Introduction: While searching for mechanisms contributing to the increased mortality of acromegaly, we have previously described an unexpected sympathoinhibition in newly diagnosed patients (Seravalle et al., Clin Endocrinol 77:262, 2012) and interpreted this finding as an adaptive phenomenon. It has also been shown that centrally administered somatostatin (SS) inhibits peripheral sympathetic outflow in rodents (Rettig et al., Am J Physiol 257:R588, 1989). Based on the above, we elected to study muscle sympathetic nerve activity (MSNA) in acromegalic patients before and during treatment with SS analogues (SSA).
Study: MSNA was directly measured by microneurography in the following groups of subjects: i) 24 newly diagnosed acromegalics (13 men and 11 women, mean age 45.5±13.0 years); ii) 22 patients on SSA, 11 of whom (seven men and four women, mean age 52.4±13.9 years) attaining biochemical control according to the currently accepted criteria and 11 (five men and six women, mean age 56.4±17.5 years) not attaining biochemical control; iii) 17 normal-weight healthy subjects serving as controls (11 men and six women, mean age 49.1±15.6 years).
Results: As expected, mean MSNA was significantly lower in untreated acromegalic patients than in control subjects (18.3±8.39 vs 37.8±6.60 bursts/min, P<0.01). Patients on SSA, either with controlled or uncontrolled disease, displayed mean MSNA values (27.4±8.24 and 31.6±3.27 bursts/min respectively) significantly lower than those shown by controls (P<0.01) but significantly higher than those found in untreated acromegalics (P<0.05). Mean MSNA values were not significantly different between controlled and uncontrolled SSA-treated patients.
Comment: The present study has confirmed the profound sympathoinhibition characterizing untreated acromegaly and has shown the reversibility of this alteration with the improvement of the disease. These preliminary data do not allow to unveil a possible role of SSA in these changes.