Antithymocyte globulin/dapsone/heparin
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Haemolytic anaemia and heparin-induced thrombocytopenia: case report A 54-year-old woman developed thrombocytopenia secondary to heparin (heparin-induced thrombocytopenia; HIT) and haemolytic anaemia secondary to dapsone. Additionally, antithymocyte globulin contributed in the development of HIT and haemolytic anaemia [routes and durations of treatments to reactions onsets not stated; not all dosages stated]. The woman had end stage renal disease secondary to polycystic kidney disease. She presented for deceased donor kidney transplantation. She had been maintained on peritoneal dialysis for approximately 2 years prior but was transitioned to hemodialysis via a tunneled catheter one week prior to transplantation due to peritoneal dialysis catheter malfunction. She started receiving anti-lymphocyte induction therapy with antithymocyte globulin [rabbit antithymocyte globulin]. After the transplant, she started receiving maintenance immunosuppressive treatment with tacrolimus, mycophenolate mofetil and unspecified steroid. Also, she started receiving treatment with dapsone, fluconazole and valganciclovir for infection prophylaxis. Immediately after the transplant, her haemoglobin level was found to be decreased from 10.1 mg/dL to 9.6 mg/dL and the platelet count was found to be decreased from 230 000 /µL to 139 000 /µL. Both hemoglobin level and platelet count continued to decrease throughout the hospital course, which was attributed to antithymocyte globulin. On post-operative day 5, she was discharged with a platelet count of 26 000 /µL and hemoglobin of 8.0 mg/dL. After two days, repeat laboratory investigation showed stable anaemia and a persistent marked thrombocytopenia with platelet count of 21 000 /µL. She was again hospitalized for further evaluation and investigations showed haemolytic anaemia. She was suspected to have dapsone-induced haemolytic anaemia. Therefore, the woman’s therapy with dapsone was discontinued, following which her haemolytic markers and anaemia improved. However, thrombocytopenia persisted. On anamnesis, it was found that she had received a heparin flush at the time of peritoneal dialysis catheter malfunction 8 days prior to the transplant and 2000 unit heparin boluses with haemodialysis treatments 7 and 5 days prior to the transplant. A detailed re-review of her medication records revealed that she had received 1000 units of heparin admixed in the antithymocyte globulin preparation on three occasions during the hospitalisation. Over the next 10 days, the reactivity in the p-selectin expression assay (low platelet factor 4) decreased, which was associated with a corresponding increase in platelet counts. She was treated with apixaban. Her allograft function and thrombocytopenia subsequently improved. At follow-up 6 weeks post-transplant, she had a serum creatinine of 1.0 mg/dL and platelet count of 298 000 /µL with no recurrence of thrombocytopenia or new thrombosis. Author comment: "Here, we describe a severe case of HIT in a renal transplant patient". "[C]linical suspicion was r
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