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Biomedical subjects

P Metcalfe

Publications and source records attributed to P Metcalfe.

69 records · Page 4Linked to original sources
PubMed1986

Use of leucocyte-poor blood components and HLA-matched-platelet donors to prevent HLA alloimmunization.

Recent studies have shown that the incidence of alloimmunization due to repeated platelet transfusions from random donors may be reduced by the use of leucocyte-poor blood components. These results were confirmed by this study, where 16% of patients with acute leukaemia undergoing initial chemotherapy and receiving leucocyte-poor blood components developed lymphocytotoxic antibodies, compared with 48% of patients in a control group receiving standard (non-leucocyte-depleted) blood components. In a third group, who received leucocyte-poor blood components and HLA-matched platelets, none of the patients developed lymphocytotoxic antibodies. There was a low incidence of platelet-specific antibodies (8%) but no difference between the three groups. Improved methods of removing leucocytes from blood components appear to offer the best approach for minimizing HLA alloimmunization, as the provision of HLA-matched platelet donors for prophylactic platelet support of all patients is not feasible.

Adolescent↗
PubMed1986

Autoimmune thrombocytopenia and neutropenia after remission induction therapy for acute leukaemia.

Patients with acute leukaemia who are exposed to intensive chemotherapy, with or without radiotherapy, may remain thrombocytopenic or neutropenic in remission. The incidence of these prolonged cytopenias was examined retrospectively in 46 patients in remission and prospectively in 14 patients. The patients were tested for the presence of autoantibodies to platelets and neutrophils using a fluorescent antihuman globulin technique with paraformaldehyde-fixed cells. In the retrospective study nine patients (20%) had neutrophil autoantibodies and seven (15%) had platelet autoantibodies; only one of the former had neutropenia and one of the latter thrombocytopenia. In the prospective study three (21%) had neutrophil autoantibodies and seven (50%) had platelet autoantibodies. One of the patients with platelet autoantibodies had transient thrombocytopenia, and shortened platelet survival was demonstrated. None of the patients with neutrophil autoantibodies had neutropenia. The rare occurrence of cytopenias in association with these autoantibodies was possibly due to bone marrow compensation for antibody-mediated cell destruction, although other possible mechanisms are discussed.

Acute Disease↗
PubMed1985

Post-transfusion purpura responding to high dose intravenous IgG: further observations on pathogenesis.

A typical case of post-transfusion purpura (PTP) is described in a 61-year-old woman. Treatment with steroids corrected the purpuric manifestations, but the patient remained thrombocytopenic in spite of steroid therapy and plasma exchange. However, an intravenous infusion of high dose IgG led to a rapid and sustained increase in the platelet count. The mechanism of thrombocytopenia in PTP is still a matter for speculation, as the platelet specific antibody usually cannot be shown to react with the patient's own platelets in vitro. Therefore, the finding of a coexistent platelet specific IgM autoantibody in this patient, first detected during the early recovery phase, is of particular interest and suggests a possible autoimmune basis for the profound thrombocytopenia.

Autoantibodies↗
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

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↗
PubMed1981

Metabolic effects of acute and prolonged growth hormone excess in normal and insulin-deficient man.

The metabolic effects of acute (4 h) and prolonged (24 h) growth hormone excess at pathophysiological concentrations were studied by growth hormone administration to normal subjects with and without somatostatin induced insulin deficiency. Acute growth hormone excess produced mild hyperinsulinaemia, but blood glucose concentrations were unaltered whereas chronic growth hormone excess caused a small (0.5 mmol/l) but significant rise in overnight-fasting blood glucose concentration together with a similar rise in fasting insulin levels (Mean +/- SEM 9 +/- 1 v 4 +/- 1 mU/l, p less than 0.01). When insulin secretion was suppressed by somatostatin, a hyperglycaemic effect of acute growth hormone excess was unmasked, and the hyperglycaemic effect of chronic growth hormone excess was exaggerated. Acute growth hormone administration without somatostatin had a mild ketogenic action despite stimulated insulin secretion but no change in plasma non-esterified fatty acid or blood glycerol levels was observed. Somatostatin magnified the ketogenic effect of acute growth hormone excess, and unmasked a lipolytic action. Prolonged growth hormone excess had a lipolytic action that was increased by somatostatin, although the ketogenic effect of growth hormone was only seen during somatostatin induced insulin deficiency. The acute hyperglycaemic, lipolytic and ketogenic actions of growth hormone in normal subjects are limited by a compensatory rise in insulin secretion although with chronic exposure hyperglycaemic and lipolytic effects are seen. In insulin-deficient states, however, elevated growth hormone levels could be important in promoting hyperglycaemia and hyperketonaemia.

Adult↗
PubMedDate not supplied

X-ray surface dose measurements using TLD extrapolation.

Surface dose measurements in therapeutic x-ray beams are of importance in determining the dose to the skin of patients undergoing radiotherapy. Measurements were performed in the 6-MV beam of a medical linear accelerator with LiF thermoluminescence dosimeters (TLD) using a solid water phantom. TLD chips (surface area 3.17 x 3.17 cm2) of three different thicknesses (0.230, 0.099, and 0.038 g/cm2) were used to extrapolate dose readings to an infinitesimally thin layer of LiF. This surface dose was measured for field sizes ranging from 1 x 1 cm2 to 40 x 40 cm2. The surface dose relative to maximum dose was found to be 10.0% for a field size of 5 x 5 cm2, 16.3% for 10 x 10 cm2, and 26.9% for 20 x 20 cm2. Using a 6-mm Perspex block tray in the beam increased the surface dose in these fields to 10.7%, 17.7%, and 34.2% respectively. Due to the small size of the TLD chips, TLD extrapolation is applicable also for intracavity and exit dose determinations. The technique used for in vivo dosimetry could provide clinicians information about the build up of dose up to 1-mm depth in addition to an extrapolated surface dose measurement.

Electrons↗
PubMedDate not supplied

Dosimetry of 6-MV x-ray beam penumbra.

The measurement of x-ray beam dose profiles in the penumbral region, using silicon diode, ionization chamber, TLD, and film dosimetry, has been investigated for a 6-MV beam defined by independent collimators. Penumbral width (80%-20%) at dmax, as measured by diode, film, and TLD was found to be 3.6, 3.6, and 3.4 mm, respectively. These results reflect the relative sensitive widths of each of the measurement systems (2.5, 2.0, and 1.0 mm, respectively). An empirical forming function was used to relate the penumbral shape measured with a finite-sized detector to that which would be measured with a point detector, the width of the point detector penumbra calculated from the diode penumbra is 3.4 mm, indicating that the TLD rods are a good approximation to a point detector. An alternative method of determining the width of a point detector penumbra is to extrapolate the penumbral widths obtained using two or more detectors of sensitive width. With this method, using Farmer and RK ionization chambers, a point detector penumbra width of 3.1 mm is obtained. An EGS4 Monte Carlo simulation, where a point source was assumed, gave a penumbral width of 2.8 mm. Negligible differences between the penumbra of beams defined by symmetric and asymmetric collimators was observed.

Biophysical Phenomena↗
PubMedDate not supplied

The penumbra of a 6-MV x-ray beam as measured by thermoluminescent dosimetry and evaluated using an inverse square root function.

Data on the dose distribution in the penumbral region of megavoltage x rays are of importance for most radiotherapy planning systems. For medical linear accelerators the distance between the points representing 20% and 80% of the central axis dose (20/80) is typically only a few millimeters. To achieve good spatial resolution a radiation detector with small physical size has to be used for penumbra measurements. The penumbra in a 6-MV therapeutic x-ray beam was investigated for field sizes of 10 x 10 cm2 and 20 x 20 cm2 at depth of maximum dose (dmax = 1.5 cm) and at 10-cm depth in a solid water phantom. In addition, the field edge of an independent jaw driven to the center of the axis of the primary collimator was investigated. LiF thermoluminescent (TL) ribbons and rods were used embedded in solid water in different geometries resulting in relative detector sizes of 1, 3.1, and 6 mm. A forming function based on an inverse square root function was used to fit the experimental penumbra measurements. For the asymmetric field an amendment to the function is proposed to give a better fit for the experimental data. From the penumbra measured with the three different detector sizes, a penumbra can be extrapolated for an infinitesimal small detector. The extrapolated penumbral width (20/80) was found to be 2.3, 3.2, and 2.7 mm at dmax for the 10 x 10-cm2 symmetric, 10 x 10-cm2 asymmetric, and 20 x 20-cm2 field sizes, respectively. The 20/80 values at 10-cm depth in the solid water phantom for the same radiation fields were 4.2, 4.3, and 4.1 mm, respectively.

Biophysical Phenomena↗