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Decrease in Carotid Intima-Media Thickness after One Year Growth Hormone (GH) Treatment in Adults with GH Deficiency¹

Service d’Endocrinologie, Hopital de l’Antiquaille (F.B.-C., A.Se., S.B, F.L., Y.R., F.B), 69005 Lyon; Service de Médecine Interne (X.D.) et de Médecine du Sport (J.P.) Hopital Lyon-Sud, 69495 Pierre-Bénite; et Service de Médecine Nucléaire (Y.K., G.S.) et Laboratoire de biochimie des lipides (A.Sa.), Hopital Neurologique; 69003 Lyon, France

Address all correspondence and requests for reprints to: Dr F. Borson-Chazot, Service d’Endocrinologie, Hopital de l’Antiquaille, 69005 Lyon, France.

An increased carotid arterial intima-media thickness (IMT) has been reported in hypopituitary adults untreated for GH deficiency. In the present study, the effect of GH replacement on IMT and cardiovascular risk factors was prospectively investigated, in GH deficiency patients treated at a mean dose of 1 UI/day during 1 yr (n = 22) and 2 yr (n = 11). The IMT measurements were performed by the same experienced physician, and the coefficient of variation (calculated in two control groups) was below 6.5%. IMT at baseline was related to conventional risk factors. After 1 yr GH treatment, IMT decreased from 0.78 ± 0.03 mm to 0.70 ± 0.03 mm (P < 0.001). The decrement was observed in 21 of 22 patients. After 2 yr GH treatment, IMT had stabilized at 0.70 ± 0.04 mm and remained significantly different from baseline values (P < 0.003). GH treatment resulted in a moderate decrease in waist circumference and body fat mass and an increase in VO₂ max. Conventional cardiovascular risk factors were unmodified except for a transient 10% decrease in low-density lipoprotein cholesterol at 6 months. The contrast between the limited metabolic effect of treatment and the importance and precocity of the changes in IMT suggests that the decrease in IMT was not exclusively attributable to a reversal in the atherosclerotic process. A direct parietal effect of GH replacement on the arterial wall might also be involved. The consequences, in terms of cardiovascular risk, should be established by randomized prospective trials.

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