Meta-analysis on anticoagulation and prevention of thrombosis and mortality among patients with lung cancer.

BACKGROUND: Venous thromboembolism (Wickham et al., 2012 [1]) is a leading cause of morbidity and mortality among patients with cancer; however, primary thromboprophylaxis is not routinely recommended. We performed a systematic review and meta-analysis of randomized control trials (RCTs) to measure the impact of primary VTE prevention and its effect on mortality among patients with lung cancer. METHODS: With assistance from a master librarian, we searched Ovid, Scopus, DARE, CINAHL, MEDLINE, EMBASE, EBM reviews-Cochrane database of systematic reviews, EBM reviews-ACP journal, and EBM Reviews-Databases for relevant studies following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We included articles addressing the role of anticoagulation in patients with lung cancer for primary VTE prevention for outpatients. The clinical outcomes were VTE occurrence, all-cause mortality, major and clinically relevant non-major bleeding. The results are presented as odds ratio (OR) and data were analyzed using R and R META package (Version 0.8-2, Author: Guido Schwarzer). RESULTS: Eleven studies with 5107 patients were included for the final analysis. We found 50% lower VTE occurrence in the prophylaxis group with low molecular weight heparin (LMWH) (OR: 0.50; 95% Confidence Interval (CI): 0.38-0.66; I2: 0%) without an increased bleeding risk (OR: 2.03; 95% CI: 0.78-5.25; I2: 71.1%). We found a mortality benefit when we grouped all VTE prevention modalities [LMWH, Warfarin, unfractionated heparin (UFH)] (OR: 0.75; 95% CI: 0.58-0.96; I2: 18.4%), but no significant difference when LMWH (OR: 0.74; 95% CI: 0.49-1.11; I2: 56.9%) and warfarin were analyzed individually (OR: 0.75; 95% CI: 0.47-1.21; I2: 0%). We found higher odds of bleeding combining all treatment modalities (OR: 3.06; 95% CI: 1.64-5.72; I2: 64.4%) with the greatest occurrence in the warfarin group (OR: 5.42; 95% CI: 3.48-8.45; I2: 45.7%). CONCLUSION: Primary VTE prophylaxis with LMWH reduces the occurrence of VTE among ambulatory patients with lung cancer, without apparent increase in bleeding risk. There is a measurable mortality benefit of anticoagulation strategies that remains elusive when the analysis is restricted to a single agent.

Bivalirudin for the treatment of patients with confirmed or suspected heparin-induced thrombocytopenia.

BACKGROUND: Heparin-induced thrombocytopenia (HIT) is an adverse immune-mediated response to unfractionated heparin and, less commonly, low molecular weight heparin. It is associated with a high thrombotic risk and the potential for limb and life-threatening complications. Argatroban is the only approved and currently available anticoagulant for HIT treatment in the USA. OBJECTIVES: To report safety and efficacy outcomes with bivalirudin for HIT treatment. METHODS: We retrospectively examined records from our registry of patients with a suspected, confirmed or previous history of HIT and who had received bivalirudin for anticoagulation in a single tertiary-care center over a 9-year period. RESULTS: We identified 461 patients who received bivalirudin: 220 (47.7%) were surgical patients, and 241 (52.3%) were medical patients. Of this population, 107 (23.2%) were critically ill, and 109 (23.6%) were dialysis-dependent. Suspected, confirmed and previous history of HIT were reported in 262, 124 and 75 patients, respectively. Of 386 patients with suspected or confirmed HIT, 223 patients (57.8%) had thrombosis at HIT diagnosis. New thrombosis was identified in 21 patients (4.6%) while they were on treatment with therapeutic doses of bivalirudin. No patient required HIT-related amputation. Major bleeding occurred in 35 patients (7.6%). We found a significant increase in major bleeding risk in the critically ill population (13.1%; odds ratio 2.4, 95% confidence interval 1.2-4.9, P = 0.014). The 30-day all-cause mortality rate was 14.5% (67 patients), and eight of 67 (1.7%) deaths were HIT-related. CONCLUSION: Bivalirudin may be an effective and safe alternative option for the treatment of both suspected and confirmed HIT, and appears to reduce the rate of HIT-related amputation.

Efecto de la infección periodontal por porphyromonas gingivalis en el desarrollo de ateroesclerosis en ratones deficientes de apolipoproteína E / Effects of porphyromona gingivalis periodontal infection upon atherosclerosis development in apolipoprotein-E

Introducción: Nuestro grupo recientemente demostró una asociación significativa entre periodontitis, placas coronarias aguda y extensión de la enfermedad coronaria aterosclerótica en pacientes con síndrome coronario agudo. Objetivo: Desarrollar un modelo experimental animal para estudiar el posible efecto pro-aterogénico de la inducción de periodontitis por Porphyromona Gingivalis (PG) en ratones deficientes en la apolipoproteína E (APO-E KO). Métodos: En 12 ratones APO-E KO mantenidos con dieta hiperlipidémica se realizaron tocaciones con PG cepa ATCC 53977 en el surco gingival de los molares mandibulares a las 8 semanas de vida. Igual número de ratones APO-E KO fue intervenido con el mismo procedimiento, pero sólo con el vehículo de las tocaciones. Estos procedimientos se repitieron a las 48, 72 y 120 hrs de la infección inicial. Luego de 4 semanas post-inoculación con PG se realizaron estudios histomorfométricos en la aorta proximal para medir la severidad de las lesiones ateromatosas y en las mandíbulas, para evaluar la pérdida del hueso alveolar. Resultados: No se observó una diferencia significativa en el daño del hueso alveolar en las mandíbulas de los animales infectados versus el grupo control. En las aortas, la razón tamaño placa/pared vascular fue mayor en el grupo infectado con PG que en el grupo control (0.132 ± 0.2 versus 0.103 ± 0.15, respectivamente), pero esta diferencia no fue estadísticamente significativa. Conclusión: El diseño experimental del presente estudio no permitió establecer si la periodontitis inducida por PG es capaz o no de acelerar el proceso aterogénico de los ratones APO-E KO. Será necesario aplicar un protocolo de infección periodontal más agresivo en estos animales para evaluar más adecuadamente el efecto de PG sobre la ateroesclerosis.