OBJECTIVETo analyze the clinical features of statin-induced myopathy.

METHODThe statin-induced myopathy case reported as adverse drug reaction (ADR) to the Beijing Center for ADR Monitoring during January 2007 to December 2012 was summarized, patients were divided to myopathy group and rhabdomyolysis group, according to the absence or presence of rhabdomylysis. The clinical characteristics, medication history and outcome were compared between the two groups.

RESULTSA total of 160 statin-induced myopathy cases (54 in rhabdomyolysis group (33.8%) and 106 cases in myopathy group (66.3%)) were collected from the database (mean age: (64.22 ± 13.55) years old, 51.2% male, n = 82). The ADR occurred immediately after the first medication and up to 4 years after medication. Observed clinical features were myalgia, myositis, asymptommatic creatine kinase (CK) elevation or rhabdomyolysis. The average age were (68.54 ± 15.41) years old in rhabdomylysis group and (62.02 ± 12.41) years old in myopathy group (P = 0.004). There was no gender difference between the rhabdomylysis group and myopathy group (P = 0.406) . Twenty-four cases (44.4%) in rhabdomyolysis group and 26 cases (16.5%) in myopathy group were treated with high dose statin (P < 0.001). Percent of simvastatin treatment was significantly higher in rhabdomyolysis group (70.4% (38/54) ) than in myopathy group (32.1% (34/106), P < 0.001). Spearman correlation analysis showed that age, high-dose statin treatment and simvastatin use were all positively correlated with rhabdomylysis (P < 0.001), and the correlation coefficients (r value) were 0.305, 0.290 and 0.364, respectively. Four patients (aged from 71 to 85 years) died because of ADR and all 4 cases received high-dose statin treatment, 3 of them suffered from complex combined diseases, acute disease progression and complex multiple drug use history.

CONCLUSIONSSevere statin-induced myopathy, like rhabdomyolysis, is more likely to occur in old patients, in patients taking high-dose statin, especially simvastatin.

Aged ; Female ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; adverse effects ; Male ; Middle Aged ; Muscular Diseases ; chemically induced ; Myositis ; chemically induced ; Rhabdomyolysis ; chemically induced ; Simvastatin ; adverse effects

Amiodarone ; adverse effects ; Female ; Humans ; Middle Aged ; Muscular Diseases ; chemically induced

Colchicine plays an important role in the treatment of gout and some other diseases. Besides gastrointestinal symptoms, myopathy has been reported as a rare side effect of colchicine in some patients. We report a case of myopathy in a patient with chronic kidney disease caused by high-dose colchicine, and then review literature on colchicine-induced myopathy, so as to provide some experience for the clinical diagnosis, treatment and medication safety. A 51-year-old male patient with 10 years of gout and 5 years of chronic kidney disease history and irregular treatment was admitted to the hospital with complaint of recurrent left wrist arthralgia and emerging lower extremities myalgia after intake of 40-50 mg colchicine in total within 20 days. Laboratory examinations showed significantly increased creatine kinase (CK) and then colchicine-induced myopathy was diagnosed preliminarily. After withdrawl of colchicine and implementation of hydration, alkalization and intramuscular injection of compound betamethasone, the symptoms of arthralgia and myalgia were relieved within 3 days and CK decreased to normal range gradually. According to literature reports, colchicine related myopathy was mostly characterized by proximal myasthenia and myalgia, accompanied by elevated CK level, which usually occurred days to weeks after initial administration of colchicine at the usual dosage in patients with renal impairment or a change in the underlying disease state in those receiving long-term therapy, and the features might remit within three to four weeks after the drug was discontinued. Electromyography of proximal muscles showed myopathy marked by abnormal spontaneous activity and muscle pathology waa marked by accumulation of lysosomes and autophagic vacuoles. Chronic kidney disease, liver cirrhosis, higher colchicine dose and concomitant cytochrome P450 3A4 (CYP3A4) inhibitors were associated with increased risk of myo-pathy. Based on the similar efficacy and lower adverse reaction rate compared with larger dosage, small dose of colchicine was recommended by many important current guidelines and recommendations in the treatment of gout. In consideration of potential risks, colchicine should be used with caution in patients with kidney or liver impairment, and in those taking CYP3A4 or P-glycoprotein inhibitors. For those patients, the drug dose should be adjusted and the latent adverse reactions should be monitored carefully.
Colchicine/adverse effects* ; Gout/drug therapy* ; Humans ; Kidney ; Male ; Middle Aged ; Muscular Diseases/chemically induced* ; Renal Insufficiency, Chronic/complications*

Infection of the central nervous system with Nocardia sp. usually manifests as supratentorial abscesses. Supratentorial and cerebellar abscesses from infection with Nocardia sp. following immunosuppression with long-term corticosteroids for idiopathic thrombocytopenia (ITP) have not been reported. An 83 years-old, human immunodeficiency virus (HIV)-negative, polymorbid male with ITP for which he required corticosteroids since age 53 years developed tiredness, dyspnoea, hemoptysis, abdominal pain, and progressive gait disturbance. Imaging studies of the lung revealed an enhancing tumour in the right upper lobe with central and peripheral necrosis, multiple irregularly contoured hyperdensities over both lungs, and right-sided pleural effusions. Sputum culture grew Nocardia sp. Neurological diagnostic work-up revealed dysarthria, dysphagia, ptosis, hypoacusis, tremor, dysdiadochokinesia, proximal weakness of the lower limbs, diffuse wasting, and stocking-type sensory disturbances. The neurological deficits were attributed to an abscess in the upper cerebellar vermis, myopathy from corticosteroids, and polyneuropathy. Meropenem for 37 days and trimethoprime-sulfamethoxazole for 3 months resulted in a reduction of the pulmonary, but not the cerebral lesions. Therefore, sultamicillin was begun, but without success. Long-term therapy with corticosteroids for ITP may induce not only steroid myopathy but also immune-incompetence with the development of pulmonary and cerebral nocardiosis. Cerebral nocardiosis may not sufficiently respond to long-term antibiotic therapy why switching to alternative antibiotics or surgery may be necessary.
Adrenal Cortex Hormones/*adverse effects/*therapeutic use ; Aged, 80 and over ; Cerebellar Diseases/*chemically induced/*diagnosis/pathology ; Humans ; Immunosuppression ; Male ; Muscular Diseases/*chemically induced/pathology ; Nocardia Infections/*diagnosis ; Purpura, Thrombocytopenic, Idiopathic/*drug therapy

OBJECTIVETo investigate the incidence of rhabdomyolysis, the relationship between striated muscular injury and myocardiac injury, and the role of elevated serum creatine kinase (CK) played in screening these two complications following acute carbon monoxide poisoning (ACOP).

METHODS280 patients with ACOP from January 2001 to April 2003 were analyzed retrospectively. According to the clinical manifestations of striated muscular injury (swelling, pain or serious myasthenia), the patients were divided into two groups: the evident injury group and non-evident injury group.

RESULTSThe abnormality rate of electrocardiogram (ECG) and cardiac troponin I (CTnI) in the evident injury group (43 patients) were significantly higher than in the non-evident injury group (73.8% vs 43.4%, P < 0.001; 77.8% vs 20.9%, P < 0.001). There was a positive correlation between peak CK and MB isoenzyme (CK-MB) in both groups, respectively (r = 0.819, r = 0.795, P < 0.01). There was no correlation in the evident injury group (P > 0.05) and only negative correlation in the non-evident injury group (r = -0.298, P < 0.01) between peak CK and MB ratio (CK-MB/CK). Multiple regression analysis indicated that peak CK and CK-MB were only related with the striated muscular injury and were not affected by the indexes of the myocardial injury (ECG and CTnI); Both peak CK and CK-MB were positively correlated with the coma time before consultation in the non-evident injury group and the latter was also affected by CTnI. The incidence of positive muscular injury symptoms increased with the elevation of CK activity. There was no significant difference either in the ECG abnormality rate between the < 5 times elevated CK level subgroup and the > 5 times elevated CK level subgroup (P > 0.05), or in the CTnI positive rate between the normal CK level subgroup and the < 5 times elevated CK level subgroup (P > 0.05).

CONCLUSIONStriated muscular injury is not a rare complication of ACOP, and always accompanied by myocardial injury. The strikingly elevated serum level of CK in patients with ACOP might be more likely to indicate the striated muscle not myocardiac injury.

Acute Disease ; Adult ; Carbon Monoxide Poisoning ; complications ; Cardiomyopathies ; chemically induced ; diagnosis ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; blood ; Electrocardiography ; Female ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Muscular Diseases ; chemically induced ; diagnosis ; Regression Analysis ; Retrospective Studies ; Troponin I ; blood

Recently apoptotic cell death has been reported in differentiated skeletal muscle, where apoptosis was generally assumed not to occur. To investigate whether apoptosis may contribute to the steroid-induced myopathy, rats treated with triamcinolone acetonide (TA) for 9 days were sacrificed for detecting apoptosis by in situ end labeling (ISEL) and electron microscopy in the soleus muscles. Immunohistochemical stainings of Fas antigen and p53 protein were performed to examine whether apoptosis-related proteins were present in the myopathy. Muscle fiber necrosis and apoptotic myonuclei appeared in the soleus muscles following administration of TA, while control muscles showed no evidences for apoptosis. Fas antigen was not detected in control muscles, but expressed in the soleus muscles of steroid-induced myopathy. Some of the Fas antigen-expressing muscle fibers were positive for ISEL. p53 protein was not detected in any muscle fibers. These findings indicate that TA can induce apoptosis in differentiated skeletal muscles, and Fas antigen might be partly related to apoptotic muscle death in steroid-induced myopathy.
Animal ; Antigens, CD95/analysis ; *Apoptosis ; Female ; Immunohistochemistry ; Microscopy, Electron ; Muscle, Skeletal/*pathology/ultrastructure ; Muscular Diseases/chemically induced/*pathology ; Protein p53/analysis ; Rats ; Rats, Sprague-Dawley ; Triamcinolone Acetonide/*toxicity

No abstract available.
Antiviral Agents/*adverse effects ; Arabinofuranosyluracil/adverse effects/*analogs & derivatives ; Female ; Guanine/*analogs & derivatives/therapeutic use ; Hepatitis B, Chronic/*drug therapy ; Humans ; Male ; Muscular Diseases/*chemically induced

OBJECTIVETo observe the intervention effect of electroacupuncture (EA) at "Weizhong" (BL 40) on rats with bupivacaine-induced multifidus muscle injury, so as to explore the action mechanism.

METHODSA total of 72 rats were randomly divided into a control group, a model group, a Weizhong group and a Shenshu group, 18 rats in each group. Each group was again randomly divided into a 4-day subgroup, a 7-day subgroup and a 14-day subgroup, 6 rats in each subgroup. Rats in the model group, Weizhong group and Shenshu group were treated with intramuscular injection of 0.5% bupivacaine (BPVC) to establish the model of multifidus muscle injury. Rats in the Weizhong group and Shenshu group were treated with EA at "Weizhong" (BL 40) and "Shenshu" (BL 23), 20 min per treatment, once a day. Each subgroup was treated for 4 days, 7 days and 14 days respectively. Rats in the control group and model group were treated with immobilization. The morphology and cross sectional area (CSA) changes of multifidus with HE and Masson staining at different time points were observed; the expression of insulin like growth factor 1 (IGF-1) and myogenic differentiation antigen (MyoD) was measured by immunohistochemical method.

RESULTSAfter the modeling, there were significant morphology changes of multifidus at different time points, which was not fully recovered after 14 days. The morphological observation in the Weizhong group and Shenshu group was superior to that in the model group. At 7th day, the CSA in the Weizhong group was higher than that in the model group (P < 0.05); at 14th day, the CSA in the Weizhong group and Shenshu group was higher than that in the model group (P < 0.01, P < 0.05). At 4th day and 7th day, the expression of IGF-1 in the model group was higher than that in the control group (both P < 0.01); at 4th day, that in the Weizhong group was higher than that in the model group (P < 0.01), and that in the Weizhong group was higher than that in the Shenshu group (P < 0.05), and that in the Shenshu group was as higher than that in the model group (P < 0.05); at 14th day, that in the Shenshu group was higher than that in the model and Weizhong group (P < 0.01). At 4th day, the expression of MyoD in the Weizhong group and Shenshu group was higher than that in the model group (P < 0.01), which was more significant in the Weizhong group (P < 0.01).

CONCLUSIONElectroacupuncture at "Weizhong" (BL 40) and "Shenshu" (BL 23) can both promote the regeneration of multifidus muscle injury. EA at "Weizhong" (BL 40) has a better effect at early phase, which may be related to the up-regulation of IGF-1 and MyoD and the completion of the proliferation of myoblast in advance.

Acupuncture Points ; Anesthetics, Local ; adverse effects ; Animals ; Bupivacaine ; adverse effects ; Electroacupuncture ; Humans ; Male ; Muscles ; injuries ; physiopathology ; Muscular Diseases ; chemically induced ; physiopathology ; therapy ; Rats ; Rats, Sprague-Dawley ; Regeneration

BACKGROUND/AIMS: Clevudine is a potent antiviral agent against HBV. However, long-term clevudine therapy may cause myopathy. This study was carried out to identify the efficacy of entecavir switching therapy in chronic hepatitis B patients experiencing clevudine-induced myopathy. METHODS: One hundred forty six patients with chronic hepatitis B treated with 30 mg of clevudine per day for 73 weeks (range, 36-132 weeks) were enrolled. Among them, clevudine-induced myopathy occurred in 21 patients (14.4%) which was diagnosed if the patients had symptoms related to myopathy with concurrent CK and AST elevation. All the patients who were diagnosed as clevudine-induced myopathy stopped the therapy, and 17 patients (81%) were switched to entecavir 0.5 mg. RESULTS: The patients with clevudine-induced myopathy were switched to entecavir 0.5 mg for median 68 weeks, and all of them showed disappearance of clinical myopathic symptoms and normalization of CK and AST level within median 2.2 months. Eight patients (47%) were HBeAg positive before entecavir treatment, and HBeAg seroconversion was achieved in 2 patients (25%). HBV DNA level was elevated in 3 patients (17.6%) at the time when the patients were diagnosed as myopathy, all of them achieved virological response with entecavir switching therapy. ALT level was elevated in 3 patients (17.6%) before entecavir treatment, all of them showed normalization of ALT level. During entecavir therapy, genotypic resistance to entecavir or virological breakthrough was not noted. CONCLUSIONS: In chronic hepatitis B patients experiencing clevudine-induced myopathy, switching to entecavir 0.5 mg per day showed a resolution of myopathy and adequate viral suppression.
Adult ; Aged ; Alanine Transaminase/analysis ; Antiviral Agents/*adverse effects/therapeutic use ; Arabinofuranosyluracil/adverse effects/*analogs & derivatives/therapeutic use ; Creatine Kinase/analysis ; DNA, Viral/blood ; Drug Resistance, Viral ; Female ; Guanine/*analogs & derivatives/therapeutic use ; Hepatitis B e Antigens/blood ; Hepatitis B virus/genetics ; Hepatitis B, Chronic/*drug therapy ; Humans ; Male ; Middle Aged ; Muscular Diseases/*chemically induced