Peripheral Vascular Disease in Older Adults with Diabetes
Medha N. Munshi, Lewis A. Lipsitz in Geriatric Diabetes, 2007
In addition to exercise and smoking cessation, some pharmacologic agents are available for this patient population. Pentoxifylline, a hemorheologic agent, was approved for treating claudication. The results of several trials, however, suggest that it does not increase walking distance to a clinically meaningful extent. Cilostazol, an oral phosphodiesterase type III inhibitor, was also approved for treating intermittent claudication. Significant benefit in increasing maximal walking time has been demonstrated in randomized trials, in addition to improving functional status and health-related quality of life (10). The use of this drug is contraindicated if any degree of heart failure is present, due to concerns about arrhythmias. Cilostazol is the drug of choice if pharmacologic therapy is necessary for the management of PAD in patients with diabetes.
Supervised Exercise, Stent Revascularization, or Medical Therapy for Claudication Due to Aortoiliac Peripheral Artery Disease: The Clever Study
Juan Carlos Jimenez, Samuel Eric Wilson in 50 Landmark Papers Every Vascular and Endovascular Surgeon Should Know, 2020
Intervention OMC was established by the 2005 ACC/AHA Guidelines for the management of patients with peripheral artery disease to promote best practices for risk factor management, use of antiplatelet therapy and use of claudication pharmacotherapy.7 All participants received cilostazol 100 mg by mouth twice daily. In addition, OMC included advice about home exercise and diet in the form of standardized verbal instruction and printed material. Cardiovascular risk factor data were collected and feedback was provided to the sites by a central risk factor committee. Risk factors were managed directly by the local study site.
Pneumonia
Thomas T. Yoshikawa, Shobita Rajagopalan in Antibiotic Therapy for Geriatric Patients, 2005
Preventing CVA may reduce the incidence of pneumonia among old people. A drug that appears to decrease the incidence of CVAs or cerebral infarction is cilostazol. It has an antithrombocyte action and an action of cerebral vasodilation. When cilostazol was administered for 3 years, it was possible to reduce the incidence of cerebral infarction by one-half, compared with a group that did not receive the drug. In addition, the incidence of pneumonia was also reduced by half (12) (Fig. 1).
Cilostazol Attenuates Retinal Oxidative Stress and Inflammation in a Streptozotocin-Induced Diabetic Animal Model
Published in Current Eye Research, 2019
Po-Ting Yeh, Yu-Hsun Huang, Shu-Wen Chang, Lu-Chun Wang, Chung-May Yang, Wei-Shiung Yang, Chung-Wu Lin, Chang-Hao Yang
Cilostazol, 6-[4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxyl]-3,4-dihydro-2-(1H)-quinolinone, is a phosphodiesterase 3 (PDE3) inhibitor which has been shown to increase intracellular cyclic adenosine monophosphate (cAMP) levels and then decrease intracellular Ca2+ levels in platelets, resulting in inhibition of platelet aggregation and vasodilation leading to a reduction in arterial pressure.17,18 Cilostazol is used to treat intermittent claudication in diabetic patients and peripheral vascular occlusive diseases because of its anti-platelet, vasodilatory, anti-proliferative and anti-atherosclerotic effects.19–21 Recent studies have shown that the potent anti-inflammatory and anti-oxidative effects of cilostazol might occur through several pathways: (a) cilostazol represses vascular cell adhesion molecule-1 (VCAM-1) gene transcription via inhibiting NF-κB binding to its recognition sequence; (b) cilostazol inhibits high glucose-mediated endothelial-neutrophil adhesion; (c) cilostazol may dose-dependently inhibit tumor necrosis factor alpha-induced NF-κB activation and pro-inflammatory gene expressions in human endothelial cells of the umbilical vein; (d) PDE3 plays a role in mediating the effect of cAMP/protein kinase A (PKA) in the inhibition of NF-κB-dependent gene expression; (e) cilostazol inhibits the cytokine-induced expression of various pro-inflammatory and adhesion molecule genes by suppressing NF-κB activity via AMP-activated protein kinase (AMPK) activation.19,22–25
Cilostazol for treatment of cerebral infarction
Published in Expert Opinion on Pharmacotherapy, 2018
Kensuke Noma, Yukihito Higashi
Cilostazol, an antiplatelet agent, is a selective PDE3A inhibitor that can inhibit the degradation of cyclic adenosine monophosphate (cAMP), resulting in an increase in the active form of protein kinase A (PKA). Therefore, cilostazol has both an inhibitory effect on platelet aggregation and a vasodilatory effect by relaxation of vascular smooth muscle cells (VSMCs) via PKA-mediated inhibition of myosin light-chain kinase [12,13]. Also, cAMP has been reported to not only upregulate p53 and p21, anti-oncogenes, subsequently inducing apoptosis in VSMCs, but also upregulate hepatocyte growth hormone (HGF), resulting in re-endothelialization and improvement of endothelial function [14,15]. In addition, cilostazol has been revealed to inhibit inflammation [16], platelet activity [17], inflammation-mediated vascular damage [18], and cerebral hypoperfusion-mediated neuronal damage [19,20]. In the US and Europe, cilostazol has been licensed for treatment of patients with intermittent claudication to improve their walking distance in the absence of tissue necrosis or rest pain. On the other hand, mainly in Asia, cilostazol is licensed for treatment of patients with peripheral artery disease (PAD) to improve their ulceration and ischemic symptoms and also for treatment of patients with cerebral thrombosis to prevent secondary ischemic events [11].
Use of big data in drug development for precision medicine: an update
Published in Expert Review of Precision Medicine and Drug Development, 2019
Tongqi Qian, Shijia Zhu, Yujin Hoshida
Accumulating evidence has demonstrated the utility of EHR data to identify potential therapeutic drug effects and drug-drug interactions. EHRs may be particularly useful when investigating therapeutic effects, owing to their continuous and longitudinal assessment of clinically relevant outcomes and medication exposures. EHR data has an additional advantage in representing the ‘real-world’ conditions of patient medication use and treatment trends, which is a great resource to uncover the clinical consequences of drug genome interactions. LePendu et al. reproduced known drug adverse events by applying natural language to a large EHR dataset, and further revealed a safety signal of rofecoxib on patients with myocardial infarction, even before this association was identified in a clinical trial [39]. The similar approach also suggested the safety signal of the claudication drug cilostazol on patients with congestive heart failure, in spite of a listed contraindication [40]. An analysis based on 31 EHR-defined drug phenotypes suggested that the use of EHRs could lead to a reduction by 72% in medical expenses, and even decrease the development period. Meanwhile, it also largely elevated the data reuse [41], supported by the evidence that data from more than 90% individuals were used repeatedly [33].
Related Knowledge Centers
- Antiplatelet Drug
- Intermittent Claudication
- Stroke
- Medication
- Peripheral Artery Disease
- Heart Failure
- Thrombocytopenia
- Leukopenia
- Pde3 Inhibitor
- Generic Drug