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Differentiation syndrome, lack of efficacy and other toxicities: case report A 77-year-old woman developed differentiation syndrome, thyroiditis, bilateral pleural effusions and hyperbilirubinaemia during treatment with enasidenib for acute myeloid leukemia (AML). Additionally, she exhibited lack of efficacy while receiving dexamethasone for hyperbilirubinaemia [routes and duration of treatments to reaction onsets not stated; not all dosages stated]. The woman presented with pancytopenia in April 2019. Her medical history was significant for paroxysmal atrial fibrillation, recurrent allergic sinusitis and hyperlipidaemia. She had been receiving apixaban, metoprolol and ezetimibe. Based on investigations, she was diagnosed with AML positive for isocitrate dehydrogenase 2 (IDH) mutation in May 2019. Consequently, she started receiving targeted therapy with azacitidine [5-azcitidine] and enasidenib 100mg. Additionally, prophylactic unspecified antiviral, antifungal and antibiotics were also initiated. Two weeks later, she reported subjective fears associated with headache, frontal sinus pressure and loss of appetite. Hence, her second cycle of chemotherapy was held. Signs of inflammatory disease were seen on CT of sinuses. She was treated with amoxicillin/clavulanic acid [Augmentin] for presumed bacterial sinusitis. After a few days, she received her second dose of chemotherapy. At a follow-up visit, hyperbilirubinaemia was noted, suggestive of differentiation syndrome. Her hyperbilirubinaemia and differentiation syndrome was attributed enasidenib. The woman started receiving dexamethasone 8mg two times a day. At her next follow-up visit, she reported to have developed dyspnoea. Examination of lungs showed diminished breath sounds at the lung bases and bilateral pitting oedema. A chest X-ray confirmed bilateral pleural effusion which was attributed to enasidenib. An ECG showed preserved left ventricular ejection fraction. She was treated with furosemide, unspecified steroids and pantoprazole. Apixaban was withdrawn due to concerns of pancytopenia. Subsequently, she was hospitalised for dehydration. ECG findings were significant for rapid atrial fibrillation. Laboratory findings showed worsening hyperbilirubinaemia along with new onset hyperthyroidism, with TSH less than 0.02 ng/mL and elevated free T4 of 2.1 ng/dL. An I-123 thyroid scan showed slightly increased uptake in the upper portion of the right thyroid lobe with no suppression in the remainder of the gland, consistent with thyroiditis. Atrial fibrillation was controlled with unspecified β-blockers and methimazole was avoided due to concerns of bone marrow suppression. Her hyperbilirubinaemia remained persistent despite treatment with dexamethasone. Consequently, the woman’s dose of enasidenib was reduced to half when her total bilirubin began to fell. At a follow-up few weeks later, she reported to have felt better and was switched to steroid taper. Her free T4 levels also began to fall. She received reduced dose of enasidenib (50mg) for third cycle of ch