Background: The occurrence of various arthropathies including carpal-tunnel syndrome (CTS) in dialysis-associated amyloidosis, a condition caused by the deposition of beta 2 microglobulin (beta 2MG), has been emphasized for several years. We attempted to analyse the pathogenesis of CTS in haemodialysis-associated amyloidosis (HA).
Methods: The expression of cell adhesion molecules and inflammatory cytokines in tenosynovial tissues was determined by using both reverse-transcriptase polymerase chain reaction (RT-PCR) and immunostaining.
Results: There was a marked expression of ICAM-1, VCAM-1, E-selectin mRNAs together with increased mRNA expression of inflammatory cytokines (IL-1 beta, TNF alpha, IL-6 and MCP-1) in proliferating synovial tissues. ICAM-1 was expressed not only on vascular endothelial cells, but also on synovial cells. In contrast, both VCAM-1 and E-selectin were exclusively expressed on endothelial cells. Mononuclear cells bearing CD13, CD14, CD33 and HLA-DR with macrophage-like morphology were accumulated in the perivascular area and expressed VLA-4, LFA-1 and Mac-1. Moreover, synovial lining cells, vascular endothelial cells and infiltrated mononuclear cells expressed chemokines such as MCP-1 and MIP-1 alpha.
Conclusions: These data suggest that upregulated expression of inflammatory cytokines and adhesion molecules promotes activation and infiltration of macrophages causing CTS in haemodialysis-associated amyloidosis patients.