Vibration-Controlled Elastography: Impact of Steatosis on Fibrosis in CHB

Chronic hepatitis B (CHB) continues to pose significant public health challenges, affecting millions worldwide and leading to substantial morbidity and mortality. One of the most critical aspects of managing CHB is assessing and staging liver fibrosis, which informs treatment decisions and predicts disease progression. Liver biopsy, historically regarded as the gold standard for fibrosis assessment, is invasive and carries risks such as pain, high costs and variability in interpretation. Consequently, non-invasive techniques like vibration-controlled transient elastography (VCTE) have gained popularity for evaluating liver stiffness measurement (LSM) as a surrogate for fibrosis staging.

However, the rise of metabolic syndromes and obesity has led to a growing prevalence of hepatic steatosis, characterised by excessive fat accumulation in the liver. This condition, often coexisting with CHB, complicates the diagnostic process as it can influence LSM values. Understanding the interplay between hepatic steatosis and LSM is crucial for accurate diagnosis and effective management of liver fibrosis in CHB patients. A recent review published in Insights into Imaging examines how hepatic steatosis affects LSM values, its impact on diagnostic accuracy and the adjustments needed to improve clinical outcomes.

Hepatic Steatosis and Its Impact on LSM Values

Hepatic steatosis is defined by the presence of fat deposits within liver cells, often associated with obesity, diabetes and metabolic syndromes. Its increasing prevalence in CHB patients has introduced complexities in liver fibrosis assessment. Research has demonstrated that hepatic steatosis significantly elevates LSM values in the early stages of liver fibrosis, such as mild (F1) and moderate fibrosis (F2). This phenomenon occurs because lipid accumulation within hepatocytes alters the mechanical properties of liver tissue. The excess fat stiffens the liver, leading to higher LSM values during VCTE.

In advanced stages of fibrosis (F3 and F4), the effects of hepatic steatosis on LSM diminish. At these stages, fibrosis-related extracellular matrix deposition and scarring become the primary determinants of liver stiffness. Therefore, while hepatic steatosis introduces variability in LSM readings in earlier stages, its influence wanes as fibrosis progresses. These findings underscore the importance of interpreting LSM values in the context of hepatic steatosis, particularly in patients with mild or moderate fibrosis.

Moreover, hepatic steatosis’s impact on LSM values can lead to potential diagnostic challenges. Elevated LSM values in the presence of steatosis might be mistaken for more severe fibrosis, increasing the risk of overestimating disease severity. This highlights the need for clinicians to carefully consider the presence of steatosis when interpreting LSM results, ensuring that patient management decisions are not based on inflated stiffness readings caused by fat deposition rather than fibrosis.

Diagnostic Efficiency of LSM in CHB Patients with Steatosis

Despite the challenges posed by steatosis-related elevation of LSM values, the diagnostic efficiency of VCTE in staging liver fibrosis remains largely unaffected. Studies have shown that the diagnostic performance of LSM, as measured by the area under the receiver operating characteristic (ROC) curve, is consistent across fibrosis stages, irrespective of whether hepatic steatosis is present. This consistency suggests that while steatosis may elevate LSM values, the increase is proportionally distributed across fibrosis stages, preserving diagnostic accuracy.

The reliability of LSM for staging fibrosis in steatosis-affected CHB patients is an encouraging finding. It means that VCTE remains a valuable tool for fibrosis assessment, even in populations with high rates of metabolic syndrome and obesity. This robustness ensures that clinicians can continue to rely on non-invasive elastography methods without compromising diagnostic outcomes.

However, it is crucial to remain vigilant about the limitations of VCTE in specific scenarios. For instance, the distribution of hepatic steatosis across different stages of fibrosis may vary, necessitating a tailored approach in interpreting LSM results. Furthermore, while the diagnostic efficiency remains intact, steatosis-related increases in LSM values could lead to higher false-positive rates (FPRs) if standard cut-off values are applied indiscriminately. This highlights the importance of refining diagnostic protocols to account for the influence of steatosis.

Adjusting LSM Cut-Offs to Enhance Diagnostic Precision

One of the most effective strategies for improving the accuracy of LSM in CHB patients with steatosis is adjusting the cut-off values used for fibrosis staging. Conventional cut-offs may result in inflated false-positive rates in this population, particularly for early and intermediate fibrosis stages. For example, using a standard cut-off of 7.0 kPa for significant fibrosis (F ≥ 2) in patients with steatosis often leads to overdiagnosis. Research indicates that raising this threshold to 7.6 kPa significantly reduces FPRs without compromising diagnostic sensitivity, specificity or accuracy.

Similarly, adjusted cut-offs for advanced fibrosis (F ≥ 3) and cirrhosis (F = 4) have been proposed. For instance, increasing the cut-off for advanced fibrosis from 8.0 kPa to 10.0 kPa in patients with hepatic steatosis reduces FPRs and enhances diagnostic precision. While this adjustment may slightly decrease sensitivity for advanced fibrosis, it avoids the potential harm of overestimating disease severity and initiating unnecessary or overly aggressive treatments.

Tailoring LSM thresholds for CHB patients with hepatic steatosis is essential for ensuring accurate and reliable fibrosis assessment. Incorporating steatosis-specific cut-offs into clinical practice guidelines could help standardise the approach, improving diagnostic outcomes and reducing variability in patient care. By addressing the unique challenges posed by hepatic steatosis, clinicians can provide more precise staging of liver fibrosis, enabling better management of CHB patients with coexisting metabolic conditions.

By increasing stiffness measurements, hepatic steatosis significantly influences LSM values, particularly in the early stages of liver fibrosis. However, its impact does not compromise the overall diagnostic efficiency of VCTE for staging fibrosis in CHB patients. Adjusting LSM cut-off values for patients with steatosis is a crucial step in mitigating false positives and enhancing diagnostic precision. These findings highlight the need for a nuanced approach to fibrosis assessment in CHB patients, accounting for the interplay between steatosis and liver stiffness. By refining diagnostic protocols and integrating steatosis-specific considerations, healthcare providers can ensure accurate staging of liver fibrosis and optimise treatment strategies for CHB patients in diverse clinical contexts.

Source: Insights into Imaging

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