Sir,We report a 51-year-old woman with coma and high-anion-gap metabolic acidosis following a supposed transdermal methanol intoxication. She had a 7-year history of epilepsy. The patient was admitted to the emergency service with an episode of tonic-clonic convulsions similar to previous attacks. Cranial computed tomography showed no abnormalities. She was discharged from hospital. Eighteen hours later, she was brought to the emergency service again with a Glasgow coma scale score of 3. The patient's vital signs included a heart rate of 105 beats/min, blood pressure of 80/60 mmHg and body temperature of 36.7 8C. Her pupils were dilated with an absent light reflex. Laboratory examinations showed the following results: serum sodium, 138 mmol/l; potassium, 4.5 mmol/l; chloride, 105 mmol/l; creatinine, 1 mg/dl; blood urea nitrogen, 20 mg/dl; glucose, 138 mg/dl. The arterial blood gases were as follows: pH 7.10; Po 2 ¼ 159 mmHg (21.2 kPa); Pco 2 ¼ 17.9 mmHg (2.4 kPa); HCO 3 ¼ 9.1 mmol/l, with an anion gap of 28 mmol/l. The lactate level was 3.7 mmol/l. Urinary ketones were negative. She was mechanically ventilated and intravenous sodium bicarbonate infusion was given to correct the acidosis. Despite bicarbonate infusion, the acidosis could not be corrected; therefore, a period of haemodialysis was performed on the third day. Salicylate and methanol analyses could not be performed in our hospital. Therefore, samples were sent to another hospital, revealing a normal S-salicylate level and an S-methanol value of 3.3 mg/dl. The patient's relatives denied oral intake of cologne, spirit or ethanol, but the patient had suffered from headache on the days prior to hospitalization, and used spirit to massage her head on several occasions. One more period of dialysis was performed. The high-anion-gap acidosis resolved, but the neurological status did not improve. She died on the fourth day of hospitalization.Fatal methanol poisoning can result from many sources and routes. Although almost all reported cases in the literature have occurred after oral ingestion, absorption via the transdermal route may lead to intoxication (1, 2). It may be difficult to make a diagnosis of methanol poisoning if no history of ingestion has been obtained. In this patient, the absence of a history of ingestion resulted in a delay in diagnosis. As the patient had a history of epilepsy, the possibility of a metabolic condition precipitating the convulsions was not considered.Various factors complicate the correlation of serum methanol concentrations with clinical effects, including differences in sampling time, individual variation in methanol metabolism, concentration of toxic metabolites and the concomitant ingestion of ethanol (3). The low serum methanol concentration in this patient can be correlated with the sampling time of 3 days after admission and the increase in elimination as a result of dialysis. In the absence of S-methanol analyses, the use of osmolal and anion gaps to establish an early diagnosis is crucial (4). In this patient, a suspi...