Depression and anxiety in individuals with axial spondyloarthritis and nonspecific low back pain who are interested in non-pharmacological therapy options: Cross-sectional study.

Psychological burden, such as depression and anxiety, may be associated with axial spondyloarthritis (axSpA) and poor prognosis of nonspecific low back pain (NSLBP). Non-pharmacological therapy is a substantial part of the management of both illnesses. Our study describes the psychological outcomes in patients with axSpA and NSLBP who were actively looking for non-pharmacological therapy. A total of 60 participants (34 with axSpA and 26 with NSLBP) were included in this cross-sectional study. Anxiety and depression were examined using the Beck Anxiety Inventory (BAI) and Beck Depression Inventory (BDI-II), respectively. The relationships between BAI and BDI-II and quality of life (EQ-5D), pain intensity (NRS pain), disease activity (AS disease activity score, ASDAS-CRP), and function (Bath AS Functional Index, BASFI) were determined. The intensity of anxiety and depression did not differ between patients with and without axSpA. In both, axSpA and NSLBP, BAI, and BDI-II scores were inversely correlated with EQ-5D, R = -0.268 (P ˂ .05) and R = -0.486 (P ˂ .0001), respectively. We found a variation in the relationship between pain intensity and psychological outcomes in NSLBP and axSpA. The pain intensity score was correlated with the BDI-II (R = 0.542, P = .001) and BAI (R = 0.489, P = .003) scores only in patients with axSpA. In patients with axSpA, BAI was inversely correlated with disease duration (R = -0.356, P = .039) and positively correlated with increased disease activity and poor function, ASDAS-CRP (R = 0.431, P = .012) and BASFI (R = 0.621, P ˂ .0001) scores. The ASDAS-CRP score was positively correlated with BDI-II (R = 0.562, P = .001), and both disease activity and female sex were identified as risk factors for poor BDI-II outcomes in axSpA patients according to multiple regression analysis. Experiences of anxiety and depression seem to be similar for patients with axSpA and NSLBP in this selected group of participants. However, pain intensity may influence psychological outcomes, mainly in patients with axSpA. Disease activity, impaired function, and female sex were risk factors for anxiety and depression in patients with axSpA.

Isokinetic Strength of Rotators, Flexors and Hip Extensors is Strongly Related to Front Kick Dynamics in Military Professionals.

Achieving the maximum possible impact force of the front kick can be related to the isokinetic lower limb muscle strength. Therefore, we aimed to determine the regression model between kicking performance and the isokinetic peak net moment of hip rotators, flexors, and hip extensors and flexors at various speeds of contraction. Twenty-five male soldiers (27.7 ± 7.2 yrs, 83.8 ± 6.1 kg, 180.5 ± 6.5 cm) performed six barefoot front kicks, where impact forces (N) and kick velocity (m∙s-1) were measured. The 3D kinematics and isokinetic dynamometry were used to estimate the kick velocity, isokinetic moment of kicking lower limb hip flexors and extensors (60, 120, 240, 300°âˆ™s-1), and stance lower limb hip internal and external rotators (30, 90°âˆ™s-1). Multiple regression showed that a separate component of the peak moment concentric hip flexion and extension of the kicking lower limb at 90°âˆ™s-1 can explain 54% of the peak kicking impact force variance (R2 = 0.54; p < 0.001). When adding the other 3 components of eccentric and concentric hip internal and external rotations at 30°âˆ™s-1, the internal and external hip rotation ratios at 30°âˆ™s-1 on the stance limb and the concentric ratio of kicking limb flexion and extension at 300°âˆ™s-1 that explained the variance of impact force were 75% (p = 0.003). The explosive strength of kicking limb hip flexors and extensors is the main condition constraint for kicking performance. The maximum strength of stance limb internal and external rotators and speed strength of kicking limb hip flexors and extensors are important constraints of kicking performance that should be considered to improve the front kick efficiency.

Changes of patient-reported outcomes and protein fingerprint biomarkers after exercise therapy for axial spondyloarthritis.

The objective of this study was to investigate the patient-reported outcomes (PROs) and matrix metalloproteinase (MMP) derived extracellular matrix (ECM) biomarkers in non-radiographic (nr)-axial spondyloarthritis (axSpA) and radiographic (r)-axSpA after exercise intervention. Forty-six axSpA patients with stable disease and treatment underwent 24 weeks long exercise intervention. The clinical and laboratory assessments were performed at baseline and at follow-up. The PROs included evaluation of patient's global disease activity (PGDA), disease activity (DA7), pain (PAIN7) and fatigue during last week and quality of life questionnaires. ELISAs for MMP-degraded collagen type II, C-reactive protein (CRPM) and citrullinated vimentin were used. The data of 23 r-axSpA and 19 nr-axSpA were analysed. The PDGA was similar for nr-axSpA (35.2 ± 18.9) and r-axSpA (33.4 ± 22.3) at baseline, improved significantly after intervention (p < 0.01) and the change of PDGA was almost identical for nr-axSpA (- 10.0 ± 15.4) and r-axSpA (- 9.8 ± 11.9). Evaluations of DA7 and PAIN7 were significantly improved only in nr-axSpA (3.5 ± 2.3 and 34.7 ± 25.6 at baseline vs. 2.1 ± 1.9 and 21.0 ± 20.5, respectively, p < 0.01). The decline of DA7 and PAIN7 was more profound, but not significantly in nr-axSpA than in r-axSpA (- 1.4 ± 1.6 and - 13.7 ± 17.4 vs. - 0.5 ± 3.1 and - 3.7 ± 3.3, respectively). The quality of life was not changed. At baseline, increased levels of CRPM were found in r-axSpA (14.85 ± 4.10) compared to nr-axSpA (11.83 ± 3.20), p < 0.05, but all three biomarkers were not influenced by exercise therapy. We found that exercise therapy mainly in the nr-axSpA improves PROs, but not ECM turnover biomarkers. This indicates that exercise therapy is important for patients' health but does not affect ECM turnover.

Clinical improvement and reduction in serum calprotectin levels after an intensive exercise programme for patients with ankylosing spondylitis and non-radiographic axial spondyloarthritis.

BACKGROUND: The efficacy of exercise therapy for ankylosing spondylitis (AS) is well-documented, but dearth of information is for non-radiographic axial spondyloarthritis (nr-axSpA). Biomarkers like serum calprotectin, interleukins IL-6, IL-17 and tumour necrosis factor (TNF)-α may reflect the disease activity of axial spondyloarthritis (axSpA). In this study, we investigated clinical and laboratory parameters of both axSpA subgroups in response to intensive physical exercise. METHODS: Altogether, 46 patients with axSpA, characterised according to the Assessment of SpondyloArthritis International Society criteria as having nr-axSpA or AS underwent 6-month exercise programme. Clinical outcomes of disease activity, Bath AS Disease Activity Index (BASDAI), AS Disease Activity Index (ASDAS-CRP), mobility, Bath AS Metrology Index (BASMI) and function, Bath AS Functional Index (BASFI) were evaluated at baseline and at the end of the exercise programme. Serum IL-6 and IL-17, TNF-α and calprotectin were measured via ELISA. The clinical and laboratory data of 29 control axSpA patients were used for the evaluation of the results. RESULTS: In all axSpA patients, the ASDAS-CRP (2.10 ± 0.12 to 1.84 ± 0.11, p <0.01) and BASMI (1.28 ± 0.14 to 0.66 ± 0.84, p <0.0001) improved after 6 months of exercise therapy. There was a significant improvement in the ASDAS-CRP in the nr-axSpA subgroup (2.01 ± 0.19 to 1.73 ± 0.16, p <0.05) and in the BASMI in both, the nr-axSpA and the AS subgroups (1.09 ± 0.12 to 0.47 ± 0.08, p <0.0001 and 1.43 ± 0.24 to 0.82 ± 0.23, p <0.0001, respectively). Both, ASDAS-CRP and BASDAI, were significantly improved in the exercise axSpA group compared to the control axSpA group (mean -0.26 vs. -0.13 and -0.49 vs. 0.12, respectively, all p <0.05). Only calprotectin was significantly reduced after the exercise programme in nr-axSpA and AS patients (from 2379.0 ± 243.20 to 1779.0 ± 138.30 µg/mL and from 2430.0 ± 269.70 to 1816.0 ± 148.20 µg/mL, respectively, all p <0.01). The change in calprotectin was more profound in the axSpA intervention group (mean -604.56) than in the control axSpA (mean -149.28, p <0.05). CONCLUSION: This study demonstrated similar efficacy for an intensive exercise programme in both nr-axSpA and AS patients. A significant decrease in serum calprotectin levels in both subgroups of axSpA patients after the exercise programme reflected an improvement in the disease activity and spinal mobility.

No effect of physiotherapy on the serum levels of adipocytokines in patients with ankylosing spondylitis.

To investigate the effect of intensive physiotherapy on disease activity and serum levels of adipocytokines in patients with ankylosing spondylitis (AS). Twenty-six patients with AS were included in this study. Intensive physiotherapy was performed twice a week for a period of 3 months. The Bath AS Disease Activity Index (BASDAI) and the Bath AS Functional Index (BASFI) were assessed at inclusion and after 3 months. Leptin, adiponectin, resistin and visfatin serum levels were analysed by ELISA assays. Patients had mild to moderate disease activity. Baseline levels of adipocytokines did not correlate with indicators of disease activity, functional status or acute-phase reactants. After the 3 months of intensive physiotherapy, BASDAI significantly decreased from 2.98 to 1.8 (p = 0.01) and BASFI improved from 2.31 to 1.37 (p = 0.05), while there were no changes in serum levels of CRP, ESR and adipocytokines. In addition, baseline levels of adipocytokines did not predict the change of disease activity or functional ability. Intensive physiotherapy effectively reduces all clinical measures of disease activity, but it is not associated with a significant change in acute-phase reactants or serum levels of adipocytokines.