Effect of etanercept on serum amyloid A protein (SAA) levels in patients with AA amyloidosis complicating inflammatory arthritis

• Published in: Clinical rheumatology Vol. 27; no. 7; pp. 923 - 925
• Main Authors: Perry, M. E., Stirling, Anne, Hunter, J. A.
• Format: Journal Article
• Language: English
• Published: London Springer-Verlag 01.07.2008; Springer Nature B.V
• Subjects: Amyloidosis - blood; Amyloidosis - drug therapy; Brief Report; Cohort Studies; Diabetes; Drug therapy; Etanercept; Female; Humans; Immunoglobulin G - therapeutic use; Male; Medicine; Medicine & Public Health; Receptors, Tumor Necrosis Factor - therapeutic use; Retrospective Studies; Rheumatology; Serum Amyloid A Protein - metabolism; Tumor Necrosis Factor-alpha - antagonists & inhibitors; Tumour necrosis factor inhibitors; Amyloidosis; Inflammation
• ISSN: 0770-3198; 1434-9949
• DOI: 10.1007/s10067-008-0875-3

We assessed changes in serum amyloid A protein (SAA) levels during treatment with etanercept in AA amyloidosis complicating inflammatory arthritis. Five women and four men with AA amyloidosis and inflammatory arthritis received etanercept. SAA levels were recorded before and after commencement of treatment. Previous immunosuppressive drugs included cyclophosphamide (four patients), azathioprine (three patients), methotrexate (two patients) and chlorambucil (in one patient). Two patients received no disease modifying drugs between the time of diagnosis of AA amyloidosis and commencement of etanercept. In seven out of nine patients the median SAA level during etanercept treatment was lower than levels before anti-tumour necrosis factor therapy. In five out of nine patients, the median post treatment level was <11 mg/l. There were no significant changes in serum creatinine or proteinuria during periods (median, 23 months; range, 1–24 months) of etanercept therapy. The etanercept was stopped in four patients because of: acute bacterial endocarditis, psoriasiform rash, psychosis and leukopenia. In two of these patients alternative biologics were commenced (adalimumab or anakinra) and one was restarted on etanercept. One patient died of cerebral haemorrhage during the study. Etanercept therapy was associated with a fall in SAA levels in seven of nine patients, five of whom achieved levels which might be expected to be associated with stable or regressing amyloid deposits. Etanercept represents a useful alternative to immunosuppressant therapy such as cyclophosphamide or chlorambucil. Further work is needed to establish whether organ damage related to AA amyloidosis is slowed by etanercept.