Usefulness of the basophil activation test in the diagnosis of hypersensitivity to amiodarone

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Guía de tratamiento del deterioro de la marcha con fampridina de liberación prolongada (Fampyra (R)) en pacientes con esclerosis múltiple / A guide to treating gait impairment with prolonged-release fampridine (Fampyra(R)) in patients with multiple sclerosis

INTRODUCCIÓN: La alteración de la marcha es frecuente en la esclerosis múltiple (EM) y tiene un gran impacto negativo en los pacientes pues conlleva a la pérdida progresiva de autonomía personal y social, y de productividad laboral. Esta guía pretende establecer recomendaciones para la evaluación del deterioro de la marcha y el uso de fampridina de liberación prolongada (fampridina-LP) como tratamiento de pacientes con EM y deterioro de la marcha en España. DESARROLLO: Fampridina-LP a dosis de 10 mg cada 12 h es actualmente el único fármaco autorizado para mejorar el trastorno de la marcha en adultos con EM. En la práctica clínica, el fármaco ha demostrado además que mejora de forma significativa la calidad de vida de los pacientes que responden al tratamiento. La respuesta se puede evaluar mediante la prueba cronometrada de la marcha de 25 pies (T25FW) o el cuestionario MSWS-12 que deben realizarse antes y después del inicio del tratamiento. El tiempo mínimo recomendado para evaluar la respuesta inicial es de 2 semanas. Para considerar a un paciente como respondedor y continuar el tratamiento debe presentar, según indica la ficha técnica, una disminución en el tiempo T25FW o mejoría en el MSWS-12. Se recomienda realizar las revaluaciones al menos cada 6 meses. En los casos en que se considere la valoración de la calidad de vida, se recomienda la utilización del cuestionario de salud Short Form-36 (SF-36) o la escala MS Impact Scale-29 (MSIS-29). Es un fármaco en general bien tolerado y con buen perfil de seguridad. Se recomienda su administración en ayunas y control periódico de la función renal. CONCLUSIONES: Estas recomendaciones permiten garantizar una prescripción eficiente y más segura, y ayudan al manejo de fampridina-LP como tratamiento del deterioro de la marcha en pacientes adultos con EM en España

INTRODUCTION: Gait impairment, a frequent sign in multiple sclerosis (MS), places a major burden on patients since it results in progressive loss of personal and social autonomy, along with work productivity. This guide aims to provide recommendations on how to evaluate gait impairment and use prolonged-release fampridine (PR-fampridine) as treatment for MS patients with gait impairment in Spain. DEVELOPMENT: PR-fampridine dosed at 10 mg every 12hours is currently the only drug approved to treat gait impairment in adults with MS. Additionally, PR-fampridine has been shown in clinical practice to significantly improve quality of life (QoL) in patients who respond to treatment. Treatment response can be assessed with the Timed 25-Foot Walk (T25FW) or the 12-item MS Walking Scale (MSWS-12); tests should be completed before and after starting treatment. The minimum time recommended for evaluating treatment response is 2 weeks after treatment onset. Patients are considered responders and permitted to continue the treatment when they demonstrate a decrease in their T25FW time or an increase in MSWS-12 scores. A re-evaluation is recommended at least every 6 months. The SF-36 (Short Form-36) and the MSIS-29 (MS Impact Scale-29) tests are recommended for clinicians interested in performing a detailed QoL assessment. This drug is generally well-tolerated and has a good safety profile. It should be taken on an empty stomach and renal function must be monitored regularly. CONCLUSIONS: These recommendations will help ensure safer and more efficient prescription practices and easier management of PR-fampridine as treatment for gait impairment in Spanish adults with MS

M3 cholinoreceptors alter electrical activity of rat left atrium via suppression of L-type Ca2+ current without affecting K+ conductance

Electrophysiological effects produced by selective activation of M3 cholinoreceptors were studied in isolated left atrium preparations from rat using the standard sharp glass microelectrode technique. The stimulation of M3 receptors was obtained by application of muscarinic agonist pilocarpine (10-5 M) in the presence of selective M2 antagonist methoctramine (10-7 M). Stimulation of M3 receptors induced marked reduction of action potential duration by 14.4 ± 2.4% and 16.1 ± 2.5% of control duration measured at 50 and 90% of repolarization, respectively. This effect was completely abolished by selective M3 blocker 4-DAMP (10-8 M). In isolated myocytes obtained from the rat left atrium, similar pharmacological stimulation of M3 receptors led to suppression of peak L-type calcium current by 13.9 ± 2.6% of control amplitude (measured at +10 mV), but failed to affect K+ currents Ito, IKur, and IKir. In the absence of M2 blocker methoctramine, pilocarpine (10-5 M) produced stronger attenuation of ICaL and induced an increase in IKir. This additive inward rectifier current could be abolished by highly selective blocker of Kir3.1/3.4 channels tertiapin-Q (10-6 M) and therefore was identified as IKACh. Thus, in the rat atrial myocardium activation of M3 receptors leads to shortening of action potentials via suppression of ICaL, but does not enhance the major potassium currents involved in repolarization. Joint stimulation of M2 and M3 receptors produces stronger action potential shortening due to M2-mediated activation of IKACh (AU)

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Bloqueo de los canales de potasio en el shock séptico, ¿otra esperanza perdida? / Blockage of potassium channels in septic shock, another lost hope?

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Effects of 5-hydroxydecanoate and ischemic preconditioning on the ischemic-reperfused heart of fed and fasted rats

This investigation aimed to assess whether the mitochondrial ATP-sensitivepotassium channel blocker 5-hydroxydecanoate (5-HD) could abolish the protectionconferred by fasting and ischemic preconditioning (IPC) and to ascertainwhether these effects are associated with glycogen breakdown and glycolytic activity.Langendorff perfused hearts of fed and 24-h fasted rats were exposed to 25 minischemia plus 30 min reperfusion. IPC was achieved by a 3 min ischemia plus a 5 minreperfusion cycle. 5-HD (100 µM) perfusion begun 5 min before IPC or 13 minbefore sustained ischemia in the non preconditioned groups. Fasting improved thereperfusion recovery of contraction, decreased the contracture and the lactate production,increased glycogenolysis and did not affect the percentage of viable tissue.5-HD abolished the effects of fasting on the contractile recovery but did not affectthe contracture. 5-HD decreased the lactate production in the fed group, increasedthe preischemic glycogen content in both nutritional groups and did not affect theischemic glycogen fall. IPC improved the contractile function but prevented thecontracture only in the fed group, reduced lactate accumulation and glycogenolysisand evoked an increase of the viable tissue. 5-HD abolished the effects of IPC on thecontractile recovery and did not affect its effect on the contracture, lactate production,glycogenolysis and viable tissue. These data suggest that the mitocondrial ATPsensitivepotassium channel is involved in the effects of fasting and IPC on the contractilefunction but the other cardioprotective and metabolic effects appear evokedthrough other mechanisms. Also suggest that besides the inhibition of the mitochondrialpotassium channel, other mechanisms mediate the effects of 5-HD (AU)

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