Hyponatremia is associated with reduced survival in patients with cirrhosis awaiting orthotopic liver transplantation (OLT). However, data are sparse regarding the impact of hyponatremia on outcome following OLT. We investigated the effect of hyponatremia at the time of OLT on mortality and morbidity following the procedure. The study included 2,175 primary OLT recipients between 1990 and 2000. Serum sodium concentrations obtained immediately prior to OLT were correlated with subsequent survival using proportional hazards analysis. Morbidity associated with hyponatremia was assessed, including length of hospitalization, length of intensive care unit (ICU) admission, and occurrence of central pontine myelinolysis (CPM). Out of 2,175 subjects, 1,495 (68.7%) had normal serum sodium (>135 mEq/L) at OLT, whereas mild hyponatremia (125-134 mEq/L) was present in 615 (28.3%) and severe hyponatremia (<125 mEq/L) in 65 (3.0%). Serum sodium had no impact on survival up to 90 days after OLT (multivariate hazard ratio ‫؍‬ 1.00, P ‫؍‬ 0.99). Patients with severe hyponatremia tended to have a longer stay in the ICU (median ‫؍‬ 4.5 days) and hospital (17.0 days) compared to normonatremic recipients (median ICU stay ‫؍‬ 3.0 days, hospital stay ‫؍‬ 14.0 days; P ‫؍‬ 0.02 and 0.08, respectively). There were 10 subjects that developed CPM, with an overall incidence of 0.5%. Although infrequent, the incidence of CPM did correlate with serum sodium levels (P < 0.01). Conclusion: Pre-OLT serum sodium does not have a statistically significant impact on survival following OLT. The incidence of CPM correlates with hyponatremia, although its overall incidence is low. Incorporation of serum sodium in organ allocation may not adversely affect the overall post-OLT outcome.

Hyponatremia is associated with an increased risk of mortality on the liver transplant (LTx) waiting list. Though incorporation of the serum sodium into the MELD score may reduce wait list mortality, concerns remain about a potential association between pre-LTx hyponatremia and decreased post-LTx survival. Furthermore, the relationship between pre-LTx hypernatremia and post-LTx survival remains unexplored. The purpose of this study was to investigate the impact of the entire spectrum pre-LTx serum sodium (Na) on post-LTx outcomes. We identified 19,537patients with serum Na that was available immediately before LTx from 2003–20010. Patients were divided into three groups including hyponatremic (Na ≤ 130 mEq/L), normonatremic (Na=131–145mEq/L) and hypernatremic (Na >145 mEq/L) groups and their post-LTx outcomes compared. There was no difference in in-hospital mortality or 90-day survival between patients with hyponatremia and normonatremia. A fraction (2.4%) of patients had hypernatremia, which was associated with increased in-hospital death (11.2% vs. 4.2%, p<0.001) and diminished 90 day survival (86.4% vs. 94.0.%, p<0.001). After adjusting for important clinical variables, the association of preLTx hypernatremia with post-transplant mortality remained significant with a HR=1.13 for each unit increase in sodium >145mEq/L (p<0.001). Length of hospitalization after LTx was significantly longer in hypernatremic patients (p < 0.001). In conclusion, hyponatremia per se does not affect post-LTx survival. Pre-LTx hypernatremia is a highly significant risk factor for post-LTx mortality.

Background:Until now, various types of combined therapy with nucleotide analogs and pegylated interferon (Peg-INF) in patients with hepatitis B patients have been tried. However, studies regarding the benefits of de novo combination, late-add on, and sequential treatment are very limited. The objective of the current study was to identify the efficacy of sequential treatment of Peg-INF after short-term antiviral treatment.Methods:Between June 2010 and June 2015, hepatitis B e antigen (HBeAg)-positive patients (n = 162) received Peg-IFN for 48 weeks (mono-treatment group, n = 81) and entecavir (ETV) for 12 weeks with a 48-week course of Peg-IFN starting at week 5 of ETV therapy (sequential treatment group, n = 81). The primary endpoint was HBeAg seroconversion at the end of follow-up period after the 24-week treatment. The primary endpoint was analyzed using Chi-square test, Fisher's exact test, and regression analysis.Results:HBeAg seroconversion rate (18.2% vs. 18.2%, t = 0.03, P = 1.000) and seroclearance rate (19.7% vs. 19.7%, t = 0.03, P = 1.000) were same in both mono-treatment and sequential treatment groups. The rate of alanine aminotransferase (ALT) normalization (45.5% vs. 54.5%, t = 1.12, P = 0.296) and serum hepatitis B virus (HBV)-DNA <2000 U/L (28.8% vs. 28.8%, t = 0.10, P = 1.000) was not different in sequential and mono-treatment groups at 24 weeks of Peg-INF. Viral response rate (HBeAg seroconversion and serum HBV-DNA <2000 U/L) was not different in the two groups (12.1% vs. 16.7%, t = 1.83, P = 0.457). Baseline HBV-DNA level (7 log10U/ml vs. 7.5 log10U/ml, t = 1.70, P = 0.019) and hepatitis B surface antigen titer (3.6 log10U/ml vs. 4.0 log10U/ml, t = 2.19, P = 0.020) were lower and predictors of responder in mono-treatment and sequential treatment groups, respectively.Conclusions:The current study shows no differences in HBeAg seroconversion rate, ALT normalization, and HBV-DNA levels between mono-therapy and sequential therapy regimens.Trial Registration:ClinicalTrials.gov, NCT01220596; https://clinicaltrials.gov/ct2/show/NCT01220596?term=NCT01220596&rank=1.

Hyponatremia, a common complication in patients with advanced liver disease and impaired free water clearance, has been shown to be an important predictor of short-term mortality. Hepatic encephalopathy, also a late complication of end-stage liver disease, has been associated with low-grade cerebral edema as a result of swelling of astrocytes. Guevara et al. hypothesized that hyponatremia and the resultant depletion of organic osmolytes (e.g., myo -inositol) from brain cells contribute to brain edema, playing an important role in the pathogenesis of hepatic encephalopathy. Using a multivariable analysis, they demonstrated that hyponatremia increased the risk of hepatic encephalopathy more than eightfold, after adjustment for serum bilirubin and creatinine concentrations and previous history of encephalopathy. Their magnetic resonance spectroscopy data correlated low brain concentrations of myoinositol with hepatic encephalopathy. As both hyponatremia and encephalopathy occur in patients with advanced liver disease, it has been diffi cult to implicate hyponatremia independently in the pathogenesis of hepatic encephalopathy. Guevara's data do suggest that hyponatremia is more likely an accomplice than an innocent bystander. Am J Gastroenterol 2009; 104:1390 -1391 doi: 10.1038/ajg.2009 published online 19 May 2009 Hyponatremia is common in patients with advanced liver disease (1) : dilutional hyponatremia results from reduction in solute-free water clearance despite increased total body water. e pathogenetic mechanism for hyponatremia in cirrhosis involves the antidiuretic hormone (arginine vasopressin). Conjugation of arginine vasopressin with its receptors (the so-called V2 receptors) located in the renal collecting duct induces production and translocation of water channel molecules (aquaporin-2), leading to reabsorption of water and reduction in excretion of free water (2) .To the degree that hyponatremia occurs in patients with advanced cirrhosis, it has been correlated with increased mortality (3,4) . Recent studies have shown that serum sodium concentration correlates with survival in patients with cirrhosis awaiting liver transplantation, even a er adjusting for the model for end-stage liver disease score. Incorporating serum sodium in organ allocation decisions will enhance the accuracy of mortality prediction and may improve the overall outcome of liver transplantation (5,6) .Physiological consequences speci cally attributable to hyponatremia in patients with advanced liver disease are difcult to study because of the pervasive e ects of portal hypertension and hepatic insu ciency that coexist in these patients. Obviously, low serum sodium concentration is associated with reduction in the osmolality of the extracellular uid, which in turn a ects osmotic balance in many cells, leading to cell swelling as water moves into the cells to attain osmotic balance (7) . Changes in cell volume are particularly important in the brain as they are directly related to intracranial pressure. One of the defe...

Background/Aims: Post-hepatectomy liver failure (PHLF) is a major concern for patients with hepatocellular carcinoma (HCC) who have undergone liver resection. The albumin-bilirubin (ALBI) score is a novel model for assessing liver function. We aimed to investigate the effectiveness of the ALBI score as a predictor of PHLF in HCC patients who have undergone hepatectomy in South Korea. Methods: Between January 2014 and November 2018, HCC patients who underwent hepatectomy and indocyanine retention rate at 15 min (ICG-R15) test were enrolled in this study. Results: A total of 101 patients diagnosed with HCC underwent hepatectomy. Thirty-two patients (31.7%) experienced PHLF. The ALBI score (OR 2.83; 95% CI 1.22-6.55; p=0.015), ICG-R15 (OR 1.07; 95% CI 1.02-1.12; p=0.007) and ALBI grade (OR 2,86; 95% CI 1.08-7.58; p=0.035) were identified as independent predictors of PHLF by multivariable analysis. The area under the receiver operating characteristic curve of the ALBI score and ICG-R15 were 0.676 (95% CI 0.566-0.785) and 0.632 (95% CI 0.513-0.752), respectively. The optimal cutoff value of the ALBI score in predicting PHLF was -2.62, with a sensitivity of 75.0% and a specificity of 56.5%. Conclusions: The ALBI score is an effective predictor of PHLF in patients with HCC, and its predictive ability is comparable to that of ICG-R15.

Background This study was conducted to determine which type and dose of sedative drugs should be given to cirrhotic patients with compensation or decompensation during esophagogastroduodenoscopy (EGD) to prevent hepatic encephalopathy (HE) after sedation. Methods We reviewed the medical records of cirrhotic patients consecutively admitted to the hospital and conducted a number connection test (NCT) before and 2 h after EGD with moderate sedation. Sedation was performed using either propofol alone, midazolam alone, or combined propofol + midazolam. Results Sixty-seven patients were admitted for a screening EGD. The NCT before and after sedation were not significantly different in the propofol alone (pre-NCT = 47.3 ± 19.71 seconds vs. post-NCT = 49.4 ± 21.79 seconds, P = 0.6389). In the midazolam alone (pre-NCT = 50.3 ± 20.56 vs. post-NCT = 63.7 ± 33.17, P = 0.0021) and in the combined propofol + midazolam (pre-NCT = 47.4 ± 20.99 vs. post-NCT = 60.0 ± 30.79, P = 0.0002), NCT were significantly delayed. The propofol alone group received 52.3 ± 16.31 mg (0.82 ± 0.29 mg/kg). In 45 (67.2%) decompensated patients, only the propofol alone was not significantly different between pre-NCT (49.2 ± 22.92) and post-NCT (52.3 ± 24.90) ( P = 0.4548). Serum sodium level was significantly correlated with delta-NCT (r = 0.3594, P = 0.0028). Conclusion Propofol alone could be the best sedation strategy for cirrhotic patients with compensation or decompensation without aggravation of covert or overt HE. Hyponatremia could be a risk factor for developing or worsening HE after EGD with sedation.

Tenofovir disoproxil fumarate (TDF) is thought to cause varying degrees of hypophosphatemia in patients with chronic hepatitis B (CHB). Therefore, we investigated factors that cause hypophosphatemia in patients treated with TDF and methods to increase serum phosphorus concentrations in clinical practice.We completed a retrospective review of patients with CHB treated with TDF initially at

Accurate diagnosis of liver cirrhosis (LC) and significant fibrosis in patients with chronic liver disease (CLD) is important. The Mac-2 binding protein glycosylation isomer (M2BPGi) has emerged as a novel serum biomarker for liver fibrosis; however, insufficient clinical data of M2BPGi are available in patients with CLD. Therefore, we performed a retrospective cohort study to investigate the clinical usefulness of serum M2BPGi for assessing LC and significant fibrosis in CLD patients. We retrospectively reviewed the CLD patients with measured serum M2BPGi at Kosin University Gospel Hospital between January 2016 and December 2019. Multivariate logistic regression analyses were conducted to identify the independent factors associated with LC. The diagnostic power of serum M2BPGi for LC and significant fibrosis (≥F2) was evaluated and compared to that of other serum biomarkers using receiver operating characteristic curve and area under the curve (AUC). A total of 454 patients enrolled in this study. M2BPGi (adjusted odds ratio [aOR], 1.77; 95% confidence interval [CI], 1.52–2.07) and fibrosis index based on four factors (aOR, 1.23; 95% CI, 1.11–1.37) were identified as significant independent factors for LC. The AUC of M2BPGi for LC (0.866) and significant fibrosis (0.816) were comparable to those of fibrosis index based on four factors (0.860, 0.773), aspartate aminotransferase-to-platelet ratio index (0.806, 0.752), and gamma-glutamyl transpeptidase-to-platelet ratio (0.759, 0.710). The optimal cut-off values for M2BPGi for LC and significant fibrosis were 1.37 and 0.89, respectively. Serum M2BPGi levels were significantly correlated with liver stiffness measurements (ρ = 0.778). Serum M2BPGi is a reliable noninvasive method for the assessment of LC and significant fibrosis in patients with CLD.