Modern rheumatology · 2025
Elevated serum heparin-binding protein levels in patients with gout flare.
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Ding Nana, Zhang Dexian, Ye Weiwei
Аннотация
OBJECTIVES: Proinflammatory substances from neutrophils play an essential role in gout flare. This study aimed to compare the levels of heparin-binding protein (HBP), released by neutrophils, among patients with gout, patients with osteoarthritis (OA), patients with asymptomatic hyperuricemia (HUA), and healthy controls (HCs).
METHODS: We enrolled 102 patients diagnosed with gout, 26 patients with OA, 25 patients with asymptomatic HUA, and 23 HCs. Serum HBP was measured by enzyme-linked immunosorbent assay.
RESULTS: We found that the level of HBP was significantly elevated in patients experiencing gout flare compared with those in patients with relieving gout after taking nonsteroidal anti-inflammatory drugs (NSAIDs), patients with intercritical gout, and other control groups. Serum HBP was significantly different between patients who experienced gout relieving after NSAIDs and patients with intercritical gout. Receiver operating characteristic curve showed HBP could distinguish gout flare from relieving gout after NSAIDs. The area under the curve (AUC) was 0.8130, sensitivity was 0.9412, and specificity was 0.6286 at the cutoff HBP value of 42.09 ng/ml. The HBP cutoff for differentiating relieving gout after NSAIDs from intercritical gout was 19.75 ng/ml, which had an AUC of 0.8971, a sensitivity of 0.8485, and a specificity of 0.9118. Moreover, serum HBP levels were positive correlated with erythrocyte sedimentation rate, C-reactive protein, white blood cell, absolute neutrophil count, and neutrophil ratio.
CONCLUSIONS: Taken together, our results showed elevated HBP levels in patients with gout flare.
METHODS: We enrolled 102 patients diagnosed with gout, 26 patients with OA, 25 patients with asymptomatic HUA, and 23 HCs. Serum HBP was measured by enzyme-linked immunosorbent assay.
RESULTS: We found that the level of HBP was significantly elevated in patients experiencing gout flare compared with those in patients with relieving gout after taking nonsteroidal anti-inflammatory drugs (NSAIDs), patients with intercritical gout, and other control groups. Serum HBP was significantly different between patients who experienced gout relieving after NSAIDs and patients with intercritical gout. Receiver operating characteristic curve showed HBP could distinguish gout flare from relieving gout after NSAIDs. The area under the curve (AUC) was 0.8130, sensitivity was 0.9412, and specificity was 0.6286 at the cutoff HBP value of 42.09 ng/ml. The HBP cutoff for differentiating relieving gout after NSAIDs from intercritical gout was 19.75 ng/ml, which had an AUC of 0.8971, a sensitivity of 0.8485, and a specificity of 0.9118. Moreover, serum HBP levels were positive correlated with erythrocyte sedimentation rate, C-reactive protein, white blood cell, absolute neutrophil count, and neutrophil ratio.
CONCLUSIONS: Taken together, our results showed elevated HBP levels in patients with gout flare.