Temporal arteritis pathophysiology

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Temporal Arteritis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Pathophysiology

The damage to the vasuclature is mediated by an attack on the internal elastica lamina by activated CD4+ T helper cells. This occurs in repsonse to the presentation of an antigen by macrophages. The inciting antigen has not been identified.

Because the disease involves only arteries with internal elastic lamina, the aortic arch and its branches are often involved. Intracranial arteries do not have internal elastic lamina and are not involved. The distribution of involved arteries are as follows:

Commonly involved sites:

  • External vertebral arteries: It is less common though for the disease to extend more than 5 mm beyond the dural penetration.

Less commonly involved sites:

Associated Conditions

The disorder may coexist (in one quarter of cases) with polymyalgia rheumatica (PMR), which is characterized by sudden onset of pain and stiffness in muscles (pelvis, shoulder) of the body and seen in the elderly. Other diseases related with temporal arteritis are systemic lupus erythematosus, rheumatoid arthritis and severe infections.

References