Lactate dehydrogenase isoenzyme 3 and hemolysis in sickle cell anemia: a possible correlation?

Mecabô, Grazielle; Yamamoto, Masahiro; Biassi, Thaís Priscila; Figueiredo, Maria Stella

doi:10.1182/blood-2015-04-641522

Cited by 5 publications

(5 citation statements)

References 9 publications

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“…LDH activity at steady state in patients with SCD is usually elevated, but the level depends on the type of SCD and on the type of disease-modifying treatments the patients are receiving 3 . As reported, long-term hydroxyurea treatment reduced LDH activity 13 . LDH significantly increases during acute painful VOC compared with steady state, whatever the severity of complications 14 .…”

Section: Discussionsupporting

confidence: 69%

Lactate dehydrogenase and hemolysis index to predict vaso-occlusive crisis in sickle cell disease

Feugray,

Dumesnil,

Grall

et al. 2023

Sci Rep

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Sickle cell disease (SCD) is an inherited hemoglobinopathy disorder associated with chronic hemolysis. A major complication is vaso-occlusive crisis (VOC), associating frequent hospitalization, morbidity and mortality. The aim of this study was to investigate whether hemolysis biomarkers were able to predict VOC risk in adult patients with SCD requiring hospitalization within 1 year. This single-center prospective study included adult patients with SCD at steady state or during VOC. A total of 182 patients with SCD were included, 151 at steady state and 31 during VOC. Among the 151 patients at steady state 41 experienced VOC within 1 year (median: 3.0 months [2.0–6.5]). We observed an increase of lactate dehydrogenase (LDH) (p = 0.01) and hemolysis index (HI) (p = 0.0043) during VOC compared to steady state. Regarding patients with VOC requiring hospitalization, LDH (p = 0.0073) and HI (p = 0.04) were increased. In unadjusted logistic regression, LDH > median (> 260 U/L) (RR = 3.6 [1.29–10.88], p = 0.0098) and HI > median (> 8 UA/L) (RR = 3.13 [1.91–5.33]; p < 0.001) were associated with VOC. The association of LDH > 260 U/L and HI > 12 UA/L presented a sensitivity of 90%, and a specificity of 72.9% to predict VOC. The association of LDH and HI cut-off was able to predict VOC risk in SCD.

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Section: Discussionsupporting

confidence: 69%

Lactate dehydrogenase and hemolysis index to predict vaso-occlusive crisis in sickle cell disease

Feugray,

Dumesnil,

Grall

et al. 2023

Sci Rep

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“…Expense, insurance approval and clinical availability, however, may hamper its availability on a routine basis. Moreover and unlike previous reports, 2,3 Mecabo et al 1 found that hydroxyurea (HU) did not show reduction of LDH or other hemolytic parameters in patients with SCA taking HU. Lactate dehydrogenase-3, however, was decreased in patients with SCA taking HU.…”

Section: To the Editorcontrasting

confidence: 67%

“…The interesting letter to the editor by Mecabo et al 1 sheds new perspective on the correlation of lactate dehydrogenase (LDH) and hemolysis in patients with sickle cell anemia (SCA). Their data show that LDH-3 seems to be the isoenzyme that is correlated with hemolysis.…”

Section: To the Editormentioning

confidence: 99%

“…4 The mean or median levels in patients with hemolysis or hyperhemolysis are usually < 1000 U/L. 1,4 Levels of LDH > 1000 U/L suggest additional sources of the enzyme with or without hemolysis or hyperhemolysis especially if other parameters of hemolysis are absent. Such high levels of LDH could be a sign of co-existent tissue damage due to SCA.…”

Section: To the Editormentioning

confidence: 99%

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Clinical Utility of Lactate Dehydrogenase in Determining the Severity of Hemolysis in Sickle Cell Anemia

Ballas

2015

Am J Clin Pathol

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“…In SCA, the RBC survival range is two to twenty-one days. Clinical markers of hemolysis-total Hb concentration, reticulocyte count, bilirubin, and lactate dehydrogenase (LDH) levels-also mirror this variability [85][86][87][88][89].…”

Section: Intravascular Rbc Hemolysis and Production Of Rnsmentioning

confidence: 98%

From Stress to Sick(le) and Back Again–Oxidative/Antioxidant Mechanisms, Genetic Modulation, and Cerebrovascular Disease in Children with Sickle Cell Anemia

Silva,

Faustino

2023

Antioxidants

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Sickle cell anemia (SCA) is a genetic disease caused by the homozygosity of the HBB:c.20A>T mutation, which results in the production of hemoglobin S (HbS). In hypoxic conditions, HbS suffers autoxidation and polymerizes inside red blood cells, altering their morphology into a sickle shape, with increased rigidity and fragility. This triggers complex pathophysiological mechanisms, including inflammation, cell adhesion, oxidative stress, and vaso-occlusion, along with metabolic alterations and endocrine complications. SCA is phenotypically heterogeneous due to the modulation of both environmental and genetic factors. Pediatric cerebrovascular disease (CVD), namely ischemic stroke and silent cerebral infarctions, is one of the most impactful manifestations. In this review, we highlight the role of oxidative stress in the pathophysiology of pediatric CVD. Since oxidative stress is an interdependent mechanism in vasculopathy, occurring alongside (or as result of) endothelial dysfunction, cell adhesion, inflammation, chronic hemolysis, ischemia-reperfusion injury, and vaso-occlusion, a brief overview of the main mechanisms involved is included. Moreover, the genetic modulation of CVD in SCA is discussed. The knowledge of the intricate network of altered mechanisms in SCA, and how it is affected by different genetic factors, is fundamental for the identification of potential therapeutic targets, drug development, and patient-specific treatment alternatives.

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Lactate dehydrogenase isoenzyme 3 and hemolysis in sickle cell anemia: a possible correlation?

Cited by 5 publications

References 9 publications

Lactate dehydrogenase and hemolysis index to predict vaso-occlusive crisis in sickle cell disease

Lactate dehydrogenase and hemolysis index to predict vaso-occlusive crisis in sickle cell disease

Clinical Utility of Lactate Dehydrogenase in Determining the Severity of Hemolysis in Sickle Cell Anemia

From Stress to Sick(le) and Back Again–Oxidative/Antioxidant Mechanisms, Genetic Modulation, and Cerebrovascular Disease in Children with Sickle Cell Anemia

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