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Background: The role of galectin-3, a pro-inflammatory mediator involved in autoimmune disorders in patients with rheumatoid arthritis (RA), is discussed in the literature.
Objectives: To clarify the relationship of clinical and laboratory manifestations of RA with galectin-3 with the ineffectiveness of basic anti-inflammatory therapy and after 12 months of treatment with biological drugs.
Methods: The study included 47pts (39 women /8 men) with RA, 51 [39,0; 63,0] years old. Pts were seropositive for IgM RF (79%) and anti-CCP (62%), with highly active RA (DAS28 5,7 [5,2; 6,4]; SDAI 35,0 [29,1; 43,6], CDAI 34,0 [25,0; 43,0]) scores, and median disease duration of 4.0 [3,0;14.0] years. All patients with RA had a history of insufficient effect or intolerance to two or more basic anti-inflammatory drugs (DMARDs). At the time of inclusion in the study, patients received DMARDs: 44% of patients received methotrexate (median dose - 15 (15; 20) mg /week), 35% - leflunomide (20 mg/day), 9.3 % - sulfasalazine (2000 mg/day), 7% - hydroxychloroquine (200 mg/day), 67.4% - glucocorticoids (5 (4;8) mg /day). Patients did not receive biological therapy at the time of inclusion in the study. Due to lack of efficacy or intolerance, patients with RA (n=21) were prescribed biological therapy: 52.4% - anti-B-cell therapy, 38% - TNF-alpha inhibitors, 9.6% - IL-6 inhibitors. The control group consisted of 20 age-matched donors without rheumatic diseases. Galectin 3 concentration was determined by ELISA (Bender MedSystems GmbH, Biocenter, Vienna Austria). The upper limit of normal when testing 20 sera from healthy donors was 5.32 ng/ml, corresponding to the 95th percentile.
Results: The serum level of galectin-3 in RA patients (n=47) and in the control group (n=20) did not differ statistically significantly (4.27 [2.3;5.26] ng/ml vs 3.83 [2.57;4.11] ng/ml (p=0.1). In the whole group of RA patients (n=47) with inefficiency (insufficient effect) of basic anti-inflammatory therapy, correlations were noted between the level of galectin-3 and age (R=0.34; p=0.02), BMI (R=0.36; p=0.02), SDAI (R=0.33; p=0.02), CDAI (R=0.31; p=0.03). RA patients were divided into 2 groups: group I (n=27) - patients with galectin-3 ≥ 5.32 ng/ml; II (n= 20) - less than <5.32 ng/ml. Group I patients were older in age (59.0 (46;67) years vs 42.5(38;53) years), had higher activity according to SDAI (38.2 (30; 48.4) vs 29.7 (26.6; 40.6)), CDAI (35.0 (29; 43) vs 27.0 (23;38)) (p<0.05 in all cases). In the group of patients (n=21) who received combination therapy (DMARDs + biological therapy) for 12 months, there was a significant decrease in clinical and laboratory activity, IgM RF levels (p<0.05 in all cases). (
| Patients with RA (n=21) with insufficient effect of basic anti-inflammatory therapy | Patients with RA (n=21) after 12 months of receiving combination therapy | Δ,% | р | |
|---|---|---|---|---|
| DAS28 | 5,6 (5,3; 6,7) | 3,97(3,36;4,63)* | -30,4 | 0,0001 |
| SDAI | 38,17 (29,5; 45,8) | 17,2(9,57;25,6) * | -54,8 | 0,0001 |
| CDAI | 35,0 (26,0; 43,5) | 17,0(9,0;23,5) * | -51,4 | 0,0001 |
| СRP,mg/l | 20,6 (11,7;34,1) | 3,15(1,2;7,2) * | -84,7 | 0,003 |
| ESR,mm/h | 27,0 (16,0;45,0) | 16,0 (10,0;23,5) * | -40,7 | 0,003 |
| IgM RF, МЕ/ml | 84,4 (20,8;163,0) | 32,2(10,6;107) * | -61,8 | 0,01 |
| Galectin-3, ng/ml | 4,2 [2,8;5,1] | 3,42 (2,56; 4,36) | -19 | 0,2 |
* -p <0.05 reliability of differences in indicators before and after 12 months of combination therapy (Wilcoxon); Δ,% - the difference in indicators between the groups by the 12th month of combination therapy.
Conclusion: There were no differences in the level of serum galectin-3 in patients with RA and with the ineffectiveness of basic anti-inflammatory therapy and in the control group. At the same time, the association of this marker with RA activity (according to the SDAI, CDAI indices) does not exclude its role in the development of clinical manifestations of rheumatoid arthritis.
Disclosure of Interests: None declared