Smoking-associated inflammation: A dual 18F-FDG PET/CT analysis of tonsillar and aortic inflammation using
Emmanouil Panagiotidis1, George Angelidis, Anna Paschali
1Nuclear Medicine Laboratory, University of Thessaly, University Hospital of Larissa, Larissa, Greece. angelidis@protonmail.ch.
Objective:
Cigarette smoking alters immune and vascular systems, yet its dual inflammatory impact on mucosal lymphoid tissues and arterial walls remains underexplored in vivo. This study employs fluorine-18-fluorodeoxyglucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) with liver-normalized maximum standardized uptake value (SUVmax) to assess metabolic inflammation in Waldeyer's ring and the thoracic aorta across smoking groups.
Subjects And Methods:
We retrospectively analyzed 18F-FDG PET/CT scans from 222 patients categorized by smoking status. Maximum SUV was recorded in the palatine, lingual, and nasopharyngeal tonsils and the thoracic aorta. Values were normalized to liver uptake. Group differences were analyzed using Kruskal-Wallis tests with Bonferroni-corrected Mann-Whitney post hoc comparisons. Pearson correlation assessed associations with cigarette consumption.
Results:
Smokers had slightly reduced tonsillar SUVmax values, especially in the lingual tonsil (mean 3.56 vs. 3.82 in non-smokers), but these differences were not statistically significant after liver normalization. In contrast, raw aortic SUVmax was highest in non-smokers (2.72), but after normalization, ex-smokers demonstrated significantly elevated aortic uptake (P=0.016). No significant associations were observed between cigarette quantity and regional SUV values, possibly due to individual variability and confounding metabolic factors such as body mass index (BMI).
Conclusion:
Fluorine-18-FDG PET/CT reveals mild immune suppression in tonsillar lymphoid tissue among smokers and persistent vascular inflammation in ex-smokers. Liver normalization is essential for identifying true inflammatory differences in metabolically heterogeneous populations. These findings suggest that inflammation is a multiparametric process influenced by factors such as BMI and metabolic status, which may mask smoking-related effects unless properly adjusted for.
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