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Increased serum levels of progranulin (PGRN) in patients with haemophilic arthropathy
Author(s) -
Kotela Andrzej,
Wojdasiewicz Piotr,
Łęgosz Paweł,
Sarzyńska Sylwia,
Drela Katarzyna,
Pulik Łukasz,
Kaleta Beata,
Kniotek Monika,
Borysowski Jan,
Poniatowski Łukasz A.,
Kotela Ireneusz
Publication year - 2019
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13054
Subject(s) - medicine , pathogenesis , synovitis , arthropathy , haemophilia , osteoarthritis , gastroenterology , stage (stratigraphy) , immunology , pathology , surgery , arthritis , paleontology , alternative medicine , biology
Summary Haemophilia A and B are rarely occurring X chromosome‐linked congenital coagulation disorders dominated by spontaneous joint bleedings and chronic synovitis, leading to development of haemophilic arthropathy (HA). Progranulin (PGRN) is a growth factor with anti‐inflammatory and immunomodulatory properties. PGRN is an important molecule in the pathogenesis of osteoarthritis (OA) and rheumatological disorders. This study was aimed at investigating the potential role of PGRN in the mechanisms underlying the pathogenesis of HA. The serum levels of PGRN were measured by enzyme‐linked immunosorbent assay (ELISA) in patients with end‐stage knee joint HA (n = 20) and end‐stage primary knee joint OA (n = 20) who met the inclusion and exclusion criteria. The clinical and radiological assessment of disease severity was evaluated by the Knee Society Score (KSS) and Kellgren‐Lawrence scale. Median PGRN levels in HA patients was 349.1 ng/mL (232.8–415.6 ng/mL) and in OA patients 148.3 ng/mL (112.1‐275.3 ng/mL) with statistically significant differences between both groups ( P  < 0.015). Further analysis revealed no correlation between PGRN levels and any of the patient demographics and clinical parameters. This study demonstrates increased PGRN serum levels in patients with HA and provides new insights into the mechanisms underlying the pathogenesis of HA indicating a new potential target for therapeutic intervention.

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