Cellular source of serum lactate dehydrogenase elevation in patients with thrombotic thrombocytopenic purpura

Cohen, Jill A.; Brecher, Mark E.; Bandarenko, Nicholas

doi:10.1002/(sici)1098-1101(1998)13:1<16::aid-jca3>3.0.co;2-c

Cited by 109 publications

(63 citation statements)

References 5 publications

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“…LDH: lactate dehydrogenase; rho; Spearman rank correlation coefficient; Cr: creatinine. 43 supports the potential involvement of HNP in the pathogenesis of TTP.…”

Section: Discussionsupporting

confidence: 64%

Human neutrophil peptides and complement factor Bb in pathogenesis of acquired thrombotic thrombocytopenic purpura

et al. 2016

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A cquired thrombotic thrombocytopenic purpura is primarily caused by the deficiency of plasma ADAMTS13 activity resulting from autoantibodies against ADAMTS13. However, ADAMTS13 deficiency alone is often not sufficient to cause acute thrombotic thrombocytopenic purpura. Infections or systemic inflammation may precede acute bursts of the disease, but the underlying mechanisms are not fully understood. Herein, 52 patients with acquired autoimmune thrombotic thrombocytopenic purpura and 30 blood donor controls were recruited for the study. The plasma levels of human neutrophil peptides 1-3 and complement activation fragments (i.e. Bb, iC3b, C4d, and sC5b-9) were determined by enzyme-linked immunosorbent assays. Univariate analyses were performed to determine the correlation between each biomarker and clinical outcomes. We found that the plasma levels of human neutrophil peptides 1-3 and Bb in patients with acute thrombotic thrombocytopenic purpura were significantly higher than those in the control (P<0.0001). The plasma levels of HNP1-3 correlated with the levels of plasma complement fragment Bb (rho=0.48, P=0.0004) and serum lactate dehydrogenase (rho=0.28, P=0.04); in addition, the plasma levels of Bb correlated with iC3b (rho=0.55, P<0.0001), sC5b-9 (rho=0.63, P<0.0001), serum creatinine (rho=0.42, p=0.0011), and lactate dehydrogenase (rho=0.40, P=0.0034), respectively. Moreover, the plasma levels of iC3b and sC5b-9 were correlated (rho=0.72, P<0.0001), despite no statistically significant difference of the two markers between thrombotic thrombocytopenic purpura patients and the control. We conclude that innate immunity, i.e. neutrophil and complement activation via the alternative pathway, may play a role in the pathogenesis of acute autoimmune thrombotic thrombocytopenic purpura, and a therapy targeted at these pathways may be considered in a subset of these patients.

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“…LDH: lactate dehydrogenase; rho; Spearman rank correlation coefficient; Cr: creatinine. 43 supports the potential involvement of HNP in the pathogenesis of TTP.…”

Section: Discussionsupporting

confidence: 64%

Human neutrophil peptides and complement factor Bb in pathogenesis of acquired thrombotic thrombocytopenic purpura

et al. 2016

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“…In addition, hE-Hb-B10 had no effect on total plasma LDH activity in either SS or HS mice ( Table 1). As plasma LDH activity increases in response to both hemolysis and tissue damage (12), the high hemolytic rates in both models may limit our ability to detect subtle changes in LDH activity that might occur as a result of changes in tissue injury.…”

Section: Resultsmentioning

confidence: 99%

A novel hemoglobin-binding peptide reduces cell-free hemoglobin in murine hemolytic anemia

Hanson

Flewelen

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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“…Platelet count and lactate dehydrogenase level have been routinely used as laboratory parameters to monitor clinical responses of TTP to therapy. While these tests do provide sensitive measurements regarding the extent of thrombotic microangiopathy, intravascular hemolysis, and organ damage from tissue ischemia, 24 the biomarkers are not specific for TTP. Many clinical conditions, including those that often coexist with TTP such as sepsis/infection, systemic lupus erythematosus, surgery or malignancy/chemotherapy, can cause low platelet counts and increased lactate dehydrogenase.…”

Section: Discussionmentioning

confidence: 99%

ADAMTS13 activity and antigen during therapy and follow-up of patients with idiopathic thrombotic thrombocytopenic purpura: correlation with clinical outcome

Yang¹,

Jin²,

Lin³

et al. 2011

Haematologica

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BackgroundThe assay for ADAMTS13 activity helps clinicians to confirm the clinical diagnosis of idiopathic thrombotic thrombocytopenic purpura. The clinical value of testing for the antigen level of ADAMTS13 protein is, however, less clear. Design and MethodsIn this study, both ADAMTS13 antigen and activity levels were measured in 835 sequential samples from 40 consecutive patients who were followed for an average of 29 months throughout the course of acute episode plasma exchange treatment and clinical remission. ResultsDuring acute episodes, ADAMTS13 activity was severely deficient while ADAMTS13 antigen levels were more variable, ranging from severely deficient to as high as within the reference range. A severe depletion of ADAMTS13 antigen level during acute disease was, however, statistically associated with disease mortality (P=0.0322). For patients who achieved initial clinical responses, ADAMTS13 antigen levels appeared to be restored faster than ADAMTS13 activity to the normal range. Further analysis demonstrated that the ADAMTS13 antigen level at the time of initial clinical recovery was significantly higher in the patients who subsequently achieved a sustained clinical remission than in the group who soon after had an exacerbation (P=0.0187). ConclusionsOur data suggest that evaluation of ADAMTS13 antigen levels during the course of therapy and follow-up may offer additional useful information for the management of patients with thrombotic thrombocytopenic purpura.Key words: thrombotic thrombocytopenic purpura, ADAMTS13, prognosis, biomarker.Citation: Yang S, Jin M, Lin S, Cataland S, and Wu H. ADAMTS13 activity and antigen during therapy and follow-up of patients with idiopathic thrombotic thrombocytopenic purpura: correlation with clinical outcome Haematologica 2011;96(10)

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Cellular source of serum lactate dehydrogenase elevation in patients with thrombotic thrombocytopenic purpura

Cited by 109 publications

References 5 publications

Human neutrophil peptides and complement factor Bb in pathogenesis of acquired thrombotic thrombocytopenic purpura

Human neutrophil peptides and complement factor Bb in pathogenesis of acquired thrombotic thrombocytopenic purpura

A novel hemoglobin-binding peptide reduces cell-free hemoglobin in murine hemolytic anemia

ADAMTS13 activity and antigen during therapy and follow-up of patients with idiopathic thrombotic thrombocytopenic purpura: correlation with clinical outcome

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