We appreciate Mironova et al.'s prospective study on non-cirrhotic portal hypertension (NCPH), which reported comparable survival rates irrespective of portal hypertension presence. While the longitudinal data on this rare condition are valuable, we posit that the study's clinical categorization methodology exhibits limitations warranting further examination.

The authors state that ‘The terms NCPH and overlap PSVD, but not entirely.’ However, the study does not clearly delineate how these entities were distinguished. This is crucial because PSVD is a specific subset of NCPH with distinct diagnostic criteria.1 The diagnosis of PSVD necessitates a multifaceted approach, incorporating clinical, vascular, aetiological and histopathological criteria, along with specific radiological or haemodynamic features. This comprehensive diagnostic framework, as elucidated in Table 1, distinguishes PSVD from other NCPH forms, highlighting the intricacy of its identification.2-5 While features of portal hypertension are important for diagnosis of PSVD, they do not alone distinguish PSVD from other forms of NCPH. The radiological features excluding cirrhosis and implying PSVD (e.g. nodular liver surface or hypertrophy of segment) were not documented. Similarly, nodular regenerative hyperplasia and obliterative portal venopathy were mentioned, but other key histological features of PSVD, such as portal vein ectasia, increased number of portal vascular channels, paraportal shunting vessels and sinusoidal dilatation were not systematically reported.2 Although hepatic venous pressure gradient (HVPG) less than 10 mmHg is suggestive for PSVD as the aetiology of NCPH,3 authors reported HVPG measurements without specifically correlating with PSVD.