Our research confirmed that using SWE to measure liver stiffness offered diagnostic performance comparable to that of TE in predicting histological staging and the risk of varices. Additionally, compared with TE, SWE excelled in distinguishing between stage 2 and stage 3 patients with PBC. Therefore, SWE can serve as a complementary clinical tool to TE, enhancing the diagnostic capability for assessing disease progression in patients with PBC.
Extensive research is ongoing regarding employing TE for staging liver fibrosis in chronic liver diseases. The EASL clinical practice guidelines suggest that vibration-controlled transient elastography is among the best alternative markers for detecting cirrhosis or severe liver fibrosis in patients with PBC [6]. Meanwhile, some researchers have begun exploring the application of SWE in patients with PBC, demonstrating its strong diagnostic efficacy in assessing PBC progression [10, 14, 15]. For instance, Yan et al. applied SWE to 157 Chinese patients with PBC, achieving a similar diagnostic performance to that observed in this study with regards to distinguishing significant fibrosis (≥ S2), severe fibrosis (≥ S3), and cirrhosis (= S4) (AUC: 0.88, 0.97, and 0.99, respectively). However, their diagnostic thresholds were notably higher than ours (10.7 kPa, 12.2 kPa, and 14.1 kPa, respectively) [14]. Similarly, Manesis et al. found that when being used to distinguish among stages ≥ 2, ≥ 3, and = 4 PBC, 2D-LSM SWE demonstrated an AUROC of 0.739, 0.688, and 0.813, respectively. Additionally, the corresponding diagnostic thresholds reported in their study, which were 7.8 kPa, 10.0 kPa, and 11.9 kPa, were similar to those in our study (6.7 kPa, 9.9 kPa, and 10.8 kPa, respectively) [15]. Nonetheless, the limited number of studies has prevented a comprehensive exploration of factors contributing to the observed differences among various studies. Consequently, further research with expanded data is necessary to define the optimal diagnostic efficacy and thresholds for SWE in predicting histological staging in PBC.
Owing to its convenience, speed, and reproducibility, TE is widely utilized in clinical practice. There is considerable research on its effectiveness in staging PBC, showing high diagnostic efficacy. A study has revealed AUROCs of 0.92, 0.91, and 0.91 for predicting PBC stages ≥ F2, ≥ F 3, and = F4, respectively, using TE [16]. However, its limitations are well-documented. Specifically, LSM values may not be obtainable in patients with ascites, abdominal distention, or excessive abdominal adiposity. Additionally, multiple studies demonstrated that elevated ALT levels consistently lead to increased LSM values [8]. SWE-LSM, on the other hand, remains unaffected by factors like fat deposition and inflammatory activity [17], the latter of which is identified as an independent predictor of LSM elevation in TE [18]. Some researchers argue that compared with SWE, TE is more susceptible to the confounding effects of inflammation when utilized solely to reflect liver elasticity [17]. Conversely, in our analysis using the corresponding SWE-LSM thresholds for PBC histological staging, we found no significant differences in transaminase and bilirubin levels among the correct estimation, overestimation, and underestimation groups. Additionally, SWE-LSM showed a low correlation with these markers, further affirming its independence from elevated transaminase and bilirubin levels, aligning with prior research findings.
Because of the dire long-term prognosis associated with variceal bleeding caused by portal hypertension in patients with PBC, where survival rates plummet to just 46% over 3 years [19], variceal screening is generally reserved for patients with PBC, primary sclerosing cholangitis, and chronic viral hepatitis who are clinically suspected of having cirrhosis [5]. Typically, portal hypertension manifests in the later stages of the disease. However, intriguingly, patients with PBC may display signs of portal hypertension even without splenomegaly or portal vein widening, possibly due to bile stasis, interface hepatitis, and portal or sinusoidal fibrosis [20]. Early detection of portal hypertension risk using noninvasive methods is crucial for the treatment and prognosis of patients with PBC. TE plays a significant role in predicting portal hypertension, with the Baveno VI criteria suggesting that compensated patients with cirrhosis with LSM > 20 kPa and platelet counts < 150 × 109/L should undergo endoscopic screening for varices. However, this method is not specifically tailored to patients with PBC, and its application in our study yielded a diagnostic accuracy of merely 61.8%. Even when disregarding factors that may affect TE, its inability to visualize LSM and avoid large vessels, bile ducts, and lesions during operation suggests that SWE may be more advantageous. In this study, the AUROC for SWE-LSM in predicting varices was 0.819, consistent with previous studies [21]. Additionally, SWE-LSM demonstrated a diagnostic accuracy of 76.4% for varices, slightly higher than that of the Baveno VI criteria. This also confirms that SWE exhibits comparable diagnostic efficacy to that of TE in assessing variceal risk. It is therefore suggested that healthcare facilities at all levels should consider the flexibility of adopting appropriate non-invasive assessment methods based on their operational capacity.
This study had some limitations. First, owing to the small sample size, the impact of transaminase and bilirubin levels on SWE-LSM could not be thoroughly analyzed. Second, the number of patients who underwent endoscopic examination was small. In the future, more participants will be included to facilitate data analysis. Finally, the technical success rate and reliability of SWE and TE measurements were not evaluated in this study.
In conclusion, our study confirmed that SWE technology is comparable to TE in assessing the risk of esophagogastric varices and in performing histological staging. When TE measurements are not feasible, SWE can serve as a complementary technique in clinical practice, thereby enhancing the diagnostic capabilities for disease progression in patients with PBC.