Relationship between disease activity level and physical activity in rheumatoid arthritis using a triaxial accelerometer and self-reported questionnaire.

OBJECTIVE: This study evaluated the relationship between rheumatoid arthritis (RA) disease activity level and physical activity (PA) by using an accelerometer and self-reported questionnaire. RESULTS: The cross-sectional study was part of a cohort study designed to determine disease activity is associated with PA in RA patients. We classified patients with a Disease Activity Score 28-erythrocyte sedimentation rate (DAS28-ESR) of less than and higher than 3.2 into the low-disease-activity (LDA) group and moderate/high-disease-activity (MHDA) group, respectively. We measured the wear time, time of vigorous-intensity PA, moderate-intensity PA, light-intensity PA, and sedentary behavior per day using a triaxial accelerometer. 34 patients were included in the study. The accelerometer-measured moderate-to-vigorous PA (MVPA) was 17.2 min/day and 10.6 min/day in the LDA group and MHDA group (p < 0.05), respectively. There was no significant association between RA disease activity level and accelerometer-measured PA with adjustment for age and Functional Assessment of Chronic Illness Therapy-Fatigue score. There was no correlation between accelerometer-measured MVPA and self-reported MVPA in the MHDA group, but these factors were correlated in the LDA group (rs = 0.57, p < 0.05). In conclusion, no significant association was noted between RA disease activity level and accelerometer-measured PA.

Therapeutic failure and eventual solution for skin necrosis and exposed tendon of the dorsum of the foot: A case report.

For the treatment of skin necrosis with exposed tendons in rheumatoid arthritis (RA) foot, we should perform microvascular free flap surgery at an early stage without conservative treatment considering the increased risk of infection and the decreased physical activity.

Posterior Tibial Artery Perforator-Based Fascial Flap for Skin Necrosis and Exposed Extensor Tendon After Revision Total Ankle Replacement.

CASE: Delayed wound-healing of anterior ankle incisions can be problematic for patients who have undergone total ankle replacement. We describe the case of a patient in whom a posterior tibial artery perforator-based fascial flap was effectively used to cover skin necrosis and to repair the extensor retinaculum in a wound following revision total ankle replacement. CONCLUSION: When a tendon is exposed in the ankle, a skin flap is generally required. The creation of a perforator-based fascial flap is a useful technique for covering a wound with an exposed tendon and is an alternative to a musculocutaneous flap.

Posterior Tibial Artery Perforator-Based Fascial Flap for Skin Necrosis and Exposed Extensor Tendon After Revision Total Ankle Replacement: A Case Report.

CASE: Delayed wound-healing of anterior ankle incisions can be problematic for patients who have undergone total ankle replacement. We describe the case of a patient in whom a posterior tibial artery perforator-based fascial flap was effectively used to cover skin necrosis and to repair the extensor retinaculum in a wound following revision total ankle replacement. CONCLUSION: When a tendon is exposed in the ankle, a skin flap is generally required. The creation of a perforator-based fascial flap is a useful technique for covering a wound with an exposed tendon and is an alternative to a musculocutaneous flap.

Hydrophilic-interaction liquid chromatography-tandem mass spectrometric determination of erythrocyte 5-phosphoribosyl 1-pyrophosphate in patients with hypoxanthine-guanine phosphoribosyltransferase deficiency.

Mutations in the gene encoding hypoxanthine-guanine phosphoribosyltransferase (HPRT) cause Lesch-Nyhan disease (LND) and its variants (LNV). Due to the technical problems for measuring the HPRT activity in vitro, discordances between the residual HPRT activity and the clinical severity were found. 5-Phosphoribosyl 1-pyrophosphate (PRPP) is a substrate for HPRT. Since increased PRPP concentrations were observed in erythrocytes from patients with LND and LNV, we have turned our attention to erythrocyte PRPP as a biomarker for the phenotype classification. In the present work, a method for determination of PRPP concentration in erythrocyte was developed using liquid chromatography-tandem mass spectrometry (LC-MS/MS) with multiple reaction monitoring (MRM). Packed erythrocyte samples were deproteinized by heating and the supernatants were injected into the LC-MS/MS system. All measurement results showed good precision with RSD <6%. PRPP concentrations of nine normal male subjects, four male patents with LND and six male patients with LNV were compared. The PRPP concentrations in erythrocyte from patients with LND were markedly increased compared with those from normal subjects, and those from patients with LNV were also increased but the degree was smaller than those with LND. The increase pattern of PRPP concentration in erythrocyte from patients with HPRT deficiency was consistent with the respective phenotypes and was correlated with the disease severity. PRPP concentration was suggested to give us supportive information for the diagnosis and the phenotype classification of LND and LNV.

Effects of antibody to receptor activator of nuclear factor κ-B ligand on inflammation and cartilage degradation in collagen antibody-induced arthritis in mice.

BACKGROUND: Rheumatoid arthritis (RA) is an inflammatory disease that leads to destruction of both articular cartilage and bone tissues. In rheumatic joints, synoviocytes and T-lymphocytes as well as bone cells produce the receptor activator of nuclear factor κ-B (RANK) ligand (RANKL), which binds to RANK on the surface of osteoclasts and their precursor cells to induce differentiation and activation of osteoclasts. Hence, inhibition of RANKL may be a promising approach to suppress osteolysis in RA. On the other hand, RANKL production by lymphocytes indicates the possibility that its inhibition would be effective to suppress inflammation in RA. In addition, it has been reported that cathepsin K, a predominant cysteine protease in osteoclasts, is involved in cartilage destruction in RA model mice. Here, we evaluated the effects of an anti-RANKL antibody on inflammation in footpads and degradation of articular cartilage in RA model mice. RESULTS: We induced arthritis in mice by injection of anti-type II collagen antibodies and lipopolysaccharide (LPS). Inhibition of RANKL by an anti-RANKL antibody (OYC1, Oriental Yeast, Tokyo, Japan) was confirmed by increased bone volume in the metaphysis of tibias. Swelling in either limb until day 14 was seen in 5 of 6 mice injected with anti-collagen antibodies and LPS without treatment with OYC1, while that was seen in 4 of 5 mice treated with OYC1. The average arthritis scores on day 14 in those groups were 2.17 and 3.00, respectively, indicating that OYC1 did not ameliorate inflammation in the limbs. Histological analyses indicated that OYC1 does not protect articular cartilage from destruction in mice with arthritis. CONCLUSIONS: Our present study failed to show the effectiveness of an anti-RANKL antibody to ameliorate inflammation in the limbs or protect articular cartilage from degradation in a collagen antibody-induced arthritis mouse model.

Characterization of synovial cell clones isolated from rheumatoid arthritis patients: possible involvement of TNF-alpha in reduction of osteoprotegerin in synovium.

To elucidate the role of the synovium in bone destruction by osteoclasts in rheumatoid arthritis (RA), primary synovial cells isolated from RA patients were cultured and characterized. The cultured primary cells did not produce RANKL (TRANCE/ODF/OPGL/TNFSF11/CD254), an inducer of osteoclast differentiation, but constitutively produced its inhibitor, osteoprotegerin (OPG). Addition of TNF-alpha to the primary cultures of synovial cells reduced the cell viability and strongly suppressed OPG production. We then established nine synovial cell clones, including SYM-1, responsible for OPG production from primary synovial cell cultures. TNF-alpha induced apoptosis of SYM-1 cells within 24h and decreased OPG levels, while infliximab, a chimerical form of the anti-TNF-alpha antibody drug, suppressed the apoptosis and restored OPG levels. These results suggest the existence of fibroblastic cells producing OPG in the synovium, while TNF-alpha suppresses OPG production by inducing apoptosis in those cells. Further, infliximab is considered to inhibit bone destruction through restoration of OPG levels in RA.