Takayasu’s arteritis diagnosed/relapsed following COVID-19 vaccine: A case report with literature review

To the best of our knowledge, this is the first case of post-COVID-19 vaccine Takayasu’s arteritis reactivation identified in the literature and which occurred 25 years after her initial unexplained symptoms.

Takayasu arteritis (TA) is a granulomatous inflammatory vasculitis of large vessels with rare incidence and unknown cause [5]. If untreated, usually results in fibrosis of the adventitia, media, and intimal layers of large vessel walls as a result of myofibroblast proliferation and arterial wall infiltration by macrophages, T lymphocytes and monocytes [5, 6]. This leads to arterial occlusion, aneurysmal dilatation, or significant arterial stenosis [6]. The majority of TA cases (80%-90%), have been reported in young females, aged ten to forty years [6]. It is more prevalent in Asia, with the highest incidence being in Japan with approximately 150 new cases of TA a year per million population. In contrast, in the United States of America and Europe, the incidence was found to be 1-3 new cases a year per million population [7].

Predominantly, TA impacts the aorta and its major branches; the pulmonary, subclavian, and common carotid arteries [6]. It is manifested clinically in two stages. Patients initially present with systemic manifestations such as headaches, fever, malaise, weight loss, arthralgia, carotidynia and myalgia which represent the early inflammatory pre-pulseless stage. In the later pulseless stage, patients usually present after months-years with symptoms associated with end-organ ischaemia which incorporate neurological manifestations and limb claudication such as systemic arterial hypertension, absent or weak peripheral pulses, arterial bruits, and aortic regurgitation [8]. Although diagnostic criteria exist [9], the lack of specific laboratory markers and the nonspecific presentation of the disease delays the diagnosis of early pre-stenotic disease leading to life-threatening outcomes [6, 8].

In our case, we confirmed the diagnosis of the TA 25 years after the initial unexplained complete occlusion of the left vertebral artery. The primary objectives of management of TA include early diagnosis and initiation of steroid treatment intending to prevent complications such as occlusive or stenotic lesions and hypertension. As the disease primarily affects women of child-bearing ages management should include a multidisciplinary approach with the contribution of rheumatologists, vascular surgeons, obstetricians, cardiologists and anesthesiologists [7]. Some TA cases need surgical intervention and the indication and timing for surgery are very important [10].

AstraZeneca (AZD1222) vaccine was developed by Oxford University and utilizes a non-replicating adenovirus chimpanzee as a transmitter (ChAdOx1) and is altered to promote the SARS-CoV-2 S protein [11].

Multiple case reports highlighted the association between the COVID vaccine and the development or reactivation of vasculitis in literature. Abdelhamid Naitlho et al, 2021, reported a case of Henoch-Schönlein Purpura (HSP), which developed 8 days following AstraZeneca COVID- 19 vaccination in a sixty-two-year-old patient [1]. Fadi Kharou et al, 2021, also reported a case of a 60-year-old male who presented 3-days following his first dose of Pfizer BioNTech COVID-19 vaccine with blurry vision, frontotemporal headaches, along with generalised weakness and diffuse arthralgia, consistent with possible temporal arteritis [4]. Moreover, Abdul-Wahab Al-Allaf et al, 2022, reported a medium vessel abdominal vasculitis associated with anterior uveitis one week following the second dose of Pfizer BioNTech COVID-19 vaccine who presented to the hospital with epigastric and right upper quadrant abdominal pain [12].

The precise post-vaccine vasculitis pathophysiology is still inadequately understood. The most revised theory is immunological, similar to the mechanism relating Polyarteritis Nodosa (PAN) to HBV Ag-Ac immune complexes [13]. In the majority of vasculitis, the causative mediator is unknown. We are proposing that the potential mechanism by which the COVID-19 vaccine triggers autoimmunity includes molecular mimicry, leading to the production of autoantibodies and there is a possible role of certain vaccine adjuvants. Previously, it has been well proposed that Influenza, hepatitis B and human papillomavirus vaccines trigger autoimmunity through molecular mimicry [2, 3, 4].

We have to keep in mind that COVID-19 infection itself could lead to the development or reactivation of autoimmune disease. It also could have significant morbidity and mortality if not prevented. The vaccine has saved many lives and altered the course of the COVID-19 pandemic. Also, the temporal relation is not proof of causation. Accordingly, we strongly advise the COVID-19 vaccine. However, we need to raise awareness of such autoimmune disease development or reactivation soon after the COVID-19 vaccines for early diagnosis and better management and outcome.