Appearance Of Myopathy Research Articles

Dealing with the most common side effect of statins

Statins are one of the key drugs in the treatment of cardiology patients. They lower LDL cholesterol levels, thereby reducing the risk of acute cardiovascular events. Statins are among the best studied drugs, and have been proven to be effective and safe in the treatment of dyslipidemia. Data presented in studies on the prevalence of statin intolerance (SI) varies widely, according to some studies, statin tolerance is the same as placebo, however, this is a common problem in clinical practice. The most common reported symptoms of SI include muscle pain. Patients are often afraid of starting satin treatment because of possible side effects. The appearance of myopathy in patients results in their discontinuation of therapy, which results in increased cardiovascular risk. In order to minimize the risk of SI, particularly statin-associated muscular pain (SI), a key role is played by discussion with the patient, exclusion of nocebo effects, identification of risk factors, dose modification and possible discontinuation of the drug. The purpose of this paper is to review the problem of the most common of the adverse effects of statins- myopathy, in terms of incidence, probable cause, and recommended treatment of patients.

P-MU005. Myopathy in primary Sjögren’s syndrome in Dr. Moewardi Hospital Indonesia

Introduction . Myopathies are disorders affecting skeletal muscle. There is a term 'overlap syndrome' when myopathies are associated with another well-defined connective tissue disease. Sjögren’s syndrome is one of the connective tissue disease characterized by hypo- function of salivary and lacrimal glands and possible systemic multi-organ manifestations. Although muscular manifestations are very common with Sjögren’s syndrome, true myopathy is very rare. Myopathy inflammatory has been reported in less than 3% of patients. The aim of the case report is to report a case of myopathy in primary Sjögren’s syndrome in Dr. Moewardi hospital Surakarta. Results . 22 years old female, with the weakness of all four extremities, arthralgia, myalgia, and shortness of breath due to respiratory failure. The weakness was heavier in the proximal. Schirmer’s test ≤5 mm/5 min in left eye. From the results of laboratory examination obtained increased CK, SGOT, and SGPT. From cerebrospinal fluid examination, no dissociation of cytoalbumin was found. There was a positive (strong) result on La / SS-B antigen. Muscle biopsy showed hyalinized muscle. Plasmapheresis was performed on this patient. The patient received intravenous methylprednisolone, azathioprine, and folic acid therapy. The patient did not improve after the plasmapheresis and immunosuppressant administration. Conclusion . Skeletal muscle involvement in primary Sjögren’s syndrome is a relatively rare complication. Some signs, symptoms, and laboratory results support the appearance of myopathy in this case. Muscle biopsy is the gold standard examination for diagnosed myopathy. In Sjögren’s syndrome, the type of myopathy that is often found is myositis. In this case, there was a hyalinized muscle that supports myopathy but no inflammatory cells were found on the muscle biopsy. Myopathy in Sjögren’s syndrome responded favorably to high- dose steroids. In this case, there was no improvement after immunosuppressant administration.

A Case of Neuromyopathy Due to Synthetic Antimalarial Drugs

Introduction: Synthetic anti malaria drugs has effectiveness in the treatment of many auto-immune diseases and principally the systemic erythematous lupus. The undesirable effects remain rare. The appearance of myopathy is considered as exceptional. We report observations which highlight the hypothesis of a double toxicity (Chloroquine and Hydroquinine). Observation: We report a case of 53 years old female patient treated chronically by Hydroquinidine and Escitalopram for Bouveret diseases which became asymptomatic. Later on, we had Chloroquine and Prednisone to the previous treatment. Prednisone was removed few months later because of a possible skin side effect. Due to the incomplete relief of joint pain we had Methotrexate to the treatment associated to Omeprazole. And the evolution was characterized by the appearance of lower limbs muscle weakness leading to the interruption of Methotrexate- Omeprazole association. Despite this interruption there was a worsening of the muscle weakness clinically and electro-physiologically diagnosed as myopathy which leads to the interruption of Chloroquine and Hydroquinidine. Other causes of myopathy have been ruled out after a large check-up and Methotrexate was re-introduced two months later with progressive regression of symptoms within six months. Discussion and conclusion: The appearance of myopathy in a patient treated by Chloroquine is extremely rare. Our observation highlights the toxicity of synthetic antimalarial drugs which can cause myopathy in some cases. The association of Chloroquine and Hydroquinidine seems potentially more toxic on muscles.

Quantitative and qualitative adaptations of muscle fibers to glucocorticoids.

The aim of this study was to understand the effects of short-term glucocorticoid administration in healthy subjects. Five healthy men received dexamethasone (8 mg/day) for 7 days. Vastus lateralis muscle biopsy and knee extension torque measurement were performed before and after administration. A large number of individual muscle fibers were dissected from the biopsy samples (pre-administration: n = 165, post-administration: n = 177). Maximal knee extension torque increased after administration (∼ 13%), whereas both type 1 and type 2A fibers had decreased cross-sectional area (type 1: ∼ 11%, type 2A: ∼ 17%), myosin loss (type 1: ∼ 18%, type 2A: ∼ 32%), and loss of specific force (type 1: ∼ 24%, type 2A: ∼ 33%), which were preferential for fast fibers. Short-term dexamethasone administration in healthy subjects elicits quantitative and qualitative adaptations of muscle fibers that precede (and may predict) the clinical appearance of myopathy in glucocorticoid-treated subjects.

Up-Regulation of MHC Class I Expression Accompanies but Is Not Required for Spontaneous Myopathy in Dysferlin-Deficient SJL/J Mice

We found that up-regulation of major histocompatibility complex (MHC) class I expression accompanies, but is not required for, appearance of spontaneous myopathy in SJL/J mice. In some neuromuscular diseases, MHC class I expression is markedly up-regulated in muscles, though the consequences of this up-regulation for pathology are not clear. To study MHC class I in myopathy, we compared muscles of SJL/J mice to muscles of SJL/J mice that were also MHC class I-deficient due to targeted mutation in the beta-2-microglobulin gene (SJL/J B2m (-/-) mice). SJL/J mice show spontaneous myopathy and have a mutation in the dysferlin gene, a gene which is also mutated in human limb-girdle muscular dystrophy type 2B (LGMD2B). Muscles of eight-month-old SJL/J mice had higher levels of MHC class I expression than muscles of either C57BL/6J (wild-type) or SJL/J B2m (-/-) mice. In contrast, the percentage of abnormal muscle fibers was similar in SJL/J and SJL/J B2m (-/-) muscles. Invading Mac-1(+) cells were most abundant in SJL/J B2m (-/-) muscles, moderately abundant in SJL/J muscles, and rare in C57BL/6J muscles. Thus, MHC class I was markedly up-regulated in SJL/J muscles, but this high level of MHC class I was not necessary for the appearance of myopathy.