Luteinizing Hormone and Follicle Stimulating Hormone-Releasing Hormone Test in Patients with Hypothalamic Pituitary-Gonadal Dysfunction

Mortimer, C. H.; Besser, G. M.; McNeilly, A. S.; Marshall, John C.; Harsoulis, P.; Tunbridge, W. M. G.; Gómez-Pan, A.; Hall, R.

doi:10.1136/bmj.4.5884.73

Cited by 181 publications

(48 citation statements)

References 12 publications

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“…cortisol) levels are normal or elevated. The reason for the peculiar susceptibility of gonadotrophins to malnutrition is unknown, and is reminiscent of the data found in anorexia nervosa (Mortimer et al, 1973).…”

Section: G O N a D O T R O P H I N S A N D G O N A D A L F U N C T I O Nmentioning

confidence: 93%

Endocrine Function in Protein‐calorie Malnutrition

Pimstone

1976

Clinical Endocrinology

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Undernutrition is widespread. In spite of the research and development being directed towards its prevention and alleviation, the weight of numbers as well as social, cultural, economic and technological considerations make eradication unlikely in the foreseeable future. Ironically, malnutrition is often endemic in areas in which sophisticated medical facilities exist; the problem clearly goes deeper than the mere availability of medical care. But this curious juxtaposition of poverty and medical sophistication has allowed numerous workers to study endocrine function in protein-calorie malnutrition (PCM). As hormones such as glucagon, insulin, growth hormone and cortisol are concerned with the efficient utilization of food, storage and expenditure of energy, and the latter three hormones with synthesis of body protein, it has been suggested that adaptive changes based on alterations in hormone secretion of function might allow for better survival of the threatened individual (Monckeberg, 1968); this conclusion, however, must be regarded as speculative at present; an alternative explanation might be that they are non-specific consequences of severe nutritional deprivation.This review is not primarily concerned with hormonal changes in prolonged fasting, nor will it refer in great depth to animal models of malnutrition which, while they have the advantage of producing more precise quantitation of the deficit, may not always be relevant to the situation in man. For infantile malnutrition is not merely the deprivation of proteins and calories ; it is inevitably associated with variable degrees of vitamin and mineral deficiency, intercurrent infection and electrolyte changes. To what extent hormonal changes are attributable to malnutrition as opposed to associated phenomena is not always apparent, but these might be very relevant in considering the pathogenesis of endocrine dysfunction in the human as opposed to the experimental context.

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Section: G O N a D O T R O P H I N S A N D G O N A D A L F U N C T I O Nmentioning

confidence: 93%

Endocrine Function in Protein‐calorie Malnutrition

Pimstone

1976

Clinical Endocrinology

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“…After an overnight fast, 100 g GnRH were administered as an iv bolus injection, and serum LH and FSH were measured at 0, 20, and 60 min. The normal range for LH is 15-42 IU/L at 20 min and 12-35 IU/L at 60 min; for FSH, the normal range is 1-11 IU/L at 20 min and 1-25 IU/L at 60 min (14,15).…”

Section: Diagnosis Of Cushing's Diseasementioning

confidence: 99%

Menstrual Abnormalities in Women with Cushing’s Disease Are Correlated with Hypercortisolemia Rather Than Raised Circulating Androgen Levels

Lado-Abeal

Rodriguez-Arnao

Newell‐Price

et al. 1998

The Journal of Clinical Endocrinology &Amp; Metabolism

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Menstrual irregularity is a common complaint at presentation in women with Cushing's syndrome, although the etiology has been little studied. We have assessed 45 female patients (median age, 32 yr; range, 16 -41 yr) with newly diagnosed pituitary-dependent Cushing's syndrome. Patients were subdivided into 4 groups according to the duration of their menstrual cycle: normal cycles (NC; 26 -30 days), oligomenorrhea (OL; 31-120 days), amenorrhea (AM; Ͼ120 days), and polymenorrhea (PM; Ͻ26 days). Blood was taken at 0900 h for measurement of LH, FSH, PRL, testosterone, androstenedione, dehydroepiandrosterone sulfate, estradiol (E 2 ), sex hormone-binding globulin (SHBG), and ACTH; cortisol was sampled at 0900, 1800, and 2400 h. The LH and FSH responses to 100 g GnRH were analyzed in 23 patients. Statistical analysis was performed using the nonparametric Mann-Whitney U and Spearman tests.Only 9 patients had NC (20%), 14 had OL (31.1%), 15 had AM (33.3%), and 4 had PM (8.8%), whereas 3 had variable cycles (6.7%). By group, AM patients had lower serum E 2 levels (median, 110 pmol/L) than OL patients (225 pmol/L; P Ͻ 0.05) or NC patients (279 pmol/L; P Ͻ 0.05), and higher serum cortisol levels at 0900 h (800 vs.602 and 580 nmol/L, respectively; P Ͻ 0.05) and 1800 h (816 vs. 557 and 523 nmol/L, respectively; P Ͻ 0.05) and higher mean values from 6 samples obtained through the day (753 vs. 491 and 459 nmol/L, respectively; P Ͻ 0.05). For the whole group of patients there was a negative correlation between serum E 2 and cortisol at 0900 h (r ϭ Ϫ0.50; P Ͻ 0.01) and 1800 h (r ϭ Ϫ0.56; P Ͻ 0.01) and with mean cortisol (r ϭ Ϫ0.46; P Ͻ 0.05). No significant correlation was found between any serum androgen and E 2 or cortisol. The LH response to GnRH was normal in 43.5% of the patients, exaggerated in 52.1%, and decreased in 4.4%, but there were no significant differences among the menstrual groups. No differences were found in any other parameter.In summary, in our study 80% of patients with Cushing's syndrome had menstrual irregularity, and this was most closely related to serum cortisol rather than to circulating androgens. Patients with AM had higher levels of cortisol and lower levels of E 2 , while the GnRH response was either normal or exaggerated. Our data suggest that the menstrual irregularity in Cushing's disease appears to be the result of hypercortisolemic inhibition of gonadotropin release acting at a hypothalamic level, rather than raised circulating androgen levels. (J Clin Endocrinol Metab 83: 3083-3088, 1998)

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“…Several earlier reports described blunted gonadotropin response to GnRH in women bearing PRL-producing adenomas (Nillius and Wide, 1972;Montimer et al, 1973;Coscia et al, 1974) . However, the tumors in these cases were large enough to destroy most of the pituitary gland.…”

Section: Discussionmentioning

confidence: 86%