An improved method for the quantification of the in vivo kinetics of a representative population of 111In-labelled human platelets

Wessels, P.; Heyns, A. du P.; Pieters, H; Mg, Lötter; Badenhorst, P. N.

doi:10.1007/bf00252745

Cited by 28 publications

(19 citation statements)

References 23 publications

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“…Uptake values on the 1st day after administration of the labelled platelets were found to be 7.4%_+ 3.0% in the liver and 43.2% _+ 14.8% in the spleen. Comparing these results with values in normal humans (Wessels et al 1985), it may be concluded that the hepatic uptake of labelled platelets is decreased in liver cirrhosis, while the splenic uptake is increased. Uptake values on the 7th day, when the state of platelet destruction was known, were found to be 13.6% _+ 8.2% in the liver and 53.7% ± 14.3% in the spleen.…”

Section: Discussionmentioning

confidence: 65%

“…Liver cirrhosis if often associated with anemia, and venesection of such a large volume of blood is therefore ethically unacceptable. Tharkur et al (1976) reported a new technique of labelling platelets with indium-111 oxine, in which only a small amount of blood was required because of a high labelling ratio, and several studies have been performed using this technique (Dewanjee et al 1981;Wessels et al 1985;Toghill and Green 1983).…”

Section: Introductionmentioning

confidence: 99%

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Mechanism of thrombocytopenia in liver cirrhosis: kinetics of indium-111 tropolone labelled platelets

1993

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Using indium-111 tropolone-labelled platelets, a study of platelet kinetics was performed on the basis of the relationship between platelet count, platelet survival time, platelet dynamics, platelet-associated immunoglobulin G (PA-IgG) and splenic volume in 31 patients with liver cirrhosis and a platelet count of less than 100 x 10(9)/l. The mean platelet count was 46.6 +/- 25.3 x 10(9)/l, and the mean platelet survival time was 6.50 +/- 1.33 days. The mean uptake into the spleen was 43.2% +/- 14.8% on the 1st day, and 53.7% +/- 14.3% on the 7th day. The mean PA-IgG level was 107.6 +/- 66.0 ng/10(7) platelets in five patients with chronic active hepatitis who were studied as controls, the mean platelet count was 197 +/- 30 x 10(9)/l, the mean platelet survival time 9.33 +/- 0.78 days, and the mean PA-IgG 21.2 +/- 2.9 ng/10(7) platelets. The former two parameters were significantly higher (P < 0.05), and the latter significantly lower (P < 0.05). In liver cirrhosis, the platelet count showed a positive correlation with the platelet survival time and a negative correlation with PA-IgG and the splenic volume. These results suggest that the increases in both the splenic platelet pool and platelet destruction in the spleen through immunological mechanisms may influence thrombocytopenia in liver cirrhosis.

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Section: Discussionmentioning

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Mechanism of thrombocytopenia in liver cirrhosis: kinetics of indium-111 tropolone labelled platelets

1993

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“…1 -9 Although these measurements are quantitative and objective, they are not readily interpreted in terms of rates of thrombus formation and dissolution. For example, platelet survival studies, which reflect all mechanisms of platelet utilization, cannot discriminate the interdependent processes of sensecent platelet removal, 16 normal platelet utilization for the maintenance of vascular integrity, 10 and additional components of platelet destruction due to vascular disease. Similarly, measurements of localized platelet depo-sition by scintillation camera imaging or other methods may have little relation to overall platelet turnover.…”

mentioning

confidence: 99%

Analysis of indium-111 platelet kinetics and imaging in patients with aortic grafts and abdominal aortic aneurysms.

et al. 1990

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To quantitatively characterize processes of platelet thrombus formation in vivo, the kinetics and incorporation into thrombus of autologous ln-111-labeled platelets were compared in six patients with aortic aneurysms and in seven patients with prosthetic aortic grafts. Although platelet survival was comparably shortened in both patient groups (mean, 5.8 days), the maximum radioactivity (percentage of whole body radioactivity) as determined by gamma camera imaging was higher in the aneurysms than in the grafts (3.3%±1.6% vs. 1.6%±1.1%, p=0.05). Maximum ln-111 uptake was also attained more quickly in the aneurysm patients (2.3±0.8 days vs. 3.5±1.3 days; p=0.07). The experimental platelet kinetic and imaging data were subsequently evaluated by compartmental analysis to estimate both normal and disease-related components of platelet destruction. This analysis indicated that deposited platelet radioactivity had a longer residence time on grafts (2.9±1.7 days vs. 1.4±0.9 days, p=0.07) but accumulated at a faster rate in aneurysms (5.0%±3.4% per day vs. 1.4%±0.9% per day, p=0.02). As determined by imaging, only a proportion of increased platelet destruction was specifically due to the aneurysms (55%±38%) or grafts (17%±11%, p=0.03). This result indicates additional components of platelet destruction unrelated to graft and aneurysm thrombus formation which, in some graft patients, may reflect a greater severity of vascular disease or other mechanisms causing a preferential shortening of platelet survival. Thus, the analytical approach described may be a useful one for discriminating components of in vivo platelet utilization including platelet removal due to normal hemostatic and senescent mechanisms, localized thrombus formation, and more generalized vascular disease.

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“…Autologous platelets were labelled with " 'Intropolone and the MPLS estimated as previously described (19,20). Radioactivity of blood samples in EDTA was determined in a well-type scintillation counter (Packard Auto-gamma 5650, United Technologies, Packard).…”

Section: Platelet Kineticsmentioning

confidence: 99%

“…This is an indirect estimate of platelet production. The in vivo distribution and sites of sequestration of labelled platelets was quantified as described in detail (20,23). Briefly, anterior and posterior images with and without a posterior and anterior placed standard radioactivity source were acquired of the thorax and abdomen using a large field of view scintillation camera interfaced with a data processing system.…”

Section: Platelet Kineticsmentioning

confidence: 99%

Kinetics of indium‐ 111‐labelled platelets in HIV‐infected patients with and without associated thrombocytopaenia

Wyk¹,

Kotzé²,

Heyns³

1999

European J of Haematology

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Seven to 12% of HIV‐infected patients have thrombocytopaenia. The pathophysiology of the thrombocytopaenia is not clear. It has been variously suggested that it may be caused by an increased peripheral platelet destruction, a defect in platelet production, or by a combination of these. The aim of the study was to elucidate the pathogenesis of HIV‐associated thrombocytopaenia. We determined the mean platelet life span (MPLS) and calculated the turnover of autologous indium‐111‐labelled platelets in 17 HIV‐positive patients, seven with thrombocytopaenia. The sites of sequestration of labelled platelets were quantified. The thrombocytopaenic patients had a very short MPLS (3.0±3.8 h) and a marked increase in platelet production (18.2±12.6× 109/l/h). The majority of these patients (5 of 7) had excessive sequestration of platelets in the spleen. Five of the patients with a normal blood platelet count had a shortened MPLS (109±23 h) and increased platelet turnover (3.8±1.2×109/l/h), i.e. the increased peripheral platelet destruction was compensated for by increased platelet production. The other five patients with a normal platelet count had normal MPLS (195±11 h) and slightly increased platelet production (2.5±0.6× 109/l/h). We conclude that patients with HIV‐associated thrombocytopaenia have increased peripheral platelet destruction. Platelet production is elevated but is insufficient to maintain a normal peripheral platelet count. In these patients platelets are predominantly sequestrated in the spleen. Patients with HIV infection and a normal blood platelet count may also have increased platelet production. This may be an early subclinical phase in the development of full‐blown HIV‐associated thrombocytopaenia.

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An improved method for the quantification of the in vivo kinetics of a representative population of 111In-labelled human platelets

Cited by 28 publications

References 23 publications

Mechanism of thrombocytopenia in liver cirrhosis: kinetics of indium-111 tropolone labelled platelets

Mechanism of thrombocytopenia in liver cirrhosis: kinetics of indium-111 tropolone labelled platelets

Analysis of indium-111 platelet kinetics and imaging in patients with aortic grafts and abdominal aortic aneurysms.

Kinetics of indium‐ 111‐labelled platelets in HIV‐infected patients with and without associated thrombocytopaenia

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