(18)F-FDG uptake on PET/CT correlated with histological assessments of inflammation and was higher in patients with symptomatic compared with asymptomatic carotid artery plaques. These results support the use of (18)F-FDG PET/CT in the detection inflammation in carotid atherosclerosis, which may be of help in the detection of vulnerable plaques.

Background. There is currently no consensus on the methodology for quantification of 18 F-FDG uptake in inflammation in atherosclerosis. In this study, we explore different methods for quantification of 18 F-FDG uptake in carotid atherosclerotic plaques and correlate the uptake values to histological assessments of inflammation.Methods and Results. Forty-four patients with atherosclerotic stenosis ‡70% of the internal carotid artery underwent 18 F-FDG PET/CT. Maximum standardized uptake values (SUV max ) from all plaque-containing slices were collected. SUV max for the single highest and the mean of multiple slices with and without blood background correction (by subtraction (cSUV) or by division (target-to-background ratio (TBR)) were calculated. Following endarterectomy 30 plaques were assessed histologically. The length of the plaques at CT was 6-32 mm. The 18 F-FDG uptake in the plaques was 1.15-2.66 for uncorrected SUVs, 1.16-3.19 for TBRs, and 0.20-1.79 for cSUVs. There were significant correlations between the different uptake values (r 5 0.57-0.99, P < 0.001). Methods with and without blood background correction showed similar, moderate correlations to the amount of inflammation assessed at histology (r 5 0.44-0.59, P < 0.02).Conclusions. In large stenotic carotid plaques, 18 F-FDG uptake reflects the inflammatory status as assessed at histology. Increasing number of PET slices or background correction did not change the correlation. (J Nucl Cardiol 2017)

CASEA 53-year-old man experienced periodic abdominal discomfort and a decreased capacity to work. His primary physician ordered a broad range of laboratory tests as part of the initial workup. The results revealed a greatly increased adrenocorticotropic hormone (ACTH) 7 concentration of Ͼ1250 pg/mL (Ͼ278 pmol/L) [reference interval Ͻ46 pg/mL (Ͻ10.2 pmol/L)]. Cortisol was within the reference interval. Repeat measurements 4 weeks later confirmed the increased ACTH. Investigators rapidly excluded 2 well-known conditions associated with increased ACTH concentrations: Cushing disease (ACTH-producing pituitary tumor) and Addison disease (adrenal insufficiency) (1, 2 ). An investigation for an ectopic source of ACTH was begun (3 ).Over the next 18 months, the patient underwent a plethora of imaging studies. A series of conventional studies failed to provide an explanation for the increased ACTH, and ultimately a positron emission tomography/computed tomography (PET/CT) scan using a relatively new radiotracer, 68 Ga-labeled 1,4,7, 10-tetraazacyclododecane-N,NЈ,NЈЈ,NЈЈЈ-tetraacetic acid-D-Phe 1 -Tyr 3 -octreotide ( 68 Ga-DOTATOC), was performed (4 ). A 3.3-cm area in the head of the pancreas with an increased uptake of radiotracer was observed ( Fig. 1). In light of the persistently increased ACTH concentration, this finding raised the suspicion of a pancreatic ACTH-secreting neuroendocrine tumor, a rare ectopic source of ACTH (3 ). Although MRI and conventional CT evaluations did not confirm the presence of a tumor, the patient was offered immediate surgical treatment. The patient declined the offer and subsequently sought second and third opinions at medical facilities in 2 different countries. In both facilities, a neuroendocrine tumor was deemed the likely cause of his problems, and surgery was again suggested. Wishing minimally invasive treatment, the patient contacted the Interventional Centre at our hospital, which offers laparoscopic resection of the pancreas.Preoperative investigations with MRI, optimized multiphase CT, and Ga-DOTATOC PET/CT evaluation were requested for reinvestigation, and surgery was postponed.Laboratory results at our hospital were comparable with the earlier results. ACTH, measured in a morning sample on the Immulite 2000 platform (Siemens Healthcare Diagnostics), was highly increased at 923 pg/mL (203 pmol/L). Cortisol, measured concurrently on the Modular E platform (Roche Diagnostics), was normal at 16.9 g/dL (467 nmol/L) [reference interval for morning samples, 8 -25 g/dL (220 -690 nmol/L)]. Results for other hormones, electrolytes, and tumor markers (neuronspecific enolase, chromogranin A, serotonin metabolites) were unremarkable. An endocrinologist could not find convincing clinical evidence of pathology in the pituitaryadrenal axis (specifically, no hyperpigmentation of the skin) to support the laboratory findings. He suggested that the persistently increased ACTH could be a laboratory artifact. Four laboratories in Norway currently offer analysis of ACTH; however, troubleshooting w...