[Giant cell arteritis manifested by bilateral arteritic Anterior Ischaemic Optic Neuropathy (AION)].
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 ofglucocorticoids, 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.
Nemec
P
P
II. Interní klinika Lékarské Fakulty MU a FN u sv. Anny Brno. petr.nemec@fnusa.cz
Jurecka
T
T
Zampachová
V
V
Masková
Z
Z
Soucek
M
M
D000368:Aged; D013700:Giant Cell Arteritis / Q000150:complications / Q000175:diagnosis* / Q000601:surgery; D006801:Humans; D008297:Male; D018917:Optic Neuropathy, Ischemic / Q000175:diagnosis / Q000209:etiology*