Acute organophosphate poisoning caused by dysfunction of pancreatic islet.docVIP

Acute organophosphate poisoning caused by dysfunction of pancreatic islet.doc

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 PAGE \* MERGEFORMAT 3 Acute organophosphate poisoning caused by dysfunction of pancreatic islet [Abstract] through the exploration of acute organophosphorus pesticide poisoning caused by high blood glucose, islet dysfunction mechanism. The results show that islet β -cell function in patients with impaired, and the poisoning of islet dysfunction re-re. After discharge from hospital should continue to avoid contact with organic phosphorus pesticides, review blood glucose. [Keywords:] organic phosphorus OGTT glucose C-peptide In recent years, studies have shown that organic phosphorus pesticide poisoning may be caused by diabetes, the existence of a potential effect of interfering with glucose metabolism in mammals, induced hyperglycemia. This paper further explore the acute organophosphorus pesticide poisoning caused by high blood glucose, islet dysfunction mechanism. 1 Data and methods 1.1 cases in our hospital in January 2006 -2,008 year in October admitted with moderate to severe acute organophosphorus pesticide poisoning patients. Exclusion criteria: ① younger than 14 years of age or greater than 50 years of age; ② the original serious underlying diseases; ③ a family history of diabetes. A total of 84 patients eligible, of which 32 cases of male and female 52 cases, aged 14-48 years old; taking pesticides volume 5-250 ml; 2 Li abuse treatment skin. Pesticide Type: DDVP 36 cases, omethoate 3 cases, dimethoate 2 cases, 13 cases of parathion, phorate, 26 cases can not clearly name of the drug in 4 cases. Cholinesterase activity continued to decrease. Moderate and severe patients were divided into two groups; moderate intoxication standard M-like symptoms aggravated, there N-like symptoms, cholinesterase activity 50% -30%; severe poisoning as having standard M, N-like symptoms, accompanied by pulmonary edema, convulsions, coma, respiratory muscle paralysis or cerebral edema, cholinesterase activity less than 30%. 1.2 Treatment of conventional treatment:

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