A man aged 38 years was admitted to hospital with fever and a soft mass in the right hypochondrium. Laboratory investigations revealed minor changes in liver enzymes, a normal plasma bilirubin and an elevated serum level of CA19.9. At the time of a barium meal radiograph, faint, tooth-like calcification was noted in the upper abdomen. A computed tomography (CT) scan revealed a cystic structure, approximately 8 cm in diameter, with a fat-fluid level and calcification in the wall (Fig. 1). Compression of the bile duct and gallbladder were noted during endoscopic retrograde cholangiography. At operation, the tumor was located in the hepatoduodenal ligament. The tumor was excised, a cholecystectomy was performed and the bile duct was reconstructed using a Roux-en-Y choledochojejunostomy. The tumor contained sebaceous material, hair and teeth (Fig. 2), and was identified histologically as a mature cystic teratoma.Teratomas are rare neoplasms that develop from the three embryonic germ layers and can potentially contain tissue of any type. They arise from totipotential cell lines and are usually located in the gonads. However, extragonadal teratomas do occur, particularly in midline structures such as the anterior mediastinum, retroperitoneum and sacrococcygeal region. To our knowledge, there is only one previous report of a teratoma in the hepatoduodenal ligament. The majority of extragonadal teratomas (60%) show calcification on plain abdominal radiographs, either calcification in the wall of the cyst or in structures such as teeth or bones. A CT scan is usually the most helpful investigation. Serum levels of alpha fetoprotein, carcinoembyronic antigen and CA19.9 are elevated in some patients but this does not appear to be helpful clinically. The most important aspect of management is careful surgical excision. Overall, approximately 25% of extragonadal teratomas are malignant but this frequency is higher in solid teratomas and lower in cystic teratomas.
A 70-year-old male was admitted to our hospital because of fever and dyspnea. The patient was seropositive for HTLV-I and ATL cells were seen in the peripheral blood in the percentage of 2-5. The proviral DNA was positive and the diagnosis of smoldering ATL was made. His chest X-ray film showed diffuse reticulo-nodular infiltrates in both lung fields. The lung tissue obtained by transbronchial lung biopsy showed the lymphocytic infiltrations in the alveolar septa and the submucosa of the bronchioles. Bronchoalveolar lavage (BAL) fluid showed an increased proportion of lymphocytes that consisted mainly of CD3+ DR+ cells and the CD4+/CD8+ ratio was 2.1 during exacerbation and 0.8 after steroid therapy. Anti-HTLV-I IgG and IgA antibodies were positive in both serum and BAL fluid by Western blotting method. It is suggested that T-lymphocyte alveolitis may occur in patients who are seropositive for HTLV-I and the immunological mechanism seems to be responsible.
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