Prohepcidin, Inflammation and Iron Homeostasis in Hemodialysis Patients With Chronic Hepatitis C

Hepatitis C Clinical Trial

Official title:

Comparison of Prohepcidin, Inflammation and Iron Homeostasis in Hemodialysis Patients With and Without Chronic Hepatitis C

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01272479
• Other study ID #: 1692
• Status: Completed
• Phase: N/A
• First received: January 6, 2011
• Last updated: January 6, 2011
• Start date: August 2008
• Est. completion date: March 2010

Study information

• Verified date: November 2009
• Source: Istanbul University
• Contact: n/a
• Is FDA regulated: No
• Health authority: Turkey: Ministry of Health
• Study type: Observational

Clinical Trial Summary

The aim of this study is to address questions regarding the link among hepcidin, hematological iron markers, inflammation and hepatitis C in HD patients. In attempt to address this issue, we planned to measure serum levels of hepcidin prohormone (pro-hepcidin), inflammatory and iron parameters.

Description:

Hepatitis C virus (HCV) infection is the most common cause of chronic liver disease in the world and also common among chronic hemodialysis (HD) patients. Patients with chronic HCV often have increased liver iron, a condition associated with reduced sustained response to antiviral therapy, more rapid progression to cirrhosis, and development of hepatocellular carcinoma; however, little is known about the mechanism of iron accumulation in the liver. Recently identified hepcidin, a 25-amino acid peptide hormone exclusively synthesized in the liver, is thought to be a key regulator for iron homeostasis and is induced by infection and inflammation. Hepcidin expression is modulated by iron stores, so that it decreases in iron deficiency to facilitate iron absorption while it increases in iron repletion to prevent pathological overload. Interleukin (IL)-6 has been proposed as a major inducer of hepcidin, via direct transcriptional activation of hepatic hepcidin expression by binding to its receptor complex containing gp130 to activate janus kinase (JAK) and activator of transcription 3 (STAT 3).

Recruitment information / eligibility

• Status: Completed
• Enrollment: 80
• Est. completion date: March 2010
• Est. primary completion date: March 2010
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: Both
• Age group: 18 Years to 85 Years

Eligibility

Inclusion Criteria:

• Chronic hemodialysis patients

Exclusion Criteria:

• Patients positive for hepatitis B virus surface antigen (HBsAg)

• Patients previously diagnosed nonrenal cause of anemia other than iron deficiency

• Patients with an evidence of active or occult bleeding

• Patients received blood transfusion within the past 4 months

• Patients with a history of malignancy, end-stage liver disease, or chronic hypoxia

• Patients with a history of recent hospitalization or infection requiring antibiotics within the past 4 weeks.

Study Design

Observational Model: Case Control, Time Perspective: Cross-Sectional

Related Conditions & MeSH terms

• Hepatitis
• Hepatitis A
• Hepatitis C
• Hepatitis C, Chronic
• Hepatitis, Chronic
• Inflammation
• Kidney Failure, Chronic
• Renal Failure Chronic Requiring Hemodialysis

Locations

Country	Name	City	State
Turkey	Division of Nephrology, Istanbul Faculty of Medicine	Istanbul

Sponsors (1)

Lead Sponsor	Collaborator
Istanbul University

Country where clinical trial is conducted

Turkey, 

References & Publications (1)

Nemeth E, Tuttle MS, Powelson J, Vaughn MB, Donovan A, Ward DM, Ganz T, Kaplan J. Hepcidin regulates cellular iron efflux by binding to ferroportin and inducing its internalization. Science. 2004 Dec 17;306(5704):2090-3. Epub 2004 Oct 28. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Association of prohepcidin and inflammation		3 months	No