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- Boustedt, Cecilia, et al.
(författare)
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Effects of a hand-joint protection programme with an addition of splinting and exercise: one year follow-up.
- 2009
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Ingår i: Clinical rheumatology. - : Springer Science and Business Media LLC. - 1434-9949 .- 0770-3198. ; 28:7, s. 793-9
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Tidskriftsartikel (refereegranskat)abstract
- Forty-two women with thumb base osteoarthritis referred to a joint protection programme (JP) were distributed into groups: one with only JP (Control group) and one with addition of splints day/night, hot pack/home exercise (SE group). Assessments of pain, stiffness, grip force, disabilities of daily activities were performed before treatment, 1 week and 1 year after treatment. The SE group had a significant decrease in pain, stiffness and an improvement in daily activities directly after the intervention and at 1-year follow-up compared to the Control group. In the SE group pain at night, pain on motion, and stiffness decreased. Grip force increased and daily activities improved. The Control group decreased in pain on motion and showed improvement in daily activities just after the intervention but not at 1-year follow up. This comparative study shows that when splinting and exercise regimen are added to a JP programme it gives a greater improvement of pain, stiffness, grip force and daily activities than the JP programme alone.
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- Grimsholm, Ola, et al.
(författare)
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BDNF in RA: Downregulated in plasma following anti-TNF treatment but no correlation with inflammatory parameters.
- 2008
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Ingår i: Clinical Rheumatology. - : Springer Science and Business Media LLC. - 0770-3198 .- 1434-9949. ; 27:10, s. 1289-1297
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Tidskriftsartikel (refereegranskat)abstract
- The involvement of brain-derived neurotrophic factor (BDNF) in rheumatoid arthritis (RA) is largely unknown. The distribution of BDNF and its associated receptors, TrkB and p75, in the synovial tissue of patients with RA was examined and contrasted with that in patients with osteoarthritis (OA). Additionally, levels of BDNF in both synovial tissue and synovial fluid were measured. Furthermore, the effects of anti-tumour necrosis factor (anti-TNF; infliximab) treatment on BDNF levels in the plasma of RA patients were analysed. Cells in the synovium showed immunoreactivity for BDNF and BDNF-, p75- and TrkB-receptor immunoreactions were seen in nerve fibres of nerve fascicles and in association with sensory corpuscles. The levels of BDNF in synovial tissue were not correlated with the number of inflammatory cells observed microscopically or with levels of TNFα. Nor did the BDNF levels in synovial fluid correlate with erythrocyte sedimentation rate (ESR) or white blood cell counts. Anti-TNF treatment lead to a decrease in plasma levels of BDNF 14 weeks after the initiation of anti-TNF therapy, i.e., 8 weeks after the last infusion. Higher levels of BDNF were observed in RA patients at baseline compared with those for healthy individuals. However, the levels of BDNF in plasma of patients treated with anti-TNF did not correlate with the changes in ESR or a disease activity score. The clinical significance of this study is that anti-TNF treatment influences plasma levels of BDNF although there was no evidence that BDNF levels correlate with inflammatory parameters in either infliximab-treated or non-infliximab-treated patients with RA. Instead it is likely that sources other than inflammatory cells, including nerve structures, are important sources of BDNF and that the effects of anti-TNF treatment on BDNF levels may be related to effects on circulating and various local cells and/or BDNF-containing neurons.
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