ABSTRACT
La poliangeitis microscópica (PM) hace parte de los procesos vasculíticos pulmonares, y aunque es una entidad rara, debe ser considerada en pacientes con cuadros de hemorragia alveolar masiva. En muchas ocasiones solo el análisis histológico permite establecer el diagnóstico preciso y con base en esto la toma de decisiones terapéuticas. Presentamos un caso clínico de PM manejado en el Hospital Universitario de San Ignacio (H.U.S.I.) yque fue confirmado con los estudios imagenológicos, inmunológicos e histopatológicos.
Subject(s)
Hemostatic Disorders/complications , Hemostatic Disorders/diagnosis , Hemostatic Disorders/immunology , Hemostatic Disorders/pathology , Hemostatic Disorders , ColombiaABSTRACT
The relationship between platelet and leukocyte activation, coagulation, and neointima development was investigated in noninjured murine blood vessels subjected to blood stasis. The left common carotid artery of C57BL/6J mice was ligated proximal to the bifurcation. Tissue-factor expression in luminal leukocytes progressively increased over 2 weeks. On day 3 after ligation, in addition to infiltrated granulocytes, platelet microthrombi and platelet-covered leukocytes as well as tissue-factor-positive fibrin deposits lined the endothelium. Maximal neointima formation in carotid artery cross sections of control mice equaled 28+/-3.7% (n=11) and 42+/-5.1% (n=8) of the internal elastic lamina cross-sectional area 1 and 2 weeks after ligation. In FVIII(-/-) mice, stenosis was significantly lower 1 (11+/-3.6%, n=8) and 2 (21+/-4.7%, n=7) weeks after ligation (both P:<0.01 versus background-matched controls). In u-PA(-/-) mice, luminal stenosis was significantly higher 1 (38+/-7.0%, n=7) and 2 (77+/-5.6%, n=6) weeks after ligation (P:<0.05 and P:<0.01, respectively, versus matched controls). In alpha(2)-AP(-/-) mice, stenosis was lower at 1 week (14+/-2.6%, n=7, P:<0.01) but not at 2 weeks. Responses in tissue-type plasminogen activator or plasminogen activator inhibitor-1 gene-deficient mice equaled that in controls. Reducing plasma fibrinogen levels in controls with ancrod or inducing partial thrombocytopenia with busulfan resulted in significantly less neointima, but inflammation was inhibited only in busulfan-treated mice. We conclude that stasis induces platelet activation, leading to microthrombosis and platelet-leukocyte conjugate formation, triggering inflammation and tissue-factor accumulation on the carotid artery endothelium. Delayed coagulation then results in formation of a fibrin matrix, which is used by smooth muscle cells to migrate into the lumen.
Subject(s)
Blood Platelets/metabolism , Carotid Arteries/metabolism , Fibrin/metabolism , Leukocytes/metabolism , Tunica Intima/metabolism , Afibrinogenemia/chemically induced , Afibrinogenemia/metabolism , Animals , Blood Coagulation/immunology , Blood Platelets/cytology , Blood Platelets/immunology , Carotid Arteries/pathology , Cell Division , Disease Models, Animal , Endothelium, Vascular/metabolism , Endothelium, Vascular/pathology , Hemostatic Disorders/immunology , Hemostatic Disorders/metabolism , Hemostatic Disorders/pathology , Inflammation/immunology , Inflammation/pathology , Leukocytes/cytology , Leukocytes/immunology , Ligation , Mice , Mice, Inbred C57BL , Mice, Knockout , Muscle, Smooth, Vascular/pathology , Platelet Activation , Thrombocytopenia/chemically induced , Thrombocytopenia/metabolism , Thromboplastin/biosynthesis , Thrombosis/immunology , Thrombosis/metabolism , Thrombosis/pathology , Tunica Intima/pathologyABSTRACT
BACKGROUND: The relationship between activated protein C resistance (APCR) and arterial stroke is uncertain. It has been speculated that multiple inherited or acquired prothrombotic conditions may alter the hemostatic balance towards thrombotic events. METHODS: Case series from a University medical center. RESULTS: In a series of 28 Caucasian patients under age 55 with cerebral ischemic events, nine were found to have activated protein C resistance. Five of nine patients (56%) had additional hematologic abnormalities. Four patients had elevated anticardiolipin IgG antibodies. Other abnormalities identified included Type I protein S deficiency, sticky platelet syndrome, and a positive lupus anticoagulant. CONCLUSIONS: Activated protein C resistance is relatively common in young adults with cerebral ischemic events and may be accompanied by other hematologic abnormalities. The constellation of hemostatic abnormalities may impact the type of and intensity of the antithrombotic regimen. There are also implications for family members of affected patients. Finding evidence of APCR should not preclude a complete hemostatic evaluation in the young stroke patient.
