Erosive esophagitis associated with metabolic syndrome,impaired liver function, and dyslipidemia

AIM:To investigate whether erosive esophagitis is correlated with metabolic syndrome and its components,abnormal liver function,and lipoprotein profiles.METHODS:We conducted a cross-sectional,case control study of subjects who underwent upper endoscopy during a health examination at the Health Management and Evaluation Center of a tertiary medical care facility located in Southern Taiwan.Metabolic syndrome components,body mass index(BMI),liver function,dyslipidemia,and cardiovascular risk factors,as defined by the ratio of total cholesterol to high-density lipoprotein cholesterol(HDL-C),and the ratio of low-density lipoprotein cholesterol to HDL-C were compared betweenindividuals with and without erosive esophagitis.Risk factors for erosive esophagitis were evaluated by multivariate logistic regression.RESULTS:Erosive esophagitis was diagnosed in 507of 5015 subjects who were individually age and sex matched to 507 esophagitis-free control subjects.In patients with erosive esophagitis,BMI,waist circumference,blood pressure,fasting plasma glucose,triglyceride levels,aspartate aminotransferase,alanine aminotransferase,the ratio of total cholesterol to HDL-C,and the ratio of low-density lipoprotein cholesterol to HDL-C were significantly higher and HDL-C was significantly lower compared to patients without erosive esophagitis(all P<0.05).In a multivariate analysis,central obesity(OR=1.38;95%CI:1.0-1.86),hypertension(OR=1.35;95%CI:1.04-1.76),hypertriglyceridemia(OR=1.34;95%CI:1.02-1.76),cardiovascular risk factors as defined by a ratio of total cholesterol to HDL-C>5(OR=1.45;95%CI:1.06-1.97),and aspartate aminotransferase(OR=1.59;95%CI:1.08-2.34)were significantly associated with erosive esophagitis.CONCLUSION:Metabolic syndrome,impaired liver function,and a higher ratio of total cholesterol to HDL-C were associated with erosive esophagitis.

IFN-a production by human mononuclear cells infected with varicella-zoster virus through TLR9-dependent and-independent pathways

Understanding the defense mechanisms of the host of an organism is important for infection control.In previous studies,we demonstrated that interferon-a(IFN-a),but not IL-12,was produced by human peripheral blood mononuclear cells infected with varicella-zoster virus(VZV).Here,we investigated what kind of cell(s)and which signal molecule(s)are involved in IFN-a production.Using cell isolation and ELISA,we found that plasmacytoid dendritic cells(pDCs)were responsible for IFN-a production during VZV infection.We also found that Toll-like receptor 9(TLR9)was involved in VZV-induced IFN-a production because inhibitory CpG oligodeoxynucleotide inhibited IFN-a production.UV-inactivated VZV-induced IFN-a production was lower than that of active VZV,indicating another TLR9-independent pathway.Further studies demonstrated that double-stranded RNA-dependent protein kinase,but not DNA-dependent protein kinase was involved in VZV-induced IFN-a production.Together,these results suggest that pDCs play an important role in IFN-a production during VZV infection through TLR9-dependent and-independent pathways.