Purpose: The hypothesis of this study is that intensive therapy by means of a sensory and motor stimulation program of the upper limb in patients with chronic hemiparesis and severe disability due to stroke increases mobility and sensibility, and improves the use of the affected limb in activities of daily living (ADL). Methods: The program consists of 16 sessions of sensory stimulation and functional activity training in the rehabilitation center, and daily sessions of tactile stimulation, mental imaginery and practice of ADL at home, during 8 weeks. An experimental group (EG) of 12 patients followed this program, compared with a control group (CG) of 9 patients under standard rehabilitation. The efficacy of the program was evaluated by Fugl Meyer Assessment (FMA), Motor Activity Log (MAL) and Stroke Impact Scale-16 (SIS-16) scores, and a battery of sensory tests. Results: The results show that in both groups, the motor FMA and the SIS-16 improved during the 8 weeks, this improvement being higher in the EG. Significant improvements were observed for the sensory tests in the EG. Conclusion: The intensive sensorimotor stimulation program for the upper extremity may be an efficacious method for improving function and use of the affected limb in ADL in chronic stroke patients.

The tapering strategy in SpA results in an important reduction of the drug administered, and the disease control remains similar to that of the patients with SpA receiving the standard regimen.

No abstract

Background The aim of our study was to investigate the influence of conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) and body mass index (BMI) on circulating drug levels and clinical response to tumour necrosis factor inhibitor (TNFi) therapy in axial spondyloarthritis (axSpA) patients. Methods Prospective observational study during 1 year with 2 cohorts (Madrid and Amsterdam) including 180 axSpA patients treated with standard doses of infliximab or adalimumab. Patients were stratified by BMI, being 78 (43%) normal weight (18.5–24.9 kg/m 2 ) and 102 (57%) overweight/obese (≥ 25.0 kg/m 2 ). After the first year of treatment, TNFi trough levels were measured by capture ELISA. Clinical response to TNFi was defined as ∆BASDAI ≥ 2 and clinical remission as BASDAI < 2 and CRP ≤ 5 mg/L. Logistic regression models were employed to analyse the association between concomitant csDMARDs and BMI with drug levels and clinical response. Results Seventy-nine patients (44%) received concomitant csDMARDs. The administration of concomitant csDMARDs (OR 3.82; 95% CI 1.06–13.84) and being normal weight (OR 18.38; 95% CI 2.24–150.63) were independently associated with serum TNFi drug persistence. Additionally, the use of concomitant csDMARDs contributed positively to achieve clinical response (OR 7.86; 95% CI 2.39–25.78) and remission (OR 4.84; 95% CI 1.09–21.36) in overweight/obese patients, but no association was found for normal-weight patients (OR 1.10; 0.33–3.58). Conclusions The use of concomitant csDMARDs with TNFi may increase the probability of achieving clinical response in overweight/obese axSpA patients. Further research studies including larger cohorts of patients need to be done to confirm it. Electronic supplementary material The online version of this article (10.1186/s13075-019-1849-3) contains supplementary material, which is available to authorized users.

Background Severe COVID-19 entails a dysregulated immune response, most likely inflammation related to a lack of virus control. A better understanding of immune toxicity, immunosuppression balance, and COVID-19 assessments could help determine whether different clinical presentations are driven by specific types of immune responses. The progression of the immune response and tissular damage could predict outcomes and may help in the management of patients. Methods We collected 201 serum samples from 93 hospitalised patients classified as moderately, severely, and critically ill. We differentiated the viral, early inflammatory, and late inflammatory phases and included 72 patients with 180 samples in separate stages for longitudinal study and 55 controls. We studied selected cytokines, P-selectin, and the tissue damage markers lactate dehydrogenase (LDH) and cell-free DNA (cfDNA). Results TNF-α, IL-6, IL-8, and G-CSF were associated with severity and mortality, but only IL-6 increased since admission in the critical patients and non-survivors, correlating with damage markers. The lack of a significant decrease in IL-6 levels in the critical patients and non-survivors in the early inflammatory phase (a decreased presence in the other patients) suggests that these patients did not achieve viral control on days 10–16. For all patients, lactate dehydrogenase and cfDNA levels increased with severity, and cfDNA levels increased in the non-survivors from the first sample (p = 0.002) to the late inflammatory phase (p = 0.031). In the multivariate study, cfDNA was an independent risk factor for mortality and ICU admission. Conclusions The distinct progression of IL-6 levels in the course of the disease, especially on days 10–16, was a good marker of progression to critical status and mortality and could guide the start of IL-6 blockade. cfDNA was an accurate marker of severity and mortality from admission and throughout COVID-19 progression.