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Treatment Options for Statin-Associated Muscle Symptoms
Statins lower the concentration of low-density lipoproteins LDL and thereby lessen the rate of cardiovascular events; the size of this effect depends on the extent of lowering of the LDL cholesterol concentration. Muscle symptoms are a clinically relevant side effect of statin treatment. This review is based on pertinent publications retrieved by a selective literature search, and on the current recommendations of the European Atherosclerosis Society.
The etiology of SAMS is heterogeneous. SAMS may seriously impair quality of life and cause complications of variable severity, up to and including rhabdomyolysis in about 1 in cases. SAMS often lead to a reduction in the prescribed dose of the statin, while also negatively affecting drug adherence. If the LDL cholesterol concentration is not adequately lowered while the patient is taking a statin in the highest tolerable dose, combination therapy is indicated.
SAMS are important adverse effects of statin treatment because they lessen drug adherence. Patients with SAMS should undergo a thorough diagnostic evaluation followed by appropriate counseling. In most cases, statins can be continued, with appropriate adjustments, even in the aftermath of SAMS.
Low-density lipoproteins LDL are causally involved in the pathogenesis of atherosclerosis e1 — e5. Both the efficacy of statins in reducing cardiovascular risk as well as their safety are undisputed 1 , 2. Statins are therefore recommended in guidelines for cardiovascular prevention e6 — e8. Nonetheless, about one-third of those undergoing long-term treatment report difficulties with routinely taking their medication 3 , 4. A reduced adherence to statin therapy is linearly associated with increased mortality 5.
Improving statin adherence is associated with a reduction in cardiovascular morbidity and mortality, making this an important aim in medical care Table 5 , e9. Data are from a retrospective study with adults, conducted by Maccabi Healthcare Services MHS in Israel between and 5.
Modified from Shalev et al. SAMS are relevant causes of reduced adherence 6 , e However, there is a striking discrepancy between incidences reported and those documented in randomized trials. The incidence of muscle symptoms in randomized trials was low, with little difference between the statin and placebo groups 7 — 9 , e15 , e16 , which could be attributed to numerous factors.
For instance, in some studies, patients were excluded if they presented muscle symptoms or statin intolerance. Slight muscle symptoms were not always systematically recorded. For observational studies without a control group, the actual incidence of SAMS can be overestimated.
SAMS are clinically heterogeneous, with patients reporting proximal, symmetric pain, tension, stiffness, or cramps, which may be accompanied by muscle weakness. From our clinical experience, it seems that people who are physically active are particularly affected Creatine kinase CK; EC 2.
SAMS has been graded differently in the literature. Our proposal for grading is given in eTable 1. CK levels that are elevated to more than ten times the upper limit of normal have an incidence of 1: Severe muscle damage with massive release of myoglobin rhabdomyolysis is even more rare about 1 per patients.
Rhabdomyolysis is accompanied by very high CK activity and myoglobinuria, and it can lead to acute renal failure and death. In this case, the values of troponin, myoglobin, lactate dehydrogenase LDH , glutamic-oxaloacetic transaminase GOT , and glutamate pyruvate transaminase GPT are within a normal range, and the CK level does not vary over time.
Macro CK can be specifically diagnosed by isoenzyme electrophoresis. For physically active patients, a control examination should be carried out following a training break of one week. The clinical procedure depends on the symptoms and the extent of the CK increase. A distinction is made between patients reporting muscle problems who have a CK increase of less than four times the upper limit of normal and those who have it above this limit.
Patients with a CK increase of more than 4 times the upper limit of normal should first discontinue their statin 2. This recommendation is not based on clinical data but rather comes from clinical experience about the potential risks of rhabdomyolysis. The pathophysiology of SAMS is not yet fully understood. Several molecular mechanisms have been proposed Box 1 12 — 18 , which include changes affecting the cellular energy metabolism, signaling protein isoprenylation, and mitochondria 11 — 20 , e18 — e Muscle biopsy analyses support the hypothesis of impaired mitochondrial function, although this has yet to be confirmed e18 — e The risk of SAMS increases with a number of clinical and constitutional factors Box 2 , and its frequency also depends on the statin dose and plasma concentration.
Using standard dosages, such as 20—40 mg of simvastatin daily, leads to pronounced symptoms in one of 10 patients annually. However, the risk increases exponentially with higher dosages. Of particular clinical relevance, the effective concentration of statins can be increased by the concomitant use of medications that interfere with statin degradation, such as macrolide antibiotics or azole antifungals, or grapefruit juice eBox 1 11 , The differential diagnosis of statin-induced and exercise-induced muscle symptoms after endurance sports such as bicycling or running or strength training is difficult, but symptoms induced by statins persist longer and often prevent a further exercise session.
Including an exercise break and then monitoring the CK values can be useful for this. Further, alcohol abuse should be excluded, as this is a common cause of CK level increases and rhabdomyolysis. In the search for causal genetic factors, a strong association between polymorphisms in the SLCO1B1 solute carrier organic anion transporter family member 1B1 gene and SAMS has been found with simvastatin 20 , e SLCO1B1 is a hepatic transporter responsible for the uptake of statins into the liver, among other things.
VA increases the blood concentrations of statins e When combined with simvastatin treatment, this genetic defect confers an increased risk for myopathy of 4. This SLCO1B1 variant affects the plasma concentrations of the following statins listed from most to least affected 21 , Further genetic variants that could potentially affect the effective concentration for statins have also been identified 15 , 23 , e27 — e In particular, patients with diabetes mellitus benefit from statin therapy e There is no correlation between diabetes mellitus and an increased risk of SAMS under statin therapy.
More appropriate laboratory parameters are not known. In our opinion, it is advisable to measure CK activity once prior to initiating therapy, to be able to better determine abnormal elevations of CK activity during therapy. Additionally, urine measurements for the thyroid stimulating hormone TSH , transaminases, a calculated glomerular filtration rate, and protein should be made There are currently no imaging methods that can detect SAMS, although clinical diagnostic algorithms have been proposed in the literature 4 , 27 , e Diagnosis is based on a detailed medical history that includes the typical form of presentation as well as a clear temporal association of symptoms with statin intake, discontinuation, and rechallenge.
Symptoms occur typically four to six weeks after therapy initiation, mostly affecting large muscle groups, such as thighs, shoulder girdle, and upper arm muscles. However, SAMS may even occur after many years of treatment. SAMS often occurs following a dose increase or if an interacting drug has been prescribed eBox 1. A pre-existing asymptomatic myopathy may be unmasked by statins e The typical characteristics of this situation are a pre-existing CK increase or a lack of a decrease in elevated CK activities after statin discontinuation.
Additionally, the delayed disappearance of muscle symptoms after discontinuation may indicate a subclinical myopathy of a different origin.
Additional differential diagnostic information on muscle symptoms and CK increases is given in Box 3a and Box 3b In the majority of cases, no identifiable specific muscle or neurological pathology, or relevant drug interaction is found 29 , 30 , e Large case series show however that patients with muscle complaints during statin therapy can still be treated with a statin. In the Cleveland Clinic Ohio, USA from to , patients with a suspected diagnosis of statin intolerance were examined; patients were subsequently able to undergo continuous statin therapy In so-called n-of-1 trials, patients took a medication break and then were individually assigned to either first a statin and then a placebo, or the reverse, in a double-blind and random manner The patient-reported symptoms were not significantly different between the statin and placebo phases, and most patients were able to return to their original medication after rechallenge.
Taken together, these data show that a very large proportion of the muscle symptoms are not specifically associated with statin therapy. These results are consistent with experiences from other areas of pain research. The challenge in everyday clinical practice is thus to distinguish perception and psychological transfer phenomena, as well as the Hawthorne Effect, from classic, organic myopathies. Only an extremely small proportion of patients will need to permanently discontinue statin medications; for instance, for the HPS participants, only 0.
However, those affected frequently do not tolerate high statin dosages. Prior to initiating a statin therapy, a detailed medical history and the basis investigations outlined should be carried out. The following advice can help prevent SAMS:. New restrictions, contraindications, and dose limitations for Zocor simvastatin to reduce the risk of injuries muscles: An Assessment of survival and Cardiovascular Events. Taking sufficient time for a patient is an important factor for the diagnosis and, in many cases, the key to success.
Many symptoms can be traced back to viral infections, unaccustomed physical activity, and drug interactions. Non—statin-associated muscle diseases also need to be considered Box 3. The doctor—patient interview should take into account fears and expectations, as well as the psychosocial situation, of the person concerned.
A large proportion of allegedly statin-associated muscle symptoms can be otherwise re-assigned. According to expert recommendations 2 , further actions should differentiate between affected patients with a CK elevation of over four times the upper limit of normal and those with no or a low elevation of CK but who are still symptomatic Figure.
In any case, the statin medication should be interrupted if the patient is symptomatic. If the CK levels exceed four times the reference range limit, a rechallenge should be done cautiously under close supervision, using a lower dose or a less potent statin. If the CK levels are not elevated or only elevated to a low level, a statin rechallenge can be carried out more quickly and with the original preparation.
This interruption and rechallenge can help the patient and doctor to determine whether the described symptoms are indeed related to the statin medication eTable 1. However, this is usually not the case. Flow-chart for statin-associated muscle symptoms modified according to Stroes et al. Clinical experience shows that it may be psychologically favorable to carry out the rechallenge with other statins.
Switching to the more potent atorvastatin is often successful, even though it shares the same degradation pathway via cytochrome P 3A4 as simvastatin. However, there are no set rules for this. In fact, some patients presenting muscle symptoms when using atorvastatin can tolerate simvastatin better.
Steroidmyopathie auf Englisch - Deutsch-Englisch Wörterbuch
CHARASH, L.: Anabolic steroids in the management of muscular dystrophy. Pediatrics and J. T. ELLIS: Debilitating muscular weakness and steroid therapy . Muscle weakness in mechanically ventilated patients with severe asthma. Respir Med ; Dekhuijzen PNR, Decramer M. Steroid- induced. 30 Oct At least 5% of patients taking statins have statin-associated muscle .. a placebo, complained of myalgia or muscle weakness at least once (8).