A 63-year-old woman with a 2-month history of dyspnea.
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Biomedical subjects
Publications and source records attributed to S E Rossi.
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OBJECTIVE: We determined the ability of 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) to differentiate benign and malignant pleural effusions in patients with non-small cell lung cancer. MATERIALS AND METHODS: Over a 6-year period, we reviewed all patients with primary non-small cell lung cancer and a pleural effusion on staging CT who underwent FDG PET. We examined 25 patients (18 men and seven women; age range, 37-86 years; mean age, 65 years). FDG PET revealed positive findings if pleural activity was greater than background mediastinal activity; FDG PET revealed negative findings if pleural activity was the same as or less than background mediastinal activity. Results of FDG PET were correlated with pathologic diagnosis determined with thoracentesis or pleural biopsy. RESULTS: All patients had effusions on the same side as the primary tumor. Twenty-two patients had a malignant pleural effusion confirmed with thoracentesis (n = 19) or biopsy (n = 3). FDG PET revealed positive findings in 21 patients and negative findings in one. Three patients had no evidence of malignancy in the pleural space determined with cytologic findings (n = 2) or biopsy results (n = 1). FDG PET uptake revealed positive findings in one of these patients and negative findings in two. Therefore, of 22 patients with positive findings on FDG PET, 21 had pleural metastases, and of three patients with negative findings on FDG PET, one had metastases. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of FDG PET for detecting pleural metastases were 95%, 67%, 95%, 67%, and 92%, respectively. CONCLUSION: This study suggests that FDG PET may be useful in improving staging evaluation in patients with non-small cell lung cancer and a pleural effusion. Increased pleural FDG uptake usually indicates pleural metastases; however, because the number of benign effusions studied was small, the relevance of negative findings on FDG PET in this setting is uncertain.
The intrathoracic manifestations of neurofibromatosis-I are protean and can, on occasion, mimic those of malignancy. Many of the intrathoracic findings are characteristic of the disease and can be expected to be present. Knowledge of the full spectrum of radiologic findings can thus be useful in preventing diagnostic error. Furthermore, an unexpected finding, such as rapid growth of a neural tumor, should be recognized as an atypical feature (suspicious for malignant degeneration) and result in further evaluation.
Pulmonary drug toxicity is increasingly being diagnosed as a cause of acute and chronic lung disease. Numerous agents including cytotoxic and noncytotoxic drugs have the potential to cause pulmonary toxicity. The clinical and radiologic manifestations of these drugs generally reflect the underlying histopathologic processes and include diffuse alveolar damage (DAD), nonspecific interstitial pneumonia (NSIP), bronchiolitis obliterans organizing pneumonia (BOOP), eosinophilic pneumonia, obliterative bronchiolitis, pulmonary hemorrhage, edema, hypertension, or veno-occlusive disease. DAD is a common manifestation of pulmonary drug toxicity and is frequently caused by cytotoxic drugs, especially cyclophosphamide, bleomycin, and carmustine. It manifests radiographically as bilateral hetero- or homogeneous opacities usually in the mid and lower lungs and on high-resolution computed tomographic (CT) scans as scattered or diffuse areas of ground-glass opacity. NSIP occurs most commonly as a manifestation of carmustine toxicity or of toxicity from noncytotoxic drugs such as amidarone. At radiography, it appears as diffuse areas of heterogeneous opacity, whereas early CT scans show diffuse ground-glass opacity and late CT scans show fibrosis in a basal distribution. BOOP, which is commonly caused by bleomycin and cyclophosphamide (as well as gold salts and methotrexate), appears on radiographs as hetero- and homogeneous peripheral opacities in both upper and lower lobes and on CT scans as poorly defined nodular consolidation, centrilobular nodules, and bronchial dilatation. Knowledge of these manifestations and of the drugs most frequently involved can facilitate diagnosis and institution of appropriate treatment.
Fibrosing mediastinitis is a rare benign disorder caused by proliferation of acellular collagen and fibrous tissue within the mediastinum. Although many cases are idiopathic, many (and perhaps most) cases in the United States are thought to be caused by an abnormal immunologic response to Histoplasma capsulatum infection. Affected patients are typically young and present with signs and symptoms of obstruction or compression of the superior vena cava, pulmonary veins or arteries, central airways, or esophagus. There may be two types of fibrosing mediastinitis: focal and diffuse. The focal type usually manifests on computed tomographic (CT) or magnetic resonance (MR) images as a localized, calcified mass in the paratracheal or subcarinal regions of the mediastinum or in the pulmonary hila. The diffuse type manifests on CT or MR images as a diffusely infiltrating, often noncalcified mass that affects multiple mediastinal compartments. CT and MR imaging play a vital role in the diagnosis and management of fibrosing mediastinitis.