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Serum Hyaluronic Acid and Interleukin‐6 as Possible Markers of Carpal Tunnel Syndrome in Chronic Hemodialysis Patients
Author(s) -
Takasu Shinji,
Takatsu Shigeko,
Kunitomo Keichi,
Kokumai Yoshiaki
Publication year - 1994
Publication title -
artificial organs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 76
eISSN - 1525-1594
pISSN - 0160-564X
DOI - 10.1111/j.1525-1594.1994.tb02227.x
Subject(s) - medicine , carpal tunnel syndrome , hyaluronic acid , rheumatoid arthritis , gastroenterology , interleukin 6 , hemodialysis , tumor necrosis factor alpha , in vivo , interleukin , inflammation , endocrinology , surgery , cytokine , microbiology and biotechnology , biology , anatomy
To elucidate the precise mechanism of carpal tunnel syndrome (CTS), serum hyaluronic acid (HA), interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α) were measured in 71 chronic hemodialysis patients with or without CTS and/or shoulder pain. Patients were divided into two groups: Group 1 (n = 40) was the control group, and Group 2 (n = 31) patients had carpal tunnel syndrome, shoulder pain, or both. None of the patients had liver disease, rheumatoid arthritis, other inflammatory disease, or cancer. Serum HA concentrations in Groups 1 and 2 were 106.0 ± 77.5 and 442.6 ± 564.7 ng/dl (mean ± SD), respectively. The difference between the groups was significant (p < 0.01). The serum concentrations of IL‐6 in Group 1 were significantly lower than in Group 2 (p < 0.05); however, there was no significant difference in serum IL‐1β and TNF‐α levels. The mechanisms regulating in vivo synthesis of HA was obscure; however, in vitro studies suggest that inflammatory cytokines may stimulate an increased production of HA. In this study, CTS might be associated with increased serum concentrations of HA, and HA production might be mediated by IL‐6.