Giant cell arteritis manifested by bilateral arteritic Anterior Ischaemic Optic Neuropathy (AION)
Authors:
P. Němec 1; T. Jurečka 2; V. Žampachová 3; Z. Mašková 2; M. Souček 1
Authors place of work:
II. interní klinika Lékařské fakulty MU a FN u sv. Anny Brno, přednosta doc. MUDr. Miroslav Souček, CSc.
1; Klinika nemocí očních a optometrie Lékařské fakulty MU a FN u sv. Anny Brno, přednosta doc. MUDr. Svatopluk Synek, CSc.
2; I. patologicko‑anatomický ústav Lékařské fakulty MU a FN u sv. Anny Brno, přednostka doc. MUDr. Markéta Hermanová, Ph. D.
3
Published in the journal:
Vnitř Lék 2008; 54(12): 1195-1205
Category:
Case Report
Summary
Giant cell arteritis (GCA) is a systemic vasculitis of unknown etiology affecting medium and large calibre vessels by granulomatous panarteritis with the formation of giant multinucleate cell granulomas. Vision is affected in 25–50% of GCA patients. Affection of vision may be the first GCA symptom or a symptom which occurs weeks or months after the initial symptoms of the disease. Eye symptoms of the disease are mostly a manifestation of occlusion of ocular and orbital blood vessels. Permanent damage to the patient’s vision is a serious consequence of visual affection provoked by GCA. Arteritic Anterior Ischaemic Optic Neuropathy (AION) is the most frequent and most serious visual manifestation of GCA. It is manifested by partial or total loss of vision. Arteritic AION therapy in GCA uses high doses of glucocorticoids, but glucocorticoid therapy has a number of adverse effects. The proofs of the effect of the therapy on the improvement of the vision of patients with visual affection in GCA are not convincing. We report a case of a 76-year old man with biopsy-verified GCA whose primary manifestation was bilateral arteritic AION resulting in a complete loss of vision in one eye and dramatic worsening of visual acuity in the other eye. Glucocorticoid therapy only improved vision in one eye, and had adverse effects. Methotrexate was added to the therapy to achieve a glucocorticoid saving effect. Glucocorticoid therapy could be discontinued after 3 years. In the course of the therapy and for the subsequent 12 months after it was finished, there was no relapse of the underlying disease.
Key words:
Arteritic Anterior Ischaemic Optic Neuropathy – glucocorticoids – giant cell arteritis – therapy – vasculitis
Zdroje
1. Hutchinson J. A peculiar form of neurotic arthritis of the aged which is sometimes productive of gangrene. Arch Surg 1890; 1: 323–327.
2. Horton BT, Magath TB, Brown GE. An underscribed form of arteritis of the temporal vessels. Mayo Clin Proc 1932; 7: 700–701.
3. Watts RA, Lane S, Bentham G et al. Is there a latitudinal variation in the incidence of giant cell arthritis? Proceeding of the American College of Rheumatology, Philadelphia, October 2000. Arthritis Rheum 2000; 43 (Suppl): S137.
4. Machado EB, Michet CJ, Ballard DJ et al. Trends in incidence and clinical presentation of temporal arteritis in Olmsted County, Minnesota, 1950–1985. Arthritis Rheum 1988; 31: 745–749.
5. Hazleman BL. Polymyalgia rheumatica and giant cell arthritis. In: Hoch-berg MC, Smolen JS, Winblatt ME et al. Rheumatology. 3rd ed. Edinburgh, London, New York, Oxford, Philadelphia, St. Louis, Sydney, Toronto: Mosby 2003: 1623–1633.
6. González-Gay MA, Garcia-Porrua C, Rivas MJ et al. Epidemiology of biopsy proven giant cell arteritis in North Western Spain: trend over an 18 year period. Ann Rheum Dis 2001; 60: 367–371.
7. Weyand CM, Hunder NN, Hicok KC et al. HLA‑DRB1 alleles in polymyalgia rheumatica, giant cell arthritis and rheumatoid arthritis. Arthritis Rheum 1994; 37: 514–520.
8. Hazleman BL. Polymyalgia rheumatica and giant cell arthritis. In: Klippel K, Dieppe PA (eds). Rheumatology. St. Louis: Mosby 1994.
9. Mattey DL, Hajeer AH, Dababneh A et al. Association of giant cell arteritis and polymyalgia rheumatica with different tumor necrosis factor microsatellite polymorphisms. Arthritis Rheum 2000; 43: 1749–1755.
10. Duhaut P, Bosshard S, Calvet A et al. Giant cell arteritis, polymyalgia rheumatica, and viral hypotheses: a multicenter, prospective case-control study. Groupe de Recherche sur l‘Artérite à Cellules Géantes. J Rheumatol 1999; 26: 361–369.
11. Cimmino MA, Grazi G, Balistreri M et al. Increased prevalence of antibodies to adenovirus and respiratory syncytial virus in polymyalgia rheumatica. Clin Exp Rheumatol 1993; 11: 309–313.
12. Salvarani C, Farnetti E, Casali B et al. Detection of parvovirus B19 DNA by polymerase chain reaction in giant cell arteritis: a case-control study. Arthritis Rheum 2002; 46: 3099–3101.
13. Rovenský J, Tuchyňová A. Polymyalgia rheumatica a obrovskobuněčná (temporální) arteritida. In: Pavelka K, Rovenský J. Klinická revmatologie. 1. vyd. Praha: Galén 2003: 317–323.
14. Cimmino MA. Genetic and environmental factors in polymyalgia rheumatica. Ann Rheum Dis 1997; 56: 576–577.
15. Malmvall BE, Bengtsson BA, Nilsson LA et al. Immune complexes, rheumatoid factors, and cellular immunological parameters in patients with giant cell arteritis. Ann Rheum Dis 1981; 40: 276–280.
16. Hayreh SS, Podhajsky PA, Zimmerman B. Ocular manifestations of giant cell arteritis. Am J Ophthalmol 1998; 125: 509–520.
17. Hayreh SS. Anterior ischaemic optic neuropathy. Differentiation of arteritic from non‑arteritic type and its management. Eye 1990; 4: 25–41.
18. Wise CM, Agudelo CA, Chmelewski WL et al. Temporal arteritis with low erythrocyte sedimentation rate: a review of five cases. Arthritis Rheum 1991; 34: 1571–1574.
19. Kyle V, Cawston TE, Hazleman BL. Erythrocyte sedimentation rate and C reactive protein in the assessment of polymyalgia rheumatica/giant cell arteritis on presentation and during follow up. Ann Rheum Dis 1989; 48: 667–671.
20. Hayreh SS, Podhajsky PA, Raman R et al. Giant cell arteritis: validity and reliability of various diagnostic criteria. Am J Ophthalmol 1997; 123: 285–296.
21. Danesh-Meyer HV, Savino PJ, Eagle RC Jr et al. Low diagnostic yield with second biopsies in suspected giant cell arteritis. J Neuroophthalmol 2000; 20: 213–215.
22. Pless M, Rizzo JF 3rd, Lamkin JC et al. Concordance of bilateral temporal artery biopsy in giant cell arteritis. J Neuroophthalmol 2000; 20: 216–218.
23. Wenger M, Calamia KT, Salvarani C et al. Do we need 18F-FDG-positron emission tomography as a functional imaging technique for diagnosing large vessel arteritis? Clin Exp Rheumatol 2003; 21 (Suppl 32): S1–S2.
24. Blockmans D. The use of (18F)fluo-ro‑deoxyglucose positron emission tomography in the assessment of large vessel vasculitis. Clin Exp Rheumatol 2003; 21 (Suppl 32): S15–S22.
25. Hunder GG, Bloch DA, Michel BA et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum 1990; 33: 1122–1128.
26. Otradovec J. Klinická neurooftalmologie. Praha: Grada 2003.
27. Jirásková N. Ischemická neuropatie optiku. In: Jirásková N. Neurooftalmologie, minimum pro praxi. Praha: Triton 2001: 26–30.
28. Arnold CA. Ischemic Optic Neuropathies. In: Yanoff M, Duker JS (eds): Ophthalmology. 2nd ed. St. Louis: Mosby 2004: 1268–1272.
29. Hayreh SS. Steroid therapy for visual loss in patients with giant-cell arteritis. Lancet 2000; 355: 1572–1573.
30. Barrier JH, Chevalet P, Ponge T. Principles of acute treatment of Horton’s disease. Role of high‑dose corticosteroid therapy. Ann Med Interne 1998; 149: 448–453.
31. Meola DC, Fierz A, Tschopp A et al. Corticosteroids in giant cell arteritis: primum nil nocere? Klin Monatsbl Augen-heilkd 2006; 223: 379–381.
32. Pipitone N, Salvarani C. Improving therapeutic options for patients with giant cell arteritis. Curr Opin Rheumatol 2008; 20: 17–22.
33. Hayreh SS, Zimmerman B, Kardon RH. Visual improvement with corticosteroid therapy in giant cell arteritis. Report of a large study and review of literature. Acta Ophthalmol Scand 2002; 80: 355–367.
34. Benucci M, Manfredi M, Puce F et al. Improvement in visual acuity in a patient with ischaemic optic neuropathy (Horton arteritis) undergoing therapy with infliximab: a case report. Recenti Prog Med 2007; 98: 624–626.
35. Pipitone N, Salvarani C. Improving therapeutic options for patients with giant cell arteritis. Curr Opin Rheumatol 2008; 20: 17–22.
36. Ahmed MM, Mubashir E, Hayat S et al. Treatment of refractory temporal arteritis with adalimumab. Clin Rheumatol 2007; 26: 1353–1355.
37. Bhatia A, Ell PJ, Edwards JC. Anti‑CD20 monoclonal antibody (rituximab) as an adjunct in the treatment of giant cell arteritis. Ann Rheum Dis 2005; 64: 1099–1100.
38. Mayrbaeurl B, Hinterreiter M, Burgstaller S et al. The first case of a patient with neutropenia and giant-cell arteritis treated with rituximab. Clin Rheumatol 2007; 26: 1597–1598.
39. Martínez-Taboada VM, Rodríguez-Valverde V, Carreño L et al. A double-blind placebo controlled trial of etanercept in patients with giant cell arteritis and corticosteroid side effects. Ann Rheum Dis 2008; 67: 625–630.
Štítky
Diabetology Endocrinology Internal medicineČlánok vyšiel v časopise
Internal Medicine
2008 Číslo 12
Najčítanejšie v tomto čísle
- New evidence‑based criteria for evaluating the appropriateness of drug regimen in seniors. Criteria STOPP (Screening Tool of Older Person’s Prescriptions) and START (Screening Tool to Alert Doctors to Right Treatment)
- Schnitzler syndrome – report on a fourteen-year course of the disease and an overview of information on the disease
- Giant cell arteritis manifested by bilateral arteritic Anterior Ischaemic Optic Neuropathy (AION)
- Guidelines for the treatment of invasive candidiasis