Validation of the Baveno VI elastography criteria for the definition of compensated advanced chronic liver disease: an individual patient meta-analysis

Tsochatzis, E.; Hiriart, Jean Baptiste; Lupșor-Platon, Monica; Bronte, F.; Boursier, Jérôme; Marra, Fabio; Payancé, Audrey; Brodkin, Edgar; Castéra, Laurent; Papatheodoridis, George V.; Arena, U.; Calès, Paul; Calvaruso, V.; Lédinghen, Victor de; Pinzani, Massimo

doi:10.1016/s0168-8278(17)30399-9

Cited by 2 publications

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“…However, the rate of clinical events observed in the follow-up is in agreement with that expected in cACLD (31) ; furthermore, we were able to confirm the predictive value of CAP independent of LSM in the subgroup of patients who have LSM greater than or equal to 15 kPa. These patients have a definite cACLD according to the Baveno VI consensus conference, (2,32) and most importantly, a LSM greater than or equal to 21 kPa, indicating that they very likely have CSPH. (7) Because liver biopsy was not available in the study population, we cannot confirm whether the CAP-increased values genuinely mirror steatosis or whether the increases are due to unknown factors in cACLD; in any case, the CAP prognostic ability remains tied to whatever components might contribute to it.…”

Section: Discussionmentioning

confidence: 98%

Prognostic Significance of Controlled Attenuation Parameter in Patients With Compensated Advanced Chronic Liver Disease

Margini

Murgia

Stirnimann

et al. 2018

Hepatology Communications

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Obesity and steatosis have been associated with liver disease progression in patients with compensated advanced chronic liver disease (cACLD) (liver stiffness measurement [LSM] ≥ 10 kPa). The controlled attenuation parameter (CAP) estimates steatosis during LSM by transient elastography. We aimed to evaluate whether CAP is associated with the development of clinically relevant events in cACLD. Consecutive patients with cACLD and CAP measurements observed between September 2013 and September 2015 were retrospectively studied. Classical decompensation and severe bacterial infections on follow‐up were recorded. A predefined CAP cut‐off for steatosis was used (220 dB/m; 90% sensitivity). The association among LSM, CAP, and events was assessed by univariate and multivariate Cox regression. Among the 193 patients (viral etiology = 58%; median Child score = 5; LSM = 15.1 kPa; CAP = 255 ± 62 dB/m) who were followed up in median for 18 months, 18 developed clinically relevant events (11 liver decompensation, 7 severe bacterial infections). Patients developing events had higher LSM (median: 30.8 versus 14.3 kPa, P < 0.001) and showed trends for higher CAP (275 ± 46 versus 252 ± 63 dB/m, P = 0.07), lower platelet count (134 ± 74 versus 167 ± 74 G/L, P = 0.07), and worse liver function versus patients remaining compensated. Body mass index was similar in the two groups. All events were more frequent in patients with CAP being greater than or equal to 220 dB/m (12.9% versus 1.6% in CAP < 220; P = 0.013), and 10 of 11 episodes of liver decompensation occurred in patients with CAP being greater than or equal to 220 dB/m. Following multivariate analysis, LSM and CAP greater than or equal to 220 dB/m remained independently associated with clinical events in the whole population and in patients with clinically significant portal hypertension. Conclusion: The CAP being greater than or equal to 220 dB/m is associated with increased risk of clinical decompensation and bacterial infections independent of LSM in patients with cACLD and allows refining the noninvasive risk stratification in this population. (Hepatology Communications 2018; 00:000‐000)

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Section: Discussionmentioning

confidence: 98%