%0 Journal Article
%T Intravenous Laser Blood Irradiation and Tocilizumab in a Patient with Juvenile Arthritis
%A Dragos Andrei Chiran
%A Michael Weber
%A Laura Marinela Ailioaie
%A Eovelina Moraru
%A Constantin Ailioaie
%A Daniela Litscher
%A Gerhard Litscher
%J Case Reports in Medicine
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/923496
%X This study presents effects of intravenous laser blood irradiation (ILBI) in a transient immunodeficiency patient with juvenile idiopathic arthritis (JIA) treated with an interleukin-6 receptor inhibitor (Tocilizumab). Biological agents induce JIA remission, but some patients do not respond favorably to this final therapeutic line of defense. ILBI was performed in a 16-year-old male patient, with JIA and transient immunodeficiency. When ILBI was introduced, the patient was receiving disease-modifying drugs, steroids, tocilizumab, and physical therapy. Because the disease was not well controlled, ILBI was applied in addition to other ongoing therapies. The patient underwent 1 session daily, and 10 successive sessions per month, repeated every 3 months, for 7 months. Patient evaluation was performed before ILBI was started and at 3, 6, 9, and 12 months after ILBI initiation, using the ACR Pediatric response. The outcome was evaluated using Pediatric 50, 70, and 90 responses and compared to initial status, after 3, 6, 9, and 12 months. At the end of study, the titre of IgA and IgG levels returned to normal. Synergistic anti-inflammatory effect of ILBI was evident, if applied additionally in combination with tocilizumab, in a patient with a therapy-resistant severe form of JIA and related subacute transient immunodeficiency. 1. Introduction Juvenile idiopathic arthritis (JIA) is an inflammatory disorder of the connective tissues, characterized by joint swelling, pain, and tenderness. Overproduction of tumor necrosis factor alpha (TNF-¦Á), interleukin-6 (IL-6), and interleukin-1 beta (IL-1¦Â) is a well-known fact in JIA. Increased levels of these cytokines, both in serum and synovial fluid, induce the production of vascular endothelial factor, triggering angiogenesis in the affected joint. IL-6 is also considered responsible for osteoclast differentiation, followed by joint destruction and osteoporosis [1]. In the last decade, the development of biological agents that target these key inflammatory cytokines or their receptors brought new horizons in JIA treatment. Disease remission became a reachable goal [2]. However, few patients develop a severe chronic rheumatic type of the disease [3]. TNF-¦Á inhibitors are the first-line biological agents used in JIA, if therapy with anti-inflammatory and disease-modifying antirheumatic drugs (DMARDs) proved to be inefficient. IL-6 receptor inhibition with Tocilizumab is a new second-line therapy for anti-TNF-¦Á nonresponding patients, based on the blockade of IL-6-regulated signaling pathways [1, 2]. The main disadvantage
%U http://www.hindawi.com/journals/crim/2014/923496/