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Koh, Jin-Sin,Park, Yongwhi,Ahn, Jong-Hwa,Kang, Min Gyu,Kim, Kye-Hwan,Bae, Jae Seok,Park, Hyun Woong,Jang, Jeong Yoon,Park, Jeong Rang,Hwang, Seok-Jae,Kwak, Choong Hwan,Hwang, Jin-Yong,Tantry, Udaya,Gu Georg Thieme Verlag KG 2019 Thrombosis and Haemostasis Vol.119 No.2
<B>Abstract</B><P>Amlodipine has a potential to reduce clopidogrel bioactivation through the cytochrome P450 3A4 enzyme in vivo, but the clinical impact of this interaction remains controversial. This randomized, open-label, two-period, crossover study was performed to evaluate the influence of amlodipine on the haemostatic profiles of high-risk patients during clopidogrel treatment. We recruited 40 Asian patients (Male/Female: n = 36/4) receiving clopidogrel (75 mg/day), aspirin (100 mg/day) and rosuvastatin for at least 6 months following percutaneous coronary intervention. Patients were randomly assigned to receive either 5 mg daily amlodipine or not for 2 weeks, and then were crossed over to the other treatment for 2 weeks. Haemostatic measurements were conducted with the VerifyNow assay and thromboelastography (TEG). Primary endpoint was P2Y12 Reaction Units (PRU) during on- versus off-amlodipine treatment. The on-amlodipine strategy showed higher level of PRU compared with the off-amlodipine strategy (176.8 ± 75.4 vs. 150.7 ± 65.5 PRU; ∆mean: 26.1 PRU; ∆95% confidence interval [CI]: 4.5-47.7 PRU; p = 0.019). Platelet-fibrin clot strength measured by TEG was lower during on- versus off-amlodipine treatment (7,712 ± 1,889 vs. 8,559 ± 2,174 dyne/cm2; ∆mean: -847 dyne/cm2; ∆95% CI: -1,632 to -62 dyne/cm2; p = 0.035). After amlodipine discontinuation, 27 patients (67.5%) showed a decrease in PRU, which was associated with ‘PRU ≥ 160 on-amlodipine’ in multivariate analysis (odds ratio: 62.014; 95% CI: 2.302-1670.328; p = 0.014). In conclusion, amlodipine increases platelet reactivity and decreases platelet-fibrin clot strength during clopidogrel treatment. In addition, the effect of amlodipine discontinuation on clopidogrel responsiveness is associated with on-amlodipine platelet reactivity.</P>
김진수,이기남,이종현,문준일,고석신 대한마취과학회 1986 Korean Journal of Anesthesiology Vol.19 No.1
Several methods for the management of intractable pain for various conditions including malignant disorders, herpes zoster, and low back pain and/or sciatica in 80 patients were described and analyzed. Neurolytic blodks of celiac plexus were given to the patienta suffering from intra-abdominal pain from malignant origin or chronic pancreatitis. Herpes zoster was treated mainly by chemical sympathectomy via paravertebral route and occassionaly corticosteroid was administered epidurally with the local anesthetic, bupivacaine. All the patients with low back pain and/or sciatica were given epidural corticosteroid one to three times. Other peripheral verve blocks and regional corticosteroid therapy were given to the rest of the patients. Fair to excellent result was obtained in 71% of the patients but the response was poor in the remaining 28% of the patients. It seems that the earlier the patients were referred to the pain clinic, the better the results were.
Leukocytosis 가 동맥혈 산소 분압에 미치는 영향
김진호,심재선,고신옥,오흥근,강신범 대한마취과학회 1990 Korean Journal of Anesthesiology Vol.23 No.4
Arterial blood gas analysis has become an integral part of the clinical evaluation of the patient with known or suspected pulmonary disease. However, when the results of the measurements show arterial hypoxemia which is out of proportion to the clinical and X-ray evidence of lung disease, we may consider potential errors in measurement involving the blood gas analyzer or methods of blood sample storage. We experienced spurious hypoxemia in a patient with extreme leukocytosis (220.0 x 10³/mm³) secondary to leukemia. The degree of PaO₂ decay was blunted by placing the blood on ice.
( Young Hoon Jeong ),( Jin Sin Koh ),( Min Kyung Kang ),( Yeon Jeong Ahn ),( In Suk Kim ),( Yong Whi Park ),( Seok Jae Hwang ),( Choong Hwan Kwak ),( Jin Yong Hwang ) 대한내과학회 2010 The Korean Journal of Internal Medicine Vol.25 No.2
Background/Aims: In patients with coronary artery stents, the cost of clopidogrel has been cited as a factor in the premature discontinuation of therapy. Thus, the introduction of lower-cost generic clopidogrel may increase patient compliance. However, platelet inhibition by generic clopidogrel has not been compared to the original clopidogrel formulation in patients with coronary artery stents. Methods: We prospectively enrolled 20 patients receiving chronic therapy with the original clopidogrel bisulfate (Plavix(R)). After assessing patient compliance with Plavix(R), maintenance therapy was switched to generic clopidogrel bisulfate (Plavitor(R)). Platelet reactivity was assessed at baseline and 30-day after the switch using conventional aggregometry and the VerifyNow P2Y12 assay. Results: All patients completed maintenance therapy with Plavitor(R). Before and after switching therapy maximal (36.5±7.9% vs. 39.8±16.2%, p=0.280) and late platelet aggregation (23.5±10.9% vs. 29.1±18.3%, p=0.156) with 5 μmol/L adenosine diphosphate (ADP) stimulus did not differ. Likewise, 20 μmol/L ADP-induced platelet aggregation and P2Y12 reaction unit in patients on Plavitor(R) therapy was comparable to that in patients on Plavix(R) therapy. However, Bland-Altman analysis showed wide limits of agreement between measured platelet reactivity on Plavix(R) vs. Plavitor(R) therapies. Conclusions: Among patients on Plavix(R) maintenance therapy with coronary stents, replacement with Plavitor(R) shows a comparable inhibition of ADP-induced platelet aggregation. However, due to poor inter-therapy agreement, between two regimens, physicians may be cautious when introducing generic clopidogrel bisulfate. (Korean J Intern Med 2010;25:154-161)