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Symptoms That May Arise in Patients With GCA

    Typical cranial
    symptoms, 80%1

  • Scalp tenderness

    Swelling and/or tenderness
    of temporal arteries2

    Scalp tenderness

  • Jaw claudation

    Mandibular pain or pain
    on chewing

    Jaw claudation

  • Headache

    Sudden or abrupt
    unilateral headache3

    Headache

  • Ischaemic complications

    Visual loss or impairment,
    transient monocular/diplopia, or
    optic neuropathy

    Ischaemic complications

    Atypical noncranial
    symptoms, 20%1

  • Extracranial symptoms (9%)

    Limb claudication or subclavian steal syndrome, increased risk of long-term vascular complications (eg, aortic aneurysm, vascular stenosis, aortic dissection)

    Extracranial symptoms (9%)

  • Systemic symptoms (9%)

    Fever, anorexia, weight loss, and fatigue. GCA has been identified as a common source of fevers of unknown origin4

    Systemic symptoms (9%)

  • Isolated PMR with vasculitis (2%)

    Asymptomatic vasculitis characterized by PMR symptoms

    Isolated PMR with vasculitis (2%)

Pathways in the
Development of GCA

GCA, also called temporal arteritis, is a systemic inflammatory vasculitis of medium- and large-sized arteries.

Pathophysiology is thought to involve an inappropriate response to vascular endothelial injury with dysregulation of the innate and adaptive immune responses.

Though the cause is unknown, it is thought that an early insult to the endothelium activates the maturation of dendritic cells in the adventitia of normal arteries.

Activated dendritic cells release proinflammatory mediators that trigger the recruitment and differentiation of CD4+ Th cells into Th17 and Th1 cells.1,2

Th1 cells

Release IFNγ and TNFα, which are mediators of chronic inflammation that cause pathological vascular remodeling.

Th17 cells

Release IL-17, IL-22, and GM-CSF, which inhibit Treg cells, stimulating acute phase reactants and other immune cells.

Disease progression is characterized by expanding areas of inflammation within the lining of the arteries. This causes intimal thickening and inflammatory infiltrates leading to luminal narrowing, intimal proliferation, and disruption of the internal lamina.

  • Immune-mediated disease resulting from a maladaptive response to endothelial injury
  • Activated dendritic cells attract CD4+ Th cells and macrophages to the arterial wall
  • Th17 cells stimulate monocyte differentiation into macrophages
  • Th1 cells influence the formation of multinucleated giant cells, releasing IL-17, which inhibits Treg cells
  • Macrophages, smooth muscle cells, and giant cells stimulate the release of PDGF, which is involved in the intimal hyperplasia, stenosis, and thrombosis of large vessels

Overview of pathological factors in GCA

gca diagram

Healthy temporal artery

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