Zollinger-Ellison syndrome is an often progressive, persistent and frequently life-threatening disease, described for the first time as characterized by ulceration of the upper jejunum, hypersecretion of gastric acid and non-beta islet cell tumors of the pancreas; this syndrome is due to the hypersecretion of gastrin. We report a case of Zollinger-Ellison syndrome presenting as severe esophagitis evolving in stenosis, which demonstrates how a delayed diagnosis may induce risk of disease spreading. In this setting new diagnostic approaches, such as somatostatin receptor scanning and positron emission tomography with 68 Ga-labeled octreotide, could be particularly useful, as well as further new therapeutic options, such as molecular targeted treatments and peptide receptor radionuclide therapy, though surgery is currently the only form of curative treatment, and the role of the therapeutic options mentioned needs to be clarified by forthcoming studies.

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A pooled analysis [1] does not found worse safety profiles in patients reaching very low values of LDL-Cholesterol (<25 and <15 mg/ dl) compared to higher LDL-Cholesterol levels. Authors concluded that aggressive alirocumab therapy seems generally well tolerated. We raise some methodological questions.First, Authors' analyses used propensity scores from regression models lacking in predictors of safety endpoints, while covariates must be associated to both outcome and exposition: associations with exposition only affect the analytical precision and do not adjust for possible confounders [2].Second, limiting the evaluation to alirocumab therapies and focusing to very-low LDL-Cholesterol values subgroups reduces the power of comparisons and increases the risk of false negatives. The apparent lack of association between the LDL-Cholesterol <25 and <15 mg/dl and the risk of neurocognitive disorders can be due to the scarce power of these analyses. Indeed, the sample size of the groups exposed to those targets [1] can demonstrate with sufficient statistical power (≥80%), only very large hypothetical increases in risk of neurocognitive events (RRs ≥2.6 and ≥3.4 respectively).