Abstract

In the presence of temporal arteritis, clinicians often refer to the diagnosis of giant cell arteritis (GCA). However, differential diagnoses should also be evoked because other types of vascular diseases, vasculitis or not, may affect the temporal artery. Among vasculitis, Anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis is probably the most common, and typically affects the peri-adventitial small vessel of the temporal artery and sometimes mimics giant cell arteritis, however, other symptoms are frequently associated and more specific of ANCA-associated vasculitis prompt a search for ANCA. The Immunoglobulin G4-related disease (IgG4-RD) can cause temporal arteritis as well. Some infections can also affect the temporal artery, primarily an infection caused by the varicella-zoster virus (VZV), which has an arterial tropism that may play a role in triggering giant cell arteritis. Drugs, mainly checkpoint inhibitors that are used to treat cancer, can also trigger giant cell arteritis. Furthermore, the temporal artery can be affected by diseases other than vasculitis such as atherosclerosis, calcyphilaxis, aneurysm, or arteriovenous fistula. In this review, these different diseases affecting the temporal artery are described.

Highlights

  • The term “temporal arteritis” is sometimes used to refer to giant cell arteritis (GCA) but this term is not appropriate

  • The involvement of this signaling pathway is highlighted by the description of a few cases of GCA occurring after treatment with immune checkpoint inhibitors (ICI) for cancer

  • Panarteritis may sometimes be present but, unlike GCA, fibrinoid necrosis may be observed within the arterial wall (Figure 3A) and cellular infiltrates rich in T lymphocytes, macrophages and eosinophils [72]

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Summary

Introduction

The term “temporal arteritis” is sometimes used to refer to giant cell arteritis (GCA) but this term is not appropriate. A recent study has reported on a defect in programmed cell Death protein ligand-1 (PD-L1) expression by vascular dendritic cells in GCA resulting in sustained activation of PD-1+ T cells and a loss of tolerance leading to vasculitis [63,64] The involvement of this signaling pathway is highlighted by the description of a few cases of GCA occurring after treatment with immune checkpoint inhibitors (ICI) for cancer. TAK is the second type of primitive large-vessel vasculitis It is a much rarer disease than GCA, which mainly occurs in females (F/H sex ratio = 9) and in patients aged

Differential Diagnoses of GCA
Necrotizing Vasculitis
Inflammatory Diseases Limited to the Adventitia
IgG4-Related Disease
Sarcoidosis
VZV Vasculitis
Atheromatous Disease
Findings
Conclusions
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