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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rhabdomyolysis can be induced by a variety of physical and chemical insults to skeletal muscle. Though there are only a few reports of myositis associated with viral diseases, and no reported cases of virus-induced rhabdomyolysis in uremic patients. Chronic uremic states have been known to potentiate a variety of metabolic and immunological abnormalities. Present case had an acute, progressive and fatal rhabdomyolysis which was thought to be induced by virus infection. A 43-year-old man had received hemodialysis therapy for 8 years. He suffered from an upper respiratory tract infection 11 days before admission. On admission, he was diagnosed as rhabdomyolysis with severe lactic acidosis and marked hyperkalemia. Although intensive care had been performed, he died of uncontrollable hyperkalemia (10.0 mEq/L) 2 days after admission. Maximum CPK and GOT levels were 105,200 and 56,800 mU/ml, respectively. Most probable cause of rhabdomyolysis was thought to be Parainfluenza type-3 infection, though histological examination failed to prove virus infection.
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PMID:A case of rhabdomyolysis in chronic renal failure. 303 62

The benefits of blood pressure lowering, lipid lowering, and glycemic control on morbidity and mortality have been established in major long-term clinical trials. The most extensive information is available for diuretics or beta-blockers in hypertension, hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) in dyslipidemia, and insulin or sulfonylureas in diabetes. Other drug classes provide similar improvements in blood pressure, lipid profile, and glycemic control, and thereby might be expected to provide comparable long-term benefits. As a result, national guidelines advocate treating patients aggressively in order to achieve control of blood pressure low-density lipoprotein (LDL) cholesterol, and blood glucose. The risks associated with drug treatment are generally class-specific. Among antidiabetic agents, sulfonylureas and insulin are associated with risk for severe hypoglycemia, metformin with risk for lactic acidosis, and troglitazone with risk for idiosyncratic hepatocellular injury. Similarly, widely used antihypertensive and lipid-lowering agents are associated with risk for serious complications, such as angioedema with angiotensin-converting enzyme inhibitors, possible increased risk for myocardial infarction and cancer with calcium antagonists, and myositis and liver dysfunction with statins. Physicians must take an aggressive approach to patient management in order to achieve a level of disease control that optimally reduces risk for morbidity and mortality. Serious adverse events may occur rarely with most drug classes; these events can be minimized by appropriately monitoring or selecting patients for treatment.
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PMID:Safety of drugs commonly used to treat hypertension, dyslipidemia, and type 2 diabetes (the metabolic syndrome): part 1. 1146 7

Lactic acidosis (LA), a rare but life-threatening adverse effect associated with antiretroviral therapy, has been reported with an increasing frequency since the mid-1990s. From June 1994 to June 2002, a total of six patients, four males and two females with a median age of 43 years (range, 30 to 74 years), had been diagnosed with LA. The estimated incidence of LA was 5.1 per 1000 patient-years (PYs) on highly active antiretroviral therapy (HAART) (95% confidence interval [95% CI], 4.5-5.5 per 1000 PYs) and 4.4 per 1000 PY on nucleoside analogues (NAs) (95% CI, 3.9-4.7 per 1000 PYs). Their median body mass index at diagnosis of LA was 17.6 kg/m(2) (range 16.3 to 22.6 kg/m(2)). The median CD4+ lymphocyte count at the initial diagnosis of HIV infection and at the onset of LA was 38 cells/ micro L (range, 4 to 103 cells/ micro L) and 108 cells/ micro L (range, 79 to 224 cells/ micro L), respectively. The most common symptoms were nausea, vomiting, and dyspnoea. All of the patients had findings suggestive of NA-related mitochondrial toxicity, such as myositis, pancreatitis, fatty hepatitis, peripheral neuropathy or lipodystrophy. The prescribed NA related to LA were stavudine in six patients, lamivudine, five, and didanosine, one. Despite treatment, all patients died of persistent circulatory collapse following LA. The median duration from diagnosis to death was eight days (range, 4-17 days). Our report highlights that clinicians caring for patients with AIDS should be alerted to the potentially fatal LA associated with antiretroviral therapy when patients present with low body mass index, lipodystrophy, unexplained abdominal symptoms, dyspnoea, or elevated aminotransferases.
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PMID:Fatal lactic acidosis associated with highly active antiretroviral therapy in patients with advanced human immunodeficiency virus infection in Taiwan. 1507 19

Apical hypertrophic cardiomyopathy (AHC) is associated with neurological abnormalities such as transient ischemic attack, stroke, limb-girdle muscular dystrophy, or eosinophilic myositis in single cases. The association of AHC and metabolic myopathy has not been reported. In an 84-year-old woman with long-standing gait disturbance, dementia, Parkinson syndrome, ptosis, ophthalmoparesis, tetraparesis, polyneuropathy, lactacidosis, polyarthralgia, dorsalgia, and osteoporosis, cardiac examination for long-standing anginal chest pain and palpitations, revealed supraventricular and monomorphic ventricular ectopic beats, hypertrophic signs, ST-depression and negative T waves on electrocardiogram (ECG), diastolic dysfunction with impaired relaxation, and AHC on transthoracic echocardiography. AHC was confirmed by cardiac magnetic resonance imaging, which additionally showed a small left ventricular apical aneurysm with a wall-thickness of only 3 mm. The patient was suspected to additionally have a multisystem disease, most likely due to impaired oxidative metabolism. This case shows that AHC may take a mild course and be associated with a number of extracardiac abnormalities.
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PMID:Apical hypertrophic cardiomyopathy in encephalomyopathy. 1816 25

A patient with a known family history of mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) due to the MT-TL1 m.3243A>G mutation presented with mild myalgia and very minor upper limb proximal muscle weakness. Muscle histology revealed low levels of cytochrome oxidase-negative fibres and non-specific myositis. Using the last "hot cycle" polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP), the MELAS MT-TL1 m.3243A>G mutation was only detected in urine, and not in hair, blood or skeletal muscle. This report highlights the need to screen various tissues to achieve an accurate mitochondrial genetic diagnosis and suggests the likelihood of myositis arising secondary to the MELAS MT-TL1 m.3243A>G mutation.
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PMID:Association of the MELAS m.3243A>G mutation with myositis and the superiority of urine over muscle, blood and hair for mutation detection. 1950 62