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

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

Status

Completed

Phases

Unknown

Study type

Observational

Source

ClinicalTrials.gov

Registry ID

NCT01272479

Enrollment

Registered

2011-01-07

Start date

2008-08-31

Completion date

2010-03-31

Last updated

2011-01-07

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Hepatitis C, Renal Failure Chronic Requiring Hemodialysis

Keywords

hemodialysis, hepatitis C, inflammation, iron stores, prohepcidin

Brief 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.

Detailed 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).

Interventions

None listed

Study design

Observational model

CASE_CONTROL

Time perspective

CROSS_SECTIONAL

Eligibility

Sex/Gender

ALL

Age

18 Years to 85 Years

Healthy volunteers

Yes

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.

Design outcomes

Primary

Measure	Time frame
Association of prohepcidin and inflammation	3 months

Countries

Turkey (Türkiye)

Outcome results