吃降血脂藥物的病人不少，必須要注意病人的酸痛是否為藥物引起。尤其是吃降血脂statins藥物。
摘要下文:
statins 類藥物引起的肌肉病變，一般來說是不會造成永久的肌肉傷害，也不需要特殊的治療。
多侵犯近端肌肉，且對稱性。
多數血中CK濃度昇高，也可能是正常的。
症狀的發生多在治療開始數周至數月，但也可能在治療的任何期間。多在停藥後數月，症狀才會消失，
The statins are increasingly used to lower the serum cholesterol concentration for both primary and secondary prevention of coronary disease.
Statins are both effective and generally safe. Although uncommon, muscle toxicity remains a concern. However, severe myopathy is unusual, affecting perhaps 0.1 percent of patients and, in patients with normal serum CK, there is no evidence of permanent or progressive muscle injury [1].
MYOPATHIC SYNDROMES ASSOCIATED WITH STATIN THERAPY - Myopathic syndromes associated with statin therapy range from myalgias to myositis to overt rhabdomyolysis, which may be associated with acute renal failure [2,3].
However, experience in clinical practice suggests that muscle side effects are relatively common, including side effects requiring discontinuation of statin therapy.
Time course of myopathy - The onset of muscle symptoms is usually within weeks to months after the initiation of statin therapy but may occur at any time during treatment. As an example, a review of 44 cases of statin-associated myopathy found a mean duration of therapy before symptom onset of 6.3 months (range 0.25 to 48 months); approximately two-thirds of patients had onset of symptoms within six months of starting therapy [7]. Myalgias and weakness resolve and serum creatine kinase concentrations return to normal over days to weeks after discontinuation of the drug. In the above study, the mean time to resolution of symptoms in 43 patients who discontinued statin therapy was 2.3 months (range 0.25 to 14 months); 58 percent had resolution of symptoms within one month and 93 percent had resolution within six months No other treatment is necessary except for supportive care in patients who develop rhabdomyolysis.
Myalgias - The incidence of "benign" myalgias in large clinical trials of statin therapy ranged from 2 to 11 percent, a value not different from placebo-treated controls [8-11]. Similarly, an elevation in serum CK above normal occurred in approximately 30 percent of both statin-treated and placebo-treated groups [9]. However, we have seen patients who had new onset myalgias and fatigability temporally related to statin therapy. The symptoms gradually resolved with statin discontinuation and recurred with statin reintroduction.
The issue of statin-associated myopathy with normal serum CK has been directly addressed in a crossover study in which 4 of 21 blinded patients who had muscle symptoms while taking a statin (aching, weakness, decreased exercise tolerance) could distinguish statin therapy from placebo because of reproducible muscle symptoms [12]. Strength testing confirmed muscle weakness during statin therapy that resolved during placebo treatment; unblinded review of muscle biopsies showed evidence of mitochondrial dysfunction that also reversed with cessation of therapy. Serum statin concentrations were not inappropriately elevated.
Statin-induced myalgia typically presents as proximal, symmetric muscle weakness and soreness [13]. There may be muscle tenderness and there may be functional impairments such as difficulty raising the arms above the head, arising from a seated position, or climbing stairs. Less often the discomfort is asymmetric. Other reported symptoms include cramping (including nocturnal cramping) and tendon pain [13].
Myositis - Clinically significant myopathy, defined as a serum CK elevation more than 10 times normal in association with muscle symptoms, occurred in less than 0.5 percent of patients in the large clinical trials [8-11]. A review of one year of records for 1014 patients taking statins in a primary care practice found that 0.9 percent of patients had CK elevations more than five times normal, and none of these appeared to be related to statin use [14]. Fourteen patients (2.1 percent) had elevations 2.5 to 5 times normal and, of these, two appeared to be potentially related to statin use.
