Large-Vessel Giant Cell Arteritis following COVID-19—What Can HLA Typing Reveal?

Author:

Stojanovic Maja12ORCID,Barac Aleksandra23ORCID,Petkovic Ana4ORCID,Vojvodic Nikola25,Odalovic Strahinja26,Andric Zorana7,Miskovic Rada12ORCID,Jovanovic Dragana12,Dimic-Janjic Sanja28ORCID,Dragasevic Sanja29ORCID,Raskovic Sanvila12,Stjepanovic Mihailo I.28

Affiliation:

1. Clinic for Allergy and Immunology, University Clinical Center of Serbia, 11000 Belgrade, Serbia

2. Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia

3. Clinic for Infectious and Tropical Diseases, University Clinical Center of Serbia, 11000 Belgrade, Serbia

4. Department of Radiology, Center of Stereotaxic Radiosurgery, Clinic of Neurosurgery, University Clinical Center of Serbia, 11000 Belgrade, Serbia

5. Clinic for Neurology, University Clinical Center of Serbia, 11000 Belgrade, Serbia

6. Center for Nuclear Medicine and PET, University Clinical Center of Serbia, 11000 Belgrade, Serbia

7. Tissue Typing Department, Blood Transfusion Institute of Serbia, 11000 Belgrade, Serbia

8. Clinic for Pulmonology, University Clinical Center of Serbia, 11000 Belgrade, Serbia

9. Clinic for Gastroenterohepatology, University Clinical Center of Serbia, 11000 Belgrade, Serbia

Abstract

Giant cell arteritis (GCA) is an immune-mediated vasculitis that affects large arteries. It has been hypothesized that viruses may trigger inflammation within the vessel walls. Genetic studies on human leukocyte antigens (HLAs) have previously reported HLA-DRB1*04 as a susceptible allele for GCA and HLA-DRB1*15 as a protective allele for GCA. Here, we discuss the clinical presentation, laboratory findings, HLA class I and class II analysis results, and management of patients with extracranial large-vessel (LV) GCA, detected at least six weeks after recovery from COVID-19. This case series encompassed three patients with LV-GCA (two males and a female with an age range of 63–69 years) whose leading clinical presentation included the presence of constitutional symptoms and significantly elevated inflammatory markers. The diagnosis of LV-GCA was confirmed by CT angiography and FDG-PET/CT, revealing inflammation in the large vessels. All were treated with corticosteroids, while two received adjunctive therapy. By analyzing HLA profiles, we found no presence of the susceptible HLA-DRB1*04 allele, while the HLA-DRB1*15 allele was detected in two patients. In conclusion, LV-GCA may be triggered by COVID-19. We highlight the importance of the early identification of LV-GCA following SARS-CoV-2 infection, which may be delayed due to the overlapping clinical features of GCA and COVID-19. The prompt initiation of therapy is necessary in order to avoid severe vascular complications. Future studies will better define the role of specific HLA alleles in patients who developed GCA following COVID-19.

Publisher

MDPI AG

Subject

Clinical Biochemistry

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