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Hyperamylasemia and acute pancreatitis following anticholinesterase poisoning

Postgraduate Institute of Medical Education and Research, Chandigarh, India, surjit51{at}hotmail.com, surjit51200{at}yahoo.co

Udaybhan Bhardwaj

Postgraduate Institute of Medical Education and Research, Chandigarh, India

Suresh k. Verma

Department of Internal Medicine and Biochemistry

Ashish Bhalla

Postgraduate Institute of Medical Education and Research, Chandigarh, India

Kirandip Gill

Department of Internal Medicine and Biochemistry

A prospective study was undertaken to find the incidence of hyperamylasemia and acute pancreatitis in patients with anticholinesterase poisoning. This was done by serial estimation of total serum amylase and pancreatic imaging by ultrasonography and confirmed, if necessary, by computerized tomography. Anticholinesterase poisoning was caused by either ingestion or accidental exposure to organophosphates or carbamates; it was diagnosed when patients presented with features of cholinergic crisis, depressed serum butrylcholinesterase activity of >50% and showed improvement following administration of atropine alone or atropine and 2-PAM. All the patients admitted with anticholinesterase poisoning between July 2001 and June 2005 were prospectively studied for elevated serum amylase. The serum amylase levels were estimated daily up to 10 days in survivors and in nonsurvivors till they survived. Ultrasonography of the abdomen was carried out in all to find swelling of the pancreas. Computerized tomography was undertaken in those who had a swollen pancreas or whose serum amylase levels were elevated significantly (800 S.U). Of the 86 patients enrolled, 79 were taken up for analysis as data were incomplete in 7. Of the 79 patients, serum amylase was found to be elevated that is, >200 S.U. in 37 patients (46.95%). In three patients it was 800 S.U. One of them showed swollen pancreas on ultrasonography, which was confirmed by computerized tomography. This patient had ingested propoxyfur. In the other two patients, evidence of acute pancreatitis was not observed (on autopsy in one who died and on imaging in the other who survived). They had ingested chlorpyriphos. There was no significant correlation between the nature of the compounds (organophosphate or carbamates), inhibition of serum BUChE at admission, duration and severity of cholinergic syndrome and increase and time course of increase in serum amylase. Except for fenthion, significant persistent increase in serum amylase was not observed with individual compounds. The other associated abnormalities were polymorphonuclear leukocytosis (TLC >11 000/cumm) in all 37 patients who had elevated amylase, hyperglycemia (6/37) and, elevated transaminases (6/37). Mild elevation of serum amylase is common in patients with anticholinesterase poisoning. However, acute pancreatitis is rare. Human & Experimental Toxicology (2007) 26, 467—471

Key Words: organophosphates • carbamates • acute poisoning • hyperamylasemia • acute pancreatitis

Human & Experimental Toxicology, Vol. 26, No. 6, 467-471 (2007)
DOI: 10.1177/0960327107076814


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