ABSTRACT
Case report Background: Giant cell arteritis (GCA) is an immune-mediated vasculitis affecting large arteries. It has been hypothesized that pathogens including viruses may trigger inflammation within the vessel walls. Human leukocyte antigens' (HLA) genetic studies have previously reported HLA-DR4 (HLA-DRB1* 04 and HLA-DRB1* 01) as susceptibility, and HLA-DR2 (HLA-DRB1* 15 and HLA-DRB1* 16) as protective alleles for GCA. Here we report two cases of large vessel (LV) GCA diagnosed in patients previously suffered from mild coronavirus disese 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV- 2). Case presentation: First case, a 69-year- old male, had a mild COVD-19 three months before the appearance of headache, malaise, and a febrile state associated with extremely increased inflammatory parameters (CRP 2847 mg/dl and IL-6 802.3 pg/ml). Computed tomography examination of the aorta (CTA) and the branches, performed in two occasions six months apart, showed an interesting picture of a migratory arteritis. HLA typing showed: HLA-A* 2,-A* 24;-B* 51,-B* 57;-DRB1* 15,-DRB1* 16;-DQB1* 05,-DQB1* 06;Second case, a 64-year- old female, was evaluated for LV-GCA two months after a mild COVID-19, when she presented with elevated CRP (183mg/dl) and systemic symptoms. Thickening of the ascending aorta and the aortic arch was seen on CTA. Typing of HLA revealed: HLA-A* 2,-A* 11;-B* 27,-B* 35;-DRB1* 14,-DRB1* 15;-DQB1* 05,-DQB1* 06;A whole-body 18F-FDG- PET/ CT performed in both cases revealed inflammation of the ascending, aortic arch, thoracic and abdominal aorta. The first patient had appearance of the inflammatory involvement of the iliac and femoral arteries, while the second patient had an additional pulmonary trunk inflammation. Corticosteroid treatment was introduced in both cases. Due to a progressive inflammatory course of LV-GCA in the first case, the IL-6 inhibitor (tocilizumab) was initiated, leading to a clinical and laboratory improvement. In conclusion, LV-GCA may be considered as an autoimmune disease triggered by SARS-CoV- 2, as one of the broad spectrum of manifestation within the post acute COVID-19. None of the previously known HLA susceptibility alleles for GCA were detected in our patients. In contrast, both patients had DRB1*15 allele, and one of them was DRB1*15/DRB1*16 carrier, suggesting a possibility of losing their protective effect in LV-GCA induced by COVID-19.
ABSTRACT
Case report Introduction: Vaccines have been recognized as agents associated with development of different forms of vasculitis. We describe the case of a leukocytoclastic vasculitis which developed after immunization with inactivated COVID-19 vaccine. Case presentation: A 68-years old female patient presented with painful purpuric papules and plaques, and areas of necrosis, dominantly localized on her feet (Figure 1), developing 12 days after she received first dose of inactivated COVID-19 vaccine (BBIBP Cor-V). There were no other symptoms except mild fatigue and low-grade temperature of 37.3degreeC. Skin biopsy showed damaged vessel wall with perivascular, neutrophilic inflammatory infiltrate, leucocytoclasia and erythrocytes extravasation (Figure 2). Thorough work-up, including broad immunoserological and virological analysis didn't reveal any other potential trigger. Three months before vaccination the patient recovered from COVID-19 pneumonia. After the four weeks course of prednisone (initially 20 mg/day) with tapering a complete resolution of skin changes was achieved. The patient was followed for one year with no relapses. Conclusion(s): COVID-19 immunization should be considered as a potential trigger for development of cutaneous vasculitis.