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Biomedical subjects

M F Murphy

Publications and source records attributed to M F Murphy.

At least 145 records · Page 8Linked to original sources
PubMed1985

Cephalosporin-induced immune neutropenia.

Neutropenia is an occasional complication of treatment with cephalosporin antibiotics. This report describes two patients who had neutropenia while receiving high doses of cephalosporins. The neutrophil counts returned to normal after stopping the drug, and cephalosporin-dependent neutrophil antibodies were demonstrated in both cases, using the granulocyte immunofluorescence test. In one patient, the immune neutropenia appeared to be due to a drug adsorption mechanism similar to penicillin-induced haemolytic anaemia, while an immune complex mechanism may have been involved in the second patient.

Adult↗
PubMed1985

Use of chloroquine-treated granulocytes and platelets in the diagnosis of immune cytopenias.

A chloroquine modification of the fluorescent antiglobulin technique has been used to demonstrate cell-specific antibodies in the presence of HLA antibodies. This is of particular value in the diagnosis of alloimmune neonatal thrombocytopenia and neutropenia, post-transfusion purpura, and in the investigation of febrile non-haemolytic transfusion reactions and of patients refractory to platelet transfusions.

Adult↗
PubMed1984

Severe megaloblastic anaemia associated with abnormal azathioprine metabolism.

Severe anaemia is a rare, unexplained, side effect of azathioprine therapy. We report here such a case associated with a previously unreported abnormality in azathioprine metabolism. A 57 year old man on azathioprine therapy, for a presumed collagen vascular disease, developed severe megaloblastic anaemia. This resolved on cessation of azathioprine treatment. A very high concentration of an azathioprine metabolite, 6-thioguanine nucleotide, was found in the patient's red blood cells and this was confirmed by subsequent rechallenge with a single dose of 50 mg azathioprine.

Anemia, Macrocytic↗
PubMed1984

Pure red cell aplasia--evidence for an inhibitory action of the bone marrow adherent cell layer.

Evidence is presented for an inhibitory action of the bone marrow adherent cell layer on erythropoiesis in a case of pure red cell aplasia. Cultures of the patient's bone marrow with autologous and normal plasma showed normal numbers of CFU-C, but total absence of BFU-E. There was no inhibition of BFU-E when normal bone marrow was cultured with the patient's plasma. T-cell depletion of the patient's bone marrow did not affect these results, but after removal of the adherent cells, normal numbers of BFU-E were cultured. These observations suggest that the adherent cells, which are predominantly macrophages, were responsible for the inhibitory action on erythropoiesis.

Aged↗
PubMed1984

Sequential development of platelet, neutrophil and red cell autoantibodies associated with measles infection.

This study describes the development of autoimmune thrombocytopenia followed by autoimmune haemolytic anaemia in a Negro woman with measles. An IgM platelet autoantibody was detected using a fluorescent labelled antiglobulin technique. The thrombocytopenia resolved spontaneously, although the platelet autoantibody persisted and platelet survival remained shortened, suggesting a compensated thrombocytolytic state. An IgG granulocyte autoantibody was present transiently although the patient was never neutropenic. The haemolytic anaemia was due to an IgM cold autoantibody (anti-I), which was active up to 30 degrees C, and an IgG warm autoantibody, which was detectable only when she was severely anaemic. After an initial blood transfusion, the anaemia resolved and the red cell autoantibodies disappeared. The platelet, granulocyte and red cell autoantibodies were cell-specific and not a single cross-reacting antibody.

Adult↗
PubMed1983

Demonstration of an immune-mediated mechanism of penicillin-induced neutropenia and thrombocytopenia.

Severe neutropenia may be a more common complication of high-dose penicillin therapy than previously recognized. This report describes five such patients, one of whom also had thrombocytopenia. The neutrophil and platelet counts rapidly increased on stopping penicillin, and the bone-marrow, which was hypocellular in some cases, became normal. Further studies on one of these patients, using a fluorescent antiglobulin technique with paraformaldehyde-fixed cells, demonstrated a complement-fixing IgG penicillin antibody reacting with the patient's granulocytes and platelets in the presence of the drug. This suggested an immune mechanism similar to the well-recognized penicillin-induced immune haemolytic anaemia. The associated bone-marrow hypoplasia may also be due to antibody-mediated suppression of penicillin-coated precursor cells.

Adult↗
PubMed1983

Thoracic vascular pathologies.

Thoracic vascular anatomy is described, and intrathoracic pathology involving both high and low pressure vasculature is reviewed.

Aortic Rupture↗
PubMed1982

Chronic cold haemagglutinin disease due to an anti-M-like autoantibody.

A case of chronic cold haemagglutinin disease due to an IgM monoclonal (kappa) autoantibody with anti-M-like specificity is described in a patient with the MN phenotype. The autoantibody was present in very high titre and active at body temperature, but haemolysis was only mild. The direct antiglobulin test was positive due to C3d on the patient's red cells, and the autoantibody was able to bind complement to normal MM and MN cells with a marked dosage effect.

Aged↗
PubMed1981

Analysis of a restriction endonuclease map for bovine papillomavirus type 2 DNA.

A physical map was constructed for bovine papillomavirus type 2 DNA by the use of restriction endonucleases. A comparison between the genomes of bovine papillomavirus types 1 and 2 in regard to location and number of cleavage sites of seven enzymes is also presented. This comparison revealed similarities between the two genomes.

Bovine papillomavirus 1↗
PubMed1981

Severe megaloblastic bone marrow change associated with unsuspected mild vitamin B12 deficiency.

Two patients are reported who developed peripheral blood abnormalities and marked megaloblastic bone marrow change within eleven days of cardiac bypass surgery. The patients were shown to have unsuspected mild vitamin B12 deficiency due to Addisonian pernicious anaemia. The megaloblastic changes were presumed to be precipitated by the increased demand for erythrocytes and platelets after surgery.

Anemia, Pernicious↗