We investigated the impact of short-term changes in general and central fatness on the risk of hepatocellular carcinoma (HCC) in a large, population-based cohort. We screened 7 221 479 subjects who underwent health examinations provided by the National Health Insurance Service of South Korea in 2009 and 2011. In total, 6 789 472 subjects were included in the final analysis. General fatness was defined as a body mass index (BMI) >= 25 kg/m(2), and central fatness was defined as a waist circumference (WC) >= 90 cm in men and >= 85 cm in women. Subjects were classified according to the change in body fatness between 2009 and 2011, as follows: (a) persistent no fatness as no fatness in both 2009 and 2011, (b) reversed fatness as fatness in 2009, but no fatness in 2011, (c) incident fatness as no fatness in 2009, but fatness in 2011 or (d) persistent fatness as fatness in both 2009 and 2011. During a median 6.4-year follow-up, we documented 9952 HCC cases. Compared to subjects with a persistent no general fatness, the risk of HCC significantly increased in those with incident (adjusted hazard ratio [aHR] = 1.10, 95% confidence interval [CI] = 1.01-1.20) and persistent (aHR = 1.28, 95% CI = 1.23-1.34) general fatness. Compared to subjects with persistent no central fatness, those with incident and persistent central fatness showed a significantly increased risk of HCC (aHR = 1.19, 95% CI = 1.11-1.27 and aHR = 1.33, 95% CI = 1.26-1.40, respectively). Taken together, these findings indicate the importance of strategies for preventing and reversing body fatness to reduce the incidence of HCC.

We investigated the association between body weight variability and the risks of cardiovascular disease and mortality in patients with nonalcoholic fatty liver disease (NAFLD) using large-scale, nationwide cohort data. We included 726,736 individuals with NAFLD who underwent a health examination between 2009 and 2010. NAFLD was defined as a fatty liver index ≥ 60, after excluding significant alcohol intake, viral hepatitis, and liver cirrhosis. Body weight variability was assessed using four indices, including variability independent of the mean (VIM). During a median 8.1-year follow-up, we documented 11,358, 14,714, and 22,164 cases of myocardial infarction (MI), stroke, and all-cause mortality, respectively. Body weight variability was associated with an increased risk of MI, stroke, and mortality after adjusting for confounding variables. The hazard ratios (HRs) (95% confidence intervals) for the highest quartile, compared with the lowest quartile, of VIM for body weight were 1.15 (1.10–1.20), 1.22 (1.18–1.26), and 1.56 (1.53–1.62) for MI, stroke, and all-cause mortality, respectively. Body weight variability was associated with increased risks of MI, stroke, and all-cause mortality in NAFLD patients. Appropriate interventions to maintain a stable weight could positively affect health outcomes in NAFLD patients.

BACKGROUND AND AIMS:It is well known that hepatocellular carcinoma (HCC) develops as a consequence of hepatic fibrosis progression. Thus, early identification of advanced liver fibrosis is very important. This study evaluated the prognostic value of FIB-4, the aspartate transaminase to-platelet ratio index (APRI), and the gamma-glutamyl transpeptidase-toplatelet ratio (GPR) for predicting HCC development using histological fibrosis stage as a reference in Asian chronic hepatitis B (CHB) patients.METHODS:A total of 444 CHB patients who underwent liver biopsy and serological tests for determining noninvasive serum fibrosis markers were enrolled. All patients were followed to monitor HCC development.RESULTS:The histological fibrosis stage showed best performance in predicting HCC development at 5 (area under the receiver operating characteristic curve [AUROC] = 0.783) and 7 years (AUROC = 0.766), followed by FIB-4 (AUROC = 0.753 at 5 years, 0.698 at 7 years), APRI (AUROC = 0.658 at 5 years, 0.572 at 7 years), and GPR (AUROC = 0.638 at 5 years, 0.603 at 7 years). When we classified risk groups according to the histological fibrosis stage (F4 vs. F0-3) and FIB-4 (FIB-4 ≥ 3.25 vs. FIB-4 < 3.25), patients in the high-risk group were found to have a significantly higher probability of developing HCC than those in the low-risk group (P=0.005 and 0.022, respectively, log-rank test).CONCLUSION:Our study demonstrated that FIB-4 is useful for the noninvasive prediction of HCC development, while APRI and GPR were less useful.

Background/Aims: Nonalcoholic fatty liver disease (NAFLD) is becoming a worldwide epidemic, and is frequently found in patients with chronic hepatitis B (CHB). We investigated the impact of histologically proven hepatic steatosis on the risk for hepatocellular carcinoma (HCC) in CHB patients without excessive alcohol intake. Methods: Consecutive CHB patients who underwent liver biopsy from January 2007 to December 2015 were included. The association between hepatic steatosis (>= 5%) and subsequent HCC risk was analyzed. Inverse probability weighting (IPW) using the propensity score was applied to adjust for differences in patient characteristics, including metabolic factors. Results: Fatty liver was histologically proven in 70 patients (21.8%) among a total of 321 patients. During the median (interquartile range) follow-up of 5.3 (2.9-8.3) years, 17 of 321 patients (5.3%) developed HCC: 8 of 70 patients (11.4%) with fatty liver and 9 of 251 patients (3.6%) without fatty liver. The five-year cumulative incidences of HCC among patients without and with fatty liver were 1.9% and 8.2%, respectively (P=0.004). Coexisting fatty liver was associated with a higher risk for HCC (adjusted hazards ratio [HR], 3.005; 95% confidence interval [CI], 1.122-8.051; P = 0.03). After balancing with IPW, HCC incidences were not significantly different between the groups (P = 0.19), and the association between fatty liver and HCC was not significant (adjusted HR, 1.709; 95% CI, 0.404-7.228; P = 0.47). Conclusions: Superimposed NAFLD was associated with a higher HCC risk in CHB patients. However, the association between steatosis per se and HCC risk was not evident after adjustment for metabolic factors.

Aims: Single-nucleotide polymorphisms (SNPs) in microRNA machinery genes might affect microRNA processing and subsequently impact tumorigenesis. The aim of this study was to investigate the associations between SNPs in microRNA machinery genes and hepatocellular carcinoma (HCC) in a Korean population. Methods: Genotyping of six SNPs in microRNA machinery genes was performed using blood samples from 147 patients with HCC and 209 healthy control subjects. Results: None of the six SNPs in microRNA machinery genes were significantly associated with HCC development. However, among the models for six polymorphic loci-DICER (rs3742330 and rs13078), DROSHA (rs10719 and rs6877842), RAN (rs14035) and XPO5 (rs11077)-one allele combination (A-A-T-C-C-C) showed synergistic effects in terms of an increased risk of HCC development (odds ratio= 8.881, 95% confidence interval [CI]=1.889-41.750; P=0.002). Multivariate Cox proportional hazard regression analysis showed a significant survival benefit for the DICER rs3742330 GG compared with the AA genotype (hazard ratio [HR], 0.352; 95% CI, 0.155-0.796; P=0.013) and for the RAN rs14035 CT compared with the CC genotype (HR, 0.599; 95% CI, 0.363-0.988; P=0.046). Conclusions: Although we found no direct association between DICER (rs3742330 and rs13078), DROSHA (rs10719 and rs6877842), RAN (rs14035) or XPO5 (rs11077) polymorphisms and HCC risk, we demonstrated that DICER (rs3742330) and RAN (rs14035) were associated with the survival of HCC patients. Future studies with larger samples are needed to determine the associations of SNPs in microRNA machinery genes with HCC risk and prognosis.

AIM:To investigate associations between the tumor necrosis factor alpha (TNF-α) -1031 T>C, -863 C>A, -857 C>T, -308 G>A, and -238 G>A polymorphisms and HCC in Korea.METHODS:Hepatocellular carcinoma (HCC) cases were diagnosed at CHA Bundang Medical Center from June 1996 to August 2008. The association between TNF-α polymorphisms and HCC was analyzed in 157 HCC patients and 201 controls using a polymerase chain reaction-restriction fragment length polymorphism assay. We investigated five TNF-α polymorphisms, which are TNF-α -1031 T>C, -863 C>A, -857 C>T, -308 G>A, and -238 G>A. The TNF-α genotype frequencies, genotype combinations and haplotypes were analyzed to disclose the association with HCC.RESULTS:None of the TNF-α polymorphisms was significantly associated with HCC. However, nine genotype combinations had associations with increased likelihood of HCC. Among them, TNF-α -1031/-857/-238 TT/CC/GA (AOR = 18.849, 95%CI: 2.203-161.246, P = 0.007), TNF-α -1031/-308/-238 TT/GG/GA (AOR = 26.956, 95%CI: 3.071-236.584, P = 0.003), and TNF-α -1031/-238 TT/GA (AOR = 21.576, 95%CI: 2.581-180.394, P = 0.005) showed marked association with HCC. There were five haplotypes of TNF-α polymorphisms which were significantly associated with HCC. They are TNF-α -1031/-863/-857/-308/-238 T-C-C-G-A (OR = 25.824, 95%CI: 1.491-447.223, P = 0.0005), TNF-α -1031/-857/-308/-238 T-C-G-A (OR = 12.059, 95%CI: 2.747-52.950, P < 0.0001), TNF-α -1031/-857/-238 T-C-A (OR = 10.696, 95%CI: 2.428-47.110, P = 0.0001), TNF-α -1031/-308/-238 T-G-A (OR = 7.556, 95%CI: 2.173-26.280, P = 0.0002) and TNF-α -1031/-238 T-A (OR = 10.865, 95%CI: 2.473-47.740, P = 0.0001). Moreover, HCC Okuda stage III cases with the TNF-α -1031 CC genotype had better survival than those with the TT genotype (AOR = 5.795, 95%CI: 1.145-29.323).CONCLUSION:Although no single TNF-α polymorphism is associated with HCC in this study, some TNF-α genotype combinations and haplotypes are associated with HCC. In addition, HCC Okuda stage III cases with the TNF-α -1031 TT genotype may have a better prognosis than those with the CC genotype.

The central venous cannulation is commonly performed in the operating rooms and intensive care units for various purposes. Although the central venous catheter (CVC) is used in many ways, the malpositioning of the CVC is often associated with serious complications. We report a case of an unexpected malposition of a CVC in the jugular venous arch via external jugular vein.

Polymyositis is a subacute inflammatory myopathy presenting as progressive and often symmetric muscle weakness. It is believed that the patients with polymyositis are sensitive to nondepolarizing muscle relaxants. The major concerns for the anesthesiologist are delayed recovery from muscle relaxation, aspiration pneumonitis, arrhythmias and cardiac failures [1]. A 26-year-old male with polymyositis, 170 cm in height and 76 kg in weight, had flap surgery of sacral pressure sore which developed during intensive care. He had progressive muscle weakness for one year. Three months ago, he was admitted to a hospital under the impression of viral hepatitis or nonalcoholic steatohepatitis due to elevated liver enzymes. However, viral studies and liver biopsy results were normal. Instead, elevated CK (> 11,000 U/L) and CK-MB (> 300 ng/ml) were found. Polymyositis was diagnosed according to clinical features, electromyography results and muscle biopsy findings. During the hospital stay, he presented pneumonia symptoms. Intravenous antibiotics were administered, but the patient was not improved. Three days later, dyspnea became more severe and arterial blood gas analysis (ABGA) showed PaO2 49 mmHg and SaO2 80%. Upon the diagnosis of acute respiratory distress syndrome, the patient was intubated. Despite of ventilator care, pulmonary status deteriorated and extracorporeal membrane oxygenation (ECMO) support was applied for five days. His pulmonary function improved enough to switch to conventional ventilator care and the care was maintained for another ten days. He was transferred to general ward after recovery of pulmonary function. On the day of surgery, the patent’s laboratory findings, chest X-ray and vital signs showed normal. In the operating room, direct arterial pressure, electrocardiography, end-tidal CO2, temperature, pulse oxymetry and peripheral nerve stimulator (TOFWatch, Organon Inc., Dublin, Ireland) were monitored. Neuromuscular relaxation was assessed by train of four (TOF) at the adductor pollicis with supramaximal stimulation of the ulnar nerve at 2 Hz every 12 seconds and was recorded continuously until end of anesthesia. Anesthesia was induced with glycopyrrolate 0.2 mg, propofol 120 mg and remifentanil infusion. The lungs were ventilated with 100% oxygen and 2.5% sevoflurane. TOF-ratio was assessed before administration of muscle relaxant as a reference value and was recorded continuously until end of anesthesia. Rocuronium 10 mg IV was slowly started and TOF-ratio decreased to 50% of reference value after 5 minutes. Rocuronium 10 mg was added and TOF-ratio was suppressed to 0 after another 5 minutes. The patient was presenting excellent intubating conditions according to the Copenhagen Consensus Conference score (abducted vocal cords, no vocal cords movement, no coughing, no limb movement). Anesthesia was maintained with 1.5 L/min O2, 1.5 L/min air, sevoflurane and remifentanil. Operation time was 250 minutes. TOF-ratio maintained 0 by 110 minutes after induction. Then TOF-ratio started to increase slowly but maintained 90% after 5 minutes. He was extubated and transferred to recovery room. There was no specific complication during the hospital stay.

To determine whether the genomic changes in hepatitis B virus (HBV) affect the clinical outcomes of hepatocellular carcinoma (HCC) in patients with HBV-associated HCC treated with curative surgical resection.