¿Mejora el control de los pacientes anticoagulados una visita presencial? / Does an in-person visit improve the control of patients with anticoagulation treatment?

Objetivo: Evaluación de un programa de control de tratamiento anticoagulante oral (TAO) en un centro de Atención Primaria de pacientes anticoagulados seguidos presencialmente en el CAP de Figueres y comparación del mismo con los resultados del control de una muestra de pacientes de similares características dosificados a distancia por el servicio de Hematología de referencia. Pacientes y método: Estudio longitudinal retrospectivo en un centro de salud urbano de 68 pacientes anticoagulados seguidos en AP (34) y Hospitalaria (34). Mediciones principales: indicaciones de anticoagulación, características de los pacientes, tiempo de seguimiento, valor del INR. Resultados: Edad media del grupo de AP, 72,8 años (77,3 en el de hematología); el 50% del grupo de AP eran mujeres (38% hematología). Indicaciones: fibrilación auricular, 76% (79% en hematología); prótesis valvulares, 14% (11% en hematología), tromboembolia venosa, 6% (3% en hematología) y otras causas, 3% (6% en hematología). Media ± DE de seguimiento en AP, 253±49 días (252±39 días en hematología); número de INR analizados, media AP=9,8 (Hematología=10,4). El 71% de los INR del grupo tratado en AP era considerado aceptable, (55% en hematología). Conclusiones: Los resultados de este estudio reflejan un control correcto de la TAO en el grupo con seguimiento presencial. La proporción relativamente baja de INR fuera de rango en la serie de AP, en comparación con la de control Hospitalario y con las consideradas por los comités de calidad, apoya la hipótesis de que es más adecuado un control presencial que uno a distancia (AU)

Objective: Evaluate the oral anticoagulation (OAC) control program in a primary care center of patients with anticoagulation who were visited in-person in the Primary Care Center of Figueres and compare them with a sample of patients having similar characteristics with doses controlled at a distance by the reference hematology department. Patients and method: A retrospective, longitudinal study carried out in an urban health care center of 68 patients with anticoagulation followed up in primary care (34) and in the hospital (34). Principal measurements were: indications of anticoagulation, characteristics of the patients, follow-up time, INR value. Conclusions: The results of this study show an appropriate control of OAC in the primary care follow-up group with in-person control. The relatively low rate of INR out of range in this group compared with the hospital control group and with the quality standard recommendations of the quality committees support the hypothesis that in-person control is more effective than at distance control (AU)

Circulating levels of colony-stimulating factor 1 as a prognostic indicator in 82 patients with epithelial ovarian cancer.

Serum samples from 82 patients with epithelial ovarian cancer, previously assayed for CA125, were assayed for circulating colony-stimulating factor 1 (CSF-1). An elevated CSF-1 concentration (> 450 U ml-1 or > 5.42 ng ml-1) was significantly associated with a worse survival (P = 0.02). The predictive value of raised CSF-1 levels was retained whether the first available sample for all patients (n = 82) or the first sample at the start of chemotherapy (n = 41) was considered. Mean CSF-1 levels (n = 14) dropped significantly during six courses of platinum-based chemotherapy (P = 0.02). Although an elevated CA125 concentration appeared to be a prognostic indicator in the total population (n = 82), it was not related to prognosis in the group of patients from whom samples had been drawn at the start of chemotherapy. In a Cox proportional hazards model, CSF-1, but not CA125, was significantly associated with outcome following adjustment for stage, grade and degree of surgical clearance.

Effect of prostaglandin E1 in brown Norway rats with mercury-induced autoimmune disease.

The effect of prostaglandin E1 on mercury-induced autoimmune disease in brown Norway rats has been investigated. Daily doses of 6 to 24 micrograms prolonged survival and significantly decreased proteinuria, deposition of immune reactants in the glomeruli, circulating anti-glomerular membrane antibody production, total serum IgE, and circulating immune complex level. A dose of 3 micrograms was also effective but to a lesser degree. These results show the efficiency of prostaglandin E1 in yet another autoimmune disease, show that the beneficial effect of prostaglandin E1 in this model is related to its immunosuppressive effects, and suggest that modification of prostaglandin-mediated suppression induced by HgCl2 might play a role in the pathogenesis of this autoimmune disease.

Effect of cyclosporine A on mercury-induced autoimmune glomerulonephritis in the Brown Norway rat.

To test the effect of cyclosporine A (CsA) in mercuric chloride (HgCl2)-induced nephritis in the Brown-Norway (BN) rat, we treated groups of intoxicated rats with varying doses of CsA for a period of 2 months. All manifestations of HgCl2-induced disease were prevented in rats treated concurrently with CsA at either 7 or 10 mg/kg/day. Partial suppression was evident at lower daily doses, but not with bi-weekly CsA administration. The initial phase of HgCl2-induced nephritis could be completely suppressed with a short, 15 day course of CsA. The later phase of the disease could be tempered by CsA administration starting on day 10 after the first HgCl2 injection. The optimal regimen of 7 mg/kg/day for 60 days was not associated with any evidence of CsA toxicity. CsA appears to interfere with the polyclonal activation of B cells observed in HgCl2-induced autoimmune disease, accounting for its striking preventive and curative effect in this model.

Effects of decomplementation on mercuric chloride-induced glomerulonephritis in Brown-Norway rats.

The course of mercuric chloride-induced immune glomerulonephritis is characterized by complement activation, intensive proteinuria, linear and then granular IgG and C3 deposits in the glomeruli. To assess the role of complement activation in the occurrence of the disease, decomplementation was achieved by intravenous injections of cobra venom factor in rats injected with mercuric chloride. In these animals, proteinuria still appeared while rats were decomplemented by cobra venom factor through the alternative pathway. These rats exhibited linear IgG deposits without detectable C3 deposits. In the rats injected with cobra venom factor alone, no proteinuria, no classical pathway complement activation and no renal IgG or C3 deposits were observed. Therefore, in Brown-Norway rats intoxicated with mercuric chloride, proteinuria appears to be at least in part complement independent.

Immune-type glomerulonephritis induced in the Brown-Norway rat with mercury-containing pharmaceutical products.

It has been shown that Brown-Norway rats develop an immune-type glomerulonephritis after treatment with various mercury-containing drugs. Anti-GBM antibodies were involved, at least in some animals. This glomerulonephritis induced a proteinuria. Strong evidence is given, suggesting that most mercury compounds, some of which, such as mercurial antiseptics, are widely used, could induce an immune-type glomerulonephritis. The question therefore arises, whether these drugs can be used any longer.