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Giant-cell arteritis

giant cell arteritis, giant cell arteritis symptoms
Giant-cell arteritis GCA, also called temporal arteritis, cranial arteritis, or Horton disease is an inflammatory disease of blood vessels most commonly involving large and medium arteries of the head, predominantly the branches of the external carotid artery The most serious complication is occlusion of the ophthalmic artery, which is a branch of the internal carotid It can create a medical emergency which can cause irreversible ischemia and blindness if not treated promptly GCA is treated with glucocorticoids steroids, which reduce the inflammation and prevent Vascular occlusion No other drugs are effective or contribute to the effect of glucocorticoids1

GCA is a form of vasculitis It typically causes inflammation of the network of small vessels vasa vasorum that supplies the larger arteries GCA affects arteries of the head and neck, including the three arteries that branch out from the arch of the ascending aorta, and their branches—the thoracic aorta, the axillary arteries, the vertebral arteries, and further on in the head in the ophthalmic and external carotid arteries the temporal and occipital arteries It can cause Vascular occlusion of the arteries and ischemia1

GCA is diagnosed with biopsy of the temporal artery While the clinical presentation, patient characteristics and blood test markers of inflammation can raise suspicion, only a temporal artery biopsy can give definite diagnosis Some cases may not involve the temporal artery, and distinguishing between a false negative and the absence of GCA is difficult1

The terms "giant-cell arteritis" and "temporal arteritis" are sometimes used interchangeably, because of the frequent involvement of the temporal artery However, it can involve other large vessels such as the aorta in "giant-cell aortitis"2 Giant-cell arteritis of the temporal artery is referred to as "temporal arteritis," and is also known as "cranial arteritis" and "Horton's disease"3 The name giant-cell arteritis reflects the type of inflammatory cell involved4 as seen on a biopsy

Contents

  • 1 Signs and symptoms
    • 11 Associated conditions
  • 2 Mechanism
  • 3 Diagnosis
    • 31 Physical exam
    • 32 Laboratory tests
    • 33 Biopsy
    • 34 Imaging studies
  • 4 Treatment
  • 5 References
  • 6 External links

Signs and symptomsedit

It is more common in women than in men by a ratio of 2:1 and more common in those of Northern European descent, as well as those residing at higher northern/southern latitudes The mean age of onset is >55 years, and it is rare in those younger than 55 years of agecitation needed

People present with:

  • bruits
  • fever
  • headache5
  • tenderness and sensitivity on the scalp
  • jaw claudication pain in jaw when chewing
  • tongue claudication pain in tongue when chewing and necrosis67
  • reduced visual acuity blurred vision
  • acute visual loss sudden blindness
  • diplopia double vision
  • acute tinnitus ringing in the ears
  • polymyalgia rheumatica in 50%8

The inflammation may affect blood supply to the eye; blurred vision or sudden blindness may occur In 76% of cases involving the eye, the ophthalmic artery is involved causing arteritic anterior ischemic optic neuropathy9

Giant-cell arteritis may present with atypical or overlapping features10 Early and accurate diagnosis is important to prevent ischemic vision loss Therefore, this condition is considered a medical emergency10

Associated conditionsedit

The Varicella-zoster virus antigen was found in 74% of temporal artery biopsies that were GCA-positive, suggesting that the VZV infection may trigger the inflammatory cascade11

The disorder may coexist in a half of cases8 with polymyalgia rheumatica PMR, which is characterized by sudden onset of pain and stiffness in muscles pelvis, shoulder of the body and is seen in the elderly GCA and PMR are so closely linked that they are often considered to be different manifestations of the same disease process Other diseases associated with temporal arteritis are systemic lupus erythematosus, rheumatoid arthritis, and severe infectionscitation needed

Giant-cell arteritis can involve branches of the aorta as well, leading to an aortic aneurysm or dissection For this reason, patients should be followed with serial chest X-rayscitation needed

Mechanismedit

The pathological mechanism seems to start when dendritic cells in the vessel wall recruit T cells and macrophages to form granulomatous infiltrates T helper 17 cells involved with interleukin IL 6, IL-17 and IL-21 play a critical part; this pathway is suppressed with glucocorticoids1

Diagnosisedit

Physical examedit

  • Palpation of the head reveals prominent temporal arteries with or without pulsationcitation needed
  • The temporal area may be tendercitation needed
  • Decreased pulses may be found throughout the bodycitation needed
  • Evidence of ischemia may be noted on fundal examcitation needed

Laboratory testsedit

  • LFTs, liver function tests, are abnormal particularly raised ALP- alkaline phosphatasecitation needed
  • Erythrocyte sedimentation rate, an inflammatory marker, >60 mm/hour normal 1–40 mm/hourcitation needed
  • C-reactive protein, another inflammatory marker, may be elevatedcitation needed
  • Platelets may also be elevatedcitation needed

Biopsyedit

Histopathology of giant cell vasculitis in a cerebral artery Elastica-stain

The gold standard for diagnosing temporal arteritis is biopsy, which involves removing a small part of the vessel and examining it microscopically for giant cells infiltrating the tissue Since the blood vessels are involved in a patchy pattern, there may be unaffected areas on the vessel and the biopsy might have been taken from these parts Unilateral biopsy of a 15–3 cm length is 85-90% sensitive 1 cm is the minimum12 A negative result does not definitively rule out the diagnosis Characterised as intimal hyperplasia and medial granulomatous inflammation with elastic lamina fragmentation with a CD 4+ predominant T cell infiltrate , currently biopsy is only considered confirmatory for the clinical diagnosis, or one of the diagnostic criteria7

Imaging studiesedit

Radiological examination of the temporal artery with ultrasound yields a halo sign Contrast-enhanced brain MRI and CT is generally negative in this disorder Recent studies have shown that 3T MRI using super high resolution imaging and contrast injection can non-invasively diagnose this disorder with high specificity and sensitivity13

Treatmentedit

Corticosteroids, typically high-dose prednisone 1 mg/kg/day, must be started as soon as the diagnosis is suspected even before the diagnosis is confirmed by biopsy to prevent irreversible blindness secondary to ophthalmic artery occlusion Steroids do not prevent the diagnosis from later being confirmed by biopsy, although certain changes in the histology may be observed towards the end of the first week of treatment and are more difficult to identify after a couple of months14 The dose of prednisone is lowered after 2–4 weeks, and slowly tapered over 9–12 months Tapering may require two or more years Oral steroids are at least as effective as intravenous steroids,15 except in the treatment of acute visual loss where intravenous steroids appear to offer significant benefit over oral steroids16 It is unclear if adding a small amount of aspirin is beneficial or not as it has not been studied17

Referencesedit

  1. ^ a b c d Solomon, Caren G; Weyand, Cornelia M; Goronzy, Jörg J 2014 "Giant-Cell Arteritis and Polymyalgia Rheumatica" New England Journal of Medicine 371 1: 50–7 PMC 4277693  PMID 24988557 doi:101056/NEJMcp1214825 
  2. ^ Walter, MA; Melzer, RA; Graf, M; Tyndall, A; Müller-Brand, J; Nitzsche, EU 2005 "18FFDG-PET of giant-cell aortitis" Rheumatology 44 5: 690–1 PMID 15728420 doi:101093/rheumatology/keh551 
  3. ^ James, William D; Berger, Timothy G; et al 2006 Andrews' Diseases of the Skin: clinical Dermatology Saunders Elsevier p 840 ISBN 0-7216-2921-0 
  4. ^ "giant cell arteritis" at Dorland's Medical Dictionary
  5. ^ Moutray, Tanya N; Williams, Michael A; Best, Jayne L 2008 "Suspected giant cell arteritis: a study of referrals for temporal artery biopsy" Canadian Journal of Ophthalmology 43 4: 445–8 PMID 18711459 doi:103129/i08-070 
  6. ^ Sainuddin, Sajid; Saeed, Nadeem R 2008 "Acute bilateral tongue necrosis – a case report" British Journal of Oral and Maxillofacial Surgery 46 8: 671–2 PMID 18499311 doi:101016/jbjoms200803027 
  7. ^ a b Zadik, Yehuda; Findler, Mordechai; Maly, Alexander; Rushinek, Heli; Czerninski, Rakefet 2011 "A 78-year-old woman with bilateral tongue necrosis" Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 111 1: 15–9 PMID 21176820 doi:101016/jtripleo201009001 
  8. ^ a b Hunder, Gene G "Polymyalgia rheumatica and giant cell temporal arteritis" uptodatecom Wolters Kluwer Retrieved 23 September 2015 
  9. ^ Hayreh April 3, 2003 "Ocular Manifestations of GCA" University of Iowa Health Care Archived from the original on 2007-10-25 Retrieved 2007-10-15 
  10. ^ a b Rana, AbdulQayyum; Saeed, Usman; Khan, OsamaA; Qureshi, Abdul; Paul, Dion 2014 "Giant cell arteritis or tension-type headache: A differential diagnostic dilemma" Journal of Neurosciences in Rural Practice 5 4: 409–11 PMC 4173245  PMID 25288850 doi:104103/0976-3147140005 
  11. ^ Gilden, Don; White, Teresa; Khmeleva, Nelly; Heintzman, Anna; Choe, Alexander; Boyer, Philip J; Grose, Charles; Carpenter, John E; Rempel, April; Bos, Nathan; Kandasamy, Balasubramaniyam; Lear-Kaul, Kelly; Holmes, Dawn B; Bennett, Jeffrey L; Cohrs, Randall J; Mahalingam, Ravi; Mandava, Naresh; Eberhart, Charles G; Bockelman, Brian; Poppiti, Robert J; Tamhankar, Madhura A; Fogt, Franz; Amato, Malena; Wood, Edward; Durairaj, Vikram; Rasmussen, Steve; Petursdottir, Vigdis; Pollak, Lea; Mendlovic, Sonia; Chatelain, Denis; Keyvani, Kathy; Brueck, Wolfgang; Nagel, Maria A 2015 "Prevalence and distribution of VZV in temporal arteries of patients with giant cell arteritis" Neurology 84 19: 1948–55 PMC 4433460  PMID 25695965 doi:101212/WNL0000000000001409 
  12. ^ Ypsilantis, E; Courtney, E D; Chopra, N; Karthikesalingam, A; Eltayab, M; Katsoulas, N; Tang, T Y; Ball, R Y 2011 "Importance of specimen length during temporal artery biopsy" British Journal of Surgery 98 11: 1556–60 PMID 21706476 doi:101002/bjs7595 
  13. ^ Bley, TA; Uhl, M; Carew, J; Markl, M; Schmidt, D; Peter, H-H; Langer, M; Wieben, O 2007 "Diagnostic Value of High-Resolution MR Imaging in Giant Cell Arteritis" American Journal of Neuroradiology 28 9: 1722–7 PMID 17885247 doi:103174/ajnrA0638 
  14. ^ Font, Ramon L; Prabhakaran, Venkatesh C 2007 "Histological parameters helpful in recognising steroid-treated temporal arteritis: an analysis of 35 cases" British Journal of Ophthalmology 91 2: 204–9 PMC 1857614  PMID 16987903 doi:101136/bjo2006101725 
  15. ^ "BestBets: Steroids and Temporal Arteritis" 
  16. ^ Chan, Colin C K; Paine, Mark; O'Day, Justin 2001 "Steroid management in giant cell arteritis" The British Journal of Ophthalmology 85 9: 1061–4 PMC 1724128  PMID 11520757 doi:101136/bjo8591061 
  17. ^ Mollan, Susan P; Sharrack, Noor; Burdon, Mike A; Denniston, Alastair K; Mollan, Susan P 2014 "Aspirin as adjunctive treatment for giant cell arteritis" The Cochrane Database of Systematic Reviews 8: CD010453 PMID 25087045 doi:101002/14651858CD010453pub2 

External linksedit

  • article from National Institute of Arthritis and Musculoskeletal and Skin Diseases
  • Hayreh, Sohan Singh; Zimmerman, Bridget 2003 "Management of Giant Cell Arteritis" Ophthalmologica 217 4: 239–59 PMID 12792130 doi:101159/000070631 

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