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Pediatria Medica e Chirurgica

[In vivo and in vitro production of interleukin-1 after febrile convulsions].

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
يتم حفظ الارتباط في الحافظة
S Miceli Sopo
B Cuomo
G Federico
M D Avantaggiato
A Pugliese
P L Navarra
A Stabile

الكلمات الدالة

نبذة مختصرة

Pathogenesis of febrile convulsions (FC) is still unknown, suggested causes include the role of antidiuretic hormone (ADH). ADH is an endogenous antypyretic and his excessive production of the consequent hyponatraemia may be the cause of FC in children with susceptibility to this type of seizure. Whereas, interleukin-1 (IL1) is a pyrogenic substances and is involved in the release of AVP. Helminen et al. have reported a significantly higher production of IL1 in culture of peripheral blood monocytes stimulated with lipopolysaccharide (LPS) of children with FC than in the others with fever but without convulsions. More recently Lahat et al. have compared plasma and cerebrospinal fluid ILI levels of children with FC with those of children with fever but without convulsions, but they did not find significant differences. The aims of this study were to determine the IL1 levels in vivo and in the supernatants of cultures of peripheral blood mononuclear cells (PBMC) stimulated or not with LPS in children with FC and in children with fever without FC and to evaluate the influence of ADH and diazepam (DZ) on IL1 production. Blood samples for PBMC cultures were obtained from 11 children with FC on the hospital admission, (group 1) and after 48 hours from treatment with DZ (group 2). The production of IL1 was measured by RIA in the supernatants of the PBMC stimulated with LPS, LPS + DDAVP (synthetic vasopressin), LPS + DZ and in vivo in plasma samples. The control groups were constituted by 9 children with fever and without convulsions (group 3), 4 of them were studied at the end of fever too (group 4), and finally by 9 children in good health (group 5). No significant differences were observed. These results do not support the hypothesis that increased production of IL1 is involved in the pathogenesis of FC in children.

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