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Lymphomas developing in the adrenal glands are rare. Twenty-one cases of primary adrenal lymphomas have been reported in the English literature, but no cytogenetic data were given. We had the opportunity to examine three cases of primary adrenal lymphoma characterized by the B cell phenotype. Samples for histologic and immunohistologic diagnosis were obtained from postmortem examination in cases 1 and 2, and with an ultrasound-guided needle biopsy in cases 2 and 3. In all 3 cases, histologic examination of adrenal masses showed diffuse medium-sized cleaved lymphoma cells, which were positive for L-26, an immunohistochemical B cell marker. Endocrine studies showed adrenal insufficiency in 1 case. Cytogenetic examination showed clonal abnormalities, including 8q24 in case 1 and 14q32 in case 2, similar to those observed in nodal B cell lymphoma.

We established IL-2-dependent T cells from an adult T-cell leukaemia (ATL) patient whose leukaemic cells changed from CD4 single-positive in the initial phase to double-negative (CD4- CD8-) at the time of exacerbation. The cells termed SO-4 were of ATL cell origin and showed the double-negative TCR alpha beta/CD3+ T-cell phenotype. SO-4 cells acquired CD4 antigen expression following stimulation with concanavalin A (ConA) or immobilized anti-CD3 antibody. The induction was inhibited by herbimycin A, an inhibitor of protein tyrosine kinase (PTK) activity. No CD4 mRNA was detectable in unstimulated SO-4 cells but a 3.0 kb signal specific for CD4 mRNA was detected after stimulation. These findings indicate that SO-4 cells return to their original phenotype (CD4 single-positive) by stimulation involving PTK. The results indicate that there is a pathway of phenotypic cycling between CD4 single-positive and double-negative T cells.

Plasma concentration of M-CSF was measured in 35 patients with adult T cell leukemia (ATL), using a radioimmunoassay (RIA). ATL patients showed elevated levels of plasma M-CSF concentration when compared with healthy adult volunteers. Higher M-CSF levels were observed in acute ATL patients than in patients with chronic or smouldering ATL (P < 0.0001). There was a significant positive correlation of M-CSF concentration with serum lactic dehydrogenase (LDL) level, a reliable marker for assessing the grade of malignancy in ATL (P = 0.0003). There was, however, no correlation of M-CSF concentration with total counts of peripheral blood ATL cells, neutrophils or monocytes, or with serum calcium levels. Although there was a significant positive correlation of M-CSF concentration with body temperature (P = 0.003), there was not a significant correlation of M-CSF concentration with C-reactive protein (CRP), a protein indicative of the severity of inflammation (P = 0.063). These results indicate that plasma M-CSF concentration reflects the disease activity of ATL, and can thus serve as a marker in the clinical subclassification of ATL patients.

Forty patients, originally diagnosed as endometrial hyperplasia, were reviewed histopathologically and evaluated for immunohistochemical staining with antibodies directed against TAG-72 and MSN-1 antigens. All patients had follow-up endometrial biospies or hysterectomies from 1 to 13 years later. The extent of regression to normal of nonhyperplastic endometrium, persistence as any type of endometrial hyperplasia, or progression to endometrial adenocarcinoma was correlated with the histologic hyperplastic subtype and immunohistochemical staining. As expected, cases of complex or atypical hyperplasia more often progressed to carcinoma than cases of simple or no hyperplasia. Interestingly, MSN-1 positivity was more prevalent in cases of higher grades than lower grades of hyperplasia and was associated with the tendency to show persistent hyperplasia or progression to carcinoma. B72.3 positivity was uncommon in the hyperplastic endometrium and was not correlated with clinical regression or progression. Although the tendency for progression of endometrial hyperplasia to endometrial carcinoma is best judged histologically, MSN-1 may add prognostic information in subgroups of hyperplasia.

This report describes three of primary bilateral adrenal lymphoma. Case 1 was an 87-year-old female. She was admitted to our hospital because of anemia. Masses in the bilateral adrenal glands were noted on abdominal computed tomography (CT). After combination chemotherapy, bilateral adrenal masses transiently showed a remarkable reduction, but they soon enlarged and she died. The pathological diagnosis at autopsy was non-Hodgkin lymphoma (diffuse medium sized cell type). Case 2 was a 77-year-old male. He visited our hospital complaining of general malaise. Masses in the bilateral adrenal glands were noted on abdominal CT and he was admitted. The left adrenal was biopsied under echo guidance. The pathological diagnosis was non-Hodgkin lymphoma (diffuse medium sized cell type). The bilateral adrenal masses transiently responded to combination chemotherapy, but soon enlarged again and he died. Case 3 was a 75-year-old male. He visited our hospital complaining of general malaise. Masses in the bilateral adrenal glands was noted on abdominal CT and he was admitted. The left adrenal was biopsied under echo guidance. The pathological diagnosis was non-Hodgkin lymphoma (diffuse medium sized cell type). Combination chemotherapy was followed by a complete remission and discharge of the patient.

The authors examined peripheral blood samples from patients with adult T-cell leukemia (ATL) using the monoclonal antibody Ki-67 which detects a nuclear antigen present in actively proliferating cells. In patients with chronic ATL, the percentage of Ki-67-positive cells was significantly lower than in acute ATL patients (median values, 3.3% versus 18.9%, P less than 0.001). Furthermore, there was a significant inverse correlation between the percentage of Ki-67-positive cells and the length of survival (P less than 0.001). Serum lactic dehydrogenase (LDH) levels also showed a significant inverse correlation with survival, but this was less strong than that for Ki-67 (0.01 less than P less than 0.02). Thus, Ki-67 positivity appears to indicate the aggressiveness of ATL, and can possibly be used for the clinical classification of ATL patients as well as for the prediction of prognosis.

A 60-year-old woman was admitted to our hospital with symmetrical arthritis of the knees. During the 2 years preceding admission, she had experienced recurrent arthritis. A histological examination of her synovial tissue showed prominent villous proliferation of the synovial cells, prominent vascularity throughout and an inflammatory infiltrate composed of abnormal mononuclear cells. Three months later, she developed fever, skin eruptions, lymphadenopathy and hepatosplenomegaly. She also had hypercalcemia and there was abnormal lymphocytosis in her blood smears. She was diagnosed as having adult T cell leukemia. Parenteral chemotherapy treatment with adriamycin and cyclophosphamide gave remission of all the manifestations of disease, including arthritis. Her leukemia recurred, however, and she died 6 months after the diagnosis was made.

The prevalence of the preleukemic state of adult T-cell leukemia (pre-ATL) was studied in Nagasaki prefecture, one of the endemic human T-lymphotropic virus type 1 (HTLV-1) areas in Japan. Pre-ATL cases have the monoclonal proliferation of abnormal lymphocytes, without signs of malignant proliferation or clinical signs and symptoms related to leukemia. HTLV-1 carriers who have monoclonal integration of HTLV-1 proviral DNA may be at high risk of developing ATL. Abnormal lymphocytes with either bilobular or large and chromatin-rich nuclei were found in 63/356 (17.7%) of HTLV-1 carriers among inhabitants. We analyzed DNA of peripheral lymphocytes from 108 carries with abnormal lymphocytes by Southern blot technique. Monoclonal integration of HTLV-1 has been detected in 12 cases (11.1%). These results lead to the conclusion that the prevalence rate of pre-ATL among all HTLV-1 carriers is about 2%. Pre-ATL is presumed to be the clinical stage which precedes ATL, although the possibility remains that the HTLV-1 carrier may develop symptoms of ATL directly, without going through the pre-ATL stage.

A 300-mg dose of UFT was administered daily for seven days prior to surgery for ovarian malignant tumors. The concentrations of FT, 5-FU and uracil in the serum, tumor tissue, adjacent normal tissue and ascitic fluid were measured. The results were as follows: 5-FU concentration in the serum was 0.008 +/- 0.006 micrograms/ml (n = 14) and the concentration in the ascitic fluid was 0.008 +/- 0.006 micrograms/ml (n = 4). The 5-FU concentration in the tumor tissue was 0.142 +/- 0.199 micrograms/g. This was approximately 3.0 times higher than the concentration in the adjacent normal tissue which was 0.048 +/- 0.030 micrograms/g and the T/B ratio (formula; see text) was approximately 17.8.

To prolong the survival of patients with chronic myeloid leukemia (CML), 19 patients were treated with busulfan to keep their leukocyte counts within normal range by controlling bone marrow hyperplasia. The duration of chronic phase in these patients was significantly longer than that in historical controls who were treated conventionally with busulfan. This prolongation was not ascribable to the difference in such prognostic factors between the two therapy groups as splenomegaly, leukocyte count and percentage of peripheral blasts. There was a significant difference again in the duration of chronic phase between the two therapy group even when restricted to each 11 patients with intermediate relative risk (0.7-1.5) according to Sokal et al. Four patients showed thrombocytopenia less than 5 x 10(4)/microliters, but all these patients recovered within 4 months and there was no further critical side effect except subcutaneous bleeding. This study suggests that maintenance of leukocyte count within normal range and suppression of granuloid hyperplasia in bone marrow with busulfan may prolong chronic phase of CML. Probability of clonal evolution may be decreased by reducing the total leukemic cell mass and suppressing cellular turnover of primitive CML stem cells. Another possibility is that prolongation of chronic phase might be dependent on the appearance of normal karyotype clone after long-term bone marrow suppression just like after intensive chemotherapy or alpha-interferon therapy.

An autopsy case of IgE myeloma, 85-year-old male is reported. He was admitted to our hospital on November 17, 1987 due to pain of left humerus. Osteolytic and osteoporotic foci were found in left humerus, ribs, spinal column and femurs. Complete blood countings were as follows: RBC 3.23 x 10(12)/L, Hb 11.3 g/dl, WBC 6.3 x 10(9)/L, platelet 173 x 10(9)/L. Blood smear showed red cell rouleaux formation without myeloma cells. Examination of bone marrow revealed hypoplasia with 52% myeloma cells which were stained with anti-IgE and antilambda antisera by peroxidase anti-peroxidase method. Total serum protein level was 7.7 g/dl. Monoclonal protein was observed at fast gamma-region by cellulose-acetate electrophoresis. On immunoelectrophoresis, this monoclonal protein made specific M-bow against anti-IgE and anti-lambda antisera. The IgE level in serum and urine were 7.8 x 10(6) IU/ml and 2.4 x 10(3) IU/ml by radio-immunoassay respectively. He was died owing to renal failure on September 7, 1988. Postmortem examination showed infiltration of myeloma cells in bone marrow, spleen, kidneys, lungs and generalized lymph nodes.