RESUMEN
Over last fifty years, intravenous (iv) phenytoin (PHT) loading dose has been the treatment of choice for patients with benzodiazepine-resistant convulsive status epilepticus and several guidelines recommended this treatment regimen with simultaneous iv diazepam. Clinical studies have never shown a better efficacy of PHT over other antiepileptic drugs. In addition, iv PHT loading dose is a complex and time-consuming procedure which may expose patients to several risks, such as local cutaneous reactions (purple glove syndrome), severe hypotension and cardiac arrhythmias up to ventricular fibrillation and death, and increased risk of severe allergic reactions. A further disadvantage of PHT is that it is a strong enzymatic inducer and it may make ineffective several drugs that need to be used simultaneously with antiepileptic treatment. In patients with a benzodiazepine-resistant status epilepticus, we suggest iv administration of levetiracetam as soon as possible. If levetiracetam would be ineffective, a further antiepileptic drug among those currently available for iv use (valproate, lacosamide, or phenytoin) can be added before starting third line treatment.
Asunto(s)
Anticonvulsivantes/administración & dosificación , Fenitoína/administración & dosificación , Piracetam/análogos & derivados , Estado Epiléptico/tratamiento farmacológico , Administración Cutánea , Administración Intravenosa , Anticonvulsivantes/efectos adversos , Exantema/inducido químicamente , Humanos , Infusiones Intravenosas , Levetiracetam , Fenitoína/efectos adversos , Piracetam/administración & dosificación , Piracetam/efectos adversos , Estado Epiléptico/diagnóstico , Resultado del TratamientoRESUMEN
The efficacy of Simvastatin to reduce plasma cholesterol is well documented. Other molecule within the lipo-lipoprotein family, such as, particularly, lipoprotein (a) -Lp(a)-, have been recently found to have a predictive and/or causative role in atherosclerosis. Based on the above consideration, we studied 20 patients (7 females and 13 males), mean age 52.4 +/- 14.2 years, affected by primary hypercholesterolemia to evaluate the effect of simvastatin on Lp(a), in addition to the classic lipidic parameters. Five weeks after suspension of lipid-lowering drugs and on a normal caloric-fat diet, were given 20 mg simvastatin/day for 12 months. Clinical and laboratory parameters, cholesterol (CH), triglycerides (TG), high density and low density lipoprotein cholesterol (HDL-CH and LDH-CH) measured enzymatically, apoproteins A1, B measured radial immunodiffusion technique and Lp(a) measured as apoprotein(a) with immunoradiometric assay and were evaluated before therapy and after 12 months of therapy. Simvastatin determined a significant reduction in total cholesterol and cholesterol-LDL (CH 327.7 +/- 44.4 vs 255.5 +/- 37.3, p < 0.0001; LDL-CH 257.1 +/- 60.9 vs 183.8 +/- 46.9, p < 0.0001) and a significant increase in HDL-CH (36.7 +/- 5.9 vs 40.2 +/- 5.7, p < 0.005); no variation was observed in triglycerides (TG) levels. Simvastatin therapy further determined a significant increase in Lp(a) plasma levels (43.8 +/- 25.6 vs 50.5 +/- 28.0, p < 0.02). The our data, in agreement with those documenting the beneficial effect of Simvastatin in greatly decreasing CH and LDL-CH, but point out the need for further studies concerning the long-ter effect of simvastatin on Lp(a), in order to fully establish its role in the secondary prevention of atherosclerosis.
Asunto(s)
Anticolesterolemiantes/uso terapéutico , Hipercolesterolemia/tratamiento farmacológico , Lovastatina/análogos & derivados , Adulto , Anciano , Anticolesterolemiantes/administración & dosificación , Apoproteínas/sangre , Colesterol/sangre , Femenino , Humanos , Hipercolesterolemia/sangre , Inmunodifusión , Lipoproteína(a)/sangre , Lipoproteínas/sangre , Lovastatina/administración & dosificación , Lovastatina/uso terapéutico , Masculino , Persona de Mediana Edad , Radioinmunoensayo , Simvastatina , Factores de Tiempo , Triglicéridos/sangreRESUMEN
Fibrinogen is a globulin of hepatic synthesis necessary for the coagulative process and is considered a risk factor of atherosclerosis disease. The increase in plasma fibrinogen seems to play an important role in the atherosclerosis disease and actually it represents a major, independent risk factor that should be considered for screening programs aimed at identifying individuals at high risk for cardiovascular disease. In the present review we'll propose to summarize current pharmacological knowledge, the relationship between fibrinogen and the best known cardiovascular factors like smoking and hypercholesterolemia. Furthermore we'll show the main mechanisms which make hyperfibrinogenaemia a pathogenetic factor of atherosclerosis. Lastly we analyse the possible fibrinogen lowering therapy.