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

Ten children, three girls and seven boys, aged 4-10 years, were admitted with benign acute childhood myositis during spring and winter months (March 1988 to March 1990). They presented with an acute onset of symmetrical calf muscle pain and tenderness, weakness and inability to walk a few days after a flu-like illness. All had raised serum creatine kinase and a normal erythrocyte sedimentation rate, and the majority had low peripheral white blood cell counts with relative lymphocytosis. Serum aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase were found to be raised in four patients. Virological studies performed in six children gave negative results. Full clinical recovery was achieved within 1-7 days. One child developed a second episode. These ten cases of benign acute childhood myositis are the first to be reported from this region.
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PMID:Benign acute childhood myositis in Kuwait. 128 48

Infused beta 2 agonists have been shown to cause focal myocardial necrosis. Serum creatine kinase activity was compared in 13 patients with brittle asthma currently being treated with subcutaneous terbutaline and an age and sex matched control group of patients with moderate asthma having inhaled treatment only. The median serum total creatine kinase activity for patients receiving subcutaneous terbutaline (211 units/l) was greater than that for the control group (120 units/l). The cardiac specific isoenzyme component of creatine kinase was not raised in either group, and the electrocardiograms and serum aspartate aminotransferase activity were normal. Electromyograms in five patients receiving subcutaneous terbutaline with high creatine kinase activity showed changes consistent with myositis in two, one of whom was subsequently shown to have a metabolic myopathy, which is thought to be long standing. No pathological changes were seen in the myocardium at necropsy in a patient who died from an acute attack of asthma while taking subcutaneous terbutaline. These results suggest that the raised creatine kinase activity seen in patients receiving this treatment is unlikely to be myocardial in origin.
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PMID:Creatine kinase activity in patients with brittle asthma treated with long term subcutaneous terbutaline. 192 27

An outbreak of muscle disease affected approximately 20 of 600 ewes in spring 1987 in south-east Scotland. The clinical signs were a flaccid paralysis of the hind limbs and in severe cases collapse. Serum creatine kinase and aspartate aminotransferase activities were increased. Clinically affected sheep had a mean reciprocal serum antibody titre in a sarcocystis immunofluorescence antibody test of 557 whereas 22 sheep from the same flock, sampled one year earlier, showed a mean reciprocal titre of only 51. Histologically a heavy infestation of sarcocysts, myodegeneration and a non-suppurative myositis centred on degenerating sarcocysts were observed in a wide range of skeletal muscles and myocardium from four affected sheep. Monensin sodium had been inadvertently included in the protein pellet used in the feed for one week before the onset of the disease.
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PMID:A myopathy of sheep associated with sarcocystis infection and monensin administration. 250 29

In 1985 and 1986, large-scale natural die-offs of sandhill cranes in Texas were attributed to fusariomycotoxicosis. These birds demonstrated a progressive loss of motor control to the neck, wings, and legs. Based on necropsy and/or histopathology of 31 cranes, the most common lesions involved skeletal muscle and included hemorrhages, granulomatous myositis, thrombosis, and vascular degeneration. Serum chemistry results revealed that levels of creatinine kinase, aspartate aminotransferase, and alanine aminotransferase were above published normals. However, only alanine aminotransferase was higher in clinically affected cranes than in normal cranes collected from the same area.
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PMID:Suspected fusariomycotoxicosis in sandhill cranes (Grus canadensis): clinical and pathological findings. 277 94

Wick catheters were used to measure intracompartmental pressures of the extensor carpi radialis muscles and long heads of the triceps brachii muscles of 7 horses maintained under halothane anesthesia during controlled ventilation. Horses were positioned in left lateral recumbency on a water bed for 4 hours. Using a crossover design, 6 of the 7 horses were subjected to normotensive and hypotensive anesthesia on separate occasions. Hypotension was achieved by increasing the inspired halothane concentration. Hematologic and biochemical measurements were determined at designated intervals before, during, and for 7 days after each anesthetic episode. Under hypotensive conditions, 2 horses developed severe generalized myositis and were euthanatized. Three of the 5 other horses developed swelling of the downside masseter muscle, 4 demonstrated mild extensor deficits of the downside forelimb, and 1 had a severe extensor deficit of the uppermost hind limb. As a group, the hypotensive horses had markedly increased activities of serum enzymes (creatine kinase, aspartate transaminase, and blood lactate) and abnormalities in calcium-phosphorus homeostasis. Lameness or enzyme alterations were not observed in normotensive horses. Although the intracompartmental pressure values were markedly increased in the muscle bellies of the compressed limbs of all horses, there was a statistically significant difference in intracompartmental pressures between the downside or compressed muscle compartments of the extensor carpi radialis of hypotensive and normotensive horses. High concentrations of halothane may predispose anesthetized horses to postanesthetic myositis, even when protective padding is used. Intracompartmental muscle pressure, as measured by the wick catheter, may not be a reliable predictor of equine postanesthetic lameness.
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PMID:Induction of equine postanesthetic myositis after halothane-induced hypotension. 293 29

Intracompartmental muscle pressures were recorded from the right and left forelimbs (extensor carpi radialis, triceps brachii) of healthy horses maintained in left lateral recumbency while under deep halothane anesthesia for 180 to 240 minutes. Cardiac output, blood pressure, blood gases, and acid-base status were monitored throughout the anesthesia, and electrolyte levels (Ca2+, P+, K+, Cl-, Na+) and enzyme activities (aspartate aminotransferase (AST), creatine phosphokinase (CPK), and blood lactate) were monitored for 7 days. Postanesthetic forelimb lameness was produced in 5 of the 6 horses with this prolonged anesthetic regime. This lameness was associated with muscle plaque formation and clinical signs which were similar to the forelimb lameness sometimes seen in horses after surgical anesthesia. Plasma protein, serum calcium, plasma sodium, and blood urea nitrogen concentrations did not change, whereas significantly increased hematocrit, plasma potassium, and serum inorganic phosphate values were seen at the end of anesthesia, along with a decrease in plasma chloride values. Blood lactate, serum AST, and serum CPK activities were significantly high in the postanesthetic period, although the sequence of the changes differed. Intracompartmental muscle pressures were higher in the left forelimb adjacent to the floor (contact limb), and in the instance of the triceps of the contact limb, the pressures were sufficiently high (greater than 30 mm of Hg) that they may have compromised capillary blood flow. However, these high intracompartmental muscle pressures did not persist when positional changes of the horses were introduced at the end of the anesthetic period. There was no correlation between the severity of postanesthetic lameness and any of the measured values. The results demonstrate an experimentally induced postanesthetic lameness which was primarily related to the development of a myositis. Although the causative factors of this myositis may be multiple, the present study implicates local hypoxia in that increased blood lactate and inorganic phosphate values preceded that increased CPK activity. Intracompartmental muscle pressure in the contact limb were possibly high enough to have restricted local capillary blood flow.
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PMID:Equine postanesthetic forelimb lameness: intracompartmental muscle pressure changes and biochemical patterns. 721 25

Plasma CK concentrations have been widely used as the primary muscle enzyme marker for diagnosis and progression of myositis. Recently, total CK and CK-MB serum concentrations have been compared to, and used in conjunction with, serum concentrations of aspartate aminotransferase in diagnosis of myositis. The algorithmic use of CK, AST, and aldolase plasma concentrations to diagnose and categorize patients with myopathy may be a useful method of diagnosing specific muscle disease without invasive procedures. CAIII, as a specific marker for skeletal muscle damage, may replace CK as the enzyme of choice in diagnosis and progression of myositis and other muscle disease. Additional studies are required to determine the usefulness of carbonic anhydrase for the diagnosis and assessment of myositis.
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PMID:Evaluation of laboratory tests as a guide to diagnosis and therapy of myositis. 785 25

Seventy-four patients with plasma low-density lipoprotein cholesterol levels > or = 160 mg/dl after an American Heart Association phase 1 diet were randomized to double-blind treatment with fluvastatin, 20 mg/day, or placebo for 6 weeks. Immediate-release niacin was then added to both treatment regimens and titrated to a maximum of 3 g/day for a further 9 weeks. After 6 weeks of fluvastatin monotherapy, low-density lipoprotein cholesterol levels decreased by 21% (p < 0.001 vs placebo), and after the addition of niacin, response was potentiated to 40% compared with 25% for the niacin control group at study end point (p < 0.001). Fluvastatin, alone and in combination with niacin, also significantly improved high-density lipoprotein cholesterol (increases of about 30%) and triglyceride profiles (decreases of approximately 28%) from baseline. Lipoprotein(a) decreased by 37% in those receiving fluvastatin-niacin but was unaltered in those receiving fluvastatin alone. No serious adverse events were ascribed to fluvastatin, and no cases of myositis were observed. Small, transient, asymptomatic increases in aspartate aminotransferase were noted with fluvastatin-niacin treatment but were not considered clinically relevant. Although the fluvastatin-niacin combination in this study was without evidence of significant transaminitis, myopathy, or rhabdomyolysis, it would seem prudent to continue to monitor its safety with longer term use. In conclusion, fluvastatin, both as monotherapy and in combination with niacin, proved to be an effective, safe, and well-tolerated therapeutic alternative for hypercholesterolemia.
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PMID:Fluvastatin with and without niacin for hypercholesterolemia. 802 79

A double-blind, randomized study was undertaken to evaluate the efficacy and safety of fluvastatin as monotherapy and as combination therapy with niacin in the treatment of hypercholesterolemia refractory to diet. Seventy-four patients with plasma low-density lipoprotein cholesterol (LDL-C) levels > or = 160 mg/dL were treated with fluvastatin, 20 mg/d, or placebo for 6 weeks. Thereafter, immediate-release niacin, at a dosage titrated to a maximum of 3 g/d, was added to both regimens for another 9 weeks. All adverse events were monitored, with particular attention to the evaluation of liver and muscle enzymes. Initial analysis of the data shows that fluvastatin and its combination with niacin was well tolerated and was not associated with any serious adverse events. Small, transient, asymptomatic rises in aspartate aminotransferase (AST) occurred in 28.9% of fluvastatin-niacin treated patients compared to 8.3% in the niacin-placebo control arm (p < 0.05). These were considered clinically insignificant in that no transaminase elevations > 3 times the upper limit of normal occurred. No evidence of myopathy, creatine kinase levels exceeding 10 times the upper limit of normal, myositis, or rhabdomyolysis were demonstrated in this short-term trial. The majority of adverse events resulting in patient withdrawals were ascribed to niacin therapy and included cutaneous vasodilatation, flushing, itching, and rash. These preliminary results suggest that fluvastatin, both alone and combined with niacin, is an effective, safe, and well-tolerated treatment for hypercholesterolemia.
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PMID:Combination therapy with fluvastatin and niacin in hypercholesterolemia: a preliminary report on safety. 819 20

In 14 patients with polymyositis (PM), 5 patients (2 males and 3 females) were positive for anti-hepatitis C virus (HCV) antibody measured by a second generation assay. We analysed the clinical characteristics and histopathological findings of the biopsied muscles from those 5 patients. They aged from 42 to 65 years averaging 53.6 years. Two asymptomatic patients visited our hospital due to elevated muscle enzyme levels, who had slight weakness in their orbicularis oculi and neck muscles on physical examination. The other 3 patients had moderate weakness of the proximal muscles. Anti-nuclear antibody was positive in 2 of the 5 patients and anti-Jo 1 antibody was negative in all patients. The serum enzymes elevated were creatine kinase (215-2, 207 (IU/l)) and glutamate oxaloacetate transaminase (40-119 (KU)). HCV-RNA was positive in the sera of 4 patients examined. All muscle biopsy specimens revealed variation in fiber size with inflammatory cellular infiltration and observed degenerating and regenerating fibers. The scant infiltration type was observed in 2 asymptomatic patients in whom the infiltrated cells were CD4 positive. The endomysial infiltration type was observed in 3 symptomatic patients; CD8 positive cells were found focally to diffusely in 2 patients examined. The expression of class 1 molecules from the major histocompatibility complex was detected mainly in infiltrated fibers to variable degrees. All of the patients showed a good response to the initial steroid therapy. The present study suggests that autoimmune reaction related to HCV infection causes myositis, therefore anti-HCV antibody should be checked in cases of PM.
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PMID:[Clinical characteristics and muscle histopathology in polymyositis positive anti-hepatitis with C virus antibody]. 921 18


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