• Korean Journal of Clinical Pharmacy
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• v.21 no.3
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• pp.270-275
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• 2011

이 증례는 드물게 보는 경우로 simvastatin과 gemfibrozil을 오랫동안 함께 복용했음에도, 특이한 문제가 발현되지 않았지만, 이들을 warfarin와 함께 치료하는 경우, 아주 높은 alanine aminotransferase (ALT), aspartate aminotransferase(AST) 혈중 농도, rhabdomyolysis, 급성 신장 장애가 발생하였다. 그 후, Simvastatin와 gemfibrozil을 복용 중단시켰더니, ALT/AST는 빠르게 정상수치로 돌아온 경우이다. 이 증례 보고서는 의료인들에게 simvastatin과 gemfibrozil을 함께 혹은 따로 warfarin과 함께 복용시켜 치료할 경우, creatine phosphokinase (CPK) 와 creatinine 혈중 수치들을 포함하여 ALT/AST 농도들을 주의 깊게 모니터하도록 경각심을 주고자 한다.

• Biomolecules & Therapeutics
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• v.3 no.2
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• pp.132-135
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• 1995

Several clofibrate congeners (bezafibrate, gemfibrozil and fenofibrate) were investigated the relationship between effects on the aggregation induced by aggregating agents (thrombin, arachidonic acid, ADP and collagen) and arachidonic acid metabolism in rabbit homogenized platelet. In platelet aggregation study, all drugs produced no significant inhibition (data not shown) in arachidonic acid and thrombin. Also platelet aggregation by ADP was not changed in bezafibrate and Inhibited dose dependently in fenofibrate and gemfibrozil. Platelet aggregation by collagen was inhibited dose dependently and significantly (from p<0.5 to p<0.001) by gemfibrozil and fenofibrate at concentrations between 20 and 400 $\mu$M. In arachidonic acid metabolism study, synthesis of thromboxane $B_2$ was not changed in rabbit platelet membranes and that of prostaglandin $E_2$ and $F_{2{\alpha}}$ was slightly increased by all drugs. It was concluded that clofibrate congeners inhibited ADP and collagen induced rabbit platelet aggregation and inhibition of collagen induced aggregation was probably mediated through some mechanism (pathway) other than arachidonic acid metabolism, judging from arachidonic acid metabolites (thromboxane $B_2$, prostaglandin $E_2$and $F_{ 2{\alpha}}$) synthesis in rabbit homogenized Platelet.

• Health Policy and Management
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• v.9 no.3
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• pp.70-94
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• 1999

This paper was performed for a cost-effectiveness analysis of pharmacologic treatment of hypercholesterolemia. Agents modeled were cholestyramine, gemfibrozil. bezafibrate, lovastatin, pravastatin, simvastatin. Pharmacologic effectiveness was estimated by regression from reported clinical trials. Pharmacologic effects were expressed as the percent change of blood cholesterol level. Cost estimates included patients' travel expenses and time loss as well as resource consumption in the health care sector. Bezafibrate was the most efficient agent for reducing total cholesterol levels, having an cost over 1 year of ￦31.400 per percent reduction in total cholesterol. Simvastatin (10mg/d) was also efficient(￦33,100 per percent reduction). Chole styramine(8g/d) was least efficient at ￦90,200. For low-density lipoprotein cholesterol. simvastatin(10mg/d) was most efficient, at ￦23,200 per percent reduction, followed by lovastatin(20mg/d) at ￦28,000. Gemfibrozil was least efficient at ￦77,800 per percent reduction. For high-density lipoprotein cholesterol. bezafibrate(400mg/d) was most efficient at ￦39,300 per percent increase of high-density lipoprotein cholesterol. Cholestyramine was least efficient at ￦514,700. Analyses combining low-density lipoprotein cholesterol and high-density cholesterol effects suggest that bezafibrate(600mg/d) and simvastatin (10mg/d) were most efficient for reducing cardiovascular risk. The cost-effectiveness analysis results show that both simvastatin and bezafibrate could be efficient treatment. Simvastatin provide more effective treatment at higher cost, whereas bezafibrate is more cost-effective, as it may be less effective, at lower cost. Therefore, clinicians should choose reasonable treatment according to the patient's needs This pharmacoeconimc analysis will provide a guideline for efficient pharmacologic treatment and also be reference data for pricing new drugs.

• The Korean journal of internal medicine
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• v.39 no.1
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• pp.77-85
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• 2024

Background/Aims: There may be many predictors of anticoagulation-related gastrointestinal bleeding (GIB), but until now, systematic reviews and assessments of the certainty of the evidence have not been published. We conducted a systematic review to identify all risk factors for anticoagulant-associated GIB to inform risk prediction in the management of anticoagulation-related GIB. Methods: A systematic review and meta-analysis were conducted to search PubMed, EMBASE, Web of Science, and Cochrane Library databases (from inception through January 21, 2022) using the following search terms: anticoagulants, heparin, warfarin, dabigatran, rivaroxaban, apixaban, DOACs, gastrointestinal hemorrhage, risk factors. According to inclusion and exclusion criteria, studies of risk factors for anticoagulation-related GIB were identified. Risk factors for anticoagulant-associated GIB were used as the outcome index of this review. Results: We included 34 studies in our analysis. For anticoagulant-associated GIB, moderate-certainty evidence showed a probable association with older age, kidney disease, concomitant use of aspirin, concomitant use of the antiplatelet agent, heart failure, myocardial infarction, hematochezia, renal failure, coronary artery disease, helicobacter pylori infection, social risk factors, alcohol use, smoking, anemia, history of sleep apnea, chronic obstructive pulmonary disease, international normalized ratio (INR), obesity et al. Some of these factors are not included in current GIB risk prediction models. such as anemia, co-administration of gemfibrozil, co-administration of verapamil or diltiazem, INR, heart failure, myocardial infarction, etc. Conclusions: The study found that anemia, co-administration of gemfibrozil, co-administration of verapamil or diltiazem, INR, heart failure, myocardial infarction et al. were associated with anticoagulation-related GIB, and these factors were not in the existing prediction models. This study informs risk prediction for anticoagulant-associated GIB, it also informs guidelines for GIB prevention and future research.

• Journal of Korean Society of Water and Wastewater
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• v.33 no.5
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• pp.367-377
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• 2019

In this study, the fate and removal of 15 pharmaceuticals (including stimulants, non-steroidal anti-inflammatory drugs, antibiotics, etc.) in unit processes of a sewage treatment plant (STP) were investigated. Mass loads of pharmaceuticals were 2,598 g/d in the influent, 2,745 g/d in the primary effluent, 143 g/d in the secondary effluent, and 134 g/d in the effluent. The mass loads were reduced by 95% in the biological treatment process, but total phosphorous treatment did not show a significant effect on the removal of most pharmaceuticals. Also, mass balance analysis was performed to evaluate removal characteristics of pharmaceuticals in the biological treatment process. Acetaminophen, caffeine, acetylsalicylic acid, cefradine, and naproxen were efficiently removed in the biological treatment process mainly due to biodegradation. Removal efficiencies of gemfibrozil, ofloxacin, and ciprofloxacin were not high, but their removal was related to sorption onto sludge. This study provides useful information on understanding removal characteristics of pharmaceuticals in unit processes in the STP.

• Journal of Korean Society of Environmental Engineers
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• v.39 no.3
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• pp.124-131
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• 2017

In this study, We investigated the effects of water temperature and empty bed contact time (EBCT) on the biodegradability of 8 blood lipid lower agents (BLLAs) in biological activated carbon (BAC) process. Experiments were conducted at three water temperatures ($8^{\circ}C$, $16^{\circ}C$ and $24^{\circ}C$) and three EBCTs (5 min, 10 min and 15 min). Increasing water temperature and EBCT increased the biodegradation efficiency of BLLAs in BAC process. Simvastatin and fenofibrate were the highest biodegradation efficiency, but atorvastatin and clofibric acid were the lowest. The kinetic analysis suggested a pseudo-first-order reaction model for biodegradation of 8 BLLAs at various water temperatures and EBCTs. The pseudo-first-order biodegradation rate constants ($k_{bio}$) of clofibric acid and atorvastatin were $0.0075min^{-1}$ and $0.0122min^{-1}$ at $8^{\circ}C$, and were $0.0540min^{-1}$ and $0.0866min^{-1}$ at $24^{\circ}C$, respectively. By increasing the water temperature from $8^{\circ}C$ to $24^{\circ}C$, the biodegradation rate constants ($k_{bio}$) were increased 7.1~7.2 times.