RESUMEN
BACKGROUND: There are inadequate data on the optimal strategy for transitioning factor Xa inhibitors (FXai; apixaban, rivaroxaban) to unfractionated heparin (UFH) infusions. OBJECTIVE: In patients transitioning from an FXai to an UFH infusion, this study compared the safety and efficacy of monitoring UFH infusions using an activated partial thromboplastin time (aPTT) titration scale versus utilizing an UFH-calibrated anti-Xa titration scale aided by a novel institutional guideline. METHODS: A retrospective cohort analysis was conducted on adult patients transitioning from an FXai to an UFH infusion at 2 medical centers from June 1, 2018, to November 1, 2020. One institution utilized aPTT while the other institution primarily used UFH-calibrated anti-Xa. The primary endpoint was a composite of death, major bleeding, or new thrombosis during the hospitalization with a planned noninferiority analysis. Secondary outcomes were also collected including the amount and duration of UFH administered between cohorts. RESULTS: The incidence rate of the primary composite endpoint was 6.3% in the anti-Xa group and 11% in the aPTT group (P < 0.001 for noninferiority, P = 0.138 for superiority) meeting noninferiority criteria. No statistical differences were seen in new thrombosis, major bleeding, or any bleeding. CONCLUSION AND RELEVANCE: This represents the first report of a comparison between aPTT versus anti-Xa monitoring in relation to clinical outcomes for patients transitioning from an FXai to an UFH infusion. A transition guideline primarily utilizing an UFH-calibrated anti-Xa assay appears to be a safe alternative to aPTT monitoring and can aid facilities in the management of patients during these complex transitions.
Asunto(s)
Inhibidores del Factor Xa , Heparina , Adulto , Anticoagulantes/efectos adversos , Monitoreo de Drogas , Factor Xa , Inhibidores del Factor Xa/efectos adversos , Fibrinolíticos/uso terapéutico , Hemorragia/inducido químicamente , Hemorragia/tratamiento farmacológico , Heparina/efectos adversos , Heparina de Bajo-Peso-Molecular , Humanos , Tiempo de Tromboplastina Parcial , Estudios Retrospectivos , Rivaroxabán/efectos adversosRESUMEN
AIM: The aim of this paper was to determine whether the injection of alcohol or phenol into the tibialis posterior nerve relive the symptoms and signs of ankle plantar flexor spasticity. METHODS: Twenty patients with hemiplegic stroke were included. Patients were randomly assigned to receive a single treatment of alcohol or phenol injection to the motor branches of tibial nerve. Clinical outcome parameters were measured before Motor branch block, immediately, and at 1, 3, and 6 months after blocking. These parameters included a. Ankle plantar flexor spasticity assessed by Modified Ashworth Scale, b. Clonus of the ankle; c. The passive range of motion changes measured by goniometer and d. Motor strength of the ankle plantar flexors measured by the Medical Research Council grades 0-5. RESULTS: In the alcohol group the spasticity score for the ankle plantar flexor was reduced in all 10 patients immediately after motor branch block and this was maintained over the 6 month follow up period in 9 patients. In the phenol group the spasticity score for the ankle plantar flexor was reduced in all 10 patients immediately after motor branch block and it was maintained over the 6 month follow up period in 7 patients. CONCLUSION: It was observed that both two methods are effective in reducing spasticity however the use of 50% alcohol as a neurolytic agent in the management of ankle plantar flexor spasticity appears to be long lasting method of regional spasticity treatment.
Asunto(s)
Etanol/administración & dosificación , Trastornos Neurológicos de la Marcha/terapia , Músculo Esquelético/inervación , Fenol/administración & dosificación , Accidente Cerebrovascular/complicaciones , Adulto , Anciano , Femenino , Trastornos Neurológicos de la Marcha/etiología , Humanos , Masculino , Persona de Mediana Edad , Rango del Movimiento Articular , Índice de Severidad de la Enfermedad , Nervio Tibial/efectos de los fármacosRESUMEN
Familial Mediterranean fever (FMF) is characterized by recurrent self-limiting flares of fever in the absence of pathogens, autoantibodies or antigen specific T cells and is inherited as an autosomal recessive trait probably deriving from common ancestors of Armenian, Jew, Turk and Arab origin. The underlying pathogenetic mechanisms of FMF have not been fully interpreted, but mutations in the gene MEFV encoding pyrin, a natural repressor of proinflammatory molecules, result in uncontrolled relapsing systemic inflammation, increased leukocyte migration to serosal membranes or joints and inappropriate response to inflammatory stimuli. FMF heterogeneous phenotypic expression could originate both from allelic heterogeneity or from the existence of modulating genes. Proper diagnosis of FMF is needed to begin both specific clinical management and treatment based on continuous prophylactic administration of colchicine, preventing flares or at least the onset of amyloidosis.
Asunto(s)
Fiebre Mediterránea Familiar/diagnóstico , Fiebre Mediterránea Familiar/tratamiento farmacológico , Periodicidad , Amiloidosis/prevención & control , Antiinflamatorios/uso terapéutico , Niño , Colchicina/uso terapéutico , Proteínas del Citoesqueleto/genética , Diagnóstico Diferencial , Fiebre Mediterránea Familiar/epidemiología , Fiebre Mediterránea Familiar/genética , Genotipo , Humanos , Mutación , Pirina , Calidad de VidaRESUMEN
Macrophage activation syndrome is a rare and potentially fatal complication of many childhood pathological settings, most frequently reported in systemic onset-juvenile idiopathic arthritis. The disruption of the macrophage-lymphocyte interaction leads to uncontrolled proliferation of highly activated macrophages and T lymphocytes. The syndrome comprises a heterogeneous group of disorders featuring sepsis-like characteristics typically combined with impaired function of natural killer cells and cytotoxic T-cells, haemophagocytosis and hypercytokinemia, often resulting in fatal multiple organ failure. The clinical picture shows high grade fever, hepatosplenomegaly, pancytopenia, lymphoadenopathy, central nervous system involvement and consumptive coagulopathy. Macrophage activation syndrome is associated with high mortality: even though diagnostic criteria have been proposed, definite diagnosis can be a challenge for clinicians, especially in early phases. There is no standardized therapeutic protocol for macrophage activation syndrome, but it is widely recognized that aggressive treatment strategies might strongly influence prognosis. First line-therapy is usually represented by parenteral administration of high dose-corticosteroids, whilst cyclosporine is added in the steroid-resistant cases. In this paper we provide clinical clues and summarize the most recent studies about pathophysiology and management suggestions for macrophage activation syndrome.