Steroid-induced Activated White Adipose Tissue on FDG PET-CT

A 58-year-old hypertensive male, known case of adenocarcinoma stomach, post 4 cycles of neoadjuvant chemotherapy 5-fluorouracil, leucovorin, oxaliplatin, docetaxel (FLOT regimen) was referred to the nuclear medicine department for an fluorine-18 fluoro D-glucose positron emission tomography computed tomography (18F-FDG PET-CT) scan for restaging. The patient underwent 18F-FDG PET-CT under standard patient preparation. PET-CT was acquired 45 min postinjection of 259 MBq of 18F-FDG. Images revealed FDG avid asymmetrical thickening in the gastric cardia along the lesser curvature, suggestive of residual primary disease. In addition, there was diffuse increased FDG uptake in the subcutaneous fat white adipose tissue (WAT) throughout the body [Figure 1]. On detailed evaluation, the patient was found to have renal biopsy-proven immune complex-mediated proliferative glomerulonephritis for which the patient was receiving supportive care along with prednisolone 30 mg daily. Thus, the uptake in the subcutaneous WAT emanated due to the altered FDG biodistribution secondary to corticosteroids.

Close

Figure 1 58-year-old male, known case of adenocarcinoma stomach and glomerulonephritis. (a) Maximum intensity projection image shows mild diffuse fluoro D-glucose (FDG) uptake throughout the body, predominantly involving lower abdomen. (b-d) Transaxial images of abdomen, pelvis and inguinal area respectively show localization of FDG in the subcutaneous white adipose tissue. Focal uptake in the right shoulder joint localized to degenerative changes in the right acromioclavicular joint

Export to PPT

The uptake and localization of FDG depend on the metabolism of the tissues. Higher uptake is noted in tissues with high metabolism, as in the case of brain parenchyma. WAT is metabolically inert, it provides energy substrate by lipolysis. Hence, shows insignificant FDG uptake.[1]

Corticosteroids are marvelous drugs and are considered jack-of-all-trades in mitigating immune responses, hence used in various inflammatory and immune-mediated conditions.[2] The effects of corticosteroids in lipid metabolism are both anabolic and catabolic in nature. It causes redistribution of body fat, adipocyte hypertrophy (anabolic lipogenesis), and facilitates agents of lipolysis.[3] Steroids induce adipocyte differentiation and increased glycolytic metabolism in the mitochondria, aided by steroid-induced hyperglycemia, secondary hyperinsulinemia and increased expression of insulin-sensitive glucose transporter transporters on WAT, leading to increased localization of FDG within the WAT.[456] It is also thought to induce a pro-inflammatory milieu and increase macrophage recruitment within WAT, further enhancing the FDG localization within the WAT.[7] This case reiterates and further confirms the findings of molecular effect of steroids in lipid homeostasis, by revealing increased FDG uptake in the WAT secondary to high-dose corticosteroid treatment in a case of immune complex-mediated glomerulonephritis in this patient. This has also been reported in the literature in HIV patients with lipodystrophy on antiretroviral therapy.[8,9]