title: Tocilizumab improves cardiac disease in a hemodialysis patient with AA amyloidosis secondary to rheumatoid arthritis.
abstract: A 58-year-old Japanese woman on hemodialysis (HD) was admitted for intractable rheumatoid arthritis. Even after HD was started due to end-stage renal failure in 2004, her arthropathy worsened. A soluble tumor necrosis factor receptor inhibitor (etanercept at 25 mg twice weekly), tacrolimus (2 mg daily), and prednisolone (10 mg daily) had been administered since 2005, but high disease activity had persisted. She was admitted to our hospital in July 2007. C-reactive protein (CRP) was 6.8 mg/dL, and the DAS-CRP score was calculated to be 8.3. The cardiothoracic ratio (CTR) was 62% on a chest radiograph, but dialysis hypotension was remarkable. Left ventricular mass (LVM) was calculated as 320 g using echocardiography. Endoscopic biopsy of the stomach and duodenum revealed heavy deposition of AA amyloid. Etanercept was discontinued and tocilizumab was started at a dose of 320 mg (8 mg/kg) monthly. Even after predonisolone and tacrolimus were tapered gradually and discontinued because of her good response, CRP and DAS-CRP became 0.0 mg/dL and 1.5, respectively. In September 2011, re-evaluation was performed. CTR was reduced to 51% and LVM was decreased to 180 g. Endoscopic biopsy of the stomach and duodenum revealed disappearance of AA amyloid. Although AA amyloidosis of the gastrointestinal tract has already been reported to be improved by tocilizumab, this is the first report on improvement of myocardial hypertrophy as well as dialysis hypotension.
authors.affiliation: Nephrology Center, Kanagawa, Okinaka Memorial Institute for Medical Research,Toranomon Hospital Kajigaya, Japan. 313hat@gmail.com
authors.forename: Yoshinari
authors.initials: Y
authors.lastname: Hattori
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Ubara
authors.forename: Keiichi
authors.initials: K
authors.lastname: Sumida
authors.forename: Rikako
authors.initials: R
authors.lastname: Hiramatsu
authors.forename: Eiko
authors.initials: E
authors.lastname: Hasegawa
authors.forename: Masayuki
authors.initials: M
authors.lastname: Yamanouchi
authors.forename: Noriko
authors.initials: N
authors.lastname: Hayami
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Suwabe
authors.forename: Junichi
authors.initials: J
authors.lastname: Hoshino
authors.forename: Naoki
authors.initials: N
authors.lastname: Sawa
authors.forename: Kenichi
authors.initials: K
authors.lastname: Oohashi
authors.forename: Kenmei
authors.initials: K
authors.lastname: Takaichi
mesh_terms: D000686:Amyloidosis / Q000175:diagnosis* / Q000188:drug therapy / Q000209:etiology; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000150:complications* / Q000188:drug therapy; D004386:Duodenum / Q000473:pathology; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis* / Q000188:drug therapy / Q000209:etiology; D007022:Hypotension / Q000188:drug therapy / Q000209:etiology; D008875:Middle Aged; D006435:Renal Dialysis; D000685:Serum Amyloid A Protein / Q000378:metabolism*; D016896:Treatment Outcome
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D000685:Serum Amyloid A Protein; C502936:tocilizumab