HOSHINO Junichi
   Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine
   Position   Professor and Division head
Article types Original article
Language English
Peer review Non peer reviewed
Title Abatacept Improves Intractable Protein-Losing Enteropathy Secondary to AA Amyloidosis in a Patient With Rheumatoid Arthritis
Journal Formal name:Mayo Clinic proceedings. Innovations, quality & outcomes
Abbreviation:Mayo Clin Proc Innov Qual Outcomes
ISSN code:25424548/25424548
Domestic / ForeginForegin
Volume, Issue, Page 4(6),pp.815-820
Author and coauthor Sawamura Masato, Sawa Naoki, Fujiwara Hideomi, Yamanouchi Masayuki, Hayami Noriko, Sekine Akinari, Mizuno Hiroki, Hasegawa Eiko, Suwabe Tatsuya, Hoshino Junichi, Kinowaki Keiichi, Fujii Takeshi, Ubara Yoshifumi
Publication date 2020/12
Summary A 71-year-old Japanese woman with a history of rheumatoid arthritis of 50 years' duration was admitted to our hospital with refractory diarrhea. Endoscopic biopsy revealed AA amyloid deposition in the large intestine. Although the patient had been prescribed 5 tumor necrosis factor inhibitors over the past 10 years, rheumatoid arthritis was poorly controlled, with a Disease Activity Score 28 using C-reactive protein score of 6.52 on admission. Treatment with tocilizumab (8 mg/kg every 2 weeks) was initiated, but this was ineffective. After 3 months, abatacept (cytotoxic T-lymphocyte-associated antigen 4 immunoglobulin) was initiated (750 mg/mo) and the patient's diarrhea began to improve. After 3 months of abatacept treatment, serum albumin, C-reactive protein, and serum amyloid A levels had all decreased to within normal ranges. After 3 years of abatacept treatment, a repeat biopsy of the large intestine revealed a marked improvement in amyloid deposition. Interleukin 6 is a key factor in AA amyloid formation, but this case suggests that T-cell activation increases the production of cytokines (including interleukin 6) via a mechanism involving cytotoxic T-lymphocyte-associated antigen 4, resulting in a second key factor of AA amyloid formation.
DOI 10.1016/j.mayocpiqo.2020.07.007
PMID 33367218