Lower Liver-related Mortality Research Articles

County-level Differences in Liver-related Mortality, Waitlisting, and Liver Transplantation in the United States.

Much of our understanding regarding geographic issues in transplantation is based on statistical techniques that do not formally account for geography and is based on obsolete boundaries such as donation service area. We applied spatial epidemiological techniques to analyze liver-related mortality and access to liver transplant services at the county level using data from the Centers for Disease Control and Prevention and Scientific Registry of Transplant Recipients from 2010 to 2018. There was a significant negative spatial correlation between transplant rates and liver-related mortality at the county level (Moran's I, -0.319; P = 0.001). Significant clusters were identified with high transplant rates and low liver-related mortality. Counties in geographic clusters with high ratios of liver transplants to liver-related deaths had more liver transplant centers within 150 nautical miles (6.7 versus 3.6 centers; P < 0.001) compared with all other counties, as did counties in geographic clusters with high ratios of waitlist additions to liver-related deaths (8.5 versus 2.5 centers; P < 0.001). The spatial correlation between waitlist mortality and overall liver-related mortality was positive (Moran's I, 0.060; P = 0.001) but weaker. Several areas with high waitlist mortality had some of the lowest overall liver-related mortality in the country. These data suggest that high waitlist mortality and allocation model for end-stage liver disease do not necessarily correlate with decreased access to transplant, whereas local transplant center density is associated with better access to waitlisting and transplant.

Association of Aspirin with Hepatocellular Carcinoma and Liver-Related Mortality

BackgroundMore information is needed about the long-term effects of low-dose aspirin (≤160 mg) on incident hepatocellular carcinoma, liver-related mortality, and gastrointestinal bleeding in persons with chronic hepatitis B or hepatitis C virus infection.MethodsUsing nationwide Swedish registries, we identified all adults who received a diagnosis of chronic hepatitis B or hepatitis C from 2005 through 2015 and who did not have a history of aspirin use (50,275 patients). Patients who were starting to take low-dose aspirin (14,205 patients) were identified by their first filled prescriptions for 90 or more consecutive doses of aspirin. We constructed a propensity score and applied inverse probability of treatment weighting to balance baseline characteristics between groups. Using Cox proportional-hazards regression modeling, we estimated the risk of hepatocellular carcinoma and liver-related mortality, accounting for competing events.ResultsWith a median of 7.9 years of follow-up, the estimated cumulative incidence of hepatocellular carcinoma was 4.0% among aspirin users and 8.3% among nonusers of aspirin (difference, −4.3 percentage points; 95% confidence interval [CI], −5.0 to −3.6; adjusted hazard ratio, 0.69; 95% CI, 0.62 to 0.76). This inverse association appeared to be duration-dependent; as compared with short-term use (3 months to <1 year), the adjusted hazard ratios were 0.90 (95% CI, 0.76 to 1.06) for 1 to less than 3 years of use, 0.66 (95% CI, 0.56 to 0.78) for 3 to less than 5 years of use, and 0.57 (95% CI, 0.42 to 0.70) for 5 or more years of use. Ten-year liver-related mortality was 11.0% among aspirin users and 17.9% among nonusers (difference, −6.9 percentage points [95% CI, −8.1 to −5.7]; adjusted hazard ratio, 0.73 [95% CI, 0.67 to 0.81]). However, the 10-year risk of gastrointestinal bleeding did not differ significantly between users and nonusers of aspirin (7.8% and 6.9%, respectively; difference, 0.9 percentage points; 95% CI, −0.6 to 2.4).ConclusionsIn a nationwide study of patients with chronic viral hepatitis in Sweden, use of low-dose aspirin was associated with a significantly lower risk of hepatocellular carcinoma and lower liver-related mortality than no use of aspirin, without a significantly higher risk of gastrointestinal bleeding. (Funded by the National Institutes of Health and others.)

Association of IFNL3 and IFNL4 polymorphisms with liver‐related mortality in a multiracial cohort of HIV/HCV‐coinfected women

African Americans coinfected with HIV and hepatitis C virus (HCV) have lower liver-related mortality than Caucasians and Hispanics. While genetic polymorphisms near the IFNL3 and IFNL4 genes explain a significant fraction of racial differences in several HCV-related outcomes, the impact of these variants on liver-related mortality has not been investigated. We conducted a cohort study of HIV/HCV-coinfected women followed in the multicentre, NIH-funded Women's Interagency HIV Study (WIHS) to investigate whether 10 polymorphisms spanning the IFN-λ region were associated with liver-related mortality by dominant, recessive or additive genetic models. We also considered whether these polymorphisms contributed to previously reported differences in liver-related death by race/ethnicity (ascertained by self-report and ancestry informative markers). Among 794 coinfected women, there were 471 deaths including 55 liver-related deaths during up to 18years of follow-up. On adjusted analysis, rs12980275 GG genotype compared to AG+AA hazards ratios [(HR) 0.36, 95% CI 0.14-0.90, P=0.029] and rs8109886 AA genotype compared to CC+AC (HR 0.67, 95% CI 0.45-0.99, P=0.047) were most strongly associated with liver-related death although these associations were no longer significant after adjusting for race/ethnicity (HR 0.41, 95% CI 0.16-1.04, P=0.060 and HR 0.78, 95% CI 0.51-1.19, P=0.25, respectively). African American women had persistently lower liver-related death independent of IFN-λ variants (HRs≤0.44, P values≤0.04). The lower risk of death among African American HIV/HCV-coinfected women is not explained by genetic variation in the IFN-λ region suggesting, that other genetic, behavioural and/or environmental factors may contribute to racial/ethnic differences in liver-related mortality.

Balanced management of hepatic trauma is associated with low liver-related mortality

Hepatic trauma is a rare surgical emergency with significant morbidity and mortality. Therapeutic strategies have been controversially discussed during the last decades. The medical records of 47 consecutive patients with hepatic trauma treated at the University Hospital of Leipzig between 2004 and 2008 were retrospectively reviewed for the severity of liver injury, management, morbidity, and mortality and compared to a preceding cohort. Logistic regression analysis was performed to identify risk factors influencing mortality. Compared to 63 patients treated between 1993 and 2003, moderate liver injuries (grades I-III) occurred more frequently (p = 0.0006), and the proportion of patients that were managed operatively decreased from 68.9% to 37.5%. Twenty patients (42.6%) were treated conservatively (all grades I to III) and 27 surgically (47.4%). In detail, five patients were treated by hepatic packing alone, 13 by suture or coagulation, five by atypical resection, and four by hemihepatectomy. The overall mortality was 8.5% with a liver-related mortality rate of 2.1%. According to severity grades I-III, IV, and V, mortality rates were 0%, 18.2%, and 50.0%, respectively. Univariate analysis identified Injury Severity Score (ISS) >30, Moore grades IV and V, hemoglobin at admission <6.0 mmol/L, and need for transfusion of >12 erythrocyte concentrates to be significant risk factors for early posttraumatic death, while multivariate analysis only ISS >30 revealed to be of prognostic significance for early postoperative survival. Compared to a previous cohort in the same hospital, more patients were treated conservatively. Management of liver injuries presented with a low liver-related mortality rate. Grades I-III injuries can safely be treated by conservative means with excellent results. However, complex hepatic injuries may often require surgical treatment ranging from packing to complex hemihepatectomy. Hence, for selection of appropriate therapeutic options, patients with hepatic injuries should be treated in a specialized institution.

Value of the Hepatic Venous Pressure Gradient to Monitor Drug Therapy for Portal Hypertension: A Meta-Analysis

The use of the hepatic venous pressure gradient (HVPG) to assess the efficacy of the pharmacological treatment of portal hypertension in cirrhosis is controversial. Our aim was to establish whether target HVPG reduction predicts variceal bleeding in cirrhotic patients receiving variceal bleeding prophylaxis. Data sources were MEDLINE, EMBASE, Cochrane Controlled Trials Register, citation lists, and abstracts (most recent search March 2006). Cohorts of patients on drug therapy from randomized and nonrandomized studies correlating variceal bleeding and HVPG change were used. Heterogeneity was explored by metaregression analysis. Ten studies totaling 595 patients undergoing two HVPG measurements were identified. The RR of bleeding was lower in patients achieving an overall (HVPG <or=12 mmHg or decrease >or=20%) (0.27, 95% CI 0.14-0.52), complete (HVPG <or=12 mmHg) (0.48, CI 0.28-0.81), or partial (HVPG decrease >or=20%) (0.41, CI 0.20-0.81) response, with significant heterogeneity. Regression analysis identified the interval between the HVPG measurements significantly associated with the RR of bleeding. Heterogeneity was no longer significant after exclusion of an outlier trial, which showed the longest interval to HVPG remeasurement and the lowest quality score. Even considering nonvaluable patients because of bleeding as HVPG responders, the RR of bleeding was lower in overall responders than in nonresponders (0.66, CI 0.51-0.86). Overall response was associated with lower liver-related mortality (RR 0.58, CI 0.37-0.91). Current evidence supports the validity of HVPG end points to monitor drug therapy efficacy for variceal bleeding prophylaxis. HVPG monitoring also provides valuable prognostic information.

Selective management of blunt hepatic injuries including nonoperative management is a safe and effective strategy

The justification and preference for operative versus nonoperative management of hepatic injuries caused by blunt trauma remains ambiguous. This review assesses the outcome of operative and nonoperative management of liver injury after blunt trauma. We retrospectively reviewed the demographics, severity of injury, severity of liver injury, associated concomitant injuries, management scheme, and outcome of patients with documented hepatic injury from 1993 to 2003. The overall mortality rate was 9.4%, with 3.7% caused by the liver injury itself. Fifty-nine percent (330 of 561) of liver injuries were of low severity (grades I and II), with an overall mortality rate of 6.6% caused by concomitant injuries and liver-related mortality of 0%. Forty-one percent (231 of 561) of liver injuries were high-severity injuries (grades III, IV, and V). Mortality for nonoperative management of high-severity liver injuries was 2.2%. If operative intervention was required because of hemodynamic instability or concomitant injuries then the mortality rate was significantly higher at 30%. Forty-two of the 378 (11%) liver injuries treated nonoperatively required an adjunctive procedure for successful management. Selective management of liver injuries presented a low liver-related mortality rate. Low-grade injuries can be managed nonoperatively with excellent results. High-grade injuries can be managed nonoperatively, if operative intervention is not required for hemodynamic instability or associated injuries, with a low mortality. In these patients, adjunctive procedures will be required selectively for successful nonoperative management of high-grade liver injuries. High-grade injuries requiring operative management because of hemodynamic instability or concomitant injuries continue to have significantly higher mortality.