Immunosuppressants
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Immunosuppressants Pancreatitis, hypertension and transplant-associated thrombotic microangiopathy: 2 case reports
In a case series, a 20-year-old woman developed hypertension during immunosuppressive treatment with unspecified steroids, cyclophosphamide, tacrolimus, methotrexate, sirolimus, ruxolitinib and basiliximab, and transplant-associated thrombotic microangiopathy during treatment with tacrolimus and sirolimus, and a 6-year-old boy developed hypertension during immunosuppressive treatment with cytarabine, cyclophosphamide, methotrexate, tacrolimus, methylprednisolone, prednisone and unspecified steroids, and pancreatitis secondary to pegaspargase [not all indications, routes, dosages and outcomes stated; duration of treatments to reactions onsets not stated]. A 20-year-old woman, who had a history of severe aplastic anaemia, diffuse large B-cell lymphoma and a persistent paroxysmal nocturnal haemoglobinuria clone, underwent haematopoietic stem cell transplant following conditioning regimen with 2 doses of cyclophosphamide 60 mg/kg and total body irradiation. Post-transplant, she received unspecified steroids, tacrolimus, and methotrexate for graft versus host disease (GVHD) prophylaxis. On day 81 post-transplant, she also received immune globulin. She developed intestinal GVHD. She received immunosuppressive therapy with tacrolimus, basiliximab, ruxolitinib, sirolimus and unspecified oral, topical and IV steroids. She developed stage I to II hypertension. Hence, she was treated with unspecified calcium channel blockers and unspecified angiotensin converting enzyme-1 inhibitors with inadequate response. She was hospitalised several times for pancytopenia episodes, pulmonary oedema, community acquired pneumonia and bloody stools [aetiologies unknown]. During these admissions, she remained hypokalaemic and hypotensive despite increase in the doses and addition of more unspecified antihypertensive medications. The transbulbar potassium gradient was 3, which was consistent with urinary potassium losses and her gastrointestinal losses. She became thrombocytopenic from day 100. Her hypokalaemia was in chronic stage. After 2 weeks, she became transfusion dependent from day 249. On day 292, angiotensin II type 1 receptor activating autoantibodies level was 16 U/mL. Subsequently, unspecified angiotensin converting enzymes-1 inhibitors were discontinued and she was treated with losartan. Her diarrhoea resolved within few days after initiation of losartan. She had been on budesonide for prolonged diarrhoea. Her serum potassium level normalised completely; however, her BP remained in the stage I hypertension range despite adjustment in the losartan dosing. After one week, the creatinine level increased to 1.32 mg/dL from 1 mg/dL. Subsequently, tacrolimus therapy was changed to sirolimus, but her acute kidney injury worsened (creatinine level at 3.2 mg/dL). She developed pulmonary haemorrhage. She was diagnosed with transplant-associated thrombotic microangiopathy, which responded well to eculizumab with improvemen
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