Methemoglobinemia is a condition in which
methemoglobin is increased and the
oxygen carrying capacity of tissues is decreased, causing a lack of
oxygen to the whole body.
RNA (
ribonucleic acid) sequencing technologies have made it possible to systematically examine how the human transcriptome responds to invasive pathologies. To our knowledge, no previous studies have reported the results of
RNA sequencing in a patient with
methemoglobinemia. We describe the analysis of RNAs from the whole blood of a patient with
methemoglobinemia.
CASE PRESENTATION: A 31-year-old Japanese man was brought to our hospital with symptoms of
dyspnea due to inhalation of gas from an
acetic acid phosphonitrate storage tank at a factory. The
nitrogen oxide concentration measured around the storage tank was over 2500 ppm, and he witnessed orange-brown
smoke at that time. After entering the area and taking a few breaths, he suddenly became unwell, with
dyspnea and
numbness in his extremities. He was evacuated from the area within a few minutes, at which time he was suffering from whole-body
cyanosis and was still aware of the above symptoms. On arrival at the hospital, his respiration rate was 18 breaths/minute, and his SpO2 ranged from 80% to 85% on 15 L/minute of
oxygen by mask (2.5 hours postexposure). Arterial blood gas testing revealed a
methemoglobin level of 23.1%. After the administration of
methylene blue, the patient's
methemoglobin level normalized and his symptoms improved. Chest X-ray and chest computed tomography showed no evidence of
pulmonary edema or
interstitial pneumonia, and no other abnormal findings were observed.
RNA sequencing was performed on the blood samples obtained at the time of the visit, with the blood sample collected on day 5 used as a control. To our knowledge, the present study is the first to describe the analysis of RNAs from the whole blood of a patient with
methemoglobinemia. The
RNA sequencing analysis showed that an activated "
hydrogen peroxide catabolic process" may be associated with the pathogenesis of
methemoglobinemia.
CONCLUSION: