RESUMO
BACKGROUND: A novel Fibroscan XL probe has recently been introduced and validated for obese patients, and has a diagnostic accuracy comparable with that of the standard M probe. The aim of this study was to analyze and understand the differences between these two probes in nonobese patients, to identify underlying causes for these differences, and to develop a practical algorithm to translate results for the XL probe to those for the M probe. METHODS AND RESULTS: Both probes were directly compared first in copolymer phantoms of varying stiffness (4.8, 11, and 40 kPa) and then in 371 obese and nonobese patients (body mass index, range 17.2-72.4) from German (n = 129) and Canadian (n = 242) centers. Liver stiffness values for both probes correlated better in phantoms than in patients (r = 0.98 versus 0.82, P < 0.001). Significantly more patients could be measured successfully using the XL probe than the M probe (98.4% versus 85.2%, respectively, P < 0.001) while the M probe produced a smaller interquartile range (21% versus 32%). Failure of the M probe to measure liver stiffness was not only observed in patients with a high body mass index and long skin-liver capsule distance but also in some nonobese patients (n = 10) due to quenching of the signal from subcutaneous fat tissue. In contrast with the phantoms, the XL probe consistently produced approximately 20% lower liver stiffness values in humans compared with the M probe. A long skin-liver capsule distance and a high degree of steatosis were responsible for this discordance. Adjustment of cutoff values for the XL probe (<5.5, 5.5-7, 7-10, and >10 kPa for F0, F1-2, F3, and F4 fibrosis, respectively) significantly improved agreement between the two probes from r = 0.655 to 0.679. CONCLUSION: Liver stiffness can be measured in significantly more obese and nonobese patients using the XL probe than the M probe. However, the XL probe is less accurate and adjusted cutoff values are required.
RESUMO
BACKGROUND: In contrast with other elastographic techniques, ascites is considered an exclusion criterion for assessment of fibrosis stage by transient elastography. However, a normal liver stiffness could rule out hepatic causes of ascites at an early stage. The aim of the present study was to determine whether liver stiffness can be generally determined by transient elastography through an ascites layer, to determine whether the ascites-mediated increase in intra-abdominal pressure affects liver stiffness, and to provide initial data from a pilot cohort of patients with various causes of ascites. METHODS AND RESULTS: Using the XL probe in an artificial ascites model, we demonstrated (copolymer phantoms surrounded by water) that a transient elastography-generated shear wave allows accurate determination of phantom stiffness up to a water lamella of 20 mm. We next showed in an animal ascites model that increased intra-abdominal pressure does not affect liver stiffness. Liver stiffness was then determined in 24 consecutive patients with ascites due to hepatic (n = 18) or nonhepatic (n = 6) causes. The cause of ascites was eventually clarified using routine clinical, imaging, laboratory, and other tools. Valid (75%) or acceptable (25%) liver stiffness data could be obtained in 23 patients (95.8%) with ascites up to an ascites lamella of 39 mm. The six patients (25%) with nonhepatic causes of ascites (eg, pancreatitis, peritoneal carcinomatosis) had a significantly lower liver stiffness (<8 kPa) as compared with the remaining patients with hepatic ascites (>30 kPa). Mean liver stiffness was 5.4 kPa ± 1.3 versus 66.2 ± 13.3 kPa. CONCLUSION: In conclusion, the presence of ascites and increased intra-abdominal pressure does not alter underlying liver stiffness as determined by transient elastography. We suggest that, using the XL probe, transient elastography can be used first-line to identify patients with nonhepatic ascites at an early stage.
