When Pulmonary Nodules Are Not Malignant: A Case Report of Granulomatosis with Polyangiitis in a Patient with Giant Cell Arteritis
Underlined: presenting author
Background
Granulomatosis with polyangiitis (GPA) can present with pulmonary nodules and renal lesions that mimic malignancy. Long-term glucocorticoid treatment for another vasculitis may also partially suppress inflammatory findings and delay recognition. Giant cell arteritis (GCA) often coexists with polymyalgia rheumatica (PMR) and requires prolonged glucocorticoid therapy. We present a patient with GCA and PMR on long-term prednisone who years later developed granulomatous pulmonary nodules and positive ANCA, revealing delayed granulomatosis with polyangiitis (GPA) initially mimicking malignancy.
Case Presentation
A 75-year-old man with GCA, PMR, low-grade prostate cancer, and a smoking history presented for evaluation of enlarging pulmonary nodules. He had received long-term prednisone for GCA/PMR, including 20 mg daily in 2022, which was later tapered. Computed tomography (CT) showed growth of a right upper lobe nodule from 4 mm to 10 mm over one year, an additional 5 mm right middle lobe nodule, and mediastinal lymphadenopathy. The findings were categorized as Lung-RADS 4B. Positron emission tomography/computed tomography demonstrated a fluorodeoxyglucose-avid 0.9 cm cavitary right upper lobe nodule with mediastinal and bilateral hilar adenopathy. Although he remained asymptomatic during serial imaging, concern for malignancy led to robotic bronchoscopy, right upper lobe wedge resection, and lymphadenectomy. Pathology showed necrotizing granulomatous inflammation with mixed acute and chronic inflammation, as well as benign sampled lymph nodes. Infectious causes, including mycobacterial disease, were excluded.
Findings
The following year, the patient developed an unintentional 20-pound weight loss, fatigue, and decreased appetite. CT of the thorax, abdomen, and pelvis showed a new 12 x 8 mm right middle lobe nodule and a 3.9 x 4.3 cm low-attenuation lesion in the upper pole of the left kidney. The renal lesion was non-enhancing and favored a chronic infectious or inflammatory process rather than malignancy. Despite the absence of sinusitis, hemoptysis, renal dysfunction, or active glomerulonephritis, he was PR3-ANCA positive. GPA was diagnosed based on PR3-ANCA positivity, prior necrotizing granulomatous lung histology, and pulmonary and renal involvement. He was still taking prednisone 10 mg daily at diagnosis. Treatment with rituximab was initiated, prednisone was tapered off, and follow-up imaging showed resolution of most of the pulmonary nodules and a significant decrease in the renal lesion.
Discussion & Conclusion
This case describes GPA closely mimicking malignancy in a patient with smoking history, low-grade prostate cancer, weight loss, FDG-avid cavitary pulmonary nodules, and a renal mass-like lesion. The absence of classic upper airway symptoms and glomerulonephritis made the diagnosis less apparent. GPA should remain in the differential diagnosis for recurrent or migratory pulmonary nodules with renal lesions, particularly when pathology shows granulomatous inflammation and the clinical course is inconsistent with malignancy. Long-term prednisone may have masked the clinical expression of GPA, although this cannot be established from a single case.