Approach to the Patient with Arthritis Articular Vs
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Acute < 6 Weeks Subacute ~ 6 Weeks Chronic >
Pain Articular Non-articular Localized Generalized . Regional Pain Disorders . Myalgias without Weakness Soft Tissue Rheumatism (ex., fibromyalgia, polymyalgia (ex., soft tissue rheumatism rheumatica) tendonitis, tenosynovitis, bursitis, fasciitis) . Myalgia with Weakness (ex., Inflammatory muscle disease) Clinical Features of Arthritis Monoarthritis Oligoarthritis Polyarthritis (one joint) (two to five joints) (> five joints) Acute < 6 weeks Subacute ~ 6 weeks Chronic > 6 weeks Inflammatory Noninflammatory Differential Diagnosis of Arthritis Differential Diagnosis of Arthritis Acute Monarthritis Acute Polyarthritis Inflammatory Inflammatory . Infection . Viral - gonococcal (GC) - hepatitis - nonGC - parvovirus . Crystal deposition - HIV - gout . Rheumatic fever - calcium . GC - pyrophosphate dihydrate (CPPD) . CTD (connective tissue diseases) - hydroxylapatite (HA) - RA . Spondyloarthropathies - systemic lupus erythematosus (SLE) - reactive . Sarcoidosis - psoriatic . - inflammatory bowel disease (IBD) Spondyloarthropathies - reactive - Reiters . - psoriatic Early RA - IBD - Reiters Non-inflammatory . Subacute bacterial endocarditis (SBE) . Trauma . Hemophilia Non-inflammatory . Avascular Necrosis . Hypertrophic osteoarthropathy . Internal derangement Chronic Monarthritis Chronic Polyarthritis Inflammatory Inflammatory . Chronic Infection . Bony erosions - fungal, - RA/Juvenile rheumatoid arthritis (JRA ) - tuberculosis (TB) - Crystal deposition . Rheumatoid arthritis (RA) - Infection (15%) - Erosive OA (rare) Non-inflammatory - Spondyloarthropathies -
Axial Spondyloarthritis
Central JSM Arthritis Review Article *Corresponding author Mali Jurkowski, Department of Internal Medicine, Temple University Hospital, 3401 North Broad Street, Axial Spondyloarthritis: Clinical Philadelphia, PA 19140, USA Submitted: 07 December 2020 Features, Classification, and Accepted: 31 January 2021 Published: 03 February 2021 ISSN: 2475-9155 Treatment Copyright Mali Jurkowski1*, Stephanie Jeong1 and Lawrence H Brent2 © 2021 Jurkowski M, et al. 1Department of Internal Medicine, Temple University Hospital, USA OPEN ACCESS 2Section of Rheumatology, Department of Medicine, Lewis Katz School of Medicine at Temple University, USA Keywords ABBREVIATIONS • Spondyloarthritis • Ankylosing spondylitis HLA-B27: human leukocyte antigen-B27; SpA: • HLA-B27 spondyloarthritis; AS: ankylosing spondylitis; nr-axSpA: non- • Classification criteria radiographic axial spondyloarthritis; ReA: reactive arthritis; PsA: psoriatic arthritis; IBD-SpA: disease associated spondyloarthritis; ASAS: Assessment of of rheumatoid arthritis [6]. AS affects men more than women SpondyloArthritis international Society; NSAIDs:inflammatory nonsteroidal bowel 79.6%, whereas nr-axSpA affects men and women equally 72.4% CASPAR: [7], independent of HLA-B27. This article will discuss the clinical for Psoriatic Arthritis; DMARDs: disease modifying anti- and diagnostic features of SpA, compare the classification criteria, rheumaticanti-inflammatory drugs; CD:drugs; Crohn’s disease; ClassificationUC: ulcerative Criteriacolitis; and provide updates regarding treatment options, including the ESR: erythrocyte sedimentation rate; CRP: C-reactive protein; developmentCLINICAL FEATURESof biologics and targeted synthetic agents. TNFi: X-ray: plain radiography; MRI: magnetic resonance imaging; CT: computed Inflammatory back pain tomography;tumor US: necrosis ultrasonography; factor-α wb-MRI:inhibitors; ESSG: European Spondyloarthropathy Study Group; IL-17i: whole-body MRI; JAKi: PDE4i: Inflammatory back pain is the hallmark of SpA, present in 70- 80% of patients [8]. -
Reactive Arthritis This Sheet Has Been Written for People Affected by Reactive Arthritis
ARTHRIINFORMATIONTI SHEETS ARTHRIINFORMATIONTI SHEETS Reactive arthritis This sheet has been written for people affected by reactive arthritis. It provides general information to help you understand how you may be affected. This sheet also covers how reactive arthritis usually resolves over time. What is reactive arthritis? It is not known why some people who get these Reactive arthritis is a condition that causes infections develop reactive arthritis and some do not. inflammation, pain and swelling of the joints. It usually A certain gene called HLA-B27 is associated with develops after an infection, often in the bowel or genital reactive arthritis, especially inflammation of the spine. areas. The infection causes activity in the immune However this is a perfectly normal gene and there are system. The normal role of your body’s immune system many more people who have this gene and do not get is to fight off infections to keep you healthy. In some reactive arthritis. people this activity of the immune system causes joints to become inflamed, however the joints themselves How is it diagnosed? are not actually infected. About one in 10 people with Your doctor will diagnose reactive arthritis from your specific types of infections will get reactive arthritis. symptoms and a physical examination. Your doctor may also order blood tests for inflammation, such as the What are the symptoms? erythrocyte sedimentation rate (ESR) and C-reactive Reactive arthritis usually begins a few weeks after an protein (CRP) tests. Blood tests may also help to rule infection. Symptoms can affect many parts of the body out other types of arthritis. -
Charcot Arthropathy: Differential Diagnosis of Inflammatory Arthritis
CHARCOT ARTHROPATHY: DIFFERENTIAL DIAGNOSIS OF INFLAMMATORY ARTHRITIS CAMILA DA SILVA CENDON DURAN (USP-SP, SÃO PAULO, SP, Brasil), CARLA BALEEIRO RODRIGUES SILVA (USP-SP, SÃO PAULO, SP, Brasil), CARLO SCOGNAMIGLIO RENNER ARAUJO (USP-SP, SÃO PAULO, SP, Brasil), LUCAS BRANDÃO ARAUJO DA SILVA (USP-SP, SÃO PAULO, SP, Brasil), LUCIANA PARENTE COSTA SEGURO (USP-SP, SÃO PAULO, SP, Brasil), LISSIANE KARINE NORONHA GUEDES (USP-SP, SÃO PAULO, SP, Brasil), ROSA MARIA RODRIGUES PEREIRA (USP-SP, SÃO PAULO, SP, Brasil), EDUARDO FERREIRA BORBA NETO (USP-SP, SÃO PAULO, SP, Brasil) BACKGROUND Charcot-Marie-Tooth Disease (CMT) is the most common hereditary neuropathy, with an estimated prevalence of 40 cases per 100,000 individuals. CMT type 2, the most common subtype, is an axonal disorder, usually beginning during the second or third decade of life. Clinical features include distal weakness, muscle atrophy, reduced sensitivity, decreased deep tendon reflexes and deformity of the foot. It may lead to the development of Charcot arthropathy, with increased osteoclastic activity and joint destruction. Ultrasonography can show effusion, synovitis, high-grade doppler activity and bone irregularities, findings that can lead to a misdiagnosis of inflammatory arthritis. CASE REPORT Male, 27-year-old, reported a history of pain and warm swelling of the left ankle and midfoot, worsening after exercise and improving with rest, that started nine years ago and persisted for one year. During this period, he self-medicated with non-steroidal anti-inflammatory drugs. He denied associated symptoms such as ocular inflammation, skin lesions, diarrhea, urethritis or fever. Ten months ago, he began to present similar symptoms in right ankle and midfoot, after a 7-year asymptomatic period. -
Confidential
CONFIDENTIAL CHILD’S MEDICAL INFORMATION The following is important information about my child’s medical condition and how the condition may affect their ability to fully participate in a regular school setting. The goal is to try to normalize every day school routines/activities while also meeting my child’s unique needs in the least disruptive manner. This document is not intended to replace any existing Individual Educational Plan (IEP) or the 504 Plan, but rather to serve as a supplement or addendum to enhance my child’s education. Medical information will be updated at the beginning of each new school year and throughout the school year as deemed necessary. “We may not look sick, but turn our bodies inside out and they will tell different stories.” Wade Sutherland CHILD’S NAME: ____________________________________________________________________________ ACADEMIC YEAR: _____________________GRADE: __________DOB: __________________AGE: _________ HOME ADDRESS: __________________________________________________________________________ PARENT/LEGAL GUARDIAN: ________________________________________________________________ PARENT/LEGAL GUARDIAN CONTACT NUMBER: ______________________________________________ SCHOOL: ________________________________________________________________________________ EMERGENCY CONTACT (2 PEOPLE) NAME: __________________________________________________________________________________ RELATIONSHIP: ____________________________ PHONE NUMBER: ________________________________ NAME: __________________________________________________________________________________ -
Approach to Polyarthritis for the Primary Care Physician
24 Osteopathic Family Physician (2018) 24 - 31 Osteopathic Family Physician | Volume 10, No. 5 | September / October, 2018 REVIEW ARTICLE Approach to Polyarthritis for the Primary Care Physician Arielle Freilich, DO, PGY2 & Helaine Larsen, DO Good Samaritan Hospital Medical Center, West Islip, New York KEYWORDS: Complaints of joint pain are commonly seen in clinical practice. Primary care physicians are frequently the frst practitioners to work up these complaints. Polyarthritis can be seen in a multitude of diseases. It Polyarthritis can be a challenging diagnostic process. In this article, we review the approach to diagnosing polyarthritis Synovitis joint pain in the primary care setting. Starting with history and physical, we outline the defning characteristics of various causes of arthralgia. We discuss the use of certain laboratory studies including Joint Pain sedimentation rate, antinuclear antibody, and rheumatoid factor. Aspiration of synovial fuid is often required for diagnosis, and we discuss the interpretation of possible results. Primary care physicians can Rheumatic Disease initiate the evaluation of polyarthralgia, and this article outlines a diagnostic approach. Rheumatology INTRODUCTION PATIENT HISTORY Polyarticular joint pain is a common complaint seen Although laboratory studies can shed much light on a possible diagnosis, a in primary care practices. The diferential diagnosis detailed history and physical examination remain crucial in the evaluation is extensive, thus making the diagnostic process of polyarticular symptoms. The vast diferential for polyarticular pain can difcult. A comprehensive history and physical exam be greatly narrowed using a thorough history. can help point towards the more likely etiology of the complaint. The physician must frst ensure that there are no symptoms pointing towards a more serious Emergencies diagnosis, which may require urgent management or During the initial evaluation, the physician must frst exclude any life- referral. -
Anaphylaxis During the Perioperative Period
REVIEW ARTICLE Anaphylaxis During the Perioperative Period David L. Hepner, MD*, and Mariana C. Castells, MD, PhD† *Department of Anesthesiology, Perioperative and Pain Medicine, and †Allergy and Clinical Immunology Training Program, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts Anesthesiologists use a myriad of drugs during the provi- perioperative period. Symptoms may include all organ sion of an anesthetic. Many of these drugs have side ef- systems and present with bronchospasm and cardiovas- fects that are dose related, and some lead to severe cular collapse in the most severe cases. Management of immune-mediated adverse reactions. Anaphylaxis is the anaphylaxis includes discontinuation of the presumptive most severe immune-mediated reaction; it generally oc- drug (or latex) and anesthetic, aggressive pulmonary and curs on reexposure to a specific antigen and requires the cardiovascular support, and epinephrine. Although a se- release of proinflammatory mediators. Anaphylactoid re- rum tryptase confirms the diagnosis of an anaphylactic actions occur through a direct non-immunoglobulin reaction, the offending drug can be identified by skin- E-mediated release of mediators from mast cells or from prick, intradermal testing, or serologic testing. Prevention complement activation. Muscle relaxants and latex of recurrences is critical to avoid mortality and morbidity. account for most cases of anaphylaxis during the (Anesth Analg 2003;97:1381–95) he term “anaphylaxis” was coined by Nobel reactions in which immune-complex formation and dep- prize recipients Portier and Richet (1) in 1902, osition leads to tissue damage (3). Anaphylactoid reac- T when they described a dog that had tolerated a tions occur through a direct nonimmune-mediated re- previous injection of actinotoxin, a jellyfish toxin, but lease of mediators from mast cells and/or basophils or reacted with bronchial spasm, cardiorespiratory ar- result from direct complement activation, but they rest, and death to a smaller dose 14 days later. -
Biological Treatment in Resistant Adult-Onset Still's Disease: a Single-Center, Retrospective Cohort Study
Arch Rheumatol 2021;36(x):i-viii doi: 10.46497/ArchRheumatol.2021.8669 ORIGINAL ARTICLE Biological treatment in resistant adult-onset Still’s disease: A single-center, retrospective cohort study Seda Çolak, Emre Tekgöz, Maghrur Mammadov, Muhammet Çınar, Sedat Yılmaz Department of Internal Medicine, Division of Rheumatology, Gülhane Training and Research Hospital, Ankara, Turkey ABSTRACT Objectives: The aim of this study was to assess the demographic and clinical characteristics of patients with adult-onset Still’s disease (AOSD) under biological treatment. Patients and methods: This retrospective cohort study included a total of 19 AOSD patients (13 males, 6 females; median age: 37 years; range, 28 to 52 years) who received biological drugs due to refractory disease between January 2008 and January 2020. The data of the patients were obtained from the patient files. The response to the treatment was evaluated based on clinical and laboratory assessments at third and sixth follow-up visits. Results: Interleukin (IL)-1 inhibitor was prescribed for 13 (68.4%) patients and IL-6 inhibitor prescribed for six (31.6%) patients. Seventeen (89.5%) patients experienced clinical remission. Conclusion: Biological drugs seem to be effective for AOSD patients who are resistant to conventional therapies. Due to the administration methods and the high costs of these drugs, however, tapering the treatment should be considered, after remission is achieved. Keywords: Adult-onset Still’s disease, anakinra, tocilizumab, treatment. Adult-onset Still’s disease (AOSD) is a rare diseases that may lead to similar clinical and systemic inflammatory disease with an unknown laboratory findings. etiology. The main clinical manifestations of It is well known that proinflammatory the disease are fever, maculopapular salmon- pink rash, arthralgia, and arthritis. -
Reactive Arthritis
PATIENT FACT SHEET Reactive Arthritis Reactive arthritis is an inflammatory disease that Most often, these bacterial infections are in the genitals occurs in reaction to infections by certain bacteria. or bowels, including the sexually transmitted infection Arthritis may show up a month after the infection. Once Chlamydia trachomatis, and bowel infections like called Reiter’s syndrome, it is a “spondyloarthropathy.” Campylobacter, Salmonella, Shigella and Yersinia. Reactive arthritis often affects men between 20 and CONDITION 50. It’s usually short in duration, but can be chronic in some people. DESCRIPTION Reactive arthritis symptoms include pain and swelling discharge from the genitals, but a urine or genital swab in knees, ankles or heels; severe swelling of toes or test can show signs of this infection. Bowel infections fingers; and persistent lower back pain that tends to may cause diarrhea. be more severe at night or in the morning. It may cause Most people with these very common infections irritated, red eyes, burning during urination, or a rash on don’t get reactive arthritis. People who test positive for the palms or soles of the feet. the HLA-B27 gene may be at higher risk for severe or To diagnose reactive arthritis, a rheumatologist may chronic arthritis, but those who test negative may get SIGNS/ look for these symptoms as well as signs of the original reactive arthritis too. People with weakened immune SYMPTOMS infection. Chlamydia may cause watery or pus-like systems from HIV or AIDS may develop reactive arthritis. Effective treatments are available for reactive arthritis. Later-stage, or chronic reactive arthritis, may be It is treated according to how far the disease has treated with disease-modifying antirheumatic drugs progressed. -
Pachydermoperiostosis As a Rare Cause of Blepharoptosis Nadir Bir Blefaroptozis Nedeni Pakidermoperiostozis
DOI: 10.4274/tjo.55707 Case Report / Olgu Sunumu Pachydermoperiostosis as a Rare Cause of Blepharoptosis Nadir Bir Blefaroptozis Nedeni Pakidermoperiostozis Özlem Yalçın Tök*, Levent Tök*, M. Necati Demir**, Sabite Kaçar***, Elif Nisa Ünlü****, Firdevs Örnek***** *Süleyman Demirel University Faculty of Medicine, Department of Ophthalmology, Isparta, Turkey **Yıldırım Beyazıt University Faculty of Medicine, Department of Ophthalmology, Ankara, Turkey ***Türkiye Yüksek İhtisas Education and Research Hospital, Department of Gastroenterology, Ankara, Turkey ****Süleyman Demirel University Faculty of Medicine, Department of Radiology, Isparta, Turkey *****Ankara Training and Research Hospital, Ministry of Health, Department of Ophthalmology, Ankara, Turkey Summary A 37-year-old male patient diagnosed with pachydermoperiostosis at another center came to our clinic to rectify his blepharoptosis. The physical examination of the patient revealed skeleton and skin symptoms typical for pachydermoperiostosis. There was thickening and extending horizontal length of the eyelids, an S-shaped deformity on the edges of the eyelids, and symmetric bilateral mechanical blepharoptosis. In order to treat the blepharoptosis, excision of the thickened skin and the orbicular muscle as well as levator aponeurosis surgery was performed. The esthetic result was satisfactory. Pachydermoperiostosis is a rare cause of blepharoptosis. Meibomius gland hyperplasia, increase of collagen substance in the dermis, mucin accumulation are reasons of thickening the eyelid and -
Differential Diagnosis of Juvenile Idiopathic Arthritis
pISSN: 2093-940X, eISSN: 2233-4718 Journal of Rheumatic Diseases Vol. 24, No. 3, June, 2017 https://doi.org/10.4078/jrd.2017.24.3.131 Review Article Differential Diagnosis of Juvenile Idiopathic Arthritis Young Dae Kim1, Alan V Job2, Woojin Cho2,3 1Department of Pediatrics, Inje University Ilsan Paik Hospital, Inje University College of Medicine, Goyang, Korea, 2Department of Orthopaedic Surgery, Albert Einstein College of Medicine, 3Department of Orthopaedic Surgery, Montefiore Medical Center, New York, USA Juvenile idiopathic arthritis (JIA) is a broad spectrum of disease defined by the presence of arthritis of unknown etiology, lasting more than six weeks duration, and occurring in children less than 16 years of age. JIA encompasses several disease categories, each with distinct clinical manifestations, laboratory findings, genetic backgrounds, and pathogenesis. JIA is classified into sev- en subtypes by the International League of Associations for Rheumatology: systemic, oligoarticular, polyarticular with and with- out rheumatoid factor, enthesitis-related arthritis, psoriatic arthritis, and undifferentiated arthritis. Diagnosis of the precise sub- type is an important requirement for management and research. JIA is a common chronic rheumatic disease in children and is an important cause of acute and chronic disability. Arthritis or arthritis-like symptoms may be present in many other conditions. Therefore, it is important to consider differential diagnoses for JIA that include infections, other connective tissue diseases, and malignancies. Leukemia and septic arthritis are the most important diseases that can be mistaken for JIA. The aim of this review is to provide a summary of the subtypes and differential diagnoses of JIA. (J Rheum Dis 2017;24:131-137) Key Words. -
Caplan's Syndrome
Int J Clin Exp Med 2016;9(11):22600-22604 www.ijcem.com /ISSN:1940-5901/IJCEM0036089 Case Report Rheumatoid pneumoconiosis (Caplan’s syndrome): a case report Wei-Li Gu, Li-Yan Chen, Nuo-Fu Zhang Department of Respiratory Medicine, State Key Laboratory of Respiratory Disease, Guangzhou Institute of Respi- ratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China Received July 18, 2016; Accepted September 10, 2016; Epub November 15, 2016; Published November 30, 2016 Abstract: Caplan’s syndrome, also referred to as rheumatoid pneumoconiosis (RP), is specific to rheumatoid arthri- tis (RA) and presents with multiple, well-defined necrotic nodules in workers exposed to dust. Here we report one case with a typical pulmonary presentation, confirmed through computed tomography (CT) and histopathological studies. A 58-year-old male patient with a diagnosis of RA, complained pain of multiple joints and mild dyspnea on exertion. He was an active smoker (40 pack-years) and worked as a shepherd for 35 years exposed to dust. High- resolution CT (HRCT) of the chest revealed bilateral, round, well-delimited nodules with peripheral distribution. After one month of treatment with corticosteroids and tripterygiumwilfordii, the patient’s pain and dyspnea improved. In the meantime, pulmonary nodules grew down gradually. The case demonstrates the clinical presentation, radiologi- cal and pathological features of Caplan’s syndrome. The effective treatment for Caplan’s syndrome is corticoste- roids and tripterygiumwilfordii. Keywords: Pneumoconiosis, rheumatoid arthritis, Caplan’s syndrome, silicosis Introduction in the lung for two years with no other initial signs of rheumatoid disease. He complained Caplan’s syndrome, also referred to as rheuma- pain of multiple joints eight months later.