ABSTRACT
AIM: To study the changes in pain syndrome and its characteristic in patients with ankylosing spondylitis (AS) who received tenoxicam after non-effective treatment with NSAIDs on the 'on-demand' basis. MATERIAL AND METHODS: Forty patients with AS, who had BASDAI ≥4.0 at baseline and after 52 weeks of NSAIDs on the 'on-demand' basis, were randomized into 2 groups: 30 patients were prescribed 20 mg of tenoxicam oraly per day, 10 patients continued previous therapy. The BASDAI, ASDAS indices were calculated in 52 and 56 weeks. RESULTS AND CONCLUSION: BASDAI and ASDAS indices decreased in patients treated with tenoxicam, the AS activity in patients with on-demand NSAID intake did not change. The change of the ineffective long-term NSAID intake in the 'on-demand' basis to permanent drug intake was associated with a rapid (within 4 weeks) decrease in the clinical activity of ankylosing spondylitis.
Subject(s)
Spondylitis, Ankylosing , Anti-Inflammatory Agents, Non-Steroidal , Humans , Piroxicam/analogs & derivatives , Severity of Illness IndexABSTRACT
AIM: To estimate changes in the concentrations of adhesion molecules and vascular endothelial growth factor A after 30-day additional use of amtolmetin guacil (AMG) in patients with active ankylosing spondylitis (AS) who were unresponsive to previous one-year treatment with nonsteroidal anti-inflammatory drugs (NSAIDs). SUBJECTS AND METHODS: 20 patients with active AS who had not reached a BASDAI score <4.0 at week 52 of NSAID therapy and 10 healthy individuals matched for cardiovascular risk factors were examined. After 52 weeks of NSAID therapy, AMG was administered orally at 1200 mg/day to patients with AS for 30 days. The concentrations of adhesion molecules (sICAM-1 and sVCAM-1) and VEGF-A were measured. BASDAI and ASDAS scores and C-reactive protein (CRP) levels were determined in AS patients. The concentrations of adhesion molecules and VEGF-A were investigated in patients with AS at baseline, at 52 weeks after NSAID treatment start, and at 30 days following AMH initiation (at week 56) and in healthy individuals at baseline and at 30 days. RESULTS: The concentration of sICAM-1 in patients with AS was 987.0±217.39, 938.98±293.31, and 364.25±363.3 ng/ml at weeks 0, 52, and 56, respectively; that in healthy individuals was 769.25±189.32 and 740.05±225.76 ng/ml at baseline and at 30 days, respectively. The differences from the baseline concentration were significant in patients with AS (p<0.05) and insignificant in healthy subjects (p≥0.05); the differences between the concentrations in patients with AS and the controls were significant at baseline and at 52 weeks (p<0.05). The concentration of sVCAM-1 in patients with AS was 364.25±160.49, 325.34±245.1, and 319.1±248.73 ng/ml at weeks 0, 52 and 56, respectively; that in healthy individuals was 245.13±40.4 and 248.73±34.42 ng/ml, respectively (p<0.05 vs baseline values and values in healthy subjects). The level of VEGF-A in AS patients was not different from that in healthy individuals, but decreased during treatment. Correlations were found between the concentration of adhesion molecules and the level of CRP (p<0.01). CONCLUSION: Elevated concentrations of adhesion molecules have been found in AS patients compared with healthy individuals. The study has demonstrated that AMG treatment is efficient in treating patients with AS. NSAID/AMG treatment is associated with lower concentrations of adhesion molecules. Decreased CRP levels serve as predictors for reduced concentration of adhesion molecules. The level of VEGF-A at baseline did not differ from that in healthy subjects, but was decreased during treatment with NSAIDs.
Subject(s)
Cardiovascular Diseases/epidemiology , Cell Adhesion Molecules/blood , Glycine/analogs & derivatives , Pyrroles/therapeutic use , Spondylitis, Ankylosing , Vascular Endothelial Growth Factor A/blood , Adult , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , C-Reactive Protein/analysis , Female , Glycine/therapeutic use , Humans , Male , Middle Aged , Patient Acuity , Predictive Value of Tests , Risk Factors , Russia/epidemiology , Spondylitis, Ankylosing/blood , Spondylitis, Ankylosing/diagnosis , Spondylitis, Ankylosing/drug therapy , Spondylitis, Ankylosing/epidemiology , Treatment OutcomeABSTRACT
AIM: To assess changes in the concentration of interleukin-17A (IL-17A) in patients with ankylosing spondylitis (AS) treated with tumor necrosis factor-α (TNFα) inhibitors during a year. SUBJECTS AND METHODS: Examinations were made in 30 patients (22 (73.3%) men) aged 38.35±9.19 years with AS (modified New-York criteria, BASDAI ≥4.0; AS duration, 11.4±9.6 years) and in 20 healthy individuals (12 (60%) men) aged 40.1±7.7 years) (a control group). All the patients were treated with infliximab (remicade, MSD) 5 mg/kg body weight during a year according to the recommended regimen. BASDAI and ASDAS were calculated; C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and TNFα and IL-17A concentrations were measured before and 52±2 weeks after TNFα inhibitors treatment. BASDAI/ASDAS improvement, ESR and CRP decreases; ASAS20/40 responses, ASAS partial remission, and an ASDAS improvement were estimated. RESULTS: In the patients with AS, the concentrations of TNFα and IL-17A were higher than those in the healthy individuals (p < 0.000). Twelve (40%) AS patients treated with TNFα inhibitors achieved ASAS partial remission. The average estimated back pain, ASDAS and BASDAI scores, and CRP and ESR substantially reduced (p<0.000 for all). The concentration of TNFα decreased from 17.8±7.6 to 7.3±3.2 pg/ml (p<0.000). The IL-17A level was 28.4±14.4 and 32.1±12.2 pg/ml before and after the treatment, respectively. The baseline level of IL-17A was lower in the patients with AS who had achieved remission than that in those who had not (p=0.01). CONCLUSION: The improvement due to one-year AS treatment with TNFα inhibitors is not associated with the reduction of IL-17A concentrations. In the patients who failed to achieve ASAS partial remission, the baseline and final serum concentrations of IL-17A were higher than in those who achieved the remission.
Subject(s)
Interleukin-17 , Spondylitis, Ankylosing , Adult , Biomarkers/blood , Blood Sedimentation , C-Reactive Protein , Humans , Infliximab , Interleukin-17/blood , Interleukin-17/therapeutic use , Male , Middle Aged , Severity of Illness Index , Spondylitis, Ankylosing/drug therapy , Spondylitis, Ankylosing/immunology , Tumor Necrosis Factor-alpha/antagonists & inhibitorsABSTRACT
AIM: To evaluate changes in the concentration of biomarkers for osteoproliferation and bone resorption in ankylosing spondylitis (AS) patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs) in different regimens. SUBJECTS AND METHODS: Forty patients with AS (according to the modified New York criteria), who had BASDAI ≥ 4.0 at baseline and at 52 weeks of on-demand NSAID treatment were examined and randomized into 2 groups: 1) 30 patients who used continuously oral tenoxicam 20 mg daily (a study group); 2) 10 patients who continued previous therapy (a comparison group). BASDAI and ASDAS were calculated; the serum levels of C-reactive protein, C-terminal type I procollagen propeptide (PICP), and C-terminal telopeptide of type I collagen (CTX-I) were measured at baseline and at 52 and 56 weeks of treatment. A control group consisted of 19 healthy volunteers. RESULTS: The continuous use of NSAIDs (tenoxicam) decreased higher baseline BASDAI and ASDAS scores. There were no changes in the indicators of AS activity in the patients who took on-demand NSAIDs. Baseline CTX-I levels did not differ between the patients with AS and the healthy individuals; those declined during continuous intake of tenoxicam and remained unchanged during on-demand administration. In the patients with AS, baseline PICP levels exceeded those in the healthy individuals. In the tenoxicam-treated patients, the concentrations of PICP at baseline and at 52 and 56 weeks were 17.1±9.0, 16.8±9.9, and 13.29±6.7 ng/ml, respectively (p=0.0001 for differences between the baseline and week 56 levels); in the comparison group, PICP levels did not change statistically significantly (p≥0.05 for all intergroup comparisons). CONCLUSION: Changing the inefficient long-term on-demand use of NSAIDs to their continuous intake is associated with a rapid decrease in clinical AS activity (within 4 weeks) with a reduction in the higher baseline concentration of the marker for osteoproliferation and in the normal level of the marker for bone resorption.
