Steatosis DeLIVERs high-sensitivity C-reactive protein.

Nonalcoholic fatty liver disease is characterized by excess accumulation of lipids within parenchymal cells of the liver (ie, hepatocellular steatosis) in the absence of excessive ethanol consumption. Fatty liver disease is widely considered to be the hepatic manifestation of metabolic syndrome and is estimated to occur in more than 25% of the Western population.1 Nonalcoholic fatty liver disease represents a continuum of histopathologic and biochemical features, progressing from simple steatosis to a more marked inflammatory condition, termed nonalcoholic steatohepatitis, which can cause liver fibrosis.2 Basic scientists and clinicians alike are significantly invested in understanding mechanisms underlying the development of steatosis, as well as identifying triggers for the transition of simple steatosis to nonalcoholic steatohepatitis, which contributes significantly to liver-related morbidity. The presence of fatty liver disease in patients has been shown to increase the risk of cardiovascular disease.3 In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Ndumele et al identify an association between hepatic steatosis, as assessed by noninvasive abdominal ultrasound, and high-sensitivity C-reactive protein (hs-CRP).4 Importantly, this association was independent of and additive to obesity and metabolic syndrome. hs-CRP is an acute phase protein that is an indicator of systemic inflammation and is used clinically to predict adverse cardiovascular events. This observation strongly suggests that inflammation sits at the crossroads between fatty liver disease and cardiovascular disease, highlighting the need for increased scientific engagement across the fields of hepatology, gastroenterology, cardiology, and endocrinology to better investigate, prevent, and manage these interconnected diseases.