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Sun Pyo Kim 3 Articles
Extracorporeal Membrane Oxygenation and Continuous Renal Replacement Therapy for Treatment of Calcium Channel Blockers, Angiotensin II Receptor Blockers, and Metformin Overdose
Jae Han Jeong, Kyung Hoon Sun, Yong Jin Park, Sun Pyo Kim
J Korean Soc Clin Toxicol. 2018;16(2):165-171.   Published online December 31, 2018
DOI: https://doi.org/10.22537/jksct.2018.16.2.165
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An overdose of antihypertensive agents, such calcium channel blockers (CCBs) and angiotensin II receptor blocker (ARBs), and the antihyperglycemic agent, metformin, leads to hypotension and lactic acidosis, respectively. A 40-year-old hypertensive and diabetic man with hyperlipidemia and a weight of 110 kg presented to the emergency room with vomiting, dizziness, and hypotension following an attempted drug overdose suicide with combined CCBs, ARBs, 3-hydroxy-3-methylglutaryl-coemzyme A reductase inhibitors, and metformins. A conventional medical treatment initially administered proved ineffective. The treatment was then changed to simultaneous extracorporeal membrane oxygenation (ECMO) and continuous renal replacement therapy (CRRT), which was effective. This shows that simultaneous ECMO and CRRT can be an effective treatment protocol in cases of ineffective conventional medical therapy for hypotension and lactic acidosis due to an overdose of antihypertensive agents and metformin, respectively.
In vitro Protective Effects of Glehnia Littoralis on Alpha-amanitin Induced Hepatotoxicity
Bo Hyun Kim, Kyung Hoon Sun, Sun Pyo Kim, Yongjin Park
J Korean Soc Clin Toxicol. 2017;15(2):107-115.   Published online December 31, 2017
DOI: https://doi.org/10.22537/jksct.2017.15.2.107
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Purpose: Glehnia littoralis has been used to treat ischemic stroke, phlegm, cough, systemic paralysis, antipyretics and neuralgia. The pharmacological mechanisms of Glehnia littoralis include calcium channel block, coumarin derivatives, anticoagulation, anti-convulsive effect, as well as anti-oxidant and anti-inflammatory effects. Alpha-amanitin (${alpha}$-amanitin) is a major toxin from extremely poisonous Amanita fungi. Oxidative stress, which may contribute to severe hepatotoxicity was induced by ${alpha}$-amanitin. The aim of this study was to investigate whether Glehnia littoralis ethyl acetate extract (GLEA) has the protective antioxidant effects on ${alpha}$-amanitin -induced hepatotoxicity. Methods: Human hepatoma cell line HepG2 cells were pretreated in the presence or absence of GLEA (50, 100 and $200{mu}g/ml$) for 4 hours, then exposed to $60{mu}mol/L$ of${alpha}$-amanitin for an additional 4 hours. Cell viability was evaluated using the MTT method. AST, ALT, and LDH production in a culture medium and intracellular MDA, GSH, and SOD levels were determined. Results: GLEA (50, 100 and $200{mu}g/ml$) significantly increased the relative cell viability by 7.11, 9.87, and 14.39%, respectively, and reduced the level of ALT by 10.39%, 34.27%, and 52.14%, AST by 9.89%, 15.16%, and 32.84%, as well as LDH by 15.86%, 22.98%, and 24.32% in culture medium, respectively. GLEA could also remarkably decrease the level of MDA and increase the content of GSH and SOD in the HepG2 cells. Conclusion: In the in vitro model, Glehnia littoralis was effective in limiting hepatic injury after ${alpha}$-amanitin poisoning. Its antioxidant effect is attenuated by antidotal therapy.
A Case of a Herbicide Poisoning Induced Methemoglobinemia Patient Treated with High-dose Vitamin C
Kyung Hoon Sun, Jun Kew Kim, Chang Yeon Ryu, Seo Jin Kim, Hyeon Kyu Jo, Tae Ho Yoo, Yong Jin Park, Sun pyo Kim
J Korean Soc Clin Toxicol. 2017;15(2):148-151.   Published online December 31, 2017
DOI: https://doi.org/10.22537/jksct.2017.15.2.148
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Methemoglobinemia is a condition in which the iron portion of hemoglobin, which binds to oxygen, is oxidized to produce methemoglobin, which increases blood concentration. There are many causes of methemoglobinemia, the most common being food, drugs, and chemicals. A 75-year-old male patient who had taken an herbicide did not notice any nonspecific symptoms. However, after 4 hours, his methemoglobin levels increased to 17.1%, while after 7 hours it increased to 26.5%, at which time intravenous administration of methylene blue 1 mg/kg (an antidote) was started. After a total of five doses of methylene blue at 1 mg/kg due to reactive methemoglobinemia for about 36 hours, the methemoglobin levels increased to 23.7%. Because no more methylene blue could be administered, 10 g of ascorbic acid (vitamin C) was administered intravenously. After 82 hours, ascorbic acid 10 g was administered six times for repeated reactive methemoglobinemia. No additional reactive methemoglobinemia was observed. The ventilator and endotracheal tube were successfully removed on day 5 after admission.

JKSCT : Journal of The Korean Society of Clinical Toxicology