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Case Reports
. 2024 Oct 31:14:1484256.
doi: 10.3389/fonc.2024.1484256. eCollection 2024.

TIPIC syndrome in a patient following sorafenib treatment for acute myeloid leukemia: a rare case report

Chang Chen #  1 , Jinman Zhong #  1 , Wanzhen Hu  1 , Jiewen Tan  1 , Dan Xiong  1
Affiliations
Case Reports

TIPIC syndrome in a patient following sorafenib treatment for acute myeloid leukemia: a rare case report

Chang Chen et al. Front Oncol. .

Abstract

Transient Perivascular Inflammation of the\ Carotid Artery (TIPIC) syndrome is uncommon, and cases of TIPIC induced by the targeted drug, sorafenib, are extremely rare. This case report describes a patient with acute myeloid leukemia carrying an FMS-like tyrosine kinase 3 mutation, who developed TIPIC syndrome, which may have been induced by sorafenib treatment. A 65-year-old woman diagnosed with acute myeloid leukemia experienced severe neck pain and sclerotic blisters on her palms and soles during sorafenib treatment. Carotid ultrasound revealed thickening of the right common carotid artery (RCCA) wall, and magnetic resonance imaging revealed perivascular tissue edema in the distal RCCA. Following clinical and imaging assessments, the patient was diagnosed with TIPIC syndrome. Treatment involved a one-week course of oral steroid therapy with dexamethasone and non-steroidal anti-inflammatory drugs, which led to complete clinical recovery. TIPIC syndrome involves transient nonspecific perivascular inflammation of the carotid adventitia; however, the precise underlying cause remains unclear. In this study, we report a rare case and explore the potential pathophysiological mechanisms through a review of the existing literature.

Keywords: FLT3; VEGFR; acute myeloid leukemia; sorafenib; transient perivascular inflammation of the carotid artery syndrome (TIPIC).

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Ultrasound and MRI imaging of right carotid artery wall thickening in TIPIC syndrome. Ultrasound imaging in axial (A), sagittal (B), and coronal (C) planes. Eccentric thickening of the arterial wall is observed from the upper right CCA to the bifurcation, particularly on the posteromedial wall. The boundary between the arterial wall and surrounding tissue is indistinct. Pre-contrast MRI vessel wall imaging in axial (D), sagittal (E), and coronal (F) planes. Mild luminal narrowing and uniform wall thickening are seen in the mid-to-distal segments of the right CCA, extending into the ICA. Post-contrast MRI vessel wall imaging in axial (G), sagittal (H), and coronal (I) planes. Significant homogeneous enhancement of the thickened vessel walls is evident.
Figure 2
Figure 2
Diagram of the potential mechanisms by which sorafenib contributes to TIPIC. The diagram illustrates how sorafenib may induce TIPIC through its pharmacological effects and hemodynamic factors. The curved red arrows represent the direction of blood flow, while the scissors symbolize the shear stress acting on the vessel wall. Together, these elements highlight how local hemodynamic forces, combined with sorafenib’s inhibition of endothelial function, contribute to vascular inflammation.
See this image and copyright information in PMC

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Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants from Guangdong Basic and Applied Basic Research Foundation (grant no.2022A1515140022), the Medical Scientific Research Foundation of Guangdong Province (grant no. A2024577), the Scientific Research Start Plan of Shunde Hospital, Southern Medical University (grant no. SRSP2021038, SRSP2023013, SRSP2023019).

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