301. Most patients who reach disease remission following anti-TNF therapy continue to report fatigue: results from the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis.
作者: Katie L Druce.;Yagnaseni Bhattacharya.;Gareth T Jones.;Gary J Macfarlane.;Neil Basu.
来源: Rheumatology (Oxford). 2016年55卷10期1786-90页
RA-related fatigue is common and debilitating, but does not always respond to immunotherapy. In the context of anti-TNF therapy, we aimed to examine whether patients achieving disease remission experienced remission of fatigue.
302. A disintegrin and metalloprotease-17 and galectin-9 are important regulators of local 4-1BB activity and disease outcome in rheumatoid arthritis.
作者: Morten Aagaard Nielsen.;Thomas Andersen.;Anders Etzerodt.;Tue Wenzel Kragstrup.;Tue Kruse Rasmussen.;Kristian Stengaard-Pedersen.;Merete Lund Hetland.;Kim Hørslev-Petersen.;Peter Junker.;Mikkel Østergaard.;Malene Hvid.;Søren K Moestrup.;Bent Deleuran.
来源: Rheumatology (Oxford). 2016年55卷10期1871-9页
Co-stimulatory T cell cytokines are important in the progression of RA. This study investigates the interplay between 4-1BB, a disintegrin and metalloprotease-17 (ADAM17) and galectin-9 (Gal-9) in RA.
303. Performance of Fibromyalgia Rapid Screening Tool (FiRST) to detect fibromyalgia syndrome in rheumatic diseases.
作者: Angelique Fan.;Anne Tournadre.;Bruno Pereira.;Zuzana Tatar.;Marion Couderc.;Sandrine Malochet-Guinamand.;Sylvain Mathieu.;Martin Soubrier.;Jean-Jacques Dubost.
来源: Rheumatology (Oxford). 2016年55卷10期1746-50页
To evaluate the performance of the Fibromyalgia Rapid Screening Tool (FiRST) self-questionnaire for the detection of FM associated with inflammatory rheumatic diseases.
304. The response to the inactivated Hepatitis A vaccine in children with autoinflammatory diseases: a prospective observational controlled study.
作者: Despoina N Maritsi.;George Vartzelis.;Lydia Kossiva.;Olga Vougiouka.;Anastasia Garoufi.
来源: Rheumatology (Oxford). 2016年55卷9期1705-6页 306. How the microbiota shapes rheumatic diseases.
作者: Tom Van de Wiele.;Jens T Van Praet.;Massimo Marzorati.;Michael B Drennan.;Dirk Elewaut.
来源: Nat Rev Rheumatol. 2016年12卷7期398-411页
The human gut harbours a tremendously diverse and abundant microbial community that correlates with, and even modulates, many health-related processes. The mucosal interfaces are particularly active sites of microorganism-host interplay. Growing insight into the characteristic composition and functionality of the mucosal microbiota has revealed that the microbiota is involved in mucosal barrier integrity and immune function. This involvement affects proinflammatory and anti-inflammatory processes not only at the epithelial level, but also at remote sites such as the joints. Here, we review the role of the gut microbiota in shaping local and systemic immune responses and how disturbances in the host-microorganism interplay can potentially affect the development and progression of rheumatic diseases. Increasing our understanding of how to promote host-microorganism homeostasis could therefore reveal novel strategies for the prevention or alleviation of rheumatic disease.
308. The brain-joint axis in osteoarthritis: nerves, circadian clocks and beyond.
Osteoarthritis (OA) is a prevalent and debilitating joint disease for which ageing, obesity and chronic inflammation are known risk factors. The central, peripheral and autonomic nervous systems are essential in all metabolic systems, and emerging evidence suggests a role for these systems in OA. In the past few years, metabolic diseases, such as obesity or diabetes, have been linked to disruption of circadian rhythms that are tightly regulated by the nervous system, whereas inflammatory and autoimmune diseases are known to be linked to disruption of the cholinergic vagus nerve reflex. Interestingly, metabolism, inflammation and circadian rhythms have all been linked to the development and progression of OA. This article reviews current knowledge of the direct and indirect roles of the nervous system and circadian system in the initiation and/or progression of OA, and highlights the directions for future research in this emerging field.
310. Tight control of disease activity fails to improve body composition or physical function in rheumatoid arthritis patients.
作者: Andrew B Lemmey.;Thomas J Wilkinson.;Rebecca J Clayton.;Fazal Sheikh.;John Whale.;Hope S J Jones.;Yasmeen A Ahmad.;Sarang Chitale.;Jeremy G Jones.;Peter J Maddison.;Thomas D O'Brien.
来源: Rheumatology (Oxford). 2016年55卷10期1736-45页
RA typically features rheumatoid cachexia [loss of muscle mass (MM) and excessive total fat mass (TFM), especially trunk FM], which contributes to physical disability. Since rheumatoid cachexia is driven by inflammation, it would be anticipated that the success of tight control of disease activity, such as treat-to-target (T2T), in attenuating inflammation would benefit body composition and physical function. This aim of this cross-sectional study was to assess the impact of T2T on body composition and objectively assessed function in RA patients.
311. BSR and BHPR guideline for the treatment of systemic sclerosis.
作者: Christopher P Denton.;Michael Hughes.;Nataliya Gak.;Josephine Vila.;Maya H Buch.;Kuntal Chakravarty.;Kim Fligelstone.;Luke L Gompels.;Bridget Griffiths.;Ariane L Herrick.;Jay Pang.;Louise Parker.;Anthony Redmond.;Jacob van Laar.;Louise Warburton.;Voon H Ong.; .
来源: Rheumatology (Oxford). 2016年55卷10期1906-10页 312. James Thomas (Tom) Scott 1926-2015.316. Incidence of ANCA-associated vasculitis in a UK mixed ethnicity population.
作者: Fiona A Pearce.;Peter C Lanyon.;Matthew J Grainge.;Reena Shaunak.;Alfred Mahr.;Richard B Hubbard.;Richard A Watts.
来源: Rheumatology (Oxford). 2016年55卷9期1656-63页
We aimed to estimate the incidence of ANCA-associated vasculitis in the UK and how this varied by ethnic group.
317. High frequency of immunodeficiency-like states in systemic lupus erythematosus: a cross-sectional study in 300 consecutive patients.
作者: Sandro F Perazzio.;Átila Granados.;Reinaldo Salomão.;Neusa P Silva.;Magda Carneiro-Sampaio.;Luis Eduardo C Andrade.
来源: Rheumatology (Oxford). 2016年55卷9期1647-55页
To determine the frequency of immunodeficiency-like states in SLE and related clinical features.
318. Intercritical circulating levels of neo-epitopes reflecting matrixmetalloprotease-driven degradation as markers of gout and frequent gout attacks.
作者: Ana M Valdes.;Tina Manon-Jensen.;Abhishek Abhishek.;Wendy Jenkins.;Anne Sofie Siebuhr.;Morten A Karsdal.;Sally Doherty.;Weiya Zhang.;Helen Richardson.;Michael Doherty.;Anne-Christine Bay-Jensen.
来源: Rheumatology (Oxford). 2016年55卷9期1642-6页
Recurrent flares constitute the main clinical burden of gout. Our aim was to assess whether biomarkers measuring MMP tissue degradation could be used as markers of frequent gout flares.
319. The metabolic role of the gut microbiota in health and rheumatic disease: mechanisms and interventions.
作者: Shahla Abdollahi-Roodsaz.;Steven B Abramson.;Jose U Scher.
来源: Nat Rev Rheumatol. 2016年12卷8期446-55页
The role of the gut microbiome in animal models of inflammatory and autoimmune disease is now well established. The human gut microbiome is currently being studied as a potential modulator of the immune response in rheumatic disorders. However, the vastness and complexity of this host-microorganism interaction is likely to go well beyond taxonomic, correlative observations. In fact, most advances in the field relate to the functional and metabolic capabilities of these microorganisms and their influence on mucosal immunity and systemic inflammation. An intricate relationship between the microbiome and the diet of the host is now fully recognized, with the microbiota having an important role in the degradation of polysaccharides into active metabolites. This Review summarizes the current knowledge on the metabolic role of the microbiota in health and rheumatic disease, including the advances in pharmacomicrobiomics and its potential use in diagnostics, therapeutics and personalized medicine.
|