Immunosuppressants
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Haemophagocytic lymphohistiocytosis: 2 case reports A case report described a 58-year-old man and a 51-year-old woman, who developed haemophagocytic lymphohistiocytosis (HLH) following immunosuppressive therapy with basiliximab, ciclosporin, everolimus, methylprednisolone, prednisone, sirolimus or tacrolimus [not all dosages and routes stated]. Patient 1: A 58-year-old man, whose medical history was notable for end-stage renal disease, underwent a kidney transplantayion in May 2016. Induction immunosuppressive therapy comprised of basiliximab and IV methylprednisolone 500mg, followed by maintenance therapy with tacrolimus 0.12 mg/kg/day, everolimus 1.25mg twice a day and prednisone 20 mg/day. His initial 6 months post-transplant were without complications. However, over the subsequent 3 months, he was hospitalised three times due to urinary infection from Escherichia coli. Thereafter, his renal function decreased, with worsening creatinine. Later, in June 2018, he was hospitalised due to diarrhoea, fever and acute kidney injury. Laboratory findings were notable for the following: WBC count 3570mm3, platelet count 94 000mm3, Hb 9.1 g/dL, serum creatinine 7.21 mg/dL, blood urea nitrogen 85 mg/dL, CRP 22.5 mg/dL, hyponatraemia with sodium 122 mEq/L, procalcitonin 7.38 ng/mL, negative fecal calprotectin, brain natriuretic peptide 176 pg/mL, sideraemia 27 µg/dL, ferritin 8889.3 µg/L, transferrin 167 mg/dL, total cholesterol 133 mg/dL, cholesterol 133 mg/dL, high-density lipoprotein 17 mg/dL and triglycerides 749 mg/dL. Epstein-Barr virus (EBV) DNA was detected at 26 34 199 copies/mL of replication on blood, with a cytomegalovirus DNA load of 87 596 copies/mL in plasma [aetiologies not specified]. Chest X-ray revealed interstitial lung involvement. Full body CT scan revealed hepatosplenomegaly. Over the subsequent days, he deteriorated, with worsening clinical conditions. Haemodialysis was initiated due to persistent acute kidney injury with oligoanuria unresponsive to medical therapy. Acute hypoxaemic and hypercapnic respiratory failure developed, requiring oxygen therapy. Due to the severe pancytopenia (WBC count 440mm3, platelet count 7000mm3 and Hb 6.7 g/dL), he underwent multiple blood and platelet pool transfusions. He also exhibited a very high ferritinaemia; hence, haematologic evaluation was requested. Medullary aspiration and bone marrow biopsy showed signs of haemophagocytosis, with a final diagnosis of HLH. He was treated with HLH-94 protocol therapy comprising etoposide, rituximab and dexamethasone. His immunosuppression therapy was modified; everolimus and tacrolimus were suspended. Ten days following initiation of the therapeutic protocol, he was discharged with remarkable improvement in his laboratory findings and clinical conditions. Haemodialysis was discontinued, and his renal function recovered. During follow-up, he reported feeling well, without fever, no dyspnoea and diarrhoea with stable hematological parameters for approximately 5 weeks after discharge. The HLH-94 protocol was prolonged, and
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