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Editorial: effect of hepatic steatosis on liver stiffness in patients with chronic hepatitis B
Although liver stiffness measurement (LSM) using transient elastography (TE) is generally accepted as a reliable method to quantify fibrotic burden in patients with chronic liver diseases, its accuracy has been challenged because of several confounders, such as high alanine aminotransferase (ALT Level, which may lead to overestimation.1,2 Hepatic steatosis is common both in the general population as well as patients with chronic viral hepatitis. 2‐ 4 The prevalence of non-alcoholic fatty liver disease (NAFLD) in Patients with chronic hepatitis B (CHB) ranges from 18% to 40%. 5,6 Thus, LSM may be influenced by the extent of hepatic steatosis, because the shear wave must propagate through the fatty liver parenchyma. Of hepatic steatosis on LSM remains controversial.7, 8In the study by Shen et al,9 the median LSM was 7.4 kPa (interquartile range [IQR]: 6.6‐8.8 kPa) for S2‐S3, which Was significantly higher than the values of 5.9 kPa (IQR: 4.7‐8.0 kPa) for S0 status and 6.3 kPa (IQR 5.3‐8.2 kPa) for S1 status (P = 0.005) among CHB patients with no significant fibrosis (F0‐ F1 status). On the other hand, no significant LSM difference was evident among F2‐F4 CHB patients according to the extent of hepatic steatosis (P = 0.7). These data are clinically relevant because the prevalence of NAFLD among real‐world Patients with CHB is high, and concomitant metabolic phenotypes (including NAFLD) are significantly associated with a higher risk of disease progression.3,10However, several critical points should be borne in mind when in‐terpreting the results.9Firstly, the rates Of S2‐S3 diagnosis based on histological findings versus controlled attenuation parameter (CAP)‐based assessments differed (n = 48 and n = 127, respectively); this may indicate that the diagnostic performance of TE for hepatic steatosis is sub
optimal. In addition, TE may inaccurately identify patients without significant fibrosis who would benefit from assessment of hepatic steatosis according to this study; it is well‐known that the diagnostic performance of TE for early stage fibrosis is suboptimal. Secondly, the potential effects of higher ALT levels (median = 56.5 and 50.0 U/L in patients with and without hepatic steatosis, respectively) were inadequately analysed. similar, the potential effects of histological necroinflammatory activity on LSM require further attention. It remains unclear whether LSM Overestimation is attributable primarily to hepatic steatosis or concomitant necroinflammation, assessed either biochemically or histologically. Third, as in previous studies, the proportions of patients of various steatosis grades were skewed, which may have led to statistical bias. In addition, little is known about the effect of coexisting fat burden on patients with chronic viral hepatitis. Thus, the results should be validated in other study populations, with different steatosis grades and the aetiologies of underlying liver diseases.In conclusion, future large, well‐designed studies are required to validate these results, and to develop a simple diagnostic algorithm allowing for accurate interpretation of the fibrotic burden, as revealed by LSM, without any risk of overestimation (especially for patients with CHB but without significant fibrosis) |
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