RESUMO
Introduction: Spondyloarthritis (SpA) is a common rheumatic inflammatory disease and can impact patients' work productivity. We aimed to evaluate the impact of pain catastrophizing and central sensitization on work outcomes in young SpA patients and determine the predictive factors of work productivity loss. Material and methods: We performed a cross-sectional study over 6 months. We included patients aged between 18 and 50 years old, diagnosed with axial or peripheral SpA. Pain catastrophizing and central sensitization were assessed using the Pain Catastrophizing Scale (PCS) and Central Sensitization Inventory (CSI) questionnaire, respectively. Impact of SpA on work productivity and activity impairment during and outside of work was measured with the Work Productivity and Activity Impairment Questionnaire (WPAI: Spondyloarthritis). Results: A total of 72 patients were enrolled, with a median age of 39 years (28.3-46), 65.3% men, and 54.4% working patients. Median scores of activity impairment outside of work, and work productivity loss were 50% (40-70), and 50% (40-60), respectively. Median absenteeism and presenteeism scores were 0% (IQR 0-7), and 100% (IQR 86.5-100), respectively. Regarding work-related outcomes: activity impairment was positively correlated with CSI and PCS; presenteeism was significantly associated with male sex (p = 0.009); and work productivity loss was positively associated with anxiety, depression, and poor quality of life. Multivariate regression analysis identified predictive factors of work productivity loss: male sex, poor quality of life, and prolonged morning stiffness. Conclusions: Assessment of the impact of pain catastrophizing and central sensitization on work-related outcomes in patients with SpA is important to understand the burden of illness and to identify early those in need of interventions in clinical practice.
RESUMO
Lung injury and respiratory distress syndrome are frequent symptoms observed in the most severe cases of scorpion envenomation. The uncontrolled transmigration of leukocyte cells into the lung interstitium and alveolar space and pulmonary edema may be the cause of death. Mast cells can release various inflammatory mediators known to be involved in the development of lung edema following scorpion venom injection. The present study was designed to determine the evidence of neurokinin 1 (NK1) receptor and the involvement of mast cell activation to induce pulmonary edema and to increase vascular permeability after Androctonus australis hector (Aah) venom administration. To this end, mast cells were depleted using compound 48/80 (C48/80). Furthermore, the involvement of tachykinin NK1 receptors expressed on mast cell membranes was elucidated by their blocking with an antagonist. On the other hand, the ability of Aah venom to increase vascular permeability and to induce edema was also assessed by measuring the amount of Evans blue dye (EBD) extravasation in bronchoalveolar lavage (BAL) fluid and in the lungs of mice. Pulmonary edema, as assessed by the levels of EBD extravasation, was completely inhibited in compound 48/80-treated animals. Depletion by stimuli non-immunological C48/80 component markedly reduced induced inflammatory response following the venom administration. The mast cells seem to play an important role in the development of lung injury and the increase of vascular permeability in mice following the subcutaneous administration of Aah scorpion venom through the NK1 receptor.
