Background and Aims

Rheumatoid Arthritis (RA) is a chronic immune -mediated disease characterized by pro-inflammatory cytokine production, synovial hypertrophy, cartilage and bone destruction resulting in severe disability. Cytokine-mediated immunity plays a major role in the pathogenesis of RA. Interleukin-33 (IL-33) is a pro-inflammatory cytokine from the IL-1 family that is expressed by tissue damage. IL-33 has been detected in high levels and has profound effects in experimental inflammatory arthritis.

The aim of the present study was to investigate the effect of IL-33 in the serum of RA patients and to evaluate the correlation of serum IL-33 with disease activity, laboratory parameters and clinical manifestations.

Methods

Sixty (44 females, 16 males) RA patients, mean age 43.53(10.88) years diagnosed according to the ACR/EULAR criteria for RA and 40 age/sex-matched healthy controls were enrolled in this study. Information on disease duration, disease severity and activity, comorbidities and medications (conventional disease modifying anti-rheumatic drugs and biological therapies) was collected. Serum levels of Il-33 were measured using an enzyme-linked immunoabsorbent assay (ELISA). Disease activity was assessed by the Disease Activity Score 28 (DAS-28).

Results

Serum Il-33 levels were significantly higher in RA patients compared to controls and correlated with disease severity, DAS28, erythrocyte sedimentation rate, C-reactive protein, rheumatoid factor (RF)-IgM, RF-IgG, anticitrullinated peptide antibodies (ACPA), TNFα and IL-6. Serum IL-33 levels decreased significantly in RA patients that had received anti-TNF and IL-6 inhibitors.

Conclusions

IL-33 appears to play a pivotal role in the pathogenesis of RA and could be a new therapeutic target. IL-33 is a reliable biomarker of disease activity and severity..

Background and Aims

Neuromyelitis optica (NMO), neuromyelitis optica spectrum disorders (NMOSD) and transverse myelitis are auto-antibody mediated chronic inflammatory demyelinating CNS diseases that can occur idiopathic or in conjunction or may overlap with autoimmune rheumatic diseases. Although rare, these immune-mediated CNS diseases pose a diagnostic and therapeutic challenge to the treating physician posing a dilemma in clinical practice.

Methods

To illustrate the difficulty and dilemma in distinguishing NPSLE from NMOSD we present a case report of a 42-year-old female with a six-year history of SLE that presented with a 2-day complaint of progressive numbness and flaccid paralysis in both legs, fatigue and a malar rash. She then developed urinary and rectal incontinence and was unable to walk or stand unassisted. Flaccid leg paralysis, lower extremity paresthesia, and a positive Babinski response on the right side were noted on physical exam.The workup included serology for antinuclear, anti-double-stranded, antiphospholipid antibodies, blood count, ESR and CRP, lumbar puncture and MRI of her spine and brain.

Results

Workup revealed strong ANA positivity, NMO-IgG antibody (antibody to aquaporin 4 IgG (AQP4-IgG)) was positive and MRI of the spine demonstrated extensive hyperintense T2 signal abnormality throughout the spinal cord.

Conclusions

This case is further evidence that they can be co-existing conditions and although demyelination can be related to SLE activity it can sometimes be difficult to distinguish NPSLE from NMOSD. Early recognition of NMOSD in patients with autoimmune rheumatic diseases presenting with a CNS event is key.The therapeutic implications of these relationships are important because they can influence the timing and selection of immunosuppressive therapy.