Blood creatine phosphokinase

Blood creatine phosphokinase (CPK) - increased Blood creatinine - increased Blood phosphate - decreased Blood potassium - decreased Blood urea nitrogen - increased... 

The longitudinal, postmarketing, observational PATRO children study (N = 1837, mean age = 9.33 years, 56.9% male) found that adverse events associated with Omnitrope with an incidence rate >0.001 (based on 2851.16 patient years) were headache, hypothyroidism, arthralgia, pain in extremity, injection-site haematoma, decreased glucose tolerance, asthenia, injection-site pain, increased blood creatine, phosphokinase and myalgia [36 -]. There were no confirmed cases of diabetes (type 1 or 2) or malignancy related to treatment and no anti-hGH antibodies have been found in a subset of 30 patients. 

Five repeated exposures of 200 ppm for 12.5 min every 4 d resulted in increased cardiac-specific creatine phosphokinase activity in the blood (pooled data measured at 2 h after the first, third, and fifth exposures) and ectopic heart beats during the first 2 min after injection of norepinephrine (after the fifth exposure) but failed to induce cardiac lesions (histopathologic examinations at 14 d postexposure) (O Flaherty and Thomas 1982). The rats were restrained and anesthetized. 

Extrapyramidal symptoms (EPS) Dystonic reactions develop primarily with the use of traditional antipsychotics. EPS has occurred during the administration of haloperidol and pimozide frequently, often during the first few days of treatment. Neuroleptic malignant syndrome (NMS) A potentially fatal symptom complex sometimes referred to as NMS has been reported in association with administration of antipsychotic drugs. Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status, and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, cardiac dysrhythmia). Additional signs may include elevated creatine phosphokinase, rhabdomyolysis, and acute renal failure. 

The essential feature of Neuroleptic Malignant Syndrome is the development of severe muscle rigidity and elevated temperature in an individual using neuroleptic medication. This is accompanied by two (or more) of the following symptoms diaphoresis, dysphagia, tremor, incontinence, changes in level of consciousness ranging from confusion to coma, mutism, tachycardia, elevated or labile blood pressure, leukocytosis, and laboratory evidence of muscle injury (e.g., elevated creatine phosphokinase [CPK].1... 

A healthy 31-year-old man developed acute renal insufficiency 18 hours after inhaling cocaine 5 g. His blood pressure was 150/100 mmHg, his serum creatinine 177 pmol/l, creatine phosphokinase activity 107 U/l, and serum potassium concentration 3.8 mmol/1. The urinary sodium concentration was 30 mmol/1 and there was a trace of protein and 1-2 red blood cells per high-power field. Immunological studies were unremarkable. Ultrasound showed kidneys of normal size with hyperechogenity of the right kidney. Over the next 10 days he recovered spontaneously. 

Therapeutic doses of morphine can alter the blood activities of amylase, lipase, lactate dehydrogenase, creatine phosphokinase, and leucine aminopeptidase, BSP retention, and urine glucose concentration (Benedict s) (57-59). 

Enzymes, which are normally produced in cells, are released into the blood when cells are injured. For example, after a heart attack, there is an increase in blood levels of creatine phosphokinase (CPK) and other enzymes such as lactate dehydrogenase (LDH). The extent of damage and the rate of recovery can be estimated by periodically measuring the levels of these enzymes. Measurement of the MB isozyme of CPK is also used as an aid in diagnosis. 

Monitor for symptoms of neuroleptic malignant syndrome (NMS) increased fever, pulse, and blood pressure, muscle rigidity, increased creatine phosphokinase, and WBC count altered mental status, acute renal failure, varying levels of consciousness pallor diaphoresis, tachycardia, and dysrhythmias. 

Disturbances in lipid metabolism also may occur, resulting in transitory increase of blood values for cholesterol and triglycerides. Liver function and serum lipids should initially be monitored, typically at baseline and at weeks 4 and 8. Serious adverse effects of isotretinoin therapy include increased creatine phosphokinase and blood glucose, as well as photosensitivity, pseudotumor cerebri, excess granulation tissue, hepatomegaly with abnormal liver function tests, bone abnormalities, arthralgias, muscle stiffness, and headaches. ... 

Myocardial infarction occurs when the blood supply to the heart muscle is blocked for an extended time. If this lack of blood supply, called ischemia, is prolonged, the myocardium suffers irreversible cell damage and muscle death, or infarction. When this happens, the concentration of cardiac enzymes in the blood rises dramatically as the dead cells release their contents into the bloodstream. Although many enzymes are liberated, three are of prime importance. These three enzymes, creatine phosphokinase (CPK), lactate dehydrogenase (LDH), and aspartate aminotransferase/serum glutamate-oxaloacetate transaminase (AST/SGOT), show a characteristic sequential rise in blood serum level following myocardial infarction and then return to normal. This enzyme profile, shown in the ac-... 

This syndrome is a combination of symptomatic effects produced by antipsychotic drug therapy. Symptoms and signs include hyperpyrexia, muscle rigidity, altered mental status (e.g., catatonia) and cardiovascular instability (e.g., unstable heart rate and blood pressure). Acute renal failure may ultimately occur. Diagnostic signs include elevated creatine phosphokinase (CPK) and myoglobinuria. 

Creatine phosphokinase (CK), one of the proteins measured to follow Ann Jeina s myocardial infarction (see Chapter 6) is present in cells as dimers (two subunits). The dimers may be homodimers (two identical subunits of either the M [muscle] isozyme or the B [brain] isozyme), or heterodimers (MB) The MB isozyme is produced only by the heart and readily released from injured cardiomyocytes into the blood (see Chapter 6). 

B. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, liver function tests, creatine phosphokinase, and arterial blood gases. 

In vitamin E-deficient rabbits, the activity of creatine phosphokinase increases, apparently in muscle first and in blood later. The administration of a-tocopherol normalizes the serum CPK levels. Because ethi-onine mimicks this effect of vitamin E, it has been proposed that vitamin E acts as a repressor of the gene responsible for the biosynthesis of creatine phosphokinase. It was also proposed that a similar mechanism could explain the increase in acid hydrolases observed in muscles of vitamin E-deficient animals. In the latter case, such an interpretation is unlikely because the appearance of the hydrolase is associated with the appearance of macrophages. 

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