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Biomedical subjects

F Lauria

Publications and source records attributed to F Lauria.

At least 145 records · Page 8Linked to original sources
PubMed1982

Staging of chronic lymphocytic leukemia.

One-hundred and eighty-eight patients with chronic lymphocytic leukemia were analyzed for prognosis based on Rai's staging system. It was found that stages I and II were not homogeneous as to prognosis. Stage II patients presenting with isolated splenomegaly had a long survival and were pooled with stage 0 patients (low risk group, 30% of cases, relative death rate 0.24, median survival greater than 10 yr). Stages I and II patients with a lymphocyte count higher than 40 x 10(9)/liter had a short survival and were pooled with stages III and IV patients (high risk group, 39% of cases, relative death rate 1.91, median survival 3.3 yr). Stages I and II patients with a lymphocyte count lower than 40 x 10(9)/liter made up an intermediate or standard risk group (31% of cases, relative death rate 1.00, median survival 6.2 yr). This modified staging system applied successfully to both old and young patients (more and less than 60 yr old, respectively).

Aged↗
PubMed1981

Increase in T gamma lymphocytes in B-cell chronic lymphocytic leukaemia. II. Correlation with clinical stage and findings in B-prolymphocytic leukaemia.

The proportion of T gamma and T mu lymphocytes was studied in 40 cases of B-chronic lymphocytic leukaemia (B-CLL) and six of B-prolymphocytic leukaemia (B-PLL). The significant increase in T gamma cells, previously reported in two small B-CLL series, was confirmed and shown to be directly correlated with the clinical stages of the disease (P less than 0.01 to less than 0.001). The normal T mu:T gamma ratio (2.3:1) was reversed in B-CLL (1:1.4) and B-PLL (1:1.9). The proportion of T mu cells was decreased but was not related to stage. Our findings suggest that the increase in T gamma cells may be responsible for the hypogammaglobulinaemia of B-CLL. This is supported by two sets of observations. First, serum Ig levels were more often normal in cases in Stages 0 and I than in Stages II-IV (P less than 0.05), while the levels of two or three Ig classes were below normal in Stages II-IV twice as frequently. Secondly, splenic irradiation in one case was followed by a fall in the absolute number of T gamma lymphocytes, a reversion to normal of the T mu: T gamma ratio and an improvement in serum Ig levels. Thus, the imbalance in ;the regulatory T-cell subsets may provide an important clue to understand the pathogenic mechanism of the immunodeficiency in the chronic B-cell leukaemias.

B-Lymphocytes↗
PubMed1981

T gamma cell deficiency in idiopathic thrombocytopenic purpura (ITP).

A significant reduction in the proportion and absolute number of circulating T gamma (suppressor) lymphocytes was observed in 15 adult patients with idiopathic thrombocytopenic purpura (ITP). The proportion of T gamma cells was also reduced in the spleen of four patients so investigated. This abnormality was not seen in 5 patients cured by splenectomy whilst it persisted in 3 who remained thrombocytopenic after splenectomy. The proportion of Tmu (helper) lymphocytes in ITP was normal. These findings, similar to those reported in systemic lupus erythematosus, suggest that an inbalance of the immunoregulatory T-cell subsets may be important in the pathogenesis of ITP.

Adult↗
PubMed1981

T-lymphocyte subsets in healthy splenectomised patients.

In 16 normal subjects who underwent splenectomy for traumatic reasons, the T-lymphocyte number (E rosette positive cells) and the proportion of T-cell subsets were assessed on peripheral blood T-lymphocytes. The findings, compared with not splenectomised normal controls, showed other than an increase in the absolute number of T-lymphocytes, mainly a significant increase of T gamma cells (21% +/- 5 vs 13% +/- 4) and a less marked decrease of T mu cells (38.7% +/- 7 vs 51.8% +/- 12). Probably this increase in T gamma cells is irrelevant on the immune response and represents only the effect of the redistribution of T-cell subsets after splenectomy. Alternatively, splenectomy, removing most of the lymphocytes that respond to antigenic stimulation, and, producing an increase in T gamma cells, may contribute to the development of an impaired B-cell response and sometimes to the development of severe infections which occur mainly in splenectomised children.

Child↗
PubMed1980

Increased proportion of Fc gamma and Fc mu positive T-lymphocytes following treatment with neuraminidase.

Membrane receptors for IgG (Fc gamma) and IgM (Fc mu) were assessed on isolated peripheral blood T-lymphocytes by rosette formation with ox-RBC coated with rabbit IgG or IgM antibodies. The mean percentage of Fc gamma and Fc mu rosettes on freshly separated T-cells was 19% (+/- 6% SD) and 4% (+/- 1% SD), respectively. These values increased significantly to 40% (+/- 9%) for Fc gamma and 34% (+/- 8%) for Fc mu after preincubation of the lymphocytes with Neuraminidase. The proportion of Fc mu, but not of Fc gamma, rosettes increased to 44% (+/- 8 SD) after overnight incubation at 37 degrees C, and less markedly after incubation for 45m at 37 degrees C (29% +/- 7). Fc gamma and Fc mu rosette formation, with or without neuraminidase, was specifically inhibited by human IgG or IgM. These findings suggest (1) that hidden receptors can be demonstrated on T-lymphocytes after Neuraminidase treatment which, in the case of Fc gamma, cannot be revealed by other means, and (2) that the proportion of T gamma lymphocytes in the peripheral blood is higher than generally believed.

Animals↗
PubMed1980

Significance of splenomegaly in childhood acute lymphoblastic leukaemia in remission.

In 5 children with acute lymphoblastic leukaemia (ALL) splenomegaly occurred or persisted after induction of haematological remission. 3 patients underwent splenectomy but the spleen was free of leukaemia in each case; these patients relapsed and died 10 to 28 months after surgery. 2 patients who were not splenectomised are alive and free of leukaemia 2 and 6 years after splenomegaly was first noted; in 1 splenomegaly regressed after cessation of antileukaemic therapy. The isolated finding of splenomegaly in children with ALL in haematological remission does not necessarily indicate a relapse; instead, it is suggested that splenic enlargement may reflect an immunological process contributing to control the leukaemia and that removal of the spleen may be harmful.

Child↗
PubMed1980

Increase in T gamma lymphocytes in B-cell chronic lymphocytic leukaemia.

A significant increase in the proportion (mean 38% +/- 9.3 SD) and absolute number of T gamma (suppressor) lymphocytes was observed in 13 patients with chronic lymphocytic leukaemia (CLL) compared with 20 normal controls (mean 19% +/- 6.5). Conversely, the proportion of T mu (helper) lymphocytes was lower in CLL (mean 27% +/- 9.3) than in the controls (mean 40% +/- 4), although the absolute numbers were normal or increased. It is suggested that an imbalance of T-lymphocyte subsets controlling B-lymphocyte differentiation may be relevant in the pathogenesis of CLL or some of its associated features.

B-Lymphocytes↗
PubMed1980

Evidence that T colony formation is a property of T mu (helper) lymphocytes.

The T-colony-forming capacity of different T lymphocyte subsets was studied in normal peripheral blood. Unfractionated lymphocytes (after 'Lymphoprep' separation) gave rise to a mean of 150 +/- 27 . 7 s.d. T colonies per 1 x 10(5) cells, while purified T lymphocytes by sheep RBC rosetting formed 110 +/- 32 . 2 colonies. Two subpopulations of T lymphocytes were further isolated according to the presence of Fc receptors for IgG (T gamma) or IgM (T mu) by ox RBC rosetting. T gamma cells were found to have a very low or absent T colony-forming capacity (23 +/- 26 . 2), while T mu cells produced normal colony numbers (106 +/- 28 . 4). Co-culture experiments showed that T gamma cells do not inhibit the T colony growth of normal T cells in our system. Our findings indicate that in human peripheral blood not all T lymphocytes are capable of forming T colonies and that this property is confined to the T mu (helper) lymphocyte subset.

Cell Separation↗
PubMed1980

T-lymphocyte colonies in human cord blood.

The capacity of human cord blood (CB) lymphocytes to form T-colonies was studied with a double layer technique. The mean number of colonies in CB was 91 +/- 70.5 SD (X 10(5) cells), significantly lower than in adult blood, mean 182 +/- 58.0 (X 10(5). In 28 of the 50 CB samples tested the colony numbers were below the normal range for adult lymphocytes. There was no direct correlation between number of colonies and percentage of E-rosette-forming cells in CB. Some CB samples with a high proportion of E-rosettes formed few T-colonies, suggesting that not all E-rosette positive cells are capable of producing T-colonies. On the other hand, some CB samples with a low proportion of E-rosettes formed normal numbers of T-colonies. Purification of two populations of T-cell enriched and T-cell depleted lymphocytes confined the T-colony growth in CB, as in adult blood, to the former fraction, excluding that T-colonies could be obtained from E-rosette negative lymphocytes. This indicates that, from birth onwards, T-lymphocyte colonies originate from E-rosette positive cells. Whether the low growth observed in CB results from lack of maturation of T-lymphocytes or from the presence of specific subsets of T-lymphocytes is not clear at the present time.

Colony-Forming Units Assay↗
PubMed1979

Immunological markers in non-Hodgkin's lymphomas.

Membrane markers of lymphomatous cells were studied in 33 patients with non Hodgkin's lymphoma and correlated with morphological diagnosis according to Rappaport's classification. Nodular lymphomas and the majority of lymphocytic lymphomas showed B cell characteristics, whereas only 6 out of 23 with diffuse pattern were B. None of the histiocytic lymphomas were B, 3 were T, and 4 non T-non B. Mixed lymphocytic/histiocytic lymphomas showed different immunological patterns (B, T, non T-non B, B and T). These results confirm the importance of functional classification, which can clarify the pathogenesis of lymphoma.

Adult↗
PubMed1979

Management of nodular sclerosis Hodgkin's disease stage I, II A and B: evidence for a beneficial effect of MOPP on the relapse rate.

85 patients with previously untreated Hodgkin's disease with stage I, II A and B nodular sclerosis were treated. 31 of them with stage I and II A were submitted to radiotherapy alone. All are alive, but 9 of them (30%) relapsed. On the contrary, 35 patients with stage I and II A, and 19 with stage I, II and IIE B were submitted to radiotherapy followed by three courses of MOPP. All 54 patients are alive and relapse-free. No severe complication related to chemotherapy was observed. The analysis of results suggests that 3 courses of MOPP can significantly (Ip < 0.00025) reduce the relapse rate in patients with stage I and II nodular sclerosis, eligible for radiotherapy, without increasing morbidity.

Adolescent↗
PubMed1978

5-year survey of methotrexate, cyclophosphamide (Endoxan), and vincristine (MEV) therapy for advanced non-Hodgkin's lymphomas.

Five courses of a combination chemotherapy regimen with methotrexate, cyclophosphamide (Endoxan), and vincristine were given to 64 patients, 37 with lymphocytic lymphoma (LL) and 27 with histocytic lymphoma (HL). Eighteen of the 37 patients with LL (48%) achieved a complete remission (CR); 12 of these 18 patients have been in CR for 20--58 months. Among the complete responders only two died. Twenty-two of the 27 patients with HL (81%) achieved CR and 12 of these patients are still in CR. Ten of the complete responders have been relapse-free for 24--70 months and five have been relapse-free for greater than 60 months. Clinical and hematologic tolerance was such that the interval between each course had to be prolonged in only three of the 64 patients and, with the exception of vincristine, the dosages were not reduced.

Adolescent↗