GH deficiency promotes atherosclerosis

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Citations: 1-3
<1>

Authors
Pfeifer M. Verhovec R. Zizek B. Prezelj J. Poredos P. Clayton RN. Institution
Department of Endocrinology, Diabetes and Metabolic Diseases, University Medical Center, Ljubljana, Slovenia.
Title
Growth hormone (GH) treatment reverses early atherosclerotic changes in GH-deficient adults. Source
Journal of Clinical Endocrinology & Metabolism. 84(2):453-7, 1999 Feb. Abstract
Hypopituitary patients have increased mortality from vascular disease, and in these patients, early markers of atherosclerosis [increased carotid artery intima-media thickness (IMT) and reduced distensibility] are more prevalent. As GH replacement can reverse some risk factors of atherosclerosis, the present study examined the effect of GH treatment on morphological and functional changes in the carotid and brachial arteries of GH-deficient (GHD) adults. Eleven GHD hypopituitary men (24-49 yr old) were treated with recombinant human GH (0.018 U/kg BW x day) for 18 months. IMT of the common carotid artery (CCA) and the carotid bifurcation (CB), and flow-mediated endothelium-dependent dilation (EDD) of the brachial artery were measured by B mode ultrasound before and at 3, 6, 12, and 18 months of treatment, and values were compared with those in 12 age-matched control men. Serum concentrations of lipids, lipoprotein(a), insulin-like growth factor I (IGF-I), and IGF-binding protein-3 (IGFBP-3) were also measured. In GHD men before treatment the IMTs of the CCA [mean(SD), 0.67(0.05) mm] and CB [0.75(0.04) mm] were significantly greater (P < 0.001) than those in control men [0.52(0.07) and 0.65(0.07) mm, respectively]. GH treatment normalized the IMT of the CCA by 6 months [0.53(0.04) mm] and that of the CB by 3 months [0.68(0.05) mm]. The IMT of the carotid artery (CCA and CB) was negatively correlated with serum IGF-I (r

• -0.53; P < 0.0001). There was a significant improvement in flow-mediated EDD of the brachial artery at 3 months, which was sustained at 6 and 18 months of GH treatment (P < 0.05). GH treatment increased high density lipoprotein cholesterol at 3 and 6 months, but did not reduce total or low density lipoprotein cholesterol and was without effect on lipoprotein(a). There was no correlation between plasma lipids and changes in IMT or EDD of the arteries examined. In conclusion, GH treatment of hypopituitary GHD men reverses early morphological and functional atherosclerotic changes in major arteries and, if maintained, may reduce vascular morbidity and mortality. GH seems to act via IGF-I, which is known to have important effects on endothelial cell function.

<2>

Authors
Marek J. Kvasnicka J. Weiss V. Markova M. Hass T. Institution
III. interni klinika 1. LF UK a VFN, Praha. Title
[Can normalization of vascular cytoadhesive activity be explained by the anti-atherosclerosis effect of growth
hormone?]. [Czech]
Source
Casopis Lekaru Ceskych. 137(22):690-3, 1998 Nov 16. Abstract
BACKGROUND: The increased mortality caused by premature atherosclerosis has been shown among patients with hypopituitarism receiving conventional hormone treatment but with unsubstituted growth hormone
deficiency. This experience belongs among the most important arguments in favour of replacement with growth hormone. The mechanisms of the antiatherogenic effect of growth hormone are poorly understood. The protective effect of growth hormone on the vascular endothel and its intervention in the clotting process, which have not been yet elucidated, may be the causative factors. METHODS AND RESULTS: The endothelial damage as given by measuring of circulating soluble cytoadhesive molecules sE-selectin, sP-selectin and intercellular adhesive molecule 1 (ICAM 1) was measured in 15 adult panhypopituitaric patients before and after 1 year treatment with recombinant human growth hormone. The blood levels of all of these cytoadhesive molecules decreased significantly (p < 0.01) during the treatment. None of the concomitantly followed coagulation tests (prothrombin time, activated partial thromboplastin time, fibrinogen, antithrombin III, von Willebrand's factor and D-dimer) was significantly changed during the treatment. The tendency to decrease (p = 0.054) was observed with antithrombin III. CONCLUSIONS: The decrease of circulating cytoadhesive molecules in blood during the treatment of growth hormone gives evidence for its
protective effect, either direct or mediated, on the vascular endothel. These findings could bring an explantation for the premature atherosclerotic changes in hypopituitarism and antiatherogenic effect of growth hormone.

<3>

Authors
Hassan HM. Kohno H. Kuromaru R. Honda S. Ueda K. Institution
Department of Paediatrics, Kyushu University, Faculty of Medicine, Japan. Title
Body composition, atherogenic risk factors and apolipoproteins following growth hormone treatment.
Source
Acta Paediatrica. 85(8):899-901, 1996 Aug. Abstract
We studied the change in atherogenic risk factors in 27 children, 21 boys and 6 girls, 6 to 14 years of age, with growth hormone deficiency during 12 months of growth hormone replacement therapy. Changes in body composition and lipid profile during growth hormone treatment were evaluated. The atherogenic index was calculated using the equation [(total cholesterol- high-density lipoprotein cholesterol)(apolipoprotein B)]/[(apolipoprotein AI)(high-density lipoprotein cholesterol)]. Body fat decreased (p < 0.01), associated with an increase in lean body mass (p < 0.01). Total cholesterol and high-density lipoprotein cholesterol showed no significant changes. The atherogenic index significantly decreased from 1.44 +/- 0.60 to 1.09 +/- 0.52 (p < 0.01) after 12 months. Apolipoproteins CII and CIII increased throughout the study period (p < 0.01). Lipoprotein(a) and apolipoproteins AI, B and B/AI ratio did not change significantly. In conclusion, growth hormone treatment improved body composition and reduced atherogenic risk factors in children with growth hormone deficiency.

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