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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results of a study involving dynamic testing of hypothalamic-pituitary function in 26 patients attending the Gynecologic Reproductive Endocrine Service at John Hopkins University are presented. Patients included women with primary amenorrhea and few if any secondary sex characteristics (Group 1), primary amenorrhea with secondary sexual development (Group 2), secondary amenorrhea (Group 3), and amenorrhea with pituitary or supracellar tumors (Group 4). Subjects received a combined luteinizing hormone-releasing hormone (LH-RH)-clomiphene test and an estrogen provocation test. 100 mcg LH-RH was administered and blood samples obtained at 15, 30, and 45 minutes and at 1, 1 1/2, 2, 2 1/2, and 3 hours. 100 mg of clomiphene citrate was given daily for 7 days (the dosage of clomiphene varied somewhat with history of preexisting conditions). Blood was assayed for serum LH and follicle stimulating hormone (FSH) In the provocation test, 1 mg of estradiol was given and blood samples drawn 48, 72, and 96 hours thereafter. In Group 1, 3 patients were unresponsive to LH-RH stimulation and were without change in the baseline after either clomiphene or Enovid suppression. 3 other patients in this group had a fairly normal delta percent peak LH response to LH-RH. However, baseline or the delta percent peak LH response to LH-RH remained unchanged after clomiphene. The 7th patient in Group 1 has an immature hypothalamus. Group 2 consisted of 3 patients. 2 were found to have elevated baseline values of LH with normal FSH levels. 1 had a poor but mature response to clomiphene of the negative estrogen feedbacK. LH peak remained unchanged in response to LH-RH after clomiphene and estrogen response was negative. 2 of these patients conceived and 1 was diagnosed as able to conceive. In Group 3, 2 patients with massive obesity showed elevated serum LH values, 2 patients were infertile after oral contraceptives and were stimulated with human chorionic gonadotropin and clomiphene, 7 had anorexia and were diagnosed with the aestrogen provocation test. The patients in Group 4 were all studied in an effort to assess the pituitary gonadotropin reserve. These tests can be useful in this regard but must be considered in light of the patient's history and physical findings. Thus initial diagnoses were further subdivided by this method of dynamic testing. It helps establish areas of further testing.
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PMID:Dynamic testing of hypothalamic-pituitary function in abnormalities of ovulation. 34 92

A case of association between hypothalamic primary amenorrhea, obesity and paraphrenia is presented in a 53 old woman. Neurological investigations, showing a diencenphalic involvement possibly on a malformative basis, lead to the hypothesis of a common pathogenesis for both endocrinological and psychiatric features of the syndrome.
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PMID:[Cases of endocrinological psychiatry. Hypothalamic primary amenorrhea with paraphrenia]. 123 41

Pulsatile GnRH administration for induction of ovulation is often ineffective in polycystic ovarian disease (PCOD) patients. To clarify and correct the endocrine mechanisms underlying this deranged response we gave pulsatile GnRH (5 micrograms, iv, every 60 min) to idiopathic hypogonadotropic hypogonadism (IHH) patients with primary amenorrhea for 19 cycles and to PCOD patients for 24 cycles before (pre-A) and for 25 cycles after (post-A) GnRH analog suppression. Compared to IHH, pre-A cycles were characterized by elevated LH, estradiol, and testosterone; reduced luteal phase progesterone; and low ovulatory (38%) and pregnancy rates (8%). Conversely, LH, estradiol, and follicular phase testosterone levels were lower in post-A than in pre-A cycles, while luteal phase progesterone was higher; the endocrine pattern of post-A cycles closely resembled the one of IHH cycles. The ovulatory and pregnancy rates of PCOD patients improved remarkably in post-A cycles (90% and 38%, respectively). Excessive body weight was associated with a lower incidence of ovulation in both pre-A (15%) and post-A cycles (75%). A worse endocrine pattern and a lower ovulatory rate (50%) were obtained when a second consecutive post-A cycle occurred without repeating GnRH analog suppression. No signs of even mild ovarian hyperstimulation and no multiple pregnancies were recorded in the post-A cycles. We conclude that in PCOD 1) deranged pituitary sensitivity, excessive ovarian androgen secretion, and obesity critically affect folliculogenesis and ovulation; 2) pituitary-gonadal suppression with a GnRH analog markedly improves the endocrine and clinical responses to pulsatile GnRH ovulation induction; 3) optimal results can be achieved only when each pulsatile GnRH cycle is preceded by GnRH analog suppression; and 4) pulsatile GnRH is highly effective and safe for ovulation induction, provided that PCOD subjects are pretreated with a GnRH analog.
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PMID:The abnormal response of polycystic ovarian disease patients to exogenous pulsatile gonadotropin-releasing hormone: characterization and management. 250 16

We have reviewed the role of insulin in ovarian physiology. Clinical observations and experimental data strongly support the hypothesis that insulin possesses gonadotropic activity, when acting alone or with FSH or LH. This idea is further supported by the recent discovery of insulin in follicular fluid. The idea that insulin has gonadotropic function can explain a variety of clinical observations, which otherwise are difficult to understand. For example, manifestations of ovarian hypofunction (primary amenorrhea, late menarche, anovulation, low pregnancy rate, and early menopause) in IDDM can be understood if it is accepted that insulin is necessary for the ovary to reach its full steroidogenic potential. The idea that insulin affects ovarian steroidogenesis also helps to understand the observation that hyperandrogenism frequently accompanies each of the various insulin-resistant states, regardless of the latter's etiology (e.g. genetic deficiency in the number of insulin receptors, antiinsulin receptor antibodies, obesity, etc.). The explanation for this association is based on the idea that hyperinsulinemia intensifies ovarian steroidogenesis, which manifests clinically as hyperandrogenism. Continuous stimulation of the ovary by insulin over a long period of time possibly produces morphological ovarian changes, such as hyperthecosis or polycystic changes; these changes commonly are observed among women with insulin resistance. The effects of insulin on ovarian cells are mediated possibly through binding of the peptide to its own receptor or to the IGF-1 receptor (the specificity spillover phenomenon). The latter could be an important mechanism in cases of insulin resistance. Potential mechanisms underlying the gonadotropic activity of insulin include direct effects on steroidogenic enzymes, modulation of FSH or LH receptor number, synergism with FSH or LH, or nonspecific enhancement of cell viability. The gonadotropic function of insulin adds yet another note to what has been termed a symphony of insulin action. Further investigation into this new area may yield greater insights not only into normal ovarian physiology, but also into the pathogeneses of such diverse entities as PCO, obesity, diabetes mellitus, and the syndromes of insulin resistance and acanthosis nigricans.
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PMID:The gonadotropic function of insulin. 330 17

Arachnoid cysts, most characteristically situated in the middle cranial fossa, have been described at other situations, in the posterior fossa and in the interpeduncular region. A case of primary amenorrhoea, obesity, with short stature, proved to be associated with a huge arachnoid cyst involving the L. middle and anterior cranial fossae; and pituitary fossa, producing panhypopituitarism with right faciobrachial paresis, normal visual fields and visual acuity. No evidence of progress of the lesion has been found after 3 years of observation, and further conservative management with regular CT scanning and oestrogen replacements is proposed.
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PMID:Hypopituitarism with arachnoid cyst. 656 32

A Caucasian female, aged 28 years, presenting with obesity and investigated for primary amenorrhoea, was found to have hydrocephalus due to a stenosis of the foramen of Magendie. Endocrine investigations showed an isolated gonadotrophin deficiency. Complete recovery was obtained by a ventricular-cardiac shunt, which led to the return of menses, a normal pregnancy, and then a return to normal weight.
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PMID:Endocrine expressions of hydrocephalus. A case of primary amenorrhoea revealing a stenosis of the foramen of Magendie. 660 Aug 67

Prader-Willi syndrome (PWS) is characterized by hypotonia at birth, hypogonadism, early childhood obesity, and mental deficiency. Hypogonadotropic hypogonadism is a major characteristic of patients with PWS, and it is speculated to be due to hypothalamic insufficiency. Two adult female patients with PWS and no prior history of menses are presented. Both of these patients were treated with fluoxetine for psychopharmacologic management of obsessive features in the form of food preoccupation and hyperphagia or for compulsive behaviors in the form of severe self-injurious behaviors. The two female patients with PWS who had primary amenorrhea developed vaginal bleeding believed to be menses following at least 6 months of treatment with fluoxetine. Mature hypothalamic function is characterized by pulsatile release of gonadotropin-releasing hormone (GnRH) in a critical range of frequency and amplitude. Central nervous system neurotransmitters may modify GnRH secretion. Fluoxetine specifically inhibits the reuptake of serotonin which may impact the hypothalamic-pituitary-ovarian system in female patients with PWS.
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PMID:Onset of menses in two adult patients with Prader-Willi syndrome treated with fluoxetine. 749 74

We report a 28-year-old-female who presented with primary amenorrhoea, absence of puberty, obesity and normal stature. The subject was clearly short as a child, with a height more than 2 SD below normal until the age of 15 years. The pubertal growth spurt failed to develop. She continued growing at a prepubertal rate until growth ceased at the age of 20 years, reaching her final adult height of 157 cm (SDS -0.86) without hormonal treatment. A combined pituitary hormone stimulation test of anterior pituitary function showed deficiencies of GH, LH and FSH, and low normal serum levels of TSH and PRL. Magnetic resonance imaging revealed a hypoplastic pituitary with markedly reduced pituitary height. In addition, a whole body dual energy X-ray absorptiometry scan showed high levels of body fat (54%). Combined pituitary hormone deficiencies with a hypoplastic pituitary suggested the diagnosis of a Prophet of Pit-1 (PROP1) gene mutation. Normal stature in this case, however, confounded this diagnosis. Sequencing of PROP1 revealed homozygosity for a single base-pair substitution (C to T), resulting in the replacement of an Arg by a Cys at codon 120 (R120C) in the third helix of the homeodomain of the Prop-1 protein. To our knowledge, this is the first report of a patient with a mutation in the PROP1 gene that attained normal height without hormonal treatment, indicating a new variability in the PROP1 phenotype, with important implications for the diagnosis of these patients. We suggest that this can be explained by (i) the presence of low levels of GH in the circulation during childhood and adolescence; (ii) the lack of circulating oestrogen delaying epiphyseal fusion, resulting in growth beyond the period of normal growth; and (iii) fusion of the epiphyseal plates, possibly as a result of circulating oestrogens originating from peripheral conversion of androgens by adipose tissue.
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PMID:A unique case of combined pituitary hormone deficiency caused by a PROP1 gene mutation (R120C) associated with normal height and absent puberty. 1215 92

In adult patients weight gain is a frequent complaint of hyperprolactinaemia and it has been associated with a high prevalence of obesity. Normalization of prolactin (PRL) levels result in weight loss. The nature of this link is poorly defined. In this report we describe a 14 year-old female with primary amenorrhea and persistent progressive weight gain. The patient's height, weight and BMI were 152 cm, 70 kg, and 30.3 kg/m2, respectively. Basal hormonal investigation showed normal free thyroxin, TSH, IGF-I, cortisol and ACTH values. Serum PRL level was very high (16,278 mIU/l; normal range 63-426 mIU/l). Magnetic resonance imaging scan showed the presence of a pituitary microadenoma. Treatment with the non-selective dopamine agonist pergolide caused a significant reduction of serum PRL concentration with a remarkable decrease of body weight. During follow-up, repeat MRI scan revealed disappearance of the microadenoma. The reduction of the daily dose of pergolide was associated with an increase of serum PRL with significant weight gain. A further reduction of body weight was subsequently observed with an increase of pergolide dosage. Serum PRL measurement may be useful as part of the endocrine work-up of obese children with a history of unexplained recent weight gain, especially if associated with pituitary-gonadal axis dysfunction. The relationship between PRL secretion and weight change needs to be examined in prospective larger studies.
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PMID:Reversible weight gain and prolactin levels--long-term follow-up in childhood. 1627 71

The word "hydrocephalus" is derived from two Greek words: hydro meaning water; and cephalus meaning head; also known as "water on the brain". Historically it is believed to result from imbalance between CSF production and absorption, with net accumulation of fluid in the cranial cavity; characterized by increase in size of the cerebral ventricles. It is classified as: Communicating hydrocephalus, in which flow is not obstructed, but CSF is inadequately reabsorbed in the subarachnoid space and the Non-communicating hydrocephalus or the Obstructive type, in which flow of CSF from the ventricles to subarachnoid space is obstructed. This type may also be sub-classified into Congenital and Acquired. The overall incidence of hydrocephalus is not known. Approximately 55% of all hydrocephalus are congenital. The etiology depends upon the age of the child. The clinical features are increase in the size of head, with wide anterior fontanelle, prominent scalp veins, sun-setting eyes, optic nerve atrophy, nystagmus and increased muscle tone in children upto 2 years. Children more than 2 years may present with these as hydrocephalus progresses; or if the fontanelles are closed, head size may be normal. These may present with optic atrophy or papilloedema, abnormal hypothalamic functions (short stature or gigantism, obesity, delayed puberty, primary amenorrhea or menstrual irregularity and diabetes inspidus) and spastic lower limbs. Performance IQ is worse than verbal IQ and learning problems are common. The diagnostic procedures include measurement of head circumference, Plain X ray of head, Ventriculography, Pneumoencephalography, Ultrasonography, Computed Tomography and Magnetic Resonance Imaging. The management may be non-surgical and surgical.
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PMID:Hydrocephalus in children. 1630 73


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