When White Fat Lights Up: Rare Corticosteroid Effect on ¹⁸F-FDG PET/CT

A 9-year-old boy with newly diagnosed B-cell Hodgkin lymphoma underwent baseline ¹⁸F-Fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) for initial staging while receiving an oral tapering corticosteroid regimen of prednisolone (approximately 2 mg/kg/day initially, gradually reduced from 60 mg to 20 mg over one month), prescribed to relieve tumour-related mediastinal compression symptoms. The scan revealed a lymph node mass in the anterosuperior mediastinum showing moderate heterogeneous FDG uptake (SUVmax = 5.3), extending to the pre-cardiac region, consistent with Ann Arbour stage II disease [Fig 1].

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Fig 1: (A) Coronal whole-body MIP PET image showing a moderately hypermetabolic mediastinal mass (red arrow) and diffuse FDG uptake in subcutaneous adipose tissue (blue arrow); (B) Sagittal PET/CT fusion demonstrating diffuse subcutaneous adipose FDG uptake (blue arrow); (C) Coronal PET/CT fusion highlighting diffuse adipose uptake in subcutaneous and visceral fat (blue arrows); (D) Axial PET image showing increased FDG uptake in subcutaneous adipose tissue (blue arrow); (E) Axial PET/CT fusion of the upper abdomen demonstrating striking FDG uptake in white adipose tissue (blue arrow); (F) Pelvic PET/CT fusion image showing diffuse adipose hypermetabolism (blue arrow). MIP: Maximum intensity projection; PET/CT: Positron emission tomography/computed tomography; FDG: Fluorodeoxyglucose

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An additional striking finding was diffuse, symmetric, and intense FDG uptake throughout subcutaneous and visceral white adipose tissue, exceeding that of skeletal muscle and surrounding soft tissues. Hepatic FDG uptake was markedly reduced (SUVmax = 0.9). Normally, white adipose tissue functions as an energy reservoir with minimal glucose metabolism, but corticosteroids can stimulate white fat glycolytic activity by promoting adipocyte hypertrophy, hyperplasia, and increased expression of insulin-sensitive glucose transporters, thereby producing diffusely increased FDG uptake.^[1,2]Steroid-induced activation of adipose tissue may both mimic and obscure pathological lesions, complicating disease interpretation.

Awareness of this pharmacologic pitfall is crucial, particularly in oncologic imaging, and repeating ¹⁸F-FDG PET/CT after corticosteroid withdrawal is advised for accurate staging. Steroid therapy can also suppress hepatic FDG uptake through enhanced hepatic glycogenesis and altered glucose utilisation, a reversible metabolic effect compatible with the known actions of glucocorticoids on liver glucose metabolism.^[3,4]

Two months later, after steroid discontinuation and completion of two chemotherapy cycles, a follow-up ¹⁸F-FDG PET/CT was performed for interim assessment. The scan demonstrated a marked metabolic response with complete resolution of both the mediastinal uptake and the previously observed diffuse adipose FDG hypermetabolism. Post-treatment images [Fig 2] confirmed the disappearance of FDG uptake in white adipose tissue, with physiological tracer distribution restored and hepatic activity normalised (SUVmax = 2.4). These findings verified that the initial diffuse fat activity was reversible and steroid-induced rather than disease-related.

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Fig 2: (A) Whole-body MIP PET (frontal view): Complete metabolic response, with resolution of the mediastinal hypermetabolic mass and no residual FDG uptake in subcutaneous or visceral adipose tissue; (B) Sagittal fused PET/CT: no residual mediastinal FDG-avid lesion and normal soft tissue background; (C) Coronal fused PET/CT: Physiological hepatic uptake, no diffuse adipose hypermetabolism; (D) Axial PET (upper abdomen): Restored hepatic activity and low background uptake in subcutaneous and visceral fat; (E) Axial fused PET/CT (liver dome): Homogeneous physiologic hepatic FDG uptake, no focal lesions or abnormal fat activity; (F) Axial fused PET/CT (pelvis): Normal pelvic structures and physiologic tracer distribution, no increased uptake in subcutaneous adipose tissue or pelvic lymph nodes. MIP: Maximum intensity projection; PET/CT: Positron emission tomography/computed tomography; FDG: Fluorodeoxyglucose.

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Other reported causes of hypermetabolic white adipose tissue include insulin therapy, obesity, metabolic syndromes such as Cushing’s syndrome, antiretroviral treatment in HIV patients, and certain herbal medicines.^[5–8] Recognition of diffusely increased adipose FDG uptake in patients on corticosteroids is essential to prevent misinterpretation and ensure accurate evaluation of disease extent and treatment response.