Aortitis which developed after the administration of granulocyte-colony stimulating factor
Tomoyuki Mukai1,2, Shinichiro Kubo3, Yoshitaka Morita1
1Department of Rheumatology, Kawasaki Medical School, Kurashiki, Japan.
Insights
Granulocyte-colony stimulating factor (G-CSF) can cause drug-induced aortitis, a rare condition. Early recognition and corticosteroid treatment are crucial for managing this side effect in cancer patients.
Area of Science:
- Cardiovascular Medicine
- Oncology
- Pharmacology
Background:
- Drug-induced aortitis is an uncommon but serious condition.
- Prompt diagnosis and treatment are essential to prevent irreversible aortic damage.
- Granulocyte-colony stimulating factor (G-CSF) is used in chemotherapy to boost white blood cell counts.
Observation:
- A 66-year-old woman developed aortitis following G-CSF administration during breast cancer chemotherapy.
- Computed tomography (CT) and magnetic resonance imaging revealed significant aortic wall thickening.
- Other potential causes of aortitis were ruled out.
Findings:
- A strong association was suspected between G-CSF use and the development of aortitis.
- Corticosteroid therapy led to rapid regression of the aortitis, confirmed by follow-up CT scans.
- Limited case reports suggest a causative role for G-CSF in aortitis development.
Implications:
- G-CSF-associated aortitis is an under-recognized condition, potentially leading to delayed diagnosis and treatment.
- Oncologists and rheumatologists must be aware of this potential adverse effect of G-CSF.
- Increased awareness can facilitate timely intervention, preventing severe aortic complications.
Abstract:
Drug-induced aortitis is rare; thus, the diagnosis of drug-induced aortitis could be delayed unless clinicians are aware of the disease entity. Herein, we describe the case of a 66-year-old woman who developed aortitis after administration of granulocyte-colony stimulating factor (G-CSF) during chemotherapy for her breast cancer. Thickening of the aortic wall was clearly detected by computed tomography (CT) and magnetic resonance imaging. After excluding the other possible aetiologies, an association between G-CSF and the development of aortitis was highly suspected. Corticosteroid treatment rapidly regressed the aortitis, as confirmed by follow-up CT examination. G-CSF analog is generally well tolerated; however, there are limited case reports of G-CSF-associated aortitis, suggesting the causative effect of G-CSF in the development of aortitis. Currently, G-CSF-associated aortitis has received little attention among rheumatologists. As the delayed diagnosis results in irreversible changes in the aorta, not only oncologists but also rheumatologists should be aware of this unrecognized disease entity, G-CSF-associated aortitis.
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