Abstract
INTRODUCTION: 3,4-methylenedioxymethamphetmamine (MDMA) is a synthetic drug that is known to be used for its euphoric effects via the release of serotonin, dopamine, and norepinephrine. It has been associated with multiple adverse effects, including seizures, serotonin syndrome, multiorgan failure, disseminated intravascular coagulation (DIC), and death. Here we report a rare case of rapidly reversible multiorgan failure after ingestion of a single tablet of MDMA and its subsequent management. CASE DESCRIPTION/METHODS: A 23-year-old female presented in a comatose state after ingesting 200 mg of MDMA. She was febrile to 109 °F, tachycardic, and hypotensive 69/42 mm Hg. Labs were initially notable for ALT 49 U/L, serum creatinine of 1.75 mg/dL, lactate 10.5 mmol/L, and an elevated anion gap metabolic acidosis. The patient was intubated for airway protection and placed under external cooling measures for hyperpyrexia. Repeat labs in the ICU revealed worsening transaminitis with AST/ALT of 2686/2239, and increasing creatine kinase of 36,350. Within 12 hours, her course worsened to acute decompensated DIC as the patient had epistaxis, platelets 35 K/uL, PT 29.3 sec, aPTT 40.7 sec, fibrinogen 129 mg/dL, and D-dimer 12,466 ng/mL, and INR 2.5 (Figure 1). Fresh frozen plasma and platelet transfusions were administered. The patient was initiated on N-acetylcysteine (NAC) infusions and transferred to a liver transplant center for further care and possible need for OLT (MELD Score 30). Her LFTs slowly improved over the next couple of weeks with overall improvement in clinical status with supportive care. She was ultimately discharged on hospital day 12. On outpatient follow-up day 21, she had complete restoration of her synthetic liver and renal function. DISCUSSION: Acute liver failure with DIC is one of many manifestations of MDMA toxicity, and it carries a 60% mortality rate. Its mechanism of hepatic injury is unclear – since a spectrum of severity exists, histology varies from a mild-moderate lobular hepatitis, to massive hepatic parenchymal collapse. The severity of liver damage appears to not be dose dependent, which suggests an idiosyncratic reaction. MDMA is primarily metabolized by the enzyme CYP2D6 and of note, the patient is Chinese – a population known to have a high prevalence of CYP2D6 polymorphisms, predisposing them to liver failure. This case is one of the few cases of full recovery from MDMA-induced multiorgan failure and it emphasizes the importance of aggressive supportive care in such patients.Figure 1.: Laboratory values by hospital day.
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