Neurosurgery is the first-line treatment for acromegaly. Whether metabolic disorders are reversible after neurosurgery is still debated. The meta-analysis aimed to address the following questions: (i) Does neurosurgery affect glycolipid metabolism? (ii) Are these effects related to disease control or follow-up length?
A meta-analysis and systematic review of the literature.
Three reviewers searched databases until August 2019 for prospective trials reporting glycometabolic outcomes after neurosurgery. Three other extracted outcomes, all assessed the risk of bias.
Twenty studies were included. Neurosurgery significantly reduced fasting plasma glucose (FPG) (effect size (ES): −0.57 mmol/L, 95% CI: −0.82 to −0.31; P < 0.001), glucose load (ES: −1.10 mmol/L, 95% CI: −1.66 to −0.53; P < 0.001), glycosylated haemoglobin (HbA1c) (ES: −0.28%, 95% CI: −0.42 to −0.14; P < 0.001), fasting plasma insulin (FPI) (ES: −10.53 mU/L, 95% CI: −14.54 to −6.51; P < 0.001), homeostatic model assessment of insulin resistance (HOMA-IR) (ES: −1.98, 95% CI: −3.24 to −0.72; P = 0.002), triglycerides (TGDs) (ES: −0.28 mmol/L, 95% CI: −0.36 to −0.20; P < 0.001) and LDL-cholesterol (LDLC) (ES: −0.23 mmol/L, 95% CI: −0.45 to −0.02 mmol/L); P = 0.030) and increased HDL-cholesterol (HDLC) (ES: 0.21 mmol/L, 95% CI: 0.14 to 0.28; P < 0.001). Meta-regression analysis showed that follow-up length – not disease control – had a significant effect on FPG, with the greatest reduction in the shortest follow-up (beta = 0.012, s.e. = 0.003; P = 0.001).
Neurosurgery improves metabolism with a significant decrease in FPG, glucose load, HbA1c, FPI, HOMA-IR, TGDs, and LDLC and increase in HDLC. The effect on FPG seems to be more related to follow-up length than to disease control.