Clinical endocrinology
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Clinical endocrinology · Dec 2003
Randomized Controlled Trial Comparative Study Clinical TrialModulation by progestogens of the effects of oestrogen on hepatic endocrine function in postmenopausal women.
Oral but not transdermal oestrogen administration reduces IGF-I, and increases GH binding protein (GHBP) reflecting effects on hepatic endocrine function in postmenopausal women. As progestogens attenuate the effects of oestrogen on circulating lipid levels according to their androgenic properties, we have investigated the impact of progestogen types on the hepatic endocrine effects of oestrogen. ⋯ Oestrogen effects on IGF-I, GHBP and SHBG are dependent on the route of administration with progestogens having variable effects. Among the progestogen types, norethisterone, the most androgenic, had the greatest effect, particularly on IGF-I. Progestogens modulate the effects of oestrogen on hepatic endocrine function in relation to their intrinsic androgenic properties. The modulatory effects of progestogens on IGF-I during oestrogen therapy may have long-term implications for lean body mass.
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Clinical endocrinology · Dec 2003
ReviewGrowth hormone, acromegaly, and heart failure: an intricate triangulation.
Short-term GH or IGF-I excess provides a model of physiological cardiac growth associated with functional advantage. The physiological nature of cardiac growth is accounted for by the following: (i) the increment in cardiomyocyte size occurs prevalently at expense of the short axis. This is the basis for the concentric pattern of left ventricular (LV) hypertrophy, with consequent fall in LV wall stress and functional improvement; (ii) cardiomyocyte growth is associated with improved contractility and relaxation, and a favourable energetic setting; (iii) the capillary density of the myocardial tissue is not affected; (iv) there is a balanced growth of cardiomyocytes and nonmyocyte elements, which accounts for the lack of interstitial fibrosis; (v) myocardial energetics and mechanics are not perturbed; and (vi) the growth response is not associated with the gene re-programming that characterizes pathologic cardiac hypertrophy and heart failure. ⋯ On the other hand, it must be stressed that GH and IGF-I activate several mechanisms that play a protective role against the development of heart failure. These include ventricular unloading, deactivation of neurohormonal components, antiapoptotic effect and enhanced vascular reactivity. Ultimately, all data available concur to hypothesize that acromegalic cardiomyopathy represents a progressive model of cardiac hypertrophy in which the cardiotoxic and pro-remodelling effect is intrinsic to the excessive and unrestrained myocardial growth.
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Clinical endocrinology · Sep 2003
Epidemiological survey of thyroid volume and iodine intake in schoolchildren, postpartum women and neonates living in Ulaan Baatar.
Although endemic goiter had been recognized in most parts of the country, there are few available data on iodine-deficiency disorders (IDDs) in Mongolia. This study aimed to characterize the current status of iodine deficiency in Ulaan Baatar, Mongolia's capital city. ⋯ The present study clearly indicates the presence of mild iodine deficiency in Mongolia. Enlarged thyroid gland and normal iodine excretion observed in schoolchildren living in Ulaan Baatar may result from the residual effects of iodine deficiency previously and presumably still exist in the city. Slight reduction in the rate of children with enlarged thyroid and low urinary iodine excretion after the onset of national iodinization programme suggests incomplete normalization of thyroid volume in children and that the correction of iodine deficiency is now in progress in Ulaan Baatar. Further nationwide surveys together with monitoring the progress of the national programme eliminating IDD are required in suburban areas surrounding the city and also in rural areas.
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Clinical endocrinology · Jul 2003
Assessment of quality of life in adults receiving long-term growth hormone replacement compared to control subjects.
There are few studies of quality of life (QOL) in adults with growth hormone deficiency (GHD) compared to matched control populations without GHD. These have shown impairments in a variety of QOL measures, which improve but do not normalize after short-term replacement with GH. There is little information on QOL in long-term treated GHD patients compared with controls without GHD. ⋯ This large population with treated GH deficiency have significant impairments in multiple aspects of QOL despite replacement with GH and other pituitary hormones for at least 1 year (mean 3 years). It is likely therefore that other factors in addition to GH deficiency must influence QOL in these patients. Further strategies to improve QOL in these individuals should therefore be considered, e.g. psychological support and treatments and physical treatments (such as exercise programmes).
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Clinical endocrinology · May 2003
The effect of growth hormone replacement therapy on adrenal androgen secretion in adult onset hypopituitarism.
Growth hormone replacement therapy in GH-deficient children is associated with enhanced adrenal androgen production, raising the possibility that GH might stimulate adrenocortical hormone secretion. This has not been extensively investigated in adults to date. GH is a potent modulator of the activity of the 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) enzyme and by altering cortisol metabolism can affect the function of the hypothalamo-pituitary-adrenal (HPA) axis and therefore potentially of adrenal androgen secretion. This study examined the effects of GH replacement in GH-deficient adults on adrenal androgen secretion. ⋯ This study shows that median serum DHEAS levels are significantly lower in GH-deficient patients, even those with intact ACTH reserve, than in aged-matched controls. GH replacement therapy is associated with a significant increase in mean serum DHEAS only in ACTH-sufficient patients. These findings are consistent with either (i) GH stimulation of adrenal androgen production in the permissive presence of ACTH or (ii) an inhibitory effect of GH on 11beta-HSD type 1 activity leading to enhanced cortisol clearance, subsequent activation of the HPA axis and ACTH-mediated androgen secretion.