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Nephritis, cerebritis, and myositis after adalimumab therapy in a patient with
rheumatoid arthritis: a case report
#MMPMID29692623
Omran NE
; Noorwali AA
Int J Gen Med
2018[]; 11
(?): 151-154
PMID29692623
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Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that
mainly affects the joints, therefore, may cause deformities and disability if
untreated. The first line of treatment is disease-modifying antirheumatic drugs
(DMARDs). When the patient fails to respond to DMARDs, mainly methotrexate, then
second-line therapy is required. Tumor necrosis factor ? (TNF?) plays an
important role in the pathogenesis of RA; however, the treatment with anti-TNF?
medications is challenging. It may trigger the autoimmune system and result in
producing antibodies that induce symptoms and signs mimic to systemic lupus
erythematosus (SLE), and in rare situations can affect vital organs with severe
and life-threatening complications. We report on a 38-year-old Saudi woman with
longstanding erosive RA, who was diagnosed based on the 1987 classification
criteria. She developed life-threatening SLE, and seroconversion of antinuclear
antibodies (ANA), anti-double-stranded DNA, with severe systemic involvement
(cerebritis, nephritis, myositis, and polyneuropathy), shortly after treatment
with adalimumab. Adalimumab was started as anti TNFa therapy (after the failure
of traditional therapy), SLE and other autoimmune diseases were ruled out by
clinical history, examination, and laboratory investigations, including negative
ANAs and anti-double-stranded DNA. When both tests turned out persistently
positive even after stopping adalimumab, specific diagnostic and therapeutic
modalities were required during her acute illness.
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