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ABCB1과 OPRM1 유전적 다형성이 수술 후 통증 조절을 위한 Fentanyl 요구량에 미치는 영향
박창신,박혜진,차영덕,강주희,최주연,박소진,정인준 대한마취통증의학회 2008 Korean Journal of Anesthesiology Vol.53 No.3
Background: Fentanyl, which is a potent synthetic μ-opioid receptor agonist, is one of the most widely used opioids in anesthesia and pain control. However, the pharmacodynamics of fentanyl show wide inter-individual variability. Therefore, this study was conducted to evaluate the influence of the blood-brain barrier transporter protein, p-glycoprotein, and μ-opioid receptor genetic polymorphism on fentanyl pharmacodynamics. Methods: Seventy-nine patients who underwent posterior lumbar interbody fusion (PLIF) were included in this study. Postoperatively, the patients received fentanyl via an intravenous patient controlled analgesia device. The cumulative fentanyl doses and other pharmacodynamic data were then recorded at 2 h, 6 h, 12 h, 24 h and 48 h after the operation. In addition, genomic DNA was isolated from the patient’s peripheral leukocytes and then evaluated for the presence of OPRM1 A118G and ABCB1 C3435T genetic polymorphism using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: The results of this study indicated that ABCB1 C3435T genetic polymorphism may be related to the cumulative fentanyl requirement for postoperative pain control. However, these findings were not statistically significant (P = 0.09). In addition, no relationship was observed between OPRM1 A118G and the cumulative postoperative fentanyl requirement. However, the cumulative postoperative fentanyl requirement was lower in the TTAA group (ABCB1 3435 TT, OPRM1 118 AA) than in the CCGG group (ABCB13435 CC, OPRM1 118 GG). Conclusions: The ABCB1 C3435T polymorphism may affect fentanyl pharmacodynamics. However, further studies are required to confirm the relationship between p-glycoprotein and fentanyl. Background: Fentanyl, which is a potent synthetic μ-opioid receptor agonist, is one of the most widely used opioids in anesthesia and pain control. However, the pharmacodynamics of fentanyl show wide inter-individual variability. Therefore, this study was conducted to evaluate the influence of the blood-brain barrier transporter protein, p-glycoprotein, and μ-opioid receptor genetic polymorphism on fentanyl pharmacodynamics. Methods: Seventy-nine patients who underwent posterior lumbar interbody fusion (PLIF) were included in this study. Postoperatively, the patients received fentanyl via an intravenous patient controlled analgesia device. The cumulative fentanyl doses and other pharmacodynamic data were then recorded at 2 h, 6 h, 12 h, 24 h and 48 h after the operation. In addition, genomic DNA was isolated from the patient’s peripheral leukocytes and then evaluated for the presence of OPRM1 A118G and ABCB1 C3435T genetic polymorphism using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: The results of this study indicated that ABCB1 C3435T genetic polymorphism may be related to the cumulative fentanyl requirement for postoperative pain control. However, these findings were not statistically significant (P = 0.09). In addition, no relationship was observed between OPRM1 A118G and the cumulative postoperative fentanyl requirement. However, the cumulative postoperative fentanyl requirement was lower in the TTAA group (ABCB1 3435 TT, OPRM1 118 AA) than in the CCGG group (ABCB13435 CC, OPRM1 118 GG). Conclusions: The ABCB1 C3435T polymorphism may affect fentanyl pharmacodynamics. However, further studies are required to confirm the relationship between p-glycoprotein and fentanyl.
Potential Targeting of Siglecs, Mast Cell Inhibitory Receptors, in Interstitial Cystitis
박창신,Bruce S. Bochner 대한배뇨장애요실금학회 2011 International Neurourology Journal Vol.15 No.2
Mast cell increases and activation are detected in the chronic inflammatory bladder disease interstitial cystitis (IC), and their proinflammatory mediators are felt to contribute to regional pelvic pain and inflammatory pathophysiology. The immunoreceptor tyrosine-based inhibition motif-containing sialic acid-binding immunoglobulin-like lectins (Siglecs) expressed in mast cells could be evaluated as in vivo signaling regulators capable of inhibiting IC-related mast cell activation.