Creatine Phosphokinase Determination Research Articles

Alcohol-induced damage to skeletal muscles in women with chronic alcohol intoxication

In Russia, there is a high level of alcohol consumption among women in doses that represent a high risk of developing alcoholic diseases, manifested, in particular, by damage to skeletal muscles.The purpose of the study. Analysis of clinical, biochemical, neurophysiological, as well as morphometric and immunohistochemical features of alcoholic skeletal muscle damage in women with chronic alcohol intoxication.Material and methods. A clinical and laboratory examination of 30 women aged 20 to 60 years with chronic alcohol intoxication was performed, which included the determination of creatine phosphokinase (CPK) and insulin-like growth factor I (IGF-I) in blood plasma, stimulation and needle electromyography (EMG), as well as morphological and immunohistochemical examination of biopsies of the quadriceps femoris.Results. Myopathic syndrome in the form of proximal para-or tetraparesis was observed in 73.3% of the examined women in combination with a decrease in IGF-1 at normal values of CPK in blood plasma. The EMG results indicated the absence of changes in the parameters of the potentials of motor units, characteristic of primary muscular lesions, and of conduction disturbances along the femoral nerve. Morphometric and immunohistochemical studies of skeletal muscle biopsies showed a decrease in the cross-sectional area of muscle fibers of types I and II without signs of muscle tissue necrosis.Conclusion. Chronic alcoholic myopathy is a common manifestation of alcoholic disease in women with long-term alcohol intoxication. The severity of the atrophic process in the skeletal muscle is comparable to the degree of proximal paresis. Violations of systemic protein synthesis and acceleration of apoptosis are considered as pathogenetic mechanisms of the atrophic process in the muscles in chronic alcoholic myopathy in women.

Incidental hypertransaminasemia in children: Potential delay in diagnosis of muscle disease

Many physicians believe that muscle disease leads either to sole elevation of aspartate aminotransferase (AST) or a disproportionate increase in AST versus alanine aminotreansferase (ALT). We herein report 25 patients with muscle disease who presented erroneously to the hepatologist with an incidental finding of elevated ALT/AST. Data of 25 patients with elevated ALT/AST who proved to have muscle disease and underwent extensive liver workup were analyzed. The time lapse until diagnosis of muscle disease and costs of unnecessary liver workup were calculated. The time interval from the incidental finding of elevated transaminases to diagnosis of skeletal muscle disease ranged between 2 months to 10 years with a median (IQR) of 2 (3.6) years. The mean ALT:AST ratio was 1.24. Creatine phosphokinase (CPK) level correlated positively and significantly with both ALT (p = 0.002) and AST (p = 0.0007). The costs of unnecessary liver workup, before muscle disease was diagnosed, ranged between 5000 and 10,000 Egyptian pounds. Unawareness of physicians with muscle origin of ALT/AST may cause delay in diagnosis of muscle disease. Early determination of CPK could save a lot of stress and money.

Myositiden

This article gives a review of the classification, diagnostic procedures and treatment of idiopathic inflammatory myopathies from a neurological point of view. The myositis syndromes can be subdivided into four groups, polymyositis (PM), dermatomyositis (DM), inclusion body myositis (IBM) and necrotizing myopathy (NM), which substantially differ clinically and pathophysiologically. Myositis may also occur in association with cancer or autoimmune systemic diseases (overlap syndrome). Diagnosis of inflammatory myopathies is based on clinical symptoms, determination of creatine phosphokinase and acute phase parameters in blood (e.g. C-reactive protein and erythrocyte sedimentation rate), electromyography results and findings of magnetic resonance imaging (MRI) in muscle. A muscle biopsy is mandatory to confirm the diagnosis. High quality randomized controlled trials of treatment regimens for inflammatory myopathies are sparse; however, empirical experience indicates a clear effectiveness of immunosuppressive treatment of PM, DM and NM.

Avaliação de diferentes híbridos suínos submetidos à insensibilização elétrica e gasosa (CO2). Parte 1: mensuração de indicadores sanguíneos de estresse

Pigs of three genetics lineages A, B and C marketed in Brazil, with alive weight from 100 to 120 kg were submitted to the manual electric stunning (Karl Schermer 220-230/250 volts, 45-60 Hz and 1.4 -1.5 A) and to the collective gaseous system (COMBI-BUTINA 90% CO2). Blood samples, for levels determination of creatine phosphokinase (CPK), lactate and cortisol, as well as samples of the semimembranosus muscle (10 g) for the determination of the gene halothane, were collected. Being compared the electric and gaseous stunning systems, the electric stunning did demonstrate to be more stressful providing larger plasmatic concentrations of cortisol ( p < 0.001) and lactate ( p < 0.001) for the genetic lineages A and C, in the studied conditions.However it didn't observe significant differences beween the sanguine indicators and stunning systems in subject when the lineage B was considered. Significant differences among the genetic lineages A, B and C were obtained being compared the plasmatic values of creatine phosphokinase (p < 0.001), lactate (p < 0.001) and cortisol (p < 0.001) when stunned with the gaseous system, however when the electric system was used only the cortisol values presented significant differences (p < 0.001). The presence of the gene halothane (Nn) was only observed in the lineage B.

Advicor (niacin extended-release and lovastatin tablets).

Advicor (niacin extended-release and lovastatin) is a newly Food and Drug Administration-approved combination medication used in addition to adjunctive treatment of primary hypercholesterolemia and mixed dyslipidemia. The drug is a combination of two familiar medications used to treat patients with elevated low-density lipoprotein (LDL) cholesterol and total cholesterol, low high-density lipoprotein (HDL) cholesterol, and elevated triglycerides. It combines extended-release niacin and lovastatin. Niacin reduces LDL cholesterol, apolipoprotein B, lipoprotein(a), triglycerides, and total cholesterol. It also increases HDL cholesterol. Lovastatin reduces both normal and elevated LDL cholesterol. Apolipoprotein B also falls with treatment. The mechanism of action of niacin is not thoroughly understood. Lovastatin is a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor that prevents the production of cholesterol. Lovastatin is a prodrug and needs to be hydrolyzed to its active metabolite, lovastatin acid. The mechanism of action of LDL reduction involves the reduction of very LDL cholesterol and induction of the LDL receptor, which leads to reduction of the production or increased catabolism of LDL cholesterol. Following a single dose of the drug, peak plasma niacin and lovastatin levels were obtained in 5 hours and 2 hours, respectively. The extent of absorption of niacin was increased with food. Lovastatin is incompletely absorbed and has considerable interindividual variability. Grapefruit juice increases the absorption by at least 30%. Niacin undergoes first-pass metabolism and is excreted in the urine. Niacin concentrations are higher in women than in men. Lovastatin also undergoes first-pass metabolism by the cytochrome P450 3A4 system and is excreted in the urine and bile. The drug can cause significant liver dysfunction; therefore, careful monitoring of hepatic function must be performed. The drug should not be substituted for equivalent doses of immediate-release niacin. The drug should be used very cautiously in patients with substantial alcohol consumption or a history of liver disease. Liver function tests should be performed on all patients at the beginning of therapy and every 6–12 weeks for at least 6 months, then periodically. The drug should be stopped if liver function values are three times the upper limits of normal. Rhabdomyolysis has been reported in patients with and without renal insufficiency. Periodic creatine phosphokinase determinations may be considered in patients suspected of developing rhabdomyolysis. The drug should be stopped if rhabdomyolysis is suspected. The use of the drug with cyclosporine or fibrates should be avoided. The drug should be stopped before giving azole antifungal agents and macrolides. Aspirin may decrease the metabolic clearance of niacin. Niacin may potentiate the effects of ganglionic blocking drugs, causing postural hypotension. The most common adverse reaction is flushing (53%–83%). The incidence of flushing can be reduced by pretreatment with aspirin or another nonsteroidal anti-inflammatory drug 1/2 hour prior to taking the drug. Other adverse reactions include infection (20%), headache (9%), nausea (7%), and pruritus (7%). The usual starting dose is 500 mg niacin extended-release and 20 mg lovastatin. The drug should be taken at bedtime with a low-fat snack. The tablet should not be broken, crushed, or split. Dosing can be increased at 4-week intervals until the desired result is achieved. The maximal dosage of the drug is 1000 mg niacin extended-release and 20 mg lovastatin. Advicor is a new combination drug consisting of niacin extended-release and lovastatin. It should be used to adjunctively treat patients with primary hypercholesterolemia and mixed dyslipidemia.

Perioperative creatine phosphokinase trends in elderly patients with hip fracture

A prospective study of the serum levels of unfractionated creatine phosphokinase (CPK) in 69 consecutive elderly patients undergoing surgery for hip fracture is reported. Serum unfractionated CPK levels were measured on admission, on the evening following surgery and daily for the first five days post-operatively. All of the CPK levels measured on admission were within the normal range for this laboratory. A gradual rise in CPK levels followed surgery. On the evening following surgery 75% of values were greater than the upper limit of the normal reference range. The peak values were seen on day 1 post-operatively but 25% of values were still less than the reference maximum. A gradual decline was seen after this and at day 5 post operatively 50% of values were within the normal reference range. A single unfractionated CPK determination is not of diagnostic benefit in the post-operative period in elderly patients with hip fracture. However, patients with intracapsular and intertrochanteric fractures do not show elevation of unfractionated CPK levels prior to surgery.

A new colorimetric method for determination of creatine phosphokinase

A new colorimetric method has been developed for the determination of creatine phosphokinase (CPK). This method is based on the reaction of creatine, formed enzymatically from creatine phosphate and ADP, with p-nitrophenylglyoxal (PNPG) under alkaline conditions to produce a colored product which absorbs maximally at 480 nm. At 25°C the reaction was complete after 10 min in 0.1 m sodium pyrophosphate, pH 12, containing 0.15 m sodium ascorbate. The colored product was stable for at least 24 h and obeyed Beer's law in the range 0.005–0.05 m m creatine. The color reaction was used to determine the activity of CPK in serum and tissue extracts. The results obtained by this method agreed well with the results obtained by other available methods for CPK determination. However, the PNPG method was more rapid and more sensitive than other colorimetric methods and required a single chromogenic reagent.

Tissue tolerance of intramuscular injectables and plasma enzyme activities in rats.

The local tissue damage after intramuscular injection caused by various commercially available injection solutions was determined in the albino rat, by measuring plasma activities of creatine phosphokinase, aspartate aminotransferase, and lactic dehydrogenase, the tissue activity of creatine phosphokinase, and macroscopic changes in the muscle at the injection site (gastrocnemius muscle). The plasma enzyme activities were determined 2, 6, 18, and 28 hr after the injection. After 28 hr the animals were sacrificed for macroscopic inspection of the injection site and for the determination of tissue enzyme activity. The tissue injury caused by the test substances correlated well with the elevated creatine phosphokinase activity (2 hr). The elevations of aspartate aminotransferase (18 hr) and lactate dehydrogenase (2 hr) activity as well as the loss of tissue creatine phosphokinase activity were less indicative of differences between test preparations. The i.p. administration of some of the test preparations caused increased enzyme activity without muscle damage, which could interfere with the test results. The creatine phosphokinase determination indicates the damage occurring immediately after the administration of the test solution, and the macroscopic inspection offers the possibility to obtain some information on the evolution of the muscular lesion.

Prediction of left ventricular function in acute anterior myocardial infarction by serum creatine kinase activity and precordial ECG mapping.

Right cardiac catheterization, serial determination of creatine phosphokinase (CPK) and of CPK-MB activities, and precordial 35-lead ECG mapping were performed in 17 consecutive patients with a first anterior acute myocardial infarction (AMI) within 6 hours of the onset of symptoms. Left ventricular function as determined by the stroke index (SI, ml/m2) to mean pulmonary capillary wedge pressure (PCWP, mmHg) ratio inversely correlated either with the total CPK and CPK-MB released and with peak enzymatic activity, or with the entity of early (6th hour ECG) ST-segment elevation. Conversely, a direct correlation was found between the SI/PCWP ratio and the ratio of R to Q+S waves from late (48th hour) ECG. Residual left ventricular function after a first anterior AMI can therefore be estimated noninvasively in the individual patient by early precordial ECG mapping and by peak enzymatic activity.

Intravenous clonidine in acute myocardial infarction in men

We studied the effects of intravenous clonidine treatment in a group of 24 patients with acute myocardial transmural anterior and/or lateral wall infarction. Clonidine, known as an antihypertonic agent, was administered as a bolus of 1–2 μg/kg body weight and repeated every 2–3 hr. However, maximal range of the time interval was 20 min to 4 hr, maximal range of doses 37 to 150 μg, depending on the hemodynamic status. The effects were measured by precordial electrocardiographic mapping as well as serial creatine phosphokinase determinations. A big decrease in ST-segment elevation was observed: ΣST reduction after 24 hr was 37% of initial value (140% in control group), after 48 hr - 30% (120% - control). NST fall after 24 hr - 45% (145% - control), after 48 hr - 41% (142% - control). NQ increased after 24 hr to 135% of initial value (156% - control), after 72 hr to 137% (167% - control). Detailed analysis revealed undoubted correlation between the dosage and favourable dynamics of precordial mapping parameters. Hemodynamic, antiarrhythmic and above all adrenolytic activity were noted. The treatment caused a distinct deterioration in daily adrenalinuria mean values to 5.99 μg in the first day (14.20 - control) and lower in the following days. No side effects were observed but sudden discontinuation of the therapy caused an unfavorable reaction. A temporal association between diminished adrenalinuria and both clinical improvement and limitation of infarct size was observed. Therapy with intravenous clonidine requires meticulous individualization of clonidine dosage depending on the patient's initial hemodynamic status.

The use of concomitant serum pyruvate-kinase (PK) and creatine-phosphokinase (CPK) for carrier detection in Duchenne's muscular dystrophy through discriminant analysis

Serum pyruvate-kinase (PK) and creatine-phosphokinase (CPK) determinations have been carried out in a sample of 30 obligate carriers for the DMD gene and 50 normal adult control females. In all the subjects under study blood samples have been collected 3 times on 3 independent occasions and the means of these 3 determinations were considered for both CPK and PK activities in the statistical analysis. Discriminant analysis has shown that in the group of 30 obligate carriers the estimated proportions of misclassification using either serum CPK, PK or both enzymes were found to be: 10 30 (33.3%) for CPK alone, 6 30 (20%) for PK alone and 5 30 (16.6%) for both enzymes. It is concluded that although a small proportion of carriers still remain undetected the concomitant use of PK and CPK determinations enhances the capability of detecting carriers for the Duchenne gene mainly when compared with CPK alone.

Mionecrosis, hemorragia y edema inducidos por el veneno de Bothrops asper en ratón blanco

Pathogenesis of the myonecrotic, hemorrhagic and edema-forming effects in white mice inoculated with Bothrops asper venom was studied at different time intervals by means of light microscopy, determination of serum levels of the enzyme creatinephosphokinase (CPK), and evaluation of edema. Although the three effects were evident in the first hour, their development was relatively independent. Myonectoric activity reached its maximum levels in the first 3 hr, as judged by serum CPK. This indicates that myonecrotic toxins have a very rapid action on muscle fibers, after which CPK levels decrease to near normal values 24 hr after venom inoculation. Histological studies showed severe myonecrosis at 3, 6, 9, 12 and 24 hr, characterized by myolytic and coagulative necrotic fibers mixed with normal fibers. Maximum hemorrhagic effect was observed between 9 and 12 hr, whereas at 6, 9, 12 and 24 hr there was an intense polymorphonuclear leucocyte infiltration. On the other hand, 1 hr after venom injection there was a local edema of 44%, reaching a maximum value of 70% within the first 24 hr, decreasing afterward. This edema is more prolonged than that induced by Agkistrodon piscivorous or Trimeresurus elegans venoms. This could have important clinical implication since local swelling contributes to tissue compression and is related to other physiological alterations. One week after venom inoculation there were fibroblasts, fragments of necrotic muscle fibers, and a mononuclear cell exudate. At this time, we did not observe hemorrhagic areas. Determination of serum levels of CPK could be a useful and powerful technique in order to quantify muscle tissue destruction due to snake bite. Since only scanty hemorrhagic and necrotic areas were observed in heart muscle, the drastic and rapid increase in CPK levels mainly reflected skeletal muscle necrosis. CPK determination is a simple and quick laboratory technique that should be used to evaluate muscle necrosis and to improve treatment in snake venom poisoning.

A Radioimmunoassay for the Measurement of Human Cardiac Myosin Light Chains

A double-antibody radioimmunoassay that specifically measures serum or urinary concentrations of human cardiac myosin light chains has been developed. The assay is both sensitive and specific for myosin light chain I. The antiserum used in the assay is capable of detecting 1--2 ng/ml of cardiac myosin light chain I and shows no cross-reaction to cardiac myosin, the heavy chains of myosin, actin, tropomyosin, or light chain II. Of 114 patients admitted to the Coronary Care Unit, 227 measurements obtained from 84 patients without myocardial infarction revealed that the serum light chain level of 2.0 +/- 0.18 ng/ml was not significantly different from that of a control group (2.1 +/- 0.17 ng/ml, n = 12). In contrast, 89 measurements from 30 patients with myocardial infarction evidence clinically, electrocardiographically, and by creatine phosphokinase determinations were found to have an average serum light chain I concentration of 10.9 +/- 1.39 ng/ml (P less than 0.001). Thus, the radioimmunoassay for human cardiac myosin light chain I provides a sensitive and specific marker for myocardial damage.

Serum pyruvate-kinase (PK) and creatine-phosphokinase (CPK) in progressive muscular dystrophies

PK and CPK have been determined in the serum from 208 individuals including 70 normal controls (61 adults and 9 children) and 138 patients with a variety of neuromuscular disorders. In adult controls the mean activity (±SE) for PK is 1.2 ± 0.05 μmol/ml/h. In normal children PK activity was about twice as high as in normal adults and decreases with increasing age. In 26 patients with Duchenne dystrophy the range of serum PK was 4.0–150.4 and in 17 individuals with the Becker type, 3.0 to 148.7. All had elevated PK and CPK levels. Eighteen of 20 patients with the facio-scapulo-humeral (FSH) from of muscular dystrophy had increased PK while only 9 had elevated CPK. Regression analyses have shown an inverse correlation between PK levels and age (or degree of disability in DMD). Kinetic and electrophoretic studies indicate that the PK isozyme found in the serum from affected patients and from heterozygotes for the DMD gene is mainly the M 1 type PK, which is the only PK isozyme found in skeletal muscle and brain and the major component from myocardium. It is concluded that the concomitant use of serum PK and CPK determinations may be very useful for clinical diagnosis of certain types of muscular dystrophies and may be of great importance in the management of affected patients and their families.

Serum Creatine Phosphokinase in Leptospirosis

Serum creatine phosphokinase (CPK) and serum glutamic oxaloacetic and pyruvic transaminase (SGOT, SGPT) levels were determined in 61 patients with leptospirosis and 16 with viral hepatitis during the acute phase of illness. The CPK value was elevated in 29 leptospirosis patients and normal in all 16 hepatitis patients. Conversely, mean SGOT and SGPT levels were lower in leptospirosis patients. The CPK determination is a simple test that may provide diagnostic information in a jaundiced patient, particularly when characteristic manifestations of leptospirosis are absent. The pattern of greatly elevated CPK levels with only modest elevations in transaminase values in an acutely jaundiced patient should strongly suggest a diagnosis of leptospirosis.

Effect of fasting, phenobarbital, or hydrocortisone on serum creatine-phosphokinase and aldolase activity in myopathic Syrian hamsters.

The hereditary polymyopathy and cardiomyopathy of inbred Syrian hamsters (UM X 7.1) are associated with a marked elevation of serum creatine phosphokinase (CPK) and aldolase levels. Fasting (overnight) further increases (+100-500%) the serum concentration of these enzymes in myopathic hamsters; however, no such effect is demonstrable in normal hamsters, or in first generation offspring produced by crossbreeding the two strains (myopathic and normal). The changes are reversible, and the enzyme values return to previous levels within 72 hr. Neither phenobarbital nor hydrocortisone prevents the rises, as shown by CPK determinations; on the contrary, hydrocortisone elicits even greater serum enzyme increases.

Effect of methylprednisolone on predicted myocardial infarction size in man.

Therapeutic manipulations designed to conserve myocardium in patients with acute myocardial infarction appear to improve prognosis. To assess the role of glucocorticoids given in pharmacologic dosage in the early treatment of patients with acute myocardial infarction, serial serum creatine phosphokinase (CPK) were obtained every 1-2 hours in 39 consecutive patients admitted with acute myocardial infarction. Determination of completed infarction size (ISc) was made using all available CPK values (range 70-160 hours). Predicted infarct size (ILp) was based on early data following the rise in CPK from baseline values: projected CPK values were obtained over a 160 hour period using a curve fitting procedure based upon nonlinear Gauss-Newton stepwise iterations. In 13 uncomplicated control patients ISp was 43.2 +/- 11.6 (mean +/- SE) CPK-gram-equivalents (CPK-q-eq), based on data from the first 7 hours following the rise in serum CPK, while ISc was 44.7 +/- 11.4 CPK-geq (r = .99, n = 13). In 7 additional control patients whose hospitals courses were complicated by clinical extension ISp was 71.8 +/- 18.0 CPK-g-eq while ISc was 118.6 +/- 31.0 CPK-g-eq (p less than .03). In 19 patients treated with 3 grams of methylprednisolone 7-14 hours following the rise in serum CPK from baseline, data from early CPK determinations (7 hours) indicated an ISp of 118.5 +/- 24.1 CPK-g-eq while total CPK data indicate an ISc of 89.6 +/- 13.2 CPK-g-Eq (p less than .04). The exponential clearance of CPK (kd) was approximated in the controls (kd = .00095 +/- .00007 min-1) and glucocorticoid treated patients (kd = .00099 +/- .00006 min-1) and found to be similar. Thus, administration of a pharmacologic dose of methylprednisolone 7-14 hours following rise in serum CPK from baseline in a group of patients with acute myocardial infarctions has resulted in salvage of myocardium.

The effect of ultrasonic energy on the creatine phosphokinase determination.

The effect of ultrasonic energy on the creatine phosphokinase determination.

An Automated Method for Measuring Creatine Phosphokinase Activity in Serum

Abstract We describe a procedure for automating the determination of creatine phosphokinase (CPK) activity in serum by use of the AutoAnalyzer. Enzyme activity is determined by measuring the creatine phosphate formed from the CPK-catalyzed reaction of creatine with adenosine triphosphate (ATP). The sensitivity of the automated procedure was comparable to that of the manual method. By use of the most favorable concentrations of creatine, ATP, and magnesium ion in the substrate, a linear relationship was obtained between enzyme concentration and enzyme activities up to 600 mU, representing a sixfold improvement over that obtained by the manual method. The degree of correlation between results obtained by the manual and automated procedures is shown.

Hypokalemic myopathy and elevation of serum enzymes.

THE MEASUREMENT of serum enzyme activities, particularly those of creatine phosphokinase (CPK), aldolase, and glutamic oxaloacetic transaminase (SGOT), is an important adjunct in the diagnosis of primary muscle disease. 1-4 Elevations have been found in patients with muscular dystrophy and polymyositis, 5-7 whereas patients with neurogenic atrophy generally have had normal levels. 8 Altered potassium metabolism has long been associated with muscle dysfunction, 9 but only a few references have appeared linking hypokalemia, myopathy, and serum enzyme elevation. 10-12 Three patients with hypokalemia and severe muscle weakness were studied; all had marked alterations in their serum enzymes, particularly CPK. Methods Creatine phosphokinase determinations were done using the method of Nielsen and Ludvigsen. 13 The normal range is 0μU to 18μU per milliliter. Glutamic oxaloacetic transaminase determinations were performed using a modification of the method of Henry and co-workers. 14 The normal values are in the range of