From: Doug Skrecky (oberon@vcn.bc.ca)
Date: Tue Jul 13 1999 - 21:44:27 MDT
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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