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  1. D. Petrovich1,
  2. D. Roggenbuck2,
  3. M. Volkava3,
  4. U. Kundzer4
  1. 1Mogilev Regional Hospital, Mogilev, Belarus
  2. 2BTU, Cottbus-Senftenberg, Germany
  3. 3BelMAPGE, Minsk, Belarus
  4. 4Liceum of BSU, Minsk, Belarus


Background: The search for new methods for predicting the effectiveness of treatment for biologics is important issue.

Objectives: To study antinuclear antibodies (ANA) levels during of AS treatment by infliximab and evaluate the influence of ANA on treatment outcome

Methods: The presence of antinuclear antibodies (ANA) in 53 ankylosing spondylitis (AS) patients (44 men (83.02%), and 9 women (16.98%), 37.19 ± 9.38 years (95% CI: 34.60-39.78) treated with infliximab was determined by indirect immunofluorescence on an automated AKLIDES system in a serum titer of 1/80 initially (before treatment with infliximab) and at week 30 (before 7 administration). Specific autoantibodies were analyzed on the AKLIDES Cytobead platform using the following antigens SS-A 52, SS-A 60, SS-B, ds-DNA, CENP-B, Sm, RNP / Sm. ANA research was carried out at the Brandenburg Technical University (Senftenberg, Germany). Evaluation of the effectiveness of infliximab therapy was carried out by determining ASDAS-CRP at baseline, at the 14th, 30th and 54th weeks.

Results: A positive nuclear type of ANA was determined initially in 2 out of 53 patients (3.77%) (in one case, the type of luminescence was nucleolar, in the other - speckled), at the 30th week of observation, 16 out of 53 patients became seropositive for ANA (30.18%). The frequency of occurrence of ANA at the 30th week of treatment was significantly higher than the baseline (p <0.0001). Positive results for the determination of specific autoantibodies to at least one nuclear antigen were found in 7 of 16 (43.75%) ANA-positive patients. In all cases, Anti-SS-A 60 (100%) was detected.

In the group of patients in whom treatment with infliximab was ineffective at the 54th week of observation, ANA positivity was observed in 10 (55.5%). In the case of treatment effectiveness at the 54th week of ANA, positivity was not observed at the 30th week. Differences in the incidence of ANA in patients with effective and ineffective treatment at week 54 were statistically significant (p <0.0001). Anti-infliximab antibodies were significantly more common in ANA-positive patients at week 30 of treatment with infliximab (p = 0.002, Fisher’s exact test).

The appearance of ANA at the 30th week of infliximab therapy was inversely related to the absence of secondary resistance at the 54th week of treatment according to the ASDAS-CRP criteria (OR 0.026; 95% CI: 0.002-0.039; p = 0.0007), which allows us to use the results of the determination of ANA at the 30th week of treatment with infliximab as a predictor of secondary resistance to treatment at the 54th week. When testing the method for predicting secondary resistance to treatment with infliximab at week 54 based on the results of determining ANA at week 30 of treatment in a control sample of 12 patients with AS, it was found that the method is statistically significant (p = 0.0015, Fisher’s exact test).

Conclusion: Assessment of ANA positivity at week 30 of treatment with infliximab can be seen a predictor of the development of secondary resistance to infliximab at the 54th week of treatment.

Disclosure of Interests: None declared

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