Growth Hormone Treatment on Atherosclerosis: Results of a 5-Year Open, Prospective, Controlled Study in Male Patients with Severe Growth Hormone Deficiency

Abstract

Background: Severe GH deficiency (GHD) is associated with, increased cardiovascular risk and intima-media thickness (IMT) at major arteries.Objective: The objective of the study was to investigate the 5-yr effects of GH replacement on common carotid IMT and insulin resistance syndrome (IRS) (at least two of the following: triglycerides levels ≥ 1.7 mmol/liter, high-density lipoprotein-cholesterol levels ≤ 1.0 mmol/liter, blood pressure above 130/85 mm Hg, fasting glucose 6.1–7 or 2 hr after glucose 7.7–11.1 mmol/liter).Design: This was an interventional, open, prospective, controlled study.Patients: Patients included 35 men with severe GHD and 35 age-matched healthy men as controls.Intervention: All patients received standard replacement therapy; GH replacement was added in 22 patients (group A) and refused by 13 others (group B).Measurements: Five-year changes in IMT and IRS prevalence were measured.Results: At baseline, IMT was higher in the patients with (P < 0.001) and without IRS (P = 0.004) than in controls. Eighteen patients (51.4%) and two controls (5.7%; P < 0.0001) had IRS. At study end, use of lipid-lowering drugs (92.3, vs. 13.6 and 34.3%, P < 0.0001), glucose-lowering drugs (69.2 vs. 31.4 and 22.7%; P = 0.016), and antihypertensive drugs (61.5 vs. 20.0 and 4.5%; P < 0.0001) was higher in group B patients than controls and group A patients. IGF-I levels normalized in all group A patients and remained lower than −1 sd score in 77% of group B patients. IMT significantly decreased only in group A and significantly increased in controls and nonsignificantly in group B patients. IRS prevalence significantly reduced only in group A patients.Conclusions: Severely hypopituitary GHD men have more frequently increased IMT at common carotid arteries and IRS than controls. After 5 years, only in GH replaced patients, IMT and prevalence of IRS decreased.