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Creatine 706 Tests

A large number of molecules have provided experimental evidence of neuroprotection in in vitro and in vivo models of Parkinson s disease and many of these putative neuroprotective substances are now the objects of clinical trials. Recently, a team of experts has identified potential neuroprotective agents to be tested in pilot studies [4]. Twelve compounds have been considered for clinical trials caffeine, coenzyme Q 10, creatine, estrogen, GPI1485, GM-1 ganglioside, minocycline, nicotine, pramipexole, ropinirol, rasagiline, and selegiline (for individual discussion see [4]). [Pg.165]

Patients with ischemic chest discomfort and suspected acute coronary syndrome are risk-stratified based upon a 12-lead electrocardiogram, past medical history, and results of the creatine kinase myocardial band and troponin tests. The diagnosis... [Pg.83]

Creatine kinase, creatine kinase myocardial band Creatine kinase (CK) enzymes are found in many isoforms, with varying concentrations depending on the type of tissue. Creatine kinase is a general term used to describe the nonspecific total release of all types of CK, including that found in skeletal muscle (MM), brain (BB) and heart (MB). CK MB is released into the blood from necrotic myocytes in response to infarction and is a useful laboratory test for diagnosing myocardial infarction. If the total CK is elevated, then the relative index (RI), or fraction of the total that is composed of CK MB, is calculated as follows RI = (CK MB/CK total) x 100. An RI greater than 2 is typically diagnostic of infarction. [Pg.1563]

Niacin requires baseline tests of liver function (alanine aminotransferase), uric acid, and glucose. Repeat tests are appropriate at doses of 1,000 to 1,500 mg/day. Symptoms of myopathy or diabetes should be investigated and may require creatine kinase or glucose determinations. Patients with diabetes may require more frequent monitoring. [Pg.123]

Am ino-1-methy 1-6-phenyl irnidazo 4,5-b]pyridine (29 PhIP), usually the most abundant product of food-derived mutagens, is formed by heating creatine and phenylalanine at 200 °C200. This compound is modestly mutagenic in the Ames test, but is a potent carcinogen in rats and mice, causing breast and colon cancers. [Pg.1033]

A number of clinical tests are available to detect kidney damage. The clinician examining a patient or the toxicologist monitoring an animal toxicity stndy collects urine and blood samples. Indications of kidney damage (which, of course, for the human patient could be related to many factors other then chemical toxicity) include urinary excretion of excessive amonnts of proteins and glucose, and excessive levels in the blood of unexcreted waste products such as urea and creatine. A number of additional kidney function tests are available to help pin down the location of kidney dysfunction. [Pg.122]

IM use May increase creatine phosphokinase levels. Use of the enzyme determination without isoenzyme separation, as a diagnostic test for acute Ml, may be compromised. [Pg.445]

Adverse events occurring in at least 3% include abnormal liver function tests, increased ALT and AST, increased creatine phosphokinase, respiratory disorder, abdominal pain, back pain, headache. [Pg.630]

Lab test abnormalities include the following ALT, AST, creatine kinase, hematuria, neutrophils, serum amylase, serum glucose, triglycerides, urine glucose. [Pg.1840]

Biocompatibility of injectable formulations with tissues can be tested by observing microscopic histology of the tissues so exposed, or by using erythrocyte hemolysis as a surrogate for these other tissues. Alternatively, one can measure the level of the cytosolic enzyme creatine phosphokinase that is released from damaged tissues (18). [Pg.277]

Degradation Creatine and creatine phosphate spontaneously cyclize at a slow, but constant, rate to form creatinine, which is excreted in the urine. The amount of creatinine excreted is proportional to the total creatine phosphate content of the body, and thus can be used to estimate muscle mass. When muscle mass decreases for any reason (for example, from paralysis or muscular dystrophy), the creatinine content of the urine falls. In addition, any rise in blood creatinine is a sensitive indicator of kidney malfunction, because creatinine is normally rapidly removed from the blood and excreted. A typical adult male excretes about 15 mmol of creatinine per day. The constancy of this excretion is sometimes used to test the reliability of collected 24-hour urine samples—too little creatinine in the submitted sample may indicate an incomplete sample. [Pg.285]

EPMEs based on carbon paste modified with antibiotics vancomycin, teicoplanin and teicoplanin modified with acetonitrile are proposed for the determination of d-2-HGA [47]. The proposed electrodes can be used reliably for enantiopurity tests of d-2-HGA using direct potentiometric method of analysis. The linear concentration ranges recorded for EPMEs are 10 7-10 3, 10 7-10 2 and 10 6-10 2 mol/L with detection limits of 1.00 x 10 8, 1.00 x 10 8 and 1.00 x 10 7 mol/L for the vancomycin, teicoplanin and teicoplanin modified with acetonitrile-based EPME, respectively. The selectivity was determined over l-2-HGA, creatine, creatinine and some inorganic cations. The proposed EPMEs were applied for the assay of d-2-HGA in urine samples. The duration of one analysis is 10 min, including the calibration of the instrument and the determination of the amount of d-2-HGA in the urine sample. [Pg.66]

Creatine is sold in powdered, liquid, tablet, capsule, and chewing-gum formulations. The most popular formulation of creatine is creatine monohydrate, which is also the creatine formula that has been most extensively tested in clinical studies. Pure creatine monohydrate is a white, odorless, crystal powder with a faintly sweet taste. Other variations of creatine supplements are available, including creatine citrate and creatine phosphate. However, the clinical data on the effectiveness of these formulas is limited. [Pg.120]

Because creatine is regulated by the FDA as a dietary supplement and not a drug, the purity of the product is a concern. A test of 100 popular nutritional supplements conducted by the International Olympic Committee (IOC) at the German Sports University in Cologne found that 16 were adulterated with nandrolone, a steroid. Nandrolone was not a listed ingredient on the product label, and most of the creatine products tested originated in the United States. [Pg.125]

In other independent tests, ConsumerLab.com, a privately held U.S. company that specializes in laboratory analysis of nutritional and herbal supplements for purity, strength, and truth in labeling, found that 15% of creatine supplements tested did not meet industry standards for creatine content, purity, and label claims. [Pg.125]

As of early 2002, creatine supplementation was not on the list of banned or prohibited supplements of the International Olympic Committee, the United States Olympic Committee, or the NCAA. However, since nutritional supplements are not closely regulated by the FDA, the United States Anti-Doping Agency (the USADA, which oversees drug testing for the USOC) warns that ingestion of any nutritional supplement is at the athlete s own risk. [Pg.126]

On June 6, this patient developed severe loin pain after he participated in two 150-m sprints at a town athletics meeting. After 5 days, he was referred to the outpatient clinic of our department. His serum creatinine and uric acid levels and FEUA, were 2.9mg/dl, 2.1 mg/dl, and 49.7%, respectively. His creatine phosphokinase (CPK) level was normal. When his serum creatinine level decreased to 1.58 mg/dl, a contrast medium was administered. A delayed computed tomography (CT) scan after 24 and 48 h confirmed patchy wedge-shaped contrast enhancement (Fig. 58). Under a diagnosis of ALPE, his body water balance (hydration) was controlled. In this patient, recovery was achieved 4 weeks after onset, and his serum creatinine and uric acid levels were then 1.0 mg/dl and 0.6 mg/dl, respectively. Furthermore, load tests with a uric acid reabsorption inhibitor (benzbromarone) and a uric acid excretion inhibitor (pyrazinamide) suggested presecretory reabsorption defect-related renal hypouricemia. A kidney biopsy 16 days after onset confirmed the recovery from acute tubular necrosis. [Pg.65]


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