{'fraction_non_alphanumeric': 0.01611170784103115, 'fraction_numerical': 0.0, 'mean_word_length': 5.705035971223022, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Evidence of the Intrinsic Coagulation Pathway and Contact System Activation in Sickle Cell Patients During Steady State

A chronic hypercoagulable state and increased risk for venous thromboembolism are prominent features of sickle cell disease (SCD). This hypercoagulable state is mediated by activation of both the intrinsic and extrinsic coagulation pathways. There is growing interest in targeting components of the intrinsic coagulation pathway (factor XII and XI) to prevent thrombotic disorders, primarily because this goal may be attainable without incurring any significant bleeding risk. In addition, FXIIa can also activate plasma prekallikrein to kallikrein (PK), which initiates the contact pathway. We have previously reported that FXIIa contributes to the prothrombotic state and vascular inflammation in sickle mice. In this study we investigated if the intrinsic and contact pathways are activated in SCD patients.