Abstract
Eight medical staff members were contaminated by the treatment agents while treating patients for organophosphate (OP) poisoning. One medical staff member who cared other emergency patients after transfer of this OP poisoning patient in the same room complained of weakness of the limbs and difficulty in walking, along with other common complaints (headache, generalized fatigue, and bleary eyesight). Serum butyrylcholine esterase (BCHE) activity was 27 IU/l (normal = 174-400 IU/l). Other laboratory data were normal. Although the level of BCHE remained under 40 IU/l, the staff member recovered fully in 5 days and returned to work. Under the suspicion of a congenital defect in BCHE synthesis, conventional genetic analysis was performed and a missense mutation at G365R (heterozygous) was confirmed. Because the abnormality was phenotypically different from that of a solitary missense mutation at G365R, another concomitant genetic mutation was thought to exist. A reduction in binding activity was thought to account for the hypersensitivity to OP by individuals with this congenital BCHE defect, and a relative increase in the concentration of OP at the neuromuscular junction was thought to account for the more severe subjective complaints by these individuals compared with personnel having normal BCHE activity. The low BCHE activity attributable to this congenital defect has been observed at our hospital. Maximal precautions are necessary to protect both medical staff members and visiting patients from secondary exposure to choline esterase inhibitors.
