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A 52-year-old woman is evaluated during a follow-up office visit. She has hypercholesterolemia that was treated with atorvastatin for 5 years. Six months ago, she developed achy thigh muscles. At that time, laboratory studies revealed a serum creatine kinase level of 430 U/L, and she was switched to cholestyramine. Since then, her creatine kinase levels have remained elevated. Her last evaluation 2 months ago revealed a creatine kinase level of 448 U/L. She has remained minimally symptomatic with myalgia during this time. She does not drink alcoholic beverages, and her only large muscle exercise includes walking approximately 1 mile daily. There is no family history of muscle disorders.
On physical examination, vital signs are normal. BMI is 31. There is no rash. On musculoskeletal examination, proximal and distal muscle strength is intact. Neurologic examination is normal.
Laboratory studies reveal a serum creatine kinase level of 550 U/L and a normal serum thyroid-stimulating hormone level.
Which of the following diagnostic studies would be warranted for this patient?
A-Aldolase
B-Antinuclear antibody
C-Erythrocyte sedimentation rate
D-MRI of the thigh muscles
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My name is smart now. So, i can answer Q?
It's tricky.
Mis Dx ..atovastatin myositis.
high cpk, myalgia, obese, daily muscle ex....Myositis
Not SLE
Not hypoTH
i got it. Aldolase A deficiency has been associated with myopathy and hemolytic anemia. Alternative splicing of this gene results in multiple transcript variants that encode the same protein.
Ans, A.
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really, do you want name change forever?
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No.. No.. I am very crazy with my name.
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yeah keep it forever and try again this stupid qs!
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So, is it polymyalgia rheumatica?... Ans , C?
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Correct Answer: D
MRI of the thigh muscles is warranted for this patient. For more than 6 months, this patient has had minor myalgia and a mildly elevated creatine kinase level despite discontinuation of atorvastatin. Statin-related myopathy usually begins within weeks to months after starting the inciting medication and may manifest as myalgia, weakness, and an elevated creatine kinase level. Some affected patients develop myalgia without elevations of the creatine kinase level. In most cases, the symptoms and laboratory abnormality associated with this condition resolve within a few days or weeks of stopping the inciting medication. Approximately 95% of cases of this condition resolve within 6 months.
This patient discontinued atorvastatin 6 months ago and does not have a history of excessive alcohol use, which may cause myopathy. Her normal thyroid-stimulating hormone level excludes hypothyroidism. In this setting, MRI of the proximal muscles, particularly the thighs, would help to assess whether muscle inflammation is present and to help localize a biopsy site.
Unlike electromyography, MRI can screen only a limited number of muscle groups. Nevertheless, MRI of the involved muscle groups, particularly the thighs, is being increasingly employed to initially evaluate a suspected myositis and to monitor disease progression. On MRI, actively inflamed muscle groups demonstrate increased edema within the muscle; this finding is not specific for myositis but does suggest a myopathic process. MRI also is a noninvasive means of localizing a muscle for biopsy. However, the role of MRI in patients with an inflammatory myopathy is still being defined, and the results of this study should be interpreted within the clinical context and should be considered complementary to results of electromyography and nerve conduction velocity studies.
Patients with active muscle disease may have an elevated aldolase level, but this enzyme is less specific for muscle damage than creatine kinase. Furthermore, the results of aldolase measurement would not influence the need to evaluate this patient for inflammatory muscle disease.
Approximately 80% of patients with an inflammatory myopathy have positive titers of antinuclear antibodies. Therefore, the absence of these antibodies would not exclude myositis, and the presence of antinuclear antibodies is not diagnostic of active muscle disease.
Similarly, patients with myositis may have an elevated erythrocyte sedimentation rate, but this finding is a nonspecific marker of inflammation and is not used to diagnose an inflammatory myopathy or to monitor disease activity.
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