Clinical meaning
Giant cell arteritis (GCA/temporal arteritis) is a systemic granulomatous vasculitis affecting medium and large arteries, predominantly the extracranial branches of the carotid artery (superficial temporal, ophthalmic, posterior ciliary arteries). It is the most common primary vasculitis in adults over 50, with peak incidence at 70-80 years. The pathogenesis involves T-cell-mediated immune activation within the arterial wall: dendritic cells in the adventitia present unknown antigens (possibly vascular wall proteins) to CD4+ T cells, which activate macrophages. These macrophages fuse to form multinucleated giant cells (the pathological hallmark) and produce matrix metalloproteinases that degrade the internal elastic lamina, pro-inflammatory cytokines (IL-6, TNF-α, IL-1β), and reactive oxygen species. The inflammatory infiltrate concentrates at the intima-media junction around the internal elastic lamina, causing intimal hyperplasia, vessel wall thickening, and progressive luminal narrowing. The most feared complication is PERMANENT VISION LOSS — anterior ischemic optic neuropathy (AION) from inflammation of the posterior ciliary arteries (branches of the ophthalmic artery) that supply the optic nerve head. Vision loss occurs in 15-20% of untreated patients and is usually IRREVERSIBLE once established. The critical clinical point: visual symptoms (amaurosis fugax, diplopia, visual field cut) in a patient with GCA represent an OPHTHALMOLOGIC EMERGENCY — high-dose steroids must be started IMMEDIATELY, before biopsy confirmation, to prevent permanent blindness. GCA is strongly associated with polymyalgia rheumatica (PMR) — 40-60% of GCA patients have concurrent PMR symptoms (bilateral shoulder and hip girdle pain/stiffness).