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)

Phosphate diabetes has been considered as rare and to occur almost exclusively in children. Upon examination of adult patients with rheumatic or kidney diseases it has, however, been found that the combination of hypophosphataemia and hyperphosphaturia is not so rare. This paper deals with 24 adult patients of this type, whom we have found during 6 months. Their mean serum phosphorus concentration was 0.7 mmol/l (range 0.5--0.8). Mean phosphate clearance was 31 ml/min/1.73 m2 (range 16--51). The diagnoses were myalgia, dorsalgia (n = 7), papillitis calcificans (n = 5), prostatitis or prostate accretions (n = 4), dizziness (n = 2), kidney stones, tubular defect, interstitial nephritis, medullary sponge kidney (1 case each), two patients had transplanted kidneys. Asthenia was a common additional diagnosis. The patients' complaints have been pain in the muscles, joints, bones (18 cases), tiredness (10 cases), dizziness (8 cases), shakyness, numbness, burning sensation (7 cases), tenderness in the muscles and bones ("the princess-on-the-pea syndrome") (7 cases). The most common findings upon examination were bone tenderness (13 cases), reduced manual power (8 cases), positive Romberg test (3 cases), slight muscle atrophy (2 cases), waddling gait (2 cases). The most common findings encountered in the laboratory, besides hypophosphataemia and hyperphosphaturia, were high pH in the urine, hyperaminoaciduria, and phosphate crystals in dried urine.
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PMID:Mild phosphate diabetes in adults. 30 93

Fatigue and myalgia are common in patients with acquired immunodeficiency syndrome (AIDS). To determine whether altered muscle metabolism or impaired activation of muscle might account for these symptoms, we utilized three different exercise protocols to produce fatigue in nine AIDS patients who complained of both fatigue and exercise-exacerbated myalgia. Five were taking azidothymidine (AZT), which may cause a mitochondrial myopathy. Simultaneous measures of force, EMG, and muscle metabolites (phosphocreatine, inorganic phosphate, adenosine triphosphate, and intracellular pH) using phosphorus nuclear magnetic resonance spectroscopy were performed during fatigue and recovery. There were no significant differences between patients and controls in terms of fatigability, muscle metabolism, or muscle activation. These results provide no support for the hypothesis that fatigue or myalgia in AIDS patients derives from altered muscle metabolism or that AZT produces mitochondrial myopathy.
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PMID:Fatigue and myalgia in AIDS patients. 192 2

Studies on a 27-year-old man with a 3-year history of exercise-induced muscle pain, passage of red urine and elevated serum creatine kinase are described. Histological examination of a biopsy from quadriceps revealed non-specific myopathic changes with occasional clusters of subsarcolemmal mitochondria. The phosphorylase stain was normal. Phosphorous nuclear magnetic resonance (NMR) spectroscopy studies of gastrocnemius and flexor digitorum superficialis muscles showed no abnormalities at rest. During aerobic exercise there was an abnormally rapid decrease in phosphocreatine concentration but the pH remained within the normal range. There was a build-up of phosphomonoester (probably glucose 6-phosphate), usually indicative of a block in glycolysis. However, a primary defect in the glycolytic pathway seemed unlikely because muscle acidified normally during ischaemic exercise. Recovery from exercise was unusual in that phosphocreatine resynthesis and inorganic phosphate disappearance followed similar prolonged time courses (in control subjects the rate of inorganic phosphate disappearance was about twice as fast as the rate of phosphocreatine resynthesis). The transport of inorganic phosphate into the mitochondria appeared to be delayed. These slow recovery data suggested that oxidative metabolism was impaired. However, with all substrates tested, isolated muscle mitochondria had rates of oxygen uptake that were similar to control values, thereby ruling out a primary defect in mitochondrial respiration. A system involving several mitochondrial transport systems, the malate-aspartate shuttle, was measured. The activity in the patient's isolated mitochondria was less than 20% of the activity present in samples from control subjects. This patient is the only one so far reported with a defect involving the malate-aspartate shuttle system.
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PMID:An unusual metabolic myopathy: a malate-aspartate shuttle defect. 344 Aug 68

Over 12 years, 49 patients with hyperparathyroidism secondary to chronic renal failure under treatment with hemodialysis were treated with total parathyroidectomy. A portion of one gland was implanted in the sternocleidomastoid muscle. The operative indications were elevation of parathormone, serum calcium, and phosphorus, levels, pruritus, bone pain, pathologic fractures, and myalgia. Special postoperative complications discussed are hyperkalemia, hemorrhage, and respiratory obstruction. There were no operative deaths. No postoperative tetany was seen. Total parathyroidectomy should be performed in chronic renal failure patients with persistent elevation of serum calcium and parathormone levels, and who have pain, fractures, or soft tissue calcification. All postoperative parathyroidectomy patients should be observed for possible hyperkalemia.
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PMID:Surgical management of renal hyperparathyroidism in the dialysis patient. 708 63

A 2-year-old male Labrador Retriever was presented to the University of Missouri Veterinary Teaching Hospital with the primary complaints of polydipsia, polyuria, and joint or muscle pain. Low blood urea nitrogen concentration, hyperchloremia, and marked proteinuria were the only abnormalities in a serum biochemical profile and urinalysis. Decreased creatinine clearance and increased renal fractional excretion of sodium, potassium, calcium, and phosphorus were detected by renal clearance studies. Increased excretion of most amino acids was found by amino acid analysis of urine, but not all amino acids were lost with equal magnitude. Amino acids with secondary amino groups or basic side chains were lost at increased rates, whereas those with acidic side chains were not. These differences could be related to defects in specific renal amino acid transport mechanisms. Identification of these transport mechanisms may allow for pharmacologic intervention at the point of renal loss to alleviate clinical signs of disease.
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PMID:Fanconi syndrome in a Labrador retriever. 788 24

Endemic skeletal fluorosis is characterized by bone, joint and muscle pain, progressive ankylosis of various joints and crippling deformities. Whole body skeletal scintigraphy with 99Tcm-methylene diphosphonate was performed for 17 symptomatic subjects suffering from this disorder. The fluoride content of drinking water ranged from 4.1 to 12.9 mg l-1 (normal < 1 mg l-1). Urinary and serum fluoride levels were markedly elevated. Serum calcium (total and ionized), inorganic phosphorus, creatinine and albumin were essentially normal while serum alkaline phosphatase was elevated in six subjects (mean +/- S.D. 206 +/- 106; range 22-1072 IU l-1). Skeletal radiology revealed a wide spectrum of bony abnormalities. Skeletal scintigraphy revealed a picture similar to metabolic 'superscan' in all subjects, i.e. increased tracer uptake in axial and appendicular skeleton, reduced soft tissue uptake, poor or absent renal images, prominent costochondral junction and 'tie' sign in sternum. Increased uptake was present in all subjects irrespective of age, water fluoride content, serum alkaline phosphatase level and radiological abnormalities. Our findings suggest the presence of a high bone turnover state in endemic skeletal fluorosis irrespective of other variables.
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PMID:Skeletal scintigraphic findings in endemic skeletal fluorosis. 851 Aug 79

Impairment of muscle glycogenolysis in McArdle's disease (myophosphorylase deficiency) leads to exercise intolerance and exercise-induced myalgia. The pathophysiology of these symptoms is not entirely clear. We used phosphorus magnetic resonance spectroscopy to measure muscle phosphate metabolite concentrations and intracellular pH during brief ischemic exercise and in the period of aerobic metabolic recovery after exercise, with special attention to cytoplasmic adenosine 5'-diphosphate (ADP). In 5 patients with McArdle's disease, calculated muscle intracellular ADP concentrations at the beginning of recovery were higher than in normal control subjects (70-425 mmol/L, control mean: 73 +/- 40 mmol/L, P < 0.05). The half-time for intracellular ADP recovery after exercise, an index of maximal mitochondrial oxidative phosphorylation, was 0.16 +/- 0.07 in normal controls and was independent of metabolic state or intracellular pH. ADP recoveries were abnormally slow in all patients with McArdle's disease (range: 0.32-0.83 min, mean = 0.2 min, P < 0.0001). These results are indicative of a limitation in the rate of oxidative phosphorylation in muscle of patients with McArdle's disease, most likely due to impaired substrate delivery to mitochondria. This impairment of mitochondrial function may contribute to the exercise-related symptoms in McArdle's disease.
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PMID:Impairment of muscle mitochondrial oxidative metabolism in McArdles's disease. 860 28

A xenobiotic, well tolerated by the majority of treated patients, can cause serious complications in patients with individual susceptibility. Based on the hypothesis that such a phenomenon may occur in rare cases of rhabdomyolysis attributed to fenoverine (DCI), we designed a protocol to look for a genetic predisposition. Six patients were included who had previously had an episode of rhabdomyolysis after taking fenoverine. A seventh patient was added, who had only experienced myalgia without cytolysis. All patients were investigated by the following tests: 31-phosphorus nuclear magnetic resonance spectroscopy, histopathological examination of the muscle, muscle contraction tests and biochemical analysis of the muscle. All patients examined proved to have muscle abnormalities. The pathology found varied greatly from patient to patient: mitochondrial myopathy, lipid storage myopathy, sensitivity to malignant hyperthermia or disorders of oxidative metabolism. The probability of finding by chance such rare muscle disorders associated with the equally rare rhabdomyolysis attributed to fenoverine is practically zero. We conclude that there is a cause and effect link between underlying abnormalities and the muscular cytolysis attributed to fenoverine.
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PMID:Research into individual predisposition to develop acute rhabdomyolysis attributed to fenoverine. 890 30

Elevated skeletal muscle phosphodiesters (PDE) have previously been reported with muscle-related disorders. Myalgia is a side effect of using statin cholesterol-lowering medications and, therefore, statin use may be associated with increased skeletal muscle PDE. The effect of cholesterol-lowering drugs on skeletal muscle phosphorus metabolites was determined with (31)P magnetic resonance spectroscopy. Resting (31)P metabolites of the anterior compartment muscles were measured in two groups (n = 20; age, 49 +/- 2 years); half were taking statins and the other half were not on these agents. Muscle PDE was 57% greater in the statin group than the control group. These data suggest that statin use increases muscle PDE. Our findings are particularly relevant due to the increasing use and higher dosing of statin medications. Further prospective studies should be performed to document a causal relationship between elevated PDE and statin use, in addition to quantifying correlates to muscle function.
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PMID:Elevated skeletal muscle phosphodiesters in adults using statin medications. 1688 Oct 62

This report describes the clinical and biologic data and bone density measurements in 19 adults seen in a rheumatology department, with phosphate diabetes defined by low serum phosphate levels and decreased tubular reabsorption of phosphate in the absence of known etiology. There were 14 males and 5 females with a mean age at disease onset of 36.7 years (20-68 years) and at diagnosis of 43.9 years (24-70 years). Axial pain was present in 17 patients (90%), radicular pain in 13 patients (68%), pain at night in 14 patients (74%), fatigue in 7 patients (37%), myalgia in 6 patients (32%), fracture in 6 patients (32%), renal colic in 4 patients (21%) and depression 10 patients (53%). Mean serum phosphorus was 2.25 mg/dL (1.08-2.76); maximum tubular reabsorption of phosphate/glomerular filtration rate was 0.58 (0.4-0.76) (n > 0.77). Calcium/creatinine > 0.48 was seen in 9 patients (47%), indicating an associated hypercalciuria. Serum calcium, sodium, magnesium, creatinine, cortisol, T3, T4, thyroid-stimulating hormone (TSH), 25 and 1,25 OH2 vitamin D3 were normal. Glucose and amino acid were absent from urine. Bone mineral density at L2-L4 level (Z-score) was -2.13 (-0.9 to -4.25), and at the femoral neck was -1.34(-1.5 to -3.2). Bone biopsy in 5 patients showed osteoporosis with minor osteoid deposition.Idiopathic phosphorus diabetes (IPD) is a rheumatic disease with chronic axial pain at night, radiculitis-like symptoms, fatigue and depression. In half of the patients, IPD is associated with hypercalciuria. Bone mineral density at L2-L4 and femoral neck level is low. Bone biopsies show osteoporosis. Chronic pain, fatigue and depression resulting from IPD may be improved by treatment with oral calcitriol and phosphorus. There might be a delay in improvement of a few months, even if the blood phosphate level is normalized. A 3% increase in bone mineral density could be measured at 6-month intervals when blood phosphate was maintained. This disease is often misdiagnosed when the maximal reabsorption rate of phosphorus is not calculated.
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PMID:Adult onset idiopathic phosphate diabetes. 1907 33


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