Clinical trial NCT01272479: Prohepcidin, Inflammation and Iron Homeostasis in Hemodialysis Patients With Chronic Hepatitis C
Official title: Comparison of Prohepcidin, Inflammation and Iron Homeostasis in Hemodialysis Patients With and Without Chronic Hepatitis C
Study type: OBSERVATIONAL
Overall status: COMPLETED
Conditions: Renal Failure Chronic Requiring Hemodialysis
Hepatitis C
Keywords: hemodialysis
hepatitis C
inflammation
iron stores
prohepcidin
Lead sponsor: Istanbul University
Sponsor class: OTHER
First posted: 2011-01-07
Enrollment: 80
Sex: ALL
Minimum age (years): 18
Maximum age (years): 85
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: yes
Observational model: CASE_CONTROL
Time perspective: CROSS_SECTIONAL
Sampling method: NON_PROBABILITY_SAMPLE
Study population: Patients on chronic hemodialysis

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).

Eligibility criteria: 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.

Primary outcomes:
measure: Association of prohepcidin and inflammation
timeFrame: 3 months
Secondary outcomes:
Other outcomes:
Locations:
city: Istanbul
country: Turkey
facility: Division of Nephrology, Istanbul Faculty of Medicine
Study officials:
affiliation: MD
name: Yasar Caliskan
role: PRINCIPAL_INVESTIGATOR
References:
citation: 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. doi: 10.1126/science.1104742. Epub 2004 Oct 28.