Background In the United States, mortality after a diagnosis of hepatocellular carcinoma (HCC) is higher in patients who are Black than in patients of other racial groups. The objective of this study was to clarify factors contributing to this disparity by analyzing liver and tumor characteristics in patients with HCC who have a history of hepatitis C virus (HCV) infection. Methods Records of patients with HCV and HCC at the authors' institution from 2003 to 2018 were retrospectively reviewed. Race and ethnicity were self‐identified. Imaging, laboratory, and pathologic features were compared between Black and non‐Black cohorts. Results Among 1195 individuals with HCC, 390 identified as Black. At the time of HCC diagnosis, Black patients had better liver function, as measured by Child‐Pugh score, Model of End‐Stage Liver Disease score, histology of nontumor tissue, and fibrosis‐4 (FIB‐4) score (all P < .05). FIB‐4 scores were <3.25 in 31% of Black patients. In addition, Black patients had less early stage HCC (20.2% vs 32.3%; P < .05), larger tumors (median [interquartile range]: 3.5 cm [2.2‐6.2 cm] vs 3.1 cm [2.1‐5.1 cm]; P < .01), more multiple tumors (median, [interquartile range]: 1 tumor [1‐3 tumors] vs 1 tumor [1‐2 tumors]; P = .03), more poorly differentiated tumors (30.3% vs 20.5%; P < .05), and more microvascular invasion (67.2% vs 56.5%; P < .05). Conclusions Black patients with HCV exposure develop HCC at earlier stages of liver disease than members of other racial groups. Nearly one‐third would not qualify for HCC screening using the common FIB‐4 cirrhosis threshold. Practice guidelines that stress HCC surveillance for cirrhotic patients with HCV may need to be revised to be more inclusive for Black patients. In addition, tumors in Black patients carry worse prognostic features, and molecular studies are needed to characterize their biologic properties.

Background Postoperative ambulation is an important tenet in enhanced recovery programs. We quantitatively assessed the correlation of decreased postoperative ambulation with postoperative complications and delays in gastrointestinal function. Methods Patients undergoing major abdominal surgery were fitted with digital ankle pedometers yielding continuous measurements of their ambulation. Primary endpoints were the overall and system-specific complication rates, with secondary endpoints being the time to first passage of flatus and stool, the length of hospital stay, and the rate of readmission. Results 100 patients were enrolled. We found a significant, independent inverse correlation between the number of steps on the first and second postoperative days (POD1/2) and the incidence of complications as well as the recovery of GI function and the likelihood of readmission ( P < .05). POD2 step count was an independent risk factor for severe complications ( P = .026). Discussion Digitally quantified ambulation data may be a prognostic biomarker for the likelihood of severe postoperative complications.

Intestinal epithelial cells (IECs) are the first to encounter luminal antigens and play an active role in intestinal immune responses. We previously reported that β‐glucans, major fungal cell‐wall glycans, induced chemokine secretion by IEC lines in a Dectin‐1‐ and Syk‐dependent manner. Here, we show that in contrast to β‐glucans, stimulation of IEC lines with Candida albicans and Saccharomyces cerevisiae did not induce secretion of any of the proinflammatory cytokines IL‐8, CCL2, CXCL1, and GM‐CSF. Commensal fungi and β‐glucans activated Syk and ERK in IEC lines. However, only β‐glucans activated p38, JNK, and the transcription factors NF‐κB p65 and c‐JUN, which were necessary for cytokine secretion. Furthermore, costimulation of IEC lines with β‐glucans and C. albicans yielded decreased cytokine secretion compared to stimulation with β‐glucans alone. Finally, ex vivo stimulation of human colonic mucosal explants with zymosan and C. albicans, leads to epithelial Syk and ERK phosphorylation, implying recognition of fungi and similar initial signaling pathways as in IEC lines. Lack of cytokine secretion in response to commensal fungi may reflect IECs’ response to fungal glycans, other than β‐glucans, that contribute to mucosal tolerance. Skewed epithelial response to commensal fungi may impair homeostasis and contribute to intestinal inflammation.

There is mounting evidence that Black patients develop more advanced liver cancers with less advanced liver disease. These findings have important implications for the future of liver cancer screening.

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