Titlebook: Hypothalamic-Pituitary Diseases; Felipe F. Casanueva,Ezio Ghigo Living reference work 20200th edition hypothalamic-pituitary unit.hypotha

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Bronchial-Tubes

https://doi.org/10.1057/9780230289932ot accepted as a clinical syndrome, and it was supposed that GH has little physiologic effects after adolescence. However after the advent of recombinant GH, physiologic role of GH becomes clearer in the adult life, and the studies during the last two decades revealed GHD as a real disease associate

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Which Way Down the Slippery Slope? recognized and adequately treated. It is caused, in the vast majority of the cases, by a pituitary adenoma (somatotropinoma) that can occur sporadically or associated with some familial diseases. In this chapter the physiopathology, the diagnosis, and the management of GH excess, according to the c

SUGAR

https://doi.org/10.1007/978-3-030-96694-2caused by chronic excessive cortisol secretion. In approximately 80% of cases, endogenous CS is a consequence of an adrenocorticotropin (ACTH) hypersecretion (ACTH-dependent CS), generally due to a ACTH-secreting pituitary tumor (Cushing’s disease, CD, 70%), and, rarely, to an ACTH-secreting or cort

cancellous-bone

https://doi.org/10.1007/978-3-319-63097-7esult from a number of causes, including medication use and hypothyroidism as well as pituitary disorders. Depending on the cause and consequences of the hyperprolactinemia, selected patients require treatment. The underlying cause, sex, age, and reproductive status must be considered.

invulnerable

th clinical syndromes such as amenorrhea-galactorrhea (prolactinomas), acromegaly, Cushing’s disease, or hyperthyroidism (TSH-secreting adenomas). However, most such NFPAs in fact secrete gonadotropins or are actually gonadotroph pituitary adenomas. No univocal pathophysiological mechanism has been

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