María José García-Fuster

Inferior Vena Cava Malformations and Deep Venous Thrombosis

We carried out a prospective study of 116 patients under 50 years of age who had deep venous thrombosis of the lower extremities to determine whether the presence of congenital anomaly of the inferior vena cava (IVC) was a risk factor for the disease. All patients were investigated by Doppler echography. Some 37 patients who had iliac vein occlusion also underwent phlebography. In 10 patients in whom the IVC was difficult to image, magnetic resonance angiography or computerized axial tomography was carried out. In all patients, studies of antithrombin, protein C and protein S deficiency, factor V Leiden, prothrombin G20210A, antiphospholipid antibodies, and acquired risk factors were also performed. Of the 37 patients who had iliac vein occlusion, six had an IVC anomaly. Two of these patients had antiphospholipid antibodies, while another had prothrombin G20210A. Two patients with an anomaly had recurrent thrombotic occlusion. In conclusion, congenital IVC anomalies were present in 16.2% (95% confidence interval, 6.2-32%) of young patients with iliac thrombosis.

Anomalías de la vena cava y trombosis venosa profunda

Resumen Estudio prospectivo de 116 pacientes menores de 50 anos con trombosis venosa profunda (TVP) de los miembros inferiores, en el que se valora la presencia de anomalias de la vena cava inferior (VCI) como factor de riesgo de la TVP. Se practico a todos una eco-Doppler; cuando tenian afeccion iliaca se realizaba tambien flebografia, y cuando el drenaje a la VCI era deficiente, se completaba el estudio con resonancia magnetica o tomografia computarizada. En todos los pacientes tambien se realizaron las siguientes determinaciones: antitrombina, deficit de proteina C y S, factor V Leiden, protrombina G20210A y anticuerpos antifosfolipidicos. Tambien se valoraron los factores de riesgo adquiridos. De los 37 pacientes con afeccion iliaca, 6 presentaron anomalias de VCI: 4 hipoplasias y 2 duplicaciones. Todos ellos eran menores de 30 anos, 2 tenian anticuerpos antifosfolipidicos y 1 protrombina G20210A. Dos presentaron recidiva trombotica tras la suspension de la anticoagulacion. En conclusion, el 16,2% (intervalo de confianza [IC] del 95%, 6,2-32) de los pacientes con trombosis iliaca presentaba anomalia de la VCI.

Estudio prospectivo de los factores de riesgo y las características clínicas de la enfermedad tromboembólica en pacientes jóvenes

Fundamento y objetivo El objetivo del presente trabajo es el estudio de los factores de riesgo de la enfermedad tromboembolica en pacientes jovenes y la descripcion de sus caracteristicas clinicas segun la etiologia Pacientes y metodo Estudio prospectivo de 100 pacientes menores de 50 anos, no afectados de neoplasias ni enfermedades cronicas, que requirieron ingreso hospitalario por enfermedad tromboembolica. El diagnostico morfologico se realizo con eco-Doppler, flebografia, gammagrafia pulmonar o tomografia computarizada. Los factores de riesgo valorados fueron deficit de antitrombina, deficit de proteina C y S, factor V Leiden, protrombina G20210A, hiperhomocisteinemia, elevacion del inhibidor del activador del plasminogeno tipo 1, del factor VIII y presencia de anticuerpos antifosfolipidicos (AAFL). Tambien se valoraron los factores adquiridos Resultados En 87% de los pacientes, la trombosis venosa se presento en los miembros inferiores. Un 37% de los pacientes tenian factores de riesgo congenitos y un 19%, AAFL. De los factores congenitos, el mas frecuente fue el factor V Leiden, seguido de la protrombina G20210A y del deficit de proteinas C y S. La mayoria de los pacientes presentaban varios factores de riesgo, siendo el grupo con AAFL el que tenia menor numero de ellos. Los antecedentes familiares tromboticos fueron significativamente mas frecuentes en el grupo con factores de riesgo congenitos Conclusiones En el 56% de los jovenes con enfermedad tomboembolica venosa se identifica una etiologia congenita o AAFL. En estos pacientes, el numero de factores adquiridos necesarios para desencadenar la trombosis es menor que en aquellos en que no se identifica una causa

Lumbar osteomyelitis and epidural abscess complicating recurrent pilonidal cyst

PURPOSE: This study was conducted to report the rare presentation of lumbar osteomyelitis and epidural abscess as a complication of a pilonidal cyst. METHODS: A case report is presented. RESULTS: We describe the rare case of a male patient with diabetes with a recurring pilonidal cyst who developed a lumbar osteomyelitis and epidural abscess three weeks after pilonidal cyst excision with epidural anesthesia, with a fatal outcome despite emergency treatment. CONCLUSIONS: Life-threatening complications should be kept in mind in high-risk patients with repetitive surgery and neurologic involvement.

CX3CR1/CX3CL1 Axis Mediates Platelet–Leukocyte Adhesion to Arterial Endothelium in Younger Patients with a History of Idiopathic Deep Vein Thrombosis

Mechanisms linking deep vein thrombosis (DVT) and subclinical atherosclerosis and risk of cardiovascular events are poorly understood. The aim of this study was to investigate the potential impact of CX3CR1/CX3CL1 axis in DVT-associated endothelial dysfunction. The study included 22 patients (age: 37.5 ± 8.2 years) with a history of idiopathic DVT and without known cardiovascular risk factors and 23 aged-matched control subjects (age: 34 ± 7.8 years). Flow cytometry was used to evaluate peripheral markers of platelet activation, leukocyte immunophenotypes and CX3CR1/CX3CL1 expression in both groups. A flow chamber assay was employed to measure leukocyte arrest under dynamic conditions. Platelet activation and the percentage of circulating CX3CR1-expressing platelets, CX3CR1-expressing platelet-bound monocytes and CD8+ lymphocytes were higher in patients with DVT than in controls. Additionally, patients with DVT had increased plasma levels of CX3CL1, soluble P-selectin and platelet factor 4/CXCL4. Interestingly, this correlated with enhanced platelet-leukocyte interaction and leukocyte adhesion to TNFα-stimulated arterial endothelial cells, which was partly dependent on endothelial CX3CL1 upregulation and increased CX3CR1 expression on platelets, monocytes and lymphocytes. In conclusion, increased CX3CR1 expression on circulating platelets may constitute a prognostic marker for long-term adverse cardiovascular events in patients with DVT. Blockade of CX3CL1/CX3CR1 axis may represent a new therapeutic strategy for the prevention of cardiovascular comorbidities associated with DVT.