AIM:To study the relationship between anti-b2-glycoprotein Ⅰ (ab2GPⅠ) antibodies and platelet activation state in patients with ulcerative colitis (UC) and its significance. METHODS:Peripheral blood samples were collected from 56 UC patients (34 males and 22 females, aged 43.5 years, range 21-66 years), including 36 at active stage and 20 at remission stage, and 25 sex-and age-matched controls. The level of ab2GPⅠ was measured by ELISA. The platelet activation markers, platelet activation complex-Ⅰ (PAC-Ⅰ) and P-selectin (CD62P) were detected by flow cytometry. RESULTS:The A value for IgG ab2GPⅠ in the active UC group was 0.61 ± 0.13, significantly higher than that in the remittent UC and control groups (0.50 ± 0.13 and 0.22 ± 0.14, P < 0.01). There was a significant difference between the two groups (P < 0.01). The A value for IgM ab2GPⅠ in the active and remittent UC groups was 0.43 ± 0.13 and 0.38 ± 0.12, significantly higher than that in the control group (0.20 ± 0.12, P < 0.01). However, there was no significant difference between the two groups (P > 0.05). The PAC-Ⅰ positive rate for the active and remittent UC groups was 30.6% ± 7.6% and 19.6% ± 7.8% respectively, significantly higher than that for the control group (6.3% ± 1.7%, P < 0.01). There was a significant difference between the two groups (P < 0.01). The CD62P positive rate for the active and remittent UC groups was 45.0% ± 8.8% and 31.9% ± 7.8% respectively, significantly higher than that for the control group (9.2% ± 2.7%, P < 0.01). There was a significant difference between the two groups (P < 0.01). In the active UC group, the more severe the state of illness was, the higher the A value for IgG ab2GPⅠ was, and the positive rate for PAC-I and CD62P was positively correlated with the state of illness (Fab2GPⅠ = 3.679, P < 0.05;FPAC-I (%) = 5.346, P < 0.01;and FCD62P (%) = 5. 418, P < 0.01). Meanwhile, in the same state of illness, the A value for IgG ab2GPⅠ was positively correlated to the positive rates for PAC-I and CD62P. CONCLUSION:ab2GPⅠ level, platelet activation state and their relationship of them are closely correlated with the pathogenesis and development of UC. AIM: To study the relationship between anti-b2-glycoprotein I (ab2GPI) antibodies and platelet activation state in patients with ulcerative colitis (UC) and its significance. METHODS: Peripheral blood samples were collected from 56 UC patients (34 males and 22 females , aged 43.5 years, range 21-66 years), including 36 at active stage and 20 at remission stage, and 25 sex-and age-matched controls. The level of ab2 GPI was measured by ELISA. The platelet activation markers, platelet activation complex RESULTS: The A value for IgG ab2GPI in the active UC group was 0.61 ± 0.13, significantly higher than that in the retentate UC and control groups (CD62P) 0.50 ± 0.13 and 0.22 ± 0.14, P <0.01). The A value for IgM ab2GPI in the active and remittent UC groups was 0.43 ± 0.13 and 0.38 ± 0.12, respectively significantly higher than that in the control group (0.20 0.12, P <0.01). The PAC-I positive rate for the active and remittent UC groups was 30.6% ± 7.6% and 19.6% ± 7.8% respectively , significantly higher than that for the control group (6.3% ± 1.7%, P <0.01). There was a significant difference between the two groups (P <0.01). The CD62P positive rate for the active and remittent UC groups was 45.0% ± 8.8% and 31.9% ± 7.8% respectively, significantly higher than that for the control group (9.2% ± 2.7%, P <0.01). There was a significant difference between the two groups group, the more severe the state of illness was, the higher the A value for IgG ab2GPI was, and the positive rate for PAC-I and CD62P were positively correlated with the state of illness (Fab2GPI = 3.679, P <0.05; FPAC- (%) = 5.346, P <0.01; and FCD62P (%) = 5. 418, P <0.01). Meanwhile, in the same state of illness, the A value for IgG ab2GPI was po sitively correlated to the positive rates for PAC-I and CD62P. CONCLUSION: ab2GPI level, platelet activation state and their relationship of them are closely correlated with the pathogenesis and development of UC.