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- The Incidence, Associated Factors and Clinical Impact of Hyperamylasemia in Self-poisoning Patients
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Min Gu Seo, Sang Hoon Oh, Jee Yong Lim, Han Joon Kim, Se Min Choi
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J Korean Soc Clin Toxicol. 2016;14(2):83-91. Published online December 31, 2016
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DOI: https://doi.org/10.22537/jksct.2016.14.2.83
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Abstract
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- 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.
- A Case of Delayed Administration of Naloxone for Morphine Intoxicated Patient
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Gun-Bea Kim, Won-Nyung Park, Hong-Du Gu
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J Korean Soc Clin Toxicol. 2012;10(1):33-36. Published online June 30, 2012
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Abstract
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- Opioids are the one of the most commonly used drugs to control cancer pain all over the world. But, we should not overlook the potential risk of opioid intoxication because they have well-known detrimental side effects. The opioid intoxication can be diagnosed thorough various clinical manifestations. The altered mental status, respiratory depression, and miosis is very representative clinical features although these symptoms don't always appear together. Unfortunately the opioid-toxidrome can be varied. A 42 years old man came to our emergency room after taking about 900 mg morphine sulfate per oral. He was nearly alert and his respiration was normal. Even though his symptoms didn't deteriorated clinically, serial arterial blood gas analysis showed increase in PaCO2. So we decided to use intravenous naloxone. Soon, he was fully awaked and his pupils size was increased. After a continuous infusion of intravenous naloxone for 2 hours, PaCO2 decreased to normal range and his pupil size also returned to normal after 12 hours. Though the levels of serum amylase and lipase increased slightly, his pancreas was normal according to the abdominal computed tomography. He had nausea, vomit, and whole body itching after naloxone continuous infusion, but conservatively treated. We stopped the continuos infusion after 1 day because his laboratory results and physical examinations showed normal. As this case shows, it is very important to prescribe naloxone initially. If you suspect opioid intoxication, we recommend the initial use of naloxone even though a patient has atypical clinical features. In addition, we suggest intranasal administration of naloxone as safe and effective alternative and it's necessary to consider nalmefene that has a longer duration for opioid intoxication.
- A Case of Lactic Acidosis after Metformin overdose
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Jung-Suk Park, Sung-Pil Chung, Han-Shick Lee, Eui-Chung Kim
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J Korean Soc Clin Toxicol. 2007;5(2):126-130. Published online December 31, 2007
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Abstract
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- Metformin is antihyperglycemic, not hypoglycemic. It causes neither insulin release from the pancreas nor hypo glycemia, even when taken in large doses. But, there are several reports of metformin-associated lactic acidosis (MALT). We present a case report of severe lactic acidosis most probably resulting from high doses of metformin in a patient with no known contraindications for metformin. A 43-year-old female was admitted to the emergency department due to a metformin overdose. She had diabetes for 6 years, well-controlled with metformin and novolet. One hour before admission, she impulsively took 50g metformin (100 mg or 100 tablets). Physical examination for symptoms revealed only irritability, and laboratory evaluation revealed only mild leukocytosis. After one hour the patient was drowsy, and arterial blood gas analysis showed severe lactic acidemia Seven hours after ED arrival, she commenced hemofiltration treatment and was admitted to the intensive care unit. Continuous venovenous hemodiafiltration was initiated. Forty-eight hours later, full clinical recovery was observed, with return to a normal serum lactate level. The patient was discharged from the intensive care unit on the third day. A progressive recovery was observed and she was discharged from the general word on the thirteenth day.