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Korean Journal of Anesthesiology 2006;50(1):84-89.
DOI: https://doi.org/10.4097/kjae.2006.50.1.84   
Influence of 5-HT3b Receptor AAG Deletion Mutation and CYP2D6*10 on the Ondansetron Treatment.
Ju Hee Kang, Helen Ki Shinn, Sung Ho Shin, Chang Shin Park, Hong Sik Lee, Jang Ho Song, Young Deog Cha, Hae Jin Park
1Department of Pharmacology, College of Medicine, Inha University, Incheon, Korea.
2Department of Anesthesiology and Pan Medicine, College of Medicine, Inha University, Incheon, Korea.
3Department of Anesthesiology, Medicine, Seoul University College of Medicine, Seoul, Korea. anesthjin@hanmail.com
Abstract
BACKGROUND
Postoperative nausea and vomiting (PONV) are common problems in patients undergoing general anesthesia. Ondansetron is widely used for this problems. But, some patients treated with ondansetron do not respond to therapy. We hypothesized that patients with genetic variation in 5-HT3b receptor and CYP2D6 gene might respond differently to ondansetron treatment.
METHODS
135 patients undergoing gynecologic surgery were given 4 mg ondansetron 15 min before extubation. The assessment of PONV was performed during < 2 hours and 2-24 hours. DNA was extracted from blood and was analyzed by using restriction fragment-length polymorphism (RFLP) and site-specific PCR.
RESULTS
In 5-HT3b AAG deletion mutation, the incidence of nausea and vomiting < 2 hr were 25% and 12.5% for wild, 23.4% and 12.2% for heteromutant. The incidence of nausea and vomiting 2-24 hr were 3.2% and 1.1% for wild, 4.9% and 2.4% for heteromutant. This showed no significant differences between two groups. In CYP2D6*10 mutation, the incidence of nausea and vomiting < 2 hr were 28.6% and 19.6% for wild, 22.8% and 8.8% for heteromutant and 23.5% and 5.9% for homomutant. The incidence of nausea and vomiting 2-24 hr were 5.4% and 1.8% for wild, 3.2% and 1.6% for heteromutant, 0% and 0% for homomutant. This showed no significant differences among three groups.
CONCLUSIONS
The incidence of PONV were not different among the genotype of CYP2D6*10 and 5HT3b AAG mutation.
Key Words: CYP2D6*10; 5-HT3b receptor; genetic polymorphism; ondansetron; PONV


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