Cyclotrimethylenetrinitramine (RDX) is a highly explosive compound frequently used for both military and civilian purposes. Previously reported cases of human RDX intoxication were limited to wartime settings and have described no human pharmacokinetic data. We report the first human intoxication to occur in a non-wartime setting. This intoxication presented with status epilepticus in a child and permitted the description of RDX human pharmacokinetics. It also suggested a strong association between central nervous system dysfunction and RDX intoxication.
Hyperphenylalaninemia in infants and children may be caused by a deficiency of dihydropteridine reductase (DHPR). Recommended therapy includes folinic acid as a source of tetrahydrofolate, a phenylalanine-restricted diet, and both dopamine and serotonin precursors. We report a child with progressive basal ganglia and other subcortical calcifications prior to the use of folinic acid. Six other reported cases of DHPR deficiency demonstrated similar calcifications prior to folinic acid therapy. Since this pattern of calcification also resembles that seen in CNS folate deficiency caused by both congenital folate deficiency and that which is methotrexate-induced, we propose that intracranial calcification in DHPR deficiency is caused by inadequate CNS tetrahydrofolate and may be prevented by the use of folinic acid. Our patient achieved excellent seizure control following the use of folinic acid, suggesting either a direct or indirect anticonvulsant effect of this compound in patients with DHPR deficiency.
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