Letter: A Prospective Study on the Prevalence of MASLD in Patients With Type 2 Diabetes and Hyperferritinaemia

We were intrigued by the study conducted by Amangurbanova et al. [1], which examined the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) in patients with type 2 diabetes mellitus (T2DM) and hyperferritinaemia. The authors proposed elevated serum ferritin as a potential biomarker for MASLD and significant fibrosis, while also elucidating the risk characteristics associated with MASLD and fibrosis in individuals with hyperferritinaemia. This pioneering work is commendable; however, certain limitations in the inclusion and exclusion criteria may affect the external validity of the findings. One notable limitation is the restricted age range of 50–80 years, which may not adequately reflect the evolving epidemiology of MASLD. Recent evidence suggests a concerning trend of earlier disease onset. A nationwide study of 5.7 million Chinese adults found that the prevalence of severe liver steatosis (grade S3) peaked between ages 35 and 39 [2]. Additionally, paediatric NAFLD rates in Asian populations increased from 4.4% (2004–2010) to 7.1% (2011–2020) [3]. Alarmingly, a long-term follow-up study reported a rise in MASLD prevalence from 0.52% to 3.4% among children aged 5–8 years [4]. Including younger patients would provide a more accurate representation of contemporary disease patterns and enhance the generalisability of results. Furthermore, we suggest refinements in the alcohol consumption exclusion criteria. While the authors defined significant alcohol intake as ≥ 14 drinks/week for men or ≥ 7 drinks/week for women over the past 2 years, the specific alcohol content per 'standard drink' was not provided. The definition of a standard drink varies internationally. For instance, in the United States, a standard drink is defined as 14 g of pure alcohol, while other countries, such as Switzerland (10–12 g) [5] and Luxembourg (12.8 g) [6], have different standards. Austria even defines a standard drink as 20 g [7]. Standardising alcohol content measurements is essential. Lastly, we would like to highlight the impact of HFE mutations (the author has noting this is one of the limitations for this study). HFE mutations are prevalent in European populations, particularly among individuals of Northern European ancestry, with frequencies reaching up to 1:250 [8]. These mutations can disrupt iron homeostasis before clinical manifestations occur. Given that both hereditary hemochromatosis and metabolic dysfunction can elevate serum ferritin levels, distinguishing between these etiologies is crucial for accurate risk stratification and patient management [9]. Moreover, HFE mutations may independently influence liver fat accumulation and fibrosis progression [10], potentially confounding the relationship between hyperferritinaemia and MASLD. Despite these limitations, the current study provides valuable insights into the interplay between hyperferritinaemia and MASLD in T2DM patients. We propose that future research should incorporate HFE mutation screening and comprehensive iron metabolism profiling to achieve more precise phenotypic characterisation. Additionally, broadening the age range of study populations and adopting standardised alcohol quantification methods would significantly enhance the external validity of the findings. Xiaojuan Liu: writing – original draft. Xueru Huang: formal analysis. Mingsi Zhang: writing – original draft. Tao Jiang: conceptualization, writing – review and editing. Guangji Zhang: conceptualization, writing – review and editing. The authors declare no conflicts of interest. This article is linked to Amangurbanova et al. papers. To view these articles, visit https://doi.org/10.1111/apt.18377 The data that support the findings of this study are available from the corresponding author upon reasonable request.