Risk Factors For Myopathy Research Articles

Body composition, muscle function, and physical performance in fibrotic interstitial lung disease: a prospective cohort study

BackgroundPatients with fibrotic interstitial lung disease (ILD) are frequently physically inactive and many ILD subtypes are characterized by risk factors for myopathy; however, the importance of body composition, muscle strength, and physical performance in this population is largely unknown.MethodsPatients were prospectively recruited from a specialized ILD clinic, baseline characteristics were collected from the clinical record, pulmonary function tests were performed per established protocols, and dyspnea was measured using the University of California San Diego Shortness of Breath Questionnaire. Dual-energy X-ray absorptiometry (DXA) was used to assess body composition; handgrip strength to determine muscle strength, and 4-m gait speed to measure physical performance.ResultsOne hundred and fifteen patients with fibrotic ILD including 40 patients with idiopathic pulmonary fibrosis were recruited. The mean age was 69+/− 10 years in men (62% of the cohort), and 66+/− 9 years in women, with mild and moderate reduction in FVC and DLCO, respectively, for both sexes. ILD severity (measured by FVC %-predicted, DLCO %-predicted, or the Composite Physiologic Index in separate models) significantly predicted muscle mass and percent body fat including with adjustment for age, sex, and weight. ILD severity was associated with grip strength and gait speed independent from body composition.ConclusionsILD severity has an important impact on body composition, particularly in men. Future studies are needed to confirm and further explore the possibility of additional pathways through which ILD directly impacts limb muscle function and physical performance.

Methamphetamine as a risk factor for myopathy

IntroductionCardiotoxic effects of methamphetamine have been proposed in many investigations, but the risk of striated muscles involvement among methamphetamine abusers is unknown.MethodsA case-control study has begun in our teaching hospital to examine the association between methamphetamine abuse and myopathy. The study population are adult clients who admit in the electrodiagnostic medicine clinic since January 2015 with complains of weakness. For each subject with myopathy, 2 controls without myopathy are randomly selected from the same population. Self-reported history of methamphetamine abuse is acceptable in both groups.ResultsA total of 56 persons with myopathy and 112 controls have been identified, of whom 5 (9 percent) and 3 (3 percent) had history of methamphetamine abuse, respectively. Persons with history of methamphetamine abuse have about three times greater chance to develop myopathy (95% CI: 1.5–5.1) as compared with controls.ConclusionThere is a misconception among some workers that some illicit drugs such as psycho stimulants can improve their ability to work. In contrast, this study demonstrates that due to harmful effect on the muscles, methamphetamine could diminish the ability to work in long time.Disclosure of interestThe author has not supplied his declaration of competing interest.

Prevalence of Myopathy in Subjects on Statin Therapy Attending the National Center for Diabetes, Endocrinology and Genetics in Jordan

Objective: This study aims to find the prevalence and risk factors of myopathy in subjects on statin therapy. Methods: Cross sectional study was conducted on 1046 subjects on statin therapy for dyslipidemia who were attending the National center for Diabetes, Endocrinology and Genetics [NCDEG] in Jordan between Sep. and Dec. 2012. Questionnaire was used to collect demographic data, medical history and muscular symptoms. Results: The prevalence of muscular symptoms among subjects taking statin was 27.9%, when subjects referred their muscular symptoms to statin the prevalence drop to 16.4%. Bivariate and multivariate analyses showed significant association between muscular symptoms and hypothyroidism, taking medication or substances that are known to interact with statin treatment [Fibrates, Verapamil, Amiodarone, Warfarin, Digoxin or Grapefruit juice [>1 quart/day]], and allopurinol therapy. Conclusions: Statin use is significantly associated with high prevalence of musculoskeletal pain [27.9%]. Although many clinicians perceive myalgia as a minor adverse effect, its clinical significance should not be underestimated, as myalgia could be a major obstacle to treatment adherence.

Inappropriate concomitant use of amlodipine and simvastatin: A report on its incidence in a primary care unit

Sir, Metabolic syndrome (diabetes mellitus, dyslipidemia, hypertension and obesity) is a common metabolic disorder that can be seen around the world. Polypharmacy can be expected in patients with this syndrome and it sometimes causes adverse effects due to drug interaction. An important concern is the inappropriate concomitant use of amlodipine and simvastatin. It is reported that concomitant use can result in double dosing of simvastatin due to common passing of the CYP3A4,[1] and this can be a risk factor for myopathy. Here, the authors report on incidence of inappropriate concomitant use of amlodipine and simvastatin in a primary care unit of a tertiary hospital (the name is blinded due to privacy). Based on the data of 600 dyslipidemic cases in this setting, 120 (20%) cases were administered high-dose simvastatin (40 mg/day). Of interest, 30 (5%) had inappropriate concomitant use of amlodipine and simvastatin. This implies that general practitioners might not know the fact that concomitant use of amlodipine and high dosage of simvastatin can be a risk factor for myopathy.

Clinical features and risk factors of creatine kinase elevations and myopathy associated with telbivudine

With the extensive use of telbivudine, more and more studies reported its association with creatine kinase (CK) elevations and myopathy. However, clinical features of these adverse effects were poorly understood. The aim of the present study was to investigate the clinical features and risk factors of CK elevations and myopathy associated with telbivudine. The serum CK levels of 200 patients who were treated with telbivudine for chronic hepatitis B (CHB) between January 2007 and July 2010 were monitored and analysed along with clinical manifestations. The 3-year cumulative incidence of CK elevations and myopathy was 84.3% and 5%, respectively. CK elevations occurred more frequently in men than in women, and patients aged ≤45 years and with negative HBeAg had higher incidence of CK elevations. There was no difference in CK elevations among patients with different HBV DNA levels. Male, younger age and HBeAg negativity were independent predictors of CK elevations by multivariate Cox regression analysis. There was no association between the occurrence of myopathy and variables including age, sex, HBeAg and HBV DNA. No risk factors of myopathy were identified. CK elevations usually occurred 21 months after starting treatment, and most patients resolved spontaneously without interruption of telbivudine therapy except three patients who had to switch to other agents. In conclusion, CK elevations are common adverse reactions associated with telbivudine therapy, while myopathy is rare. Male, younger age and HBeAg negativity might be risk factors of CK elevations.

Propranolol and the risk of hospitalized myopathy: Translating chemical genomics findings into population-level hypotheses

A recent large-scale, chemical screening study raised the hypothesis that propranolol may increase the risk of myopathy. We tested this hypothesis in a large population to assess whether (1) propranolol use is associated with an increased risk of myopathy and (2) the concurrent use of propranolol with a statin may further increase risk of myopathy. New users of propranolol and other beta-blockers (BBs) aged >/=65 were identified using data from Medicare and drug benefit programs in 2 states (1994-2005). The primary end point studied was hospitalization for myopathy or rhabdomyolysis. We used stratified Cox proportional hazards regression to estimate the multivariate-adjusted effect of propranolol compared to other BBs and controlled for demographic variables, risk factors for myopathy, other comorbidities, and health service use measures. We also assessed whether co-use of propranolol and statin further increases the risk, by including an interaction term for use of propranolol and statins. We identified 9,304 initiators of propranolol and 130,070 initiators of other BBs and found 30 cases of hospitalized myopathy in 15,477 person-years (PYs) of propranolol use and 523 in 343,132 PYs of other BB use. Comparing propranolol with other BB users, the adjusted hazard ratio was 1.45 (95% CI 1.00-2.11) for myopathy and 1.48 (95% CI 0.82-2.67) for rhabdomyolysis. We could not detect interaction between propranolol and statins due to limited power. Similar results were observed when propranolol users were compared to other antihypertensive drug users. Propranolol may be associated with a 45% increased risk of hospitalized myopathy in the elderly. Our study illustrates how results from in vitro chemical screens can be translated into hypotheses about drug toxicity at the population level.

Statin myopathy: Incidence, risk factors, and pathophysiology

3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are generally well-tolerated lipid-lowering drugs. However, they are associated with myopathy, and incidence rates of muscle-related complaints predicted from clinical trials may underestimate rate of occurrence of these side effects in clinical practice. The development of a standardized system for description and documentation of statin-associated myopathy that includes the entire spectrum of muscle complaints would provide valuable data for researchers and clinicians seeking to better understand statin-induced muscle complaints. Among the risk factors for myopathy are polypharmacy, high-dose statin treatment, aging, and diabetes. The etiology of statin-induced myopathy is not well understood, but potential contributing mechanisms include decreases in mevalonate pathway products, mitochondrial dysfunction, alterations in gene expression related to apoptosis and protein degradation, and genetic predisposition.