Case Report: a hypermetabolic mediastinal mass (SUVmax 16.7) mimicking malignancy with spontaneous resolution: an inflammatory myofibroblastic proliferation and diagnostic pitfall
Background Hypermetabolic mediastinal masses on 2-deoxy-2-[18F]fluoro-D-glucose ([18F]FDG) positron emission tomography/computed tomography (PET/CT) are presumed malignant until proven otherwise. However, benign inflammatory and organizing processes may exhibit equally intense metabolic activity, posing a diagnostic challenge—particularly when the lesion abuts major vascular structures and limits safe tissue sampling. Case summary A 55-year-old male smoker presented with cough, right-sided chest pain, low-grade fever, and mild dysphagia. Contrast-enhanced CT identified an ill-defined mass in the retrotracheal region of the superior mediastinum (within the tracheoesophageal groove), measuring 1.8×2.6×3.2 cm, with poorly defined margins against the esophagus and heterogeneous enhancement (precontrast attenuation 17–41 Hounsfield units (HU)). [18F]FDG PET/CT demonstrated markedly elevated [18F]FDG uptake (maximum standardized uptake value [SUVmax], 16.7), raising strong suspicion for malignancy. Serum tumor markers, procalcitonin, interleukin-6, and total immunoglobulin E (IgE) were within normal limits; sputum acid-fast, fungal, and bacterial cultures were negative, as were Epstein–Barr virus, cytomegalovirus, and a respiratory virus panel. Endobronchial ultrasound (EBUS)-guided aspiration did not yield a diagnostic specimen. CT-guided core needle biopsy was safely performed despite proximity to the superior vena cava and aortic arch, without complications. Histopathology revealed fibrocollagenous tissue with lymphoplasmacytic infiltration and foamy histiocytes, without malignant cells. Immunohistochemistry showed anaplastic lymphoma kinase (ALK) negativity, smooth muscle actin (SMA) positivity, and immunoglobulin G4 (IgG4) sparse focal weak positivity (below the threshold for IgG4-related disease), and a Ki-67 index of approximately 30% that labeled predominantly inflammatory cells rather than spindle cells, consistent with an inflammatory myofibroblastic proliferation. No antineoplastic, further targeted antimicrobial, or immunosuppressive therapy was administered. Follow-up CT at approximately 2.5 months demonstrated complete spontaneous resolution of the mass. A repeat chest CT in July 2026, approximately 2 months after the scan that first documented complete resolution, continued to show no residual or recurrent mediastinal lesion. Taken together, the findings favored an inflammatory myofibroblastic proliferation with an organizing, self-limiting course, while acknowledging that complete distinction from an ALK-negative inflammatory myofibroblastic tumor cannot be made with absolute certainty on limited core-biopsy material alone. Conclusion An inflammatory myofibroblastic proliferation in the mediastinum may exhibit extreme FDG avidity (SUVmax 16.7) indistinguishable from malignancy on imaging. A Ki-67 index of ~30% that labels predominantly inflammatory cells supports reactive proliferative activity as a histological correlate of the elevated metabolic signal, whereas complete spontaneous resolution sustained on repeat CT supports a self-limiting inflammatory course. When tissue sampling and subsequent clinical evolution make malignancy and active infection less likely, short-interval imaging surveillance may be an appropriate strategy in carefully selected patients.