A 59-year-old Chinese female was referred to the chest clinic of the First Affiliated Hospital, College of Medicine, Zhejiang University (Hangzhou, China) in April 2011 due to a two-month history of cough, hemoptysis and general fatigue. A CT scan of the chest revealed a nodule in the left lower lung with mild enhancement in the lesion. The nodule progressed during the two-month follow-up period under treatment with anti-infection drugs. No other significant history was noted. The patient’s physical examination was unremarkable, and hematological and biochemical parameters were within normal limits.\nA dual phase FDG PET/CT scan was performed following six hours of fasting. FDG (5.5 MBq/kg) was injected intravenously through an antecubital vein while the patient remained at rest. Image acquisition was subsequently conducted using a Siemens Biograph 16 PET-CT scanner (Siemens Medical Solutions USA, Inc., Malvern, PA, USA). The PET/CT images revealed a 1.83×1.40 cm slightly lobulated nodule, with burr-like margins in the left lower lung, exhibiting moderately increased F-18 FDG uptake (maximum SUV of 2.6) in the initial images (1 h following the FDG injection), and more intense FDG uptake with an SUV of 3.5 (26.9% increase) in the delayed images (2 h following the injection) (). Based on the dual phase FDG PET/CT imaging findings, morphological features, contrast-enhanced chest CT imaging and medical history (progression of the nodule during the two-month follow-up period), lung malignancy was highly suspected. A percutaneous CT-guided thoracoscopic biopsy was subsequently performed. Histological examination revealed that the specimens contained amorphous, homogeneous material with a number of polyclonal plasma cells, lymphocytes and giant cells. Eosinophilic material exhibited apple-green birefringence under polarizing microscopy. Immunohistochemically, congo red staining was positive, and trichrome staining was negative, confirming the deposition of amyloid within the specimen (). Therefore, a diagnosis of primary nodular parenchymal pulmonary amyloidosis was determined, and the patient was discharged without chemotherapy and other treatment. After May 2011, the patient was followed up every 3 months and was in good clinical condition at the time of writing.
A 71-year-old woman was investigated for a one-year history of deteriorating dyspnoea on a background of well-controlled asthma. Other co-morbidities included cutaneous systemic lupus erythematosus, rheumatoid arthritis and Sjogren’s syndrome. High-resolution computerised tomography (HRCT) showed multiple cysts, solid nodules and aggregate masses – the largest (2 × 1.5 cm) in the peripheral left lower lobe with fine-needle aspiration suggestive of amyloid. Serum biochemistry showed a polyclonal elevation of IgG, no detectable monoclonal band and normal serum-free light chains. Immunohistochemistry showed no specific staining for kappa or lambda antibodies. Mass spectrometry was not performed. Echocardiography excluded cardiac involvement and no visceral uptake by 123I SAP scintigraphy. Pulmonary function tests demonstrated a restrictive pattern, and a further HRCT raised suspicion of lymphocytic interstitial pneumonitis. FDG-PET/CT demonstrated similar low-grade uptake in all lung nodules (). A mini-thoracotomy was performed to obtain tissue from the largest nodule showing evidence of amyloid but too few infiltrating cells were present to confirm clonality.\nA low-grade lymphoplasmocytic lymphoma (LPL) was presumed to be driving the pulmonary amyloid, based on the assumption of low-grade B-cell clonal disorders that can occur with Sjogren’s syndrome. A trial of R-CVP (Rituximab – Cyclophoshamide, Vincristine, Prednisolone) chemotherapy was commenced for four months resulting in no progression of symptoms and stable lesions.