Abstract Any opacity on a chest radiograph has a wide differential diagnosis. Plain radiography and computed tomography may help to differentiate whether bone, intercostal soft tissue or mediastinum are involved. Bronchoscopy is often negative with peripheral lesions. This leaves the physician with a diagnostic problem. We examined ultrasonically 30 patients with juxta-pleural lesions and performed cutting biopsy in 27. Twenty-four of these produced positive histology (90%). The three that were not biopsied were anechoic and had pulsatile lesions due to vascular abnormalities. There were four benign lesions all with hypoechoic appearances and the 20 malignant cases showed a wide spectrum of echogenicity. Of the malignant lesions, 90% showed pleural line disruption with reduced respiratory movement suggesting chest wall invasion. There were no complications, despite using cutting biopsy.
Endothelial cell injury resulting in vascular leak syndrome (VLS) is one of the most widely noted phenomenons in a variety of clinical diseases. In the current study we used IL-2-induced VLS as a model to investigate the role of cytolytic lymphocytes in the cytotoxicity of endothelial cells. Administration of IL-2 (75,000 U/mouse, three times a day for 3 days) into BL/6 wild-type mice triggered significant VLS in the lungs, liver, and spleen. Interestingly, perforin-knockout (KO) mice exhibited a marked decrease in IL-2-induced VLS in all three organs tested. Also, Fas ligand-defective (gld) mice and Fas-deficient (lpr) mice exhibited decreased VLS in the liver and spleen, but not in the lungs. The decreased VLS seen in perforin-KO, gld, and lpr mice was not due to any defect in lymphocyte migration or homing to various organs because histopathologic studies in these mice demonstrated significant and often greater perivascular infiltration of lymphocytes compared with the IL-2-treated wild-type mice. Ultrastructural studies of the lungs demonstrated significant damage to the endothelial cells in IL-2-treated wild-type mice and decreased damage in perforin-KO mice. IL-2 administration caused up-regulation of CD44 in all strains of mice tested and triggered increased LAK activity against an endothelial cell line in wild-type and gld mice, but not in perforin-KO mice. The current study demonstrates for the first time that perforin and Fas ligand may actively participate in endothelial cell injury and induction of VLS in a variety of organs.
Extramedullary haematopoiesis is an uncommon finding in the adult patient. Many sites have been described, the liver and spleen being more common. The ultrasound appearances have not been well documented. Two cases of extramedullary haematopoiesis in the liver and spleen are presented. A 58-year-old man presented with a history of a cough, haemoptysis, dyspnoea and weight loss. On examination he had finger clubbing, no significant chest signs and hepatomegaly. A bronchial neoplasm was suspected clinically and the initial chest radiograph demonstrated a right lung mass adjacent to the hilum. Full blood count was normal and the erythrocyte sedimentation rate was raised at 52 mm/h. Bronchoscopy revealed extrinsic compression of the right upper lobe bronchus but biopsy was unsuccessful. Ultrasound examination of the abdomen demonstrated multiple echogenic lesions in an enlarged liver (Fig. 1). Some of these lesions contained central echo-poor areas. The spleen was of normal size, and contained one echogenic mass similar to those in the liver. No other abnormality was shown in the remainder of the abdomen and pelvis. The most likely diagnosis for these lesions was metastatic carcinoma. Ultrasound-guided Trucut biopsy was performed. The lesion chosen was peripheral and without any central echopoor area. Histology revealed immature and mature cells of the myeloid and erythroid series with occasional megakaryocytes. Dilated sinusoids and portal tracts contained pleomorphic infiltrate. These are the features of hepatic extramedullary haematopoiesis. An isotope bone scintigram using 99Tcm MDP revealed multiple hot spots in the femora, ribs, skull and spine, interpreted as being metastases.
Abstract The previously unreported sonographic anatomy of the intraglandular parotid ducts is described, and how this aids tumour localization is illustrated. Forty patients underwent ultrasonography and computed tomography (CT) sialography for the evaluation of parotid tumours. Ultrasound identified two extra unsuspected 5 mm tumours in the superficial lobe, which could not be seen at CT. Both techniques produced similar results for deep and mixed lobe lesions. Ultrasound had one false positive mixed lesion, which surgery subsequently found to be confined to the deep lobe. The full extent of invasion in three deep lobe tumours was revealed only by CT to be parotid invasion by nasopharyngeal carcinomas. We conclude that parotid sonography with reference to the intraglandular ducts is highly accurate in localizing parotid tumours and should probably be the first-line imaging technique. Computed tomography should only be necessary for visualization of deep lobe tumour extent and in those cases where the complete tumour boundary cannot be seen by ultrasound alone.
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