Myopathy is possibly the most clinically relevant statin-induced side effect.
We report a case of a 63-year-old healthy male with mixed dyslipidemia. He developed bilateral myalgia of the forearms with fluvastatin 40 mg/day, pravastatin 20 mg/day, and combination of atorvastatin 10 mg and ezetimibe 10 mg/day. The only hypolipidemic treatment that was tolerable was the combination of pitavastatin 1 mg and ezetimibe 10 mg/day.
Pitavastatin demonstrated less potential for the development of myalgia compared to the so far considered most tolerable statins (i.e., fluvastatin and pravastatin). All the tested statins were used at the lowest approved dose for clinical use.
The combination of pitavastatin 1 mg and ezetimibe appears to be a promising treatment choice for individuals who are intolerant to statin therapy due to muscle complaints.

Statins represent the elective lipid-lowering strategy in hyperlipidemic and high cardiovascular-risk patients. Despite excellent safety and tolerability, reversible muscle-related and dose-dependent adverse events may decrease a patient\'s compliance. Large meta-analyses, post-hoc and genetic studies showed that statins might increase the risk of new-onset diabetes (NOD), particularly in insulin-resistant, obese, old patients. Race, gender, concomitant medication, dose and treatment duration may also contribute to this effect. Based on this evidence, to warn against the possibility of statin-induced NOD or worsening glycemic control in patients with already established diabetes, FDA and EMA changed the labels of all the available statins in the USA and Europe. Recent meta-analyses and retrospective studies demonstrated that statins\' diabetogenicity is a dose-related class effect, but the mechanism(s) is not understood. Among statins, only pravastatin and pitavastatin do not deteriorate glycemic parameters in patients with and without type 2 diabetes mellitus. Interestingly, available data, obtained in small-scale, retrospective or single-center clinical studies, document that pitavastatin, while ameliorating lipid profile, seems protective against NOD. Beyond differences in pharmacokinetics between pitavastatin and the other statins (higher oral bioavailability, lower hepatic uptake), its consistent increases in plasma adiponectin documented in clinical studies may be causally connected with its effect on glucose metabolism. Adiponectin is a protein with antiatherosclerotic, anti-inflammatory and antidiabetogenic properties exerted on liver, skeletal muscle, adipose tissue and pancreatic beta cells. Further studies are required to confirm this unique property of pitavastatin and to understand the mechanism(s) leading to this effect.