**Figure 1.**

*Pathomechanisms involved in hemorrhage in aPL patients. CAPS, catastrophic antiphospholipid syndrome; DIC, disseminated intravascular coagulation; F, factor; vWF, von Willebrand factor; \* most common pathomechanisms.*

#### *Bleeding in Patients with Antiphospholipid Antibodies DOI: http://dx.doi.org/10.5772/intechopen.97856*

might occasionally manifest as a hemorrhagic event with various clinical severity or combined thrombo-hemorrhagic syndrome. The latter is common in catastrophic APS (CAPS), a rare but often fatal variant with excessive activation of hemostasis, consumption of its components, and micro-thrombotic damage in multiple organs.

aPL can interact with different blood and vascular components and cause hemorrhage through several mechanisms (**Figure 1**) [1]. Firstly, aPL-positive patients frequently develop thrombocytopenia. Secondly, acquired immune-mediated coagulation factor deficiencies, such as hypoprothrombinemia, can appear after the interaction between aPL and coagulation factors.

Thirdly, the microvascular system damage with an extensive thrombotic or inflammatory insult via the monocyte, endothelial, and complement activation can result in secondary bleeding to the affected tissue. Thrombotic microangiopathies (TMAs) such as CAPS, as well as diffuse alveolar hemorrhage (DAH) and adrenal hemorrhage (AH), the pathognomic complications of APS, are representative examples of this pathomechanism. Since the antithrombotic therapy remains a mainstay of management of aPL, the extensive use of antithrombotics, typical for patients afflicted with their presence, can contribute to bleeding events and represents the fourth cause. Severe thrombocytopenia (platelet count lower than 50000/μL) and prothrombin deficiency are the most prominent causes of bleeding [4]. The discussion of the given pathomechanisms follows.
