SMT is effective for the treatment of chronic nonspecific LBP. To obtain long-term benefit, this study suggests maintenance SM after the initial intensive manipulative therapy.
The aim of the study was to examine whether weight reduction can result in improvement of fibromyalgia impact questionnaire (FIQ) in the patients with fibromyalgia syndrome (FMS). This study was a randomized controlled trial. Obese patients with fibromyalgia were randomly assigned to 6-month dietary weight loss (n = 41) and no weight loss (n = 42) groups. Patients were assessed at baseline and at 6 months. The primary outcome measure was FIQ. Secondary measures included the tender point (TP) examination, Beck Depression Inventory-II, and Pittsburg Sleep Quality Index. Compared to the control group, patients who underwent weight reduction obtained significantly better FIQ (p = 0.007), lower mean TP count (p = 0.015), and lower mean TP pain rating in the lower body (p < 0.001). Patients who lost weight had less depression and better sleep quality than the controls. Patients who lost weight had significantly lower interleukin 6 and C-reactive protein levels than those in the control group (p = 0.034 and p = 0.007, respectively). Weight loss in obese patients with FMS leads to significant improvement in the quality of life as shown by the decrease in the FIQ score. Depression, sleep quality, and tender point count are also significantly improved by weight loss in obese patients with fibromyalgia. Our results suggest that weight reduction should be a part of fibromyalgia treatment.
Patients with fibromyalgia syndrome (FMS) have impaired mobility and therefore get less sunlight exposure, we postulated that they may be at increased risk of developing osteoporosis (OP). The aim of this study was to assess and compare serum vitamin D level and bone mineral density (BMD) value in patients with primary FMS (PFMS) and healthy controls. A total of 50 patients with PFMS participated in this case-control study, and 50 healthy females who were age-matched to the patients were used as the control group. Venous blood samples collected from all subjects were used to evaluate serum 25-hydroxyvitamin D3 (25-OHD). BMD was measured at the lumbar spine (L2-L4) anteroposterior, femoral neck and forearm by dual-energy X-ray absorptiometry. Patients with PFMS had significantly lower serum 25-OHD than controls (15.1 ± 6.1 and 18.8 ± 5.4 ng/ml, respectively, p = 0.0018). Apart from the BMD in the lumbar spine, which was significantly lower in the PFMS patients compared with controls (p = 0.0012), no significant difference was found in other measures of BMD. Compared to PFMS patients who had serum level of the 25-OHD >20 ng/ml, the patients with 25-OHD ≤20 ng/ml are more likely to have impaired short memory (46.4 vs. 13.6%, respectively, p = 0.0136), confusion (50 vs. 18.2%, respectively, p = 0.0199), mood disturbance (60.7 vs. 27.3%, respectively, p = 0.0185), sleep disturbance (53.6 vs. 22.7%, respectively, p = 0.0271), restless leg syndrome (57.1 vs. 27.3%, respectively, p = 0.0346) and palpitation (67.9 vs. 36.4%, respectively, p = 0.0265). Serum level of the 25-OHD is inversely correlated with visual analogue scale (VAS) of pain (p = 0.016), Beck score for depression (p = 0.020) and BMD at lumbar spine (p = 0.012). The lumbar BMD inversely correlated with VAS of pain (p = 0.013) and Beck score for depression (p = 0.016). This study confirmed high prevalence of hypovitaminosis D among in patients with PFMS. This study confirmed the concept that FMS is a risk factor for OP. Based on this, an early nutrition program rich in calcium and vitamin D, appropriate exercise protocols, and medical treatment should be considered in these patients in terms of preventing OP development.
Reports suggest leptin, which was initially described as a hormone that regulates food intake and energy balance, has an intimate relationship, and interacts with the immune system. Leptin consumption in the synovial cavity in patients with rheumatoid arthritis (RA) reported to have protective effect against erosion. To determine the difference in serum leptin and synovial/serum leptin ratio between RA and control and to assess whether these parameters correlate with systemic inflammation in RA. Also, the hypothesis that synovial/serum leptin ratio could be linked to joint erosion in RA was evaluated. The study subjects consisted of 40 consecutive patients with RA, 30 patients of them had knee effusion, and 30 controls. Ten of these controls had acute knee injury and their synovial fluid was obtained for comparison of synovial/serum leptin ratio with patients with RA. The mean serum leptin in patients with RA was significantly higher than controls. Also, the synovial leptin and synovial/serum leptin ratio in the RA patients with effusion was significantly higher than in the 10 control subjects with traumatic effusion. Serum leptin in the 30 RA patients with effusion was higher than the matched synovial leptin. In RA patients with effusion, synovial/serum leptin ratio was also significantly higher in RA patients with erosion than RA patients without erosion. Serum leptin level and synovial/serum leptin ratio are significantly correlated with the RA duration, DAS28, ESR, CRP, TNF-α, and IL-6. Finally, in regression analysis, only the synovial/serum leptin ratio was positively associated with erosion in patients with RA. In RA, there is a significant increase in circulating leptin levels and synovial/serum leptin ratio compared to non-RA controls. Serum leptin and synovial/serum leptin ratio are significantly in erosive RA than non-erosive RA. Both parameters are correlated with disease duration and parameters of RA activity. In regression analysis, only the synovial/serum leptin ratio was positively associated with erosion in patients with RA. These results indicate that local consumption of leptin in the joint cavity has a protective role against the destructive course of RA.
Since vascular risk factors that predispose to vertebrobasilar ischemia are common findings in elderly, cervical spondylosis-which is also common in such age group-as a cause of vertigo is sometimes considered as a myth. The purpose of this study is to investigate the effect of cervical spondylosis on blood flow velocity of VAs during cervical rotation and to identify the possible association of vertigo with the decreased blood flow velocity through VAs during head rotation in these patients. The incidence of cervical spondylosis was estimated in patients with and without vertigo. Patients with vertigo proved to have spondylosis are further compared with patients having spondylosis but not complaining of vertigo and patients who neither have spondylosis nor complain of vertigo who served as controls. Plain cervical radiography was used to evaluate cervical degenerative changes using cervical degenerative index. Color duplex sonography was used to measure vertebral artery blood flow with the cervical spine in the neutral position then with 60° rotation and 30° extension to measure the opposite vertebral artery. A significantly higher prevalence of cervical spondylosis was found among patients complaining of vertigo than those in non-vertigo group (71.4% vs. 32.9%, respectively). Furthermore, among patients with cervical spondylosis, patients having vertigo showed significantly more evident degenerative changes (P = 0.003). Despite Doppler ultrasound examination with head in neutral position was similar in all groups; cervical spondylosis patients with vertigo had statistically significant lower blood flow parameters with contralateral head rotation in the left and right vertebral arteries than cervical spondylosis patients without vertigo and controls. The decreased vertebral artery blood flow that occurs with cervical rotation can be observed in patients with cervical spondylosis. In patients with high-grade cervical spondylosis with more extensive osteophyte formation, the decreased blood flow becomes prominent and symptomatic presenting as vertigo.
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