![]() ![]() She had 1 younger sibling with autism spectrum disorder. She was taking her regular diet and drinking city water. She was shown a bottle of cetirizine and confirmed the ingestion of the particular drug. She denied ingestion of medications other than cetirizine during or before this episode or any recent intake of green beans, carrots, beets, or spinach. She admitted to 1 episode of attempted self-harm with a knife approximately 6 years ago. There was no past history of surgical procedures, illnesses, or any other drug intake. ![]() ![]() She attributed those symptoms to her traumatic childhood. In the past, she had received counseling and behavioral therapy for anxiety and depression but no medication. She denied any suicidal thoughts, ideation, or intention behind the ingestion. She was brought to the emergency department by her father. Shortly afterwards, she started experiencing nausea and worsening abdominal pain. She took an additional 10 to 16 tablets of 10 mg each within the next hour as the pain persisted. She took 2 tablets (20 mg) of cetirizine, reportedly for alleviation of pain, which she had bought over the counter for seasonal allergies. We describe the first report documenting cetirizine as a causative agent for drug induced MHb.Īn 18-year-old African American female with a past history of anxiety and depression developed abdominal pain while moving into her dormitory room. It is reduced and eliminated through other oxidation and conjugation pathways, 4 which can potentially release by-products that act as powerful reducing agents like free radicals, such as superoxide or hydrogen peroxide, and can oxidize hemoglobin into Fe +3 containing methemoglobin. 4 Cetirizine does not undergo metabolism via the cytochrome P450 enzyme system. The reported adverse effects of cetirizine are headache, somnolence, tremor, anxiety, nausea, abdominal pain, cough, hyperventilation, and hematuria among others. Having greater affinity for H1 receptors than other muscarinic acetylcholine receptors, its anticholinergic side effects are insignificant. Unique from older antihistaminic receptor agents, it less readily crosses the blood-brain barrier and causes minimal sedation or amnesic effects. 1 – 3Ĭetirizine, commonly used to treat allergic symptoms is a selective antagonist of the histamine H1 receptor. 1 – 3 Physiologically, the protective enzymes, namely cytochrome-b5 reductase (nicotin-amide adenine dinucleotide methemoglobin reductase) via the major and nicotinamide adenine dinucleotide phosphate (NADPH) reductase via the minor pathway, reduce methemoglobin and maintain it at an insignificant homeostatic level of approximately 1%. In normal circumstances, methemoglobin is spontaneously formed within the red blood cells from imperfect intracellular reactions through the process of auto-oxidation and electron dissociation, which leads to release of free superoxide radicals and production of Fe +3 in heme groups. This results in tissue hypoxia and a shift of oxygen-hemoglobin dissociation curve to left. 1 Fe +3 has an increased affinity for oxygen, which makes it ineffective to release and deliver oxygen at tissue sites. Methemoglobinemia is defined by the presence of elevated levels of oxidized heme groups that contain iron (Fe) in ferric form (Fe +3) as opposed to the physiological ferrous form (Fe +2). In this case, an unusually high systemic load of the drug speculatively saturated and overwhelmed the protective enzyme systems, which resulted in clinical manifestation of MHb. The metabolism could potentially create by-products, like superoxide or hydrogen peroxide, which could act as strong reducing agents and oxidize hemoglobin into ferric containing methemoglobin. Cetirizine, a selective histamine H1 receptor antagonist is eliminated via oxidation and conjugation processes, which use pathways other than cytochrome P450 enzyme system. To the best of our knowledge, this is the first documentation of cetirizine as a causative agent for drug induced MHb. The exact enzymatic deficiency could not be ascertained as the patient refused to undergo complete testing. There was a history of recurrent, spontaneously remitting, unprovoked “blue discoloration of hands.” Investigations confirmed the diagnosis of MHb, and the patient responded to ascorbic acid and methylene blue, although the baseline methemoglobin level remained slightly high. The patient presented with anxiety and tremors and rapidly developed central cyanosis unresponsive to oxygen supplementation. A case of methemoglobinemia (MHb) in a teenage woman, triggered by an acute ingestion of approximately 120 to 180 mg of cetirizine, allegedly, with no suicidal intent is described. ![]()
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