Nephritis, cerebritis, and myositis after adalimumab therapy in a patient with rheumatoid arthritis: a case report
International Journal of General Medicine
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Nephritis, cerebritis, and myositis after
adalimumab therapy in a patient with rheumatoid
arthritis: a case report
This article was published in the following Dove Press journal:
International Journal of General Medicine
Narges E Omran 1
Abdulsalam A Noorwali 2
1
Department of Internal Medicine
and Rheumatology, Al-Noor Specialist
Hospital, Makkah, Saudi Arabia;
2
Department of Internal Medicine
and Rheumatology, Umm Al Qura
University Hospital, Makkah, Saudi
Arabia
Introduction
Correspondence: Narges E Omran
Department of Internal Medicine and
Rheumatology, Al-Noor Specialist
Hospital, PO Box 6251, Makkah 21955,
Saudi Arabia
Tel +966 59 442 1399
Email
Early diagnosis and treatment of rheumatoid arthritis (RA) is very important. The use
of disease-modifying antirheumatic drugs (DMARDs) during the first few months of
the disease minimizes the adverse sequelae of RA.2 For non-responders, biological
agents are recommended.3 Although the treatment with antitumor necrosis factor alpha
(anti-TNFα) had been shown to trigger autoimmune responses, such as a lupus-like
syndrome,1 the clinical presentation of immune-mediated complications induced by
adalimumab treatment, especially a lupus-like syndrome, is very rare,17 with various
signs and symptoms, including the less common induction of systemic lupus erythematosus (SLE) with end-organ damage.4 Written informed consent has been provided
by the patient to have the case details and pictures published.
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http://dx.doi.org/10.2147/IJGM.S154835
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Abstract: 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 α (TNFα) plays an important role in the pathogenesis of RA; however, the
treatment with anti-TNFα 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.
Keywords: rheumatoid, arthritis, tumor necrosis factor, adalimumab, anti-TNF, systemic lupus
erythematosus
Omran and Noorwali
International Journal of General Medicine downloaded from https://www.dovepress.com/ by 175.212.112.4 on 04-Jun-2020
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Case presentation
A 38-year-old Saudi woman presented to the emergency
department with generalized fatigue and weakness. She had
been affected by RA for 13 years, RA was diagnosed based on
the 1987 diagnostic criteria,5 according to which, the patient
had bilateral hand polysymmetric inflammatory arthritis with
morning stiffness for more than 1 hour and positive rheumatoid radiographic abnormalities on X ray (periarticular
osteopenia, decreased joint space, and marginal erosions).
She developed bilateral hand irreversible deformities within
the first 2 years of her disease (ulnar deviation, Z deformity,
swan neck, and boutonniere deformities), with restricted
wrists movement and impaired hand grip (Figure 1).
She had no previous history of skin rash, malar rash,
muscle weakness, numbness, and no cardiopulmonary symptoms or any symptoms or signs suggestive of SLE or other
associated autoimmune diseases.
She was treated for several years with DMARDs; methotrexate 15 mg/week, hydroxychloroquine 200 mg twice daily,
and steroid with a maintenance dose of prednisolone 7.5
mg daily (she was given frequent short courses of steroid),
as well as calcium, vitamin D, and alendronate. During the
course of the treatment, there were periods of remission and
flare up. Due to persistent and active inflammatory arthritis
for almost 6 months, she was followed up in the rheumatology clinic with the following: number of swollen joints:10;
number of tender joints: 15; morning stiffness for more than 1
hour; high erythrocyte sedimentation rate (ESR); and positive
C-reactive protein. Her disease activity assessment (28) score
of 5.2 meant that she had highly active disease.6 Adalimumab
was added to her treatment as second-line therapy after the
failure of traditional DMARDs based on the American Col-
Figure 1 Rheumatoid arthritis of the hand with deformity.
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lege of Rheumatology treatment guidelines.3 Initial laboratory results showed normal liver and kidney function, mild
normocytic normochromic anemia, high ESR of 50 mm/h,
C-reactive protein 4 mg/dL, rheumatoid factor 456, and anticyclic citrullinated peptide being strongly positive. Hepatitis
B and C serology were normal, with a negative antinuclear
antibody (ANA) of 0.3 IU/mL (<1), a negative anti-DNA
15 IU/mL (<30), a negative purified protein derivative test,
and normal chest X-ray. Her arthritic symptoms improved
dramatically. However, 6 weeks after the administration of
adalimumab, she (...truncated)