Patologia de l'hormona del creixement (GH) en adults: del defecte a l'excés de GH. Marcadors inflamatoris i factors de risc cardiovascular.

by Sesmilo León, Gemma

Abstract (Summary)
ENGLISH ABSTRACT: "Physiopathology of growth hormone (GH) deficiency and GH excess clinical conditions. Exploring inflammatory markers and cardiovascular risk factors". SUBJECT: GH deficiency and GH excess clinical human models are associated with increased cardiovascular mortality AIMS: We aimed to study: 1) Effects of GH replacement on inflammatory and other cardiovascular risk markers, homocysteine, folate and thyroid hormones. 2) Effects of GH discontinuation on body composition, bone mineral density (BMD) and cardiovascular risk markers. 3) Androgen levels and cardiovascular risk markers in women with hypopituitarism. 4) Cardiovascular risk markers in patients with acromegaly before and after treatment with Pegvisomant. METHODS: 1) Randomized controlled trial 18 months duration- of GH vs placebo in men with adult onset GH deficiency (GHD). 2) Longitudinal study -18 months duration- after GH replacement withdrawal, of patients who had received GH replacement during 18 months, focusing on body composition, BMD and cardiovascular risk markers. 3) Observational study in women with hypopituitarism compared to controls focusing on androgen levels, inflammatory and other cardiovascular risk markers. 4) Observational study in patients with active acromegaly compared to controls analysing cardiovascular risk markers. 5) Randomized controlled trial of Pegvisomant treatment in acromegaly, focusing on cardiovascular risk markers. 6) Longitudinal open study of Pegvisomant treatment in acromegaly. CONCLUSIONS: 1) GH negatively modulates C-reactive protein (CRP) concentrations. CRP is high in GH deficiency and low in acromegaly. CRP decreases with GH replacement and increases with Pegvisomant treatment in acromegaly. 2) GH replacement decreases central fat but increases insulin-resistance. 3) GH replacement decreases homocysteine, a putative cardiovascular risk marker. The mechanism and significance of this is unknown but it could be mediated by the effect of GH on thyroid hormones. 4) GH discontinuation increases fat and decreases lean body mass. However, bone mineral density increases further. 5) GH discontinuation increases central fat, CRP and homocysteine levels. However it decreases glucose and insulin consistent with an improvement on insulin-resistance. 6) GH modulates lipoprotein (a) levels; they increase with GH replacement and decrease with Pegvisomant treatment of acromegaly. 7) The overall cardiovascular effect of GH replacement must be assessed in appropriate clinical studies.
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Bibliographical Information:

Advisor:Gomis de Barbarà, Ramon; Klibanski, Anne

School:Universitat de Barcelona

School Location:Spain

Source Type:Master's Thesis



Date of Publication:06/10/2002

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