Summary:Background: The incidence of status epilepticus (SE) in Asian children, including Japanese, has not been reported.Methods: In 2003, we performed an epidemiological study of SE on Japanese children (31 days or older to <15 years of age) in Okayama City by ascertaining all lifetime first episodes of SE.Results: Thirty-seven patients (22 males and 15 females) were identified. The annual incidence of SE was 38.8 per 100,000 population (95% CI: 24.5-49.5). Febrile SE in the absence of CNS infection accounted for 17. Acute symptomatic etiologies other than febrile SE were observed in eight patients, including three cases of influenza encephalitis/encephalopathy. Five were classified as remote symptomatic and the remaining seven as cryptogenic. The highest incidence (155.1/100,000) was seen in the age range of 31 days or older to <1 year, followed by 101.5/100,000 in the age range of one year, and the incidence decreased after eight years. In 26 of the 37 patients, SE was their first seizure. As for seizure types, 32 had convulsive SE, including tonic status in one. Five others showed nonconvulsive SE, including complex partial SE in four and absence status in one. No one died of SE. Two patients who brought on SE because of influenza encephalitis/encephalopathy suffered from motor disturbance with or without mental disturbance after SE.Conclusions: The incidence of SE tended to be higher in Japanese children than reported in Caucasians. The Japanese had an age-specific incidence pattern similar to that of Caucasians.
Based on the clinical features and the TNFRSF1A mutation, both siblings were given a diagnosis of TRAPS. The serum levels of soluble TNFRSF1A, measured along with the CRP level, may be a useful screening marker for differentiating TRAPS from systemic JIA.
Antibody‐dependent cellular cytotoxicity (ADCC) and natural killer (NK) ativity were examined using MT‐2 cells persistently infected by HTLV‐1 as target cells, and mononuclear cells as effector cells, from helathy one‐week‐old newborn babies, infants, children and adults. More than 10% of ADCC was observed in 17 newborn babies out of 22 (77.3%) and in all 67 healthy one‐month‐old babies to adults, by adding serum from anti‐HTLV‐1 positive carriers. When anti‐HTLV‐1 negative serum was added, less than 10% of ADCC was observed. If infants without anti‐HTLV‐1 antibodies were breast‐fed they had the possibility of HTLV‐1 vertical transmission. There was no significant decrease in NK activity between 90 healthy newborn babies, infants, children, or adults. These results suggest that ADCC and NK activity protect against the transmission of HTLV‐1 from mother to child.
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