Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016053 (fibromyalgia)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine the prevalence of musculoskeletal disorders in patients with chest pain and angiographically normal coronary arteries. The authors studied 40 consecutive patients with chest pain presenting at an Internal Medicine Clinic who had undergone coronary angiography and were found to have < 30% stenosis of all major coronary arteries. Patients with any known noncardiac cause of chest pain were excluded from the study. Each patient underwent a complete rheumatologic examination with x-rays and blood tests when indicated. The diagnosis of fibromyalgia was based on the presence of at least eight paired tender points. The diagnosis of costochondritis was made when palpation of the costal cartilages elicited tenderness. In the normal coronary artery group, 30% of the patients had fibromyalgia and 10% had costochondritis. In the control group of 40 patients with coronary artery disease, only 1 patient had fibromyalgia and none had costochondritis (P < 0.04). Other rheumatologic disorders were uncommon, with no statistical difference between the two groups. The authors conclude that many patients with chest pain and angiographically normal coronary arteries suffer from rheumatologic disorders with fibromyalgia being the most common.
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PMID:The prevalence of rheumatologic disorders in patients with chest pain and angiographically normal coronary arteries. 774 27

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health, disease, and aging. A wide range of seemingly unrelated disorders, such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis, have underlying pathophysiological mechanisms in common, namely reactive oxygen species (ROS) production, the accumulation of mitochondrial DNA (mtDNA) damage, resulting in mitochondrial dysfunction. Antioxidant therapies hold promise for improving mitochondrial performance. Physicians seeking systematic treatments for their patients might consider testing urinary organic acids to determine how best to treat them. If in the next 50 years advances in mitochondrial treatments match the immense increase in knowledge about mitochondrial function that has occurred in the last 50 years, mitochondrial diseases and dysfunction will largely be a medical triumph.
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PMID:Mitochondrial dysfunction and molecular pathways of disease. 1723 70

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis. Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have stain medications, analgesics such as acetaminophen, and many others. While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine) hold promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies. This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.
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PMID:Medication-induced mitochondrial damage and disease. 1862 87