Evolution of laboratory parameters during sickle cell painful crisis

Evidence compatible with dense red cell sequestration without thrombosis

Henny H. Billett, R. L. Nager, M. E. Fabry

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

We find that during 51 episodes of sickle cell painful crisis indirect bilirubin fell 52% from its steady state value of 2.3 ± 1.9 mg% to a value of 1.1 ± 0.37 mg% at the end of crisis (p < .00000085). The indirect bilirubin decline correlates with a decrease in the dense sickle cells during crisis (r = .31, p < .0009). During steady state, both indirect bilirubin and lactic acid dehydrogenase correlate significantly with number of dense red cells (r = .62, p < .000002 and r = .32, p < .02 respectively). Platelet counts, β-thromboglobulin, Platelet Factor 4, and Fibrinopeptide A levels all were elevated during steady state and did not change during the evolution of crisis. These data demonstrate that elevated indices usually associated with platelet activation are a feature of the steady state of sickle cell disease but argue against thrombosis as a factor in the progression of a sickle cell painful crisis episode. The parallel decline of both dense cells and bilirubin during painful crisis indicates that the disappearance of dense cells during crisis is not caused by hemolysis and supports the hypothesis that dense red cell sequestration, in the absence of evidence of thrombosis, is an intrinsic component of the evolution of sickle cell painful crisis.

Original languageEnglish (US)
Pages (from-to)293-298
Number of pages6
JournalAmerican Journal of the Medical Sciences
Volume296
Issue number5
StatePublished - 1988

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Thrombosis
Bilirubin
Fibrinopeptide A
Platelet Factor 4
Platelet Activation
Sickle Cell Anemia
Hemolysis
Platelet Count
Lactic Acid
Oxidoreductases

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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title = "Evolution of laboratory parameters during sickle cell painful crisis: Evidence compatible with dense red cell sequestration without thrombosis",
abstract = "We find that during 51 episodes of sickle cell painful crisis indirect bilirubin fell 52{\%} from its steady state value of 2.3 ± 1.9 mg{\%} to a value of 1.1 ± 0.37 mg{\%} at the end of crisis (p < .00000085). The indirect bilirubin decline correlates with a decrease in the dense sickle cells during crisis (r = .31, p < .0009). During steady state, both indirect bilirubin and lactic acid dehydrogenase correlate significantly with number of dense red cells (r = .62, p < .000002 and r = .32, p < .02 respectively). Platelet counts, β-thromboglobulin, Platelet Factor 4, and Fibrinopeptide A levels all were elevated during steady state and did not change during the evolution of crisis. These data demonstrate that elevated indices usually associated with platelet activation are a feature of the steady state of sickle cell disease but argue against thrombosis as a factor in the progression of a sickle cell painful crisis episode. The parallel decline of both dense cells and bilirubin during painful crisis indicates that the disappearance of dense cells during crisis is not caused by hemolysis and supports the hypothesis that dense red cell sequestration, in the absence of evidence of thrombosis, is an intrinsic component of the evolution of sickle cell painful crisis.",
author = "Billett, {Henny H.} and Nager, {R. L.} and Fabry, {M. E.}",
year = "1988",
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journal = "American Journal of the Medical Sciences",
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T1 - Evolution of laboratory parameters during sickle cell painful crisis

T2 - Evidence compatible with dense red cell sequestration without thrombosis

AU - Billett, Henny H.

AU - Nager, R. L.

AU - Fabry, M. E.

PY - 1988

Y1 - 1988

N2 - We find that during 51 episodes of sickle cell painful crisis indirect bilirubin fell 52% from its steady state value of 2.3 ± 1.9 mg% to a value of 1.1 ± 0.37 mg% at the end of crisis (p < .00000085). The indirect bilirubin decline correlates with a decrease in the dense sickle cells during crisis (r = .31, p < .0009). During steady state, both indirect bilirubin and lactic acid dehydrogenase correlate significantly with number of dense red cells (r = .62, p < .000002 and r = .32, p < .02 respectively). Platelet counts, β-thromboglobulin, Platelet Factor 4, and Fibrinopeptide A levels all were elevated during steady state and did not change during the evolution of crisis. These data demonstrate that elevated indices usually associated with platelet activation are a feature of the steady state of sickle cell disease but argue against thrombosis as a factor in the progression of a sickle cell painful crisis episode. The parallel decline of both dense cells and bilirubin during painful crisis indicates that the disappearance of dense cells during crisis is not caused by hemolysis and supports the hypothesis that dense red cell sequestration, in the absence of evidence of thrombosis, is an intrinsic component of the evolution of sickle cell painful crisis.

AB - We find that during 51 episodes of sickle cell painful crisis indirect bilirubin fell 52% from its steady state value of 2.3 ± 1.9 mg% to a value of 1.1 ± 0.37 mg% at the end of crisis (p < .00000085). The indirect bilirubin decline correlates with a decrease in the dense sickle cells during crisis (r = .31, p < .0009). During steady state, both indirect bilirubin and lactic acid dehydrogenase correlate significantly with number of dense red cells (r = .62, p < .000002 and r = .32, p < .02 respectively). Platelet counts, β-thromboglobulin, Platelet Factor 4, and Fibrinopeptide A levels all were elevated during steady state and did not change during the evolution of crisis. These data demonstrate that elevated indices usually associated with platelet activation are a feature of the steady state of sickle cell disease but argue against thrombosis as a factor in the progression of a sickle cell painful crisis episode. The parallel decline of both dense cells and bilirubin during painful crisis indicates that the disappearance of dense cells during crisis is not caused by hemolysis and supports the hypothesis that dense red cell sequestration, in the absence of evidence of thrombosis, is an intrinsic component of the evolution of sickle cell painful crisis.

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