Muerte súbita en un niño de 2 años con enfermedad de Kawasaki / Sudden death in a two-year-old child with Kawasaki disease

La enfermedad de Kawasaki es una vasculitis sistémica que afecta a arterias de pequeño o mediano calibre, y es la principal causa de cardiopatía adquirida en la infancia. La afectación coronaria es frecuente y se produce en forma de aneurismas. Sin embargo la trombosis de estos aneurismas con infarto de miocardio y/o muerte súbita es rara. Presentamos el caso de un paciente de 2 años diagnosticado de enfermedad de Kawasaki tratado con gammaglobulina iv y AAS, que presentó a los 2 meses un síndrome coronario agudo con trombosis de la arteria descendente anterior en el que se indicó reperfusión con rTPA intravenoso. Dos meses después es traído a urgencias en parada cardiorrespiratoria de la que se recupera. En la necropsia se encontró un aneurisma gigante trombosado en la arteria coronaria izquierda (AU)

The Kawasaki syndrome or disease is a systemic vasculitis affecting medium- or small-calibre arteries and is the main cause of acquired heart disease in childhood. Coronary involvement is frequent and manifestas as aneurysmata. However, thrombosis of these aneurysmata with acute myocardial infarction and/or sudeen death is uncommon. We report the case of a two-year-old male patient with a diagnosis of Kawasaki disease and under therapy with i.v. gammaglobulin and acetylsalicylic acid, who after two months evidenced an acute coronary artery syndrome with anterior descending artery thrombosis, for which reperfusion with intravenous rTPA was indicated. Two months later he was brought to the Emergency Department in a state of carduiorespiratory arrest; the necropsy studies disclosed a thrombosed giant aneurysm in the left coronary artery (AU)

Parkinsonism and Parkinson's disease associated with long-term administration of sertraline.

Sertraline, a serotonin reuptake inhibitor, has been used to treat depression and has rarely been associated to Parkinsonism. The disease usually appears in old people a few days after sertraline administration and disappears very quickly after its withdrawal. We report a case of a woman, 81-year-old, who presented with hemiparkinsonism after long-term administration of sertraline at a dose of 100 mg/day. The symptoms disappeared 3 months after the withdrawal of the drug. However, without further administration of the drug for 14 months, the patient presented with Parkinson's disease, but responded well to levodopa.

Influence of calcium antagonist drugs in myasthenia gravis in the elderly.

A number of drugs have been reported to cause neuromuscular blockade and/or to increase weakness in myasthenia gravis. We report on two patients, treated with felodipine and nifedipine for arterial hypertension, who presented with an exacerbation of their myasthenia gravis and a myasthenic syndrome or exacerbation of myasthenia gravis, respectively. The mechanism of action of calcium antagonist drugs at the neuromuscular junction is not yet well established, but it could be located at both presynaptic and postsynaptic levels.

Effect of probenecid and benzbromarone on gluconeogenesis in isolated rat liver cells.

The effect of benzbromarone on gluconeogenesis from several gluconeogenic substrates in isolated rat liver cells is reported. Benzbromarone inhibited glucose synthesis from all substrates employed when the drug was used at concentrations half to ten times greater than its therapeutic plasma levels. This inhibition was more pronounced from lactate and pyruvate than from fructose and glycerol. The results are compared with those obtained for probenecid, a classical uricosuric drug. We found that probenecid inhibited the pathway in the same way as benzbromarone.

Inhibition of purine catabolism by benzbromarone in isolated rat liver cells. Comparison with allopurinol and probenecid.

Benzbromarone, a potent uricosuric agent, inhibited allantoin production in isolated hepatocytes at concentrations half to ten times greater than therapeutic plasma levels of the drug. In addition, the drug at these concentrations also markedly inhibited xanthine oxidase (EC 1.2.1.37), an enzyme involved in the regulation of this pathway. We found that allopurinol is several times superior to benzbromarone in the lowering of allantoin production (if they are compared in terms of their relative therapeutic levels), and that probenecid had no effect on it.