Thrombosis research · 2019
Elevated plasma levels of soluble C-type lectin-like receptor 2 (CLEC2) in patients with thrombotic microangiopathy.
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Yamashita Yoshiki, Suzuki Kei, Mastumoto Takeshi, Ikejiri Makoto, Ohishi Koji, Katayama Naoyuki, Suzuki-Inoue Katsue, Wada Hideo
Аннотация
BACKGROUND: Thrombotic microangiopathy (TMA) is caused by activated platelets. The plasma C-type lectin-like receptor 2 (CLEC2) levels in 58 patients with TMA were examined and compared with those in healthy volunteers and other diseases.
MATERIALS AND METHODS: The plasma levels of soluble platelet surface glycoprotein VI (GPVI) and CLEC2 were measured in patients with TMA.
RESULTS: Plasma CLEC2 levels in patients with DIC and TMA were significantly higher (p < 0.001) than those in thrombocytopenic patients with other hematological diseases, but no significant differences in the plasma CLEC2 levels were observed among patients with thrombotic thrombocytopenic purpura, hemolytic uremic syndrome (HUS), atypical HUS and other TMA. The plasma CLEC2 levels after the remission were significantly lower than those before treatment (p < 0.001). The plasma CLEC2 levels were poorly correlated with the levels of soluble GPVI in the plasma of patients with TMA. The plasma CLEC2 levels were not significantly differ between survivor and non-survivor in TMA patients, but were significantly higher in non-survivor in overall population (p < 0.001).
CONCLUSION: The measurement of the plasma CLEC2 level is considered to be important for the diagnosis and evaluation of TMA.
MATERIALS AND METHODS: The plasma levels of soluble platelet surface glycoprotein VI (GPVI) and CLEC2 were measured in patients with TMA.
RESULTS: Plasma CLEC2 levels in patients with DIC and TMA were significantly higher (p < 0.001) than those in thrombocytopenic patients with other hematological diseases, but no significant differences in the plasma CLEC2 levels were observed among patients with thrombotic thrombocytopenic purpura, hemolytic uremic syndrome (HUS), atypical HUS and other TMA. The plasma CLEC2 levels after the remission were significantly lower than those before treatment (p < 0.001). The plasma CLEC2 levels were poorly correlated with the levels of soluble GPVI in the plasma of patients with TMA. The plasma CLEC2 levels were not significantly differ between survivor and non-survivor in TMA patients, but were significantly higher in non-survivor in overall population (p < 0.001).
CONCLUSION: The measurement of the plasma CLEC2 level is considered to be important for the diagnosis and evaluation of TMA.