The Incidence, Associated Factors and Clinical Impact of Hyperamylasemia in Self-poisoning Patients
2
조회
0
다운로드
1
인용
0
참고문헌
키워드
초록
Purpose: This study was conducted to investigate the incidence, associated factors and clinical impact of hyperamylasemia in self-poisoning patients. Methods: This study was based on a toxicology case registry of patients treated from 2009 to 2013 at a tertiary care university hospital. We retrospectively investigated the demographics, clinical variables, laboratory variables and intoxicants. Hyperamylasemia was defined as an elevation in serum amylase level to above the upper normal limit within 24 hours after admission. We analyzed the predisposing factors and clinical outcomes of patients in the hyperamylasemia group. Results: Hyperamylasemia was identified in 49 (13.3%) of the 369 patients. Using multivariate logistic regression, the odds ratios for HA were 3.384 (95% confidence interval, 1.142-8.013, p=0.014), 3.261 (95% confidence interval, 1.163-9.143, p=0.025) and 0.351 (95% confidence interval, 0.154-0.802, p=0.013) for pesticides, multi-drug use and sedatives, respectively. In the hyperamylasemia group, the peak amylase levels during 72 hours were correlated with the peak lipase levels (r=0.469, p=0.002) and peak aspartate aminotransferase levels (r=0.352, p=0.013). Finally, none of these patients had confirmed acute pancreatitis. Conclusion: Hyperamylasemia occurred rarely in these self-poisoning patients, and pesticide and multi-drug use were independent predictors of hyperamylasemia. Peak amylase levels were correlated with the peak lipase and aspartate aminotransferase levels.
Abstract
Purpose: This study was conducted to investigate the incidence, associated factors and clinical impact of hyperamylasemia in self-poisoning patients. Methods: This study was based on a toxicology case registry of patients treated from 2009 to 2013 at a tertiary care university hospital. We retrospectively investigated the demographics, clinical variables, laboratory variables and intoxicants. Hyperamylasemia was defined as an elevation in serum amylase level to above the upper normal limit within 24 hours after admission. We analyzed the predisposing factors and clinical outcomes of patients in the hyperamylasemia group. Results: Hyperamylasemia was identified in 49 (13.3%) of the 369 patients. Using multivariate logistic regression, the odds ratios for HA were 3.384 (95% confidence interval, 1.142-8.013, p=0.014), 3.261 (95% confidence interval, 1.163-9.143, p=0.025) and 0.351 (95% confidence interval, 0.154-0.802, p=0.013) for pesticides, multi-drug use and sedatives, respectively. In the hyperamylasemia group, the peak amylase levels during 72 hours were correlated with the peak lipase levels (r=0.469, p=0.002) and peak aspartate aminotransferase levels (r=0.352, p=0.013). Finally, none of these patients had confirmed acute pancreatitis. Conclusion: Hyperamylasemia occurred rarely in these self-poisoning patients, and pesticide and multi-drug use were independent predictors of hyperamylasemia. Peak amylase levels were correlated with the peak lipase and aspartate aminotransferase levels.
참고문헌 (37)
- Salt WB 2nd, "Amylase--its clinical significance:a review of the literature", Medicine (Baltimore), 55, pp.269~289 (1976)
- Buchman AL, "Total serum amylase but not lipase correlates with measured glomerular filtration rate", J Clin Gastroenterol, 16, pp.204~206 (1993)
- Pezzilli R, "Serum pancreatic enzyme concentrations in chronic viral liver diseases", Dig Dis Sci, 44, pp.350~355 (1999)
- Vinicor F, "Hyperamylasemia in diabetic ketoacidosis: sources and significance", Ann Intern Med, 91, pp.200~204 (1979)
- Yagi C, "Hyperamylasemia associated with endometrioid carcinoma of the ovary: case report and immunohistochemical study", Gynecol Oncol, 25, pp.250~255 (1986)
- Benedetti G, "Challenging problems in malignancy: case 1. Presentation of small-cell lung cancer with marked hyperamylasemia", J Clin Oncol, 22, pp.3826~3828 (2004)
- Frulloni L, "Pancreatic hyperenzymemia: clinical significance and diagnostic approach", JOP, 6, pp.536~551 (2005)
- Sahin I, "The prevalence of pancreatitis in organophosphate poisonings", Hum Exp Toxicol, 21, pp.175~177 (2002)
- Lee WC, "The clinical significance of hyperamylasemia in organophosphate poisoning", J Toxicol Clin Toxicol, 36, pp.673~681 (1998)
- Ku JE, "A case of survival after chlorfenapyr intoxication with acute pancreatitis", Clin Exp Emerg Med, 2, pp.63~66 (2015)
- Brahmi N, "Acute pancreatitis subsequent to voluntary methomyl and dichlorvos intoxication", Pancreas, 31, pp.424~427 (2005)
- Mofenson HC, "Acetaminophen induced pancreatitis", J Toxicol Clin Toxicol, 29, pp.223~230 (1991)
- Yang CC, "Pancytopenia, hyperglycemia, shock, coma, rhabdomyolysis, and pancreatitis associated with acetaminophen poisoning", Vet Hum Toxicol, 43, pp.344~348 (2001)
- Moreno Escobosa MC, "Pancreatitis due to codeine", Allergol Immunopathol, 33, pp.175~177 (2005)
- Hastier P, "A new source of drug-induced acute pancreatitis: codeine", Am J Gastroenterol, 95, pp.3295~3298 (2000)
- Srivastava R, "Hyperamylasaemia: not the usual suspects", BMJ, 331, pp.890~891 (2005)
- Lankisch PG, "Drug induced acute pancreatitis: incidence and severity", Gut, 37, pp.565~567 (1995)
- Sekimoto M, "JPN Guidelines for the management of acute pancreatitis: epidemiology, etiology, natural history, and outcome predictors in acute pancreatitis", J Hepatobiliary Pancreat Surg, 13, pp.10~24 (2006)
- Vinklerová I, "Incidence, severity, and etiology of drug-induced acute pancreatitis", Dig Dis Sci, 55, pp.2977~2981 (2010)
- Andersen V, "Spontaneous reports on drug-induced pancreatitis in Denmark from 1968 to 1999", Eur J Clin Pharmacol, 57, pp.517~521 (2001)
- Bronstein AC, "2011 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 29th Annual Report", Clin Toxicol (Phila), 50, pp.911~1164 (2012)
- Tenner S, "American College of Gastroenterology guideline: management of acute pancreatitis", Am J Gastroenterol, 108, pp.1400~1415 (2013)
- Dressel TD, "Pancreatitis as a complication of anticholinesterase insecticide intoxication", Ann Surg, 189, pp.199~204 (1979)
- Ikizceli I, "Effect of interleukin-10 on pancreatic damage caused by organophosphate poisoning", Regul Toxicol Pharmacol, 42, pp.260~264 (2005)
- Bulera SJ, "Acetaminophen-arylated proteins are detected in hepatic subcellular fractions and numerous extra-hepatic tissues in CD-1 and C57B1", 6J mice, 1996, pp.109, 85~99
- Badalov N, "Drug-induced acute pancreatitis: an evidencebased review", Clin Gastroenterol Hepatol, 5, pp.648~661 (2007)
- Lancashire RJ, "Discrepancies between population-based data and adverse reaction reports in assessing drugs as causes of acute pancreatitis", Aliment Pharmacol Ther, 17, pp.887~893 (2003)
- Martín Rubí JC, "Poisoning caused by organophosphate insecticides. Study of 506 cases", Rev Clin Esp, 196, pp.145~149 (1996)
- Clavien PA, "Acute pancreatitis and normoamylasemia. Not an uncommon combination", Ann Surg, 210, pp.614~620 (1982)
- Lankisch PG, "Underestimation of acute pancreatitis: patients with only a small increase in amylase", lipase levels can also have or develop severe acute pancreatitis, 1999, pp.44, 542~
- Clavien PA, "Acute pancreatitis and normoamylasemia", Ann Surg, 210, pp.614~620 (1982)
- Ranson JH, "Diagnostic standards for acute pancreatitis", World J Surg, 21, pp.136~142 (1997)
- Vissers RJ, "Amylase and lipase in the emergency department evaluation of acute pancreatitis", J Emerg Med, 17, pp.1027~1037 (1997)
- Suzuki K, "Salivary-type hyperamylasemia in theophylline poisoning", Pediatr Int, 47, pp.209~210 (2005)
- Donaldson LA, "Amylase activity in human bile", Gut, 20, pp.216~218 (1979)
- Rosenblum JL, "Hepatobiliary and pancreatic clearance of circulating pancreatic amylase", Am J Physiol, 243, pp.21~27 (1982)
- Coté GA, "The role of etiology in the hyperamylasemia of acute liver failure", Am J Gastroenterol, 104, pp.592~597 (2009)
