Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0231528 (myalgia)
 6,565 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Creatine kinase activity was measured in 28 patients in the steady state of sickle cell disease and ranged from 4-45 IU/l, comparable with that found in healthy adult caucasians. Creatine kinase activity was also measured in 14 patients admitted consecutively for the treatment of vaso-occlusive sickle cell crises. Creatine kinase activity remained within the normal range in eight of these 14 patients throughout their admission; none had muscle pain or a chest syndrome. In the remaining six, three with muscle pain and three with a chest syndrome, increased activity was found on one or more days. A further 17 patients with vaso-occlusive sickle cell crises, associated with muscle pain, were studied. Creatine kinase activity was significantly raised in all 17, the mean creatine kinase activity for men was 578.8 IU/l and 210.6 IU/l for women, with the highest values (up to 1790 IU/l) found in those who had exercised before admission. Measurement of creatine kinase activity may therefore be a useful marker of muscle perturbation due to sickling.
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PMID:Creatine kinase activity in sickle cell disease. 276 Feb 31

We studied a family in which seven individuals in three generations had slowly progressive weakness without atrophy, myalgia, cramps, or episodic weakness. Creatine kinase was normal, and EMG showed only slight "myopathic" changes. Neuromuscular transmission was undisturbed. Muscle biopsies were performed in three patients. About 60 to 90% of all fibers contained tubular aggregates. There was a marked variation in fiber size and a marked type II fiber atrophy. Biopsy of an asymptomatic family member was normal. The nature of the underlying disease was obscure.
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PMID:A dominantly inherited myopathy with excessive tubular aggregates. 668 78

Muscle pain is the presenting symptom in patients with a wide variety of conditions. Such patients often pose problems in diagnosis and management and a rational scheme for their investigation is needed. The results of muscle biopsy, electromyography, exercise and strength testing and blood measurements in 109 consecutive patients presenting with myalgia are reported. By determining the sensitivity and specificity of the tests in identifying patients with specific muscle abnormalities, a rational investigative protocol has been constructed. Creatine kinase and erythrocyte sedimentation rate are the most useful screening tests and if either is abnormal, muscle biopsy, electromyography, muscle strength and exercise testing are then performed. Despite exhaustive investigation, specific muscle abnormalities were found in only one-third of the patients; whilst many of the remaining patients undoubtedly had a psychogenic component to their pain, it is likely that a number of unidentified specific metabolic defects remain as causes of myalgia.
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PMID:Investigative strategies for muscle pain. 684 60

Three patients with eosinophilia-myalgia syndrome linked to consumption of L-tryptophan supplement developed a severe sensorimotor axonal neuropathy. All three had myalgia, elevated eosinophil count, and later developed fasciitis. Neuropathy was found at all stages of the illness and resulted in disability which was irreversible despite cessation of L-tryptophan. Nerve conduction studies showed reduced motor and sensory evoked response amplitudes with select sparing of some nerves and the arms were more involved than the legs. Cerebrospinal fluid protein content was increased in one of two patients so tested. Creatine kinase was normal and muscle biopsy showed perimysial inflammation. Sural nerve biopsy in one case showed epineural perivascular inflammation. Our data showed that a severe sensorimotor axonal neuropathy occurs in eosinophilia-myalgia syndrome, suggestive of mononeuritis multiplex.
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PMID:Axonal neuropathy in eosinophilia-myalgia syndrome. 810 5

A 78-year-old woman was admitted to our hospital on September 14, 1992, because of systemic myalgia and stiffness, joint pain, and gait disturbance. She had begun to feel headache and pain in the neck and shoulder in the middle of August, 1992. The pain became systemic, and was accompanied by a low-grade fever, which was unresponsive to NSAIDs. On admission, she had no joint swelling or deformities in the extremities. Neurological examination revealed weakness in the right leg, hypoalgesia below the left C4 level, hyperreflexia in the right extremities, and right Babinski's sign. The erythrocyte sedimentation rate was very high (100 mm/h). Levels of other acute phase reactants were also high. Tests for antinuclear antibody and anti-cardiolipin antibody were positive, but a test for rheumatoid factor was negative. Creatine kinase activity was within normal limits. A T1-weighted magnetic resonance image of the cervical spine at 0.5 T showed an intramedullary low signal. A T2-weighted image showed a borderless spindle-like high signal. Four nodules enhanced by Gd DTPA were seen at C1-C4. The age at onset, myalgia, stiffness, and erythrocyte sedimentation rate were considered to be consistent with a diagnosis of polymyalgia rheumatica. Glucocorticoid treatment was therefore started, and a dramatic clinical improvement was evident within a few days. The patient was discharged from hospital on November 30, 1992. To our knowledge, myelopathy complicated by polymyalgia rheumatica has never been reported previously. Recently, some patients with polymyalgia rheumatica have been reported to have anti-cardiolipin antibody in serum. In the present case anti-cardiolipin antibody may have played a role in the formation of microemboli or in angitis of the cervical spine.
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PMID:[Polymyalgia rheumatica and myelitis associated with anti-cardiolipin antibody]. 1021 70

McArdle's disease or myophosphorylase deficiency is one of the most common muscle glycogenoses and typically presents in childhood or adolescence with exercise intolerance, myalgia, myoglobinuria, and cramps in exercising muscle. We describe an elderly man who developed asymmetric proximal arm weakness at age 73. He had no history of exercise-induced cramps, myalgias, or myoglobinuria. Creatine kinase levels were elevated, serum lactate did not rise on ischemic exercise testing, and muscle biopsy showed a vacuolar myopathy with absent myophosphorylase activity. This unusual case demonstrates that McArdle's disease may present with fixed, asymmetric proximal weakness at an advanced age and should be considered in this clinical setting, especially when a history of poor exercise tolerance can be elicited.
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PMID:McArdle's disease presenting with asymmetric, late-onset arm weakness. 1071 77

The effect of continuous propofol administration on creatine kinase and suxamethonium-induced postoperative myalgia was evaluated in 50 patients randomised into two groups of 25 patients each. Induction of anaesthesia was identical in all patients. Anaesthesia was maintained with 66% nitrous oxide in oxygen supplemented by either isoflurane 1% or continuous propofol. Creatine kinase was measured before and after operation. Myalgia was evaluated postoperatively by a blinded observer. The median level of myalgia was reduced significantly in the continuous propofol group (p = 0.011). The median creatine kinase value increased significantly in the isoflurane group (from 90 to 160 IU, p = 0.001).
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PMID:Continuous propofol administration for suxamethonium-induced postoperative myalgia. 1054 96

Myositis and rhabdomyolysis with influenza are rare, but sometimes serious complications. Patients with myositis more commonly have influenza B infection than influenza A. On the other hand, rhabdomyolysis are more frequently recognized in patients with influenza A infection than those with influenza B. Upper respiratory symptoms usually precede myositis, while rhabdomyolysis occurs simultaneously or shortly after the respiratory symptoms. Creatine kinase levels are elevated in myositis mildly and in rhabdomyolysis markedly. Influenza myositis improve spontaneously within 6 weeks, but influenza rhabdomyolysis sometimes induce renal failure with fatal outcome. Although the true incidence of myositis and rhabdomyolysis in the influenza infection remains unknown, careful medical care is necessary when patients have muscle pain and weakness.
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PMID:[Myositis and rhabdomyolysis with influenza infection]. 1122 17

The purpose of this study was to examine the effects of vitamin E (VE) supplementation (1200 IU/day) on recovery responses to repeated bouts of resistance exercise. Non-resistance trained men were assigned to supplement with VE (n = 9) or placebo (PL; n = 9) for 3 weeks and then perform 3 resistance exercise sessions separated by 3 days of recovery (EX-1, EX-2, and EX-3). Performance was assessed at EX-1, EX-2, and EX-3. Fasting morning blood samples and perceived muscle soreness were obtained before EX-1 and for 10 consecutive days. Muscle soreness peaked after EX-1 and gradually returned to baseline values by day 6. Lower and upper body maximal strength and explosive power were significantly (p < or = 0.05) decreased at EX-2 and EX-3 (approximately 10%). Plasma malondialdehyde (MDA) was significantly elevated on days 7 and 8. There were no significant differences between VE and PL in muscle soreness, performance measures, or plasma MDA. Creatine kinase (CK) area under the curve from day 1 to day 10 was significantly greater for VE because of a nearly 2-fold greater increase in CK after EX-1 in VE, compared with PL (404 +/- 146 and 214 +/- 179 U/L, respectively). VE supplementation was not effective at attenuating putative markers of membrane damage, oxidative stress, and performance decrements after repeated bouts of whole-body concentric/eccentric resistance exercise.
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PMID:Effects of vitamin E supplementation on recovery from repeated bouts of resistance exercise. 1463 5

Rippling muscle disease (RMD) is a rare muscle disorder characterised by muscle stiffness, exercise induced myalgia, and cramp-like sensations. It is genetically heterogeneous and can be acquired, but most cases show autosomal dominant inheritance due to mutations in the caveolin-3 (CAV3) gene. We report a novel heterozygous missense mutation in CAV3 in a Belgian family with autosomal dominant RMD. A 40 year old woman complained of fatigue, exercise induced muscle pain, and muscle cramps since the age of 35. Neurological examination revealed percussion induced rapid muscle contractions (PIRCs) and localised muscle mounding on percussion; muscle rippling was not observed. Creatine kinase (CK) was elevated but electromyography and nerve conduction studies were normal. Fluorescence immunohistochemistry revealed reduced caveolin-3 and dysferlin staining in a quadriceps muscle biopsy. Western blot analysis confirmed severely reduced caveolin-3 levels, whereas dysferlin was normal. Sequence analysis of the two coding exons of CAV3 revealed a hitherto unreported heterozygous C82A transversion in the first exon, predicting a Pro28Thr amino acid exchange. Thr patient's first degree relatives did not present with neuromuscular complaints, but PIRCs, muscle mounding, and muscle rippling were found in the mother, who also carried the CAV3 mutation.
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PMID:Novel missense mutation in the caveolin-3 gene in a Belgian family with rippling muscle disease. 1531 33


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