Asunto(s)
Aceites de Pescado/uso terapéutico , Diálisis Renal/efectos adversos , Trombosis/prevención & control , Ensayos Clínicos como Asunto , Endotelio Vascular/fisiología , Endotelio Vascular/fisiopatología , Humanos , Hiperplasia , Modelos Biológicos , Músculo Liso Vascular/patología , Distribución Aleatoria , Trombosis/etiología , Venas/patologíaRESUMEN
Metabolic pathways and toxic effects of long-term selenium exposure in animal models and humans have both similarities and significant differences. In animal models the target organ is the liver, in which chronic cirrhosis develops. In man the target organ appears to be the lung, which manifests acute "rose cold," or, as in our patient, a chronic granulomatous hypersensitivity. Our data indicate not only a different target organ than would have been predicted from animal models, but also a difference in the distribution of selenium in human tissues. Long-term use of selenium favors production of dimethylselenide, which is excreted by the lungs and should be considered a pulmonary toxin. The ramifications of these findings may require a change in the monitoring techniques of long-term industrial exposure and mandate a close follow-up of selenium as a health fad.