Spleen volume is independently associated with non-alcoholic fatty liver disease, liver volume and liver fibrosis.

Non-alcoholic fatty liver disease (NAFLD) can lead to irreversible liver damage manifesting in systemic effects (e.g., elevated portal vein pressure and splenomegaly) with increased risk of deadly outcomes. However, the association of spleen volume with NAFLD and related type 2-diabetes (T2D) is not fully understood. The UK Biobank contains comprehensive health-data of 500,000 participants, including clinical data and MR images of >40,000 individuals. The present study estimated the spleen volume of 37,066 participants through automated deep learning-based image segmentation of neck-to-knee MR images. The aim was to investigate the associations of spleen volume with NAFLD, T2D and liver fibrosis, while adjusting for natural confounders. The recent redefinition and new designation of NAFLD to metabolic dysfunction-associated steatotic liver disease (MASLD), promoted by major organisations of studies on liver disease, was not employed as introduced after the conduct of this study. The results showed that spleen volume decreased with age, correlated positively with body size and was smaller in females compared to males. Larger spleens were observed in subjects with NAFLD and T2D compared to controls. Spleen volume was also positively and independently associated with liver fat fraction, liver volume and the fibrosis-4 score, with notable volumetric increases already at low liver fat fractions and volumes, but not independently associated with T2D. These results suggest a link between spleen volume and NAFLD already at an early stage of the disease, potentially due to initial rise in portal vein pressure.
Competing Interests: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Håkan Ahlström reports financial support was provided by the Swedish Heart Lung Foundation. Håkan Ahlström reports financial support was provided by the Swedish Research Council. Joel Kullberg reports financial support was provided by the Swedish Research Council. Sambit Tarai, Taro Langner, Elin Lundström, Joel Kullberg, Håkan Ahlström and Lars Johansson report a relationship with Antaros Medical AB that includes: consulting or advisory, employment, and equity or stocks. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(© 2024 Published by Elsevier Ltd.)