BackgroundWe assessed the efficacy of serial interferon-gamma release assays (IGRAs) for the diagnosis of latent tuberculosis infection (LTBI) in patients receiving immunosuppressive agents for treatment of rheumatic diseases in Korea.MethodsOf 276 patients who underwent consecutive screening with one of two IGRAs [QuantiFERON-TB Gold or QuantiFERON-TB Gold In-Tube], 66 patients were evaluated by the serial IGRA for detection of LTBI during therapy with immunosuppressive agents. Information on clinical diagnosis, medication, previous TB, blood cell count, tuberculin skin test, and interferon-gamma (IFN-γ) level measured by IGRA was collected.ResultsOf the 66 patients, the initial IGRA was positive in 24.2%, negative in 65.2%, and indeterminate in 10.6%. Forty-six patients (69.7%) showed consistent IGRA results during follow-up, and 13 patients (19.7%) had consistently positive results. IGRA conversion rate was 12.1% (8/66) and reversion rate was 4.5% (3/66). Conversion of IGRA results was only observed in ankylosing spondylitis patients, and the median interval between the two tests in patients with conversion was 8.5 months. The mean IFN-γ level in the group of patients with consistently positive IGRA results was higher than that in the group with inconsistently positive results, although this trend was not statistically significant (P=0.293). Indeterminate results were observed most frequently in patients with systemic lupus erythematosus.ConclusionsIn patients receiving immunosuppressive agents, both IGRA conversions and reversions were observed. Serial IGRA testing may not be needed in patients with a positive initial IGRA result showing high IFN-γ levels, because of high consistency in the test results.

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This study designed to assess the relationship between tumor necrosis factor (TNF)-α promoter polymorphisms and disease susceptibility to human leukocyte antigen (HLA)-B27-positive ankylosing spondylitis (AS). One hundred and nineteen HLA-B27(+) AS patients, 95 HLA-B27(+) healthy controls, and 135 random healthy controls were enrolled in this study. Six single nucleotide polymorphisms (SNPs) of the TNF-α promoter at positions -1031T/C, -863C/A, -857C/T, -646G/A, -308G/A, and -238G/A were analyzed. Differences between groups were evaluated using the chi-square test or Fisher's exact test. Haplotypes from each SNP were constructed, and differences in haplotypic frequencies between groups were evaluated. There were significant differences in the allelic and genotypic frequencies of 1031T/C, -863C/A, and -857C/T TNF-α promoters polymorphisms between HLA-B27(+) AS patients and random controls, but not between patients with AS and HLA-B27(+) healthy individuals. TNF-α polymorphisms did not influence the extra-spinal clinical features in patients with AS. The haplotypic sequence -1031T/-863C/-857C/-308G increased the risk of susceptibility to AS compared to random controls (P (corr) < 0.001, OR = 2.756, 95% CI = 1.894-4.010), whereas the sequence -1031C/-863A/-857C/-308G appeared to be associated with decreased susceptibility to AS compared to random controls (P (corr) = 0.006, OR = 0.396, 95% CI = 0.231-0.679). This study indicates that TNF-α promoter polymorphism between controls and AS patients with HLA-B27(+) genetic background is not associated with susceptibility to AS. However, TNF-α polymorphism, irrespective of HLA-B27, increases risk of susceptibility to AS in general population.

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Behçet's disease (BD) is a multisystem disorder characterized by vasculitis. Pulmonary vascular problems such as pulmonary artery aneurysms (PAA) are reported to indicate poor prognosis and high mortality. We describe a 43-year-old man who presented with life threatening bilateral PAA and thromboembolic disease due to BD. He was treated with prednisone and pulse cyclophosphamide and was poorly responsive to the conventional immunosuppression. The introduction of adalimumab therapy stabilized his PAA. We report that the inhibition of TNF-alpha using the neutralizing monoclonal antibody adalimumab has the potential to induce rapid, complete, and long-lasting remission in a life-threatening manifestation of BD.