Lamotrigine
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Haemophagocytic lymphohistiocytosis and Takotsubo cardiomyopathy: case report A 45-year-old woman developed haemophagocytic lymphohistiocytosis (HLH) and Takotsubo cardiomyopathy during treatment with lamotrigine for recurrent major depression. The woman, who had generalised anxiety and major depression disorder presented with influenza-like symptoms including fevers and neck stiffness of 1-week duration. Seventeen days prior to the presentation, she started receiving lamotrigine [route and dosage not stated] for recurrent major depression. She had been receiving various other medications concomitantly. The woman’s lamotrigine therapy was stopped. Initial laboratory data showed acute anaemia, thrombocytopenia, transaminitis, elevated inflammatory markers with ferritin 29 101 ng/mL, lactate dehydrogenase (LDH) 1101 U/L and Ddimer 62 365 ng/mL. Initial vital signs showed a body temperature 38.8°C and tachycardia. A physical examination showed a mildly anxiety, sinus tachycardia, clear lung fields, no palpable splenomegaly or lymphadenopathy. A maculopapular rash was noted on her trunk and bilateral lower extremities. An abdominal ultrasound (US) revealed hepatomegaly with increased echogenicity thought to be fatty liver and spleen size of 11–12cm. A CT scan of her chest showed bibasilar opacifications thought to be atelectasis and small bilateral pleural effusions. She was admitted for sepsis and acute hypoxic respiratory failure and treated with vancomycin, ceftazidime and metronidazole. Peripheral blood smear was notable for band neutrophils with prominent toxic granulation, anisocytosis and poikilocytosis. Based on findings (severe hyperferritinaemia >50 000 ng/mL, coagulopathy with elevated prothrombin time (PT)/partial thromboplastin time (PTT), uptrending liver function tests and low fibrinogen with markedly elevated D-dimer and LDH), she was suspected to have HLH. Initially, her serum triglycerides was mildly elevated but quickly up trended to >3000 mg/dL. Soluble interleukin-2 (IL-2) receptor had been elevated to 10 270 pg/mL. She started receiving empiric treatment for HLH due to development of multiorgan failure, rapidly rising ferritin and worsening of liver function tests and creatinine. The protocol comprises an 8-week induction therapy of etoposide and dexamethasone. A bone marrow biopsy revealed a hypercellular marrow with no evidence of haematologic malignancy but two foci of haemophagocytosis. The morning after dexamethasone initiation, she experienced a witnessed ventricular fibrillation and cardiac arrest, and Code Blue team was activated. Immediately, the critical medical emergency team was activated and was able to achieve a return to spontaneous circulation and thereafter, she was intubated for airway protection. Her ICU course was complicated by acute renal failure requiring intermittent dialysis, liver failure (progressive transaminitis) and an acute drop in left ventricular ejection fraction with a transthoracic echocardiogram revealing Takotsubo cardiomyopathy. HLH-directed therapy was co
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