Nurse and Patient Perceptions and Preferences for Subcutaneous Autoinjectors for Inflammatory Joint or Bowel Disease: Findings from a European Survey.

INTRODUCTION: Imraldi™ is a biosimilar of the anti-tumor necrosis factor (TNF) monoclonal antibody adalimumab and was recently approved in Europe for the treatment of various inflammatory conditions. Imraldi is administered via an autoinjector device that features distinct design attributes compared with other biologic TNF inhibitor autoinjectors, such as the Humira (adalimumab) Pen® and Enbrel® (etanercept) MyClic® Pen were developed by the relevant pharmaceutical companies. The aim of this study was to evaluate patients' and nurses' preferences for the Imraldi versus Humira or Enbrel MyClic autoinjectors in the UK and Germany. METHODS: Patients with inflammatory joint or bowel disease and nurses with experience in educating patients with these conditions on self-injection participated in two survey studies, the first comparing the Imraldi and Humira autoinjectors and the second comparing the Imraldi and Enbrel MyClic autoinjectors. RESULTS: Overall, 101 nurses (UK, n = 50; Germany, n = 51) and 151 patients (UK, n = 90; Germany, n = 61) participated in both studies. In the first study, 85% of nurses and 78% of patients preferred the Imraldi autoinjector over the Humira autoinjector (P < 0.001); in the second study, 86% of nurses and 79% of patients preferred the Imraldi autoinjector over the Enbrel MyClic autoinjector (P < 0.001). Top reasons for preferring the Imraldi autoinjector included ease of use, ease of grip, and its button-free initiation mechanism. Most nurses indicated they would recommend the Imraldi autoinjector over the Humira and Enbrel MyClic autoinjectors, and most patients indicated they would choose the Imraldi autoinjector over the Humira and Enbrel MyClic autoinjectors to continue treatment. CONCLUSION: Nurses and patients in the UK and Germany preferred the Imraldi autoinjector over both the Humira and Enbrel MyClic autoinjectors, which may be a consideration, along with other factors, for treatment decisions in the management of patients with inflammatory joint or bowel disease. FUNDING: Biogen International GmbH.

Class I histone deacetylase inhibition modulates metalloproteinase expression and blocks cytokine-induced cartilage degradation.

OBJECTIVE: To examine the ability of a broad-spectrum histone deacetylase (HDAC) inhibitor to protect cartilage in vivo, and to explore the effects of class-selective HDAC inhibitors and small interfering RNA (siRNA)-induced knockdown of HDACs on metalloproteinase expression and cartilage degradation in vitro. METHODS: A destabilization of the medial meniscus (DMM) model was used to assess the in vivo activity of the HDAC inhibitor trichostatin A (TSA). Human articular chondrocytes (HACs) and SW-1353 chondrosarcoma cells were treated with cytokines and TSA, valproic acid, MS-275, or siRNA, and quantitative reverse transcription-polymerase chain reaction was performed to determine the effect of treatment on metalloproteinase expression. HDAC inhibitor activity was detected by Western blotting. A bovine nasal cartilage (BNC) explant assay was performed to measure cartilage resorption in vitro. RESULTS: Systemically administered TSA protected cartilage in the DMM model. TSA, valproic acid, and MS-275 repressed cytokine-induced MMP1 and MMP13 expression in HACs. Knockdown of each class I HDAC diminished interleukin-1-induced MMP13 expression. All of the HDAC inhibitors prevented degradation of BNC, in which TSA and MS-275 repressed cytokine-induced MMP expression. CONCLUSION: Inhibition of class I HDACs (HDAC-1, HDAC-2, HDAC-3) by MS-275 or by specific depletion of HDACs is capable of repressing cytokine-induced metalloproteinase expression in cartilage cells and BNC explants, resulting in inhibition of cartilage resorption. These observations indicate that specific inhibition of class I HDACs is a possible therapeutic strategy in the arthritides.