Hypertrophic pachymeningitis in rheumatoid arthritis after adalimumab administration.
Tumor necrosis factor-a (TNF-a) inhibition, used in the treatment of rheumatoid arthritis (RA), is associated with central nervous system (CNS) events including new onset and/or exacerbations of pre-existing demyelinating neurological diseases. We describe a patient with refractory RA where adalimumab, a fully humanized IgG1 monoclonal antibody against TNF-a, may have contributed to the development of meningoencephalitis, with brain biopsy suggestive of hypertrophic pachymeningitis, a rare complication of this disease. The patient had recurrence of neurological symptoms upon repeated administration of adalimumab, and resolution of symptoms after withdrawal.
Ahmed
Mansoor
M
Division of Immunology, Department of Medicine, University of Cincinnati Medical Center, 231 Albert Sabin Way, Cincinnati, OH 45267, USA.
Luggen
Michael
M
Herman
Jerome H
JH
Weiss
Kenneth L
KL
Decourten-Myers
Gabrielle
G
Quinlan
John G
JG
Khanna
Dinesh
D
D000068879:Adalimumab; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage; D000911:Antibodies, Monoclonal / Q000009:adverse effects*; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000009:adverse effects*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D006651:Histocytochemistry; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008581:Meningitis / Q000139:chemically induced* / Q000175:diagnosis / Q000188:drug therapy; D011241:Prednisone / Q000008:administration & dosage
D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D000068879:Adalimumab; D011241:Prednisone