Endocrine Abstracts

Acromegaly is known to be associated to an increased cardiovascular risk, due to the increased prevalence of glucose intolerance and dyslipidemia and pre-atherosclerotic lesions. The aim of this study was to evaluate the effect of treatment with the GH receptor antagonist pegvisomant on cardiovascular risk and atherosclerosis in patients with acromegaly resistant to somatostatin analogues. Twelve patients (4 m, 8 f, 28–58 yrs) and 24 sex-, age- and BMI-matched controls entered the study. The patients were evaluated before and after 18 months of treatment with pegvisomant at the dose of 10–40 mg/day. In all patients and controls, serum total, LDL and HDL cholesterol, triglycerides, glucose, insulin and fibrinogen levels, total/HDL cholesterol ratio and HOMA index, as well as common carotid intima-media thickness (IMT) were measured and correlated with serum GH and IGF-I levels. At baseline, increased GH and IGF-I levels were confirmed in all patients. HDL-cholesterol were significantly lower (P<0.05) whereas total/HDL-cholesterol ratio (P<0.001), glucose levels (P<0.05), HOMA index (P<0.001) and fibrinogen levels (P<0.001) were significantly higher in patients than controls. Moreover, maximal IMT were significantly higher in patients than in controls (1.13±0.55 vs 0.69±0.1 mm; P<0.001). At 18-month follow-up, serum IGF-I levels were normalized in 9 (75%) patients and significantly reduced in the remaining patients. Both serum glucose levels (5.62±1.33 vs 4.86±0.73; P<0.05) and HOMA index (3.31±2.24 vs 1.10±0.22; P<0.05) were significantly decreased after treatment. A trend to a decrease in maximal IMT (1.13±0.55 vs 0.96±0.16 mm) was also found after 18 months of treatment with pegvisomant. A significant correlation was found between the changes in serum IGF-I levels and maximal IMT (P<0.05). The results of the current study demonstrated that the treatment with pegvisomant is able to improve the cardiovascular risk, especially through the improvement of glucose tolerance, and prevent the progression of atherosclerosis in patients with acromegaly resistant to somatostatin analogues.