BACKGROUND Patient blood management (PBM) programs are associated with improved patient outcomes, reduced transfusions and costs. In 2008, the Western Australia Department of Health initiated a comprehensive health‐system–wide PBM program. This study assesses program outcomes. STUDY DESIGN AND METHODS This was a retrospective study of 605,046 patients admitted to four major adult tertiary‐care hospitals between July 2008 and June 2014. Outcome measures were red blood cell (RBC), fresh‐frozen plasma (FFP), and platelet units transfused; single‐unit RBC transfusions; pretransfusion hemoglobin levels; elective surgery patients anemic at admission; product and activity‐based costs of transfusion; in‐hospital mortality; length of stay; 28‐day all‐cause emergency readmissions; and hospital‐acquired complications. RESULTS Comparing final year with baseline, units of RBCs, FFP, and platelets transfused per admission decreased 41% (p < 0.001), representing a saving of AU$18,507,092 (US$18,078,258) and between AU$80 million and AU$100 million (US$78 million and US$97 million) estimated activity‐based savings. Mean pretransfusion hemoglobin levels decreased 7.9 g/dL to 7.3 g/dL (p < 0.001), and anemic elective surgery admissions decreased 20.8% to 14.4% (p = 0.001). Single‐unit RBC transfusions increased from 33.3% to 63.7% (p < 0.001). There were risk‐adjusted reductions in hospital mortality (odds ratio [OR], 0.72; 95% confidence interval [CI], 0.67‐0.77; p < 0.001), length of stay (incidence rate ratio, 0.85; 95% CI, 0.84‐0.87; p < 0.001), hospital‐acquired infections (OR, 0.79; 95% CI, 0.73‐0.86; p < 0.001), and acute myocardial infarction‐stroke (OR, 0.69; 95% CI, 0.58‐0.82; p < 0.001). All‐cause emergency readmissions increased (OR, 1.06; 95% CI, 1.02‐1.10; p = 0.001). CONCLUSION Implementation of a unique, jurisdiction‐wide PBM program was associated with improved patient outcomes, reduced blood product utilization, and product‐related cost savings.

The World Health Organization (WHO) has declared coronavirus disease 2019 (COVID-19), the disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a pandemic. Global health care now faces unprecedented challenges with widespread and rapid human-to-human transmission of SARS-CoV-2 and high morbidity and mortality with COVID-19 worldwide. Across the world, medical care is hampered by a critical shortage of not only hand sanitizers, personal protective equipment, ventilators, and hospital beds, but also impediments to the blood supply. Blood donation centers in many areas around the globe have mostly closed. Donors, practicing social distancing, some either with illness or undergoing self-quarantine, are quickly diminishing. Drastic public health initiatives have focused on containment and “flattening the curve” while invaluable resources are being depleted. In some countries, the point has been reached at which the demand for such resources, including donor blood, outstrips the supply. Questions as to the safety of blood persist. Although it does not appear very likely that the virus can be transmitted through allogeneic blood transfusion, this still remains to be fully determined. As options dwindle, we must enact regional and national shortage plans worldwide and more vitally disseminate the knowledge of and immediately implement patient blood management (PBM). PBM is an evidence-based bundle of care to optimize medical and surgical patient outcomes by clinically managing and preserving a patient’s own blood. This multinational and diverse group of authors issue this “Call to Action” underscoring “The Essential Role of Patient Blood Management in the Management of Pandemics” and urging all stakeholders and providers to implement the practical and commonsense principles of PBM and its multiprofessional and multimodality approaches.

While there may be compelling reasons to reduce reliance on patients, cadavers, and animals for surgical training, none of the methods of simulated training has yet been shown to be better than other forms of surgical training.

Modest (1-70 g per week) alcohol consumption, particularly wine in a non-binge pattern, is associated with lower fibrosis in patients with NAFLD. Prospective longitudinal studies into fibrosis progression, cardiovascular outcomes, and mortality are required before clinical recommendations can be made.

Genetic factors account for a significant proportion of the phenotypic variance of nonalcoholic fatty liver disease (NAFLD); however, very few predisposing genes have been identified. We aimed to (1) identify novel genetic associations with NAFLD by performing a genome-wide association study (GWAS), and (2) examine the biological expression of the strongest genetic associations in a separate cohort. We performed GWAS of a populationbased cohort (Raine Study) of 928 adolescents assessed for NAFLD by ultrasound at age 17. Expression of genes with single nucleotide polymorphisms (SNPs) that were associated with NAFLD at a significance level of P < 10 25 was examined in adults with NAFLD and controls by quantifying hepatic messenger RNA (mRNA) expression and serum levels of protein. After adjustment for sex and degree of adiposity, SNPs in two genes expressed in liver were associated with NAFLD adolescents: group-specific component (GC) (odds ratio [OR], 2.54; P 5 1.20 3 10 26 ) and lymphocyte cytosolic protein-1 (LCP1) (OR, 3.29; P 5 2.96 3 10 26 ). SNPs in two genes expressed in neurons were also associated with NAFLD: lipid phosphate phosphatase-related protein type 4 (LPPR4) (OR, 2.30; P 5 4.82 3 10 26 ) and solute carrier family 38 member 8 (SLC38A8) (OR, 3.14; P 5 1.86 3 10 26 ). Hepatic GC mRNA was significantly reduced (by 83%) and LCP1 mRNA was increased (by 300%) in liver biopsy samples from patients with NAFLD compared to controls (P < 0.05). Mean serum levels of GC protein were significantly lower in patients with NAFLD than controls (250 6 90 versus 298 6 90, respectively; P 5 0.004); GC protein levels decreased with increasing severity of hepatic steatosis (P < 0.01). Conclusion: The association between GC and LCP1 SNPs and NAFLD as well as altered biological expression implicate these genes in the pathogenesis of NAFLD. (HEPATOLOGY 2013;57:590-600) T he development of nonalcoholic fatty liver disease (NAFLD) is closely related to increasing adiposity and insulin resistance, largely attributed to excess caloric intake and reduced energy expenditure. It is increasingly recognized that there are strong genetic influences in the development of NAFLD. The underlying risk factors for NAFLD of diabetes mellitus and obesity have numerous predisposing genetic polymorphisms. 1,2 Furthermore, the heritability of hepatic steatosis has been estimated at 39% after controlling for factors such as age, gender, race, and body mass index (BMI). 3 Identifying genetic Abbreviations: BMI, body mass index; C-RP, c-reactive protein; GC, group-specific component; GWAS, genome wide association study; HDL, high-density lipoprotein; HPRT1, hypoxanthine phosphoribosyltransferase 1; LCP-1, lymphocyte cytosolic protein-1; LPPR4, lipid phosphate phosphatase-related protein type 4 gene; NAFLD, nonalcoholic fatty liver disease; PNPLA3, patatin-like phospholipase domain containing 3; PPIA, peptidylprolyl isomerase A; SDHA, succinate dehydrogenase complex, subunit A flavoprotein; SLC38A8, solute carrier family 38 member 8; SNP, sing...