Maxillary artery 18F-FDG uptake as a new finding on PET/CT scan in a cohort of 41 patients suspected of having giant cell arteritis.

Abstract

Dear Editor, Giant cell arteritis (GCA) is a medium to large vessel vasculitis which commonly involves branches of the external carotid artery (ECA). It has been hypothesized that maxillary arteritis with associated demand ischemia to the muscles of mastication may underpin the cardinal GCA symptom of jaw claudication.1 However, to date, there has been limited imaging or pathological evidence to support this. We describe a new finding of increased fluorine-18 fluoro-2-deoxyglucose (18F-FDG) uptake on positron emission tomography/computed tomography (PET/CT) scan of the internal maxillary artery in a cohort of patients with suspected GCA. The internal maxillary artery is one of the two terminal branches of the ECA, arising proximal to the superficial temporal artery. It has a deep course and via its three parts (mandibular, pterygoid and pterygopalatine) it supplies the internal structures of the face and muscles of mastication. While its involvement in GCA is supported by its proximity and structural similarity to the adjacent superficial temporal artery, only a handful of studies have described maxillary artery imaging findings. These include a case report of a GCA patient with angiographic internal maxillary artery narrowing,2 a report of maxillary artery beading on magnetic resonance angiogram3 and a magnetic resonance imaging study of the deep temporal branch of the internal maxillary artery in 61 GCA patients which found abnormal enhancement in 21 (34%) patients.1 Traditionally, PET/CT scan has not had sufficient resolution to assess the branches of the external carotid artery. However, newer generation scanners have recently detected arteritis of the superficial temporal and occipital vessels.4, 5 Our group is currently assessing the diagnostic utility of PET/CT in a cohort of suspected GCA patients using a new protocol that permits enhanced visualization of the cranial and cervical vessels (clinicaltrials.gov ID: NCT02771483). All patients must meet two or more of the 1990 American College of Rheumatology classification criteria for GCA.6 Patients are scanned within 72 hours from starting corticosteroids and before temporal artery biopsy using a Siemens Biograph mCT time-of-flight PET/CT scanner with 1 mm CT slice reconstruction. For the purposes of this series, temporal artery biopsies were reported positive if there was inflammatory cell infiltrate within the artery wall (intima, media and/or adventitia). The study was approved by our institution's Human Research Ethics Committee (HREC/16/HAWKE/68). Among our first 41 patients enrolled and scanned, 12 (29%) had increased FDG uptake in the internal maxillary artery. Uptake was visualized in the proximal pterygopalatine part of the artery at the fat plane adjacent to the pterygomaxillary fissure. A representative image is shown in Figure 1. For these 12 patients, 33% had symptoms of jaw claudication or masticatory pain on chewing a piece of gum for five minutes.7 Fifty percent had a positive temporal artery biopsy and 75% were assessed at 2-week follow-up as having definite or probable (≥50% chance) GCA by the treating clinician. Comparison to patients without maxillary uptake is shown in Table 1. This finding is highly significant if, as we suspect, the uptake represents active inflammation of the maxillary artery. It further defines the extent of vessels that are affected by GCA and may improve the diagnostic accuracy of PET/CT for this vision-threatening condition. In addition, it could help to explain one of the mechanisms of jaw claudication in GCA for cases where arteritis is severe enough to cause a hemodynamically significant stenosis. We would encourage other groups using PET/CT in GCA to look for increased internal maxillary artery FDG uptake as a possible marker of arteritis. We are continuing our study of this protocol and long-term follow-up should help to clarify the significance and diagnostic utility of this new finding in patients suspected of having GCA. Author contributions: Dr Sammel: Study design, patient follow-up and manuscript preparation. Dr Hsiao: Study design, PET/CT reporting and manuscript preparation. Dr Nguyen: Patient follow-up, data analysis and manuscript preparation. Dr Schembri: Study design, PET/CT reporting and manuscript preparation. Dr Laurent: Study design and manuscript preparation. The authors would like to acknowledge the funding support from an Arthritis Australia Translational research grant and the contributions from the Giant Cell Arteritis and PET Scan (GAPS) study research team, including Professors L. Schrieber, P. Youssef, P. Roach, D. Bailey, C. Fraser, C. Little, Drs B. Janssen, H. Dunn, M. Wei, E. Bailey, C. Kuo, J. Brewer, H. Soh, Ms S. Smith and Mr N. Hall.