New reliability criteria for transient elastography increase the number of accurate measurements for screening of cirrhosis and portal hypertension

Schwabl, Philipp; Bota, Simona; Salzl, Petra; Mandorfer, Mattias; Payer, BA; Ferlitsch, Arnulf; Stift, Judith; Wrba, Friedrich; Trauner, Michael; Peck‐Radosavljevic, Markus; Reiberger, Thomas

doi:10.1111/liv.12623

Cited by 134 publications

(101 citation statements)

References 61 publications

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“…[24][25][26] All relevant confounding factors for the TE-based assessment of liver fibrosis induce false-high liver stiffness results leading to an overestimation of liver fibrosis stage. 27 Thus, they cannot explain the very low prevalence of liver fibrosis !F3 observed in our study. Since sample size limits the conclusions of our study, collaborative efforts are required to perform large international studies.…”

Section: Discussionmentioning

confidence: 99%

Liver disease in adults with α1‐antitrypsin deficiency

et al. 2018

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Background: The natural history of adult liver disease due to a1-antitrypsin deficiency (A1AD) remains poorly understood. Objective: We investigated whether heterozygosity for the Z-allele predisposes for the development of clinically significant portal hypertension (CSPH). Moreover, we aimed to non-invasively assess the prevalence of liver fibrosis and hepatic steatosis in adults with A1AD treated by pulmonologists. Methods: SERPINA1 rs28929474 (Z-allele) was genotyped in 315 patients with CSPH (hepatic venous pressure gradient !10 mmHg; cases) and 248 liver donors (controls). In addition, 31 adults with A1AD (Pi*ZZ/Pi*SZ) and 11 first-degree relatives (Pi*MZ/Pi*MS) underwent liver stiffness and controlled attenuation parameter (CAP) measurement. Results: Heterozygosity for the Z-allele was observed in 6.7% of patients with CSPH and 2.8% of liver donors. Thus, harboring the Z-allele was associated with increased odds of CSPH (odds ratio: 2.47; 95% confidence interval: 1.03-5.9; P ¼ 0.042). Among Pi*ZZ/Pi*SZ patients, 23%/3% had liver stiffness values indicative of liver fibrosis ( !F2/ !F3). Interestingly, 65%/52% of Pi*ZZ/Pi*SZ patients had CAP values indicative of hepatic steatosis ( !S1/ !S2). Conclusions: Heterozygosity for the Z-allele predisposes for the development of CSPH, confirming its role as a genetic (co)factor in liver disease. Pi*ZZ/SZ patients rarely develop liver fibrosis !F3 during adulthood; however, liver fibrosis !F2 is common. Elevated CAP values hint at underlying hepatic steatosis, which might promote liver fibrosis progression.

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Section: Discussionmentioning

confidence: 99%

Liver disease in adults with α1‐antitrypsin deficiency

et al. 2018

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“…All patients were infected with HCVsubtype 1a and had the IL28B C/T genotype. [19]. Advanced liver fibrosis and cirrhosis were defined by liver stiffness values > 9.5 kPa and > 12.5 kPa, respectively [20].…”

Section: Characteristics Of Patients With Boc Add-onmentioning

confidence: 99%

Treatment intensification with boceprevir in HIV-positive patients with acute HCV-genotype 1 infection at high risk for treatment failure

Mandorfer

Steiner

Schwabl

et al. 2015

Wien Klin Wochenschr

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“…TE has been validated in different liver diseases and has been shown to be accurate in diagnosing fibrosis in the F3-F4 stages with a specificity of 72 % and sensitivity of 86 % [5]. Previous studies have demonstrated that the patient's anthropometric characteristics and etiology of liver disease are factors that can influence the reliability of TE measurements and that these factors may influence the diagnosis of liver fibrosis [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%