{'fraction_non_alphanumeric': 0.029110936270653028, 'fraction_numerical': 0.013375295043273014, 'mean_word_length': 5.235294117647059, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[FDG-PET findings of nodular pulmonary amyloidosis with a long-term observation].

A 60-year-old woman was referred to our hospital because of an abnormal chest radiograph in May, 2000. She was found to have rheumatoid arthritis in March, 1998, and pharmacologic therapy with anti-rheumatic drug was started. The chest CT scan revealed bilateral multiple lung nodular lesions of various sizes up to 30 mm. F-18 fluorodeoxyglucose positron emission tomography (FDG-PET) demonstrated a lesion with intense FDG activity in the right lung with a standardized uptake value (SUV) of 10.1. Fiberoptic bronchoscopy revealed no endobronchial lesions. Video-assisted thoracoscopic surgery was done to ascertain the pathological diagnosis. Histological examination showed that the pulmonary nodules were composed of amyloid A (AA) protein. Secondary Sjögren syndrome was subsequently diagnosed. A diagnosis of localized nodular pulmonary amyloidosis with AA type amyloid protein was made, and therapy with anti-rheumatic drugs was continued. After six years of therapy, the size of pulmonary amyloidoma was reduced, and the accumulation of FDG returned to normal. We reported this interesting case in which FDG-PET apparently reflected the disease activity of pulmonary amyloidosis.