Hemostatic balance between pro‐ and anticoagulant is maintained during glucocorticoid treatment

• Published in: Pediatric blood & cancer Vol. 71; no. 3; pp. e30812 - n/a
• Main Authors: Yamashita, Atsuki, Nagae, Chiai, Umezawa, Yotaro, Mori, Mika, Ashikaga, Tomoko, Akita, Mieko, Suzuki, Noriko, Yamazaki, Satoshi, Takayama, Shigenobu, Taki, Masashi
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.03.2024
• Subjects: Anticoagulants; Anticoagulants - therapeutic use; Antithrombin; Blood Coagulation Factors; Coagulation factors; glucocorticoid; Glucocorticoids; Glucocorticoids - adverse effects; hemostatic balance; Hemostatics; Humans; Idiopathic thrombocytopenic purpura; Pediatrics; Protein C; Protein C - metabolism; Purpura, Thrombocytopenic, Idiopathic; Thrombin; Thrombin - metabolism; thrombin generation; Thrombocytopenia; Thromboplastin; Thrombosis; Von Willebrand factor; anticoagulants; glucocorticoid; thrombin generation; hemostatic balance; coagulation factors
• ISSN: 1545-5009; 1545-5017
• DOI: 10.1002/pbc.30812

Background Glucocorticoids are associated with an increased risk of venous thrombosis. Glucocorticoid treatment increases coagulation factor and anticoagulant levels; however, its effect on hemostatic function remains unclear. This study aimed to investigate the changes in comprehensive coagulation profiles after glucocorticoid treatment in noninflammatory diseases to elucidate the direct contribution of glucocorticoids to hemostatic function. Procedure Patients diagnosed with primary immune thrombocytopenia requiring glucocorticoid treatment were prospectively enrolled in this study. Changes in coagulation factors and anticoagulants during glucocorticoid treatment and changes in thrombin generation potential were determined in the absence and presence of soluble thrombomodulin (sTM). Results Seven treatment cases (four for steroid pulse therapy and three for oral glucocorticoid therapy) in six patients with immune thrombocytopenia were examined. After glucocorticoid treatment, activated partial thromboplastin time significantly shortened, and activities of factor VIII, IX, XI, and XII significantly increased, except for von Willebrand factor antigen. Moreover, antithrombin and protein C (PC) activities significantly increased after glucocorticoid treatment. Two major parameters of thrombin generation potential, endogenous thrombin potential (ETP) and peak thrombin (Peak), significantly increased in the absence of sTM after glucocorticoid treatment. However, no significant increases in either parameter were observed in the presence of sTM. ETP‐TM and Peak‐TM ratios, which represent resistance to the anticoagulant effect of the PC pathway, significantly decreased after glucocorticoid treatment, suggesting that anticoagulant function via the PC pathway is elevated after glucocorticoid treatment. Conclusions As glucocorticoids increase intrinsic coagulation factor and anticoagulant levels, hemostatic balance between pro‐ and anticoagulant functions is maintained.