Development of Descending Thoracic Aortic Aneurysm in a Psoriasis Patient Under Guselkumab Treatment

Psoriasis is a systemic inflammatory disease that frequently presents with several comorbidities, including cardiovascular diseases (CVD) beyond cutaneous symptoms. Aortic aneurysm (AA) is a localized, abnormal bulge or ballooning in the wall of the aorta and is recognized as one of the CVDs. Here, we report a case of psoriasis in a patient who developed thoracic AA (TAA) during guselkumab treatment. The patient was a 75-year-old male who had been diagnosed with psoriasis 15 years earlier and had been treated with topical agents, but with insufficient response. His past history included pulmonary tuberculosis diagnosed 9 years prior. He was taking sacubitril valsartan sodium hydrate and nifedipine for hypertension, and his blood pressure was well controlled. He had a smoking history of one pack a day for 40 years and did not stop smoking during our psoriasis treatment. On clinical examination, infiltrated hyperkeratotic erythematous plaques were observed on the buttocks, elbows, and lower extremities (Figure 1A). Prominent nail changes were noted in both thumbnails (Figure 1B). Apremilast was initiated but subsequently discontinued due to diarrhea. Furthermore, narrowband UVB therapy failed to adequately improve his skin lesions, and we started guselkumab. The Psoriasis Area and Severity Index (PASI) score was 22 at the initiation of treatment. Baseline chest computed tomography (CT) showed no evidence of pulmonary tuberculosis or aortic aneurysm (Figure 1C). The administration of guselkumab resulted in the remission of erythematous plaques by 12 weeks, and the PASI score had improved to 0.3. The patient continued treatment without recurrence of skin lesions; however, follow-up chest CT 1 year later for biologic use accidentally revealed a descending TAA measuring 5.2 cm in maximum diameter (Figure 1D, arrow head). Compared to the prior imaging, the aortic diameter had increased by 2.0 cm over the course of approximately 1 year. The patient was referred to cardiovascular surgery, and thoracic endovascular aortic repair was performed. He became nearly bedridden, and therefore guselkumab was discontinued. The causes of AA involve a complex of chronic inflammation and degenerative changes of elastin and collagen, leading to weakening and dilation of the aortic wall. Abdominal AA (AAA) is deeply associated with atherosclerosis, and a smoking history, hypertension, and male gender are its risk factors. In contrast, TAA may also be associated with other congenital or acquired conditions, such as bicuspid aortic valves, congenital vascular disorders, vasculitis involving the aorta, and infectious aortitis [1]. According to cohort studies, the risk of AAA or TAA/AAA has also been reported to be significantly increased in patients with psoriasis, particularly among those with severe disease [2, 3]. Interestingly, TAA developed after the administration of guselkumab in our case. Anti-IL-23 antibodies are reported to decrease the risk of CVD in psoriasis [4]. In addition, anti-IL-23p19 antibody suppresses elastase-induced AAA mouse model [5]. Thus, smoking, psoriasis, hypertension, and previous tuberculosis but not guselkumab may contribute to the development of TAA in cooperation in our case. The careful monitoring of CVD including AA may be recommended even after the administration of biologics in patients with severe psoriasis and patients with additional CVD risks. Tomomitsu Miyagaki is an Associate Editor and Takafumi Kadono is an Editor-in-Chief of the Journal of Dermatology. They are coauthors of the current article. To minimize bias, they were excluded from all editorial decision-making related to the acceptance of this article for publication. There are no other conflicts of interest to be declared. The data that support the findings of this study are available from the corresponding author upon reasonable request.