Aortitis is classified as either non-infectious or infectious. Although the mechanisms of aortitis are not fully understood, non-infectious aortitis might be triggered by increased neutrophil-mediated damage and pro-inflammatory reactions (3). G-CSF stimulates proliferation and differentiation of neutrophil precursors [4] and the resulting immunological reactions can cause aortitis [5].

In the case reported here, we excluded autoimmune disease because all ANA, MPO-ANCA, and PR3-ANCA values were within normal ranges. Since viral antibody tests were also negative and no bacterial growth was observed in blood and urine cultures, we concluded that G-CSF was the most suspicious cause of this aortitis.

Corticosteroids are commonly used to treat patients with suspected autoimmune diseases, such as Takayasu arteritis (TAK). However, there is no established treatment for G-CSF-associated aortitis. In general, G-CSF-associated aortitis has good prognosis and often resolves spontaneously without the administration of corticosteroids [6]. Moreover, previous reports show that there is no difference in the therapeutic effect and the time to remission of G-CSF-associated aortitis with or without corticosteroids [7]. The cases of G-CSF-associated aortitis reported in recent years are listed in Table 3 [6,7,8,9,10,11,12,13].

Table 3 Reported cases of G-CSF-associated aortitis in recent years

Aortitis caused by PEG-G tended to develop within 2 weeks of G-CSF administration and to resolve spontaneously within 3 weeks, as in the present case. We hypothesized that this common period of time was due to the duration of action of PEG-G, and that once the effects of PEG-G wore off, the aortitis would spontaneously abate. What is also interesting about this case is that despite the extensive lesions, the disease resolved quickly and spontaneously without corticosteroid treatment. This suggests that the extent of the lesions is not related to the need for corticosteroid treatment. On the other hand, it has been reported that G-CSF-associated aortitis lasting more than 3 weeks was relieved by corticosteroid administration, and we believe that corticosteroids should be considered in cases of long-term lack of improvement.

Although there are reports of G-CSF re-administration after symptom improvement in patients with G-CSF-associated aortitis, caution is required because some patients had recurrent aortitis [6, 14]. In this case, at the patient’s request, we shifted to endocrine therapy without re-administering PEG-G, and aortitis recurrence was not observed for 15 months after the onset of symptoms.

In breast cancer patients, dose-dense chemotherapy involving more frequent administration of chemotherapy agents than in standard chemotherapy significantly improved clinical outcomes [15, 16]. The addition of G-CSF to chemotherapy regimens to prevent chemotherapy-induced febrile neutropenia yields favorable clinical outcomes in breast cancer patients [17, 18]. Therefore, physicians should be aware that because most breast cancer patients undergo chemotherapy with PEG-G, aortitis may easily develop.

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