Some people find symptom relief with coenzyme Q However, small clinical trials haven't substantiated the positive effects. Get your doctor's advice about taking either of these. Change your prescription. If, after a few weeks of statin use, you're still experiencing muscle pain or cramping, you and your doctor might consider going to a lower statin dose or switching to a different statin, possibly one that is designed to be taken less frequently.
Adding another type of cholesterol-lowering drug called ezetimibe Zetia , which hasn't been associated with muscle pain, may also allow your doctor to lower your statin dosage. As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date of last review or update on all articles.
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Get helpful tips and guidance for everything from fighting inflammation to finding the best diets for weight loss Stay on top of latest health news from Harvard Medical School. Recent Blog Articles. A person who experiences muscle pain alongside any other concerning symptoms should seek guidance from a doctor immediately. The exact cause of SAMS is unknown. However, there are many risk factors that may contribute to it, such as having a lower muscle mass or a vitamin D deficiency.
A person experiencing statin muscle pain should contact a healthcare professional to discuss what course of action is best. Statins are drugs that can reduce levels of cholesterol in the blood. Learn about the types, their uses, and the risks of taking statins here.
Taking statins with alcohol has no direct risks, but people should be cautious as alcohol may increase the side effects and complications of statins…. Statins are medication people take to lower their cholesterol and treat heart disease. They may interact with compounds in grapefruit juice. Some cholesterol-lowering drugs work best when a person takes them in the evening, while others are equally effective in the morning. Learn more about…. Statins are a medical treatment for high cholesterol, while fish oil is a dietary supplement.
Learn how fish oil and statins differ. What causes statin muscle pain, and will it go away? Causes Symptoms Risk factors Will it go away? Pain relief Statin alternatives Complications Contacting a doctor Summary Statins are a type of drug that lowers cholesterol levels in the blood. What causes statin muscle pain? What does it feel like? Risk factors for statin side effects. Will the muscle pain go away? How to reduce pain. Statins seem to modulate membrane cholesterol in different tissues, including skeletal muscle Reduction of the cholesterol content of skeletal muscle cell membranes might make them unstable A change in membrane fluidity may affect different ion channels, such as sodium, potassium, and chloride channels, and thus modify muscle membrane excitability.
For example, a dose-dependent reduction of membrane chloride conductance was recorded in muscle fibers of simvastatin-treated rats. Again, the hydrophilic pravastatin had no such effect However, since, as previously mentioned, myotoxicity does not occur in vitro when cholesterol is lowered by inhibiting squalene synthetase, this mechanism seems less plausible. Statins may cause myopathy via impairing calcium signaling. Simvastatin has been shown to trigger mitochondrial depolarization and calcium efflux through the permeability transition pore and sodium-calcium exchanger.
Statins have been shown to trigger a massive calcium release from the sarcoplamsic reticulum via ryanodine receptors. In addition, simvastatin induced long-lasting fura-2 calcium transients in human skeletal muscle that led to activation of calpain and caspaces 3 and 9.
Calcium chelation and ryanodine, via inhibition of calcium-induced calcium release, have been shown to abrogate these effects. These may lead first to an elevated cytoplasmic calcium concentration and consequently to sarcoplasmic reticulum calcium overload resulting in calcium waves There are several case reports of induction of inflammatory myopathies i. These cases are characterized by large elevations of CK levels, a myopathic pattern on electromyogram, and a muscle biopsy showing inflammatory infiltrates.
Discontinuation of statin therapy and immunosuppressive therapy e. Such cases, however, are rare, and in most myopathies there is no evidence of an inflammatory component. More recently, 25 cases of a histologically distinct statin myopathy have been described, in which muscle biopsy demonstrated necrotizing myopathy without significant inflammation. These cases presented with proximal muscle weakness and elevated CK levels that persisted despite discontinuation of the statin and responded to immunosuppressive agents Major histocompatibility complex-I staining was upregulated in nonnecrotic fibers in eight patients with such necrotizing myopathy It is postulated that previously restricted epitopes are exposed by statins and this may trigger an autoimmune myopathy.
Indeed, there is a report of autoantibodies against HMG-CoA reductase in patients with this kind of myopathy In the PRIMO study, the strongest independent risk factor for muscular symptoms in multivariate analysis was a history of myopathy while receiving another lipid-lowering therapy odds ratio Interestingly, although depression current or in the past was not associated with a risk of myopathy, the use of antidepressant medications was associated with a significantly lower prevalence of muscular symptoms 0.
Although there was no effect of sex on the prevalence of myopathy in the PRIMO study, female sex is sometimes considered a risk factor 6. Women are also considered to be at lower risk of developing coronary heart disease, at least before menopause. However, all risk-assessment models take sex into consideration, and meta-analyses of statin trials show that women derive benefit from treatment similar to benefit in men Therefore, the same principles regarding treatment initiation and management should be used in both sexes.
Although the role of the aforementioned genetic polymorphisms in predisposing to statin myopathy is a subject of interest, at present there are insufficient data to warrant pharmacogenetic testing of patients to determine such risk 6.
In the vast majority of cases, CK levels will be normal or only mildly elevated. The presence of contributing factors, such as strenuous exercise and consumption of grapefruit juice, should be assessed.
Depending on the statin used, the use of medications that inhibit CYP3A4 such as azole antifungals, macrolide antibiotic, fibrates, and calcium channel blockers , or CYP2C9 such as amiodarone should be ruled out. Thyroid function should be assessed, as subclinical hypothyroidism may contribute to statin-associated myopathy.
Vitamin D deficiency should also be ruled out and treated if found, as it may cause myalgia. Several small studies have found that correction of vitamin D deficiency may enable patients with a history of statin-associated myopathy to tolerate statins The importance of lifestyle measures, including diet and exercise, should be stressed. Supplements such as CoQ10, vitamin E, and magnesium are often tried, but as previously mentioned, there are very little data to support their use.
Since statins are the only agents with a robust body of evidence proving reduction in clinical end points, every effort should be made to keep high-risk patients on a statin-based regimen. Switching statins may be efficacious. Considering the results of the PRIMO study, the use of statins associated with a lower risk of myopathy, such as fluvastatin or pravastatin, may be considered 4 , although these statins may not be potent enough if a large reduction of LDL cholesterol is needed to reach target values.
Another approach evaluated in several studies involves the use of long-acting statins, mainly rosuvastatin, in low doses or at a reduced frequency 1—3 times a week. For example, in a retrospective analysis of 51 patients with a statin, alternate-day rosuvastatin at a mean dose of 5.
When no statin is tolerated or the maximal tolerable dose of statins fails to reduce LDL cholesterol to target levels, nonstatin therapies should be used. The most commonly used drug is ezetimibe.
It should be noted that currently there are no studies that demonstrate ezetimibe's efficacy in reducing cardiovascular morbidity and mortality. Colesevelam has a better side effects profile and may lead to better patient compliance Given as monotherapy in the Coronary Drug Project study, niacin reduced cardiovascular morbidity and mortality Niacin can also be used in combination with BAS and ezetimibe in statin-intolerant patients requiring a large reduction in LDL cholesterol In extreme cases, when both cardiovascular risk and LDL cholesterol are high despite maximal tolerable drug therapy, LDL apheresis can be used Most statins are lipophilic, which means they passively diffuse into the muscle.
A little statin is better than none, so try taking the lowest dose of a hydrophilic statin once a week. For example, start with rosuvastatin 2. If you can tolerate it, add 2. Another option is to stay on the twice-weekly schedule and raise the dose to 5 mg.
Cho says. These powerful drugs can lower LDL to rock-bottom levels without triggering muscle pain. The only disadvantage is price.
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