Tacrolimus
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Tacrolimus-induced thrombotic microangiopathy: case report A 67-year-old man developed tacrolimus-induced thrombotic microangiopathy (TMA) during immunosuppressive treatment with tacrolimus. The man had a medical history of liver transplantation, heart failure, atrial fibrillation, hypertension and type 2 diabetes mellitus. He had been receiving immunosuppressive therapy with tacrolimus [route and dosage not stated] and prednisone. Additionally, he had been receiving apixaban concomitantly for atrial fibrillation. He was admitted to an outside hospital with painful and necrotic ulcerations of the left first metatarsal and fifth toes 4 months previously. During this hospitalisation, he was diagnosed with bilateral pulmonary emboli, subclavian clots, and thrombocytopenia. Skin biopsy showed intravascular clots and shaggy perivascular deposits of C4d. Then, he was diagnosed with tacrolimus-induced TMA [duration of treatment to reaction onset not stated]. The man was treated with 7 sessions of plasmapheresis. An improvement in thrombocytopenia and some of his lower extremity ulcerations was noted. However, he did require amputation of his left great toe. Due to concern for tacrolimus-induced TMA, tacrolimus was switched to ciclosporin [cyclosporine]. However, he developed thrombocytopenia associated with ciclosporin. Thus, ciclosporin was switched to everolimus. After 2 weeks, he was admitted hospital with worsening necrotic lesions and ulcerations of the left first metatarsal and fifth toes with significant spread to his bilateral lower extremities (current presentation). At the time of examination, he was in mild distress. Investigations showed the following: body temperate 99.3 °F, BP 103/73mm Hg, pulse rate 117 beats per minute and oxygen saturation 94% on 6 liters of O2 via nasal cannula. Jugular vein dilatation and bilateral lower extremity oedema was noted. The left foot was cool and dusky with oedema and the first left great toe was amputated-pulses present. His amputation site was dry and black and the tip of the third toe was black. Large open wounds were present on the bilateral shins. The left lateral leg ulcer (8 × 3cm) was also observed. The wound base was moist, yellow, and black. The right medial leg ulcer (6.5 × 5.5cm) at the skin level with a dry and black wound base. Bilateral arms had ecchymosis with a left arm ulcer (3 × 1.5 × 0.2cm). The wound base was moist and yellow with scant discharge. Laboratory investigations showed the following: haemoglobin 9.0 g/dL, platelet count 30,000 /µL, creatinine 1.33 mg/ dL, prothrombin time 17.9 seconds, INR 1.6, partial thromboplastin time 27.2 seconds, haptoglobin 463 mg/dL, lactate dehydrogenase 407 U/L, CRP 192.7 mg/L, proteinuria 5.7g per 24 hours and sedimentation rate 49 mm/h. He was continued on prednisone and everolimus. Computed tomography angiogram of the bilateral lower extremities showed
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