Adult T-cell leukemia-lymphoma.

Adult T-cell leukemia-lymphoma, an aggressive T-cell leukemia, is characterized by the presence in the peripheral blood of malignant T cells that have highly indented or lobulated nuclei. Phenotypically the cells are usually helper T cells, but functionally they behave as suppressor cells. Patients have skin and lung involvement, hepatosplenomegaly, moderate lymphadenopathy sparing the mediastinum, and various metabolic abnormalities such as hypercalcemia. The clinical course may be chronic or acute, usually followed by a rapidly progressive terminal course. Adult T-cell leukemia-lymphoma is now known to be caused by human T-cell lymphotropic virus type I, which has been identified in the cells of patients with the disease.     

Adult T-cell leukemia with an unusual phenotype, Leu-2a positive and Leu-3a negative

A case of adult T-cell leukemia (ATL) with an unusual phenotype is presented. Leukemia cells of this patient reacted with anti-Leu-2a monoclonal antibody, although most of ATL cases are reported to show the phenotype of helper/inducer T-cell. It is indicated that the surface phenotype of ATL is rather heterogeneous.     

Joint and tendon subclinical involvement suggestive of gouty arthritis in asymptomatic hyperuricemia: an ultrasound controlled study

Introduction  

In this study, we aimed to investigate ultrasonographic (US) changes suggestive of gouty arthritis in the hyaline cartilage, joints and tendons from asymptomatic individuals with hyperuricemia.     

Ultrastructural cytochemistry of chronic T-cell leukaemias. A study with four acid hydrolases

The ultrastructural localization of four acid hydrolases (acid phosphatase, beta-glucuronidase, beta-glucosaminidase and alpha-naphthylacetate esterase) has been studied in lymphocytes from 16 patients with three types of chronic T-cell leukaemia, namely, T-prolymphocytic leukaemia (T-PLL), T-chronic lymphocytic leukaemia (T-CLL) and adult T-cell lymphoma leukaemia (ATLL). Different patterns of enzyme distribution were observed in the leukaemic T-cells from these disorders. In T-PLL, reactivity for the four acid hydrolases was confined to single or a few large granules. Gall bodies were reactive for beta-glucuronidase, b-glucosaminidase and alpha-naphthylacetate esterase but apparently unreactive for acid phosphatase. In T-CLL, scattered small- to medium-size cytoplasmic granules and many parallel tubular arrays were strongly reactive for acid phosphatase, beta-glucuronidase and beta-glucosidase but showed no reactivity for alpha-naphthylacetate esterase. Intermediate features were observed in ATLL. The observed differences in enzyme reactivity reflect a different content of lysosomal granules in the various types of leukaemic T-cells. They also suggest that similar differences may be found in normal T-lymphocyte subsets.     

Blast transformation in chronic myeloid leukemia with synovial involvement

In a patient with chronic myeloid leukemia in blastic transformation, the blast cells in a knee joint effusion were identical morphologically to those in the marrow. Cytochemical and immunocytochemical studies showed that these blasts were primitive erythroblasts and not granulocytic or monocytic precursors. The combined use of cytologic, cytochemical and immunocytochemical techniques will help to accurately identify cells in joint effusions and to elucidate the mechanism of synovial involvement by hematologic disorders.     

The involvement of protein kinase C in activation-induced cell death in T-cell hybridoma.

T-cell hybridoma activated by a variety of stimuli such as anti-cell surface antigen, notably CD3 and T-cell receptors, and Con A undergoes a cell lysis process called activation-induced cell death (AICD). It was found that the major protein kinase C (PKC) isoform in the 2B4.11 T-cell hybridoma, PKC(alpha), was translocated from the cytosolic to the particulate fraction when these hybridoma cells were induced to die by plastic-adsorbed anti-CD3 antibodies. Inhibitors of protein phosphorylation rescued 2B4.11 cells from AICD as determined by the analysis of cellular metabolism and the proportion of living cells. Furthermore, PKC(alpha) down-regulation by phorbol ester treatment abolished AICD, and the degree of PKC down-regulation correlated well with the degree of AICD abolishment, suggesting that PKC activation represents an essential step in the molecular mechanisms underlying AICD in this T-cell hybridoma.     

Asymmetric papilledema in an asymptomatic patient with pseudotumor cerebri

A 58-year-old, obese, asymptomatic female was found to have asymmetric disc swelling with a unilateral optociliary shunt vessel on routine ophthalmological examination. Subsequent ultrasonography, neuroimaging and cerebrospinal fluid evaluations were consistent with the diagnosis of pseudotumor cerebri. This case demonstrates that pseudotumor cerebri may present in a variety of forms including asymmetric papilledema.