Daily physical activity in ankylosing spondylitis:validity and reliability of the IPAQ and SQUASH and the relation with clinical assessments

Introduction: The aim of this study was to investigate the construct validity and test-retest reliability of the International Physical Activity Questionnaire (IPAQ; long form) and the Short QUestionnaire to Assess Health-enhancing physical activity (SQUASH) and to investigate the relation between daily physical activity and clinical assessments in patients with ankylosing spondylitis (AS). Methods: For validity, the self-report questionnaires IPAQ and SQUASH were compared with daily physical activity assessed with the ActiGraph accelerometer during 7 consecutive days in 63 AS outpatients. For reliability, the IPAQ and SQUASH were administered twice approximately 1 week apart in 52 AS outpatients. In all 115 patients, clinical assessments were performed at the outpatient clinic. Results: IPAQ and SQUASH total scores correlated significantly with accelerometer outcome: rho = 0.38 and r = 0.35, respectively. Intraclass correlation coefficients between first and second assessments of the IPAQ and SQUASH were 0.83 and 0.89, respectively. Bland-Altman analyses showed no systemic bias, but in particular for the IPAQ the 95% limits of agreement were wide. Daily physical activity assessed by accelerometer, IPAQ, and SQUASH correlated significantly with disease activity, physical activity, and quality of life. A relation with spinal mobility was found only for the accelerometer and SQUASH. The direction of these correlations indicates that higher daily physical activity is related to lower disease activity and better physical function, spinal mobility and quality of life. Conclusions: Both physical activity questionnaires showed modest construct validity. The SQUASH showed good test-retest reliability, superior to the IPAQ. These results indicate that the SQUASH is more suitable than the IPAQ to assess daily physical activity in AS population studies. However, it is desirable to add questions on AS-specific physical activity. Further studies are needed to investigate the causality of the relation between daily physical activity and clinical assessments

Systemic autoimmune disease and Raynaud's phenomonen.

Systemic autoimmune diseases (AID) are clinically characterized by the involvement of multiple organ systems in the desease process, and immunologically by immune responsiveness against "self". The constitute a heterogenous group of disorders wich are presented to the clinician in a wide variety of clinical syndromes. Overlap between these sydromes occurs frequently and great differences in disease acivity take place in course of time. ... Zi: Summary and conclusion

Vasculitis syndromes: Peripheral neuropathy in AAV--when vasculitis hits a nerve

Peripheral neuropathy can be a manifestation of small-vessel vasculitides such as antineutrophil cytoplasmic antibody-associated vasculitis. Diagnosing vasculitic neuropathy is, however, difficult in many cases. Early treatment focused on achieving remission of the underlying vasculitic process is important as chronic neuropathy has a major influence on a patient's quality of life

Refractory disease in antineutrophil cytoplasmic antibodies associated vasculitis

Purpose of review Induction treatment of antineutrophil cytoplasmic antibodies (ANCA) associated vasculitis (AAV) is not always successful and nonresponding patients are considered refractory. Recent findings Refractory disease should be subdefined to the treatment that was received. Cyclophosphamide refractory AAV occurs in up to 5% of patients. Many more patients develop contraindications to cyclophosphamide or relapse frequently. The latter two patient groups might also benefit from treatment used for cyclophosphamide refractory AAV. Summary The most promising drug for treating refractory AAV is rituximab

Infectious triggers for vasculitis

PURPOSE OF REVIEW: Infections have been suggested to contribute to disease induction and reactivation in many of the idiopathic vasculitides. This review describes and evaluates the evidence that microbes are involved in the etiopathogenesis of these diseases. RECENT FINDINGS: Large-vessel vasculitis has recently been associated with two specific bacteria. Mycobacterium tuberculosis is thought to have an inducing role in Takayasu arteritis and a Burkholderia bacterium might be involved in giant cell arteritis. Hepatitis B and C viruses have been linked to polyarteritis nodosa. In antineutrophil cytoplasmic autoantibody-associated vasculitis, and more specifically granulomatosis with polyangiitis (GPA), Staphylococcus aureus has been the focus of many studies. Chronic nasal carriage of S. aureus is related to endonasal activity and disease relapses in GPA patients. Moreover, antibacterial treatment is known to reduce the risk for disease relapses. If and how pathogens trigger vasculitis is still unclear, but several potential mechanisms have been suggested and are briefly reviewed here. SUMMARY: Although many observations suggest a link between infections and the development of vasculitis, no direct proof exists. Transcriptomic and proteomic studies of the pathogens involved could aid in identifying specific or common traits of pathogens that are relevant for the development and reactivation of vasculitis

FoxP3(+) CD4(+) T cells in systemic autoimmune diseases:the delicate balance between true regulatory T cells and effector Th-17 cells

Breakdown of tolerance is a hallmark of autoimmune diseases. Over the past 10 years, there has been increased interest in the role of FoxP3(+) regulatory T cells (T-Regs) in maintaining peripheral tolerance. Dysfunction of these cells is considered to play a major role in the development of autoimmune diseases. Besides their suppressive function, a fraction of these cells has the capacity to differentiate into IL-17-producing cells (Th-17), a phenomenon associated with autoimmune inflammation. The revealed plasticity of T-Regs, therefore, has obvious implications when designing therapeutic strategies for restoring tolerance in autoimmune diseases using T-Regs. In this review, we discuss development, classification, molecular characterization and mechanisms of suppression by T-Regs. In addition, we describe recent data on their potential conversion into Th-17 cells in human systemic autoimmune diseases. We also outline a new strategy for T-Reg-based therapy via isolation, expansion and re-infusion of highly pure FoxP3(+) T-Regs free of contaminating effector T cells