We report the largest single institution experience of LT for NASH. Over a 10-year period, the frequency of LT for NASH has increased 5-fold. Although outcomes are comparable with LT for other indications, health care resources are stressed significantly by this new and increasing group of transplant candidates.

Background Psoriasis, a chronic inflammatory disease associated with an accelerated risk of MI, provides an ideal human model to study inflammatory atherogenesis in vivo. We hypothesized that the increased cardiovascular risk observed in psoriasis would be partially attributable to an elevated subclinical coronary artery disease (CAD) burden composed of non-calcified plaques with high-risk features. However, inadequate efforts have been made to directly measure CAD in this vulnerable population. As such, we sought to compare total (TB) and non-calcified (NCB) coronary plaque burden, and high-risk plaque (HRP) prevalence, between psoriasis patients (n=105), hyperlipidemic patients eligible for statin therapy under NCEP-ATP III guidelines (n=100) who were ~10 years older, and non-psoriasis healthy volunteers (HV) (n=25). Methods Patients underwent coronary computed-tomography angiography (CCTA) for TB and NCB quantification, and HRP identification, defined as low-attenuation (<30 HU), positive remodeling (>1.10), and spotty calcification. A consecutive sample of the first 50 psoriasis patients were scanned again at 1 year following therapy. Results Despite being younger and at lower traditional risk than hyperlipidemic patients, psoriasis patients had increased NCB (mean±S.D.:1.18±0.33 vs 1.11±0.32, p=0.02), and similar HRP prevalence (p=0.58). Furthermore, compared to HV, psoriasis patients had increased TB (1.22±0.31 vs 1.04±0.22, p=0.001), NCB (1.18±0.33 vs 1.03±0.21, p=0.004), and HRP prevalence beyond traditional risk (OR=6.0, 95% CI: 1.1–31.7; p=0.03). Finally, amongst psoriasis patients followed for 1-year, improvement in psoriasis severity associated with improvement in TB (β=0.45, 0.23–0.67; p<0.001) and NCB (β=0.53, 0.32–0.74; p<0.001) beyond traditional risk factors. Conclusions Psoriasis patients had greater NCB and increased HRP prevalence than HV. Additionally, psoriasis patients had elevated NCB and equivalent HRP prevalence as older, hyperlipidemic patients. Finally, modulation of target organ inflammation (eg. skin) associated with an improvement in NCB at 1 year, suggesting that control of remote sites of inflammation may translate into reduced CAD risk.

An accurate clinical assessment of hepatic steatosis before transplantation is critical for successful outcomes after liver transplantation, especially if a pathologist is not available at the time of procurement. This prospective study investigated the surgeon's accuracy in predicting hepatic steatosis and organ quality in 201 adult donor livers. A steatosis assessment by a blinded expert pathologist served as the reference gold standard. The surgeon's steatosis estimate correlated more strongly with large-droplet macrovesicular steatosis [ld-MaS; nonparametric Spearman correlation coefficient (r S ) 5 0.504] versus small-droplet macrovesicular steatosis (sd-MaS; r S 5 0.398). True microvesicular steatosis was present in only 2 donors (1%). Liver texture criteria (yellowness, absence of scratch marks, and round edges) were mainly associated with ld-MaS (variance 5 0.619) and were less associated with sd-MaS (variance 5 0.264). The prediction of 30% ld-MaS versus <30% ld-MaS was excellent when liver texture criteria were used (accuracy 5 86.2%), but it was less accurate when the surgeon's direct estimation of the steatosis percentage was used (accuracy 5 75.5%). The surgeon's quality grading correlated with the degree of ld-MaS and the surgeon's steatosis estimate as well as the incidence of poor initial function and primary nonfunction. In conclusion, the precise estimation of steatosis remains challenging even in experienced hands. Liver texture characteristics are more helpful in identifying macrosteatotic organs than the surgeon's actual perception of steatosis.