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Various toxicities and off-label use: case report A 43-year-old man developed BK viremia and viruria during treatment with antithymocyte-globulin for acute cellular rejection post-kidney transplantation, and pink eye during immunosuppression therapy with mycophenolate-mofetil, prednisone, tacrolimus, dexamethasone, and off-label venetoclax treatment for light chain deposition disease [not all dosages stated; routes, durations of treatments to reactions onsets and outcomes not stated]. The man presented with a serum creatinine of 3.7 mg/dL, proteinuria and sudden-onset lower extremity oedema in 2011. Based on further investigation, he was diagnosed with light chain deposition disease secondary to monoclonal gammopathy of renal significance (MGRS). Therefore, he was started on bortezomib, cyclophosphamide, and dexamethasone induction therapy and achieved a very good partial response (VGPR). Subsequently, he had undergone an autologous stem cell transplantation conditioned with melphalan. One month after the transplantation, he developed a rash with 31% peripheral eosinophilia and a slight elevation in creatinine was noted. His prophylaxis treatment with penicillin was switched to doxycycline and he was initiated on prednisone treatment. Despite treatment, his creatine level was elevated. So, he was initiated on haemodialysis. Thereafter, in 2013, he underwent total thyroidectomy for papillary thyroid carcinoma successfully. In 2016, he had undergone a living donor kidney transplant under maintenance therapy with tacrolimus, mycophenolate mofetil and prednisone. Three months after the kidney transplant, a marked drop in the serum-free light chain (sFLC) and lambda were noted. Six months post-kidney transplant, an episode of acute cellular rejection was diagnosed, which was treated with antithymocyte-globulin [anti-thymocyte antibody]. However, he developed BK viremia and viruria secondary to antithymocyte-globulin. In view of BK viremia and viruria, the man’s immunosuppression therapy was reduced. Later, due to the prevention of the development of light chain deposition disease, he was started on ixazomib, cyclophosphamide and dexamethasone 20mg weekly. For infection prophylaxis, aciclovir [acyclovir] and cotrimoxazole [trimethoprim/sulfamethoxazole] were added in his treatment. During the first 6 months of therapy, he received only 1 cylce of ixazomib due to insurance issue and elevation in his sFLC and kappa to lambda ratio were noted, which was continued after receiving regular ixazomib therapy. He denied IV or SC medications. Therefore, he was started on off-label treatment with venetoclax [initial dosages not stated] and achieved a dose of 800mg daily by rapid escalation protocol. His cyclophosphamide treatment was immediately stopped. After 1 cylce, he achieved a complete response with improvement in sFLC kappa to lambda ratio were noted. Later, his ixazomib treatment was discontinued and he was started on dexamethasone 8mg weekly along with the continuation of venetoclax. However, he developed an episode o