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עמוד בית
Sun, 14.07.24

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October 2015
September 2015
Lihi Atzmony MD, Hana Feuerman MD, Yair Molad MD, Yelena Didkovsky MD and Emmilia Hodak MD
April 2015
Jana Petríková MD PhD, Peter Jarčuška MDPhD, Marián Švajdler MD, Daniel Pella MD PhD and Želmíra Macejová MD PhD MPH
February 2015
Attila Kovacs MD PhD, Adelina G. Siminischi MD, Beáta Baksay MD, Andras Gall MD, Maria Takacs MD and Zoltan Szekanecz MD PhD
Abdulla Watad MD, Marina Perelman MD, Ribhi Mansour MD, Yehuda Shoenfeld MD FRCP MaACR and Howard Amital MD MHA
January 2015
Przemyslaw Kotyla MD PhD, Katarzyna Jankiewicz-Ziobro MD PhD, Aleksander Owczarek MD PhD and Eugene J. Kucharz MD PhD

Background: Targeted anti-tumor necrosis factor-alpha (TNFα) therapy in patients with rheumatoid arthritis (RA) has resulted in dramatic improvement in the course of the disease and prognosis. One of the features of RA is hyperplasia of synovial cells, particularly RA synovial fibroblasts (RA-SF), caused partially by impaired apoptosis of RA-SF cells. It has been shown that TNFα may inhibit apoptosis in RA-SF cells and this process may be reversed by the use of TNFα antagonists.

Objectives: To determine the influence of etanercept, an anti-TNFα agent, on sFas (CD 95) receptor.

Methods: We analyzed serum levels of sFaS and TNFα in a group of 26 patients with high RA disease activity who were selected to start treatment with etanercept. Assessment of sFas receptor and TNFα levels was performed before and 6 months after treatment with etanercept.

Results: Treatment with etanercept resulted in increased TNFα levels (log TNFα 0.602 vs. 1.17, P < 0.05) but no change in sFas levels (log sFas 3.17 vs. 3.11, P = 0.37). As expected, treatment resulted in significant reduction in both disease activity and levels of inflammatory markers.

Conclusions: Etanercept may increase TNFα levels in patients with RA. We also speculate that the Fas pathway is not the main apoptotic pathway in patients with RA treated with etenercept, since sFas, a marker of apoptotic activity, remained unchanged and was not influenced by disease activity and concomitant treatment. 

December 2014
Yael Weintraub MD, Noa Rabinowicz MD, Penny Hanuka, Michal Rothschild MD, Shulamit Kotzki and Yosef Uziel MD

Background: Intra-articular corticosteroid injection (IACI), a common procedure in juvenile idiopathic arthritis, is usually associated with anxiety and pain. In a previous study, we concluded that nitrous oxide (NO2) provides effective and safe sedation for such procedures. Following the introduction of medical clowns in our hospital, we added them as an integral part of the team performing IACI.

Objectives: To prospectively evaluate the effect of a medical clown on pain perception during intra-articular corticosteroid injection for juvenile idiopathic arthritis using NO2 conscious sedation.

Methods: Patients scheduled for IACI first met and interacted with the medical clown. During the procedure, the rheumatologist and the medical clown worked in parallel to create distraction. NO2 was administered. The patient, parent, physician, medical clown and nurse completed a visual analog scale (0–10) for pain. Change in heart rate ≥ 15% was recorded to evaluate physiologic response to pain and stress.

Results: A total of 46 procedures were performed in 32 children: 23 girls, 9 boys, with a mean age of 10.9 ± 3.6 years. The median visual analog scale pain score for the patients, parents, physicians, medical clown and nurses was 2, 2, 1, 1 and 1, respectively. Five patients had increased heart rate and experienced increased pain.

Conclusions: Active participation of a medical clown during IACI with nitrous oxide for juvenile idiopathic arthritis further decreases pain and stress and results in a positive patient experience. 

October 2014
Carlo Perricone MD, Elias Toubi MD, Guido Valesini MD and Yehuda Shoenfeld MD FRCP (Hon.) MaACR
Orit Barrett MD, Ella Abramovich MD, Jacob Dreiher MD MPH, Victor Novack MD PhD and Mahmoud Abu-Shakra MD
Piercarlo Sarzi-Puttini MD and Fabiola Atzeni MD PhD
M. Galeazzi, L. Bazzichi, G.D. Sebastiani, D. Neri, E. Garcia Gonzalez, N. Ravenni, L. Giovannoni, J. Wilton, M. Bardelli, C. Baldi, E. Selvi, A. Iuliano, G. Minisola, R. Caporali, E. Prisco and S. Bombardieri
September 2014
Smadar Gertel MD and Howard Amital MD MHA

The major autoantigens in the inflamed synovium in rheumatoid arthritis (RA) are citrullinated peptides. Citrullinated peptides are employed in diagnostic kits for detection of anti-citrullinated protein antibodies (ACPA), a serological marker with high specificity and sensitivity in the diagnosis of RA, and have been included in the new ACR/EULAR classification criteria for RA. ACPA-positive RA patients suffer from an erosive and more aggressive disease compared to ACPA-negative patients. In view of the mounting indications that ACPA plays a seminal role in the pathogenesis of RA, it might be valuable to pursue a specific treatment aiming ACPA as a target. We found that citrullinated peptides, which contain a unique amino acid, citrulline, alter the protein structure within the connective tissue, leading to tolerance breakdown and triggering the autoimmune response in RA. However, with different doses and routes of administration, citrullinated peptides can promote immune tolerance rather than induction of disease. 

May 2014
April 2014
Marina Pekar, Gilad Twig MD, Alex Levin MD and Howard Amital MD MHA
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