A 56-year-old woman presents to the emergency department complaining of progressive weakness for the past 3 weeks. Prior to the onset of her symptoms, she was able to ambulate without assistance, and she was fully independent with all her daily activities. Approximately 3 weeks ago, she noted some weakness in her arms and legs on both sides which has progressed to a point where she is having trouble walking up the stairs or lifting any heavy objects. She says it has been difficult for her to get herself up from a chair as well. She has been mostly sitting on her couch or bedbound in the past couple days. She says she has been taking lisinopril for hypertension and atorvastatin for hyperlipidemia for the past five months. On review of systems, she denies fever, recent travel, recent vaccination, sick contacts, chest pain, difficulty breathing, recent trauma or injury, or urinary and bowel incontinence. She denies alcohol or substance use. She works as a gardener. Physical examination shows bilateral weakness in her proximal arms and legs with 3/5 strength in the affected areas. Her brachial and patellar reflexes are 2+. Distal pulses are 2+. Laboratory findings show elevated creatine kinase of 2300 IU/L. TSH is within normal limits.
Considering the most likely diagnosis, which of the following is the most appropriate next step in management?
B) Discontinue atorvastatin
This patient’s clinical presentation is most consistent with statin-induced myopathy. Complaints such as difficulty walking up the stairs, lifting heavy objects, and standing up from a chair are classic presentations of proximal muscle weakness, which is a characteristic finding in patients with statin-induced autoimmune myopathy. There is generally no correlation between the onset of autoimmune activity and how long a patient has been taking a statin. Symptoms may occur soon after the initiation of a statin or they may also appear years after. The mechanism is due to the development of autoantibodies against HMG-CoA reductase, which can be ordered if suspicion is high. However, the most appropriate next step for treatment is discontinuation of the suspected eliciting agent for the most likely differential. Spontaneous improvement in symptoms should be expected within days to weeks. Creatine kinase should be reassessed in 8 weeks to ensure resolution of muscle damage.
Answer choice A: Consult Neurology, is incorrect. Although evaluation by a specialist is important down the line, the first step would be to stop the suspected eliciting agent.
Answer choice C: Obtain anti–acetylcholine receptor antibody, is incorrect. Anti-acetylcholine receptor antibody is associated with myasthenia gravis, which presents as muscle weakness after repetitive use. Most patients describe weakness that is worse at the end of the day. Associated symptoms include ptosis, diplopia, dysphagia, and dysarthria which are absent in this patient.
Answer choice D: Obtain anti-HMG-CoA reductase autoantibody, is incorrect. As described above, anti-HMG-CoA reductase autoantibody should be obtained if suspicion for statin induced myopathy is high. However, the most appropriate next step is discontinuation of the eliciting agent prior to further work up. As long as the patient remains on the medication, it could lead to further muscle damage.
Answer choice E: Obtain CT of the head, is incorrect. The patient’s symmetrical proximal muscle weakness is less likely due to an acute stroke process. Suspicion is low.
Key Learning Point
Although statin-induced myopathy is very rare, when a patient presents with proximal muscle weakness or muscle pain while they are taking a statin, check for creatine kinase level. Discontinue statin if the level is elevated.
