Creatine phosphokinase half life,body supplement india,clickbank affiliate program knihy - Step 3

08.04.2014, admin  
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15.De Wilde V, Vogelaers D, Colardyn F, Vanderstraeten G, Van den Neucker K, De Bleecker J et al. 20.Soltaninejad K, Shadnia S, Afkhami-Taghipour M, Saljooghi R, Mohammadirad A, Abdollahi M. In 2007, The American Association of Poison Control Centers received 96,307 calls (3.4% of all human exposures) related to pesticide exposures, many of which involved OP agents and 80 uses of Pralidoxime (2-PAM).
2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Organophosphate exposures in the United States: a longitudinal analysis of incidents reported to poison centers. Poison control, training and research center, Institute of Internal Medicine, Government General Hospital, Madras Medical College, Chennai, India.
The kinetic study of the inhibition of human cholinesterases by demeton-S-methyl shows that cholinesterase-based titration methods are not suitable for this organophosphate.
Impairment in clinical indices in acute organophosphate insecticide poisoning patients in India.
Biochemical changes associated with muscle fibre necrosis after experimental organophosphate poisoning. Sarcoplasmic lipase and non-specific esterase inhibition in myofibers of rats intoxicated with the organophosphate isofenphos. Albumin, a new biomarker of organophosphorus toxicant exposure, identified by mass spectrometry.
Blood â-glucuronidase as a suitable biomarker at acute exposure of severe organophosphorus poisoning in human. Measurement of paraoxonase (PON1) status as a potential biomarker of susceptibility to organophosphate toxicity. Paraoxonase (PON1) polymorphism and activity as the determinants of sensitivity to organophosphates in human subjects.
Use of Biomarkers to Indicate Exposure of children to organophosphate pesticides: Implications for a longitudinal study of children's environmental health. Acid-base interpretation can be the predictor of outcome among patients with acute organophosphate poisoning before hospitalization. Effects of acidosis on the activity of creatine phosphokinase and its isoenzymes in the serum of newborn infants.

OP poisoning causes what is known as the "suicide impulse" which leads to high level of suicides in some sectors of the agricultural industry. Massive OP intoxication from suicidal and accidental events, such as the Jamaican ginger palsy incident in 1930, led to the discovery of the mechanism of action of OPs. They act by inhibiting the acetylcholinesterase enzyme (AchE) at muscarinic and nicotinic receptors, producing an array of symptoms like miosis, bradycardia, increased gastrointestinal motility, emesis, sweating, tachypnea, salivation, lacrimation, altered sensorium, fasciculation, bronchospasm, blurred vision, photophobia, urination and defecation.
Complications include acidosis, respiratory paralysis, acute renal failure, seizures, arrythmias, aspiration, coma and even death. A delay of initiation of treatments limits not only outcome, but also the opportunity to use 2-PAM (cholinesterase re-activator) which prevents "aging" of the enzyme. Till now, investigations comprised serum erythrocyte cholinesterase (EchE) and plasma cholinesterase (PchE) estimation, the levels of which are reduced in OP poisoning. But estimation of their levels is costly and not regularly performed in most laboratories of our country. Besides, the kinetic study of inhibition of human AchEs by Demeton-S-methyl has shown that cholinesterase-based titration methods are not suitable for the estimation of OPs. Several animal model studies on rat liver and fresh-water snails indicate the association between OP poisoning and CPK levels.
It was a prospective and observational study conducted from 1 st January 2010 to 30 th June 2010. Clinical severity was categorized according to Peradeniya organophosphorus poisoning (POP) scale as shown in [Table 1].
Sample was collected aseptically by a single prick after initial resuscitation, from a peripheral vein without tying any tourniquet.
The total dose of atropine (mg) until the final clinical outcome (complete recovery or death) was calculated for each patient.
Just before discharging the patients from our institution or at the end of one completed week, the levels of serum CPK was re-evaluated and the responses were tabulated. Student's t-test and Pearson's Correlation coefficient were used for the assessment of statistical significance.
The morbidity and mortality outcome depends on time lag between exposure and the onset of management. With increase in use of OP compounds for agricultural and industrial purposes and due to easy access and low cost, they are becoming a major source of health hazard.

Identification, risk stratification, early diagnosis and prompt treatment of OP poisoning victims are equally vital.
Symptoms are classified into muscarinic and nicotinic receptors based on the receptor involved. Muscarinic features include excessive salivation, lacrimation, urination, diarrhea, gastrointestinal cramps, emesis, blurred vision, miosis, bradycardia, and wheezing.
Nicotinic features include fasciculation, paresis or paralysis, hypertension and tachycardia. Type I is due to continued depolarization at neuro-muscular junction, type II due to intermediate syndrome and type III due to delayed polyneuropathy.The presence of muscle fiber necrosis in OP poisoning has been already demonstrated in animal experimental studies by Calore et al. It has been shown that there is rhabdomyolysis in "intermediate syndrome" and consequently there is raised CPK level.
If there is ongoing injury to the muscle due to development of complications, the CPK level continues to be elevated.
Since half-life of CPK is about 1.5 days, it normalizes within 5-6 days of a single insult to the muscle. This approach is likely to cause difficulties as severe OP poisoning may cause either central respiratory depression with a reduced respiratory rate or tachypnea in the context of bronchorrhea, bronchoconstriction or respiratory muscle weakness.
OP-labeled albumin in human plasma and blood b-glucuronidase have been suggested by some researchers. These markers are also costly and their estimation is difficult in developing countries.Acidosis is a frequently encountered complication of OP poisoning, and it was previously suggested that both the degree and type of acidosis can be a predictor of outcome in OP poisoning. It is documented that acidosis itself can cause modest elevations in CPK levels in blood, which implies that CPK can be falsely high in case of acidosis. So, serial measurement of serum CPK level might be helpful in predicting as well as assessing the prognosis of patients of OP poisoning. So, exclusion of other causes of raised CPK in a patient of acute OP poisoning is required. It can be of particular importance in developing countries, where other costly biomarkers are difficult to estimate.

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