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January 1, 2009Circulation Journal32 citationsOpen Access

Effect of Cilostazol Treatment on Adiponectin and Soluble CD40 Ligand Levels in Diabetic Patients With Peripheral Arterial Occlusion Disease

CHChing‐Jung HsiehPWPei‐Wen Wang

Key Result

Cilostazol significantly decreased hs-CRP (p=0.001) and sCD40L (p=0.05) levels and increased adiponectin (p=0.004) compared to placebo in type 2 diabetic patients with peripheral arterial occlusion disease.

Study Design

Type

RCT (n=192)

Blinding

Single-blinded

Randomization

Randomly assigned

Multicenter

No

Structured PICO

Does cilostazol improve serum levels of sCD40L, adiponectin, and hs-CRP in patients with type 2 diabetes and peripheral arterial occlusion disease?

P
Population
192 patients with type 2 diabetes, including 92 with peripheral arterial occlusion disease and 100 without, randomized to cilostazol or placebo for 6 months.
I
Intervention
Cilostazol 100 mg oral twice daily for 6 months
C
Comparator
Matching placebo for 6 months
O
Outcome
Changes in serum levels of soluble CD40 ligand (sCD40L), adiponectin, and high-sensitivity C-reactive protein (hs-CRP) at 6 monthssurrogate

Cilostazol improves inflammatory and atherogenic biomarker profiles (hs-CRP, sCD40L, adiponectin) in patients with type 2 diabetes and peripheral arterial disease, suggesting a potential role in delaying atherogenesis.

Main Result

Absolute Event Rate: 4.6% vs 8.9%

p-value: p=0.001

Limitations

  • Office blood pressure may not be a good measure of blood pressure control.
  • Available lipid profile data were insufficient for defining dyslipidemia.
  • HOMA IR may erroneously conclude poor beta-cell function in patients taking high doses of antidiabetic agents.
  • No significant change in resting ABI after 6 months, indicating a possible need for a longer study duration.
  • ABI <0.9 may underestimate the prevalence of PAOD in the general elderly population.
  • Office BP may not be a good measure of BP control
  • Insufficient lipid profile data for defining dyslipidemia
  • HOMA IR or HbA1c may not be adequate for assessing diabetes control
  • 6 months may be too short to see changes in resting ABI
  • ABI <0.9 may underestimate PAOD prevalence

Abstract

BACKGROUND: Peripheral arterial occlusion disease (PAOD) is caused mainly by chronic inflammation and endothelium dysfunction, and is often treated with cilostazol. However, because this drug's influence on atherogenic cytokines is still not well known, this study examined the effect of cilostazol on the serum levels of soluble CD40 ligand (sCD40L), adiponectin and high-sensitivity C-reactive protein (hs-CRP) in patients with type 2 diabetes and PAOD. METHODS AND RESULTS: The 92 type 2 diabetics with PAOD and 100 non-PAOD diabetics were enrolled and randomly assigned to a group receiving either cilostazol or placebo for 6 months. The atherogenic cytokines were measured at the beginning and completion of the study. In the PAOD groups, those in the cilostazol group had significant changes in the levels of hs-CRP, sCD40L and adiponectin (P=0.001, P=0.05, P=0.004, respectively). Changes in the levels of adiponectin and sCD40L were more significant in the PAOD group treated with cilostazol than in the non-PAOD group also treated with the drug (P=0.01 and P=0.008, respectively). CONCLUSIONS: Cilostazol can decrease hs-CPR and sCD40L levels and increase that of adiponectin, and then delay the progression of atherogenesis and chronic inflammation in type 2 diabetics, especially those with PAOD.

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Cite This Study

Hsieh et al. (2009) conducted an RCT in Type 2 diabetes mellitus with and without peripheral arterial occlusion disease (n=192). Cilostazol vs. Placebo was evaluated on Change in serum high-sensitivity C-reactive protein (hs-CRP) levels in PAOD patients (p=0.001). Cilostazol significantly decreased hs-CRP (p=0.001) and sCD40L (p=0.05) levels and increased adiponectin (p=0.004) compared to placebo in type 2 diabetic patients with peripheral arterial occlusion disease.

synapsesocial.com/papers/6a88259c729e8aa7bb583987https://doi.org/10.1253/circj.cj-08-0905
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