Letter on ‘Clinical Features of Portal Hypertension and Their Prognostic Implications in Patients With Autoimmune Hepatitis’

We read with great interest the article by Burghart et al. [1] entitled ‘Clinical Features of Portal Hypertension and Their Prognostic Implications in Patients with Autoimmune Hepatitis (AIH)’. This is a very well-conducted and clearly presented study that addresses a major issue, as few data exist on the prognostic role of clinically significant portal hypertension (CSPH) in AIH. We fully agree with the authors' conclusions that all features of CSPH are associated with an increased risk of hepatic decompensation and liver transplantation or death, while achieving complete biochemical response (CBR) certainly confers a protective effect. This finding is of paramount importance, as in patients with compensated or even decompensated advanced chronic liver disease (cACLD and dACLD), CBR may lead to substantial reversal of fibrosis or cirrhosis. Of particular interest is the authors' application of the Baveno VII criteria to rule out CSPH in AIH [2]. In this cohort, patients with liver stiffness measurement (LSM) < 15 kPa and platelet counts ≥ 150 × 109/L showed a significantly lower risk of decompensation, as well as better liver transplant-free survival compared to those exceeding these thresholds. However, in AIH, previous studies have shown that LSM may underestimate the degree of fibrosis and even the presence of CSPH. In fact, Llovet et al. [3] showed that up to 52% of AIH patients with CSPH had LSM values below the traditional cutoffs (12.5–16 kPa) used for the diagnosis of cirrhosis. In addition, a progressive decrease in LSM values was observed from the moment of AIH diagnosis, yet increasing the probability of misdiagnosing patients with significant fibrosis or cirrhosis over time. These findings raise concerns about the underestimation of the risk of CSPH when relying on liver elastography alone. As the authors correctly used the LSM obtained 6 months after treatment initiation to minimise the inflammatory confounding [4, 5], it would be valuable to know how many patients in their cohort fulfilled the Baveno VII criteria based on LSM ≥ 15 kPa and platelet count < 150 × 109/L alone, or both. Such a breakdown would clarify whether platelet count alone, rather than LSM, accounted for the classification of the majority of patients at risk. This could support the notion that platelet count alone outperforms LSM for the prediction of CSPH and that additional parameters, such as spleen stiffness measurement, might provide more accurate noninvasive identification of CSPH in AIH. Finally, we would like to congratulate the authors for their important contribution, which provides new insights into the prognostic implications of portal hypertension in AIH and opens new avenues for refining noninvasive risk stratification of the disease. Marlene Padilla-Lopez: writing – original draft, writing – review and editing, investigation. María Carlota Londoño: conceptualization, writing – original draft, writing – review and editing, supervision. Pinelopi Arvaniti: investigation, writing – original draft, writing – review and editing. This article is linked to Burghart et al paper. To view this article, visit http://doi.org/10.1111/apt.70349. The data that support the findings of this study are available upon request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.