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Objetivo: Evaluar la densidad mineral ósea (DMO) y parámetros de 3D-Shaper a nivel de fémur proximal (FP) en adultos con hipofosfatasia (HPP) confirmada genéticamente y compararlos en aquellos sujetos con y sin fracturas. Material y métodos: Análisis transversal de datos densitométricos y de arquitectura ósea de la visita basal de un estudio longitudinal en el que se incluyeron pacientes con HPP. Se realizó un estudio densitométrico (Lunar Prodigy, GE iDXA) en FP y se empleó el software 3D-Shaper (version 2,7. Galgo Medical). Resultados: Se incluyeron 33 adultos con HPP con mutaciones en heterocigosis. Un 63,6% (21/33) fueron mujeres (42,9% postmenopáusicas), y 8 de los varones (66,6%) fueron mayores de 50 años. La media de edad fue 50,56±15,08 años, el 30,3% (10/33) tuvieron fracturas previas traumáticas, y un 15,2% (5/33), de estrés. La prevalencia de osteoporosis en CF fue del 11,8% (2/17) y de osteopenia, 82,4% (14/17). En premenopáusicas y varones jóvenes se detectó baja masa ósea para la edad en un 12,5% (2/16). Al comparar sujetos con fracturas de estrés y sin ellas, así como con traumáticas, no hubo diferencias en DMO. El 3D-Shaper mostró disminución del grosor cortical (mm) en pacientes con fracturas de estrés [1,8 (1,77-1,89)] frente a sujetos sin ellas [1,94 (1,87-2,03, p=0,03)] y en comparación con los que tuvieron fracturas traumáticas [1,97 (1,88-2,04), p=0,03]. Conclusiones: Estos datos reflejan una discreta repercusión densitométrica en formas más leves del adulto. Estudios de arquitectura ósea pudieran resultar de interés para determinar pacientes susceptibles de presentar fracturas de estrés.

Abstract Introduction No definitive data are available regarding the value of switching to an alternative TNF antagonist in rheumatoid arthritis patients who fail to respond to the first one. The aim of this study was to evaluate treatment response in a clinical setting based on HAQ improvement and EULAR response criteria in RA patients who were switched to a second or a third TNF antagonist due to failure with the first one. Methods This was an observational, prospective study of a cohort of 417 RA patients treated with TNF antagonists in three university hospitals in Spain between January 1999 and December 2005. A database was created at the participating centres, with well-defined operational instructions. The main outcome variables were analyzed using parametric or non-parametric tests depending on the level of measurement and distribution of each variable. Results Mean (± SD) DAS-28 on starting the first, second and third TNF antagonist was 5.9 (± 2.0), 5.1 (± 1.5) and 6.1 (± 1.1). At the end of follow-up, it decreased to 3.3 (± 1.6; Δ = -2.6; p > 0.0001), 4.2 (± 1.5; Δ = -1.1; p = 0.0001) and 5.4 (± 1.7; Δ = -0.7; p = 0.06). For the first TNF antagonist, DAS-28-based EULAR response level was good in 42% and moderate in 33% of patients. The second TNF antagonist yielded a good response in 20% and no response in 53% of patients, while the third one yielded a good response in 28% and no response in 72%. Mean baseline HAQ on starting the first, second and third TNF antagonist was 1.61, 1.52 and 1.87, respectively. At the end of follow-up, it decreased to 1.12 (Δ = -0.49; p < 0.0001), 1.31 (Δ = -0.21, p = 0.004) and 1.75 (Δ = -0.12; p = 0.1), respectively. Sixty four percent of patients had a clinically important improvement in HAQ (defined as ≥ -0.22) with the first TNF antagonist and 46% with the second. Conclusion A clinically significant effect size was seen in less than half of RA patients cycling to a second TNF antagonist.

To update and integrate the recommendations for ankylosing spondylitis and the recommendations for the use of tumour necrosis factor inhibitors (TNFi) in axial spondyloarthritis (axSpA) into one set applicable to the full spectrum of patients with axSpA. Following the latest version of the European League Against Rheumatism (EULAR) Standardised Operating Procedures, two systematic literature reviews first collected the evidence regarding all treatment options (pharmacological and non-pharmacological) that were published since 2009. After a discussion of the results in the steering group and presentation to the task force, overarching principles and recommendations were formulated, and consensus was obtained by informal voting. A total of 5 overarching principles and 13 recommendations were agreed on. The first three recommendations deal with personalised medicine including treatment target and monitoring. Recommendation 4 covers non-pharmacological management. Recommendation 5 describes the central role of non-steroidal anti-inflammatory drugs (NSAIDs) as first-choice drug treatment. Recommendations 6-8 define the rather modest role of analgesics, and disprove glucocorticoids and conventional synthetic disease-modifying antirheumatic drugs (DMARDs) for axSpA patents with predominant axial involvement. Recommendation 9 refers to biological DMARDs (bDMARDs) including TNFi and IL-17 inhibitors (IL-17i) for patients with high disease activity despite the use (or intolerance/contraindication) of at least two NSAIDs. In addition, they should either have an elevated C reactive protein and/or definite inflammation on MRI and/or radiographic evidence of sacroiliitis. Current practice is to start with a TNFi. Switching to another TNFi or an IL-17i is recommended in case TNFi fails (recommendation 10). Tapering, but not stopping a bDMARD, can be considered in patients in sustained remission (recommendation 11). The final two recommendations (12, 13) deal with surgery and spinal fractures. The 2016 Assessment of SpondyloArthritis international Society-EULAR recommendations provide up-to-date guidance on the management of patients with axSpA., Competing Interests: Competing interests: DvdH received consulting fees from AbbVie, Amgen, Astellas, AstraZeneca, BMS, Boeringer Ingelheim, Celgene, Daiichi, Eli-Lilly, Galapagos, Gilead, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi-Aventis, UCB and is Director of Imaging Rheumatology BV. RL received consulting fees from AbbVie, Ablynx, Amgen, AstraZeneca, Bristol-Myers Squibb, Celgene, Janssen, Galapagos, GlaxoSmithKline, Novartis, Novo-Nordisk, Merck, Pfizer, Rhoche, Schering-Plough, TiGenix, UCB and is Director of Rheumatology Consultancy BV. XB received consulting fees and research grants from AbbVie, Bristol-Myers Squibb, Celgene, Janssen, Novartis, Pfizer, Roche, MSD and UCB. FVdB received consulting and/or speaker fees from AbbVie, BMS, Celgene, Eli-Lilly, Janssen, Merck, Novartis, Pfizer and UCB. AC received consulting fees from AbbVie, Celgene, Eli-Lilly, Janssen-Cilag, Merck Sharp & Dohme, Novartis, Pfizer and UCB. MD received consulting fees from AbbVie, BMS, Boeringer Ingelheim, Celgene, Eli-Lilly, Galapagos, Janssen, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi-Aventis and UCB. FvG received consulting fees from Pfizer, MSD, AbbVie and Novartis. PG received consulting fees from AbbVie and Roche. IvdH-B received consulting fees from AbbVie, UCB and MSD and received unrestricted grants for investigator initiated studies from MSD, Pfizer and AbbVie. RDI received consulting fees from Amgen, Janssen, AbbVie, Novartis. UK received consultancy fees as well as grant and research support from AbbVie, Chugai, MSD, Novartis, Pfizer, Roche and UCB. TKK received consulting fees from AbbVie, Biogen, BMS, Boehringer Ingelheim, Celltrion, Eli-Lilly, Epirus, Janssen, Merck-Serono, MSD, Mundipharma, Novartis, Oktal, Orion Pharma, Hospira/Pfizer, Roche, Sandoz and UCB Pharma. PM received speaker/consulting fees from AbbVie, Centocor, Janssen, MSD, Novartis and Pfizer. HM-O received consulting fees from AbbVie, Celgene, Janssen, MSD, Novartis, Pfizer and UCB and grants from Janssen and Pfizer. AM received consulting fees and/or grants from AbbVie, Merck Pfizer and UCB. VN-C received consulting fees from AbbVie, BMS, Novartis, Pfizer, Roche and UCB. SO received consulting fees, speaking fees and/or honoraria from AbbVie, Pfizer, UCB, Merck Sharp & Dohme and Novartis. FMP-S received consulting fees from AbbVie, Celgene, Janssen, Novartis, Pfizer, Roche, Merck Sharp & Dohme, UCB, Biogen. JR received consulting fees from Janssen and is a participant in clinical trials of Janssen and Eli-Lilly. MR received consulting or speaking fees from AbbVie, Bristol-Myers Squibb, Celgene, Chugai, Janssen, Novartis, Merck, Pfizer, Roche, UCB. JS received consulting fees from AbbVie, Boeringer Ingelheim, Eli-Lilly, Galapagos, Janssen, Merck, Novartis, Pfizer, Roche, UCB. PS-B received consulting fees from AbbVie, Janssen, Novartis, Pfizer, Roche, UCB. JB received research grants, honoraria, speaker fees and consultancy payments from AbbVie (Abbott), Amgen, Biogen, Boehringer Ingelheim, BMS, Celgene, Celltrion, Centocor, Chugai, EBEWE Pharma, Epirus, Hospira, Janssen, Medac, MSD (Schering-Plough), Mundipharma, Novartis, Pfizer (Wyeth), Roche, Sanofi-Aventis and UCB., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)