Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because patients with stable coronary artery disease are at continued risk of major atherosclerotic events despite effective secondary prevention strategies, there is a need to continue to develop additional safe, effective and well-tolerated therapies for secondary prevention of cardiovascular disease. RATIONALE AND DESIGN: The LoDoCo (Low Dose Colchicine) pilot trial showed that the anti-inflammatory drug colchicine 0.5 mg once daily appears safe and effective for secondary prevention of cardiovascular disease. Colchicine's low cost and long-term safety suggest that if its efficacy can be confirmed in a rigorous trial, repurposing it for secondary prevention of cardiovascular disease would have the potential to impact the global burden of cardiovascular disease. LoDoCo2 is an investigator-initiated, international, multicentre, double-blind, event driven trial in which 5522 patients with stable coronary artery disease tolerant to colchicine during a 30-day run-in phase have been randomized to colchicine 0.5 mg daily or matching placebo on a background of optimal medical therapy. The study will have 90% power to detect a 30% reduction in the composite primary endpoint: cardiovascular death, myocardial infarction, ischemic stroke and ischemia-driven coronary revascularization. Adverse events potentially related to the use of colchicine will also be collected, including late gastrointestinal intolerance, neuropathy, myopathy, myositis, and neutropenia. CONCLUSION: The LoDoCo2 Trial will provide information on the efficacy and safety of low-dose colchicine for secondary prevention in patients with stable coronary artery disease.
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PMID:The effect of low-dose colchicine in patients with stable coronary artery disease: The LoDoCo2 trial rationale, design, and baseline characteristics. 3170 44

A 74-year-old man, with inflammatory arthritis, recently commenced on adalimumab, presented with a 4-week history of left-sided chest pain, malaise and shortness of breath. Admission ECG showed age-indeterminate left bundle branch block. Troponin T was 4444 ng/L (normal range <15 ng/L) and acute coronary syndrome treatment was commenced. Catheter angiogram revealed mild-burden non-obstructive coronary disease. Cardiac magnetic resonance (CMR) was performed to refine the differential diagnosis and demonstrated no myocardial oedema or late gadolinium enhancement. Extracardiac review highlighted oedema and enhancement of the left shoulder girdle muscles consistent with acute myositis. Creatine kinase was subsequently measured and significantly elevated at 7386 IU/L (normal range 30-200 IU/L in men). Electrophoresis clarified that this was of predominantly skeletal muscle origin. Myositis protocol MRI revealed florid skeletal muscle oedema. The MR findings, together with positive anti-Scl-70 antibodies, suggested fulminant immune-mediated necrotising myopathy presenting as a rare mimic of myocardial infarction with non-obstructive coronary arteries, diagnosed by careful extracardiac CMR review.
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PMID:Fulminant immune-mediated necrotising myopathy (IMNM) mimicking myocardial infarction with non-obstructive coronary arteries (MINOCA). 3313 59

Patients with systemic lupus erythematosus (SLE) presenting with chest pain pose a unique diagnostic challenge, with causes ranging from cardiopulmonary disease to esophageal disorders and musculoskeletal chest wall pain. The most common biomarkers for myocardial injury are cardiac troponin T and I (cTnT and cTnI) due to their high sensitivity for the early detection of myocardial infarction. In the idiopathic inflammatory myopathies, cTnT is commonly elevated, and this reflects skeletal muscle breakdown rather than myocardial damage. Similar observations have not been reported in SLE myositis to date. We present two cases of patients with SLE and associated myositis who presented with chest pain and elevated cTnT. Both patients had a normal cTnI, transthoracic echocardiogram, and cardiac magnetic resonance imaging, likely indicating noncardiac chest pain. Clinicians should be aware that the specificity of cTnT might be lower in SLE myositis and that cTnI elevation may be more specific in detecting myocardial insult.
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PMID:Elevated Cardiac Troponin T in Patients with Lupus Myositis Presenting with Noncardiac Chest Pain. 3314 55


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