Editorial: Refining the Natural History of MASLD by Imaging‐Based Markers: The GOLDMINE Study. Authors' Reply

We thank Drs Perna and Armandi for their comprehensive editorial [1] addressing the rationale, design and potential implications of the GOLDMINE study. We greatly appreciate their thoughtful synthesis of the existing literature supporting magnetic resonance (MR)–based biomarkers in metabolic dysfunction‐associated steatotic liver disease (MASLD) and their articulation of the unmet need for longitudinal, outcome‐driven data.

As highlighted in the editorial, the GOLDMINE consortium was established to address several key limitations of prior studies through an international effort spanning three continents and enrolling approximately 1000 adults across the full spectrum of MASLD [2]. The study incorporates centralized review of both liver histology and MR imaging, alongside adjudicated clinical outcomes. This study design enables standardized assessment across participating sites while simultaneously providing a robust framework to evaluate the prognostic utility of imaging‐based non‐invasive tests.

A particular strength of GOLDMINE is its ability to evaluate both established and emerging MR‐based biomarkers coupled with prolonged follow‐up of up to 10 years. The acquisition of three serial MR examinations over time—paired with annual vibration‐controlled transient elastography—allows for detailed longitudinal assessment of fibrosis dynamics and the correlation with major adverse liver outcomes. These study features are intended to complement emerging therapeutic paradigms and support a more precise alignment of non‐invasive imaging markers with clinical outcomes of interest in an increasingly biopsy‐free clinical landscape [3].

In addition, we appreciate the authors' recognition of the value of paired biospecimen collection within GOLDMINE. The longitudinal banking of serum and plasma will facilitate future biomarker and multi‐omics investigations, enabling integration of imaging‐based measures with circulating blood‐based markers. We anticipate that this combined approach will also help inform future mechanistic studies.

Finally, we thank the authors for highlighting the GOLDMINE study in the broader MASLD research landscape and for emphasizing the importance of standardized, scalable tools to refine our understanding of disease natural history—and ultimately advance the management of MASLD.

The authors' declarations of personal and financial interests are unchanged from those in the original article [2].

Author Contributions

Suzanne Sharpton: conceptualization, writing – original draft, writing – review and editing. Luis Antonio Diaz: writing – review and editing. Rohit Loomba: supervision, writing – review and editing, conceptualization, funding acquisition.

Funding

The authors have nothing to report.

Linked Articles

This article is linked to Sharpton et al. papers. To view these articles, visit https://doi.org/10.1111/apt.70696 and https://doi.org/10.1111/apt.70714.

Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.