Study suggests link between peripheral blood α-L-fucosidase and rheumatoid arthritis progression

A cross-sectional study, recently published in the Annals of Joint, has revealed a significant  association between peripheral blood α-L-fucosidase (AFU) levels and the progression of rheumatoid arthritis (RA). The research suggests that changes in peripheral blood AFU activity might coincide with the advancement of RA in patients, potentially leading to abnormal glucose and lipid metabolism. 

Zhou and colleagues compared the levels of AFU activity in the peripheral blood of 96 RA patients with those of 94 age-matched healthy individuals.  The study results revealed that AFU activity in the peripheral blood of RA patients was significantly lower compared to healthy controls. Moreover, a significant inverse relationship was observed between AFU activity and the duration of RA, suggesting that higher AFU levels may be associated with shorter disease duration. 

Further analysis indicated that RA patients exhibited higher activity levels of lactate dehydrogenase, an enzyme involved in cellular metabolism, compared to healthy individuals. Conversely, the activity of acetylcholinesterase, an enzyme crucial for nerve signal transmission, was found to be lower in RA patients. Notably, AFU activity displayed a negative correlation with lactate dehydrogenase activity and a positive correlation with acetylcholinesterase activity, indicating the potential interplay between these enzymes in the context of RA. 

AFU is a lysosomal acid hydrolase initially discovered in cytolysosomes, primarily responsible for hydrolyzing fucose-containing carbohydrate complexes. Its fundamental physiological role involves catalyzing the breakdown of fucosyl oligosaccharides, glycoproteins, glycopeptides, and glycosides. AFU is widely distributed across various tissues, cells, and bodily fluids in humans. Studies indicate a significant association between AFU and chronic inflammatory conditions in pediatric cohorts, suggesting its potential as a biomarker for chronic inflammation and autoimmunity. Moreover, alterations in plasma AFU levels have shown significant correlations with the onset of Sjögren’s syndrome. 

While the etiology of RA remains unclear, the present study underscores the importance of investigating peripheral blood AFU activity as a potential biomarker for disease progression. Further research is warranted to elucidate the link between AFU activity and RA pathogenesis, which may open new avenues for therapeutic intervention and personalized management strategies.  

Reference 

Zhou XG, He H, Yuan K. Changes of peripheral blood α-L-fucosidase activity in patients with rheumatoid arthritis: a cross-sectional study. Ann Jt. 2024;9:13. 

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