Reactions Weekly | 2019

Bevacizumab

 

Abstract


IgA vasculitis and thrombotic microangiopathy: case report A 67-year-old man developed IgA vasculitis and thrombotic microangiopathy during treatment with bevacizumab for metastatic rectal cancer. The man, who was diagnosed with T4N2M1 stage IV rectal adenocarcinoma, underwent resection of the low anterior rectum. He had a history of hyperuricaemia and wellcontrolled hypertension. He also had a history of proteinuria and haematuria, which improved in the past 2 years. One month after the resection, he started receiving bevacizumab 660mg [route and frequency not stated], along with gimeracil/ oteracil/tegafur [S-1] and oxaliplatin. Six months later, he developed oedema and purpura. The following month, he was transferred to the nephrology clinic. He had gained weight of 7Kgs and developed painful purpuras scattered from the toes to the distal femurs. Concomitantly, he had been receiving various medications for hypertension. Urinalysis revealed a spot urine protein/creatinine ratio of 15 g/g creatinine, and RBC of 50 to 99 /high-power field with fatty, granular, waxy and epithelial casts. Additionally, hypoproteinaemia and hypoalbuminaemia was noted. His serum creatinine level was 1 mg/dL, and serum IgA level was 424 mg/dL. Subsequently, a renal biopsy was performed, and histological examination showed endocapillary hypercellularity with lymphocyte and neutrophil infiltration. Also, mild mesangial hypercellularity was noted. Some of the glomeruli revealed double contour of the glomerular basement membrane and mesangiolysis, which indicated thrombotic microangiopathy. An arterial vessel revealed mild sclerosis with interstitial fibrotic and tubular atrophic changes. Immunofluorescence revealed granular mesangial deposition of galactose-deficient-IgA1, IgA and complement component 3 (C3). Electron microscopy revealed inflammatory cell infiltration and mesangial cell proliferation. He also had purpuric ulcerated lesions on the left ankle. A skin biopsy revealed several neutrophils around vessels with nuclear fragments, which were consistent with leucocytoclastic vasculitis. Therefore, he was diagnosed with bevacizumab-induced IgA vasculitis and nephrotic syndrome. Hence, the man’s therapy with bevacizumab was stopped, and subsequently, proteinuria and purpura improved. Also, the spot urine protein/creatinine ratio and creatinine levels improved. Author comment: To our knowledge, this is the first case of bevacizumab-related immunoglobulin A vasculitis with nephritis, as evidenced by galactose-deficient immunoglobulin A1. [Thrombotic microangiopathy] as well as [immunoglobulin A vasculitis with nephritis] are considered as the causes of nephrotic syndrome.

Volume 1784
Pages 64 - 64
DOI 10.1007/s40278-019-72783-x
Language English
Journal Reactions Weekly

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