scholarly journals Global Hypertrophic Calcification of Shoulder Joint Capsule

2021 ◽  
Vol 14 ◽  
pp. 117954762110253
Author(s):  
Abdulkarim Yousef Aldehaim ◽  
Abdurhman Saud Alarfaj

Background: Calcification around the shoulder joint usually occur inside or around the tendons of the rotator cuff. We herein report on a case of global hypertrophic calcification of shoulder joint capsule in a patient with Rheumatoid arthritis. Case Report: An 86 years-old male with a long-standing history of seropositive Rheumatoid arthritis. The treatment for his Rheumatoid arthritis included Methotrexate and Hydroxychloroquine initially, but due lack of control, adalimumab was added with excellent control of his arthritis. He has progressively experienced an increasing pain and stiffness in his shoulders, in addition to an increasing limitation of shoulder movement. Magnetic Resonance Imaging revealed severe arthritis with remoulding deformity with extensive capsular calcification, intra-articular loose-bodies. Discussion: This phenomenon of calcification of shoulder capsule has not been reported before. The pathophysiology of calcific tendinopathy of the shoulder remains controversial. The calcific deposits consist of poorly-crystallized hydroxyapatite. Conclusion: Global hypertrophic calcification of shoulder joint capsule is unique and unreported in the literature. We can postulate that the long-standing inflammation of the synovial lining of the capsules had a major part. Moreover, Diabetes Mellitus, smoking, and repetitive manoeuvres are recognized contributing factors as well for similar conditions. Genetic predisposition seems to play a role as well. We think all those have played part in the development of this unprecedented presentation. Management should be tailored to target specific symptoms for pain, rigidity, and decreasing calcification size. Several options are available, including Kinesiotherapy, electrotherapy modalities, iontophoresis, electroshock wave therapy, and finally surgical approaches for progressive and refractory cases.

2009 ◽  
Vol 29 (S 01) ◽  
pp. S87-S89 ◽  
Author(s):  
I. Music ◽  
M. Novak ◽  
B. Acham-Roschitz ◽  
W. Muntean

SummaryAim: In children, screening for haemorrhagic disorders is further complicated by the fact that infants and young children with mild disease in many cases most likely will not have a significant history of easy bruising or bleeding making the efficacy of a questionnaire even more questionable. Patients, methods: We compared the questionnaires of a group of 88 children in whom a haemorrhagic disorder was ruled out by rigorous laboratory investigation to a group of 38 children with mild von Willebrand disease (VWD). Questionnaires about child, mother and father were obtained prior to the laboratory diagnosis on the occasion of routine preoperative screening. Results: 23/38 children with mild VWD showed at least one positive question in the questionnaire, while 21/88 without laboratory signs showed at least one positive question. There was a trend to more specific symptoms in older children. Three or more positive questions were found only in VWD patients, but only in a few of the control group. The question about menstrual bleeding in mothers did not differ significantly. Sensitivity of the questionnaire for a hemostatic disorder was 0.60, while specifity was 0.76. The negative predictive value was 0.82, but the positive predictive value was only 0.52. Conclusions: Our small study shows, that a questionnaire yields good results to exclude a haemostatic disorder, but is not a sensitive tool to identify such a disorder.


GYNECOLOGY ◽  
2018 ◽  
Vol 20 (6) ◽  
pp. 77-80
Author(s):  
M R Orazov ◽  
V E Radzinsky ◽  
M B Khamoshina ◽  
A O Dukhin ◽  
L R Toktar ◽  
...  

Pelvic pain syndrome associated with adenomyosis is a common disease in women of reproductive age. Frequency of detection in the population varies from 10 to 53%. The aim - to study the clinical and anamnestic risk factors of pelvic pain, with adenomiose. Materials and methods. The study included 120 (n=120) patients with diffuse adenomyosis with pain and painless form of the disease who underwent examination and treatment in the gynecological Department of the Central clinical hospital №6 of Russian Railways in Moscow. Each patient was provided with an individual card, which was encrypted 171 sign. The studied parameters reflected the passport and anthropometric data, information about education, social status, presence of occupational hazards, complaints, illness. Results. Burdened gynecological and somatic histories, manifested a low health index, a more pronounced hereditary a family history of neoplastic diseases are contributing factors, and high prevalence of postponed surgeries, chronic, long-term ongoing inflammatory processes of the pelvic organs to create a favorable background for the further progression of chronic pelvic pain syndrome in adenomiose.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 426.1-426
Author(s):  
T. Hügle ◽  
S. Nasi ◽  
D. Ehirchiou ◽  
P. Omoumi ◽  
A. So ◽  
...  

Background:Fibrin(ogen) maintains inflammation in various disorders but has never been linked to cartilage damage in rheumatoid arthritis (RA) or other forms of inflammatory arthritis.Objectives:To investigate the role of fibrin deposition on cartilage integrity in arthritis.Methods:Fibrin deposition on knee cartilage was analyzed by immunohistochemistry in RA patients and in murine adjuvant-induced arthritis (AIA). In chondrocytes, fibrinogen expression (Fgα, Fgβ, Fgγ) and procoagulant activity were evaluated by qRT-PCR and turbidimetry respectively. Fibrin-induced catabolic genes were assessed by qRT-PCR in chondrocytes. Fibrin-mediated chondro-synovial adhesion (CSA) with subsequent cartilage tears was studied in co-cultures of human RA cartilage with autologous synoviocytes, in the AIA model, and by MRI. The link between fibrin and calcification was examined in human RA cartilage stained for calcific deposits and in vitro in fibrinogen-stimulated chondrocytes.Results:Fibrin deposition on cartilage correlated with the severity of cartilage damage in human RA explants and in AIA wildtype (WT) mice, while fibrinogen deficient (Fg-/-) mice were protected. Accordingly, fibrin upregulated catabolic enzymes (Adamts5 and Mmp13) in chondrocytes. Secondly, CSA was present in fibrin-rich and damaged cartilage in AIA WT but not in Fg-/- mice. In line, autologous human synoviocytes, cultured on RA cartilage explants, adhered exclusively to fibrin-positive degraded areas. Gadolinium-enhanced MRI of human joints showed contrast-enhancement along cartilage surface in RA patients but not in controls. Finally, fibrin co-localized with calcification in human RA cartilage and triggered chondrocyte mineralization inducing pro-calcification genes (Anx5, Pit1, Pc1) and cytokine (IL-6). Although at a much lesser extent, we observed similar fibrin-mediated mechanisms in osteoarthritis (OA).Conclusion:Fibrin deposition directly impacts on cartilage integrity via induction of catabolism, mechanical stress, and calcification. Potentially, fibrin is a key factor of cartilage damage occurring in RA as a secondary consequence of inflammation.Disclosure of Interests:None declared


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 540.3-540
Author(s):  
A. Munir ◽  
C. Sheehy

Background:Corneal melt is a rare inflammatory disease of the peripheral cornea; it may lead to perforation of the globe and visual failure. Corneal melt can be a manifestation of systemic vasculitis in patients with RA and other conditions, such as cancer. Without early and aggressive treatment it may be associated with a poor visual outcome and a high mortality. It has been reported in patients with stable RA.Objectives:A case report in a patient with long standing but well controlled Rheumatoid Arthritis (RA) and metastatic disease.Methods:A 75 year old male with a background of sero positive Rheumatoid Arthritis for more than 10 years presented to the Eye Casualty with a two week history of a painful left red eye. His other medical history was significant for Stage IIB poorly differentiated cancer of the left lower lobe. Left lower lobectomy with a patch of diaphragm resected. Intratumoural lymphovascular invasion noted. He completed Adjuvant Carboplatin/Vinorelbine chemotherapy September, 2017. He had DVT proximal left leg 22ndof September, 2017. Follow up CT in 2018 demonstrated a right renal upper pole lesion for which he was awaiting biopsy with?metastatic lung disease vs primary renal carcinoma. His RA was well controlled on Methotrexate 10mg weekly. He had been treated by the ophthalmology team for left marginal Keratitis for the prior 2 months with steroid eye drops without significant improvement. On presentation to ED, he described sharp eye pain, waking him from the sleep, associated with watery discharge and photophobia. Examination showed corneal melt in left eye involving 25% of inferior portion of the cornea and spastic entropion with injecting eye lashes. He had no active joints and there were no other signs of vasculitis. CRP was 4.1. He had a negative ANA and ANCA; viral swabs were negative. He was admitted under the medical team. Intravenous Methyl Prednisolone was started. The patient felt better after 5 days of Methyl Prednisolone. Left temporary tarsorrhaphy was done by Ophthalmology. Cyclophosphamide was initiated after discussion with Oncologist pending the result of the renal biopsy. Patient was discharged after 5 days of admission in the hospitalResults:The renal biopsy was positive for metastatic Squamous cell carcinoma of lung. Cyclophosphamide was withdrawn and he was started on Carboplatin/Gemcitabine. The corneal melt improved with complete resolution of his visual symptoms.Conclusion:In this case, although the history of RA was felt by the ophthalmology team to be the most likely association with the corneal melt, we would argue the oncological diagnoses were likely the driving force behind the presentation.References:[1]Sule A, Balakrishnan C, Gaitonde S, Mittal G, Pathan E, Gokhale NS, et al. Rheumatoid corneal melt. Rheumatology (Oxford)2002;41:705–6.[2]S. Yano, K. Kondo, M. Yamaguchi et al., “Distribution and function of EGFR in human tissue and the effect of EGFR tyrosine kinase inhibition,” Anticancer Research, vol. 23, no. 5, pp. 3639–3650, 2003.Disclosure of Interests:None declared


Rheumatology ◽  
2021 ◽  
Vol 60 (Supplement_1) ◽  
Author(s):  
Malika A Swar ◽  
Marwan Bukhari

Abstract Background/Aims  Osteoporosis (OP) is an extra-articular manifestation of rheumatoid arthritis (RA) that leads to increased fracture susceptibility due to a variety of reasons including immobility and cytokine driven bone loss. Bone loss in other populations has well documented risk factors. It is unknown whether bone loss in RA predominantly affects the femoral neck or the spine. This study aimed to identify independent predictors of low bone mineral density (BMD) in patients RA at the lumbar spine and the femoral neck. Methods  This was a retrospective observational cohort study using patients with Rheumatoid arthritis attending for a regional dual X-ray absorptiometry (DEXA) scan at the Royal Lancaster Infirmary between 2004 and 2014. BMD in L1-L4 in the spine and in the femoral neck were recorded. The risk factors investigated were steroid use, family history of osteoporosis, smoking, alcohol abuse, BMI, gender, previous fragility fracture, number of FRAX(tm) risk factors and age. Univariate and Multivariate regression analysis models were fitted to explore bone loss at these sites using BMD in g/cm2 as a dependant variable. . Results  1,527 patients were included in the analysis, 1,207 (79%) were female. Mean age was 64.34 years (SD11.6). mean BMI was 27.32kg/cm2 (SD 5.570) 858 (56.2%) had some steroid exposure . 169(11.1%) had family history of osteoporosis. fragility fracture history found in 406 (26.6%). 621 (40.7%) were current or ex smokers . There was a median of 3 OP risk factors (IQR 1,3) The performance of the models is shown in table one below. Different risk factors appeared to influence the BMD at different sites and the cumulative risk factors influenced BMD in the spine. None of the traditional risk factors predicted poor bone loss well in this cohort. P129 Table 1:result of the regression modelsCharacteristicB femoral neck95% CIpB spine95%CIpAge at scan-0.004-0.005,-0.003<0.01-0.0005-0.002,0.00050.292Sex-0.094-0.113,-0.075<0.01-0.101-0.129,-0.072<0.01BMI (mg/m2)0.0080.008,0.0101<0.010.01130.019,0.013<0.01Fragility fracture-0.024-0.055,0.0060.12-0.0138-0.060,0.0320.559Smoking0.007-0.022,0.0350.650.0286-0.015,0.0720.20Alcohol0.011-0.033,0.0 5560.620.0544-0.013,0.1120.11Family history of OP0.012-0.021,0.0450.470.0158-0.034,0.0650.53Number of risk factors-0.015-0.039,0.0080.21-0.039-0.075,-0.0030.03steroids0.004-0.023,0.0320.030.027-0.015,0.0690.21 Conclusion  This study has shown that predictors of low BMD in the spine and hip are different and less influential than expected in this cohort with RA . As the FRAX(tm) tool only uses the femoral neck, this might underestimate the fracture risk in this population. Further work looking at individual areas is ongoing. Disclosure  M.A. Swar: None. M. Bukhari: None.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1253.2-1254
Author(s):  
T. Formánek ◽  
K. Mladá ◽  
M. Husakova

Background:Cohort studies using nationwide health registers have shown an increased risk for affective and anxiety disorders in people with ankylosing spondylitis (AS) and rheumatoid arthritis (RA) (1-3). Moreover, a nationwide cohort study demonstrated an increased risk for mental disorders in people with rheumatic diseases (4).Objectives:We aimed to investigate the risk for psychiatric hospitalization following a hospitalization for rheumatic disease.Methods:Using data from the Czech nationwide register of all-cause hospitalizations, we obtained 4 971 individuals hospitalized (index hospitalization) between 2004 and 2012 for rheumatic diseases - RA, spondyloarthritis (including AS, psoriatic arthritis and undifferentiated spondyloarthritis), systemic lupus erythematosus and systemic sclerodermia, with no history of psychiatric and rheuma-related hospitalization in the previous 10 years from the index hospitalization. On these individuals, we randomly matched (on age, gender and year of index hospitalization) controls that were hospitalized in the same time period for a non-rheumatic disease and have no history of psychiatric and rheumatic hospitalization in the last 10 years from their index hospitalization, in the ratio of 1:5. We employed conditional logistic regression for assessing the risk for psychiatric hospitalization in the subsequent 3 years from the index hospitalization. To strengthen our results, we repeated the matching step 100 times and run the analysis on each resulting dataset separately, and pooled the results. The findings are expressed as odds ratios (OR) with 95% confidence intervals (95% CI).Results:We identified an elevated risk for psychiatric (OR = 1.34, 95% CI = 1; 1.78) and for affective disorders (OR = 2.19, 95% CI = 1.17; 4.1) in people hospitalized for rheumatic diseases. We did not find a statistically significant association with organic, psychotic and anxiety disorders.Conclusion:There is an increased risk for experiencing a psychiatric disorder in the period of 3 years after a rheuma-related hospitalization.References:[1]Shen C-C, Hu L-Y, Yang AC, Kuo BI-T, Chiang Y-Y, Tsai S-J. Risk of Psychiatric Disorders following Ankylosing Spondylitis: A Nationwide Population-based Retrospective Cohort Study. The Journal of Rheumatology. 2016;43(3).[2]Park J-S, Jang H-D, Hong J-Y, Park Y-S, Han K, Suh S-W, et al. Impact of ankylosing spondylitis on depression: a nationwide cohort study. Scientific Reports. 2019;9(1):6736.[3]Hsu C-C, Chen S-C, Liu C-J, Lu T, Shen C-C, Hu Y-W, et al. Rheumatoid Arthritis and the Risk of Bipolar Disorder: A Nationwide Population-Based Study. PLOS ONE. 2014;9(9).[4]Sundquist K, Li X, Hemminki K, Sundquist J. Subsequent Risk of Hospitalization for Neuropsychiatric Disorders in Patients With Rheumatic Diseases: A Nationwide Study From Sweden. Archives of General Psychiatry. 2008;65(5):501-7.Acknowledgments:Supported by the project (Ministry of Health Czech Republic) for conceptual development of research organization 00023728 (Institute of Rheumatology).Disclosure of Interests:Tomáš Formánek: None declared, Karolina Mladá: None declared, Marketa Husakova Speakers bureau: Novartis


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Nobunori Takahashi ◽  
Shuji Asai ◽  
Tomonori Kobayakawa ◽  
Atsushi Kaneko ◽  
Tatsuo Watanabe ◽  
...  

AbstractThis study aimed to evaluate the short-term effectiveness and safety profiles of baricitinib and explore factors associated with improved short-term effectiveness in patients with rheumatoid arthritis (RA) in clinical settings. A total of 113 consecutive RA patients who had been treated with baricitinib were registered in a Japanese multicenter registry and followed for at least 24 weeks. Mean age was 66.1 years, mean RA disease duration was 14.0 years, 71.1% had a history of use of biologics or JAK inhibitors (targeted DMARDs), and 48.3% and 40.0% were receiving concomitant methotrexate and oral prednisone, respectively. Mean DAS28-CRP significantly decreased from 3.55 at baseline to 2.32 at 24 weeks. At 24 weeks, 68.2% and 64.1% of patients achieved low disease activity (LDA) and moderate or good response, respectively. Multivariate logistic regression analysis revealed that no previous targeted DMARD use and lower DAS28-CRP score at baseline were independently associated with achievement of LDA at 24 weeks. While the effectiveness of baricitinib was similar regardless of whether patients had a history of only one or multiple targeted DMARDs use, patients with previous use of non-TNF inhibitors or JAK inhibitors showed lower rates of improvement in DAS28-CRP. The overall retention rate for baricitinib was 86.5% at 24 weeks, as estimated by Kaplan–Meier analysis. The discontinuation rate due to adverse events was 6.5% at 24 weeks. Baricitinib significantly improved RA disease activity in clinical practice. Baricitinib was significantly more effective when used as a first-line targeted DMARDs.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 206.1-207
Author(s):  
C. Grönwall ◽  
L. Liljefors ◽  
H. Bang ◽  
A. Hensvold ◽  
M. Hansson ◽  
...  

Background:Seropositive rheumatoid arthritis (RA) is characterized by the presence of rheumatoid factor (RF) and anti-citrullinated protein autoantibodies (ACPA) with different fine-specificities. Yet, other serum anti-modified protein autoantibodies (AMPA), e.g. anti-carbamylated (Carb), anti-acetylated (KAc), and anti-malondialdehyde acetaldehyde (MAA) modified protein antibodies, have been described. By using RA patient single-cell derived monoclonal antibodies we have previously shown that individual ACPA clones recognize small distinct citrulline-containing epitopes giving them extensive multireactivity when these epitopes are found in many peptides and proteins. Moreover, certain CCP2+ multireactive ACPA clones bind also to cabamylated and acetylated autoantigens [1].Objectives:To provide a comprehensive evaluation of serum IgG and IgA autoreactivity to different post-translational modifications in RA.Methods:We analyzed 30 different IgG and IgA AMPA reactivities to modified antigens by ELISA and autoantigen arrays, in N=1985 newly diagnosed RA patients and population controls. The study utilized both previously established (i.e IgG and IgA CCP2; IgG ACPA fine-specificities; IgG anti-Carb fibrinogen and Carb FCS; IgG and IgA Cit/Carb/KAc/Orn(Ac)-vimentin), and novel assays (e.g. IgG anti-MAA and IgG anti-acetylated histones). Association with patient characteristics such as smoking and disease activity were explored. The newly developed assays were also evaluated in SLE disease controls and CCP2+ RA-risk individuals without arthritis.Results:Carb and KAc reactivities by different assays were primarily seen in patients also positive for citrulline-reactivity. Modified vimentin (mod-Vim) peptides were used for direct comparison of different AMPA reactivities, revealing that IgA AMPA recognizing mod-Vim was mainly detected in subsets of patients with high IgG anti-Cit-Vim levels and a history of smoking. IgG acetylation reactivity was mainly detected in a subset of patients with Cit and Carb reactivity. Anti-acetylated histone 2B reactivity was RA-specific and associated with high anti-CCP2 IgG levels, multiple ACPA fine-specificities, and smoking. This reactivity was also found to be present in CCP2+ RA-risk individuals without arthritis. Our data further demonstrate that IgG autoreactivity to MAA was increased in RA compared to controls with highest levels in CCP2+ RA, but was not RA-specific, and showed low correlation with other AMPA. Anti-MAA was instead associated with disease activity and was not significantly increased in CCP2+ individuals at risk of RA. Notably, RA patients could be subdivided into four different subsets based on their AMPA IgG and IgA reactivity profiles.Conclusion:We conclude that autoantibodies exhibiting different patterns of ACPA fine-specificities as well as Carb and KAc reactivity are present in RA and may be derived from multireactive B-cell clones. Anti-Carb and anti-KAc could be considered reactivities within the “Cit-umbrella” similar to ACPA fine-specificities, while MAA is distinctly different.References:[1]Sahlström P, Hansson M, Steen J, Amara K, Titcombe PJ, Forsström B, Stålesen R, Israelsson L, Piccoli L, Lundberg K, Klareskog L, Mueller DL, Catrina AI, Skriner K, Malmström V, Grönwall C. Different Hierarchies of Anti-Modified Protein Autoantibody Reactivities in Rheumatoid Arthritis. Arthritis Rheumatol. 2020 Oct;72(10):1643-1657. PMID: 32501655Caroline Grönwall: None declared, Lisa Liljefors: None declared, Holger Bang Employee of: Employee at ORGENTEC Diagnostika GmbH, Aase Hensvold: None declared, Monika Hansson: None declared, Linda Mathsson-Alm Employee of: Employee at Thermo Fisher Scientific, Lena Israelsson: None declared, Anna Svärd: None declared, Cyril CLAVEL: None declared, Elisabet Svenungsson: None declared, Iva Gunnarsson: None declared, Guy Serre: None declared, Saedis Saevarsdottir: None declared, Alf Kastbom: None declared, Lars Alfredsson: None declared, Vivianne Malmström: None declared, Johan Rönnelid: None declared, Anca Catrina: None declared, Karin Lundberg: None declared, Lars Klareskog: None declared


2009 ◽  
Vol 79 (4) ◽  
pp. 804-811 ◽  
Author(s):  
Kenichi Sasaguri ◽  
Rika Ishizaki-Takeuchi ◽  
Sakurako Kuramae ◽  
Eliana Midori Tanaka ◽  
Takashi Sakurai ◽  
...  

Abstract A 32-year-old Japanese female patient consulted the authors' dental clinic with a 4.5-year history of rheumatoid arthritis (RA). She complained of pain during mouth opening and difficulty in eating due to masticatory dysfunction caused by an anterior open bite. Imaging showed severe erosion and flattening of both condyles. RA stabilized after pharmacological therapy and became inactive during the orthodontic therapy aimed at reconstructing an optimal occlusion capable of promoting functional repositioning of the mandible. At present, 4 years and 2 months postretention, the reconstructed occlusion remains stable, and both condyles continue to be remodeled. The distance from reference position to intercuspal position has gradually decreased throughout the 4-year posttreatment and postretention periods. Orthodontic therapy that comprehensively reconstructs occlusion and enhances the functioning of the mandible can induce remodeling of eroded condyles, even those with a history of rheumatoid arthritis.


Author(s):  
Balaji Zacharia ◽  
Arun Prakas ◽  
Subramanian Vaidyanathan ◽  
Antony Roy ◽  
Mohammed Komalam Ayyub

AbstractInstability of the shoulder joint is common but most of the time it is unrecognized by the treating surgeon. The symptoms can vary from subtle pain to shoulder dislocation. In many cases, there is no history of trauma. The shoulder joint is stabilized by both static and dynamic factors, and treatment is complex, with recurrence more common in young athletic individuals. Open and arthroscopic techniques of stabilization are available with specific indications for each of these methods. In this narrative review of shoulder instability, we describe the pathological anatomy, evaluation, natural history, classification, and treatment of shoulder instability.


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