The significance of iron status as a possible risk factor for a first febrile seizure (FFS) was investigated at Jordan University and King Hussain Medical Center, Irbid, Jordan. Mean ferritin level in this prospective study of 75 children with FFS (29,5 +/- 21.3 mcg/L) and 75 matched controls (53.3 +/- 37.6 mcg/L) was significantly decreased (P=0.0001). A plasma ferritin level of <30 mcg/L was significantly more prevalent among children with FFS (49 of 75) than controls (24 of 75). Mean levels of Hgb, MCV, and MCH were lower in FFS cases, and a higher proportion of FFS cases had an Hgb <110 g/L, MCV <72 fL, and MCH <24 pg, but differences were not significant. The findings suggest a possible role for iron insufficiency in FFS. [1]

COMMENT. Plasma ferritin is used as a reliable measure of iron deficiency and total body iron status. Decreased plasma ferritin levels in children with a first febrile seizure are not explained by fever, since the mean peak temperature on admission was similar in patients and controls. Other neurologic disorders in which iron-deficiency anemia may play a role include breath-holding spells developmental delay, and behavior and attention disorders.

Iron metabolism and Hallervorden-Spatz syndrome are reviewed in Ped Neur Briefs October 2001:15:75-76.

Genetics of febrile seizures. A splice-site mutation in the GABRG2 gene has been described that causes a nonfunctional truncation of the GABA receptor g-subunit, and contributes susceptibility to childhood absence epilepsy and febrile convulsions in a single family [2]. The association of a missense mutation in the GABRG2 gene and susceptibility to febrile seizures is a rare finding, previously reported and cited by the authors in only one other family [3].