The proliferative response of fresh peripheral blood leukemic cells from eight adult T cell leukemia (ATL) patients to interleukin-4 (IL-4) was studied to determine the possibility that the ...IL-4-mediated T-cell growth pathway is involved in the cell growth of leukemic cells in ATL. Resting lymphocytes from ten normal individuals did not proliferate in response to IL-4. Leukemic cells from two ATL patients did not respond to interleukin-2 (IL-2) or IL-4. Leukemic cells from two patients did respond to IL-2. but not to IL-4. In contrast, a strong proliferative response was observed in the IL-4 culture, but not in the IL-2 culture in the remaining four patients. Chromosome analysis of mitotic cells, performed in one of four patients, confirmed that the cells dividing in response to IL-4 were leukemic cells, but not activated normal lymphocytes. These results indicate the activation of IL-4/IL-4 receptor system in leukemic cells from some ATL patients and suggest the possible involvement of the system in the proliferation of leukemic cells and the leukemogenesis in ATL.
We studied the change in cytoplasmic free calcium ion concentration (Ca2+i) in the peripheral blood leukemic cells from adult T-cell leukemia (ATL) patients stimulated by anti-T3 (CD3) or anti-T11 ...(CD2) antibodies in order to see whether there is an abnormal response in the early activation processes following T3 or T11 antigen stimulation. Peripheral blood mononuclear cells (PBMC) from four T-cell chronic lymphocytic leukemia (T-CLL) patients showed a rapid and clear increase in Ca2+i (from 165 +/- 26 nM to more than 299 nM) when stimulated by OKT3 antibody and anti-mouse IgG antibody. This response was comparable to that of PBMC from 10 normal individuals (from 151 +/- 20 nM to 252 +/- 34 nM). In contrast, PBMC from 10 ATL patients showed only a slight increase in Ca2+i (from 137 +/- 21 nM to 176 +/- 32 nM) following T3 stimulation. The experiments with higher concentrations of OKT3 antibody suggested that this attenuated increase in Ca2+i in ATL cells was not exclusively due to impaired expression of T3 antigen. The Ca2+i increase in ATL cells induced by the stimulation with two anti-T11 antibodies recognizing different epitopes of the T11 antigen, however, was comparable to that of normal PBMC. The abnormal response of Ca2+i to the T-cell receptor/T3 antigen stimulation in ATL may be related to dysfunction or leukemogenesis of HTLV-I-infected cells.
We studied cell proliferation and interleukin-2 (IL-2) receptor upregulation mediated by exogenous IL-2 in leukemic cells from adult T-cell leukemia (ATL) patients to characterize some aspects of ...abnormal IL-2 receptor expression in ATL. Leukemic cells from 7 ATL patients examined showed no or very poor proliferative response to IL-2 though they expressed IL-2 receptors without any stimulation. In contrast, ATL leukemic cells cultured with IL-2 for 2 days expressed about twice as many IL-2 receptors as those of cells cultured without IL-2. Thus, in ATL leukemic cells, there seems to be a dissociation between the signal(s) for two different effects mediated by IL-2, cell proliferation and IL-2 receptor upregulation.
A 46-year-old man had acute leukemia with two cell populations of lymphoblasts and monoblasts (L1 and M5-b in FAB classification, respectively), which were characterized by morphological, ...cytochemical and cell marker studies. At the time of diagnosis about 80% blasts were terminal deoxynucleotidyl transferase (TdT) positive lymphoid cells, while the rest were TdT negative monocytoid cells. After induction chemotherapy of vindesine and prednisolone for 15 days, almost all blasts were TdT negative monocytoid cells. Therefore, an additional course of the chemotherapy with the protocol for acute nonlymphocytic leukemia was given and one month later the patient achieved complete remission.
We report a case of primary aldosteronism in a -- woman without - or any other characteristic symptoms. The condition was first suspected by hypokalemia (2.6 mEq/liter), which was incidentally found ...by routine checkup. There was evidence of suppressed plasma renin activity (PRA) and elevated plasma aldosterone levels. However, the blood pressure never reached a hypertensive level, and the circulating blood volume was within a normal range. A functioning right adrenal tumor was diagnosed by adrenal scintigraphy, computerized x-ray tomog-raphy, and adrenal venography. Adrenal venous catheterization suggested an aldosteronoma, which was confirmed by lateralized hypersecretion of aldosterone. After removal of the benign adenoma, the biochemical abnormalities were corrected, yet the blood pressure remained much the same. - is not necessarily a sign of primary aldosteronism.
A 35-year-old woman, who had been hypertensive for about 17 years and had lacked menarche, showed hypokalemia, low plasma cortisol and aldosterone levels, suppressed renin activity, and marked ...elevation of plasma corticosterone. The patient was diagnosed as having 17α-hydroxylase deficiency from functional studies. In addition, a right adrenal tumor was found by adrenal venography. Adrenal venous sampling showed that this tumor might be secreting corticosterone and possibly also deoxycorticosterone (DOC). The genotype was 46, XY, so she was diagnosed as having male pseudohermaphroditism. Right adrenalectomy and contralateral adrenal biopsy were done. The retained testicles were removed. Dexamethasone administration normalized the blood pressure and serum potassium. This is the first report of 17Q-hydroxylase deficiency with a right adrenal tumor.
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