Comparing bromism with methyl bromide toxicity

To the Editor:

We would like to comment on the recently published case report by Lin and colleagues entitled “Myoclonic jerks due to acute bromovalerylurea intoxication.”¹ The authors describe a patient who had ingested an acutely toxic dose of the bromide-containing hypnotic-sedative bromovalerylurea and presented at the Emergency Department with myoclonic jerks. Blood bromide levels were remarkably low, reported to be 81.0 mg/L. As the author correctly stated, blood bromism generally occurs when patients have blood bromine levels in excess of 500 mg/L. Commenting on their patient's low halide concentration, Lin and colleagues suggest acute bromism may differ from chronic toxicity and cite papers associated with methyl bromide intoxication resulting in similarly elevated bromide blood levels to what was reported for the bromovalerylurea overdose patient.

Unfortunately, these authors have confused bromism with methyl bromide intoxication, they are two separate and distinct toxodromes. The intact methyl bromide molecule acts directly as an alkylating agent on amino acids and bioactive proteins that contain sulfhydryl groups, leading to a permanent cytotoxic effect.² In contrast, bromide ions temporarily displace chlorine ions in neuronal cells that can lead to impaired neurotransmission.³ Furthermore, blood bromide levels cannot be correlated with severity of methyl bromide symptoms. Deaths have occurred with patients with blood bromide levels as low as 83 mg/L,⁴ whereas others suffered only dizziness at 125 mg/L.⁵ Comparing bromism with methyl bromide toxicity is therefore not valid and an alternate hypothesis must be considered to explain the anomaly between low bromide levels and reported neurological symptoms.