Lactate dehydrogenase in sickle cell disease

Lactate dehydrogenase (LDH) activity is elevated in many pathological states. Interest in LDH activity in sickle cell disease (SCD) has developed out of an increased comprehension of the pathophysiological process and the clinical course of the disease. Elevated LDH activity in SCD comes from variou...

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Bibliographic Details
Published in:Clinica chimica acta 2016-07, Vol.458, p.99-102
Main Authors: Stankovic Stojanovic, Katia, Lionnet, François
Format: Article
Language:English
Subjects:
Anemia, Sickle Cell - diagnosis
Anemia, Sickle Cell - enzymology
Hemolysis
Humans
L-Lactate Dehydrogenase - metabolism
Lactate dehydrogenase
Prognosis
Sickle cell disease
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Summary:Lactate dehydrogenase (LDH) activity is elevated in many pathological states. Interest in LDH activity in sickle cell disease (SCD) has developed out of an increased comprehension of the pathophysiological process and the clinical course of the disease. Elevated LDH activity in SCD comes from various mechanisms, especially intravascular hemolysis, as well as ischemia-reperfusion damage and tissular necrosis. Intravascular hemolysis is associated with vasoconstriction, platelet activation, endothelial damage, and vascular complications. LDH has been used as a diagnostic and prognostic factor of acute and chronic complications. In this review we have evaluated the literature where LDH activity was examined during steady-state or acute conditions in SCD. •Lactate dehydrogenase is a marker of intravascular hemolysis in SCD associated with vascular damage.•During acute vaso-occlusive crisis, LDH has been correlated with the severity of pain and clinical state worsening.•Very high LDH activity during acute painful vaso-occlusive crisis should suggest specific life-threatening complications.•Elevated LDH activity at steady-state is a predicting component of the “hyper hemolytic phenotype”.•A decline of LDH level during hydroxyurea therapy is associated with better survival.
ISSN:0009-8981
1873-3492
DOI:10.1016/j.cca.2016.04.035