Hepatobiliary and Pancreatic: Atrophy-hypertrophy complex of the liverA man, aged 42, was investigated because of a gradual increase in dyspnea with exercise. His past history included a car accident 18 years previously that resulted in trauma to his abdomen and chest. As a chest x-ray was abnormal, a computed tomography (CT) scan was performed that showed a diaphragmatic hernia including herniation of the liver. Various blood tests including liver function tests were normal. At operation, he had a large defect in the right hemidiaphragm with herniation of multiple organs including the liver, right colon, distal stomach and proximal duodenum. After repositioning the organs in the abdomen, the defect in the right diaphragm was closed using surgical mesh. The right lobe of the liver (RL) was small and seemed cirrhotic while the left lobe (LL) was greatly enlarged (Figure 1). A follow-up CT scan confirmed the presence of atrophy-hypertrophy complex of the liver (Figure 2). The right lobe was small and was recognized on only the most cranial CT sequences. The lateral segment of the left lobe (segment 3) was greatly enlarged, segment 4 was shown and the gallbladder (*) was in a retrohepatic position. The portal vein (white arrow), hepatic artery (thin white arrow) and common hepatic duct (thick white arrow) were also in unusual positions because of clock-wise rotation of hilar structures.The radiological features described above are typical of right lobe atrophy associated with left lobe hypertrophy. This atrophy-hypertrophy complex of the liver is almost always due to biliary obstruction or to occlusion of the portal vein. Hilar or intrahepatic causes of biliary obstruction include benign and malignant neoplasms and benign strictures including Caroli's disease. Vascular causes include hilar or intrahepatic portal vein occlusion by neoplasms, cavernous transformation of the portal vein and congenital stenosis of the portal vein. Embolism into the right portal vein is also being used to enlarge the left lobe of the liver prior to surgical or other therapies for neoplasms in the right lobe of the liver. In animal models, a compromised portal venous blood flow is a much stronger stimulus for atrophy-hypertrophy than biliary obstruction. In the patient described above, we have attributed the atrophy-hypertrophy complex to herniation of the liver causing distortion of the right portal vein and a reduction in right portal blood flow.
Introduction. Mediastinal ectopic thyroid tissue (ETT) rep-resents a rare entity. Clinically, it can manifest with thyroid gland dysfunction or with symptoms and signs caused by a compressive effect on the surrounding structures, but in most cases it is an asymptomatic condition and incidental finding. All pathologic processes, including malignancy that can occur in the orthotopic thyroid gland can also develop in the ETT. Case report. We presented a case of a 17-year-old female with incidentally found mediastinal ETT. Besides ETT, the patient had an orthotopic thyroid gland and was euthyroid. During follow-up, mild compressive symptoms developed. Magnetic resonance imaging examination showed a non-significant increase of the mediastinal mass volume, but due to its morphological changes, a suspicion of another etiology was raised. A discrepancy between the positive technetium-99m pertechnetate and negative 131 iodine radionuclide imaging of the mediastinal mass was highly suspicious for malignancy. Surgery was performed and the pathologist confirmed that it was a colloid goiter in the mediastinal ETT. Conclusion. Mediastinal ectopic thyroid tissue should be taken into account in the differential diagnosis of the mediastinal tumor mass. An increase in the size of the mediastinal ETT, development of compressive symptoms or suspected malignant alteration require surgical treatment.
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