OBJECTIVES:Limitations of the Model for End-Stage Liver Disease (MELD) score include its failure to assess the nutritional and functional status of cirrhotic patients. Our objectives were to evaluate the impact of sarcopenia in cirrhosis and whether the inclusion of muscularity assessment within MELD could improve the prediction of mortality in patients with cirrhosis.METHODS:We included 669 cirrhotic patients who were consecutively evaluated for liver transplantation. Skeletal muscle index at the third lumbar vertebra (L3 SMI) was measured by computed tomography, and sarcopenia was defined using previously published gender and body mass index–specific cutoffs. Using Cox proportional hazards regression, a novel MELD-sarcopenia score was derived.RESULTS:Sarcopenia was present in 298 patients (45%); sarcopenic patients had shorter median survival than non-sarcopenic patients (20±3 vs. 95±24 months, P<0.001). By Cox regression analysis adjusted for age, gender, and hepatocellular carcinoma, both MELD (hazard ratio (HR) 1.08, 95% confidence interval (CI) 1.06–1.10, P<0.001), and the L3 SMI (HR 0.97, 95% CI 0.96–0.99, P<0.001) were associated with mortality. Overall, the c-statistics for 3-month mortality were 0.82 (95% CI 0.78–0.87) for MELD and 0.85 (95% CI 0.81–0.88) for MELD-sarcopenia (P=0.1). Corresponding figures for 1-year mortality were 0.73 (95% CI 0.69–0.77) and 0.77 (95% CI 0.73–0.80), respectively (P=0.03). The c-statistics for 3-month mortality in patients with MELD<15 (0.85 vs. 0.69, P=0.02) and refractory ascites (0.74 vs. 0.71, P=0.01) were significantly higher for MELD-sarcopenia compared with MELD.CONCLUSIONS:Modification of MELD to include sarcopenia is associated with improved prediction of mortality in patients with cirrhosis, primarily in patients with low MELD scores. External validation of this prognostic index in larger cohorts of cirrhotic patients is warranted.

BackgroundLiver stiffness measurement (LSM) by transient elastography (TE, FibroScan) is a validated method for noninvasively staging liver fibrosis. Most hepatic complications occur in patients with advanced fibrosis. Our objective was to determine the ability of LSM by TE to predict hepatic complications and mortality in a large cohort of patients with chronic liver disease.MethodsIn consecutive adults who underwent LSM by TE between July 2008 and June 2011, we used Cox regression to determine the independent association between liver stiffness and death or hepatic complications (decompensation, hepatocellular carcinoma, and liver transplantation). The performance of LSM to predict complications was determined using the c-statistic.ResultsAmong 2,052 patients (median age 51 years, 65% with hepatitis B or C), 87 patients (4.2%) died or developed a hepatic complication during a median follow-up period of 15.6 months (interquartile range, 11.0–23.5 months). Patients with complications had higher median liver stiffness than those without complications (13.5 vs. 6.0 kPa; P<0.00005). The 2-year incidence rates of death or hepatic complications were 2.6%, 9%, 19%, and 34% in patients with liver stiffness <10, 10–19.9, 20–39.9, and ≥40 kPa, respectively (P<0.00005). After adjustment for potential confounders, liver stiffness by TE was an independent predictor of complications (hazard ratio [HR] 1.05 per kPa; 95% confidence interval [CI] 1.03–1.06). The c-statistic of liver-stiffness for predicting complications was 0.80 (95% CI 0.75–0.85). A liver stiffness below 20 kPa effectively excluded complications (specificity 93%, negative predictive value 97%); however, the positive predictive value of higher results was sub-optimal (20%).ConclusionsLiver stiffness by TE accurately predicts the risk of death or hepatic complications in patients with chronic liver disease. TE may facilitate the estimation of prognosis and guide management of these patients.

SUMMARY BackgroundNorth American data are lacking on the effect of nucleos(t)ide analogues (NA) in preventing chronic hepatitis B (CHB)-related hepatocellular carcinoma (HCC).

FibroScan failure and poorly reliable LSM are uncommon. The most important determinants of poorly reliable results are older age, obesity, higher liver stiffness and the operator, the latter emphasizing the need for adequate training.

The middle-third of the patellar tendon (PT) is well-established as a potential graft for cruciate ligament reconstruction, but there is little anatomical basis for its use. Although studies on PT vascular anatomy have focused on the risk to tendon pedicles from surgical approaches and knee pathophysiology, the significance of its blood supply to grafting has not been adequately explored previously. This investigation explores both the intrinsic and extrinsic arterial anatomy of the PT, as relevant to the PT graft. Ten fresh cadaveric lower limbs underwent angiographic injection of the common femoral artery with radio-opaque lead oxide. Each tendon was carefully dissected, underwent plain radiography and subsequently schematically reconstructed. The PT demonstrated a well-developed and consistent vascularity from three main sources: antero-proximally, mainly by the inferior-lateral genicular artery; antero-distally via a choke-anastomotic arch between the anterior tibial recurrent and inferior medial genicular arteries; and posteriorly via the retro-patellar anastomotic arch in Hoffa's fat pad. Two patterns of pedicles formed this arch: inferior-lateral and descending genicular arteries (Type-I); superior-lateral, inferior-lateral, and superior-medial genicular arteries (Type-II). Both types supplied the posterior PT, with the majority of vessels descending to its middle-third. The middle-third PT has a richer intrinsic vascularity, which may enhance its ingrowth as a graft, and supports its conventional use in cruciate ligament reconstruction. The pedicles supplying the PT are endangered during procedures where Hoffa's fat pad is removed including certain techniques of PT harvest and total knee arthroplasty.