Intra-Articular Injections of Infliximab in the Treatment of Inflammatory Rheumatic Diseases: Case Reports and Review of Literature

Abstract

Inflammatory chronic diseases involving joints together with other organs are usually treated with a systemic approach. In a few cases, where arthritis is not responsive to traditional treatments, an intraarticular (I.A.) therapy could be useful. Furthermore, patients not eligible for systemic therapy with anti-TNF or other DMARDs, as well as patients with an initial arthritis with the involvement of a single joint, such as the knee or hip joint, could use the I.A. injection therapy. In this article we report our experience with five patients affected by rheumatic inflammatory diseases, not responding to traditional systemic DMARDs-based therapies or not eligible for systemic use of biological response modifiers who underwent ultrasound-guided I.A. injection of Infliximab. Three of 5 patients showed a positive and long-lasting response to treatment with local Infliximab. Safety profile was good according to literature data. Moreover, in this article we review the literature on this therapeutic approach. This is the first report of I.A. use of Infliximab in the hip joint.

Microarray Analysis of NF-κB Signaling Pathways in PBMC of Mice Infected by Trichinella Spiralis

“…Cytokine that binds to TNFrsflaITNFrl and TNFrsflbl TNFbr. may indicate the persistence of infection as parasites have developed several strategies for manipulating the NF-KB signaling pathway in order to escape the host immune response and subsequently ensure their survival (32,(53)(54)(55)(56)(57). The post-infection upregulated genes according to our results are the TNF, Litaf and Map3kl4.…”

Cholesterol: An Inflammatory Compound

“…The shoulder region of plaques as well as areas of foam cell accumulation contain MMP-9, a member of the gelatinase class of the rnetalloproteinase family (18)(19)(20)(21)(22). Human plaque analysis has revealed that MMP-9 is catalytically active and may thus contribute to the dysregulation of extracellular matrix that leads to plaque rupture during the complication of atherothrombosis (23)(24)(25)(26). Further evidence suggests that local overexpression of MMP-9 promotes intravascular thrombus formation through increased tissue factor expression and tissue factor-mediated activation of the coagulation cascade (27)(28)(29)(30) These data support an important role for MMP-9 in several stages of atherosclerosis.…”

IL-31 a TH2 Cytokine Involved in Immunity and Inflammation

“…Recent studies revealed that IL-31 stimulates inflammatory responses in myofibroblasts and induces the generation of chemokines such as IL-8, GRO-u, MCP-3, CXCL3, CCLl3, CCLl5, IL-6, IL-16 and IL-32, and matrix metalloproteinases (MMP-I, MMP-3, MMP-25 and MMP-7) (14). In epithelial cells, IL-31 can activate p38 MAPK, ERK and JNK, and also increases protein expressions of epidermal growth factor (EGF), vascular endothelial growth factor (VEGF) and MCP-I (39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50).…”