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CLINICAL STUDY |
1 Section of Endocrinology and 2 Department of Medical Biochemistry, The National University Hospital, N-0027 Oslo, Norway, 3 Medical Department, Section of Endocrinology, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway, 4 Department of Endocrinology, Aker University Hospital, Oslo, Norway and 5 Global Endocrine Care, Pfizer Inc, New York, New York, USA
(Correspondence should be addressed to J Bollerslev; Email: jens.bollerslev{at}klinmed.uio.no)
Objective: GH deficiency is associated with an increased cardiovascular mortality. Fifty-five patients with adult-onset GH deficiency (AO-GHD) (24 female, 31 male, mean age 49 years) were enrolled in a placebo-controlled double-blind crossover study to investigate the effects of GH therapy on a variety of cardiovascular risk factors representing different aspects of atherogenesis, including apolipo-proteins (Apo A-1, Apo B), markers of subclinical inflammation (high-sensitivity C-reactive protein (CRP) and interleukin-6) and markers of endothelial function (intercellular adhesion molecule-1, von Willebrand factor and sCD40L (a pro-atherogenic factor and marker for plaque destabilization)).
Methods: GH therapy was individually dosed to obtain an IGF-I concentration within the normal range for age and sex. GH and placebo were administered for 9 months each, separated by a 4 month washout period.
Results: The final mean dose of GH was 50% higher for women and IGF-I increased to the same level in both sexes. Compared with placebo, substitution with GH showed a significant effect on Apo B (mean change –0.15 (–0.22 to –0.08) mg/l) and CRP (–1.8 (–3.3 to –0.3) mg/l). The baseline level of and change in IGF-I during treatment with GH contributed significantly to the improvement in both markers. No effects were found on interleukin-6 or Apo A-1, or on markers of endothelial function. No gender differences were observed for any of the markers at baseline or following intervention.
Conclusions: GH substitution to naïve patients with AO-GHD at a low, individually titrated dose aiming at normalizing IGF-I was followed by significant reductions in Apo B and CRP, indicating a positive effect of GH on cardiovascular risk.
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