DOCSLIB.ORG

VASCULITIS 156 Final24/07Xwendy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
VASCULITIS 156 Final24/07Xwendy Letters to the Editors Signifi cant improvement of axillary artery stenosis in a ▼ 67-year-old woman with giant ▼ cell arteritis ▼ Sirs, We describe a 67-year-old woman with giant cell arteritis (GCA) presented with a month’s history of intermittent claudica- tion of the upper limbs and newly appeared Raynaud’s phenomenon. The patient did not complain of headaches, shoulder or pel- vic pain, nor did she have jaw claudication or visual impairment. Her past medical history was unremarkable. ▼ The physical examination revealed absence ▼ of radial and brachial pulses bilaterally. ▼ Temporal arteries appeared normal on ex- amination. Blood pressure was unrecordable in the upper limbs. The laboratory evalua- tion showed high erythrocyte sedimentation rate (ESR) (70 mm/h) and C-reactive pro- tein (CRP) (80 mg/dl), as well as hypochro- mic and microcytic anemia (Hemoglobin 8.8 gr/dl). The rest of the laboratory tests were within normal limits. The color Dop- Fig. 1. Doppler ultrasound studies showed right axillary artery stenosis (A) and left axillary artery stenosis (B). After pler ultrasound study revealed a signifi cant a year of treatment a signifi cant degree of improvement were noted of both axillary arteries (C and D respectively). degree of bilateral axillary artery stenosis with excessively thickened endothelium Color Doppler ultrasonography demon- enables a good clinical response and avoid- Fig. 1A and B). The angiography of the aor- strates a characteristic picture in GCA show- ance of large-artery complications. tic arch and its branches also showed exten- ing a hypoechoic mural thickening in the sive smooth appearance of stenoses of the acute phase of the disease due to edema of C.G. PAPADOPOULOS1, MD axillary arteries bilaterally. The biopsy of the vessel wall with subtotal or total occlu- P.V. VOULGARI1, MD A. ZIOGA2, MD the left temporal artery revealed histologi- sion of the involved vessel. In the chronic 1 cal lesions suggesting GCA. stage or after treatment, the mural thicken- G.A. MILTIADOUS , MD, P. NICOLOPOULOS3, MD, Treatment with prednisolone 60 mg/day and ing becomes hyperechoic due to fi brosis. M.S. ELISAF1, MD, Prof. methotrexate (MTX) 10 mg/week was start- Thus, Doppler ultrasonography permits ac- A.A. DROSOS1, MD, FACR, Prof. ed Four weeks later, the ESR and CRP had curate assessment of the involved vessels at Departments of 1Internal Medicine, 2Pathology fallen to normal values (ESR 3 mm/h, CRP specifi c sites (4). and 3Radiology, Medical School, University of 1 mg/dl). and hemoglobin also returned to Angiography, computed tomography, and Ioannina, Ioannina, Greece. normal values, so the dose of prednisolone magnetic resonance angiography delineate Address correspondence and reprint requests to: was tapered. One year later, her symptoms characteristic patterns in large-vessel GCA Alexandros A. Drosos, MD, FACR, Department improved impressively, the blood pressure (5). of Internal Medicine, Medical School, was recordable in both limbs and the color High-dose of corticosteroids is the treatment University of Ioannina, 45110 Ioannina, Greece. Doppler ultrasound studies showed a sig- of choice for large-vessel GCA (2). Early E-mail: [email protected] nifi cant improvement of the axillary artery diagnosis and treatment enables a good Competing interests: none declared. stenosis (Fig. 1C and D). At this time the response avoiding vascular complications. dose of prednisolone was 10 mg every other However, angioplastic revascularization is References day plus 10 mg MTX/week. required in cases with arterial occlusion not 1. NUENNINGHOFF DM, HUNDER GG, CHRISTIAN- GCA targets extracranial branches of the responsive to corticosteroid therapy, while SON TJ, MCCLELLAND RL, MATTESON EL: Incid- carotid arteries preferentially but also af- the addition of aspirin may help maintain- ence and predictors of large-artery complication fects the large arteries and especially the ing the angioplastic results (6). Despite a (aortic aneurysm, aortic dissection, and/or large- artery stenosis) in patients with giant cell arteritis: carotid, subclavian, and axillary arteries in tendency to restnoses, balloon angioplasty a population-based study over 50 years. Arthritis almost a quarter of patients (1). The clini- of the upper-extremity artery, in combina- Rheum 2003; 48: 3522-31. cal presentation of the large vessel involve- tion with immunosuppressive treatment, is 2. VAN DAMME H, FOURNY J, ZICOT M, LIMET R: ment includes claudication of the arms, ab- an effi cient method for the treatment of ex- Giant cell arteritis (Horton’s disease) of the axillary sent or asymmetrical pulses, paresthesias, tracranial GCA (7, 8). Although the use of artery--case reports. Angiology 1989; 40: 593-601. Raynaud’s phenomenon and occasionally, MTX in temporal arteritis is controversial, 3. LONG A, BRUNEVAL P, LAURIAN C, CORMIER JM, CAMILLERI JP, FIESSINGER JN: Extratem- peripheral gangrene (2, 3). Patients with the it seems to be an effective corticosteroid- poral Horton’s disease: diagnosis using subclavian large-vessel variant of GCA may lack the sparing agent for the treatment of GCA (9, biopsy. 4 cases. Arch Mal Coeur Vaiss 1989; 82: clinical evidence of cranial involvement, 10). However, the most important fi nding 1727-31. as happened with our patient. Almost 50% in this case is the signifi cant improvement 4. SCHMIDT WA, KRAFT HE, BORKOWSKI A, of temporal artery biopsies are negative for of axillary artery stenosis after a year of GROMNICA-IHLE EJ: Color duplex ultrasonog- early treatment with prednisone and MTX. raphy in large-vessel giant cell arteritis. Scand J vasculitis. In addition, large artery involve- Rheumatol 1999;1999; 28:28: 3374-6.74-6. ment in GCA may be complicated by aortic Thus, in patients with upper limb ischemia, 5. AGARD C, PONGE T, FRADET G et al.: Giant cell aneurysm, artery stenosis and/or aortic dis- the possibility of large-vessel GCA must be arteritis presenting with aortic dissection: two cases section increasing mortality (1). considered. Early diagnosis and treatment and review of the literature. Scand J Rheumatol S-151 Letters to the Editors 2006; 35: 233-6. count of 357x103/mm3. Serum IgA were L. CANTARINI1, MD, PhD 6. AMANN-VESTI BR, KOPPENSTEINER R, RAIN- slightly increased. C-reactive protein, eryth- A. BROGNA2, MD 3 ONI L, PFAMATTER T, SCHNEIDER E: Immediate rocyte sedimentation rate, kidney function A. FIORAVANTI , MD and long-term outcome of upper extremity balloon M. GALEAZZI1, MD, Prof. angioplasty in giant cell arteritis. J Endovasc Ther and urine sediment were normal. Antistrep- 1 2003; 10: 371-5. tolysin was not increased. Antinuclear anti- Interdepartmental Research Center of Systemic 7. BOTH M, ARIES PM, MULLER-HULSBECK S et al.: Autoimmune and Autoinfl ammatory Diseases, bodies, cryoglobulins and antineutrophilic 2 Balloon angioplasty of arteries of the upper extrem- Unit of Rheumatology, Department of cytoplasmic antibodies (perinuclear and Paediatrics, Obstetrics and Reproductive ities in patients with extracranial giant-cell arteritis. cytoplasmic patterns) were negative. Ann Rheum Dis 2006; 65: 1124-30. Medicine, Neonatal Intensive Care Unit, 3 8. BOTH M, JAHNKE T, REINHOLD-KELLER E et al.: The patient had started treatment with pi- Department of Clinical Medicine and Percutaneous management of occlusive arterial dis- dotimod 400 mg per day eight days before Immunologic Sciences, Unit of Rheumatology, ease associated with vasculitis: a single center experi- her visit due to recurring tonsil infections Policlinico Le Scotte, University of Siena, ence. Cardiovasc Intervent Radiol 2003;2003; 26:26: 19-26.19-26. and adenoid-tonsillar hypertrophy. Siena, Italy. 9. HOFFMAN GS, CID MC, HELLMANN DB et al.: She had had her last infection three months Address correspondence and reprint requests to: A multicenter, randomized, double-blind, placebo- earlier, and she was living with her parents Luca Cantarini, MD, Institute of Rheumatology, controlled trial of adjuvant methotrexate treatment Policlinico “Le Scotte”, University of Siena, for giant cell arteritis. Arthritis Rheum 2002; 46: who were in good health. Viale Bracci 1, 53100 Siena, Italy. 1309-18. Pidotimod ((R)-3-[(S)-(5-oxo-2-pyrrolidi- E-mail: [email protected] 10. DASGUPTA M, HASSAN N; BRITISH SOCIETY nyl) carbonyl]-thiazolidine-4-carboxylic Competing interests: none declared. FOR RHEUMATOLOGY GUIDELINES GROUP: Gi- acid, PGT/1A, CAS 121808-62-6) is a syn- ant cell arteritis: recent advances and guidelines for thetic biological response modifi er which management. Clin Exp Rheumatol 2007;2007; 2525 (Suppl.(Suppl. References 44): S62-5. acts by stimulating cell-mediated immunity 1. CALVINO MC, LLORCA J, GARCIA-PORRUA C, (5) and which has been shown to enhance FERNANDEZ-INGLESIAS JL, RODRIGUEZ-LEDO several immune parameters in humans, P, GONZALEZ-GAY MA: Henoch-Schönlein pur- both in vitro and in vivo (6, 7). Pidotimod pura in children from northwestern Spain: a 20-year is active on T-lymphocytes in early matura- epidemiologic and clinical study. Medicine 2001; tion stage (8) and is able to enhance periph- 80: 279-90. Henoch-Schönlein purpura 2. TRAPANI S, MICHELI A, GRISOLIA F et al.: associated with pidotimod eral blood mononuclear cell proliferation Henoch-Schönlein purpura in childhood: epidemio- through an increased interleukin-2 produc- logical and clinical analysis of 150 cases over a 5- therapy tion (IL-2) (7). IL-2 has been shown to in- year period and review of literature. Semin Arthritis duce interleukin-5 (IL-5) production by T- Rheum 2005; 35: 143-53. Sirs, lymphocytes, in a dose-dependent manner, 3. SAULSBURY FT: Henoch-Schönlein purpura. Curr Henoch-Schönlein purpura (HSP) is a Opin Rheumatol 2001;2001; 113:3: 35-40.35-40. and IL-5 induces IgA production from B- 4. SAULSBURY FT: Clinical update: Henoch-Schön- small-sized vasculitis affecting mainly lymphocytes and is also recognized by its lein purpura. Lancet 2007; 369: 976-8. children and young adults. The mean age activity as an IgA-enhancing factor (9). 5. COPPI G, MANZARDO S: Experimental immuno- of patients is six years; 90% of patients are She was diagnosed with drug related HSP logical screening tests on Pidotimod.
Load more

Recommended publications
  • ANCA--Associated Small-Vessel Vasculitis
    ANCA–Associated Small-Vessel Vasculitis ISHAK A. MANSI, M.D., PH.D., ADRIANA OPRAN, M.D., and FRED ROSNER, M.D. Mount Sinai Services at Queens Hospital Center, Jamaica, New York and the Mount Sinai School of Medicine, New York, New York Antineutrophil cytoplasmic antibodies (ANCA)–associated vasculitis is the most common primary sys- temic small-vessel vasculitis to occur in adults. Although the etiology is not always known, the inci- dence of vasculitis is increasing, and the diagnosis and management of patients may be challenging because of its relative infrequency, changing nomenclature, and variability of clinical expression. Advances in clinical management have been achieved during the past few years, and many ongoing studies are pending. Vasculitis may affect the large, medium, or small blood vessels. Small-vessel vas- culitis may be further classified as ANCA-associated or non-ANCA–associated vasculitis. ANCA–asso- ciated small-vessel vasculitis includes microscopic polyangiitis, Wegener’s granulomatosis, Churg- Strauss syndrome, and drug-induced vasculitis. Better definition criteria and advancement in the technologies make these diagnoses increasingly common. Features that may aid in defining the spe- cific type of vasculitic disorder include the type of organ involvement, presence and type of ANCA (myeloperoxidase–ANCA or proteinase 3–ANCA), presence of serum cryoglobulins, and the presence of evidence for granulomatous inflammation. Family physicians should be familiar with this group of vasculitic disorders to reach a prompt diagnosis and initiate treatment to prevent end-organ dam- age. Treatment usually includes corticosteroid and immunosuppressive therapy. (Am Fam Physician 2002;65:1615-20. Copyright© 2002 American Academy of Family Physicians.) asculitis is a process caused These antibodies can be detected with indi- by inflammation of blood rect immunofluorescence microscopy.
    [Show full text]
  • A Review of Primary Vasculitis Mimickers Based on the Chapel Hill Consensus Classification
    Hindawi International Journal of Rheumatology Volume 2020, Article ID 8392542, 11 pages https://doi.org/10.1155/2020/8392542 Review Article A Review of Primary Vasculitis Mimickers Based on the Chapel Hill Consensus Classification Farah Zarka ,1 Charles Veillette ,1 and Jean-Paul Makhzoum 2 1Hôpital du Sacré-Cœur de Montreal, University of Montreal, Canada 2Vasculitis Clinic, Department of Internal Medicine, Hôpital du Sacré-Coeur de Montreal, University of Montreal, Canada Correspondence should be addressed to Jean-Paul Makhzoum; [email protected] Received 10 July 2019; Accepted 7 January 2020; Published 18 February 2020 Academic Editor: Charles J. Malemud Copyright © 2020 Farah Zarka et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Primary systemic vasculitides are rare diseases that may manifest similarly to more commonly encountered conditions. Depending on the size of the vessel affected (large vessel, medium vessel, or small vessel), different vasculitis mimics must be considered. Establishing the right diagnosis of a vasculitis mimic will prevent unnecessary immunosuppressive therapy. 1. Introduction 2. Large-Vessel Vasculitis Mimics Vasculitides are rare heterogenous diseases that affect vessel Large-vessel vasculitis (LVV) is an inflammatory vascu- walls as the main site of inflammation. Organs affected vary lopathy affecting large arteries; giant cell arteritis (GCA) depending on the type and size of blood vessels involved and Takayasu’s arteritis (TAK) are the two main docu- [1]. Autoimmune vasculitis can be primary (idiopathic) or mented variants, each with their own characteristic fea- secondary to an underlying disease.
    [Show full text]
  • Rheumatology 2 Objectives
    1 RHEUMATOLOGY 2 OBJECTIVES Know and understand: • How the clinical presentations of rheumatologic diseases can vary • Components of a thorough physical examination for investigating rheumatoid complaints • How to differentiate between different rheumatologic diseases • Evidence-based management of rheumatologic diseases 3 TOPICS COVERED • Osteoarthritis • Rheumatoid Arthritis • Gout • Calcium Pyrophosphate Deposition Disease • Polymyalgia Rheumatica • Giant Cell Arteritis (Temporal Arteritis) • Systemic Lupus Erythematosus • Sjögren Syndrome • Polymyositis and Dermatomyositis • Fibromyalgia 4 OSTEOARTHRITIS (OA): OVERVIEW • Principal cause of knee, hip, and back pain in older adults, and most common source of chronic pain • Avoid the reflexive conclusion that all joint pain in older adults is the result of OA • Can develop in any joint that has suffered injury or other disease • Hallmark: cartilage degeneration Ø But not purely a degenerative disease; subchondral bone abnormalities and focal synovial inflammation are also seen in pathologic specimens 5 OA: DIAGNOSIS • Differential diagnosis: inflammatory and crystal arthritides, septic arthritis, bone pain due to malignancy • Bony enlargement and crepitus suggest OA Ø In the fingers, bony enlargement occurs in the distal interphalangeal joint (Heberden nodes) and in the proximal interphalangeal joints (Bouchard nodes) Ø Osteophytes are the radiographic counterpart of this enlargement, and asymmetric joint space narrowing is common • Joint tenderness and warmth may appear, but true synovitis
    [Show full text]
  • Guideline-Management-Giant-Cell
    Arthritis Care & Research Vol. 73, No. 8, August 2021, pp 1071–1087 DOI 10.1002/acr.24632 © 2021 American College of Rheumatology. This article has been contributed to by US Government employees and their work is in the public domain in the USA. 2021 American College of Rheumatology/Vasculitis Foundation Guideline for the Management of Giant Cell Arteritis and Takayasu Arteritis Mehrdad Maz,1 Sharon A. Chung,2 Andy Abril,3 Carol A. Langford,4 Mark Gorelik,5 Gordon Guyatt,6 Amy M. Archer,7 Doyt L. Conn,8 Kathy A. Full,9 Peter C. Grayson,10 Maria F. Ibarra,11 Lisa F. Imundo,5 Susan Kim,2 Peter A. Merkel,12 Rennie L. Rhee,12 Philip Seo,13 John H. Stone,14 Sangeeta Sule,15 Robert P. Sundel,16 Omar I. Vitobaldi,17 Ann Warner,18 Kevin Byram,19 Anisha B. Dua,7 Nedaa Husainat,20 Karen E. James,21 Mohamad A. Kalot,22 Yih Chang Lin,23 Jason M. Springer,1 Marat Turgunbaev,24 Alexandra Villa-Forte, 4 Amy S. Turner,24 and Reem A. Mustafa25 Guidelines and recommendations developed and/or endorsed by the American College of Rheumatology (ACR) are intended to provide guidance for particular patterns of practice and not to dictate the care of a particu- lar patient. The ACR considers adherence to the recommendations within this guideline to be voluntary, with the ultimate determination regarding their application to be made by the physician in light of each patient’s individual circumstances. Guidelines and recommendations are intended to promote beneficial or desirable outcomes but cannot guarantee any specific outcome.
    [Show full text]
  • PMR) / Giant Cell Arteritis (GCA
    Arthritis and Rheumatology Clinics of Kansas Patient Education Polymyalgic Rheumatica (PMR) / Giant Cell Arteritis (GCA) Introduction: PMR and GCA are related conditions affecting adults over the age of 50. Both are inflammatory diseases, with PMR involving the large joints of the hips and/or shoulders and GCA involving large and medium sized blood vessels. PMR occurs in about 30 individuals over the age of 50 per 100,000 population per year, while GCA is roughly half as common. Both conditions are about twice as common in women as in men and are seen most commonly in those of Northern European descent. The average age of onset is about 70 for both conditions, and with the aging population the prevalence of these disorders is expected to increase in the next few decades. While the cause of these conditions is unknown, the fact that they tend to occur in cooler climates and in clusters of cases every several years suggests that infections may trigger PMR and GCA. Having certain genes also seems to increase the risk of developing either of these disorders. Features of PMR: Patients with PMR tend to experience widespread pain in the regions of the shoulders, upper arms, neck, hips, buttock, and thighs. These symptoms may be sudden in onset and are accompanied by up to several hours of morning stiffness. While swelling of knees, elbows, or wrists may occur, there is most often no visible joint swelling but only difficulty with movement of the larger joints. A small percentage of patients may experience swelling of the entire hand and foot with edema, or excess fluid accumulation.
    [Show full text]
  • Versus Arthritis Vasculitis Information Booklet
    Condition Vasculitis Vasculitis This booklet provides information and answers to your questions about this condition. Arthritis Research UK booklets are produced and printed entirely from charitable donations. What is vasculitis? Vasculitis means inflammation of the blood vessels. There are several different types of the condition, many with unknown causes, but treatments can be very effective. In this booklet we’ll briefly explain the main types of vasculitis, how they’re diagnosed and treated, what you can do to help yourself and where to get more information. At the back of this booklet you’ll find a brief glossary of medical words – we’ve underlined these when they’re first used. www.arthritisresearchuk.org Page 2 of 32 Vasculitis information booklet Arthritis Research UK What’s inside? 2 Vasculitis at a glance 5 Who diagnoses and treats 15 What is the outlook? vasculitis? 15 How is vasculitis diagnosed? 6 What is vasculitis? – What tests are there? 8 What are the symptoms 17 What treatments are there for vasculitis? of vasculitis? – Drugs 9 What types of vasculitis 20 Self-help and daily living are there? – Exercise – Takayasu arteritis (TA) – Diet and nutrition – Giant cell arteritis (temporal arteritis) – Stop smoking – Polyarteritis nodosa (PAN) – Keep warm – Kawasaki disease 22 Research and new – Granulomatosis with polyangiitis developments (Wegener’s granulomatosis) 23 Glossary – Behçet’s syndrome – Eosinophilic granulomatosis 26 Where can I find out more? with polyangiitis (Churg–Strauss 28 We’re here to help syndrome) – Microscopic polyangiitis – Cryoglobulin-associated vasculitis – Immunoglobulin A vasculitis (Henoch–Schönlein purpura) 14 Who gets vasculitis? 15 What causes vasculitis? Page 3 of 32 Vasculitis information booklet At a glance Vasculitis There are several different types of vasculitis but all are treatable.
    [Show full text]
  • Immune-Mediated Diseases in a Nutshell
    Immune-Mediated Diseases In a Nutshell Objectives Describe the epidemiology, clinical presentation, pathogenesis and pathologic changes of autoimmune diseases, including lupus erythematosis, rheumatoid arthritis, vasculitis, temporal arteritis and Wegener's granulomatosis Systemic Lupus Erythematosus Systemic lupus erythematosus: clinical features Febrile, multisystem inflammatory disease Variably affects wide range of organs and tissues, especially skin, kidneys, serosal surfaces, joints, heart Clinical course highly variable, often with multiple exacerbations and remissions Especially prevalent in young women, black Americans Prevalence: up to 1 to 2,500 persons Systemic lupus erythematosus: pathogenesis Autoantibodies develop against a variety of antigens: Nucleoproteins / nucleic acids DNA histones nonhistone RNA-binding proteins Blood cells erythrocytes platelets lymphocytes Phospholipids (e.g., “lupus anticoagulant”) Systemic lupus erythematosus: pathogenesis Antigen-antibody Antibody bound to immune complexes cells leads to lysis form via complement- mediated Complexes deposit in cytotoxicity or numerous sites, ADCC initiate complement cascade, and trigger inflammation Type III Hypersensitivity Type II Hypersensitivity Systemic lupus erythematosus: pathogenesis Possible causes of autoantibody production Intrinsic B cell defect Excessive helper T cell activity Deficient suppressor T cell activity Rheumatoid Arthritis Rheumatoid arthritis: clinical features Systemic, chronic inflammatory disease Principally affects joints: severe,
    [Show full text]
  • Vasculitis Factsheet Dr Laurence Knott Dr David Kluth
    Author Peer Reviewer Vasculitis Factsheet Dr Laurence Knott Dr David Kluth This is a leaflet for people who want general information about vasculitis. Vasculitis is a medical term meaning inflammation of blood vessels. It can be primary (occurring on its own) or secondary (occurring as part of another condition). Some people with vasculitis test positive for antibodies to constituents of certain white blood cells (anti-neutrophil cytoplasmic antibodies or ANCA) and are said to have ANCA vasculitis. Who gets vasculitis? Vasculitis is an uncommon illness. About 20 in every 100,000 people get ANCA vasculitis every year in the UK. Vasculitis can affect all age groups. Some are mostly diseases of childhood (e.g. Kawasaki), whilst others persist throughout adult life (ANCA systemic vasculitis). Some principally affect the elderly (e.g. giant cell arteritis). What causes vasculitis? In most cases the cause is not known. Many experts think that the illness is the result of infection in people who were born with a certain genetic predisposition. Vasculitis can also be caused by illnesses which trigger inflammation in the body such as rheumatoid arthritis and inflammatory diseases of the bowel. Medicines associated with vasculitis include certain types of antibiotics (e.g. quinolones, sulphonamides,beta-lactams), a nti-inflammatories, the contraceptive pill, some types of fluid tablets (thiazides) and flu vaccines. Rare types of cancer (paraproteinaemia, lymphoproliferative disorder) can occasionally cause vasculitis. Are there different types of vasculitis? There are many different types of vasculitis and various ways of classifying them. Vasculitis occurring in one part of the body is known as localised vasculitis.
    [Show full text]
  • Giant Cell Arteritis Overlapping with Rheumatoid Arthritis and Sjögren's
    ogy iol : Op r B e a n l A u c c c e l e Wang et al., Mol Biol 2019, 8:2 o s s M Molecular Biology: Open Access ISSN: 2168-9547 Case Report Open Access Giant Cell Arteritis Overlapping with Rheumatoid Arthritis and Sjögren’s Syndrome Jing Wang1#, Lingyan Zhou2# and Jing Gao2* 1Department of Rheumatology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, P.R. China 2Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, P.R. China #These authors have contributed equally to this work Abstract Background: Giant cell arteritis (GCA) is an autoimmune vasculitis involving large and medium arteries, but the relationship with other autoimmune diseases is unclear. We reported a case of an 85-year-old woman who was diagnosed with GCA, Sjögren’s syndrome (SS) and rheumatoid arthritis (RA) simultaneously, and discussed the potential link between these diseases. Case presentation: An 85-year-old Chinese woman was admitted to hospital with aggravation of pain in two knees with headache and blurred vision. She had a history of rheumatoid arthritis and rheumatoid heart disease for 30 years and atrial fibrillation for 1 year. On admission, she had bilateral temporal pain accompanied by blurred vision. Physical examination showed dry tongue and decreased coating on the tongue. Initial laboratory results showed that C-reactive protein (CRP) was 24.89 mg/L (normally 0-5), and erythrocyte sedimentation rate (ESR) was 42.4 mm/h (normally 0-20), both of them were significantly elevated. Results: The anti-nuclear antibody (ANA) and anti-centromere antibody (ACA) was positive in serum.
    [Show full text]
  • Giant Cell Arteritis
    GIANT CELL ARTERITIS What is giant cell arteritis (GCA)? Giant cell arteritis (GCA) is a form of vasculitis—a family of rare disorders characterized by inflammation of the blood vessels, which can restrict blood flow and damage vital organs and tissues. Also called temporal arteritis, GCA typically affects the arteries in the neck and scalp, especially the temples. It can also affect the aorta and its large branches to the head, arms and legs. GCA is the most common form of vasculitis in adults over the age of 50. The most common symptoms of GCA include persistent, throbbing headaches, tenderness of the temples and scalp, jaw pain, fever, joint pain, and vision problems. Early treatment is vital to prevent serious complications such as blindness or stroke. GCA is typically treated with high doses of corticosteroids such as prednisone, sometimes in combination with other medications that suppress the immune system. Prompt treatment usually relieves symptoms, however GCA is a chronic condition with periods of relapse and remission, so ongoing medical care is usually necessary. Patients with GCA may also have symptoms of polymyalgia rheumatica (PMR), a closely related inflammatory disorder. Causes The cause of GCA is not yet fully understood by researchers. Vasculitis is classified as an autoimmune disorder—a disease which occurs when the body’s natural defense system mistakenly attacks healthy tissues. Researchers believe a combination of factors may trigger the inflammatory process. Studies have linked genetic factors, infectious agents, and a prior history of cardiovascular disease to the development of GCA. Who gets GCA? GCA is the most common form of vasculitis in older adults, affecting people over 50 years of age, with an average onset of 74 years of age.
    [Show full text]
  • Giant Cell Arteritis
    NANOS Patient Brochure Giant Cell Arteritis Copyright © 2017. North American Neuro-Ophthalmology Society. All rights reserved. These brochures are produced and made available “as is” without warranty and for informational and educational purposes only and do not constitute, and should not be used as a substitute for, medical advice, diagnosis, or treatment. Patients and other members of the general public should always seek the advice of a physician or other qualified healthcare professional regarding personal health or medical conditions. Giant Cell Arteritis What is Giant Cell Arteritis (GCA)? Giant cell arteritis (also called temporal arteritis) is inflammation of blood vessels. It tends to affect arteries which supply the head and neck, though can also affect blood vessels throughout the body supplying other organs and large muscle groups. GCA almost only affects people older than 50 years of age, with an average age of 70 years. It affects both men and women and can occur in any race or ethnicity. The cause of GCA remains unknown, though increasing age increases the risk of developing this condition. Some experts believe that giant cell arteritis is autoimmune, meaning that the body’s immune system is creating antibodies against itself, similar to fighting against a bacteria or virus. GCA may be an extreme form of the autoimmune condition polymyalgia rheumatic (PMR), which causes joint aches and stiffness in the limbs and torso. Because GCA can involve the blood vessels which go to the eye and the brain, the condition may cause permanent vision loss in one or both eyes in up to 20-50% of patients.
    [Show full text]
  • Conditions Where LDN Could Be of Benefit
    Conditions Where LDN Could Be of Benefit Acute disseminated encephalomyelitis Acute CREST syndrome hemorrhagic leukoencephalitis Addison's Disease Crohns Disease (one of two types of idiopathic Agammaglobulinemia inflammatory bowel disease "IBD") Alopecia areata Cushing's Syndrome Amyotrophic Lateral Sclerosis Cutaneous leukocytoclastic angiitis Ankylosing Spondylitis Dego's disease Anti-GBM/TBM Nephritis Antiphospholipid Dercum's disease syndrome Antisynthetase syndrome Dermatitis herpetiformis Asthma Dermatomyositis Atopic allergy Diabetes mellitus type 1 Atopic dermatitis Diffuse cutaneous systemic sclerosis Autoimmune aplastic anemia Autoimmune Discoid lupus erythematosus cardiomyopathy Autoimmune enteropathy Dressler's syndrome Autoimmune hemolytic anemia Autoimmune Eczema hepatitis Enthesitis-related arthritis Autoimmune inner ear disease Autoimmune Eosinophilic fasciitis lymphoproliferative syndrome Autoimmune Eosinophilic gastroenteritis pancreatitis Epidermolysis bullosa acquisita Autoimmune peripheral neuropathy Erythema nodosum Autoimmune polyendocrine syndrome Essential mixed cryoglobulinemia Autoimmune progesterone dermatitis Evan's syndrome Autoimmune thrombocytopenic purpura Fibrodysplasia ossificans progressiva Fibromyalgia Autoimmune urticaria (FB) Autoimmune uveitis Fibrosing aveolitis Balo disease/Balo concentric sclerosis Bechets Gastritis Syndrome Gastrointestinal pemphigoid Berger's disease Giant cell arteritis Bickerstaff's encephalitis Glomerulonephritis Blau syndrome Goodpasture's syndrome Bullous pemphigoid Graves'
    [Show full text]