• Anna Bazylewicz, Tomasz Kłopotowski, Mariusz Kicka, Łukasz Miśkiewicz, and Sebastian Picheta.
• Instytut Medycyny Pracy i Zdrowia, Srodowiskowego w Sosnowcu, Oddzia Toksykologii Klinicznej z Regionalnym Ośrodkiem Ostrych Zatruć. annazboj@poczta.onet.pl
• Prz. Lek. 2010 Jan 1; 67 (8): 636-9.

AbstractMethemoglobin is an oxidized derivative of hemoglobin. It is generated by oxidization the ferrous form of iron (Fe2+) in the heme molecule to the ferric form (Fe3+). A molecule of methemoglobin is incapable of binding and carrying of oxygen. Methemoglobinemia, an increased concentration of methemoglobin in the blood above 2%, may be congenital due to deficiency or lack of specific enzymes protecting hemoglobin from oxidization or abnormal structure of hemoglobin molecule. More often methemoglobinemia is acquired as a result of accidental or intentional poisoning due to chemical substances oxidizing hemoglobin. Some of them may induce hemolysis. Cyanosis resistant to oxygen therapy and dyspnea occur in patients with the methemoglobin concentration above 20%. Consciousness disorders, respiratory and circulatory failure, liver and kidney damage may occur in patients with high methemoglobin levels greater than 50%. Fatal cases have also been reported. In the paper we present two cases of patients who were admitted to our hospital ward. First of them regards a 21-year-old woman with the methemoglobin level of 38.3% induced by accidental inhalation exposure to aniline. The other case concerns a 49-year-old man who developed methemoglobinemia of 42.7% after suicidal ingestion of an urea-substituted herbicide containing linuron. We observed hemolysis in both of these cases. They were treated symptomatically and with a specific antidote--methylene blue.

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