Relapsing Polychondritis
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Sexually Transmitted Disease (STD) Case Definitions (Source: Centers for Disease Control and Prevention
Sexually Transmitted Disease (STD) Case Definitions (Source: Centers for Disease Control and Prevention. Case definitions for infectious conditions under public health surveillance, 1997. MMWR Morb Mortal Wkly Rep. 1997;46(No. RR-10).) STD Conditions Reportable in Arizona Chancroid (Revised 9/96) Clinical description A sexually transmitted disease characterized by painful genital ulceration and inflammatory inguinal adenopathy. The disease is caused by infection with Haemophilus ducreyi. Laboratory criteria for diagnosis Isolation of H. ducreyi from a clinical specimen Case classification Probable: a clinically compatible case with both a) no evidence of Treponema pallidum infection by darkfield microscopic examination of ulcer exudate or by a serologic test for syphilis performed ≥7 days after onset of ulcers and b) either a clinical presentation of the ulcer(s) not typical of disease caused by herpes simplex virus (HSV) or a culture negative for HSV. Confirmed: a clinically compatible case that is laboratory confirmed Chlamydia Infection (Revised 6/09) Clinical description Infection with Chlamydia trachomatis may result in urethritis, epididymitis, cervicitis, acute salpingitis, or other syndromes when sexually transmitted; however, the infection is often asymptomatic in women. Perinatal infections may result in inclusion conjunctivitis and pneumonia in newborns. Other syndromes caused by C. trachomatis include lymphogranuloma venereum (see Lymphogranuloma Venereum) and trachoma. Laboratory criteria for diagnosis Isolation of C. trachomatis -
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. -
WO 2014/134709 Al 12 September 2014 (12.09.2014) P O P C T
(12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2014/134709 Al 12 September 2014 (12.09.2014) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 31/05 (2006.01) A61P 31/02 (2006.01) kind of national protection available): AE, AG, AL, AM, AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, (21) International Application Number: BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, PCT/CA20 14/000 174 DO, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, (22) International Filing Date: HN, HR, HU, ID, IL, IN, IR, IS, JP, KE, KG, KN, KP, KR, 4 March 2014 (04.03.2014) KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, (25) Filing Language: English OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, (26) Publication Language: English SC, SD, SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, (30) Priority Data: ZW. 13/790,91 1 8 March 2013 (08.03.2013) US (84) Designated States (unless otherwise indicated, for every (71) Applicant: LABORATOIRE M2 [CA/CA]; 4005-A, rue kind of regional protection available): ARIPO (BW, GH, de la Garlock, Sherbrooke, Quebec J1L 1W9 (CA). GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, SZ, TZ, UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, TJ, (72) Inventors: LEMIRE, Gaetan; 6505, rue de la fougere, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, Sherbrooke, Quebec JIN 3W3 (CA). -
2012 Case Definitions Infectious Disease
Arizona Department of Health Services Case Definitions for Reportable Communicable Morbidities 2012 TABLE OF CONTENTS Definition of Terms Used in Case Classification .......................................................................................................... 6 Definition of Bi-national Case ............................................................................................................................................. 7 ------------------------------------------------------------------------------------------------------- ............................................... 7 AMEBIASIS ............................................................................................................................................................................. 8 ANTHRAX (β) ......................................................................................................................................................................... 9 ASEPTIC MENINGITIS (viral) ......................................................................................................................................... 11 BASIDIOBOLOMYCOSIS ................................................................................................................................................. 12 BOTULISM, FOODBORNE (β) ....................................................................................................................................... 13 BOTULISM, INFANT (β) ................................................................................................................................................... -
Diagnostic Issues in Systemic Lupus Erythematosis
266 Postgrad Med J 2001;77:266–285 Postgrad Med J: first published as 10.1136/pmj.77.906.268 on 1 April 2001. Downloaded from SELF ASSESSMENT QUESTIONS Diagnostic issues in systemic lupus erythematosis N Sofat, C Higgens Answers on p 274. A 24 year old woman was diagnosed with sys- (4) What other tests (apart from 24 hour urine temic lupus erythematosis (SLE) based on a creatinine clearance) are available to measure few months’ history of a photosensitive skin the glomerular filtration rate? rash, predominantly on her face, arthralgia The patient had a 24 hour urinary protein col- involving both hands and wrists, a positive lection, which showed a 24 hour protein measure- antinuclear antibody (ANA) test and a raised ment of 1.8 g. There was no evidence of cellular antinative double stranded DNA antibody casts on urine microscopy. Her blood results were binding level. She was treated with oral as below (normal values are in parentheses): hydroxychloroquine 400 mg daily and short x Sodium 134 mmol/l (135–145) courses of prednisolone during flare-ups. x Potassium 4.5 mmol/l (3.5–5.0) She was reviewed in clinic for her regular x Urea 7.0 mmol/l (2.5–6.7) follow up appointment when she was found to x Creatinine 173 µmol/l (70–115) be hypertensive on repeated measurements of x Haemoglobin 108 g/l (115–160) her blood pressure, an average value being x White cell count 4.5 × 109/l (4.0–11.0) 150/90 mm Hg. She was also urine dipstick x Platelets 130 × 109/l (150–400) positive for blood and protein. -
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 -
Ear-Nose-Throat Manifestations in Inflammatory Bowel Diseases ANNALS of GASTROENTEROLOGY 2007, 20(4):265-274X Xx 265X
xx xx Ear-nose-throat manifestations in Inflammatory Bowel Diseases ANNALS OF GASTROENTEROLOGY 2007, 20(4):265-274x xx 265x Review Ear-nose-throat manifestations in Inflammatory Bowel Diseases C.D. Zois, K.H. Katsanos, E.V. Tsianos going activation of the innate immune system driven by SUMMARY the presence of luminal flora. Both UC and CD have a Inflammatory bowel diseases (IBD) refer to a group of chron- worldwide distribution and are common causes of mor- ic inflammatory disorders involving the gastrointestinal tract bidity in Western Europe and northern America. and are typically divided into two major disorders: Crohn’s The extraintestinal manifestasions of IBD, however, disease (CD) and ulcerative colitis (UC). CD is characterized are not of less importance. In some cases they are the first by noncontiguous chronic inflammation, often transmural clinical manifestation of the disease and may precede the with noncaseating granuloma formation. It can involve any onset of gastrointestinal symptoms by many years, playing portion of the alimentary tract and CD inflammation has of- also a very important role in disease morbidity. As multi- ten been described in the nose, mouth, larynx and esopha- systemic diseases, IBD, have been correlated with many gus in addition to the more common small bowel and colon other organs, including the skin, eyes, joints, bone, blood, sites. UC differs from CD in that it is characterized by con- kidney, liver and biliary tract. In addition, the inner ear, tiguous chronic inflammation without transmural involve- nose and throat should also be considered as extraintesti- ment, but extraintestinal manifestations of UC have also been nal involvement sites of IBD. -
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. -
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. -
Emtree Terms Changed in May 2018
Emtree Terms Changed in May 2021 1 Emtree Terms Added and Changed (May 2021) This is an overview of new terms added and changes made in the second Emtree release in 2021. Overall, Emtree has grown by 1150 preferred terms (140 drug terms and 1010 non-drug terms) compared with the previous version released in January 2021. In total Emtree now counts 90095 preferred terms. Because the terms added include replacements for existing preferred terms (which become synonyms of the new terms) as well as completely new concepts, the number of terms added exceeds the net growth in Emtree. Other changes could include the merging of two or more existing preferred terms into a single concept. The terms added and changed are summarized below and specified in detail on the following pages. Emtree Terms Added in May 2021 1228 new terms (including 78 replacement terms and promoted synonyms) have been added to Emtree as preferred terms in version May 2021 (compared to January 2021): ◼ 179 drug terms (terms assigned to the Chemicals and Drugs facet). ◼ 1049 non-drug terms (terms not assigned as Chemicals and Drugs). The new terms (including the replacement terms and the promoted synonyms) are listed as Terms Added on the following pages. Note that many of these terms will have been indexed prior to 2021 (typically as candidate terms), sometimes for several years, before they were added to Emtree. Emtree Terms Changed in May 2021 78 terms (39 drug terms and 39 non-drug terms) from Emtree January 2020 have been replaced by 76 different terms in May 2021 (39 drug terms and 37 non-drug terms). -
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. -
Autoimmune PUK Is Usually Unilateral and Sectoral
1 Q Concerning PUK circumferential Autoimmune PUK is usually unilaterallaterality and sectoralextent . 2 A Concerning PUK Autoimmune PUK is usually unilateral and sectoral 3 Concerning PUK Autoimmune PUK 4 Q Concerning PUK Autoimmune PUK is usually unilateral and sectoral improvement vs It often heralds exacerbationworsening of systemic disease 5 A Concerning PUK Autoimmune PUK is usually unilateral and sectoral It often heralds exacerbation of systemic disease 6 Q Concerning PUK With what general category of autoimmune dz is PUK associated? Autoimmune PUKConnective-tissue is usually dz, unilateral especially vasculitides and sectoral It often heralds exacerbation of systemic disease 7 A Concerning PUK With what general category of autoimmune dz is PUK associated? Autoimmune PUKConnective-tissue is usually dz, unilateral especially vasculitides and sectoral It often heralds exacerbation of systemic disease 8 Q Concerning PUK With what general category of autoimmune dz is PUK associated? Autoimmune PUKConnective-tissue is usually dz, unilateral especially vasculitides and sectoral It often heralds exacerbation of systemic disease With which connective-tissue diseases (CTDs) and/or vasculitides has PUK been associated? Pretty much all of them Which three conditions are most likely to present with PUK? Rheumatoid arthritis, Wegener’s granulomatosis, and polyarteritis nodosa If a PUK pt does not carry a CTD/autoimmune diagnosis, what should the ophthalmologist do? Initiate a diagnostic workup (or promptly arrange for a rheumatologist