Platelet-to-White Blood Cell Ratio Is Associated with Adverse Outcomes in Cirrhotic Patients with Acute Deterioration.

Background: The platelet-to-white blood cell ratio (PWR) is a hematologic marker of the systemic inflammatory response. Recently, the PWR was revealed to have a role as an independent prognostic factor for mortality in patients with hepatitis B virus (HBV)-related acute-on-chronic failure (ACLF) and HBV-related liver cirrhosis (LC) with acute decompensation (AD). However, the prognostic role of the PWR still needs to be investigated in LC patients with AD. In this study, we analyzed whether the PWR could stratify the risk of adverse outcomes (death or liver transplantation (LT)) in these patients. Methods: A prospective cohort of 1670 patients with AD of liver cirrhosis ((age: 55.2 ± 7.8, male = 1226 (73.4%)) was enrolled and evaluated for 28-day and overall adverse outcomes. Results: During a median follow-up of 8.0 months (range, 1.9−15.5 months), 424 (25.4%) patients had adverse outcomes (death = 377, LT = 47). The most common etiology of LC was alcohol use (69.7%). The adverse outcome rate was higher for patients with a PWR ≤ 12.1 than for those with a PWR > 12.1. A lower PWR level was a prognostic factor for 28-day adverse outcomes (PWR: hazard ratio 1.707, p = 0.034) when adjusted for the etiology of cirrhosis, infection, ACLF, and the MELD score. In the subgroup analysis, the PWR level stratified the risk of 28-day adverse outcomes regardless of the presence of ACLF or the main form of AD but not for those with bacterial infection. Conclusions: A lower PWR level was associated with 28-day adverse outcomes, indicating that the PWR level can be a useful and simple tool for stratifying the risk of 28-day adverse outcomes in LC patients with AD.

Type-specific human papillomavirus distribution in invasive cervical cancer in Korea, 1958-2004.

OBJECTIVE: To describe the HPV genotype distribution and to investigate the underlying secular trend in the relative contribution of HPV types 16-18 in invasive cervical cancer (ICC) over a period of 47 years (1958-2004) in South Korea. METHODS: Paraffin embedded ICC samples were obtained from historical archives of two hospitals in Korea. HPV detection and genotyping was performed by SPF10 PCR, DEIA and LiPA25 assays (version 1). RESULTS: Of 874 ICC cases, 742 were considered suitable for HPV DNA testing after histological evaluation. Squamous cell carcinoma was the major histological type (93.0%). HPV was detected in 674 of the 742 specimens (90.8%). The five most common types identified as single types among HPV-positive cases were HPV16 (63.1%), HPV18 (8.5%), HPV33 (4.5%), HPV58 (3.9%) and HPV31 (3.0%). Multiple infections were detected in 5%. HPV16-18 together accounted for 72% of all HPV-positive cervical cancers with no statistically significant differences by time at diagnosis (adjusted model-p>0.05). CONCLUSION: This present study confirmed the role of HPV infection as the main factor in cervical cancer in Korea. HPV16-18 accounted for more than 70% in cervical cancer and there was no statistically significant secular trend for the past 50 years.

Sulindac prevents esophageal adenocarcinomas induced by gastroduodenal reflux in rats.

PURPOSE: It is known that cyclooxygenase (COX)-2 expression is increased in Barrett's esophagus and esophageal adenocarcinomas. We studied COX-2 expression and the effect sulindac has on the genesis of Barrett's esophagus and adenocarcinoma in rats undergoing esophagogastroduodenal anastomosis (EGDA). MATERIALS AND METHODS: Fifty-one rats were divided into a control group (n=27), a 500 ppm sulindac-treated group (n=15) and 1000 ppm sulindac-treated group (n=9). Randomly selected rats were killed by diethyl ether inhalation at 20 and 40 weeks after surgery. RESULTS: At 40 weeks, rats treated with 1000 ppm sulindac showed narrower esophageal diameter and milder inflammation than the control rats. At 40 weeks, the incidence of Barrett's esophagus was similar between control and sulindac-treated groups, but the incidence of adenocarcinoma was significantly lower in the 1000 ppm sulindac-treated group than either the control or 500 ppm sulindac-treated groups. COX-2 was significantly increased in the lower esophagus of control rats killed at 40 weeks. Cyclin D1 expression was negligible in the sulindac- treated group compared with the control group. CONCLUSION: We suggest that the chemopreventive effect of sulindac is related to decreased COX-2 and cyclin D1 expression, which may be influenced by reduced inflammation.