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AB0468 Relapsing and systemic nature of temporal arteritis
  1. M. Bély1,
  2. Á. Apáthy2
  1. 1Department of Pathology, Policlinic of the Order of the Brothers of Saint John of God
  2. 2Department of Rheumatology, St. Margaret Clinic, Budapest, Hungary


Background Temporal arteritis (TA) with or without polymyalgia rheumatica (PMR) is a systemic disorder involving different size of arteries and even veins with a predilection for branches of temporal arteries. Some authors distinguish three histologic patterns of TA: classic, atypical, and healed (1).

Objectives The aim of this study was to identify the histologic characteristics of TA and to verify the relapsing nature of the disease.

Methods: TA in association with PMR was analysed histologically in 71 patients (23.74%) (females 61, average age 71.8 years, range 88-43; males 10, average age 71.9 years, range 86-51). PMR was clinically diagnosed according to the criteria of Bird et al (2). TA was histologically diagnosed.

Results Histologically TA existed in different (acute, subacute, subchronic, and/or chronic) stages of vasculitis.

Intensively active vasculitis was present in 32 (45.1%) of 71 patients, characterized by sectorial or segmental cellular infiltration. The inflammatory infiltration was dominated by T lymphocytes and histiocytes with or without multinucleated giant cells of Langhans type. The inflammatory infiltration was always accompanied by chronic fibromuscular and/or intimal proliferation, and adventitial fibrosis (classic type of TA).

In 23 (32.4%) of 71 patients the chronic structural changes of the vessel walls were accompanied by only moderate inflammation (atypical type of TA).

In the remaining 16 (22.5%) cases only chronic structural changes were present in the vessel wall without or only with sporadic inflammatory infiltration (healed type of TA).

Giant cells of Langhans type were present only in 10 of 71 patients with TA. The relationship between TA and presence of giant cells was significant (c2=32.4, p<0.0001).

TA was occasionally accompanied by phlebitis (TP), not as an extension of the inflammation from adjacent arteries, in 10 of 71 patients. In 6 of 10 patients intensive temporal phlebitis (TP) was associated with intensive temporal arteritis (TA) in blood vessels of different sizes. The association between TP and TA was significant (c2=5.8, p<0.01).

Conclusions: TA, like any type of autoimmune vasculitis, is a recurrent pathological process. Sectorial or segmental cellular infiltration in different stages of inflammation and chronic structural changes of the vessel wall exist side by side and indicate the relapsing nature of inflammation (3). We interpret the three histologic patterns of TA to represent the same pathological process characterized by progressive chronic structural changes in combination with florid (classic type), moderate (atypical form) or subsided inflammation (healed stage).

Recurrent inflammation, spontaneous or due to failed steroid therapy, may occur and the structural changes in this repetitive process accumulate and a new exacerbation of TA may lead to occlusion not only of the temporal artery but of the ophthalmic artery as well causing loss of vision.

TA is a manifestation of systemic vasculitis. Accompanying inflammatory infiltration of medium size veins indicates the systemic nature of TA caused by circulating immune complexes returning on the venous side.

  1. Flood TA, Burke AP: Temporal Arteritis Pathology

  2. Bird HA et al: An evaluation of criteria for polymyalgia rheumatica. Ann Rheum Dis 1979; 38:434-439

  3. Bély M, Apáthy Á: Histologic characteristics of systemic vasculitis in rheumatoid arthritis. Ann Rheum Dis 2002; 61 (Suppl 1):394-395

Disclosure of Interest None Declared

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