Relationships Between Vitamin D Status and Cytokine: Results from Interferon-Based Therapy in Non-Cirrhotic, Treatment-Naïve Patients with Chronic Hepatitis C Infection.

BACKGROUND: Vitamin D contributes to bone health and extra-skeletal effects. The mechanisms underlying vitamin D metabolism have not been extensively evaluated. The relationships between vitamin D and inflammatory cytokines are debated. Our objective was to investigate whether supplemental interferons are associated with longitudinal change of vitamin D status in humans. METHODS: A total of 48 patients with 24 or 48 weeks of pegylated interferon-α plus ribavirin therapy were examined for serum 25-hydroxyvitamin D (25[OH]D) level before treatment, at the end of treatment, and 24 weeks after treatment. In addition, we analyzed publicly available RNA sequencing data from accession GSE42697 and GSE7123 in the Gene Expression Omnibus. FINDINGS: The overall sustained virologic response (SVR) rate was 62.5%. There was no statistically significant association between baseline 25(OH)D concentrations and liver fibrosis. In patients with SVR, serum 25(OH)D increased markedly at end-of-treatment and decreased markedly by the end of the 24-week follow-up period. In the non-SVR group, this treatment-dependent change was lost. In gene expression analysis, the vitamin D biosynthesis process was activated in subjects with SVR, but not in patients without SVR. Furthermore, vitamin D receptor (VDR) signaling in peripheral blood mononuclear cells (PBMCs) was triggered in marked responders but not in poor responders. CONCLUSION: In the aggregate, these data suggest that interferons have a regulatory influence on vitamin D status that can contribute to VDR signaling in PBMCs.

Risk factors for the development of pulmonary oil embolism after transcatheter arterial chemoembolization of hepatic tumors.

Pulmonary oil embolism (POE) is a rare fatal complication after transcatheter arterial embolization (TAE) and transcatheter arterial chemoembolization (TACE). As risk factors have not been clearly delineated, the aim of the present study was to identify the risk factors for development of POE after TACE. A retrospective analysis was carried out on patients with unresectable hepatocellular carcinoma who received TAE or TACE at the Tri-Service General Hospital (Taiwan) between January 2005 and December 2008. The diagnosis of TAE-induced or TACE-induced POE was based on development of respiratory signs and symptoms relatively soon after the procedure, as well as based on characteristic radiographic findings. Of the 219 enrolled patients in this study, 20 were diagnosed with POE after TAE or TACE. On univariate logistic regression analysis, patients developing POE were found to be older (67.95±15.95 vs. 61.44±12.59 years, P=0.033), with a lower serum albumin level (3.25±0.58 vs. 3.62±0.57 g/dl, P=0.009), a higher grade of liver cirrhosis as classified on the basis of Child's criteria (P<0.006), a larger tumor size (8.55±4.52 vs. 4.78±3.97 cm in diameter, P<0.001), a higher lipioidol dose (22.35±11.01 vs. 13.69±7.66 ml, P=0.003), and a higher doxorubicin dose (50.27±7.05 vs. 40.75±13.61 mg, P<0.001). Following multivariate logistic regression analysis, only lipiodol dose was found to be a significant risk factor for POE (odds ratio=1.133, 95% confidence interval: 1.004, 1.279; P=0.044). The receiver operator characteristic curve cutoff point for lipiodol dose level was 14.5 ml, with a sensitivity of 80% and a specificity of 66.3%. In conclusion, the lipiodol dose could be considered as a predictive factor for POE after TAE or TACE in hepatic malignant tumor patients. On the basis of this retrospective study, the safe lipiodol dose to minimize the risk for POE is 14.5 ml or lower; however, larger, prospective studies are needed to determine the optimally safe and yet efficacious dose.

An unusual complication following transarterial chemoembolization: acute myocardial infarction.

Transarterial chemoembolization has been widely used to treat unresectable hepatocellular carcinoma. Various complications have been reported, but they have not included acute myocardial infarction. Acute myocardial infarction results mainly from coronary artery occlusion by plaques that are vulnerable to rupture or from coronary spasm, embolization, or dissection of the coronary artery. It is associated with significant morbidity and mortality. We present a case report that describes a patient with hepatocellular carcinoma who underwent transarterial chemoembolization and died subsequently of acute myocardial infarction. To our knowledge, there has been no previous report of this complication induced by transarterial chemoembolization for hepatocellular carcinoma. This case illustrates the need to be aware of acute myocardial infarction when transarterial chemoembolization is planned for the treatment of hepatocellular carcinoma, especially in patients with underlying coronary artery disease.