Background and Objectives: Angiopoietin-like protein 3 (ANGPTL3) is a secretory protein regulating lipid metabolism. This study evaluated the relationship between serum ANGPTL3 level and peripheral arterial stiffness (PAS) in patients with coronary artery disease (CAD). Materials and Methods: Fasting blood samples were collected from 95 CAD patients. PAS was defined as left or right brachial-ankle pulse wave velocity (baPWV) > 18.0 m/s by an oscillometric method. Serum ANGPTL3 levels were assessed using a commercial enzyme-linked immunosorbent assay kit. Results: Seventeen CAD patients (17.9%) had PAS. Patients with PAS had a significantly higher percentage of diabetes (p = 0.002), older age (p = 0.030), higher systolic blood pressure (p = 0.016), higher fasting glucose (p = 0.008), serum C-reactive protein (p = 0.002), and ANGPTL3 level (p = 0.001) than those without PAS. After multivariable logistic regression analysis, serum ANGPTL3 level (Odds ratio (OR): 1.004, 95% confidence interval (CI): 1.000–1.007, p = 0.041) is still independently associated with PAS in CAD patients. The receiver operating characteristic curve for PAS prediction revealed that the area under the curve for ANGPTL3 level was 0.757 (95% CI: 0.645–0.870, p < 0.001). Conclusions: Serum fasting ANGPTL3 level is positively associated with PAS in CAD patients. Further studies are required for clarification.
Objective: Sclerostin is associated with endothelial inflammation and vascular calcification and therefore contributes to atherosclerosis disease. Hypertension is one of risk factors of peripheral arterial occlusive disease (PAOD), is associated with increased mortality in patients with hypertension. The aim of this study was to determine the relationship between serum sclerostin level and PAOD in patients with hypertension. Design and method: Fasting blood samples and baseline characteristics were obtained from 92 hypertensive patients. ABI values were measured using an automated oscillometric device. Patients with ABIs of <0.9 were categorized into the low ABI group. The serum sclerostin and dickkopf-1 (DKK1) concentrations were determined using commercially available enzyme-linked immunosorbent assays. Results: In total, 14 patients with hypertension (15.2%) were in the low ABI group. When compared to those in the normal ABI group, the low ABI group had high rates of diabetes mellitus (P = 0.044) as well as the high serum C-reactive protein levels (P = 0.001) and sclerostin levels (P < 0.001), but the serum DKK1 level did not find this association (P = 0.639). The multivariable logistic regression analysis revealed that serum levels of sclerostin (odds ratio [OR]: 1.052, 95% confidence interval [CI]: 1.018–1.088, P = 0.002) was independently associated with PAD in patients with hypertension. Conclusions: Serum levels of sclerostin, but not DKK1, were associated with PAOD in patients with hypertension.
Objective: Trimethylamine N-oxide (TMAO) is a metabolite derived from gut microbial metabolism and dietary intake and plays important roles in cardiovascular disease pathogenesis. Endothelial dysfunction is associated with risk factors of cardiovascular disease in patients with hypertension. The present study aimed to determine the correlation between serum TMAO and endothelial function, measured by vascular reactivity index (VRI) in patients with hypertension. Design and method: The present study collected fasting blood samples from 110 patients with hypertension. Serum TMAO levels were determination of by high-performance liquid chromatography–mass spectrometry. The endothelial function and VRI values were measured using digital thermal monitoring test, and VRI values of >2.0, 1.0–1.9 and <1.0 indicated good, intermediate and poor vascular reactivity, respectively. Results: Ten hypertensive patients (9.1%) were categorized as poor vascular reactivity (VRI < 1.0), 57 hypertensive patients (51.8%) were categorized as intermediate vascular reactivity (1.0 < VRI < 2.0), and 43 hypertensive patients had good vascular reactivity. Older age (P = 0.010), higher levels of serum total cholesterol (TCH, P = 0.007), low-density lipoprotein cholesterol (LDL-C, P = 0.009), and TMAO levels (P < 0.001) were associated with poor vascular reactivity. Furthermore, after multivariable forward stepwise linear regression analysis noted that logarithmically transformed serum level of TMAO (log-TMAO, adjusted R2 change = 0.274, P < 0.001) was significantly and independently associated with VRI values in hypertensive patients. Compared with good vascular reactivity index, patients with vascular reactivity dysfunction (intermediate vascular reactivity and poor vascular reactivity; odds ratio (OR) = 1.100; 95% confidence interval (CI) = 1.047–1.155; P < 0.001) or poor vascular reactivity (OR = 1.580, 95% CI = 1.002–2.492, P = 0.049) also noted TMAO was positively associated with poor vascular reactivity after multivariate logistic regression analysis. Conclusions: Serum TMAO levels were negatively associated with VRI and associated with endothelial dysfunction in patients with hypertension.
Immune thrombocytopenic purpura (ITP) is a life-threatening complication following pegylated interferon alpha (PEG-IFN) plus ribavirin treatment, the standard treatment for hepatitis C virus (HCV) infection. We reported a rare case with late-onset ITP after withdrawal of PEG-IFN treatment.A 53-year-old male with hepatitis C developed massive gum bleeding and a severe, reversible, immune thrombocytopenia 2 weeks after cessation of PEG-IFN treatment for HCV due to anemia and depression. The platelet count decreased to 4000 cells/μL. The HCV viral load was undetectable at the end of PEG-IFN treatment and during follow-up for 5 months. Other potential autoimmune disorders were ruled out. Late-onset ITP associated with PEG-IFN treatment was diagnosed.The patient was treated successfully with steroid and azathioprine. Platelet count gradually increased to 117 × 103 cells/μL on the 18th day after admission.ITP is a rare complication in patients with hepatitis C or in patients who received PEG-IFN treatment. The particular case supported that it may occur even after withdrawal of PEG-IFN treatment. Physicians should be aware of this late-onset complication.
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