Characteristics of benign adrenocortical adenomas with 18F-FDG PET accumulation

Abstract

Introduction: Although 18F-FDG PET was originally developed to evaluate benign and malignant tumors, the frequency of detection of benign adrenocortical adenomas showing FDG-PET accumulation has increased. However, the details of FDG-PET-accumulated benign adrenocortical adenomas have not been elucidated. Methods: To elucidate the pathophysiology of FDG-PET-positive cortisol-producing adrenal tumors, we performed clinicopathological and genetic analyses of adrenocortical adenomas examing FDG-PET in 30 operated patients with unilateral cortisol-producing adrenal tumors (26 adrenal adenomas and 4 adrenal cancers). Results: All adrenocortical carcinomas and 17/26 (65%) benign adrenocortical adenomas showed high FDG accumulation (SUVmax ≥ 3). In adrenocortical adenomas with high FDG accumulation (SUVmax ≥ 3), SUVmax showed a positive correlation with the CT Hounsfield units. A higher SUVmax showed a clear black adenoma appearance with predominantly compact cells, which exhibited high T1 and T2 signals, a lack of signal drop on out-of-phase imaging on MRI, and less accumulation on 131-I adsterol scintigraphy. Furthermore, RNA-sequencing analysis revealed significant increases in the lysosomal and autophagy pathways and metabolic pathways, including glycolysis through glucose transporter (GLUT) 1 and 3, in black adenomas with high-level FDG accumulation. Discussion: A black adenoma is blackish due to lipofuscin, which accumulates as a result of damaged mitochondria or proteins that escape lysosomal degradation or autophagy. Since FDG in PET is taken up via GLUTs, alteration of the intracellular metabolic dynamics associated with mitochondrial damage in black adenomas may increase PET accumulation. Conclusion: Black adrenal adenomas should be considered with adrenal tumors showing PET accumulation and low lipid contents.

Increasing Catecholamine Secretion Through NPY in Pheochromocytomas With False-Negative 123I-MIBG Scintigraphy

“…Each read was mapped to human genome hg38 using STAR v2.7.5 and default settings. After normalization of RPM using default settings, scatter plots were generated based on gene expression patterns 21,22 . The differentially expressed genes (DEGs) obtained from RNA-seq were analyzed by the online application RaNA-seq (https://ranaseq.eu/login).…”

Glucocorticoids and mineralocorticoids in blood plasma as markers of early diagnostic adrenal cortical tumors

“…In addition, dyshormonal changes under the conditions of adrenocortical adenomas may indicate metabolic disorders not only in the hypothalamic-pituitary-adrenal system, but also in the reninangiotensin-aldosterone system [6]. Violations of biochemical processes in these systems will be accompanied by changes in the physiological characteristics of the human bodydisturbances in the regulation of blood pressure and blood volume in the body, changes in sodium and water reabsorption in the kidneys, regulation of carbohydrate metabolism [7]. Hormonally active tumours of the adrenal glands have a wide range of clinical manifestations, while inactive incidentalomas do not manifest themselves [7].…”

“…Violations of biochemical processes in these systems will be accompanied by changes in the physiological characteristics of the human bodydisturbances in the regulation of blood pressure and blood volume in the body, changes in sodium and water reabsorption in the kidneys, regulation of carbohydrate metabolism [7]. Hormonally active tumours of the adrenal glands have a wide range of clinical manifestations, while inactive incidentalomas do not manifest themselves [7]. The first step after detecting an adrenal tumour should be to determine its hormonal status.…”