RESUMEN
We studied the role of oligoantigenic diets in 63 children with epilepsy; 45 children had epilepsy with migraine, hyperkinetic behavior, or both, and 18 had epilepsy alone. Of the 45 children who had epilepsy with recurrent headaches, abdominal symptoms, or hyperkinetic behavior, 25 ceased to have seizures and 11 had fewer seizures during diet therapy. Headaches, abdominal pains, and hyperkinetic behavior ceased in all those whose seizures ceased, and in some of those whose seizures did not cease. Foods provoking symptoms were identified by systematic reintroduction of foods, one by one; symptoms recurred with 42 foods, and seizures recurred with 31; most children reacted to several foods. Of 24 children with generalized epilepsy, 18 recovered or improved (including 4 of 7 with myoclonic seizures and all with petit mal), as did 18 of 21 children with partial epilepsy. In double-blind, placebo-controlled provocation studies, symptoms recurred in 15 of 16 children, including seizures in eight; none recurred when placebo was given. Eighteen other children, who had epilepsy alone, were similarly treated with an oligoantigenic diet; none improved.
Asunto(s)
Epilepsia/dietoterapia , Hipersensibilidad a los Alimentos/complicaciones , Trastornos Migrañosos/dietoterapia , Adolescente , Niño , Preescolar , Método Doble Ciego , Electroencefalografía , Epilepsia/etiología , Epilepsia/fisiopatología , Estudios de Seguimiento , Humanos , Hipercinesia/etiología , Trastornos Migrañosos/etiología , Recurrencia , Pruebas CutáneasRESUMEN
Selected immunologic functions were assessed in 14 patients with the Shwachman syndrome. Nine patients were neutropenic and four had low levels of IgA or of IgM. Neutrophil mobility was significantly defective in the group of patients as a whole (in 12 it was below the lower limit of normal) and in their parents. No other consistent abnormality in immunity was found. These results suggest that the defective neutrophil mobility is a feature of Shwachman syndrome which may contribute to the vulnerability of these patients to frequent infections. The defect appears to be a primary genetic one, inherited as an autosomal recessive characteristic consistent with the assumed inheritance of Shwachman syndrome.