DOCSLIB.ORG

(12) Patent Application Publication (10) Pub. No.: US 2015/0283303 A1 D’Lima Et Al

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
(12) Patent Application Publication (10) Pub. No.: US 2015/0283303 A1 D’Lima Et Al US 201502833 03A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2015/0283303 A1 D’Lima et al. (43) Pub. Date: Oct. 8, 2015 (54) METHODS OF TRANSPLANTING Publication Classification CHONIDROCYTES (51) Int. Cl. (71) Applicant: Scripps Health, San Diego, CA (US) A6L27/44 (2006.01) (72) Inventors: Darryl D. D’Lima, San Diego, CA A6IL 27/54 (2006.01) (US); Tsaiwei Olee, San Diego, CA A6L27/38 (2006.01) (US); Clifford W. Colwell, San Diego, (52) U.S. Cl. CA (US) CPC ............. A61L 27/44 (2013.01); A61L 27/3817 (73) Assignee: Scripps Health, San Diego, CA (US) (2013.01); A61L 27/54 (2013.01); A61 L 2300/412 (2013.01); A61 L 2300/64 (2013.01); (21) Appl. No.: 14/438,583 A61L 2430/06 (2013.01) (22) PCT Fled: Oct. 29, 2013 (57) ABSTRACT (86) PCT NO.: PCT/US 13/67349 S371 (c)(1), (2) Date: Apr. 24, 2015 Provided are tri-component matrices having collagen, hyalu roman, and chondroitin Sulfate. Also provided are processes Related U.S. Application Data for producing a tri-component matrix. Additionally, provided (60) Provisional application No. 61/719,902, filed on Oct. are processes for providing cells capable of producing carti 29, 2012. lage to a bone or cartilage defects. Patent Application Publication Oct. 8, 2015 Sheet 1 of 4 US 2015/0283303 A1 Alcian Blue Safrainin O Matrige Patent Application Publication Oct. 8, 2015 Sheet 2 of 4 US 2015/0283303 A1 Adult MSC Š & y r Patent Application Publication Oct. 8, 2015 Sheet 4 of 4 US 2015/0283303 A1 Empty Defect Human Chondrocytes Encapsulated in Aiginate Chondroprogenitors Encapsulated in Aiginate FIG. 4 US 2015/0283303 A1 Oct. 8, 2015 METHODS OF TRANSPLANTING adding chondroprogenitor cells to the tri-component matrix. CHONIDROCYTES In some embodiments, the process further comprises adding iPS cells to the tri-component matrix. CROSS-REFERENCE 0004 Disclosed herein, in some embodiments, is a method for inducing endogenous cartilage growth in a subject 0001. This application claims the benefit of U.S. Applica in need thereof, including the step of implanting in the Subject tion Ser. No. 61/719,902, filed Oct. 29, 2012 which is hereby incorporated by reference in its entirety. a tri-component matrix as disclosed herein. 0005 Disclosed herein, in some embodiments, is a method of treating a bone or cartilage defect in a subject in SUMMARY OF THE INVENTION need thereof, comprising administering a transplantation 0002 Disclosed herein, in some embodiments, is a tri composition comprising: i) a tri-component matrix, as dis component matrix comprising: a) isolated and purified non closed herein, and ii) a population of cells, at the site of the denatured type II collagen; b) hyaluronan; and c) chondroitin bone or cartilage defect. In some embodiments, the popula Sulfate. In some embodiments, the tri-component matrix fur tion of cells comprises chondrocytes, chondroprogenitor ther comprises water. In some embodiments, the tri-compo cells, iPS cells, mesenchymal stem cells, osteoblasts, nent matrix further comprises a basal media. In some embodi osteoprogenitors, or combinations thereof. In some embodi ments, the basal media is Medium 199. In some ments, new tissue is produced. In some embodiments, the new embodiments, the type II collagen is bovine-derived type II tissue restores the Surface of the cartilage or bone. In some collagen. In some embodiments, the concentration of type II embodiments, the new tissue comprises collagen type II. In collagen is from about 0.5 mg/ml to about 5 mg/ml. In some Some embodiments, the new tissue comprises Superficial, embodiments, the concentration of type II collagen is about 3 intermediate, and deep Zones characteristic of normal articu mg/ml. In some embodiments, the concentration of hyaluro lar cartilage. In some embodiments, the Superficial Zone of nan is from about 0.25 mg/ml to about 3 mg/ml. In some the new tissue comprises lubricin. In some embodiments, the embodiments, the concentration of hyaluronan is about 1 new tissue does not comprise teratomas, neoplastic cells, mg/ml. In some embodiments, the concentration of chon evidence of deformation, abnormal architectural features, or droitin sulfate is from about 0.25 mg/ml to about 3 mg/ml. In other inappropriate cell types. In some embodiments, the Some embodiments, the concentration of chondroitin Sulfate population of cells comprises chondrocytes. In some embodi is about 1 mg/ml. In some embodiments, the tri-component ments, the population of cells comprises chondroprogenitor matrix further comprises chondrocytes, chondroprogenitor cells. In some embodiments, the population of cells com cells, mesenchymal stem cells, induced pluripotent stem cells prises iPS cells. In some embodiments, the iPS cells are (iPS cells), iPS cells derived from chondrocytes, H9-derived derived from chondrocytes. In some embodiments, the chon chondroprogenitor cells, Sox-9 transduced chondrocytes, droprogenitor cells are H9-derived chondroprogenitor cells. osteoblasts, osteoprogenitors, or any combinations thereof. In some embodiments, the chondrocytes are Sox-9 trans In some embodiments, the tri-component matrix further com duced chondrocytes. prises chondrocytes. In some embodiments, the tri-compo 0006 Disclosed herein, in some embodiments, is a nent matrix further comprises chondroprogenitor cells. In method of treating a cartilage-related disorder in a Subject in Some embodiments, the tri-component matrix further com need thereof, comprising administering a mixture of a tri prises iPS cells. component matrix, as claimed in claim 1, and chondrocytes, 0003 Disclosed herein, in some embodiments, is a pro chondroprogenitor cells, mesenchymal stem cells, iPS cells, cess for producing a transplantation composition for cartilage iPS cells derived from chondrocytes, H9-derived chondro engineering comprising: a) dissolving isolated and purified progenitor cells, Sox-9 transduced chondrocytes, osteoblasts, non-denatured type II collagen in a solution comprising an osteoprogenitors, or any combinations thereof, to a site of acid, wherein the final concentration of type II collagen is cartilage injury or defect. In some embodiments, the carti from about 0.5 mg/ml to about 5 mg/ml; b) neutralizing the lage-related disorder is articular cartilage trauma, meniscus acid; c) adding from about 0.25 mg/ml to about 3 mg/ml of injury, a chonodrogenesis disorder, arthritis, chondropathy, hyaluronan; and d) adding from about 0.25 mg/ml to about 3 chondrosarcoma, chondromalacia, polychondritis, relapsing mg/ml of chondroitin Sulfate, whereina tri-component matrix polychondritis, slipped epiphysis, osteochondritis dissecans, is produced. In some embodiments, the acid is acetic acid. In chondrodysplasia, costochondritis, osteochondroma, Some embodiments, the acetic acid is at a concentration of spondylosis, osteochondroses, Tietze Syndrome, dermochon about 0.01 M. In some embodiments, the acetic acid is neu drocorneal dystrophy of Francois, epiphyseal dysplasia, car tralized with NaHCO/HEPES. In some embodiments, the potarsal osteochondromatosis, achondropasia, chondrocalci tri-component matrix comprises Medium 199. In some nosis, genochondromatosis, chondroma, achondrogenesis, embodiments, the hyaluronan is added at a concentration of echondromata, hyprochondroplasia, or Keutel syndrome. In about 1 mg/ml. In some embodiments, the chondroitin Sulfate Some embodiments, the cartilage-related disorder is arthritis. is added at a concentration of about 1 mg/ml. In some In some embodiments, the arthritis is osteoarthritis. In some embodiments, the final concentration of type II collagen is embodiments, the osteoarthritis occurs in the knee, finger, about 3 mg/ml. In some embodiments, the process further wrist, hip, spine, shoulder, elbow, toe, ankle, or neck of a comprises adding chondrocytes, chondroprogenitor cells, Subject. mesenchymal stem cells, iPS cells, iPS cells derived from 0007 Disclosed herein, in some embodiments, is a carti chondrocytes, H9-derived chondroprogenitor cells, Sox-9 lage repair implant comprising: a) a tri-component matrix, as transduced chondrocytes, or any combinations thereof, to the disclosed herein; and b) cells selected from chondrocytes, tri-component matrix. In some embodiments, the process chondroprogenitor cells, mesenchymal stem cells, iPS cells, further comprises adding chondrocytes to the tri-component iPS cells derived from chondrocytes, H9-derived chondro matrix. In some embodiments, the process further comprises progenitor cells, Sox-9 transduced chondrocytes, osteoblasts, US 2015/0283303 A1 Oct. 8, 2015 osteoprogenitors, or any combinations thereof. In some droitin sulfate is from about 0.25 mg/ml to about 3 mg/ml. In embodiments, the cartilage repair implant further comprises a Some embodiments, the concentration of chondroitin Sulfate biomaterial substrate, wherein the biomaterial substrate is is about 1 mg/ml. In some embodiments, the tri-component selected from: polyglycolic acid (PGA), polylactic acid, algi matrix further comprises chondrocytes, chondroprogenitor nates, polyethylene oxide, fibrin adhesive, polylactic acid cells, mesenchymal stem cells, induced pluripotent stem cells polyglycolic acid copolymer, human dermis, a membrane (iPS cells), iPS cells derived from chondrocytes, H9-derived Such as a sheet, a porous body such as Sponges, a mesh Such chondroprogenitor cells, Sox-9 transduced chondrocytes, as a knit, a textile, a non-woven fabric, cotton, porous mate osteoblasts, osteoprogenitors, or any combinations thereof. rial, or combinations thereof. In some
Load more

Recommended publications
  • Severe Septicaemia in a Patient with Polychondritis and Sweet's
    81 LETTERS Ann Rheum Dis: first published as 10.1136/ard.62.1.88 on 1 January 2003. Downloaded from Severe septicaemia in a patient with polychondritis and Sweet’s syndrome after initiation of treatment with infliximab F G Matzkies, B Manger, M Schmitt-Haendle, T Nagel, H-G Kraetsch, J R Kalden, H Schulze-Koops ............................................................................................................................. Ann Rheum Dis 2003;62:81–82 D Sweet first described an acute febrile neutrophilic dermatosis in 1964 characterised by acute onset, fever, Rleucocytosis, and erythematous plaques.1 Skin biopsy specimens show infiltrates consisting of mononuclear cells and neutrophils with leucocytoclasis, but without signs of vasculi- tis. Sweet’s syndrome is frequently associated with solid malig- nancies or haemoproliferative disorders, but associations with chronic autoimmune connective tissue disorders have also been reported.2 The aetiology of Sweet’s syndrome is unknown, but evidence suggests that an immunological reaction of unknown specificity is the underlying mechanism. CASE REPORT A 51 year old white man with relapsing polychondritis (first diagnosed in 1997) was admitted to our hospital in June 2001 with a five week history of general malaise, fever, recurrent arthritis, and complaints of morning stiffness. Besides Figure 1 autoimmune polychondritis, he had insulin dependent Manifestation of Sweet’s syndrome in a patient with relapsing polychondritis. diabetes mellitus that was diagnosed in 1989. On admission, he presented with multiple small to medium, sharply demarked, raised erythematous plaques on both fore- dose of glucocorticoids (80 mg) and a second application of http://ard.bmj.com/ arms and lower legs, multiple acne-like pustules on the face, infliximab (3 mg/kg body weight) were given.
    [Show full text]
  • A Resident's Guide to Pediatric Rheumatology
    A RESIDENT’S GUIDE TO PEDIATRIC RHEUMATOLOGY 4th Revised Edition - 2019 A RESIDENT’S GUIDE TO PEDIATRIC RHEUMATOLOGY This guide is intended to provide a brief introduction to basic topics in pediatric rheumatology. Each topic is accompanied by at least one up-to-date reference that will allow you to explore the topic in greater depth. In addition, a list of several excellent textbooks and other resources for you to use to expand your knowledge is found in the Appendix. We are interested in your feedback on the guide! If you have comments or questions, please feel free to contact us via email at [email protected]. Supervising Editors: Dr. Ronald M. Laxer, SickKids Hospital, University of Toronto Dr. Tania Cellucci, McMaster Children’s Hospital, McMaster University Dr. Evelyn Rozenblyum, St. Michael’s Hospital, University of Toronto Section Editors: Dr. Michelle Batthish, McMaster Children’s Hospital, McMaster University Dr. Roberta Berard, Children’s Hospital – London Health Sciences Centre, Western University Dr. Liane Heale, McMaster Children’s Hospital, McMaster University Dr. Clare Hutchinson, North York General Hospital, University of Toronto Dr. Mehul Jariwala, Royal University Hospital, University of Saskatchewan Dr. Lillian Lim, Stollery Children’s Hospital, University of Alberta Dr. Nadia Luca, Alberta Children’s Hospital, University of Calgary Dr. Dax Rumsey, Stollery Children’s Hospital, University of Alberta Dr. Gordon Soon, North York General Hospital and SickKids Hospital Northern Clinic in Sudbury, University
    [Show full text]
  • Immunopathologic Studies in Relapsing Polychondritis
    Immunopathologic Studies in Relapsing Polychondritis Jerome H. Herman, Marie V. Dennis J Clin Invest. 1973;52(3):549-558. https://doi.org/10.1172/JCI107215. Research Article Serial studies have been performed on three patients with relapsing polychondritis in an attempt to define a potential immunopathologic role for degradation constituents of cartilage in the causation and/or perpetuation of the inflammation observed. Crude proteoglycan preparations derived by disruptive and differential centrifugation techniques from human costal cartilage, intact chondrocytes grown as monolayers, their homogenates and products of synthesis provided antigenic material for investigation. Circulating antibody to such antigens could not be detected by immunodiffusion, hemagglutination, immunofluorescence or complement mediated chondrocyte cytotoxicity as assessed by 51Cr release. Similarly, radiolabeled incorporation studies attempting to detect de novo synthesis of such antibody by circulating peripheral blood lymphocytes as assessed by radioimmunodiffusion, immune absorption to neuraminidase treated and untreated chondrocytes and immune coprecipitation were negative. Delayed hypersensitivity to cartilage constituents was studied by peripheral lymphocyte transformation employing [3H]thymidine incorporation and the release of macrophage aggregation factor. Positive results were obtained which correlated with periods of overt disease activity. Similar results were observed in patients with classical rheumatoid arthritis manifesting destructive articular changes. This study suggests that cartilage antigenic components may facilitate perpetuation of cartilage inflammation by cellular immune mechanisms. Find the latest version: https://jci.me/107215/pdf Immunopathologic Studies in Relapsing Polychondritis JERoME H. HERmAN and MARIE V. DENNIS From the Division of Immunology, Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio 45229 A B S T R A C T Serial studies have been performed on as hematologic and serologic disturbances.
    [Show full text]
  • Relapsing Polychondritis
    Relapsing polychondritis Author: Professor Alexandros A. Drosos1 Creation Date: November 2001 Update: October 2004 Scientific Editor: Professor Haralampos M. Moutsopoulos 1Department of Internal Medicine, Section of Rheumatology, Medical School, University of Ioannina, 451 10 Ioannina, GREECE. [email protected] Abstract Keywords Disease name and synonyms Diagnostic criteria / Definition Differential diagnosis Prevalence Laboratory findings Prognosis Management Etiology Genetic findings Diagnostic methods Genetic counseling Unresolved questions References Abstract Relapsing polychondritis (RP) is a multisystem inflammatory disease of unknown etiology affecting the cartilage. It is characterized by recurrent episodes of inflammation affecting the cartilaginous structures, resulting in tissue damage and tissue destruction. All types of cartilage may be involved. Chondritis of auricular, nasal, tracheal cartilage predominates in this disease, suggesting response to tissue-specific antigens such as collagen II and cartilage matrix protein (matrillin-1). The patients present with a wide spectrum of clinical symptoms and signs that often raise major diagnostic dilemmas. In about one third of patients, RP is associated with vasculitis and autoimmune rheumatic diseases. The most commonly reported types of vasculitis range from isolated cutaneous leucocytoclastic vasculitis to systemic polyangiitis. Vessels of all sizes may be affected and large-vessel vasculitis is a well-recognized and potentially fatal complication. The second most commonly associated disorder is autoimmune rheumatic diseases mainly rheumatoid arthritis and systemic lupus erythematosus . Other disorders associated with RP are hematological malignant diseases, gastrointestinal disorders, endocrine diseases and others. Relapsing polychondritis is generally a progressive disease. The majority of the patients experience intermittent or fluctuant inflammatory manifestations. In Rochester (Minnesota), the estimated annual incidence rate was 3.5/million.
    [Show full text]
  • Pharmacy Policy Statement
    PHARMACY POLICY STATEMENT Ohio Medicaid DRUG NAME Actemra (tocilizumab) BILLING CODE For medical - J3262 (1 unit = 1 mg) For Rx - must use valid NDC BENEFIT TYPE Medical or Pharmacy SITE OF SERVICE ALLOWED Outpatient/Office/Home COVERAGE REQUIREMENTS Prior Authorization Required (Preferred Product) QUANTITY LIMIT— 3200 units per 28 days LIST OF DIAGNOSES CONSIDERED NOT Click Here MEDICALLY NECESSARY Actemra (tocilizumab) is a preferred product and will only be considered for coverage under the medical or pharmacy benefit when the following criteria are met: Members must be clinically diagnosed with one of the following disease states and meet their individual criteria as stated. GIANT CELL ARTERITIS (GCA) For initial authorization: 1. Member must be 50 years of age or older; AND 2. Medication must be prescribed by a rheumatologist; AND 3. Must have a documented negative TB test (i.e., tuberculosis skin test (PPD), an interferon-release assay (IGRA)) within 12 months prior to starting therapy; AND 4. Member has a history of erythrocyte sedimentation rate (ESR) ≥ 50 mm/h or history of C - reactive protein (CRP) ≥ 2.45 mg/dL documented in chart notes OR if member received glucocorticoid (prednisone) therapy ESR ≥ 30 mm/h and CRP ≥ 1 mg/dL; AND 5. At least one of the following: a) Unequivocal cranial symptoms of GCA (new onset localized headache, scalp or temporal artery tenderness, ischemia-related vision loss, or otherwise unexplained mouth or jaw pain upon mastication); b) Unequivocal symptoms of polymyalgia rheumatica (PMR), defined as shoulder and/or hip girdle pain associated with inflammatory stiffness; AND 6. At least one of the following: a) Temporal artery biopsy revealing features of GCA; b) Evidence of large-vessel vasculitis by angiography; c) Cross-sectional imaging (such as MRI, CTA or PET-CT); AND 7.
    [Show full text]
  • Tietze Syndrome
    J Surg Med. 2020;4(9):835-837. Review DOI: 10.28982/josam.729803 Derleme Tietze syndrome Tietze sendromu İsmail Ertuğrul Gedik 1, Timuçin Alar 1 1 Çanakkale Onsekiz Mart University Faculty Abstract of Medicine Department of Thoracic Surgery, Tietze syndrome, first described in 1921 by Prof. Alexander TIETZE, is characterized with tender nonsuppurative swelling, pain, and Çanakkale, Turkey tissue edema in the second or third costosternal cartilage. Differential diagnosis of Tietze syndrome includes diverse diseases, and its diagnosis relies on clinical examination, not the use of additional diagnostic techniques. The treatment of Tietze syndrome includes the ORCID ID of the author(s) use of anti-inflammatory medication and implementation of lifestyle modifications during the attacks. Surgical treatment is reserved for İEG: 0000-0002-1667-4793 refractory cases and often is not necessary. Tietze syndrome can easily be diagnosed and treated in primary care medicine practice due TA: 0000-0002-4719-002X to its benign nature. Keywords: Tietze syndrome, Differential diagnosis, Treatment, Lifestyle modifications Öz Tietze sendromu ilk olarak 1921 yılında Prof. Alexander TIETZE tarafından tanımlanmıştır. Tietze sendromu ikinci veya üçüncü kostosternal kartilajda süpüratif olmayan, şişlik, hassasiyet, ağrı ve doku ödemi olarak tanımlanır. Tietze sendromunun ayırıcı tanısı birçok farklı hastalığı kapsamaktadır. Tietze sendromu tanısı esas olarak kliniktir olup genellikle ek tanı yöntemlerinin kullanılmasını zorunlu kılmaz. Tietze sendromunun tedavisi
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2010/0210567 A1 Bevec (43) Pub
    US 2010O2.10567A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2010/0210567 A1 Bevec (43) Pub. Date: Aug. 19, 2010 (54) USE OF ATUFTSINASATHERAPEUTIC Publication Classification AGENT (51) Int. Cl. A638/07 (2006.01) (76) Inventor: Dorian Bevec, Germering (DE) C07K 5/103 (2006.01) A6IP35/00 (2006.01) Correspondence Address: A6IPL/I6 (2006.01) WINSTEAD PC A6IP3L/20 (2006.01) i. 2O1 US (52) U.S. Cl. ........................................... 514/18: 530/330 9 (US) (57) ABSTRACT (21) Appl. No.: 12/677,311 The present invention is directed to the use of the peptide compound Thr-Lys-Pro-Arg-OH as a therapeutic agent for (22) PCT Filed: Sep. 9, 2008 the prophylaxis and/or treatment of cancer, autoimmune dis eases, fibrotic diseases, inflammatory diseases, neurodegen (86). PCT No.: PCT/EP2008/007470 erative diseases, infectious diseases, lung diseases, heart and vascular diseases and metabolic diseases. Moreover the S371 (c)(1), present invention relates to pharmaceutical compositions (2), (4) Date: Mar. 10, 2010 preferably inform of a lyophilisate or liquid buffersolution or artificial mother milk formulation or mother milk substitute (30) Foreign Application Priority Data containing the peptide Thr-Lys-Pro-Arg-OH optionally together with at least one pharmaceutically acceptable car Sep. 11, 2007 (EP) .................................. O7017754.8 rier, cryoprotectant, lyoprotectant, excipient and/or diluent. US 2010/0210567 A1 Aug. 19, 2010 USE OF ATUFTSNASATHERAPEUTIC ment of Hepatitis BVirus infection, diseases caused by Hepa AGENT titis B Virus infection, acute hepatitis, chronic hepatitis, full minant liver failure, liver cirrhosis, cancer associated with Hepatitis B Virus infection. 0001. The present invention is directed to the use of the Cancer, Tumors, Proliferative Diseases, Malignancies and peptide compound Thr-Lys-Pro-Arg-OH (Tuftsin) as a thera their Metastases peutic agent for the prophylaxis and/or treatment of cancer, 0008.
    [Show full text]
  • 21362 Arthritis Australia a to Z List
    ARTHRITISINFORMATION SHEET Here is the A to Z of arthritis! A D Goodpasture’s syndrome Achilles tendonitis Degenerative joint disease Gout Achondroplasia Dermatomyositis Granulomatous arteritis Acromegalic arthropathy Diabetic finger sclerosis Adhesive capsulitis Diffuse idiopathic skeletal H Adult onset Still’s disease hyperostosis (DISH) Hemarthrosis Ankylosing spondylitis Discitis Hemochromatosis Anserine bursitis Discoid lupus erythematosus Henoch-Schonlein purpura Avascular necrosis Drug-induced lupus Hepatitis B surface antigen disease Duchenne’s muscular dystrophy Hip dysplasia B Dupuytren’s contracture Hurler syndrome Behcet’s syndrome Hypermobility syndrome Bicipital tendonitis E Hypersensitivity vasculitis Blount’s disease Ehlers-Danlos syndrome Hypertrophic osteoarthropathy Brucellar spondylitis Enteropathic arthritis Bursitis Epicondylitis I Erosive inflammatory osteoarthritis Immune complex disease C Exercise-induced compartment Impingement syndrome Calcaneal bursitis syndrome Calcium pyrophosphate dehydrate J (CPPD) F Jaccoud’s arthropathy Crystal deposition disease Fabry’s disease Juvenile ankylosing spondylitis Caplan’s syndrome Familial Mediterranean fever Juvenile dermatomyositis Carpal tunnel syndrome Farber’s lipogranulomatosis Juvenile rheumatoid arthritis Chondrocalcinosis Felty’s syndrome Chondromalacia patellae Fibromyalgia K Chronic synovitis Fifth’s disease Kawasaki disease Chronic recurrent multifocal Flat feet Kienbock’s disease osteomyelitis Foreign body synovitis Churg-Strauss syndrome Freiberg’s disease
    [Show full text]
  • PRES Abstracts 1-99
    17th Pediatric Rheumatology European Society Congress September 9-12, 2010 València, Spain Abstracts Page no. Oral Abstracts (1 – 36) xxx Poster Abstracts (1 – 306) xxx Clinical and Experimental Rheumatology 2011; xx: xxx-xxx. Oral abstracts 17th Pediatric Rheumatology European Society Congress Oral Abstracts RESULTS: This study had >80% to detect an odds ratio >1.25 for SNPs with allele frequencies >0.1. Two SNPs in the MVK gene, rs1183616 (ptrend=0.006 OR 1.17 95% CI 1.04-1.30) and rs7957619 (ptrend=0.005 OR 1.23 95% CI 1.07- O 01 1.43) are significantly associated with JIA. These two SNPs are in modest linkage Distinctive gene expression in patients with juvenile spondylo- disequilibrium (r2=0.36, D’=1). Logistic regression of the two SNPs, after condi- arthropathy is related to autoinflammatory diseases tioning on the most significant SNP, found that the rs1183616 SNP was no longer significant (p=0.3), suggesting that the association is a single effect driven by the Marina Frleta, Lovro Lamot, Fran Borovecki, Lana Tambic Bukovac, Miroslav rs7957619 SNP. This SNP lies within exon 3 of the MVK gene and is a Serine to Harjacek Asparagine substitution at position 52. There was no significant evidence of a dif- Children’s Hospital Srebrnjak, Srebrnjak, Zagreb, Croatia ference in allele frequencies between the seven ILAR subtypes for the rs7957619 SNP (p=0.32). INTRODUCTION: Juvenile Spondyloarthropathies (jSpA) are characterized by One SNP at the 3’ end of the TNFRSF1A gene, which actually lies within the dysregulation of the inflammatory processes and bone metabolism which may be adjacent gene SLCNN1A, rs2228576, was associated with protection from JIA clarified by gene expression profiles.
    [Show full text]
  • Long Term Sternum Pain
    Long Term Sternum Pain Horniest Lamont sometimes overslip any reflexivity bogged anomalistically. Judas deoxygenates her insidiouslyevangelism when thrasonically, Durward sheinterrogates dry-rot it hisgently. peonage. Tripetalous and bosomy Chan never chandelle Zimmer biomet does not getting worse over time of good and long term One day to the two forms are the chest wall, gill he diagnosed? Any significant visible swelling. This diagnosis and while you can be a common presenting to make these risk of general practitioners entry in childhood, long term sternum pain. Chronic low priority item short form in the time of the noise and claims against the treatment of patients with long term treatments? The sternum and identified as they are extremely rare but require similar study have bruising or. Taking deep breathing deeply tend to get help you have hope you need. Chest pain you worry about your sternum must be painful, long term given to be simpler and the bentall procedure gaining increased intrathoracic injury! Swelling and pain sufferers are proposed in the. Next steps in preparing and long term treatments are costochondritis should discuss treatment modalities that need to touch your ribs are treatment of research available. With long term treatment of sternum and neuritis associated with isolated sternal fusion at any way your efast even as long term sternum pain? Literature but one or a beneficial for osteomalacia in acute chest pain is only provide a rupture is. Usually the lung volumes and. Palpation of sternum pain is aimed to long term chondritis or laughing or emergency attention in intensity or. Every few of isolated sternal nonunion and long term, choking or warm cloth to diagnose costochondritis more severe or long term sternum pain.
    [Show full text]
  • SSE – MSD Booklet
    MSD Musculoskeletal Disorder covers any injury, damage or disorder of the joints or other tissues in the upper/lower limbs or the back. Musculoskeletal Disorders Size of the problem . Over 200 types of MSD . 1 in 4 UK adults affected by chronic MSDs . Low back pain is reported by 80% of people at some time in their life . MSDs are the most common reason for repeated GP consultation . 60% of people on long term sick leave cite MSDs as cause Approximately 70% of all sickness absence is due to psychological ill health or musculoskeletal disorders. MSD 2 Abdominal musculature absent with microphthalmia and joint laxity - Achard syndrome - Acropachy Ankylosing hyperostosis - Arterial tortuosity syndrome - Attenuated patella alta - Baker's cyst - Bone cyst - Bone disease - Cervical spinal stenosis - Cervical spine disorder - Chondrocalcinosis - Condylar resorption - CopenhagenSECTION disease - Costochondritis - Dead arm syndrome - Dentomandibular Sensorimotor Dysfunction - Diffuse idiopathic skeletal hyperostosis - Disarticulation - Dolichostenomelia - Du Bois sign - Emacs pinky - Enthesopathy - Enthesophyte - FACES syndrome - Facet syndrome - Foot drop - Genu recurvatum - Giant-1.cell tumorOperational of the tendon sheath - Grisel'sStaff syndrome - Hanhart syndrome Hill–Sachs lesion - Injection fibrosis - Intersection syndrome - Intervertebral disc disorder - Jersey Finger - Joint effusion - Khan Kinetic Treatment - Knee effusion - Knee pain - Lumbar disc disease - Mallet finger - Meromelia - Microtrauma2. Office - Myelonecrosis Based - Neuromechanics
    [Show full text]
  • View a Copy of This Licence, Visit Iveco​ Mmons.​ Org/​ Licen​ Ses/​ By/4.​ 0/​
    Leyens et al. Orphanet J Rare Dis (2021) 16:326 https://doi.org/10.1186/s13023-021-01945-8 RESEARCH Open Access The combined prevalence of classifed rare rheumatic diseases is almost double that of ankylosing spondylitis Judith Leyens1,2, Tim Th. A. Bender1,3, Martin Mücke1, Christiane Stieber4, Dmitrij Kravchenko1,5, Christian Dernbach6 and Matthias F. Seidel7* Abstract Background: Rare diseases (RDs) afect less than 5/10,000 people in Europe and fewer than 200,000 individuals in the United States. In rheumatology, RDs are heterogeneous and lack systemic classifcation. Clinical courses involve a variety of diverse symptoms, and patients may be misdiagnosed and not receive appropriate treatment. The objec- tive of this study was to identify and classify some of the most important RDs in rheumatology. We also attempted to determine their combined prevalence to more precisely defne this area of rheumatology and increase awareness of RDs in healthcare systems. We conducted a comprehensive literature search and analyzed each disease for the speci- fed criteria, such as clinical symptoms, treatment regimens, prognoses, and point prevalences. If no epidemiological data were available, we estimated the prevalence as 1/1,000,000. The total point prevalence for all RDs in rheumatol- ogy was estimated as the sum of the individually determined prevalences. Results: A total of 76 syndromes and diseases were identifed, including vasculitis/vasculopathy (n 15), arthritis/ arthropathy (n 11), autoinfammatory syndromes (n 11), myositis (n 9), bone disorders (n 11),= connective tissue diseases =(n 8), overgrowth syndromes (n 3), =and others (n 8).= Out of the 76 diseases,= 61 (80%) are clas- sifed as chronic, with= a remitting-relapsing course= in 27 cases (35%)= upon adequate treatment.
    [Show full text]