Rheumatology-Rhumatologie
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RHUMATOLOGIE - RHEUMATOLOGY

Obviously a topic of interest for so many people:

for the patient, it includes aching muscles, tendons and joints..

for MDs and researchers, it covers degenerative diseases as well as arthritis, often associated with various autoimmune diseases (see autoimmunity http://www.scoop.it/t/autoimmunity)

fortunately, new diagnostic tools are available

https://www.scoop.it/t/rheumatology-rhumatologie?q=diagnosis

and new biotherapies 

https://www.scoop.it/t/rheumatology-rhumatologie?q=therapy

allowed to improve the prognosis and the quality of life of patients

Gilbert C FAURE's insight:

January 2016

still few viewers (#650) for this topic, but >1280 posts and 2000 views

much less than other immunology topics, but growing!


October 2016 1500 scoops and almost 3K views

January 2018 1700 scoops and #5K views

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Altered composition and phenotype of mucosal-associated invariant T cells in early untreated rheumatoid arthritis | Arthritis Research & Therapy | Full Text

Altered composition and phenotype of mucosal-associated invariant T cells in early untreated rheumatoid arthritis | Arthritis Research & Therapy | Full Text | Rheumatology-Rhumatologie | Scoop.it
Mucosal-associated invariant T (MAIT) cells are innate-like T cells that recognise bacterial metabolites presented by MHC class I-related protein 1 (MR1). Bacterial dysbiosis has been implicated in auto-inflammatory disease development.
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KCa1.1 and Kv1.3 channels regulate the interactions between fibroblast-like synoviocytes and T lymphocytes during rheumatoid arthritis | Arthritis Research & Therapy | Full Text

KCa1.1 and Kv1.3 channels regulate the interactions between fibroblast-like synoviocytes and T lymphocytes during rheumatoid arthritis | Arthritis Research & Therapy | Full Text | Rheumatology-Rhumatologie | Scoop.it
Fibroblast-like synoviocytes (FLS) and CCR7− effector memory T (TEM) cells are two of the major cell types implicated in the progression of rheumatoid arthritis (RA). In particular, FLS become highly invasive, whereas TEM cells proliferate and secrete proinflammatory cytokines, during RA.
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Cell migration: implications for repair and regeneration in joint disease

Cell migration: implications for repair and regeneration in joint disease | Rheumatology-Rhumatologie | Scoop.it
Improved understanding of cell migration in the synovial joint, including the associated cellular and environmental factors, might reveal new therapeutic strategies for joint diseases such as rheumatoid arthritis and osteoarthritis and have important implications for tissue engineering of the joint.

Via Krishan Maggon
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Epigenetics and Cartilage Regeneration | IntechOpen

Epigenetics and Cartilage Regeneration | IntechOpen | Rheumatology-Rhumatologie | Scoop.it
Regenerative cartilage therapy has great potential for the treatment of debilitating diseases such as osteoarthritis and rheumatoid arthritis. Recent advances in the field of epigenetics have enabled us to understand more clearly the role of micro RNAs, DNA methylations and histone modification in...
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Anemia of inflammation

Anemia of inflammation | Rheumatology-Rhumatologie | Scoop.it
Anemia of inflammation (AI), also known as anemia of chronic disease (ACD), is regarded as the most frequent anemia in hospitalized and chronically ill patients. It is prevalent in patients with diseases that cause prolonged immune activation, including infection, autoimmune diseases, and cancer.
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Social Media as a Creative/Disruptive Force in Rheumatology (or Why I Now Tweet)

Social Media as a Creative/Disruptive Force in Rheumatology (or Why I Now Tweet) | Rheumatology-Rhumatologie | Scoop.it
Healio Rheumatology | I have been reflecting on the amazing American College of Rheumatology meeting held in Chicago — also known as #ACR18, a hashtag that those of you in the social media universe immediately recognize as a metadata tag. For the rest of you who don’t recognize this as the hashtag of the meeting itself, I urgently counsel that perhaps it is time to join the ACR social media community. I
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Tophus resolution in patients with chronic refractory gout who have persistent urate-lowering responses to pegloticase | Arthritis Research & Therapy | Full Text

Tophus resolution in patients with chronic refractory gout who have persistent urate-lowering responses to pegloticase | Arthritis Research & Therapy | Full Text | Rheumatology-Rhumatologie | Scoop.it
Pegloticase is a recombinant mammalian uricase conjugated to polyethylene glycol approved in the United States for treatment of chronic refractory gout. It can profoundly decrease serum urate to < 1 mg/dl. In patients receiving pegloticase who did not generate high-titer antidrug antibodies (responders), the serum urate remained low for the duration of therapy, 6 months in the phase III clinical trials plus the open-label extension. The objective of this study was to assess the velocity of tophus resolution in subjects treated with pegloticase. Data from two randomized controlled trials of pegloticase in chronic refractory gout were analyzed. Tophi were assessed by computer-assisted measurements of standardized digital photographs. Subjects were designated as responders and nonresponders based on maintenance of serum urate < 6 mg/dl at months 3 and 6 of treatment. The projected time of complete resolution of all tophi was determined by linear regression analysis. The mean total tophus area at baseline was 585.8 mm2 for responders, 661.5 mm2 for nonresponders, and 674.4 mm2 for placebo-treated patients. Complete resolution at 6 months of at least one tophus was achieved by 69.6% of 23 responders, 27.9% of 43 nonresponders, and 14.3% of 21 patients who received placebo. Complete resolution of all photographed tophi was achieved by 34.8% of biochemical responders, 11.6% of nonresponders, and 0% of placebo-treated patients. The mean velocity of resolution of all tophi was 60.1 mm2/month in responders with a mean projected time of complete resolution of 9.9 months (4.6–32.6 months). There was a significant inverse correlation between serum urate AUC and tophus resolution velocity (r = − 0.40, P = 0.0002), although considerable heterogeneity in the velocity of resolution was noted. The only patient characteristic that correlated with the velocity of tophus resolution was the baseline tophus area. Pegloticase treatment caused a rapid resolution of tophi in responders that correlated with the serum urate lowering associated with this therapy.
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ExchangeCME :: Online Activities

ExchangeCME :: Online Activities | Rheumatology-Rhumatologie | Scoop.it
This activity is jointly provided by Global Education Group and Integritas Communications.   Based on a live symposium supported by an educational grant from Gilead Sciences, Inc. Target Audience This activity has been designed to meet the educational needs of health care professionals involved in the diagnosis, treatment, or management of patients with rheumatoid arthritis. Educational Objectives After completing this activity, the participant should be better able to: Discuss the latest insights into RA immunopathology with a focus on JAK enzyme activation Evaluate patients with RA longitudinally based on an understanding of treat-to-target recommendations and appropriate disease activity measures Describe the mechanistic profiles and clinical trial data for current and emerging targeted synthetic DMARDs Integrate targeted synthetic DMARDs into treatment regimens for patients with RA based on current clinical practice guidelines and evidence for efficacy and safety Faculty Rieke Alten, MD (Course Chair) Professor of Medicine Department Head Internal Medicine, Rheumatology, Clinical Immunology, and Osteology Schlosspark-Klinik University Medicine Berlin Berlin, Germany Joel Kremer, MD, FACP Pfaff Family Professor of Medicine Albany Medical College Director of Research The Center for Rheumatology Albany, New York, USA Josef Smolen, MD Professor of Medicine Chair, Division of Rheumatology Department of Medicine III Medical University of Vienna Vienna, Austria Agenda Pathophysiology: A Focus on JAK Enzymes Josef Smolen, MD Long-term Assessment of Patients With RA: Understanding Treatment Targets as a Foundation for Therapeutic Tailoring Joel Kremer, MD Targeted Synthetic DMARDs in the Treatment of RA Rieke Alten, MD Case Study Panel Discussion: Putting the Evidence to Practice Moderated by: Rieke Alten, MD Program Overview Rheumatoid arthritis (RA) is a chronic inflammatory joint disease that can cause bone and cartilage damage and lead to disability.1 RA affects about 24.5 million people, with 5 and 50 per 100,000 people newly developing the condition each year.1,2 RA has resulted in increased mortality in recent years, creating a need for an understanding of treat-to-target recommendations and appropriate disease activity measures.3 Adopting treat-to-target strategies in RA patients has shown great promise in improving RA outcomes.4 Treatments for RA continue to emerge along with advances in the understanding of its pathologic mechanisms and the development of drugs that target them.5 Many cytokines involved in controlling cell growth and the immune response in RA function by binding to and activating cytokine receptors, which in turn rely on the Janus kinase (JAK) family of enzymes for signal transduction. Disease-modifying antirheumatic drugs (DMARDs) inhibit the activity of these JAK enzymes and block cytokine signaling.6  Identifying the mechanistic profiles and clinical trial data for current and emerging targeted synthetic DMARDs can assist health care providers in optimizing RA patient outcomes.7 In this Clinical Issues™ program, an expert faculty panel will discuss and debate the latest insights into RA immunopathology with a focus on JAK enzyme activation, increase participants’ understanding of treat-to-target recommendations and appropriate disease activity measures, and describe the mechanistic profiles and clinical trial data for current and emerging targeted synthetic DMARDs. Attendees will leave this engaging program with new information and a fresh perspective on the evolving best practices for managing patients with RA.  References Smolen JS, et al. Lancet. 2016;388(10055):2023-2038. GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016;388 (10053): 1545-1602. GBD 2013 Mortality and Causes of Death, Collaborators. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;385 (9963): 117-171. Bykerk VP, et al. Tocilizumab in patients with active rheumatoid arthritis and inadequate responses to DMARDs and/or TNF inhibitors: a large, open-label study close to clinical practice. Ann Rheum Di. 2012;71(12): 1950-1954. Kahlenberg JM, Fox DA. Advances in the medical treatment of rheumatoid arthritis. Hand Clin. 2011;27(1):11-20. Kontzias A, et al. Jakinibs: a new class of kinase inhibitors in cancer and autoimmune disease. Curr Opin Pharmacol. 2012;12(4):464-470. Ramiro S, et al. Safety of synthetic and biological DMARDs: a systematic literature review informing the 2016 update of the EULAR recommendations for management of rheumatoid arthritis. Ann Rheum Dis. 2017;76(6):1101-1136. Physician Accreditation Statement This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of Global Education Group (Global) and Integritas Communications. Global is accredited by the ACCME to provide continuing medical education for physicians. Credit Designation Global Education Group designates this enduring activity for a maximum of 1.0 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Global Contact Information For information about the accreditation of this program, please contact Global at 303-395-1782 or cme@globaleducationgroup.com. Fee Information There is no fee for this educational activity. Disclosure of Conflicts of Interest Global Education Group (Global) requires instructors, planners, managers, and other individuals and their spouses/life partners who are in a position to control the content of this activity to disclose any real or apparent conflict of interest they may have as related to the content of this activity. All identified conflicts of interest are thoroughly vetted by Global for fair balance, scientific objectivity of studies mentioned in the materials or used as the basis for content, and appropriateness of patient care recommendations. The faculty reported the following financial relationships or relationships to products or devices they or their spouses/life partners have with commercial interests related to the content of this CME activity: Rieke Alten, MD: Grants/Research Support: Gilead Sciences, Inc., and Pfizer Inc. Honoraria/Consultation fees: Eli Lilly & Company, and Pfizer Inc. Speakers Bureau: Eli Lilly & Company, and Pfizer Inc. Joel Kremer, MD, FACP: Grants/Research Support: AbbVie Inc., Genentech, Inc., Eli Lilly & Company, and Novartis Pharmaceuticals Corporation. Stock Shareholder: Corrona Josef Smolen, MD: Grants/Research Support: AbbVie Inc., AstraZeneca, Janssen Pharmaceuticals, Inc., Eli Lilly & Company, F. Hoffmann-La Roche Ltd, Merck Sharp Dohme Corp., and Pfizer Inc. Honoraria/Consultation fees:  AbbVie Inc., Amgen Inc., AstraZeneca, Astro-Pharma GmbH, Bristol-Myers Squibb, Celgene Corporation, Celltrion Inc., Chugai Pharmaceutical Co., Ltd., Eli Lilly & Company, Gilead Sciences, Inc., GlaxoSmithKline, F. Hoffmann-La Roche Ltd, ILTOO Pharma, Janssen Pharmaceuticals, Inc., Medimmune, LLC, Merck Sharp Dohme Corp., Pfizer Inc., Sandoz International GmbH, Samsung Pharmaceutical Co., Ltd., Sanofi, and UCB S.A. The planners and managers reported the following financial relationships or relationships to products or devices they or their spouse/life partner have with commercial interests related to the content of this CME activity: Lindsay Borvansky: Nothing to disclose Andrea Funk:  Nothing to disclose Liddy Knight:  Nothing to disclose Jim Kappler, PhD:  Nothing to disclose Disclosure of Unlabeled Use This educational activity may contain discussion of published and/or investigational uses of agents that are not indicated by the FDA. Global Education Group (Global) and Integritas do not recommend the use of any agent outside of the labeled indications. The opinions expressed in the educational activity are those of the faculty and do not necessarily represent the views of any organization associated with this activity. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings. Disclaimer Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed in this activity should not be used by clinicians without evaluation of patient conditions and possible contraindications on dangers in use, review of any applicable manufacturer’s product information, and comparison with recommendations of other authorities. Instructions to Receive Credit In order to receive credit for this activity, the participant must score 70% on the posttest and complete the program evaluation
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Ma Vie de Spondy Accueil

Ma Vie de Spondy Accueil | Rheumatology-Rhumatologie | Scoop.it
Ce Site s’adresse à toute personne intéressée par la pathologie de la spondylarthrite ankylosante (également dénommée « SA » ou « spondy »). Il a pour but d’apporter des informations (notamment à caractère médical et scientifique), conseils, témoignages sur la maladie aux utilisateurs du site, qu’ils soient atteints de cette pathologie ou proches de personnes souffrant de SA.
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Meniscal Tears And ‘Mechanical Symptoms’ – An Unsolved Puzzle

Meniscal Tears And ‘Mechanical Symptoms’ – An Unsolved Puzzle | Rheumatology-Rhumatologie | Scoop.it
Mechanical symptoms in combination with a meniscal tear on MRI is currently a strong indication for arthroscopic meniscal surgery. We recently conducted several studies that...
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Adding baseline protein biomarkers to clinical predictors does not enhance prediction of treatment response to a methotrexate strategy in early rheumatoid arthritis

Adding baseline protein biomarkers to clinical predictors does not enhance prediction of treatment response to a methotrexate strategy in early rheumatoid arthritis | Rheumatology-Rhumatologie | Scoop.it
Recently, we identified baseline higher disease activity score assessing 28 joints, current smoking and no alcohol consumption as predictors of inadequate response (IR) to methotrexate (MTX), used with or without other conventional synthetic disease modifying anti-rheumatic drugs, here designated...

Via Krishan Maggon
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Case Report: The Hairdresser Who Couldn't Comb Hair

Case Report: The Hairdresser Who Couldn't Comb Hair | Rheumatology-Rhumatologie | Scoop.it
Polymyalgia rheumatica (PMR) is an inflammatory rheumatic condition characterized by pain and morning stiffness at the neck, shoulders and hip girdle. It can be associated with giant cell arteritis (GCA); in fact, the two disorders may represent a continuum of the same disease process. This case describes a patient who initially refused treatment for PMR... [Read More]
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A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis

A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis | Rheumatology-Rhumatologie | Scoop.it
ELMO1 is a protein centrally involved in controlling the engulfment of apoptotic cells. Ravichandran and colleagues demonstrate a noncanonical role for ELMO1 in the promotion of neutrophil migration and inflammatory arthritis.
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Effects of B-cell directed therapy on the preclinical stage of rheumatoid arthritis: the PRAIRI study

Effects of B-cell directed therapy on the preclinical stage of rheumatoid arthritis: the PRAIRI study | Rheumatology-Rhumatologie | Scoop.it
Objectives We explored the effects of B-cell directed therapy in subjects at risk of developing autoantibodypositive rheumatoid arthritis (RA), who never experienced inflammatory arthritis before, and explored biomarkers predictive of arthritis development.
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Stem cell signal drives new bone building

Stem cell signal drives new bone building | Rheumatology-Rhumatologie | Scoop.it
In experiments in rats and human cells, Johns Hopkins Medicine researchers say they have added to evidence that a cellular protein signal that drives both bone and fat formation in selected stem cells can be manipulated to ...

Via Krishan Maggon
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Article: Macrophage activation syndrome with lung involvement complicating adult-onset Still's disease (full text) - December 2018 - NJM

Article: Macrophage activation syndrome with lung involvement complicating adult-onset Still's disease (full text) - December 2018 - NJM | Rheumatology-Rhumatologie | Scoop.it
Full text KEY WORDS Adult-onset Still’s disease, AOSD, macrophage activation syndrome, pulmonary involvement INTRODUCTION Adult-onset Still’s disease (AOSD) was first reported in 1971 by Eric Bywaters in 14 adult patients who failed to fulfill the criteria of classic rheumatoid arthritis.1 It is a rare systemic auto-inflammatory disorder with high spiking fever, evanescent skin rash, arthralgia/arthritis, neutrophilic leukocytosis and marked hyperferritinemia.2,3 Despite a usually favorable prognosis in AOSD, patients can experience disease flares which involve vital organs, or present specific clinical features, such as macrophage activation syndrome (MAS).4 Here, we report on an AOSD patient with MAS-related pulmonary parenchymal involvement who was successfully managed by high-dose corticosteroids and pulse cyclophosphamide therapy. CASE REPORT A 19-year-old Han Chinese female was presented with polyarthritis affecting her wrists, knees and ankles, and a recurrent maculopapular erythematous rash over her trunk and limbs during febrile spikes (above 390C). Laboratory tests revealed leukocytosis (10,600 to 15,800/µl) with dominant neutrophil classification (82 to 92%), elevated liver enzyme levels, absence of autoantibody profiles and negative microbiological examinations. One year later, she visited the outpatient rheumatology clinic with a series of clinical, laboratory and radiological surveys, leading to the diagnosis of AOSD by exclusion of infection, malignancy or other rheumatologic diseases. She was brought to the emergency department one month later due to a cough and dyspnea, where radiological images demonstrated diffuse peribronchovascular infiltrates, multiple ground-glass opacities and consolidations in her lower lungs without pleural effusion (figures 1A and B), as well as hepatosplenomegaly. Hemogram was hemoglobin = 8.0 g/dl, platelet count = 25,000/µl and leukocyte count = 9,300/µl (neutrophils 63%), and bone marrow examination revealed hemophagocytosis. She exhibited elevated levels of aspartate aminotransferase (1,115 U/l), alanine aminotransferase (311 U/l), ferritin (9,655 ng/mL), triglycerides (388 mg/dl) and impaired estimated glomerular filtration rate (22 ml/min/1.73 m2 ) with unremarkable urinalysis. Pathogenic microorganisms were not isolated despite extensive cultures. MAS complication was identified with the prescription of methylprednisolone 20 mg, every eight hours by injection. However, bloody sputum with a significant drop of hemoglobin led to a suspicion of diffuse alveolar hemorrhage. Multiple petechiae and hematuria with global coagulation tests fulfilled the disseminated intravascular coagulation criteria, followed by attacks of generalized tonic-clonic seizure; both are distinct AOSD-related MAS presentations.4 A monthly pulse cyclophosphamide 750 mg infusion was initiated due to progressive pulmonary infiltration (figure 1C) and persistent multi-organ abnormalities. The patient had a complete recovery of lung involvement (figure 1D) and other systemic dysfunction with daily corticosteroids replaced by weekly methotrexate therapy during outpatient follow-up. DISCUSSION Unlike other rheumatology disorders involving multiple organs with known respiratory abnormalities, little attention has been paid to lung involvement in AOSD.5 By excluding the infectious etiology, pulmonary infiltrates have been observed in fewer than one-tenth of AOSD patients, with its acute nature accompanied by pleural effusion during disease exacerbation and a fast response to corticosteroids usage.6 In a recent literature review including 18 AOSD cases with parenchymal lung involvement, two with MAS were successfully managed by corticosteroids alone.7 In another review with nine cases of corticosteroid-resistant AOSD-associated MAS significant responses were observed in all 5 patients receiving cyclophosphamide injection, despite no associated pulmonary parenchymal involvement.8 In the reported patient with progressive pulmonary infiltration under the high-dose corticosteroid therapy, adding cyclophosphamide resulted in complete recovery. Notably, biologics have proven to be safe and effective in the long-term management of AOSD, particularly in cases with systemic involvement.9 Since MAS is characterized by a cytokine storm with overproduction of pro-inflammatory cytokines, anti-cytokine agents are an attractive approach in treating this complication.10 Indeed, in young female victims, cytokine blockades as alternative therapeutics can avoid the well-known cyclophosphamide-related gonadal toxicity. DISCLOSURES All authors declare no conflict of interest. There was no funding or financial support in this report. REFERENCES Bywaters EG. Still’s disease in the adult. Ann Rheum Dis. 1971;30:121-33.  Gerfaud-Valentin M, Jamilloux Y, Iwaz J, Sève P. Adult-onset Still’s disease. Autoimmun Rev. 2014;13:708-22.  Meijvis SC, Endeman H, Geers AB, ter Borg EJ. Extremely high serum ferritin levels as diagnostic tool in adult-onset Still’s disease. Neth J Med. 2007;65:212-4.  Efthimiou P, Kadavath S, Mehta B. Life-threatening complications of adult-onset Still’s disease. Clin Rheumatol. 2014;33:305-14.  Cheema GS, Quismorio FP Jr. Pulmonary involvement in adult-onset Still’s disease. Curr Opin Pul Med. 1999;5:305-9.  Reginato AJ, Schumacher HR, Baker DG, O’Connor CR, Ferreiros J. Adult onset Still’s disease: experience in 23 patients and literature review with emphasis on organ failure. Semin Arthritis Rheum. 1987;17:39-57.  Gerfaud-Valentin M, Cottin V, Jamilloux Y, et al. Parenchymal lung involvement in adult-onset Still disease: ASTROBE-compliant case series and literature review. Medicine (Baltimore). 2016;95:e4258.  Kumakura S, Murakawa Y. Clinical characteristics and treatment outcomes of autoimmune-associated hemophagocytic syndrome in adults. Arthritis Rheumatol. 2014;66:2297-307.  Cavalli G, Franchini S, Aiello P, et al. Efficacy and safety of biological agents in adult-onset Still’s disease. Scand J Rheumatol. 2015;44:309-14.  Grom AA, Horne A, De Benedetti F. Macrophage activation syndrome in the era of biologic therapy. Nat Rev Rheumatol. 2016;12:259-68.
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Ankylosing spondylitis - chalk stick fracture | Radiology Case | Radiopaedia.org

Ankylosing spondylitis - chalk stick fracture | Radiology Case | Radiopaedia.org | Rheumatology-Rhumatologie | Scoop.it

Patients with ankylosing spondylitis are prone to chalk stick fractures, often through the ossified disk. 
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Involvement of tumor necrosis factor alpha in steroid-associated osteonecrosis of the femoral head: friend or foe? | Stem Cell Research & Therapy | Full Text

Involvement of tumor necrosis factor alpha in steroid-associated osteonecrosis of the femoral head: friend or foe? | Stem Cell Research & Therapy | Full Text | Rheumatology-Rhumatologie | Scoop.it
The etiology and pathology osteonecrosis of the femoral head (ONFH) are not completely clarified. As a cytokine participating in systemic inflammation, tumor necrosis factor alpha (TNFα) has been shown to be involved in the pathogenesis of ONFH.
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Immune-related adverse events with immune checkpoint inhibitors affecting the skeleton: a seminal case series | Journal for ImmunoTherapy of Cancer | Full Text

Immune-related adverse events with immune checkpoint inhibitors affecting the skeleton: a seminal case series | Journal for ImmunoTherapy of Cancer | Full Text | Rheumatology-Rhumatologie | Scoop.it
The use of immune checkpoint inhibitors is increasing in cancer therapy today. It is critical that treatment teams become familiar with the organ systems potentially impacted by immune-related adverse events associated with these drugs. Here, we report adverse skeletal effects of immunotherapy, a phenomenon not previously described. In this retrospective case series, clinical, laboratory and imaging data were obtained in patients referred to endocrinology or rheumatology with new fractures (n = 3) or resorptive bone lesions (n = 3) that developed while on agents targeting PD-1, CTLA-4 or both. The average age of patients was 59.3 (SD 8.6), and five were male. Cancer types included melanoma, renal cell carcinoma and non-small cell lung cancer. All fracture patients had vertebral compression, and two of the three had multiple fracture sites involved. Sites of resorptive lesions included the shoulder, hand and clavicle. Biochemically, elevated or high-normal markers of bone resorption were seen in five of the six patients. Erythrocyte sedimentation rate was elevated in three of the four patients where checked. This case series represents the first description of potential skeletal adverse effects related to immune checkpoint inhibitors. These findings are important for providers caring for patients who experience musculoskeletal symptoms and may merit additional evaluation.
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LACC1 Regulates TNF and IL-17 in Mouse Models of Arthritis and Inflammation

LACC1 Regulates TNF and IL-17 in Mouse Models of Arthritis and Inflammation | Rheumatology-Rhumatologie | Scoop.it
Both common and rare genetic variants of laccase domain-containing 1 ( LACC1 , previously C13orf31) are associated with inflammatory bowel disease, leprosy, Behcet disease, and systemic juvenile idiopathic arthritis.
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Immunodeficiency Diseases and the Rheumatologist: It’s Not Just About Infection –

Immunodeficiency Diseases and the Rheumatologist: It’s Not Just About Infection – | Rheumatology-Rhumatologie | Scoop.it
Primary immunodeficiency disorders (PID) have a growing spectrum of noninfectious complications. Vasculitis is one. Here’s what rheumatologists should take away from recent research.
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Impact of Cyclic Citrullinated Peptide Antibody Level on Progression to Rheumatoid Arthritis in Clinically Tested CCP‐Positive Patients Without RA - Ford - - Arthritis Care & Research - Wiley O...

Objective We investigated risk of progression to rheumatoid arthritis (RA) in patients who were cyclic citrullinated antibody positive (CCP+) without RA at initial presentation. Methods We performed a retrospective cohort study of CCP+ individuals seen at a US tertiary care system between 2009‐2018 who were without RA or other systemic rheumatic disease by medical record review at time of CCP positivity. Progression to classifiable RA was determined through medical record review. We investigated risk of progression to RA overall and stratified by CCP level (low: >1 to 2 times upper limit of normal [x ULN]; medium: >2 to 3x ULN; high: >3x ULN). Multivariable Cox regression estimated the hazard ratio (HR) and 95% confidence interval (95%CI) for RA by CCP level. Results We identified 340 CCP+ patients who were without RA or other rheumatic disease at baseline. During 1047 person‐years of follow‐up, 73 (21.5%) patients developed RA. Risk of progression to RA increased with CCP level, with 46.0% (95%CI 34.7‐55.3) of high level CCP patients progressing to RA by 5 years. Compared to low CCP, medium (HR 3.00, 95%CI 1.32‐6.81) and high (HR 4.83, 95%CI 2.51‐9.31) CCP levels were strongly associated with progression to RA, adjusting for age, sex, body mass index, smoking, family history of RA, and rheumatoid factor level. Conclusion Among CCP+ patients without RA, risk for progression to RA increased substantially with increasing CCP level. This study provides further support for close monitoring for development of RA among CCP+ patients and identifying strategies to mitigate this risk. This article is protected by copyright. All rights reserved.

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Online Courses | Pathoaetiology of shoulder conditions, clinical and imaging diagnosis

Online Courses | Pathoaetiology of shoulder conditions, clinical and imaging diagnosis | Rheumatology-Rhumatologie | Scoop.it
Shoulder Screening Course In this course you will learn how to systematically work through a process of screening the patient for red flags, other causes of shoulder pain, obtaining appropriate diagnostic imaging, and then classifying shoulder pain into categories that guide management.    Modules: Red Flags You will learn to screen for red flag indicators of potentially serious pathology and refer the patient for necessary evaluation within an appropriate time-frame. Click here to register Health Screening You will learn current health guidelines for alcohol, tobacco and physical activity, and how to screen for risk factors and atypical symptoms and signs of medical conditions that may present with shoulder symptoms. Click here to register Pain and Psychosocial Modifiers In this module you will learn the pathoaetiology and features of various pain states, including the mechanisms behind persistent pain. You will learn how to screen for and manage psychosocial factors and learn about their relationship to persistent pain. Click here to register Cervical Spine and Neurological Examination In this module you will learn about the difference between somatic and radicular pain and how to examine the cervical spine to identify local, or referred pain. You will learn the diagnostic features of cervical radiculopathy, how to perform an accurate and thorough neurological examination. Click here to register Shoulder Imaging In this module you will learn about the strengths and limitations of imaging modalities, indications for imaging, prevalence of imaged pathology and how to read and interpret basic shoulder x-ray views. Click here to register Diagnostic Classification of Shoulder Conditions This module defines “diagnosis”, highlights the importance of the diagnostic process, provides a brief overview of diagnostic accuracy and presents a clinical classification system for shoulder conditions that forms the basis of the modules in the “Diagnosis and Non-Surgical Management” Course. Click here to register Course Aim To produce practitioners who can: Accurately screen patients presenting with shoulder girdle symptoms for red flags, and other causes of symptoms that may require additional investigations or treatment in the primary contact setting. Read basic shoulder x-ray views and interpret findings in the context of patient symptoms.  Classify patients with shoulder symptoms into diagnostic categories that help guide management. Learning Outcomes By the end of the course, the participant will be able to: Identify red flag indicators of serious pathology and refer appropriately. Undertake an efficient and effective health screen for lifestyle and health risk factors, and symptoms and signs of systemic medical conditions presenting with shoulder pain and refer appropriately. Describe the features of different pain states, the mechanisms underpinning persistent pain, and explain the relationship of psychosocial factors to persistent pain. Competently perform an examination of the cervical spine and neurological examination of the upper limb to identify pain referred from the cervical spine or evidence of neurological compromise. Appropriately refer for diagnostic imaging, and describe the strengths and limitations of basic shoulder x-ray views for identifying specific shoulder pathology. Describe the diagnostic classification of the main categories of shoulder conditions that can be identified clinically to guide management. Social Learning Online Forum Those enrolled in all modules in this course will be invited to attend the online forum led by Dr Angela Cadogan, The purpose of this informal online forum is to ask any questions you have from the online learning material and to discuss any patient cases. A link to the forum will be sent to all those enrolled the full course closer to the time. See the SMS website for online forum dates. Facebook Group Those who complete all modules in this course will be invited to join the “Stiff Shoulder” Facebook Group upon completion of the course. Membership to this Group is indefinite. This Group contains social learning units where latest research and updates are organised by topics that align with the modules in this course. You can check off the items you complete and use this for CPD purposes. Continuing Education Certificates After completion of the Course, you will receive a Certificate of Completion. If you score more than 75% in the quizzes, you will receive a Certificate of Achievement. Copyright Notice The materials provided in this course are protected by copyright and are to be used solely for educational purposes by students enrolled in Southern Musculoskeletal Seminars courses and its teachers. You may not sell, alter or further reproduce or distribute any part of this material to any other person. Where provided to you in electronic format, you may only print from it for your own private study and research. Failure to comply with the terms of this warning may expose you to legal action for copyright infringement. Before you begin It is recommended you follow SMS on Twitter or Facebook, or check the SMS website to receive notifications of new lessons, updates and clinical resources related to the Shoulder Course Series.
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