Abstract

Potential conflict of interest: Nothing to report. To the Editor: Kim and colleagues report that a high liver stiffness value (≥13 kPa) is an independent risk factor for hepatocellular carcinoma in patients with treated and untreated chronic hepatitis B viral infection.1 The problem is that the liver stiffness value is a function of fibrosis and necroinflammation2 and that liver stiffness may decrease when the latter is controlled.3 In our center, 627 patients with chronic hepatitis B viral infection underwent liver stiffness measurement between 2006 and 2014 and 16 (2.5%) developed hepatocellular carcinoma after a median follow‐up of 35 (interquartile range 17‐65) months. Considering the entire cohort, the liver stiffness value was correlated to hepatocellular carcinoma development with an area under the receiver operating characteristic curve of 0.87 (P < 0.0001). Nevertheless, a 13‐kPa threshold for prediction of hepatocellular carcinoma had a sensitivity and specificity at 31% and 95%, respectively. Among patients under treatment, the sensitivity and specificity for the same threshold were 36% and 91%, respectively, corresponding to seven patients with a median liver stiffness value of 7.4 (interquartile range 5.4‐9) kPa before the development of hepatocellular carcinoma. Moreover, three (43%) of them had overt cirrhosis or biopsy‐proven “occult” cirrhosis at the time of hepatocellular carcinoma. It is likely that a growing number of clinicians will perform serial liver stiffness measurements in their patients with chronic hepatitis B viral infection, including those under treatment, and that evidence‐based proven management of these patients will be inferred from such measurements. At the individual level, the liver stiffness value does not accurately predict the risk of hepatocellular carcinoma and liver stiffness measurement should not be used as a follow‐up tool. Patients at risk of hepatocellular carcinoma should comply with recommended follow‐up.4

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