Seven Cases of Late-Life Depression Treated With Cilostazol-Augmented Therapy
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Baba, Hajime MD, PhD; Kubota, Yuki MD; Suzuki, Toshihito MD, PhD; Arai, Heii MD, PhD Author InformationKeywords:
Cilostazol
Depression
목적: Cilostazol은 phosphodiesterase (PDE) III를 선택적으로 차단하는 항혈소판 제제로 혈관 내막증식 억제 작용을 함께 가지고 있다. 최근의 임상연구에서 관상동맥 내 BMS 삽입 후 cilostazol을 포함한 삼제 병합치료(aspirin+clopido-grel+cilostazol)를 하였을 경우 표준치료(aspirin+clopidogrel+placebo)에 비하여 유의한 재협착률 감소를 나타내었다. 본 연구는 DES 삽입 후 저용량의 cilostazol을 포함한 6개월 간의 항혈소판 삼제 병합요법의 효과를 알아보고자 하였다. 방법: 2004년 6월부터 2006년 1월까지 순천 성가롤로 병원에서 관상동맥 내 DES 삽입술을 시행 받은 환자를 대상으로 6개월간 저용량의 cilostazol (50 mg/BID) 복용 여부에 따라 I군(aspirin+clopidogrel+cilostazol)과 II군(aspirin+clopidogrel)으로 나누어 추적 관상동맥 조영술 및 임상결과를 전향적으로 비교하였다. 결과: 대상 환자는 109명이었으며 I군은 56명(67.3±10.8세, 남자 37명), II군은 53명(67.6±10.5세, 남자 26명)이었다. 대상 환자 중 80명(74%)에서 6개월 후 추적 관상동맥 조영술을 시행하였고, 임상 추적관찰은 모든 환자에서 실시되었다. 추적 관상동맥 조영술상 양 군 간에 최소 혈관 내경(I군: 2.25±0.63 mm, II군: 2.30±0.56 mm, p=0.742), 후기 손실(I군: 0.47±0.47 mm, II군: 0.52±0.53 mm, p=0.747)과 재협착률 (I군: 7.2%; II군: 5.6%, p=0.611)의 유의한 차이는 없었다. 또한 임상 추적 결과상 스텐트 혈전증은 일어나지 않았고, 양군간에 심장관련 사고나 출혈성 합병증 발생률의 유의한 차이는 없었다. 결론: DES 삽입 후 저용량의 cilostazol을 포함한 6개월 간의 항혈소판 삼제 병합치료는 출혈성 합병증을 증가시키지 않고 비교적 안전하게 사용할 수 있지만 보다 큰 최소혈관 내경을 얻고 재협착률을 감소시키는데 효과가 없었다.
Cilostazol
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Cilostazol
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본 연구의 최종 목표는 한방제제인 심적환과 심혈관계 양방 치료제인 cilostazol과 병용 투여 효과에 대한 포괄적이고 통합의학 측면에서 정확한 정보를 얻는 것이다. Cilostazol은 말초 동맥질환 치료제로 개발 된 항 혈소판 및 혈관확장제이다. 사이클릭 AMP protein kinase A를 활성 시켜 세포내 사이클릭 AMP (cAMP) 증가를 통하여 내피세포의 NO생산을 활성화 시킨다. 심적환을 단 회 또는 반복 투여 후 cilostazol의 약물 동태학적 효과를 평가하기 위하여 순수한 증류수 단회 용량과 증류수에 심적환 콜로이드 현탁액을 각각 대조군과 시험군에 투여 하여 30분 후, 두 그룹에 cilostazol를 투여하였다. 혈청은 cilostazol 약물 투여 30분 전에 수집 하였으며, cilostazol 약물 처리 후 0.25, 0.5, 0.45 및 1, 2, 4, 6, 8, 24시간 후에 각각 수집 하였다. 그 다음 실험군과 및 테스트 그룹 사이에 실로 스타 졸에서 관찰 된 약동학 적 변화를 평가 하였다. 통계적으로 유의 한 차이는 심적관 단독 투여와 반복투여군 그룹의 약물 동태 학에서 관찰되지 않았다. 이러한 연구 결과는 만성 질환 환자에서 한약제인 심적환의 투여는 cilostazol의 약동학에 영향을 미치지 않았음을 보여 주었다. 본 연구에서 얻어진 결과는 만성 혈관질환 환자에서 심적환과 cilostazol의 병용 투여를 제안하며 두 약물간의 잠재적 인 약물 상호 작용에 대한 cilostazol의 생체 이용률에 영향을 미치지 않을 것이라 판단된다. The object of this study was to obtain accurate information about the co-administration effects of cardiotonic pills on the pharmacokinetics of cilostazol were observed as a process of the comprehensive and integrative medicine. Cilostazol is a synthetic anti-platelet and vasodilator agent developed for the treatment of intermittent claudication resulting from peripheral arterial disease. By increasing intracellular cyclic adenosine monophosphate (cAMP), cilostazol induces the activation of protein kinase A, which activates endothelial nitric oxide synthase. In order to evaluate the effect of a single or repeated cardiotonic pill dose on the pharmacokinetics of cilostazol, a single dose of pure_distilled water or a colloidal suspension of distilled water and cardiotonic pills were administered to the control and test groups, respectively. After 30 min, both groups were administered cilostazol. Plasma was collected 30min before administration, and 0.25, 0.5, 0.45, 1, 2, 4, 6, 8, and 24h after the end of cilostazol treatment. We then evaluated the pharmacokinetic changes observed with cilostazol between the control and test groups. No statistically significant differences were observed. These findings demonstrated that a single dose of cardiotonic pills did not affect the pharmacokinetics of cilostazol. The results obtained in this study suggest that co-administration of cardiotonic pills and cilostazol may not affect the bioavailability of cilostazol as a potential drug interaction.
Cilostazol
Phosphodiesterase 3
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: Cilostazol is a unique platelet inhibitor that has been used clinically for more than 20 years. As a phosphodiesterase type III inhibitor, cilostazol is capable of reversible inhibition of platelet aggregation and vasodilation, has antiproliferative effects, and is widely used in the treatment of peripheral arterial disease, cerebrovascular disease, percutaneous coronary intervention, etc. This article briefly reviews the pharmacological mechanisms and clinical application of cilostazol.
Cilostazol
Vasodilator agents
Phosphodiesterase 3
Phosphodiesterase inhibitor
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Cilostazol is a phosphodiesterase-3 inhibitor that functions as a platelet aggregation inhibitor and is used for treating peripheral artery diseases and ischemic stroke. Dendritic cells (DCs) play an active role in the immunological processes related to atherosclerosis. Cilostazol has anti-atherogenic and anti-inflammatory effects, but the effects of cilostazol on DC maturation remain unknown. The purpose of this study was to determine the effects of cilostazol on lipopolysaccharide (LPS)-induced maturation of DCs. DC2.4 cells were treated with cilostazol for 12 h and subsequently stimulated with LPS to induce maturation. Cilostazol reduced the expression of maturation-associated markers induced by LPS, such as CD40, CD86, and MHCII, improved the endocytotic function, and decreased production of the tumour necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) of these cells. To further elucidate the mechanisms responsible for the inhibition of DC2.4 maturation by cilostazol, we investigated the effect of cilostazol on LPS-stimulated nuclear factor-kappa B (NF-κB) activation. Our results indicated that cilostazol treatment decreased IκBα degradation and inhibited NF-κB p65 translocation, and the inhibitory effects of cilostazol were cAMP-independent. Therefore, inhibition of NF-κB by cilostazol might result in the suppression of DC maturation. In conclusion, cilostazol suppressed LPS-stimulated DC maturation, which might contribute to its anti-atherosclerosis effect.
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Phosphodiesterase 3
CD86
Proinflammatory cytokine
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Purpose Drug-eluting stents (DESs) play an important role in endovascular therapy (EVT) for femoropopliteal (FP) lesions. Cilostazol improves patency after bare-metal nitinol stent (BNS) implantation for femoropopliteal lesions. This study aimed to establish whether cilostazol is effective in improving the patency of DESs and determine whether BNS or DESs with or without cilostazol are more effective in improving the 12-month patency after EVT for FP lesions. Materials and methods In this prospective, open-label, multicenter study, 85 patients with symptomatic peripheral artery disease due to de novo FP lesions were enrolled and treated with DESs with cilostazol from eight cardiovascular centers between April 2018 and May 2019. They were compared with 255 patients from the DEBATE SFA study, in which patients were randomly assigned to the BNS, BNS with cilostazol, or DES groups. The primary endpoint was the 12-month patency rate using duplex ultrasound (peak systolic velocity ratio < 2.5). This study was approved by the ethics committee of each hospital. Results The 12-month patency rates for the BNS, BNS with cilostazol, DES, and DES with cilostazol groups were 77.6%, 93.1%, 82.8%, and 94.2%, respectively (p = 0.007). The 12-month patency rate was higher in the DES with cilostazol group than in the DES group (p = 0.044). In small vessels, the DES with cilostazol group had a higher patency rate than the DES group (100.0% vs. 83.4%, p = 0.023). Conclusions DES with cilostazol showed better patency than DES alone. Cilostazol improved patency after EVT with DES in FP lesions and small vessels. Clinical trial registration University Hospital Medical Information Network Clinical Trials Registry (no. UMIN 000032473 ).
Cilostazol
Bare-metal stent
Clinical endpoint
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Cilostazol is a phosphodiesterase III inhibitor that has been shown to be effective for treatment of symptomatic intermittent claudication. It is generally well tolerated, but is contraindicated in patients with severe heart failure because of the potential detrimental effects demonstrated by other agents in the same class. Additional studies are required to examine the long-term benefits of cilostazol therapy.
Cilostazol
Intermittent claudication
Vasodilator agents
Claudication
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To investigate the midterm safety and effectiveness of cilostazol treatment in claudicant patients undergoing endovascular therapy.The Sufficient Treatment of Peripheral Intervention by Cilostazol (STOP-IC) study ( ClinicalTrials.gov identifier NCT00912756; University Hospital Medical Information Network identifier UMIN000002091) enrolled 200 patients (mean age 73 years; 131 men) treated for femoropopliteal disease from March 2009 to April 2011 at 13 cardiovascular centers in Japan. The participants were randomized 1:1 to receive oral aspirin with or without cilostazol. Of the 100 patients assigned to the 2 treatment groups, 7 patients in the cilostazol group and 2 patients in the no-cilostazol group were withdrawn from the study without undergoing endovascular treatment, leaving 93 patients in the cilostazol group and 98 patients in the no-cilostazol group for follow-up analysis. The primary outcome measure was primary patency; secondary outcome measures were freedom from clinically-driven target lesion revascularization (CD-TLR) and overall survival. Outcomes were analyzed on an intention-to-treat basis using the Kaplan-Meier method; estimates were compared with the log-rank test.The median follow-up was 38.1 months (interquartile range 25.1, 47.7). Among the 93 subjects in the cilostazol group, 7 died and 26 withdrew from administration 1 year after the endovascular procedure. Discontinuation of cilostazol was not a significant factor for restenosis. Primary patency was significantly higher in the cilostazol group than in the no-cilostazol group (69% vs 54%, p=0.026) at 3 years. The cilostazol group also had better 3-year freedom from CD-TLR (78% vs 63%, p=0.014), although overall survival estimates did not differ significantly (p=0.95).These results suggest that the safety and effectiveness of cilostazol treatment were sustained in patients with femoropopliteal disease undergoing endovascular treatment.
Cilostazol
Interquartile range
Intermittent claudication
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Cilostazol is being developed for the treatment of intermittent claudication due to peripheral arterial disease (PAD). In this study, we measured the serum cilostazol concentrations and platelet aggregations induced by adenosine diphosphate (ADP) and collagen, and also investigated the pharmacokinetics and pharmacodynamics of cilostazol in inpatients receiving cilostazol therapy. No significant difference was observed in C/D (serum trough concentration/dose) between males and females. A trend toward increasing the serum cilostazol concentration by increasing the dose (mg/kg) was observed (P<0.05). The interindividual variation of the C/D for cilostazol was found to be very large. No significant difference was observed between the C/D for cilostazol and the age, GPT or Ccr. A statistical correlation was observed between the serum cilostazol concentration and the maximum extent of aggregation (%) induced by ADP and collagen (P<0.05).
Cilostazol
Pharmacodynamics
Intermittent claudication
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