Dexamethasone/lenalidomide
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Various toxicities: case report A case report described a woman in her 80s [exact age at the time of reaction onset not stated], who developed a paradoxical worsening of N-terminale-pro hormone B-type natriuretic peptide (NT-proBNP), congestive heart failure and anasarca during treatment with lenalidomide for immunoglobulin heavy-and-light-chain amyloidosis (AH/AL Amyloidosis). Additionally, she developed fluid overload during treatment with dexamethasone for AH/AL Amyloidosis. The woman sought care in April 2016, at the age of 83 years, for painful lower extremity sensory neuropathy. She had undergone bilateral carpal tunnel release a few years previously. Examination revealed IgG-λ monoclonal gammopathy with an additional monoclonal free λ component. No amyloidosis was noted. The cardiac biomarker troponin I was normal, but NTproBNP had elevated to 1464 pg/mL. By January 2018, haemoglobin had dropped to 9.9 g/dL, and stage 3 chronic kidney disease with proteinuria were identified. By June 2018, she developed shortness of breath on minimal exertion, and NTproBNP had increased to 3397 pg/mL. At this point, a renal biopsy was performed, which showed amyloid with predominant staining for IgG heavy chain with a smaller amount of signal for λ light chain (LC) by immunofluorescence. These findings were consistent with either immunoglobulin heavy chain amyloidosis (AH) with some nonspecific trapping of lambda LC or an IgG lambda AH/AL. After further investigations, she was diagnosed with AH/AL. She started receiving cyclophosphamide, bortezomib and dexamethasone (CyBorD) therapy and achieved a partial haematologic response in 3 months. However, due to worsening peripheral neuropathy and myelosuppression (aetiology unknown), the CyBorD therapy was discontinued in September 2018. Thereafter, she started receiving lenalidomide 10mg daily and dexamethasone 20mg weekly (Rd) therapy [routes not stated]. However, this treatment was complicated by the paradoxical increase in underlying elevated NT-proBNP, along with congestive heart failure and anasarca. It was thought that, dexamethasoneinduced fluid overload might have played a role in her clinical decompensation [durations of treatments to reactions onsets not stated]. The woman’s treatment with lenalidomide and dexamethasone was discontinued. Both anasarca and congestive heart failure resolved with the discontinuation of lenalidomide and dexamethasone. In October 2018, the woman was started on dexamethasone and daratumumab. She experienced complete haematologic response after 8 doses. At the time of this report, she was receiving daratumumab maintenance therapy every 8 weeks, and her disease was in complete remission. She had received 30 doses of daratumumab without complications. She had also experienced complete renal and cardiac response with the normalisation of proteinuria and NT-proBNP. Chaulagain CP, et al. How We Manage Systemic Immunoglobulin Heavy Chain Amyloidosis (AH Amyloidosis) and Immunoglobulin Heavy-and-Light-Chain Amyloidosis 803507754 (AH/AL Amyloidos
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