Like mutations with loss of function in the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene, inhibitors of PCSK9 (PCSK9i) may potentially favor the manifestation of diabetes. RESEARCH DESIGN AND METHODS A meta-analysis of phase 2/3 randomized clinical trials (RCTs) assessed PCSK9i versus placebo in the primary hypercholesterolemia setting. Statins and ezetimibe were used in 98.4% of these studies and balanced between PCSK9i and placebo. We calculated relative risks (RRs) and 95% CIs using random-and fixed-effect models. RESULTS We included 68,123 participants (20 RCTs) with median follow-up of 78 weeks. PCSK9i increased fasting blood glucose (weighted mean difference 1.88 mg/dL [95% CI 0.91-2.68]; I 2 = 0%; P < 0.001) and HbA 1c (0.032% [0.011-0.050]; I 2 = 15.5%; P < 0.001) when compared with placebo. This effect was not sufficient to increase incidence of diabetes (RR 1.04 [0.96-1.13]; I 2 = 0%; P = 0.427). Exploratory meta-regression analyses indicated an association between the increased risk of diabetes and the potency (P = 0.029) and duration (P = 0.026) of PCSK9i treatment. CONCLUSIONS In the short term, PCSK9i therapy favors a small but significant increase in plasma glycemia and HbA 1c .

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Our data confirm the current validity of the reference values obtained in 1981, which continue to be significantly different from those of the UniCAP method for Swedish donors. The population of allergic subjects can be divided into two subgroups: subjects with total IgE levels similar to those of the donors, which we refer to as LRs, and which represent 44% of all allergic subjects, and a second subgroup with total IgE values above those of the donors (HRs), who would therefore be the only subjects that would be identified by individual serum IgE study.