Preliminary study on the dynamic positron emission tomography imaging with 11C‐ER176 to delineate macrophage activation in diabetic gastroparesis

Author:

Maalouf Elisia1,Khasawneh Hala23,Karbhari Aashna2,AlAsfoor Shefaa1,Breen‐Lyles Margaret1,Bernard Cheryl1,Rajan Elizabeth1,Farrugia Gianrico1,Lowe Val2,Goenka Ajit2,Grover Madhusudan1ORCID

Affiliation:

1. Division of Gastroenterology and Hepatology Mayo Clinic Rochester Minnesota USA

2. Department of Radiology Mayo Clinic Rochester Minnesota USA

3. Department of Radiology UT Southwestern Medical Center Dallas Texas USA

Abstract

AbstractBackgroundAnimal models and human data have suggested macrophage‐driven immune dysregulation in diabetic gastroparesis (DG). Translocator protein (TSPO) upregulation has been suggested to indicate activated state of macrophages and ER176 is a high affinity third generation TSPO‐specific radioligand. The aim of this study was to determine feasibility of dynamic 11C‐ER 176 PET to identify macrophage activation in DG.MethodsTwelve patients, all females, were recruited (4 DG, 4 diabetics, and 4 healthy volunteers) for 11C‐ER 176 PET/CT scanning. The standardized uptake value (SUVmax) in the gastric fundus, body, pylorus, and descending part of the duodenum were compared between three groups using Kruskal‐Wallis test to perform the comparisons, and a p‐value of 0.05 was considered statistically significant.Key ResultsAge was comparable among the three groups with a median of 53 years. The uptake was higher in pylorus in diabetics compared to DG and healthy (SUVmax healthy 4.6 ± 0.2, diabetics 8.4 ± 4.1, DG 5.5 ± 1.0, p = 0.04). The uptake was similar in gastric fundus (9.0 ± 1.6, 13.1 ± 8.3, 7.8 ± 1.9 respectively, p = 0.3), body (7.7 ± 1.9, 13 ± 9.2, 7.8 ± 1.9 respectively, p = 0.8), and duodenum (6.2 ± 2.1, 9.5 ± 6.8, 7.0 ± 1.8 respectively, p = 0.6). No correlation was observed between SUVmax uptake and either HbA1C or fasting blood glucose.Conclusions and InferencesFemale diabetic gastroparesis patients did not demonstrate increased TSPO ligand 11C‐ER 176 uptake in the stomach. Possible explanations include lack of specificity of ligand for specific macrophage phenotypes in DG, sex effect, or small sample size. Further studies investigating non‐invasive ways of analyzing immune dysregulation in neurogastrointestinal disorders are warranted.

Funder

National Institutes of Health

Publisher

Wiley

Reference18 articles.

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