Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the differential diagnosis of intermittent claudication some rare myopathies have to be considered. The most frequent is phosphorylase deficiency (McArdle's disease). Exercise-induced muscular pain, weakness, contractures and occasionally myoglobinuria are the most prominent clinical signs. Serum creatine phosphokinase, aldolase and lactic dehydrogenase may be elevated after exertion. In the ischemic forearm test there is no rise of serum lactic acid. The enzyme deficiency can be demonstrated by histochemical and biochemical examination of a muscle specimen. Further, but more infrequent, enzymatic disturbances of glycolysis are phosphofructokinase deficiency and phosphohexoisomerase inhibitor, which also yield an abnormal ischemic forearm test and must be demonstrated histochemically and biochemically. Apart from muscular signs, myopathy with lactic acidosis is associated with palpitation, dyspnea and exhaustion, and a disproportionate rise in serum lactic acid level after exertion. Histochemically and electronmicroscopically demonstrable fat accumulation in the muscle can be a sign of a disturbance in lipid metabolism. This type of exercise-induced myopathy has been reported only in a few cases with carnitine-pylmityltransferase deficiency, which has to be demonstrated biochemically. Muscular contractures also exercise-induced but painless and reversible within seconds may be due to deficient uptake of sarcoplasmic calcium in the tubular system. Dyskalemic paralysis causes painless paresis within minutes of hours after exertion, which disappears within hours to a few days. Myopathy with tubular aggregates can be differentiated from other exercise-induced myopathies by morphology. Myotonia combined with painful contractures characterizes myopathia myotonica.
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PMID:[Exercise-induced muscular weakness, myalgia and contractures. I. A clinical review]. 13 80

Technetium-99m-stannous pyrophosphate (99mTc-PYP) accumulates in acutely infarcted myocardium and can be detected by scintiscanning. The clinical value of 99mTc-PYP scintiscanning was studied in 83 patients 6 hours to 21 days after the onset of acute chest pain. In 12 patients with normal electrocardiograms and serum enzyme values no uptake of 99mTc-PYP was detected on the scintigrams. Of 44 patients with electrocardiographic or enzyme evidence, or both, of acute myocardial infarction the scintigrams were positive in 31, "questionable" in 2 and negative in 11; no positive scan was obtained within 12 hours of the onset of pain, and the scans generally remained positive for up to 5 days. In 24 patients with evidence of prolonged myocardial ischemia the scans were positive in 2, questionable in 4 and negative in 18. The scans were negative in each of three patients with acute or constrictive pericarditis. Localization by electrocardiography and scintiscanning correlated nearly perfectly for transmural infarcts but subendocardial infarcts could not always be localized precisely by scintiscanning. The infarct area (total area of 99mTc-PYP uptake) correlated well with the peak serum value of creatine phosphokinase.
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PMID:Technetium pyrophosphate scanning in the detection of acute myocardial infarction: clinical experience. 18 87

1. Coronary insufficiency is a pathophysiologic state that can initiate lethal cardiac arrhythmias in the absence of myocardial necrosis. Patients with suspected coronary insufficiency should be monitored until they are stabilized and a diagnosis is confirmed. 2. Early and adequate intravenous antiarrhythmic prophylaxis with lidocaine to raise the fibrillation threshold in the setting of coronary insufficiency can prevent primary ventricular fibrillation. Classic "warning arrhythmias" are not predictive of ventricular fibrillation. Their persistence during adequate antifibrillatory prophylaxis does not indicate therapeutic failure. 3. The isoenzyme of creatine phosphokinase, CPK-MB, is an extremely sensitive and specific indicator of myocardial necrosis if measured serially during the 24 hours following the onset of symptoms suggesting coronary insufficiency. It may prove most useful in eliminating the false positive diagnosis of myocardial infarction in difficult clinical cases. 4. The management of heart failure in myocardial infarction requires an understanding of the relationship between ventricular preload and the cardiac output. The treatment of clinical manifestations of an elevated ventricular preload in asymptomatic patients is not justified and may be detrimental. In symptomatic patients, however, judicious manipulation of ventricular preload should be the first therapeutic consideration, and an optimal filling pressure should be achieved and maintained when other determinants of the cardiac output are manipulated. 5. Indications for the prophylactic insertion of a temporary transvenous pacing electrode for heart block associated with myocardial infarction must be individualized. Most authorities agree that prophylactic pacing may be justified in patients with evidence of new infranodal block involving two of the three fascicles. Patients with bifascicular block who progress to complete heart block transiently may benefit from permanent transvenous pacemaker insertion before discharge. 6. Hospitalized patients with persistent pain of suspected cardiac origin but without evidence of myocardial infarction can be studied safely with coronary angiography. A small percentage will be normal or have diffuse disease that is inoperable. Of those with operable disease, short-term mortality appears to be similar for medical and surgical therapy. 7. Patients with an uncomplicated myocardial infarction may be safely discharged from thehospital by day 7-10. 8. Experimental evidence indicates that modification of infarct size is possible. Application of these concepts to human subjects presently is limited by the absence of a proved method of measuring infarct size in vivo in humans.
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PMID:The management of acute coronary insufficiency. 32 38

We investigated the activity kinetics of CK-total and CK-MB in 83 patients with proven myocardial infarctions. Serial serum samples were taken at intervals of 2--6 h. The activity of isoenzym CK-MB was determined by means of the immunological inhibition method. CK-MB activity was determined in all patients. The mean peak activity of CK-MB was 65 U/l (range: 9-241 U/l). At the time of peak CK-MB activity the mean percentage CK-MB activity was 13.2% (range: 3.4--21.7%). The CK-MB activity reached its peak at 17.4 h (range: 3.0--32.5 h) after the onset of retrosternal pain. This is 1.4 h after peak CK-total activity. The mean disappearance rate constant for CK-MB (n = 31) was found to be 9.3 X 10(-4) U/min with a large individual variation. This value corresponds to a half life of 12.5 h (CK-total: 15.5 h). The determination of CK-MB activity is therefore only of diagnostic significance within 48 h of possible myocardial occurrence. Moreover, isoenzyme CK-MB is not found exclusively in myocardium. For this reason it is better to use the percentage CK-MB activity in the differential diagnosis of myocardial infarction. With 80% of the patients this value is greater than 6% within 36 h of proven myocardial infarction.
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PMID:[Studies of activity kinetic of isoenzyme CK-MB in serum after myocardial infarction (author's transl)]. 56 53

The clinical picture of toxic rhabdomyolysis after alcohol and drug intoxications is characterized by severe pain, swelling, and inability to move the affected muscle group. The disintegration of necrotic muscle tissue leads to hyperkalaemia, excessive increase of creatine kinase in serum, and a myorenal syndrome with anuria. Pathogenetically the combined effects of toxic vascular damage and local pressure and cold influence are assumed to occur. In anuria, resistant to conventional medication, early and repeated plasma exchanges are considered to be a therapeutic alternative to haemodialysis.
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PMID:[Toxic rhabdomyolysis after alcohol and drug intoxications (author's transl)]. 62 51

Six patients developed persistent muscular cramps, aching pain, and fatigability after an influenza-like illness. Electromyography showed myopathic changes, although results of routine laboratory investigations were normal in all but one patient, whose serum creatine kinase concentration was slightly increased. All but one of the patients improved: three were asymptomatic within one to two years. The syndrome was probably a benign form of polymyositis.
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PMID:Benign postinfection polymyositis. 70 4

A patient with a long history of exercise-unduced pain developed myoglobinuria and respiratory failure following extensive exercise (football). Although muscle histochemistry was normal, tissue oxidation of 14C-labeled palmitate was decreased, and muscle carnitine palmityltransferase (CPT) activity was one-tenth of normal. During fasting, his creatine kinase (CK) rose from 127 mu/ml to 278 mu/ml and blood ketones failed to exhibit a normal rise. Triglycerides were normal, as was fatty-acid mobilization. Prolonged exercise resulted in an inordinately increased CK with only moderate elevations in lactate. Treatment with medium-chain triglycerides did not alter his symptoms or improve exercise performance. Pain on exercise is a common complaint, but the occurrence of myoglobinuria points to a defect of energy metabolism; Screening for defects of fat utilization may be accomplished by the prolonged-exercise test, invitro oxidation of 14C-labeled substrates, and prolonged fasting.
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PMID:Biochemical and physiologic consequences of carnitine palmityltransferase deficiency. 75 Sep 17

An outbreak of acute crural myalgia in children is reported. The severe calf pain followed an influenza-like episode, with subsequent complete recovery. Laboratory studies in most cases showed elevated creatine phosphokinase and SGOT values, with a low peripheral white blood cell count. Electromyographic studies were normal. Results of one muscle biopsy were normal. This postviral myalgia is a distinctive syndrome only recently being recognized in the United States.
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PMID:Acute postinfectious crural myalgia in children. 85 Aug 7

In order to investigate the relation between the release of creatine kinase (CK) in acute myocardial infarction and the evolution of infarction, the appearance functions of CK (release of CK from the heart into the circulation) were calculated by the modified method of Sobel and associates from the serial determinations of serum CK activity in 50 patients with acute myocardial infarction. The relation of the time between the onset of infarction and the peak value of the appearance function to the duration of the evolution of abnormal Q waves in 14 patients with inferior infarction and to the duration of pain in all patients was investigated. The duration of CK release from the heart averaged 37-2+/-2-4 hours and correlated well with the total CK released (R=0.665) which represents the infarct size. The mean per cent of the total CK eventually released by the time of maximum sigmaQ (sum of the amplitude of Q wave in leads II, III, and aVF) was 80-0+/-6-4 per cent and that of CK released while pain persisted was 72-0+/-3-9 per cent. These results strongly suggest that the appearance function of CK reflects the evolution of myocardial infarction.
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PMID:Evaluation of evolution of myocardial infarction by serial determinations of serum creatine kinase activity. 86 Oct 91

Serum creatine phosphokinase (CPK) concentrations were determined in healthy volunteers for the first 48 hours after intramuscular injection of 50 mg chlordiazepoxide hydrochloride or of its solvent alone. Intramuscular injection of both the drug solution and its solvent was painful and caused CPK elevations. The CPK rise due to the drug solution was 33 per cent higher than that due to the solvent alone, but the difference was not significant. The pH of the solvent preparation is low and it contains high concentrations of propylene glycol. The pain and muscle damage due to injection of the solvent could be due to its acidity and its high osmolarity. Problems associated with intramuscular injections of water-insoluble drugs are not resolved by the use of such solvent preparations.
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PMID:Serum creatine phosphokinase concentrations after intramuscular chlordiazepoxide and its solvent. 94 24


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