Lymph nodes were examined from four patients with incipient adult T-cell leukemia-lymphoma (ATLL) who had mild lymphadenopathy, fatigue, no or a few atypical lymphocytes in their peripheral blood, and integrated proviral human T-cell lymphotrophic virus type I (HTLV-I) DNA in the nodes. The HTLV-I DNA was detected by southern blot analysis and/or polymerase chain reaction in the lymph nodes of all cases. The nodal architecture was preserved. Some scattered or aggregated highly lobular, cerebriform, or Reed-Sternberg-like giant cells were observed, with occasional mitoses and diffuse infiltration of small to medium-sized lymphocytes, with no or minimal nuclear abnormalities in the enlarged paracortex. The giant cells were usually positive for Ki-1 and also for UCHL-1 and other T-cell markers but negative for Ber-H2. Rearrangement and/or deletion of T-cell receptors were found in three of four patients. All patients died within 2 years, with transformation to overt leukemia-lymphoma occurring in three patients, and pulmonary carcinoma in one. The incipient or prelymphomatous phase of ATLL should be differentiated from Hodgkin's disease because of the distinctly different prognoses of these two diseases.

Aim: Postprandial hyperlipidemia (PH) is thought to be caused by the impaired postprandial metabolism of triglycerides (TG)-rich lipoproteins in both endogenous and exogenous pathways; however, there is no consensus. It is difficult to estimate the presence of PH without performing a time-consuming oral fat loading (OFL) test, so postprandial lipoprotein metabolism was analyzed by measuring the postprandial levels of apolipoprotein (apo) B-48 and apo B-100, and the correlation between postprandial TG increase and fasting apoB-48 levels was assessed to establish a good marker of PH without performing an OFL test. Methods: Ten male normolipidemic subjects were loaded with a high-fat (HF, 1045 kcal) or standard (ST, 566 kcal) meal, and the lipids, apolipoproteins and lipoprotein profiles were analyzed after each meal. Results: TG, apo B-48, remnant-like particles (RLP)-cholesterol and RLP-TG levels were increased and their levels were significantly higher after intake of the HF meal than the ST meal; however, there was no postprandial increase in apo B-100 and LDL-C levels. Postprandial increases in TG levels of CM, VLDL, LDL and HDL were significantly higher after intake of the HF meal than the ST meal. Fasting apo B-48 levels were strongly correlated with the incremental area under the curve of TG after intake of the HF meal, but not the ST meal. Conclusion: Postprandial TG increase was mainly due to increased CM and CM-R, but not VLDL. Measurement of fasting serum apo B-48 may be a simple and useful method for assessment of the existence of PH.

Histopathologic changes in lymph nodes were examined from ten patients with mild lymphadenopathy, a few atypical lymphocytes in their peripheral blood, skin lesions, and proviral DNA of human T‐cell leukemia virus type I (HTLV‐I) in their nodes. The proviral DNA of HTLV‐I was detected by southern blot analysis, in situ hybridization, and/or polymerase chain reaction techniques. The lymph nodes showed preserved nodal architecture with diffuse infiltration of small to intermediate‐sized lymphocytes in association with scattered transformed lymphocytes and a few immunoblast‐like cells in the enlarged paracortex. The infiltrating lymphocytes were positive for CD4, but neither rearrangement nor deletion of T‐cell receptors and immunoglobulin heavy chain genes was detected. Eight of ten patients received no therapy, and all patients were alive and healthy more than 5 months after the biopsies. The histologic findings resembled those of a viral infection and could be distinguished from HTLV‐I associated lymphomas.

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apillary fibroelastomas, which are generally found on the valvular endocardium, are relatively uncommon benign tumors and the next most common of the primary cardiac tumors after myxomas and lipomas. 1,2 However, they can cause lethal embolisms resulting in myocardial infarction, cerebral infarction and pulmonary embolism. 2 The number of patients diagnosed with papillary fibroelastomas has increased since the advent of echocardiography, but cases of recurrence have not been reported and multiple occurrence is rare. [3][4][5][6][7][8][9][10][11] We present a case of double papillary fibroelastoma of the aortic valve with aortic regurgitation and mitral periprosthetic leakage occurring 4 years after resection of an initial left ventricular papillary fibroelastoma with mitral and tricuspid valvular disease. Case ReportIn 1997, a 52-year-old man presented to hospital with dyspnea and a medical history that included atrial fibrillation in 1993. Cardiac catheterization revealed mild pulmonary hypertension of 45/22 mmHg, elevated wedge pressure of 22 mmHg, and obstruction of the posterior descending artery. Transthoracic echocardiography confirmed the presence of a left ventricular tumor (Fig 1A), and revealed moderate mitral stenosis and regurgitation, tricuspid regurgitation and trivial aortic regurgitation. Mitral valve replacement (29 mm Carbomedics Valve), tricuspid annuloplasty (32 mm Carpentier Ring) and tumor excision without blood transfusion were performed. The tumor, found on the anterior wall of the left ventricle near the apex of the heart, was pale yellow and 7 mm in maximum length. It was excised through the mitral valve (Fig 2A). Pathology showed papillary growth with myxoid stroma and the