H epatitis C viral infection is a common cause of chronic liver disease, with a worldwide prevalence of 3%. About 140 million people worldwide and 4 million in the United States are infected with HCV. An estimated 65% to 80% of the individuals infected with HCV develop persistent infection. As many as 20% to 50% of these individuals develop cirrhosis and 5% develop hepatocellular carcinoma. 1,2 The rate of disease progression varies widely, and unknown factors other than alcohol use, obesity, and age may influence the longterm clinical outcome of the disease. In recent years many efforts have been made to identify receptors involved in viral entry into host cells. Two molecules are proposed to function as HCV receptors, namely, the low-density lipoprotein receptor (LDLR) and CD81. [3][4][5] Experiments in vitro showed competitive inhibition of binding between HCV and LDLR by purified LDL. 3 If similar inhibition occurs in vivo, the serum concentration of beta-lipoproteins may influence HCV proliferation because cell infection is required for replication of the virus. 6 Serum HCVAg levels negatively correlated with serum beta-lipoproteins, supporting the concept that LDLR is the HCV receptor and that beta-lipoproteins competitively inhibit infection of hepatocytes with HCV. 6 Additional in vivo evidence has been reported by in situ hybridization studies on keratinocytes obtained from vasculitic lesions of patients with type II cryoglobulinemia. 3 These keratinocytes with upregulation of LDL receptors were found to have the positive HCV RNA strand compared to keratinocytes obtained from normal skin of the same person with low levels of LDL receptors. In those with chronic HCV infection, polymorphisms of the LDLR can influence the severity of fibrosis (single-nucleotide polymorphism [SNP] in exon 8), clearance of virus (SNP in exon 10), Abbreviations: LDLR, low-density lipoprotein receptor; VLDL, very-low-density lipoprotein; HDL, high-density lipoprotein; EVR, early viral response; ETR, endof-treatment response.

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AIMTo determine whether there is an increased risk of gastric adenocarcinoma associated with vitamin D deficiency (VDd).METHODSA retrospective case control study was performed of all patients diagnosed with gastric adenocarcinoma between 2005 and 2015. After we excluded the patients without a documented vitamin D level, 49 patients were included in our study.RESULTSThe average age of patients with gastric adenocarcinoma and documented vitamin D level was 64 years old (95%CI: 27-86) and average vitamin D level was 20.8 mg/dL (95%CI: 4-44). Compared to a matched control group, the prevalence of VDd/insufficiency in patients with gastric adenocarcinoma was significantly higher than normal vitamin D levels (83.7% vs 16.3%). Forty-one patients (83.7%) with adenocarcinoma showed VDd/insufficiency compared to 18 (37%) patients with normal vitamin D level without gastric cancer (OR: 8.8, 95%CI: 5-22, P value < 0.0001). The average age of males with gastric adenocarcinoma diagnosis was 60 years old vs 68 years old for females (P = 0.01). Stage II gastric adenocarcinoma was the most prevalent in our study (37%).CONCLUSIONWe reported a positive relationship between VDd and gastric adenocarcinoma, that is to say, patients with decreased VDd levels have an increased propensity for gastric adenocarcinoma.