Abstract
Purpose: Liver iron is frequently elevated in chronic hepatitis C and may contribute to liver injury. The pathophysiology behind this phenomenon may involve hepcidin, a gene that is up-regulated in the liver by inflammation and iron. Inappropriately low hepcidin is important to the pathophysiology of hereditary hemochromatosis. However, the role of hepcidin in the iron loading of patients with hepatitis C is unknown. Subjects and Methods: To determine whether liver hepcidin mRNA correlates with markers of hepatic inflammation and iron status in patients with hepatitis C, we extracted total RNA from liver biopsy specimens of patients with chronic hepatitis C and quantified hepcidin mRNA. Liver hepcidin mRNA levels were then correlated with aspartate aminotransferase, alanine aminotransferase, ferritin, viral load, fibrosis, hepatic iron concentration, and Hepatic Activity Index (HAI). Results: Among patients with hepatitis C, there was a significant correlation of hepcidin mRNA expression in the liver with hepatic iron concentration and serum ferritin (r = 0.72, P = 0.006, and r = 0.60, P = 0.01, respectively). Hepcidin mRNA expression in the liver did not correlate with aspartate aminotransferase, alanine aminotransferase, HAI, or viral load. No differences in hepcidin mRNA were found based on viral genotype or the presence of fibrosis. Conclusion: In contrast to other inflammatory states, hepcidin mRNA expression in the liver was independent of markers of inflammation in hepatitis C. Instead, our results suggest that iron stores in patients with hepatitis C regulate hepcidin expression and that iron loading in chronic hepatitis C is not due to inappropriate hepcidin expression.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 71-74 |
| Number of pages | 4 |
| Journal | Journal of Clinical Gastroenterology |
| Volume | 39 |
| Issue number | 1 |
| State | Published - Jan 2005 |
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Keywords
- Hepatitis C
- Hepcidin
- Iron
ASJC Scopus subject areas
- Gastroenterology
Cite this
Liver hepcidin mRNA correlates with iron stores, but not inflammation, in patients with chronic hepatitis C. / Aoki, Christopher A.; Rossaro, Lorenzo; Ramsamooj, Rajendra; Brandhagen, David; Burritt, Mary E.; Bowlus, Christopher.
In: Journal of Clinical Gastroenterology, Vol. 39, No. 1, 01.2005, p. 71-74.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Liver hepcidin mRNA correlates with iron stores, but not inflammation, in patients with chronic hepatitis C
AU - Aoki, Christopher A.
AU - Rossaro, Lorenzo
AU - Ramsamooj, Rajendra
AU - Brandhagen, David
AU - Burritt, Mary E.
AU - Bowlus, Christopher
PY - 2005/1
Y1 - 2005/1
N2 - Purpose: Liver iron is frequently elevated in chronic hepatitis C and may contribute to liver injury. The pathophysiology behind this phenomenon may involve hepcidin, a gene that is up-regulated in the liver by inflammation and iron. Inappropriately low hepcidin is important to the pathophysiology of hereditary hemochromatosis. However, the role of hepcidin in the iron loading of patients with hepatitis C is unknown. Subjects and Methods: To determine whether liver hepcidin mRNA correlates with markers of hepatic inflammation and iron status in patients with hepatitis C, we extracted total RNA from liver biopsy specimens of patients with chronic hepatitis C and quantified hepcidin mRNA. Liver hepcidin mRNA levels were then correlated with aspartate aminotransferase, alanine aminotransferase, ferritin, viral load, fibrosis, hepatic iron concentration, and Hepatic Activity Index (HAI). Results: Among patients with hepatitis C, there was a significant correlation of hepcidin mRNA expression in the liver with hepatic iron concentration and serum ferritin (r = 0.72, P = 0.006, and r = 0.60, P = 0.01, respectively). Hepcidin mRNA expression in the liver did not correlate with aspartate aminotransferase, alanine aminotransferase, HAI, or viral load. No differences in hepcidin mRNA were found based on viral genotype or the presence of fibrosis. Conclusion: In contrast to other inflammatory states, hepcidin mRNA expression in the liver was independent of markers of inflammation in hepatitis C. Instead, our results suggest that iron stores in patients with hepatitis C regulate hepcidin expression and that iron loading in chronic hepatitis C is not due to inappropriate hepcidin expression.
AB - Purpose: Liver iron is frequently elevated in chronic hepatitis C and may contribute to liver injury. The pathophysiology behind this phenomenon may involve hepcidin, a gene that is up-regulated in the liver by inflammation and iron. Inappropriately low hepcidin is important to the pathophysiology of hereditary hemochromatosis. However, the role of hepcidin in the iron loading of patients with hepatitis C is unknown. Subjects and Methods: To determine whether liver hepcidin mRNA correlates with markers of hepatic inflammation and iron status in patients with hepatitis C, we extracted total RNA from liver biopsy specimens of patients with chronic hepatitis C and quantified hepcidin mRNA. Liver hepcidin mRNA levels were then correlated with aspartate aminotransferase, alanine aminotransferase, ferritin, viral load, fibrosis, hepatic iron concentration, and Hepatic Activity Index (HAI). Results: Among patients with hepatitis C, there was a significant correlation of hepcidin mRNA expression in the liver with hepatic iron concentration and serum ferritin (r = 0.72, P = 0.006, and r = 0.60, P = 0.01, respectively). Hepcidin mRNA expression in the liver did not correlate with aspartate aminotransferase, alanine aminotransferase, HAI, or viral load. No differences in hepcidin mRNA were found based on viral genotype or the presence of fibrosis. Conclusion: In contrast to other inflammatory states, hepcidin mRNA expression in the liver was independent of markers of inflammation in hepatitis C. Instead, our results suggest that iron stores in patients with hepatitis C regulate hepcidin expression and that iron loading in chronic hepatitis C is not due to inappropriate hepcidin expression.
KW - Hepatitis C
KW - Hepcidin
KW - Iron
UR - http://www.scopus.com/inward/record.url?scp=11144280608&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=11144280608&partnerID=8YFLogxK
M3 - Article
C2 - 15599216
AN - SCOPUS:11144280608
VL - 39
SP - 71
EP - 74
JO - Journal of Clinical Gastroenterology
JF - Journal of Clinical Gastroenterology
SN - 0192-0790
IS - 1
ER -