ABSTRACT
Background/Aims@#Shear wave elastography (SWE) is used for liver fibrosis staging based on stiffness measurements. It can be performed using endoscopic ultrasound (EUS) or a transabdominal approach. Transabdominal accuracy can be limited in patients with obesity because of the thick abdomen. Theoretically, EUS-SWE overcomes this limitation by internally assessing the liver. We aimed to define the optimal technique for EUS-SWE for future research and clinical use and compare its accuracy with that of transabdominal SWE. @*Methods@#Benchtop study: A standardized phantom model was used. The compared variables included the region of interest (ROI) size, depth, and orientation and transducer pressure.Porcine study: Phantom models with varying stiffness values were surgically implanted between the hepatic lobes. @*Results@#For EUS-SWE, a larger ROI size of 1.5 cm and a smaller ROI depth of 1 cm demonstrated a significantly higher accuracy. For transabdominal SWE, the ROI size was nonadjustable, and the optimal ROI depth ranged from 2 to 4 cm. The transducer pressure and ROI orientation did not significantly affect the accuracy. There were no significant differences in the accuracy between transabdominal SWE and EUS-SWE in the animal model. The variability among the operators was more pronounced for the higher stiffness values. Small lesion measurements were accurate only when the ROI was entirely situated within the lesion. @*Conclusions@#We defined the optimal viewing windows for EUS-SWE and transabdominal SWE. The accuracy was comparable in the non-obese porcine model. EUS-SWE may have a higher utility for evaluating small lesions than transabdominal SWE.
ABSTRACT
Brief SummaryCOVID-19 is one of the most consequential pandemics in the last century, yet the biological mechanisms that confer disease risk are incompletely understood. Further, heterogeneity in disease outcomes is influenced by race, though the relative contributions of structural/social and genetic factors remain unclear.1,2 Very recent unpublished work has identified two genetic risk loci that confer greater risk for respiratory failure in COVID-19: the ABO locus and the 3p21.31 locus.3 To understand how these loci might confer risk and whether this differs by race, we utilized proteomic profiling and genetic information from three cohorts including black and white participants to identify proteins influenced by these loci. We observed that variants in the ABO locus are associated with levels of CD209/DC-SIGN, a known binding protein for SARS-CoV and other viruses,4 as well as multiple inflammatory and thrombotic proteins, while the 3p21.31 locus is associated with levels of CXCL16, a known inflammatory chemokine.5 Thus, integration of genetic information and proteomic profiling in biracial cohorts highlights putative mechanisms for genetic risk in COVID-19 disease.
