Prenatal diagnosis of Fanconi's anemia.
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Anemia, Aplastic↗
Biomedical subjects
A D Heyns
Publications and source records attributed to A D Heyns.
IgD myeloma. A report of 4 new cases.
IgD myeloma is relatively rare. We wish to report 4 new cases investigated in this laboratory during the past 18 months. Extra-osseous involvement was present in 2 patients. Total serum protein concentrations were normal in all cases, while serum paraprotein peaks were inconspicuous in 2 patients. Bence Jones proteinuria of the lambda type was present in all, while free light chains could be detected in the blood in 3 patients.
Aged↗
Kinetics and fate of indium 111 oxine-labeled platelets in patients with aortic aneurysms.
The survival and sites of sequestration of indium 111 oxine-labeled autologous platelets were studied quantitatively in six patients with aortic aneurysms. The in vivo distribution was quantitated daily with a scintillation camera and a computer-assisted imaging system. Data of platelet survival curves were fitted to a gamma function model. Mean platelet survival was shortened and the disappearance curves were exponential in all but two patients who had normal platelet survival. Platelet radioactivity in the aneurysm was 5.1 +/- 3% of whole-body radioactivity at the end of platelet survival. Platelet were sequestered in the spleen, liver, and bone marrow. Accumulation of platelets, presumably due to microembolization, was prominent in the lower limbs. This indicates that although platelets were deposited in the aneurysm, many are damaged and are eventually sequestered in the reticuloendothelial system.
Aged↗
Kinetics and sites of destruction of 111Indium-oxine-labeled platelets in idiopathic thrombocytopenic purpura: a quantitative study.
Kinetics and quantification of the sites of destruction of 111-Indium-oxine-labeled autologous platelets were investigated in eight patients with idiopathic thrombocytopenic purpura. The mean platelet count was 17 +/- 9 X 10(9)/liter; platelets were separated by differential centrifugation and labeled with 5.6 +/- 2.5 MBq 111In. Whole body and organ 111In-platelet distribution was quantitated with a scintillation camera and a computer-assisted imaging system acquisition matrix. Areas of interest were selected with the computer and organ 111In-radioactivity expressed as a percentage of whole body activity. Mean platelet survival was 49.5 +/- 29.6 hr and the survival curves were exponential. Equilibrium percentage organ 111In-radioactivity was (normal values in parentheses): spleen 33.7 +/- 8.8 (31.1 +/- 10.2); liver 16.1 +/- 9.5 (13.1 +/- 1.3); thorax 22.8 +/- 3.7 (28.2 +/- 5.6). Percentage organ 111In-activity at the time when labeled platelets had disappeared from the circulation was: spleen 44.5 +/- 16.4 (40 +/- 16); liver 16.0 +/- 11.5 (32.4 +/- 7.2); thorax 19.7 +/- 6.0 (17.7 +/- 10.3). Thorax activity corresponds to bone marrow radioactivity. Three patterns of platelet sequestration were evident. Three patients had mainly splenic sequestration, two mainly hepatic sequestration, and three diffuse reticuloendothelial system sequestration with a major component of platelets destroyed in the bone marrow. Splenectomy was performed in two patients. The pattern of 111In-platelet sequestration was not predictive of response of glucocorticoid therapy or indicative of the necessity for splenectomy. Quantitative 111In-labeled autologous platelet kinetic studies provide a new tool for the investigation of platelet disorders.U
Adolescent↗
Quantification of the distribution of 111In-labelled platelets in organs.
A single and practical approach to the in vivo quantification of 111indium-oxine labelled blood platelets with a scintillation camera and computer assisted imaging system was evaluated. Radioactivity of the 172 and 247 keV energies was measured in a phantom at various source distances from the collimator and the accuracy of anterior and posterior mode measurements compared with that of the geometrical mean (GM) method, with and without correction for Compton scatter (CS). Organ radioactivity, expressed as a percentage of whole body radioactivity, was determined in vivo in five baboons and the accuracy of the methods verified by post mortem quantification in the animals. Measurements in the anterior mode significantly overestimates hepatic and underestimates splenic radioactivity; posterior mode quantification reverses these results. Correction with the GM method made the accuracy and reproducibility very acceptable. Further correction for anterior-posterior attenuation and/or CS did not improve results materially. The GM method could readily be applied in five human subjects. This study showed that the GM method is an accurate and practical method for the in vivo quantification of organ and regional distribution of 111In-labelled platelets.
Animals↗
The influence of the 'collection injury' on the survival and distribution of indium-111-labeled canine platelets.
The extent of the 'collection injury' sustained by platelets during labelling with In-111-oxine was investigated in three matched pairs of beagle dogs. The influence of the procedure on the survival, kinetics, in vivo distribution and fate of the labelled platelets was determined by serial blood sampling and quantitative computerized scintillation camera studies. Injured labelled platelets were removed in the matched dog acting as a biological filter. The survival, distribution and fate of the 'filtered' and 'unfiltered' platelets were compared. The mean platelet lifespan of the 'filtered' and 'unfiltered' platelets did not differ significantly, but the shape of the survival curve of the filtered platelets fitted a linear function more closely than that of the unfiltered platelets. Radioactivity in the different organs and regions was serially quantitated and expressed as a percentage of whole body radioactivity. Splenic and hepatic radioactivity of filtered and unfiltered platelets did not differ significantly at equilibrium or at the end of platelet lifespan. It is concluded that the currently employed isolation and labelling techniques for platelets are suitable for quantitative in vivo studies with a computerized scintillation camera system. The shape of platelet survival curves should, however, be interpreted with some caution as it may be influenced by these procedures.
Animals↗
Quantification of in vivo distribution of platelets labeled with indium-111 oxine.
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Animals↗
A quantitative study of indium-111-oxine platelet kinetics in acute and chronic renal transplant rejection.
Thirteen patients were investigated on 22 occasions at times varying from 1 day to 10 years after living family donor or cadaver renal transplantation. Platelet survival in the circulation, and in vivo platelet distribution and sites of deposition and sequestration was quantitatively determined with Indium-111-oxine (In-111-oxine) labelled platelets and a scintillation camera interfaced with a computer assisted imaging system. In all patients platelet survival was shortened and the platelet survival curve exponential. In patients with no evidence of transplant rejection and those with chronic rejection, there was no measurable or visible accumulation of labelled platelets in the kidney. The sequestration pattern of In-111 labelled platelets at the end of platelet life span was within normal limits and located in the reticuloendothelial system. In those patients with acute transplant rejection, platelet survival was shortened. Labelled platelets accumulated in the kidney: this was clearly visualized on scintigraphy and reflected by a significant increase in the radioactivity count density of the kidney. Platelets not deposited in the transplant were sequestrated in the reticuloendothelial system. This study demonstrates the diagnostic value of In-111 labelled platelet kinetics in the investigation of acute renal failure after renal transplantation. This investigation appears of limited clinical value in chronic rejection.
Adult↗
Unsuitability of evacuated tubes for monitoring heparin therapy by activated partial thromboplastin time.
Activated partial thromboplastin times (APTT) for monitoring heparin therapy for venous thromboembolism tended to be inappropriately short if blood was collected in commercially available evacuated glass tubes. Five types of evacuated tubes marketed under the trade names Vacutainer and Venoject were examined. The APTT of heparinized blood collected in these tubes correlated poorly (r = 0.04 to 4 = 0.25) with that of blood samples from the same patients collected in plastic tubes. Most of the evacuated tube APTT were shorter than that of blood collected in plastic or siliconised glass tubes, but the results were unpredictable and varied from tube to tube and from batch to batch. This effect on heparin is apparently due to an unidentified substances which is eluted from the rubber stoppers of the tubes. Heparin control according to the APTT blood collected in these evacuated tubes is hazardous.
Blood Coagulation Tests↗
Kinetics and sites of sequestration of indium 111-labeled human platelets during cardiopulmonary bypass.
A new approach for the study of the kinetics and quantification of the in vivo and ex vivo sites of sequestration of platelets during cardiopulmonary bypass (CPB) is described. Autologous platelets of four patients were labeled with 111In-oxine and reinfused on the day prior to CPB for coronary artery bypass grafting. Changes in blood 111In-labeled platelet radioactivity and blood platelet counts were monitored during the operation. In vivo 111In-labeled platelet redistribution was quantified with a scintillation camera and a computer-assisted imaging system before and after CPB. Sequestration of 111In-labeled platelets in the bubble oxygenator was measured. 111In-labeled platelet activity in the blood decreased by 46% +/- 5% within 5 minutes of CPB, but this decrease was mostly due to hemodilution; the true loss of platelets from the circulation was 13% +/- 4%. Intraoperatively, whole body 111In activity decreased by oxygenator 10.8% +/- 1.3% of administered platelets were sequestered, especially in the innermost active layers of the defoaming mesh of the bubble oxygenator. Mean survival time of circulating platelets was 58 +/- 8 hours and fitted an exponential function best. The bleeding time increased to 40 minutes during operation and returned to normal within 24 hours. During operation 111In-labeled platelets accumulated somewhat in the liver (10.7%) but not in the spleen, thorax, or head. In the 48 hours after operation, platelets were sequestered mainly in the liver. The scintillation camera with computer-assisted imaging allows in vivo quantitative studies of platelet kinetics of a type which has not been possible with previous techniques.
Blood Platelets↗
[Severe Rh-isoimmunization and intensive plasma exchange during pregnancy].
Intensive plasma exchange was performed with a continuous-flow centrifuge in 2 pregnant women severely immunized to the Rh(D) iso-antigen. Plasma exchange was started at 17 and 18 weeks of gestation and a total of 220 litres and 185 litres plasma was replaced with plasma protein fraction over a period of 14 and 12 weeks respectively. There was a marked lowering of the anti-D antibody concentration in one patient, and the expected increase in antibody level during pregnancy was prevented in the other. Serum IgG and IgA levels were decreased by the exchange, but the continuous hypogammaglobulinaemia had no adverse effects. The serum IgM concentration was also lowered, but plasma levels returned to normal between plasma exchange procedures. The successful outcome in both cases suggests that intensive plasma exchange may reduce fetal haemolysis and that it may be an useful adjunct to amniocentesis, intra-uterine transfusions and premature delivery in the prenatal management of haemolytic disease in newborn infants.
Adult↗
Kinetics and fate of (111)Indium-oxine labelled blood platelets in asplenic subjects.
The survival, tissue distribution and fate of (111)Indium-oxine labelled autologous platelets was studied in four asplenic subjects with serial blood sampling, scintillation camera and computer-assisted imaging. Mean (111)In-platelet recovery in the circulation was 89 /+- 13% (/+- 1 SD). Platelet survival curves fitted a linear function best and was 238 /+0 41 h. The shape of the survival curves of normal and asplenic subjects differed: in the asplenic subjects the curve was linear whereas that of normal subjects was significantly more curvilinear if analyzed by least squares computer fitting to a gamma function. Early hepatic (111)In-activity was significant and transient and ascribed to the "collection injury". As labelled platelets disappeared from the circulation, (111)In-activity in the liver increased progressively and linearly to reach 42.5 /+- 14.1% of whole body activity at 240 h. Radioactivity also accumulated in the bone marrow, but could not be demonstrated in the vasculature of the lower limbs. These results would indicate that in asplenic subjects the majority sites of destruction of senescent platelets are the liver and bone marrow.
Adult↗
Kinetics and in vivo redistribution of (111)Indium-labelled human platelets after intravenous protamine sulphate.
The pathogenesis of thrombocytopenia induced by intravenous protamine sulphate was studied in six patients who underwent cardiopulmonary bypass surgery, and in three normal volunteers. Autologous platelets were labelled with (111)Indium-oxine. Platelet lifespan was determined. In vivo (111)In-platelet localization, organ redistribution and sites of destruction were quantitated with a scintillation camera and a computer-assisted imaging system. Protamine induced a transient thrombocytopenia, maximal 5-10 min after injection, and 30-40 min in duration. . The thrombocytopenia was accompanied by a transient accumulation of platelets in the liver. The splenic platelet pool remained unaltered and no platelets accumulated in the lungs. Platelet survival, measured in two volunteers, was slightly longer than normal and fitted a linear function best. There was a severe transient neutropenia during the period of thrombocytopenia. We conclude that protamine-induced thrombocytopenia is caused by hepatic accumulation of "activated" platelets or platelet aggregates, the process is reversible, and in the two normal volunteers studied, platelet survival was not affected.
Blood Platelets↗
A South African family with antithrombin III deficiency.
Antithrombin III is the most important natural inhibitor of coagulation. Reduced levels of antithrombin III are a well-documented cause of hypercoagulability. Several families have been described with hereditary antithrombin III deficiency, including one from South Africa. We report a second South African family with this defect.
Antithrombin III↗
Metamorphosis of chronic granulocytic leukaemia, lytic bone lesions and hypercalcaemia. A case report.
Chronic granulocytic leukaemia may undergo metamorphosis characterized by diffuse granulocytic sarcomas resulting in lytic bone lesions and hypercalcaemia. A patient with this rare complication is reported.
Adult↗
Preparation of a viable population of indium-111-labelled human blood platelets.
Factors influencing labelling of human platelets with 111Indium-8-hydroxyquinoline ([111In]-oxine) in a physiological saline medium were investigated. The efficiency of labelling is influenced by time of incubation, concentration of oxine, and pH of the incubating medium. It was found that a viable platelet population could be labelled under the following conditions: (1) centrifugation of platelet rich plasma in polystyrene conical tubes at 800 g for 15 min; (2) resuspension of the platelet pellet in saline, pH 5.5; (3) incubating for 30 min at 22 degrees C with [111In]-oxine at a concentration of 6.25 mg oxine/litre platelet suspension; (4) washing once with platelet poor autologous plasma (PPP); and (5) finally resuspending the platelets in PPP. The labelled platelets aggregated normally with collagen and ADP. Electron microscopy, done immediately after labelling, showed internal organelle reorganization characteristic of activated platelets. These ultrastructural features were reversible on incubation in PPP at 37 degrees C for 30 min. The 111In is not released from aggregated platelets and the label does not elute from incubated platelets for at least five hr. We conclude that human platelets thus labelled are suitable for in vivo kinetic studies.
Blood Platelets↗
Kinetics, distribution and sites of destruction of 111indium-labelled human platelets.
The survival, tissue distribution and fate of 111In-oxine labelled autologous platelets in six normal humans were studied with serial blood sampling, scintillation camera and computer-assisted imaging, whole body profile scanning, and rectilinear scanning. 111In-platelets recovery in the circulation was 72+/-16% and survival was 216+/-17 h. Platelet survival curves fitted a linear function best. Initially platelets pooled rapidly in the spleen as a single exponential function, and at 90 min 26% of the injected 111In was located in this organ. Early hepatic uptake was also significant and at 90 min constituted 16% of total body 111In-activity. As labelled platelets disappeared from the circulation there was a threefold increase of radioactivity in the liver to reach 39% of whole body activity at 216 h. Radioactivity also increased significantly in the spleen (33.3% at 216 h). There was significant residual radioactivity in the thoracic and lower abdominal regions at 216 h, suggesting that platelets are also sequestered in the bone marrow. Radioactivity in the lower limbs almost disappeared with time (0.7% at 216 h), indicating that utilization of platelets in the peripheral vasculature is not marked in normal subjects.
Adult↗
Kinetics, distribution, and sites of destruction of canine blood platelets with In-111 oxine.
In five normal dogs we have studied the survival, tissue distribution, and fate of autologous platelets labeled with indium- 111 oxine. The methods include blood sampling, computer-assisted scintigraphy, and whole-body profile scanning. Mean In- 111-platelet recovery in the circulation was 45 +/- 22.5 (s.d.) and survival 124.6 +/- 10.5 hr. Platelet survival curves fitted a linear function best. Initially platelets pooled rapidly in the spleen with a single exponential function, and at zero-time equilibrium (35 +/- 4)% of the injected In- 111 was located in this organ. Early hepatic uptake was also significant, and constituted (20 +/- 4)% of total-body radioactivity. As labeled platelets disappeared from the circulation, In- 111 activity in the spleen increased progressively and linearly to reach (59 +/- 9)% of the body activity at 120 hr. Hepatic radioactivity decreased with time but to a lesser extent than that of the heart. The results indicate that in the dog the major site of destruction of platelets is the spleen, with the liver playing a less important role.
Animals↗