and Mcfarlane (Arch. Ophthalmol., 74, 1965). The patient was shown to be growth hormone deficient, with hypopituitarism as part of the syndrome. Adjuvant growth hormone did not influence her ovarian responses to exogenous gonadotrophins during assisted conception treatment, as reflected by the required total number of ampoules of human menopausal gonadotrophin, the number of developing follicles, the rate of follicular growth and the serum oestradiol concentrations.

Topics: Adult; Chorionic Gonadotropin; Embryo Transfer; Estradiol; Female; Fertilization in Vitro; Growth Hormone; Humans; Hypopituitarism; Infertility, Female; Menotropins; Ovulation Induction; Pregnancy; Puberty, Delayed; Syndrome

Forty-three ovulation cycles stimulated with human menopausal gonadotropin were examined in 31 patients with hypogonadotropic amenorrhea. Peripheral blood estradiol and luteinizing hormone were radioimmunoassayed. The findings indicate the possibility of recovery of adenohypophyseal gonadotropin autosecretion in the presence of human menopausal gonadotropin administration.

Topics: Adult; Amenorrhea; Chronic Disease; Estradiol; Female; Gonadotropins, Pituitary; Humans; Hypopituitarism; Luteinizing Hormone; Menotropins; Ovulation Induction; Stimulation, Chemical

A 33-year-old man with hypopituitarism is documented. He was born at breech presentation without asphyxia. He was the shortest in his class throughout his school days. He kept slowly growing and reached 172.8 cm at the age of 33. He was devoid of secondary sexual characteristics. Endocrinological studies showed panhypopituitarism with elevated levels of plasma TSH (15.0 microU/ml). TRH administration resulted in a marked increase in plasma TSH. Posterior pituitary function was normal. MR imaging showed transection of the pituitary stalk and the presence of ectopic and eutopic posterior lobes. The replacement of corticosteroid was initiated, and exaggerated response of TSH to TRH disappeared. Delayed bone maturation due to hypogonadism and hypothyroidism was one of the reasons why he had normal height without GH therapy. The significance of his peculiar MRI findings remains to be determined.

Topics: Adult; Body Height; Chorionic Gonadotropin; Humans; Hydrocortisone; Hypopituitarism; Magnetic Resonance Imaging; Male; Menotropins; Pituitary Gland; Thyrotropin

This case report describes an infertile male patient with panhypopituitarism, presumably caused by traumatic breech delivery. Previous hMG/hCG treatment had failed to induce spermatogenesis. Initiation of the production of motile and morphological normal sperm, despite persisting significant oligozoospermia was established with s.c. pulsatile LH-RH treatment. Spermatogenesis could be maintained with i.m. hCG injections bi-weekly. Later, fruitful in vitro fertilization (IVF) resulted in the birth of a healthy daughter.

Topics: Adult; Chorionic Gonadotropin; Fertilization in Vitro; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Humans; Hypopituitarism; Infertility, Male; Luteinizing Hormone; Male; Menotropins; Oligospermia; Spermatogenesis; Testosterone

A hypogonadotropic patient with primary pituitary insufficiency who has been previously treated for four cycles with hMG/hCG for ovulation induction is described. The hMG consumption was 76 to 96 ampules/cycle. Addition of GH (16 to 24 units/cycle) to hMG treatment was associated with a significant diminution in hMG consumption (35 to 36 ampules/cycle). The patient conceived on the second cycle of combined hMG/GH/hCG treatment. The possible role of GH as an adjunct to gonadotropin treatment is discussed, as well as the possible mechanisms of GH effects on the ovary.

Topics: Adult; Amenorrhea; Chorionic Gonadotropin; Drug Synergism; Female; Fertilization; Growth Hormone; Humans; Hypopituitarism; Infertility, Female; Menotropins; Ovarian Follicle; Stimulation, Chemical

Topics: Adult; Chorionic Gonadotropin; Humans; Hypopituitarism; Infertility, Male; Male; Menotropins; Sexual Maturation; Testosterone

Topics: Adult; Diabetes Insipidus; Female; Humans; Hypopituitarism; Menotropins; Ovulation Induction; Pregnancy; Pregnancy Complications

The case of a patient who developed partial hypopituitarism (hypogonadotropism and growth hormone deficiency) following transphenoidal removal of a prolactinoma is described. Hypogonadotropism persisted despite restoration of normoprolactinemia with bromocriptine therapy. Successful induction of ovulation with human menopausal gonadotropin (hMG) and bromocriptine suppression of the hyperprolactinemia was carried out, resulting in a pregnancy. The pros and cons of operative and nonoperative management of hyperprolactinemia are discussed.. A case report is presented of the need for both bromocriptine and human menopausal gonadotropin (hMG) for induction of ovulation in a patient who developed partial hypopituitarism and persistent hyperprolactinemia even after a transsphenoidal pituitary microadenectomy. The patient, a 27-year old white female, initially presented in 1979 with a history of amenorrhea and galactorrhea after discontinuing oral contraceptives (OCs). Her menstrual cycles had been regular since her menarch at age 13 until she began taking OCs at age 20. Preoperative endocrine evaluation in 1979 revealed serum luteinizing hormone (LH), 9.1 mIU/ml; serum follicle stimulating hormore (FSH), 6.4 mIU/ml; serum thyroid stimulating hormone (TSH), 3.8 mIU/ml; serum prolactine (PRL), 300 ng/ml; serum thyroxine (T4), 6.4 mcg/dl; and an attenuated PRL response to thyrotropin releasing hormone (TRH). Radiographic studies revealed a pituitary tumor of approximately 1 cm in diameter. In July 1979 a transsphenoidal hypophysectomy was performed. Pathologic examination revealed a pituitary adenoma with a monomorphic basophilic cell population with fibrosis and chronic inflammation. The patient required prednisone therapy postoperatively for 3 months secondary to compromised adrenal status. Prednisone therapy was discontinued in October 1979 after a normal cortisol (F) response to induced hypoglycemia was documented. The patient's serum PRL levels remained elevated at 111 ng/ml in August 1979 and 269 ng/ml in October 1979. Her amenorrhea and galactorrhea persisted. Bromocriptine therapy, 2.5 mg 3 times daily, was instituted in October 1979. She became normoprolactinemic, with a serum PRL of 6 ng/ml, and the galactorrhea disappeared but the amenorrhea persisted. In February 1981 she was referred for further consultation on her fertility status. Bromocriptine therapy was discontinued. In April 1981 she underwent a thorough endocrine evaluation. The results indicate that GnRH stimulation was unable to elicit a pituitary gonadotropin response anywhere near normal levels of FSH and LH, thus suggesting pituitary hypogonadotropism. Growth hormone release was subnormal in response to the insulin induced hypoglycemia and L-dopa ingestion. Hyperprolactinemia was obvious but the patient's serum TSH, T4, and adrenocorticotropin (ACTH) levels were normal. A diagnosis of hyperprolactinemia with partial hypopituitarism and gonadotropin deficiency was made. Bromocriptine therapy was reinstitu

Topics: Adult; Bromocriptine; Female; Follicle Stimulating Hormone; Growth Hormone; Humans; Hypopituitarism; Luteinizing Hormone; Menotropins; Ovulation Induction; Pituitary Neoplasms; Prolactin

Thyrotropic involvement is considered to be constant in Sheehan's syndrome. In this study, plasma thyroid stimulating hormone (TSH) levels were similar to those of normal women (respectively: 1.01 +/- 0.54 ng/ml and 0.54 +/- 0.27 ng/ml). The pituitary response to the administration of TRH was nul in 63.8% of cases. In one patient, thyrotrophic function was normal. Twelve patients had a minimal or moderate reserve of TRH. By order of prevalence, thyrotrophic involvement succeeds that of the somatotrophic and lactotrophic axes. There is no correlation with involvement of other axes which would make it possible to define a sequential course of pituitary lesions. These results are discussed in the light of the existing literature. The TRH test does not offer certain evidence of hypothalamic involvement.

Topics: Adrenocorticotropic Hormone; Adult; Female; Gonadotropin-Releasing Hormone; Humans; Hypopituitarism; Luteinizing Hormone; Menotropins; Prolactin; Thyrotropin; Thyrotropin-Releasing Hormone

Successful treatment of primary sterility in a woman having the rare association of panhypopituitarism with Fredrickson's Type V hyperlipemia is described. Replacement therapy with l-thyroxine, prednisone and a low fat diet cleared the patient's blood of the excessive chylomicrons and very low density lipoproteins. Ovulation was induced with human gonadotrophins, and triplets (two normal girls and a boy) were born.

Topics: Adult; Chorionic Gonadotropin; Chylomicrons; Drug Therapy, Combination; Female; Humans; Hyperlipidemias; Hypopituitarism; Infertility, Female; Lipoproteins, VLDL; Menotropins; Triglycerides

Topics: Adult; Amenorrhea; Chorionic Gonadotropin; Clomiphene; Estradiol; Estrogens; Female; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Humans; Hypopituitarism; Hypothalamo-Hypophyseal System; Luteinizing Hormone; Menotropins; Pregnancy; Progesterone; Radioimmunoassay; Syndrome

Topics: Adolescent; Adult; Amenorrhea; Capillary Permeability; Chiari-Frommel Syndrome; Female; Follicle Stimulating Hormone; Gonadotropins, Pituitary; Humans; Hypopituitarism; Infertility, Female; Menotropins; Ovarian Diseases; Ovulation; Pregnancy; Stimulation, Chemical

Topics: Adolescent; Adult; Amenorrhea; Body Temperature; Dose-Response Relationship, Drug; Drug Interactions; Female; Follicle Stimulating Hormone; Gonadotropins, Pituitary; Humans; Hypopituitarism; Luteinizing Hormone; Menotropins; Ovarian Follicle; Ovulation; Polycystic Ovary Syndrome