ECE2017 Eposter Presentations: Pituitary and Neuroendocrinology Pituitary - Clinical (145 abstracts)
1Department of Experimental Medicine Sapienza University of Rome, Rome, Italy; 2Department of Neuroscience- Fatebenefratelli Hospital-Isola Tiberina-Rome, Rome, Italy.
Introduction: Glucose metabolism impairment is a common complication of acromegaly. Somatostatin analogs (SSAs) are used as both first and second line treatment. The effect of SSAs on glucose metabolism in acromegaly is still debated.
Aim: To address the following questions: 1) do SSAs affect glucose metabolism? 2) does the effect correlate with disease control? 3) do different SSAs Lanreotide (LAN) and octreotide LAR (OCT) affect metabolism differently?
Methods: We performed a meta-analysis of prospective interventional studies reporting the use of SSAs for the treatment of acromegaly. We searched MEDLINE, EMBASE, and SCOPUS for English-language studies. Inclusion criteria: minimum 6-month follow-up, glyco-metabolic outcomes before and after SSA treatment. The pooled estimate of a weighted mean was obtained for all outcomes using a random effects model.
Results: Forty-one studies have been included, 20 for LAN (354 patients) and 21 for OCT (569 patients). LAN treatment induced a significant decrease in fasting plasma insulin (FPI) (effect size −8.32, 95% CI: −10.44 to −6.20; P<0.001) and HOMAi (−2.11, 95% CI: −3.54 to −0.69; P=0.004), without changes of fasting plasma glucose (FPG), HbA1c, triglyceridemia, weight and BMI. OCT induced a small increase in HbA1c (+0.146, 95% CI: 0.0430.249; P=0.005), a borderline rise of glucose during OGTT (0.47, 95% CI: −0.01 to 0.95; P=0.053) and significant decrease in FPI (−6.78, 95% CI:−9.37 to −4.18; P<0.001), triglyceridemia (−0.41, 95% CI −0.55 to −0.28; P<0.001), HOMAi (−1.44, 95% CI:−2.54 to −0.34; P=0.010) and HOMAβ (−36.65, 95% CI:−63.21 to −10.08; P=0.007), without any change of FPG. Meta-regression analysis revealed an association between the degree of GH reduction and lowering of HbA1c (P=0.03). Meta-regression also showed a worse post-therapy Hb1Ac outcome with increasing pre-therapy IGF1 levels (P=0.002). The percentage of patients at target for GH and baseline IGF1 explained up to 58% of variance of HbA1c.
Conclusions: LAN and OCT induce a significant decrease in FPI and in HOMAi, without adverse change in FPG. OCT seems to reduce HOMAβ and increase HbA1c, while reducing trygliceridemia. IGF1 and GH-response partially explain the metabolic effect of SSAs.