Statins are effective drugs to reduce cardiovascular events secondary to dyslipidemia; however, they cause frequent undesirable side effects. The incidence of statin-induced myotoxicity is presented by 7% to 29% of patients. These changes can be responsible for fatigue, myalgia, cramps, and elevation of serum creatine kinase.3 In this letter, Dr. Jankovic reminded us that statin-induced MSP should be added to the list of causes of pain experienced by patients with PD.
We posit 2 explanations for answering why the proportion of patients with PD taking statins was higher than that of control group: First, patients with PD were more likely to have significant comorbidities such as dyslipidemia4 compared to non-PD patients (16.12% vs 9.85%, P < 0.0001) and statins were the commonly prescribed medication for dyslipidemia. Second, some patients with PD take statins not only for their anti-lipid properties but also as potential disease-modifying therapies. Supporting this therapy are findings in some studies that there is an inverse association between statin use and the risk of PD.1
To validate potential influence of statins, we compared the crude and adjusted HR for MSP among patients with PD with all-kind of statin use, high-risk statin use (simvastatin, atorvastatin, fluvastatin, and lovastatin),2 and nonuse using Cox proportional hazard regression models with adjustment for potential confounders, including sex, age, insurance premium, urbanization level, comorbidities (including hypertension, diabetes, hyperlipidemia, coronary heart disease, congestive heart failure, nephritis, nephrotic syndrome, and nephrosis, anemia, thyroid disease, rheumatoid arthritis, gout, osteoporosis, chronic obstructive pulmonary disease, depression, any types of cancer, and anxiety disorders) and co-medications (including diuretics, renin-angiotensin system inhibitors, calcium channel blockers, beta blockers, insulin, oral antidiabetics, aspirin, opioid analgesics, steroids, estrogens, antidepressants, and anticonvulsant medications). We noted that 39 (7.96%) of 490 patients with PD in our data took statins and 35 (7.14%) of 490 patients with PD took high-risk statins. The analysis failed to find significant associations between MSP and use of statins (adjusted HR = 0.70; P-value = 0.2320; 95% confidence interval 0.39-1.26) and between MSP and use of high-risk statins (adjusted HR = 0.76; P-value = 0.4081; 95% confidence interval 0.42-1.42) in patients with PD (Table 1). However, the weak association may be due to small sample size and thus further investigation is warranted.
The extent to which statin contributes to MSP in patients with PD, to our knowledge, has not been systematically explored. However, given the potential overlap of symptoms between PD-related pain and statin-related muscle and joint pains, we concluded that further studies are need to identify individual risk factors that predict MSP because of the use of statins, especially in PD.