Platelet sparing effect of COX II inhibition used with pegylated interferon alfa-2a for the treatment of chronic hepatitis C: A short term pilot study

Magdalene M. George, S. David Li, Ayse L. Mindikoglu, Mehdi H. Baluch, Sonu Dhillon, Deborah Farr, David H. Van Thiel

Research output: Contribution to journalArticle

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Abstract

The role of a cyclooxygenase (COX) II inhibitor in reducing microvascular inflammation and the platelet count associated with interferon (IFN) plus ribavirin therapy of chronic hepatitis C (HCV) was assessed. Three plasma mediators (biomarkers) associated with platelet activation, inflammation and fibrosis were measured. Eighteen IFN naïve patients were studied. Nine were treated with pegylated IFN alfa-2a (PEG-IFN α-2a) plus ribavirin and rofecoxib; nine were treated with PEG-IFN α-2a plus ribavirin. A complete blood count, liver panel and HCV-RNA were assayed weekly. Human soluble P-selectin (hs-P-selectin), human interleukin-8 (IL-8), human interleukin-13 (IL-13) and human thrombopoietin (TPO) were assayed at 4 week intervals. The COX II inhibitor reduced the platelet reduction experienced with PEG-IFN α-2a treatment of HCV despite a reduction in the plasma TPO level. Hs-P-selectin was increased in both groups. In contrast, human IL-8 levels declined to undetectable levels in virologic responders. Similarly, human IL-13 levels declined with therapy (P<0.001). These data suggest that: (1) a COX II inhibition is associated with an increase in the platelet count despite a reduction in the TPO level; (2) human IL-8 and human IL-13 but not hs-P-selectin levels decline in those who experience an early virologic response.

Original languageEnglish (US)
Pages (from-to)159-165
Number of pages7
JournalCytokine
Volume27
Issue number6
DOIs
StatePublished - Sep 21 2004

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Chronic Hepatitis C
Prostaglandin-Endoperoxide Synthases
Platelets
Thrombopoietin
Ribavirin
Blood Platelets
Interleukin-8
P-Selectin
Cyclooxygenase Inhibitors
Platelet Count
Interferons
Inflammation
Plasmas
Cyclooxygenase 1
Blood Cell Count
Platelet Activation
Biomarkers
Therapeutics
Liver
Fibrosis

Keywords

  • alanine aminotransferase
  • ALT
  • aspartate aminotransferase
  • AST
  • blood urea nitrogen
  • BUN
  • COX
  • COX II
  • cyclooxygenase
  • EIA
  • enzyme immunoassay
  • G-CSF
  • granulocyte colony stimulating factor
  • HCV
  • Hepatitis C
  • hepatitis C virus
  • IL-8
  • Interferon
  • interleukin-8
  • Platelets

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Biochemistry
  • Hematology
  • Molecular Biology

Cite this

Platelet sparing effect of COX II inhibition used with pegylated interferon alfa-2a for the treatment of chronic hepatitis C : A short term pilot study. / George, Magdalene M.; Li, S. David; Mindikoglu, Ayse L.; Baluch, Mehdi H.; Dhillon, Sonu; Farr, Deborah; Van Thiel, David H.

In: Cytokine, Vol. 27, No. 6, 21.09.2004, p. 159-165.

Research output: Contribution to journalArticle

George, Magdalene M. ; Li, S. David ; Mindikoglu, Ayse L. ; Baluch, Mehdi H. ; Dhillon, Sonu ; Farr, Deborah ; Van Thiel, David H. / Platelet sparing effect of COX II inhibition used with pegylated interferon alfa-2a for the treatment of chronic hepatitis C : A short term pilot study. In: Cytokine. 2004 ; Vol. 27, No. 6. pp. 159-165.
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AU - George, Magdalene M.

AU - Li, S. David

AU - Mindikoglu, Ayse L.

AU - Baluch, Mehdi H.

AU - Dhillon, Sonu

AU - Farr, Deborah

AU - Van Thiel, David H.

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N2 - The role of a cyclooxygenase (COX) II inhibitor in reducing microvascular inflammation and the platelet count associated with interferon (IFN) plus ribavirin therapy of chronic hepatitis C (HCV) was assessed. Three plasma mediators (biomarkers) associated with platelet activation, inflammation and fibrosis were measured. Eighteen IFN naïve patients were studied. Nine were treated with pegylated IFN alfa-2a (PEG-IFN α-2a) plus ribavirin and rofecoxib; nine were treated with PEG-IFN α-2a plus ribavirin. A complete blood count, liver panel and HCV-RNA were assayed weekly. Human soluble P-selectin (hs-P-selectin), human interleukin-8 (IL-8), human interleukin-13 (IL-13) and human thrombopoietin (TPO) were assayed at 4 week intervals. The COX II inhibitor reduced the platelet reduction experienced with PEG-IFN α-2a treatment of HCV despite a reduction in the plasma TPO level. Hs-P-selectin was increased in both groups. In contrast, human IL-8 levels declined to undetectable levels in virologic responders. Similarly, human IL-13 levels declined with therapy (P<0.001). These data suggest that: (1) a COX II inhibition is associated with an increase in the platelet count despite a reduction in the TPO level; (2) human IL-8 and human IL-13 but not hs-P-selectin levels decline in those who experience an early virologic response.

AB - The role of a cyclooxygenase (COX) II inhibitor in reducing microvascular inflammation and the platelet count associated with interferon (IFN) plus ribavirin therapy of chronic hepatitis C (HCV) was assessed. Three plasma mediators (biomarkers) associated with platelet activation, inflammation and fibrosis were measured. Eighteen IFN naïve patients were studied. Nine were treated with pegylated IFN alfa-2a (PEG-IFN α-2a) plus ribavirin and rofecoxib; nine were treated with PEG-IFN α-2a plus ribavirin. A complete blood count, liver panel and HCV-RNA were assayed weekly. Human soluble P-selectin (hs-P-selectin), human interleukin-8 (IL-8), human interleukin-13 (IL-13) and human thrombopoietin (TPO) were assayed at 4 week intervals. The COX II inhibitor reduced the platelet reduction experienced with PEG-IFN α-2a treatment of HCV despite a reduction in the plasma TPO level. Hs-P-selectin was increased in both groups. In contrast, human IL-8 levels declined to undetectable levels in virologic responders. Similarly, human IL-13 levels declined with therapy (P<0.001). These data suggest that: (1) a COX II inhibition is associated with an increase in the platelet count despite a reduction in the TPO level; (2) human IL-8 and human IL-13 but not hs-P-selectin levels decline in those who experience an early virologic response.

KW - alanine aminotransferase

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KW - aspartate aminotransferase

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KW - blood urea nitrogen

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KW - EIA

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KW - granulocyte colony stimulating factor

KW - HCV

KW - Hepatitis C

KW - hepatitis C virus

KW - IL-8

KW - Interferon

KW - interleukin-8

KW - Platelets

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