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Introduction: Elevated fibroblast growth factor-21 (FGF-21) levels are related to carotid intima-media thickness (CIMT), a well-established marker of atherosclerosis. Acromegaly has also been linked to increased CIMT. There has been no data considering the association between FGF-21 levels and atherosclerosis in acromegaly patients. This study aimed to evaluate FGF-21 levels and CIMT in acromegalic patients in relation to atherosclerotic complications. Design: Case–control study. Materials and methods: The study group included 70 acromegaly patients and 72 healthy volunteers from the Department of Endocrinology and Metabolism Disease, Marmara University Medical School. FGF-21, growth hormone, insulin-like growth factor I, lipids, glucose, insulin levels were assessed. CIMT was measured from the common carotid artery wall on B-mode ultrasound. Results: Median FGF-21 levels were significantly lower in the acromegaly group than in the control group. CIMT was higher in acromegaly patients compared to controls. Although there was no correlation between FGF-21 levels and CIMT in patients with acromegaly, a positive correlation was found between high-density lipoprotein-cholesterol and FGF-21 levels. Glucose metabolic markers were the determining factors of the FGF-21 levels in acromegaly patients. Conclusion: Our study is the first to examine the relationship between serum FGF-21 levels and atherosclerosis in acromegaly patients. The lower serum FGF-21 levels in acromegaly subjects might be associated with the improving effects of growth hormone on liver fat. Acromegaly was linked to higher CIMT, but there was no correlation between FGF-21 levels and CIMT. The role of FGF-21 in acromegaly as a marker of atherosclerosis requires additional research.

Acromegaly is caused by a pituitary adenoma that releases excess growth hormone (GH) and a concomitant increase in insulin-like growth factor 1 (IGF-1). Acromegaly results not only in phenotypic changes, but also in neurologic complications as peripheral neuropathy and cognitive dysfunction. This study aimed to compare depressive mood and cognitive function in patients with acromegaly and in healthy controls as well as to determine the factors underlying cognitive dysfunction in the acromegalic patients. This study included 42 patients with acromegaly that were receiving somatostatin analogue therapy and 44 healthy controls. Memory, attention, visuospatial function, inhibitory function, abstract thinking, verbal fluency, and depressive mood were measured in the patients and controls. Patients with acromegaly had lower learning (p= 0.01), planning (p= 0.03), complex attention and inhibitory function (p= 0.04) scores than the controls. There was no significant difference in depressive mood between the patients and controls (p> 0.05). Gamma knife radiosurgery did not negatively affect cognitive function (p> 0.05). The present findings show that acromegaly negatively affects learning, attention, and planning.

Acromegaly is known to affect peripheral nervous system (PNS) causing carpal tunnel syndrome (CTS) and polyneuropathy. The frequency of these disorders and the evaluation methods vary among studies. In the present study, we aimed to examine PNS of acromegaly patients under somatostatin analogue (SSA) therapy. Forty-eight acromegaly patients (26 F/22 M, 45.58 ± 11.6 years) under SSA treatment and 44 healthy controls (25 F/19 M, 47.46 ± 8.7 years) were assessed by symptom questionnaires, neurologic examination and electrophysiological studies. 87.5 % of the acromegaly patients had at least one abnormal finding regarding PNS. With the incorporation of palm–wrist median nerve conduction velocity method, we detected CTS in 50 % of patients. Polyneuropathy was less frequent (29.2 %). Both conditions were independent from the coexisting diabetes mellitus (p= 0.22 for CTS, p= 0.71 for polyneuropathy). Polyneuropathy but not CTS was more common among biochemically uncontrolled acromegaly patients rather than those under control (p= 0.03; p= 0.68, respectively). Our findings emphasize the high prevalence of peripheral nervous system involvement in acromegaly patients under SSA therapy and importance of neurological evaluation of these patients. Early diagnosis and treatment of the disease may reduce the PNS involvement.

Aim: Increased asymmetrical dimethylarginine (ADMA) is known to disturb endothelial function. ACE inhibitors decrease plasma ADMA levels in diseases associated with endothelial dysfunction. The effects of ACE inhibition on endothelial function and plasma ADMA levels in Type 1 diabetic patients was evaluated in the study. Methods: Thirty Type 1 diabetic patients [29±6 yr; females (F)/males (M): 18/12] and 29 controls (30±6 yr; F/M: 16/13) were recruited. Flow-mediated dilatation (FMD), plasma ADMA and thiobarbituric acid reactive substances (TBARs) were determined at baseline, on day 15 and 90 of 0.5 mg qd trandolapril therapy. Results: Compared to controls, baseline FMD levels were lower (4.7±2.0% vs11.2±3.9%) (p<0.001), plasma ADMA (271.1±48.1 nmol/l vs237.5±25.1 nmol/l) (p<0.05) and TBARs levels [4517.1±2366.9 nmol/malondialdehyde (MDA) vs1775.9±598.7 nmol/MDA] (p<0.001) were higher in diabetic patients. On day 90 of trandolapril treatment, FMD (8.6±4.1%) (p<0.01) increased, ADMA levels (229.6±42.9 nmol/l) (p<0.001) decreased and TBARs levels (1531.8±1036.0 nmol/MDA) (p<0.001) decreased significantly. FMD was negatively correlated with plasma ADMA (r=-0.228, p<0.01), and TBARs levels (r=−0.244, p=0.02), whereas ADMA and TBARs levels were correlated positively (r=0.399, p<0.0001). Conclusions: In conclusion, endothelial dysfunction is associated with elevated plasma ADMA levels in Type 1 diabetic patients. Low-dose ACE inhibition improves endothelial dysfunction and reduces ADMA levels. The antioxidant action of ACE inhibitors may play role in this process.