thromboplastin and Eosinophilia

It is known that peripheral blood eosinophilia (PBE) is a normal hematopoietic response to several parasitic diseases, but it is less known that PBE promotes a hypercoagulable state that may favor thrombosis. Scope of this article is to explore which parasitic infestations are most likely to be complicated by thrombosis and to highlight the pathogenetic contribution of PBE to vascular occlusions in this setting. A review of the world literature revealed 18 cases in which PBE was associated with vascular occlusion though no specific surveys were dedicated to this topic. The eosinophil exerts its thrombogenic potential by inhibition of the natural anticoagulant pathways and release of tissue factor with enhanced coagulation activation leading to vascular occlusion. It is hoped that this review contributes to the awareness of the link between PBE and thrombosis in parasitic disorders to foster research in this area.

Topics: Adult; Aged; Blood Coagulation; Eosinophilia; Eosinophils; Female; Humans; Male; Middle Aged; Parasitic Diseases; Thrombophilia; Thromboplastin; Thrombosis

An increased risk of thrombosis has been described in patients with hypereosinophilic syndromes, including Churg-Strauss syndrome (CSS). We report the case of a 43-year-old man with CSS who presented with asthma, pansinusitis, blood eosinophilia (9650/microL), peripheral neuropathy, cutaneous eosinophilic vasculitis, and a positive result for antineutrophil cytoplasmic antibodies. An analysis of plasma during active disease revealed elevated levels of prothrombin fragment 1+2 (marker of thrombin generation) (832 pM; normal range, 68-229 pM) and D-dimer (marker of fibrin degradation) (2300 ng/mL; normal range, 130-250 ng/mL), which indicate an increased risk of thrombosis. Both parameters returned to normal values during remission after immunosuppressive treatment. Skin histology showed leukocytoclastic vasculitis with numerous eosinophils in the dermal infiltrate. Immunohistochemistry revealed expression of tissue factor by skin-infiltrating eosinophils, as confirmed by colocalization with eosinophil cationic protein, a classic marker of eosinophil granulocytes. In conclusion, we present a patient with active CSS and a prothrombotic state that reverted during remission achieved by immunosuppressive therapy.

Topics: Adult; Churg-Strauss Syndrome; Eosinophilia; Fibrin Fibrinogen Degradation Products; Humans; Immunosuppressive Agents; Male; Peptide Fragments; Prothrombin; Skin Diseases; Thromboplastin; Thrombosis

Bullous pemphigoid (BP) is a blistering skin disease caused by autoantibodies to hemidesmosomal proteins, with eosinophils participating in blister formation. Eosinophils are a source of tissue factor (TF), an initiator of blood coagulation.. To evaluate the local and systemic activation of coagulation in BP.. We studied 20 patients with active BP (eight re-evaluated during remission) and 40 controls. The coagulation markers prothrombin fragment F1+2 and d-dimer were measured in the plasma of all subjects and in both plasma and blister fluid of patients with BP. TF was evaluated immunohistochemically in skin specimens from the 20 patients and in 20 normal samples.. F1+2 and d-dimer levels were higher in plasma of patients with BP (649 +/- 96 pmol L(-1) and 18.52 +/- 3.44 nmol L(-1), respectively) than in plasma of controls (157 +/- 7 pmol L(-1) and 1.42 +/- 0.06 nmol L(-1); P = 0.0001), and were very high in blister fluid (40 449 +/- 3491 pmol L(-1) and 1532.32 +/- 262.81 nmol L(-1); P = 0.0001). Plasma and blister fluid F1+2 and d-dimer levels paralleled blood and tissue eosinophilia and disease severity. In the eight patients re-evaluated during remission, there was a marked reduction in F1+2 (from 1127 +/- 144 to 287 +/- 52 pmol L(-1); P = 0.005) and d-dimer (from 24.03 +/- 4.08 to 4.69 +/- 1.51 nmol L(-1); P = 0.029). Immunohistochemistry revealed strong TF reactivity in BP skin (P = 0.0001), and colocalization studies confirmed eosinophils as a source of TF.. The coagulation cascade is activated in BP and correlates with the severity of the disease and with eosinophilia, indicating that eosinophils play a role in coagulation activation via TF. The hypercoagulability may contribute to inflammation, tissue damage, blister formation and possibly thrombotic risk in BP.

Topics: Aged; Aged, 80 and over; Autoantibodies; Blister; Blood Coagulation; Eosinophilia; Eosinophils; Female; Fibrin Fibrinogen Degradation Products; Humans; Immunohistochemistry; Immunologic Factors; Male; Middle Aged; Pemphigoid, Bullous; Peptide Fragments; Prothrombin; Skin; Thromboplastin