Suppression of the Hypothalamic-Pituitary-Ovarian Axis in Normal Women by Glucocorticoids

Saketos, M.; Sharma, Neelam; Santoro, Nanette

doi:10.1097/00006254-199408000-00020

Cited by 35 publications

(43 citation statements)

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“…X70. trous cycle, were also consistent with effects described for synthetic glucocorticosteroids in the dog (23). Inhibition of ovulation due to glucocorticosteroid-induced suppression of luteinizing hormone (LH) release (ie, preovulatory LH surge) has been described for rodents and women (4,12,13,38). Inhibition of the preovulatory LH surge in female rabbits has also been demonstrated with medroxyprogesterone acetate (31).…”

Section: Methodssupporting

confidence: 75%

Chronic Effects of the Novel Glucocorticosteroid RPR 106541 Administered to Beagle Dogs by Inhalation

Miller¹,

Valerio²,

Pino³

et al. 2000

Toxicol Pathol

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Section: Methodssupporting

confidence: 75%

Chronic Effects of the Novel Glucocorticosteroid RPR 106541 Administered to Beagle Dogs by Inhalation

Miller¹,

Valerio²,

Pino³

et al. 2000

Toxicol Pathol

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“…In healthy women, high-dose cortisol causes either a decrease (12,13) or no change (16) in LH pulsatility, and Rickenlund et al (15) have reported an inverse correlation between cortisol and menstrual frequency. AN is associated with hypercortisolemia in adults (27) and adolescents (4), and it is tempting to postulate that hypercortisolemia may contribute to hypogonadotropic hypogonadism associated with AN.…”

Section: Discussionmentioning

confidence: 99%

“…Cortisol in high doses decreases gonadotropin-releasing hormone (GnRH) secretion and LH pulse frequency in healthy women (12,13), and inverse associations have been noted between cortisol and LH pulse frequency (14) as well as between cortisol and menstrual frequency (15). Samuels et al (16), conversely, did not observe a decrease in gonadotropin pulsatility following hydrocortisone administration.…”

mentioning

confidence: 98%

Role of Cortisol in Menstrual Recovery in Adolescent Girls with Anorexia Nervosa

et al. 2006

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Neuroendocrine abnormalities in anorexia nervosa (AN) include hypercortisolemia, hypogonadism, and hypoleptinemia, and neuroendocrine predictors of menstrual recovery are unclear. Preliminary data suggest that increases in fat mass may better predict menstrual recovery than leptin. High doses of cortisol decrease luteinizing hormone (LH) pulse frequency, and cortisol predicts regional fat distribution. We hypothesized that an increase in fat mass and decrease in cortisol would predict menstrual recovery in adolescents with AN. Thirty-three AN girls 12-18 y old and 33 controls were studied prospectively for 1 y. Body composition [dual energy x-ray absorptiometry (DXA)], leptin, and urinary cortisol (UFC) were measured at 0, 6, and 12 mo. Serum cortisol was measured overnight (every 30 min) in 18 AN subjects and 17 controls. AN subjects had higher UFC/cr·m 2 and cortisol area under curve (AUC), and lower leptin levels than controls. Leptin increased significantly with recovery. When menses-recovered AN subjects were compared with AN subjects not recovering menses and controls, menses-recovered AN subjects had higher baseline cortisol levels and greater increases in leptin than controls and greater increases in fat mass than AN subjects not recovering menses and controls (adjusted for multiple comparisons). In a logistic regression model, increasing fat mass, but not leptin, predicted menstrual recovery. Baseline cortisol level strongly predicted increases in the percentage of body fat. We demonstrate that 1) high baseline cortisol level predicts increases in body fat and 2) increases in body fat predict menses recovery in AN. (Pediatr Res 59: [598][599][600][601][602][603] 2006) A N, a model of severe undernutrition, is associated with hypogonadotropic hypogonadism resulting in primary or secondary amenorrhea or delayed menarche. Weight recovery occurs in up to 50% of adolescents with AN and should result in recovery of the hypothalamo-pituitary-gonadal (H-P-G) axis (1). However, a temporal association between weight gain and menstrual recovery is not always observed (2,3). Not all adolescents with AN who resume menses are weight recovered, and not all weight-recovered adolescents with AN resume menstrual function. In addition, neuroendocrine predictors of menstrual recovery are unclear.We have demonstrated higher cortisol (4) and lower leptin levels (3,5) in AN girls compared with healthy adolescents.Leptin is an adipocytokine, and leptin-deficient or -resistant mice (6,7) and humans with leptin and leptin receptor mutations (8,9) are hypogonadal. In a recent study, leptin administration was associated with resumption of menses in five of eight women with hypothalamic amenorrhea (10). These data suggest that leptin is an important regulator of the H-P-G axis and that an increase in leptin along with an increase in fat mass may predict recovery of the H-P-G axis in AN. Conversely, Golden et al. (11) observed no differences in fat mass between AN girls who recovered menses and those who did not.In add...

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“…It is known that hypercortisolemia can lead to hypogonadism. Patients with Cushing syndrome have decreased LH and FSH levels (Luton et al 1977) and even short-term hydrocortisone therapy in normally menstruating women results in suppression of gonadotropin levels (Saketos et al 1993).…”

Section: Discussionmentioning

confidence: 99%

Hypogonadotropic Hypogonadism in Males with Glycogen Storage Disease Type 1

et al. 2017

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Background: Glycogen storage disease type 1 is an autosomal recessive disorder with an incidence of 1 in 100,000. Long-term complications include chronic blood glucose lability, lactic academia, short stature, osteoporosis, delayed puberty, gout, progressive renal insufficiency, systemic or pulmonary hypertension, hepatic adenomas at risk for malignant transformation, anemia, vitamin D deficiency, hyperuricemic nephrocalcinosis, inflammatory bowel syndrome (type 1b), hypertriglyceridemia, and irregular menstrual cycles. We describe hypogonadotropic hypogonadism as a novel complication in glycogen storage disease (GSD) type 1.Case Studies and Methods: Four unrelated patients with GSD 1a (N ¼ 1) and 1b (N ¼ 3) were found to have hypogonadotropic hypogonadism diagnosed at different ages. Institutional Research Ethics Board approval was obtained as appropriate. Participant consent was obtained. A retrospective chart review was performed and clinical symptoms and results of investigations summarized as a case series. Results: All patients were confirmed biochemically to have low luteinizing hormone (LH) and follicular stimulating hormone (FSH), and correspondingly low total testosterone. Clinical symptoms of hypogonadism varied widely. Investigations for other causes of hypogonadotropic hypogonadism were unremarkable. In addition, all patients were found to have disproportionately low bone mineral density at the lumbar spine compared to the hip. Common to all patients was erratic metabolic control, including recurrent hypoglycemia and elevated lactate levels. Discussion: Recurrent elevations in cortisol in response to hypoglycemia may be the underlying pathology leading to suppression of gonadotropin-releasing hormone (GnRH) release. Incorporating clinical and/or biochemical screening of the hypothalamic-pituitary-gonadal axis may be important in the management of this disease. Testosterone therapy however needs to be carefully considered because of the risk of hepatic adenomas.

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Suppression of the Hypothalamic-Pituitary-Ovarian Axis in Normal Women by Glucocorticoids

Cited by 35 publications

References 0 publications

Chronic Effects of the Novel Glucocorticosteroid RPR 106541 Administered to Beagle Dogs by Inhalation

Chronic Effects of the Novel Glucocorticosteroid RPR 106541 Administered to Beagle Dogs by Inhalation

Role of Cortisol in Menstrual Recovery in Adolescent Girls with Anorexia Nervosa

Hypogonadotropic Hypogonadism in Males with Glycogen Storage Disease Type 1

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