Liver stiffness increases acutely during sickle cell vaso-occlusive crisis

Christopher Koh, Tiffany Turner, Xiongce Zhao, Caterina P. Minniti, Jordan J. Feld, Jennifer Simpson, Mary Demino, Anna K. Conrey, Mary J. Jackson, Catherine Seamon, David E. Kleiner, Gregory J. Kato, Theo Heller

Research output: Contribution to journalArticle

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Abstract

Acute vaso-occlusive crisis (VOC) in sickle cell disease (SCD) is an important cause of end-organ damage. It is estimated that 10-39% of VOC occurs with hepatic involvement. Current assessments of hepatic involvement during VOC are unsatisfactory. We investigated transient elastography (TE) as a marker of hepatic involvement, its relationship with histology, and biochemical markers during VOC. SCD patients were evaluated with biochemical markers and TE at steady-state and during VOC. Change in TE and biochemical markers were correlated with length of hospital stay. When available, liver biopsy and tricuspid regurgitation velocity (TRV) at steady-state were correlated with TE. Twenty-three patients were evaluated (mean age=34.3 years, standard deviation=7.96). In 15 patients with liver biopsies, TE correlated with fibrosis (P=0.01) and TRV (P=0.0063), but not hepatic iron. Hemolysis biomarkers changed during VOC (P<0.022), but not alanine aminotransferase (ALT). Paired comparison of TE at steady-state and during VOC showed an increased from 6.2 to 12.3 kPa (P=0.0029). Increasing TE during VOC associated with increasing ALT and alkaline phosphatase (P=0.0088 and 0.0099, respectively). At steady-state, increasing inflammation on biopsy (P=0.0037) and TRV (P=0.0075) correlated with increasing TE during VOC. Increased hospital stay was associated with higher ALT (P=0.041), lower albumin (P=0.046), hemoglobin/hematocrit (P<0.0021) but not TE. TE may identify patients with hepatic involvement during VOC independent of biochemical measures. Increase in TE may reflect both hepatic passive congestion and hepatic involvement during VOC. TE may serve as a physiological biomarker for hepatic features of VOC. Am. J. Heamtol. 88:E250-E254, 2013.

Original languageEnglish (US)
JournalAmerican Journal of Hematology
Volume88
Issue number11
DOIs
StatePublished - Nov 2013
Externally publishedYes

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Elasticity Imaging Techniques
Liver
Biomarkers
Tricuspid Valve Insufficiency
Alanine Transaminase
Length of Stay
Sickle Cell Anemia
Biopsy
Matched-Pair Analysis
Hemolysis
Hematocrit
Alkaline Phosphatase
Albumins
Histology
Fibrosis

ASJC Scopus subject areas

  • Hematology

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Liver stiffness increases acutely during sickle cell vaso-occlusive crisis. / Koh, Christopher; Turner, Tiffany; Zhao, Xiongce; Minniti, Caterina P.; Feld, Jordan J.; Simpson, Jennifer; Demino, Mary; Conrey, Anna K.; Jackson, Mary J.; Seamon, Catherine; Kleiner, David E.; Kato, Gregory J.; Heller, Theo.

In: American Journal of Hematology, Vol. 88, No. 11, 11.2013.

Research output: Contribution to journalArticle

Koh, C, Turner, T, Zhao, X, Minniti, CP, Feld, JJ, Simpson, J, Demino, M, Conrey, AK, Jackson, MJ, Seamon, C, Kleiner, DE, Kato, GJ & Heller, T 2013, 'Liver stiffness increases acutely during sickle cell vaso-occlusive crisis', American Journal of Hematology, vol. 88, no. 11. https://doi.org/10.1002/ajh.23532
Koh, Christopher ; Turner, Tiffany ; Zhao, Xiongce ; Minniti, Caterina P. ; Feld, Jordan J. ; Simpson, Jennifer ; Demino, Mary ; Conrey, Anna K. ; Jackson, Mary J. ; Seamon, Catherine ; Kleiner, David E. ; Kato, Gregory J. ; Heller, Theo. / Liver stiffness increases acutely during sickle cell vaso-occlusive crisis. In: American Journal of Hematology. 2013 ; Vol. 88, No. 11.
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abstract = "Acute vaso-occlusive crisis (VOC) in sickle cell disease (SCD) is an important cause of end-organ damage. It is estimated that 10-39{\%} of VOC occurs with hepatic involvement. Current assessments of hepatic involvement during VOC are unsatisfactory. We investigated transient elastography (TE) as a marker of hepatic involvement, its relationship with histology, and biochemical markers during VOC. SCD patients were evaluated with biochemical markers and TE at steady-state and during VOC. Change in TE and biochemical markers were correlated with length of hospital stay. When available, liver biopsy and tricuspid regurgitation velocity (TRV) at steady-state were correlated with TE. Twenty-three patients were evaluated (mean age=34.3 years, standard deviation=7.96). In 15 patients with liver biopsies, TE correlated with fibrosis (P=0.01) and TRV (P=0.0063), but not hepatic iron. Hemolysis biomarkers changed during VOC (P<0.022), but not alanine aminotransferase (ALT). Paired comparison of TE at steady-state and during VOC showed an increased from 6.2 to 12.3 kPa (P=0.0029). Increasing TE during VOC associated with increasing ALT and alkaline phosphatase (P=0.0088 and 0.0099, respectively). At steady-state, increasing inflammation on biopsy (P=0.0037) and TRV (P=0.0075) correlated with increasing TE during VOC. Increased hospital stay was associated with higher ALT (P=0.041), lower albumin (P=0.046), hemoglobin/hematocrit (P<0.0021) but not TE. TE may identify patients with hepatic involvement during VOC independent of biochemical measures. Increase in TE may reflect both hepatic passive congestion and hepatic involvement during VOC. TE may serve as a physiological biomarker for hepatic features of VOC. Am. J. Heamtol. 88:E250-E254, 2013.",
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T1 - Liver stiffness increases acutely during sickle cell vaso-occlusive crisis

AU - Koh, Christopher

AU - Turner, Tiffany

AU - Zhao, Xiongce

AU - Minniti, Caterina P.

AU - Feld, Jordan J.

AU - Simpson, Jennifer

AU - Demino, Mary

AU - Conrey, Anna K.

AU - Jackson, Mary J.

AU - Seamon, Catherine

AU - Kleiner, David E.

AU - Kato, Gregory J.

AU - Heller, Theo

PY - 2013/11

Y1 - 2013/11

N2 - Acute vaso-occlusive crisis (VOC) in sickle cell disease (SCD) is an important cause of end-organ damage. It is estimated that 10-39% of VOC occurs with hepatic involvement. Current assessments of hepatic involvement during VOC are unsatisfactory. We investigated transient elastography (TE) as a marker of hepatic involvement, its relationship with histology, and biochemical markers during VOC. SCD patients were evaluated with biochemical markers and TE at steady-state and during VOC. Change in TE and biochemical markers were correlated with length of hospital stay. When available, liver biopsy and tricuspid regurgitation velocity (TRV) at steady-state were correlated with TE. Twenty-three patients were evaluated (mean age=34.3 years, standard deviation=7.96). In 15 patients with liver biopsies, TE correlated with fibrosis (P=0.01) and TRV (P=0.0063), but not hepatic iron. Hemolysis biomarkers changed during VOC (P<0.022), but not alanine aminotransferase (ALT). Paired comparison of TE at steady-state and during VOC showed an increased from 6.2 to 12.3 kPa (P=0.0029). Increasing TE during VOC associated with increasing ALT and alkaline phosphatase (P=0.0088 and 0.0099, respectively). At steady-state, increasing inflammation on biopsy (P=0.0037) and TRV (P=0.0075) correlated with increasing TE during VOC. Increased hospital stay was associated with higher ALT (P=0.041), lower albumin (P=0.046), hemoglobin/hematocrit (P<0.0021) but not TE. TE may identify patients with hepatic involvement during VOC independent of biochemical measures. Increase in TE may reflect both hepatic passive congestion and hepatic involvement during VOC. TE may serve as a physiological biomarker for hepatic features of VOC. Am. J. Heamtol. 88:E250-E254, 2013.

AB - Acute vaso-occlusive crisis (VOC) in sickle cell disease (SCD) is an important cause of end-organ damage. It is estimated that 10-39% of VOC occurs with hepatic involvement. Current assessments of hepatic involvement during VOC are unsatisfactory. We investigated transient elastography (TE) as a marker of hepatic involvement, its relationship with histology, and biochemical markers during VOC. SCD patients were evaluated with biochemical markers and TE at steady-state and during VOC. Change in TE and biochemical markers were correlated with length of hospital stay. When available, liver biopsy and tricuspid regurgitation velocity (TRV) at steady-state were correlated with TE. Twenty-three patients were evaluated (mean age=34.3 years, standard deviation=7.96). In 15 patients with liver biopsies, TE correlated with fibrosis (P=0.01) and TRV (P=0.0063), but not hepatic iron. Hemolysis biomarkers changed during VOC (P<0.022), but not alanine aminotransferase (ALT). Paired comparison of TE at steady-state and during VOC showed an increased from 6.2 to 12.3 kPa (P=0.0029). Increasing TE during VOC associated with increasing ALT and alkaline phosphatase (P=0.0088 and 0.0099, respectively). At steady-state, increasing inflammation on biopsy (P=0.0037) and TRV (P=0.0075) correlated with increasing TE during VOC. Increased hospital stay was associated with higher ALT (P=0.041), lower albumin (P=0.046), hemoglobin/hematocrit (P<0.0021) but not TE. TE may identify patients with hepatic involvement during VOC independent of biochemical measures. Increase in TE may reflect both hepatic passive congestion and hepatic involvement during VOC. TE may serve as a physiological biomarker for hepatic features of VOC. Am. J. Heamtol. 88:E250-E254, 2013.

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