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M J Deegan

Publications and source records attributed to M J Deegan.

At least 19 recordsLinked to original sources
PubMed1992

A clinicopathologic study of familial chronic lymphocytic leukemia.

The familial occurrence of chronic lymphocytic leukemia was studied using morphologic, immunophenotypic, cytogenetic, and immunoglobulin gene rearrangement analyses. Three of six siblings developed chronic lymphocytic leukemia. One (patient 1) died 9 years after the diagnosis of chronic lymphocytic leukemia at age 67 years. The other two patients, ages 64 and 68 years (patients 2 and 3, respectively), are alive after chronic lymphocytic leukemia was diagnosed 11 and 4 years ago, respectively. Using the Rye classification, patient 2 and patient 3 had Stage I and Stage O disease, respectively. In contrast, patient 1 had Stage IV disease. The bone marrow of patient 2 was 90% cellular, with sheets of mature lymphocytes, and that of patient 3 was 70% cellular, with a nodular pattern of similar cells. Both patients 2 and 3 had normal karyotypes. Immunophenotyping studies revealed that patient 3 had an expanded population of B cells with minimal to no detectable expression of surface immunoglobulins and membrane-bound light chains. In contrast, the B-cell population of patient 2 expressed immunoglobulins M, D, and Kappa light chains. Gene rearrangement studies performed on these two patients revealed different but distinct patterns of heavy chain rearrangement. This may represent an evolution of two different clones of chronic lymphocytic leukemia in this family.

Aged↗
PubMed1990

Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases.

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.

Adult↗
PubMed1989

Membrane antigen analysis in the diagnosis of lymphoid leukemias and lymphomas. Differential diagnosis, prognosis as related to immunophenotype, and recommendations for testing.

The immunophenotypic features of lymphoid leukemias and non-Hodgkin's lymphomas are reviewed. Emphasis is placed on the more recent literature, particularly the insights provided by monoclonal antibodies specific for T and B lymphocytes, and the contributions of flow cytometry. Characteristic immunophenotypes for T- and B-lineage acute lymphoblastic leukemia, the non-Hodgkin's lymphomas, chronic B- and T-cell lymphoproliferative disorders, and multiple myeloma are described. The importance of this information in the diagnostic process and in providing prognostic information concerning disease progression is considered. Limitations associated with monoclonal antibody reagents and flow technology are noted. Representative panels of monoclonal antibodies as used in the author's laboratory for characterizing these disorders are presented and discussed in light of the author's experience.

Antigens, Neoplasm↗
PubMed1987

Recurrent stroke associated with thymoma and anticardiolipin antibodies.

A 44-year-old woman developed recurrent thrombotic cerebral cortical infarctions. IgG and IgM anticardiolipin antibodies were found, as was a thymoma. To our knowledge, these antiphospholipid antibodies, which may inhibit prostacyclin formation and alter platelet function, have not been previously associated with this thymic neoplasm, an association we believe is not coincidental.

Adult↗
PubMed1986

Nonsecretory multiple myeloma with osteoporosis: immunocytologic and bone resorptive studies.

Two patients, ultimately found to have advanced nonsecretory multiple myeloma, presented with skeletal pain, diffuse skeletal demineralization, and fractures. The correct diagnosis was initially obscured by the absence of typical hematologic findings and discrete lytic bone lesions. Bone marrow examination was diagnostic. Intracytoplasmic IgA or IgD kappa was demonstrated in the myeloma cells of each case. Decreased quantitative polyclonal serum immunoglobulins and hypercalcemia were important clinical clues. The demonstration of increased osteoclast activating factor (OAF) derived from the cultured myeloma cells from each case suggests that the secretion of OAF and immunoglobulin are unrelated.

Bone Resorption↗
PubMed1985

Frozen RPMI 8402 cells: a reliable source of terminal deoxynucleotidyl transferase positive control material.

A reliable source of positive control material is needed for immunoperoxidase or immunofluorescent terminal deoxynucleotidyl transferase (TdT) assays. The cell line RPMI 8402 was obtained from a patient with acute lymphoblastic leukemia and is positive for nuclear TdT. The kinetics of TdT expression in a series of cultured RPMI 8402 cells and the effect of cryopreservation on TdT expression were evaluated. The highest percentage of TdT+ cells was detected on days 5-8 of RPMI 8402 cell cultures. TdT positivity was preserved for more than 3 years in cells stored in suspension at -70 degrees C, and at least 76 days on slide preparations when fixed with methanol prior to freezing. We conclude that when RPMI 8402 cells with maximum TdT positivity are stored at -70 degrees C, aliquots can be used as a constant source of positive control material thereby eliminating the necessity and expense of a continuing culture system.

Cell Cycle↗
PubMed1984

Differentiation of chronic lymphocytic leukemia cells after in vitro treatment with Epstein-Barr virus or phorbol ester. I. Immunologic and morphologic studies.

Leukemic cells from ten patients with "nonsecretory," B-type chronic lymphocytic leukemia (CLL) were cultured alone or in the presence of Epstein-Barr virus (EBV) or a phorbol ester (12-0-tetradecanoylphorbol-13-acetate; TPA) for 7 days. At periodic intervals the cell morphology, cytoplasmic immunoglobulin content (direct immunofluorescence) and capacity for immunoglobulin secretion (hemolytic plaque assay) were assessed. A variable but significant number of the TPA-treated CLL cells from all patients expressed cytoplasmic immunoglobulin of a single light-chain type at some stage, usually within the first 3 days. EBV induced similar changes in seven of eight cases tested. Untreated cell cultures were negative or contained a few cytoplasmic immunoglobulin-positive cells. Cells from five of nine cases secreted immunoglobulin of a single light-chain type. In every instance this was identical to the surface and cytoplasmic immunoglobulin. Cytologic changes were observed in the leukemic cells after treatment with one or both agents in nine of ten cases. The major feature was an increase in cell size associated with immunoblastic or plasma-cytoid features. Mitotic figures and binucleate cells were also present. These studies indicate that EBV and TPA are effective at inducing immunoglobulin synthesis and secretion in "nonsecretory" B cell neoplasms and are useful tools for studying the maturation potential inherent in these tumors. The study also suggests that the secreted immunoglobulin is a monoclonal product.

Aged↗
PubMed1984

High incidence of monoclonal proteins in the serum and urine of chronic lymphocytic leukemia patients.

Chronic lymphocytic leukemia (CLL) is generally considered a nonsecretory B cell immunoproliferative disorder. Conventional electrophoretic and immunoelectrophoretic methods have revealed serum monoclonal proteins in less than 10% of these patients. However, there is increasing experimental evidence from in vitro studies demonstrating that CLL cells may secrete immunoglobulins, particularly free light chains. We examined the serum and urine of 36 consecutive CLL patients for monoclonal proteins using sensitive immunochemical methods (high resolution agarose gel electrophoresis combined with immunofixation). The results obtained were correlated with the Rai stage, quantitative immunoglobulin levels, and lymphocyte membrane immunoglobulin phenotype of the leukemic cells. Twenty-three monoclonal proteins were identified in the serum or urine of 22 patients, an incidence of 61%. Six patients had serum monoclonal proteins, seven had only urinary monoclonal proteins, and nine had monoclonal proteins in serum and urine. In every instance the monoclonal protein was the same light chain type as expressed on the leukemic cells. Our findings suggest that the monoclonal proteins observed in the serum or urine of CLL patients are secretory products of the tumor cells and that their discovery is a function of the sensitivity of the method used for their detection.

B-Lymphocytes↗
PubMed1983

Sheep erythrocyte rosette formation by B chronic lymphocytic leukemia cells as a consequence of monoclonal surface immunoglobulin with "Forssman-like" antibody activity.

Peripheral blood and splenic lymphocytes from an elderly man with chronic lymphocytic leukemia (Rai stage 4) were shown to have monoclonal surface immunoglobulin (IgM+, IgD+, kappa+), Ia-like antigen and receptors for unsensitized sheep red blood cells. The sheep red blood cell receptor was not blocked by monoclonal antibodies that bind to the classic T lymphocyte rosette receptor (OKT-11 and Lyt-3) or by anti-human IgG or antilambda antibodies. However, the sheep red blood cell receptor was blocked by antihuman IgM and kappa antisera and by soluble guinea pig kidney antigen (Forssman antigen). It is concluded from these and other observations that our patient has a B-cell lymphoproliferative disorder expressing monoclonal surface immunoglobulin with anti-"Forssman-like" antibody activity.

Aged↗
PubMed1981

Cold dependent activation of complement in systemic lupus erythematosus. A unique cause for a discrepancy between clinical and laboratory parameters.

A 31-year-old woman with systemic lupus erythematosus (SLE) was studied because she developed markedly reduced total hemolytic complement activity at a time when her disease was clinically inactive. Functional assays demonstrated reduced activities of C1, C4, and C2, but normal concentrations of C3 and the terminal (C5-9) components were present. Antigenic concentrations of C1, C4, and C2 were normal. Plasma or serum obtained from blood allowed to clot at 37 degrees C had normal complement activity. Complement activity was depleted when the patient's serum was incubated in the cold. At reduced temperatures, the patient's serum (or purified IgG) depleted complement activity of normal human sera. A second patient with SLE was also demonstrated to have this same phenomenon. Cryoglobulins were not detectable in these patients. These data indicate that in vivo the patients' complement was normal and that the observed in vitro reduction was caused by cold dependent activation of the classical pathway.

Adolescent↗
PubMed1981

Undetected IgM paraproteins on serum protein electrophoresis.

Sera from three patients initially evaluated by cellulose acetate electrophoresis demonstrated apparent application "artifacts." On agarose gel electrophoresis, each had a definite paraprotein "spike." The immunoglobulin classes of the paraproteins were determined by immunoelectrophoresis, with and without reduction by dithiothreitol. The immunoglobulin class was confirmed by immunofixation electrophoresis on agarose gel. All three abnormal immunoglobulins were IgM-kappa-type paraproteins. Agarose electrophoresis with immunofixation was superior in the identification of these paraproteins compared with the standard method of cellulose acetate electrophoresis coupled with immunoelectrophoresis.

Aged↗
PubMed1980

Immunoglobulins in heroin users.

Concentrations of the serum immunoglobulins IgG, IgM, and IgA as well as rheumatoid factor were studied in a group of 80 intravenous and non-parenteral heroin users who were US soldiers serving in Vietnam and who were unique in their use of unadulterated heroin. Significant elevations of IgM out of normal range and IgG above controls were found in intravenous heroin users, while significant elevations of IgA above controls were found in non-parenteral heroin users. Rheumatoid factor was not found in either group. Evidence is presented to support the hypothesis that IgM elevation may be due to bacterial or other contamination but not to liver disease. The higher IgA in non-parenteral heroin users is postulated to reflect local antibody synthesis. The failure to detect rheumatoid factor in this study supports the view that the stimulation of rheumatoid factor is due to excipients or contaminants not found in the "uncut" drug.

Adolescent↗
PubMed1980

Systemic lupus erythematosus. Some contemporary laboratory aspects.

A summary of some of the important laboratory features of systemic lupus erythematosus (SLE) is presented. Emphasis is given to the sensitivity and specificity of the antinuclear antibody test, the relevance of particular antinuclear antibody patterns, and the status of testing for antibodies to DNA. Serum complement abnormalities in the patient with SLE are briefly reviewed, and the utility of the total hemolytic complement assay is stressed. The increasing evidence for disordered immune regulation in SLE is considered. Particular attention is given to the role of antilymphocyte antibodies and in vitro assays that permit an assessment of functional lymphocyte subsets. The heterogeneity of the SLE patient population and the influence of treatment and/or disease activity on laboratory results is repeatedly emphasized.

Antibodies, Antinuclear↗