Dapsone
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Methaemoglobinaemia following drug toxicity: case report A 28-year-old woman developed episodes of methaemoglobinaemia following drug toxicity during treatment with dapsone for suspected dermatitis herpetiformis. The woman presented to the emergency room due to acute hypoxic respiratory distress. She had been experiencing progressive dyspnoea and had multiple fainting episodes. A pulse oximeter showed an oxygen saturation of 80–85%. Her peripheral and central cyanosis did not improve with supplemental oxygen provided using a non-rebreather mask. Therefore, she was quickly intubated and mechanically ventilated with pressure support. However, her oxygen saturation did not improve despite fraction of inspired oxygen of 100%. A transthoracic ultrasound showed normal ventricular function without cardiac shunting. A CT scan ruled out intraparenchymatous abnormalities and pulmonary embolism. Arterial blood was chocolate brown coloured. A blood gas analysis revealed almost 15 times higher methaemoglobin level than the cut-off normal value. Anamnesis revealed that her medical history was significant for coeliac disease and suspected dermatitis herpetiformis. She had been receiving dapsone tablet and dosage was increased from 50 to 100mg once a day 4 days prior to this presentation [route not stated]. On the basis of clinical presentation and medical history, she was diagnosed with dapsone-induced methaemoglobinaemia [duration of treatment to reaction onset not stated]. The woman was treated with methylene blue resulting in decreased methaemoglobin level.Shortly thereafter, she was extubated due to significant clinical improvement with normal blood oxygen level. Her dapsone was discontinued and she disposed the remaining dosages as well. However, during the following two days, she had asymptomatic increase in methaemoglobin level. She was again treated with methylene blue resulting in normal methaemoglobin level. Four days after presentation, she was discharged home. However, 12 days after dapsone discontinuation and 7 days after discharge, she presented again with progressive dyspnoea. Her methaemoglobin level was fond to be elevated. She was admitted again and successfully treated with two doses of methylene blue. On the same day, a serum dapsone level was found to be within the toxic range. Toxicological analysis was not performed during the first admission. She had not taken further dapsone, any other medication or drugs of abuse influencing pharmacokinetics of dapsone. The toxicological study and Naranjo score of 7 confirmed that dapsone was the most likely cause of relapse of methaemoglobinaemia. The delayed renal clarance, delayed metabolism and glucose-6-phosphate dehydrogenase deficiency was ruled out as a cause of relapse of methaemoglobinaemia. Due to the toxic level of dapsone, it was hypothesised that dapsone, which is a lipophilic drug, remained in blood for prolonged period due to distribution of dapsone from the peripheral tissue to the blood. Additionally, a metabolite of dapsone (hydroxylamine), can be
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