Lipid extract from hard-shelled mussel (Mytilus coruscus) improves clinical conditions of patients with rheumatoid arthritis: a randomized controlled trial.

Yuanqing Fu,Xiaojie Hu,Gengyan Xing,Lifeng Yang,Guipu Li,Xinhua Zhang,Duo Li

doi:10.3390/nu7010625

Abstract

Studies have suggested a lipid extract from hard-shelled mussel (Mytilus coruscus) (HMLE) possessed strong anti-inflammatory activity in arthritis model of rats. This study investigated whether HMLE could improve clinical conditions of rheumatoid arthritis patients. Fifty rheumatoid arthritis patients (28–75 years) were randomly assigned to receive HMLE capsules or receive placebo capsules for 6 months. Forty-two subjects and 50 subjects were included in per-protocol and intention-to-treat analysis, respectively. Significant differences in changes on disease activity score (DAS28) and clinical disease activity index (CDAI) after 6-month intervention (p < 0.01) were observed in both analyses with more evident efficacy shown in per-protocol population (∆DAS28 = 0.47; ∆CDAI = 4.17), which favored the benefits of the HMLE group. TNF-α (tumor necrosis factor α), interleukin (IL)-1β and PGE2 (prostaglandin E2) but not IL-6, were significantly decreased in both groups, and the decrements were much larger in the HMLE group for TNF-α and PGE2 after 6 months from baseline (p < 0.05). IL-10 was significantly increased in both groups and the change was much more evident in the HMLE group (p < 0.05). In conclusion, HMLE exhibited benefits for the clinical conditions of rheumatoid patients in relation to improvement in the balance between pro- and anti-inflammatory factors, which indicated its potential to serve as adjunctive treatment for rheumatoid arthritis. (ClinicalTrials.gov NCT02173587).

Highlights

Rheumatoid arthritis (RA) is a chronic, progressive, systemic autoimmune disorder, characterized by abnormal immune responses, inflammation of joints with severe pain and swelling, and irreversible destruction of cartilage and bone in the joints [1,2,3,4,5]
It is well known that inflammatory factors regulated a broad range of inflammatory processes that are implicated in the pathogenesis of rheumatoid arthritis
Increased levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were found in the joint tissues of patients suffering from RA [8], which indicated the positive association between these inflammatory mediators and RA pathogenesis

Summary

Introduction

Rheumatoid arthritis (RA) is a chronic, progressive, systemic autoimmune disorder, characterized by abnormal immune responses, inflammation of joints with severe pain and swelling, and irreversible destruction of cartilage and bone in the joints [1,2,3,4,5]. It is well known that inflammatory factors regulated a broad range of inflammatory processes that are implicated in the pathogenesis of rheumatoid arthritis. Increased levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were found in the joint tissues of patients suffering from RA [8], which indicated the positive association between these inflammatory mediators and RA pathogenesis. TNF-α and IL-1β were reported to be participating in the macrophage-dependent inflammation, and the activation of macrophages led to cyclooxygenase 2 (COX-2) stimulation with consequent prostaglandin E2 (PGE2)

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Conclusion