Three Faces of Methemoglobinemia: Drug-induced, Herbal-associated, and Congenital: A Case Series

Methemoglobinemia is a rare, potentially life-threatening disorder caused by oxidation of hemoglobin’s iron from ferrous (Fe 2+ ) to ferric (Fe 3+ ), impairing oxygen delivery. It may be congenital or, more commonly, acquired after exposure to oxidizing agents such as dapsone, nitrates, sulfonamides, or rasburicase. Clinical manifestations depend on methemoglobin (MetHb) levels, ranging from asymptomatic cases to severe hypoxia with end-organ dysfunction. We describe three patients with varied etiologies. A 37-year-old woman with immune thrombocytopenia in remission developed dyspnea, palpitations, and desaturation after self-administering high-dose dapsone. Co-oximetry revealed MetHb 11.2%. She was managed conservatively with oxygen and monitoring, achieving complete recovery without methylene blue. A 43-year-old man without comorbidities presented with cyanosis and breathlessness following ingestion of an ayurvedic preparation. His MetHb was 18.1%, and he was treated with intravenous methylene blue followed by oral ascorbic acid, leading to rapid recovery. A 16-year-old male presented with exertional dyspnea and peripheral cyanosis. Hemoglobin was 20 g/dL, hematocrit 54%, and co-oximetry showed MetHb 46.9% with normal partial pressure of oxygen, suggesting congenital methemoglobinemia with secondary polycythemia. Intravenous methylene blue reduced levels to 7% with symptomatic improvement. This series illustrates the spectrum of acquired and congenital methemoglobinemia, emphasizing timely recognition, co-oximetry-based diagnosis, and severity-guided management.