We are interested in a recent article, which is the first to address the potential impact of metabolic dysfunction-associated steatotic liver disease (MASLD) on the treatment response and prognosis of primary biliary cholangitis (PBC) patients and demonstrates that concomitant MASLD worsens the prognosis of PBC patients [1]. We appreciate the innovative work of the authors as the significant prevalence of MASLD within the general population [2]. Drawing upon these results and the literature, we contend that this represents a significant opportunity to elucidate the potential impact of visceral obesity in the management of PBC.

The regional distribution of adipose tissue has been demonstrated to serve as a more accurate predictor of health risks than overall excessive adiposity. The abnormal accumulation of visceral fat can result in visceral fatty obesity, trigger an inflammatory response and dysfunction within visceral adipose tissue, and is closely associated with the pathogenesis of MASLD [3]. A total of 106 PBC patients from West China Hospital, Sichuan University, were included in this retrospective study. All patients received treatment with ursodeoxycholic acid (UDCA) at a dosage of 13–15 mg/kg per day after the diagnosis of PBC. The response to UDCA was evaluated after 1 year of UDCA therapy according to the Paris II criteria. Image analysis of pretreatment abdominal CT scans was performed by a clinically trained radiologist (LB). Visceral obesity was defined as a visceral fat area (VFA) > 100 cm² for both sexes. The chi-square test was used to compare the proportions of patients with or without response across groups. In total, 43.4% (46/106) of the patients were classified as poor response to UDCA. Representative patient images are shown in Figure 1A,B. According to the data shown in Figure 1C, the proportion of visceral obesity among patients who were poor responders was greater (p < 0.05). Therefore, we suppose that the coexistence of visceral obesity may be related to poor response in our PBC cohort. Our results were also similar to the findings in cirrhosis, which demonstrated a negative impact of coexisting visceral adiposity on long-term mortality among patients with cirrhosis [4]. Recent studies have indicated that the impact of liver-based interorgan communication on liver diseases, for example, VEGF-B signalling in white adipose tissue, enhances the progression of nonalcoholic fatty liver disease [5], which means that improving visceral obesity might be a potential therapeutic target for PBC.

In conclusion, in this primary study, for the first time, we provide clinical evidence that the presence of visceral obesity may be related to a poor response in PBC patients. However, larger cohorts are needed for validation in future studies.

我们对最近的一篇文章感兴趣，该文章首次讨论了代谢功能障碍相关脂肪性肝病 （MASLD） 对原发性胆汁性胆管炎 （PBC） 患者治疗反应和预后的潜在影响，并证明伴随的 MASLD 会使 PBC 患者的预后恶化 [1]。我们感谢作者的创新工作，因为 MASLD 在普通人群中的患病率很高 [2]。借鉴这些结果和文献，我们认为这代表了阐明内脏肥胖对 PBC 管理的潜在影响的重要机会。

脂肪组织的区域分布已被证明比总体过度肥胖更准确地预测健康风险。内脏脂肪的异常积累可导致内脏脂肪肥胖，引发内脏脂肪组织内的炎症反应和功能障碍，与 MASLD 的发病机制密切相关 [3]。本回顾性研究共纳入来自四川大学华西医院的 106 例 PBC 患者。所有患者在诊断为 PBC 后接受了熊去氧胆酸 （UDCA） 治疗，剂量为每天 13-15 mg/kg。根据 Paris II 标准，在 UDCA 治疗 1 年后评估对 UDCA 的反应。治疗前腹部 CT 扫描的图像分析由受过临床培训的放射科医生 （LB） 进行。内脏肥胖定义为两性的内脏脂肪面积 （VFA） > 100 cm²。采用卡方检验比较各组有或无反应的患者比例。总共 43.4% （46/106） 的患者被归类为对 UDCA 反应不佳。代表性患者图像如图 1A、B 所示。根据图 1C 所示的数据，反应不佳的患者内脏肥胖的比例更大 （p < 0.05）。因此，我们假设内脏肥胖的共存可能与我们的 PBC 队列反应不佳有关。我们的结果也与肝硬化的发现相似，后者表明共存的内脏肥胖对肝硬化患者长期死亡率有负面影响 [4]。 最近的研究表明，基于肝脏的器官间通讯对肝脏疾病的影响，例如，白色脂肪组织中的 VEGF-B 信号传导，会加速非酒精性脂肪肝的进展 [5]，这意味着改善内脏肥胖可能是 PBC 的潜在治疗靶点。

总之，在这项主要研究中，我们首次提供了临床证据，表明内脏肥胖的存在可能与 PBC 患者的不良反应有关。然而，在未来的研究中需要更大的队列进行验证。