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Uveitis is a form of intraocular inflammation that can occur as a result of infection, injury, vaccination, or as a systemic manifestation of autoimmune or inflammatory diseases including sarcoidosis. Sarcoidosis is an inflammatory disease that involves the formation of abnormal granulomas in multiple organ systems. The hallmark of sarcoidosis is a non-caseating granuloma seen on biopsy. Here, we present a case report of a healthy 56-year-old Caucasian female who presented with uveitis sarcoidosis that was presumably initiated after administration of the Shingrix vaccine. Shingrix is a new attenuated subunit vaccine for Varicella Zoster Virus with an AS01B adjuvant that can result in a potent immune response. The Shingrix vaccine is made using Chinese hamster ovary cells which can contaminate the final vaccination product. Together, through the process of molecular mimicry and strong induction of the immune response, administration of Shingrix may have caused or exasperated this patient’s autoimmune etiology.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by inflammation and pannus formation, with subsequent joint and cartilage degradation. Treatment commonly targets inflammatory cytokines, including tumor necrosis factor (TNF) alpha, which is a potent inflammatory cytokine required for cell signaling, regulation, and apoptosis, as well as for other cellular functions including immune response. TNF alpha inhibitors have demonstrated benefits in improving RA patient outcomes in terms of immune function and symptomatology. While TNF alpha inhibitors are generally beneficial, some studies have demonstrated that TNF alpha inhibitors may increase the risk of adverse cardiovascular events. While this continues to be debated, our study investigates the role of Tumor Necrosis Factor Receptor 1 (TNFR1) and Tumor Necrosis Factor Receptor 2 (TNFR2) in cardiac tissue. TNFR1 is an apoptotic receptor and its inhibition by TNF alpha inhibitors is subsequently cardioprotective. However, TNF alpha inhibitors may be inhibiting TNFR2 receptors even more so than TNFR1 receptors. TNFR2 is primarily a cardioprotective receptor and its greater inhibition results in the cardiovascular morbidity associated with TNF alpha inhibitors.

Giant cell arteritis (GCA) is a large vessel vasculitis with a pathogenesis that involves two CD4 T-helper cell lineages, Th1 and Th17. The goal of GCA treatment is to achieve clinical remission and prevent complications, especially vision loss. Despite recent advances in treatment and diagnostic modalities for GCA, there continues to be a gap in the medical literature in addressing treatment and follow-up for patients with GCA after clinical remission is achieved. Of the most important issues to address in this patient population by rheumatologists and primary care physicians alike, is that of cardiovascular disease (CVD) risks in GCA patients associated with the vasculitis and its mainstay of treatment with high-dose glucocorticoids over a prolonged period of time. Physicians must be aware of the CVD events that have been observed in a higher proportion compared to the general population in GCA patients, including strokes, thoracic aortic aneurysms and dissections, myocardial infarctions, and peripheral vascular disease. This review will focus on the risk of CVD in GCA patients, with recommendations for management and follow-up.

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