STUDY OF THE PREVALENCE OF HEREDITARY HEMOCHROMATOSIS (HFE) AND SECONDARY CAUSES OF HYPERFERRITINEMIA IN PATIENTS TREATED IN A BLOODLETTING PROGRAMME.

Authors

Agustin Castiella, Ane Arteaga, Iñigo Garaizabal, Mª-José Sánchez-Iturri, Iratxe Urreta, Eva Zapata

Published in

Clinics and research in hepatology and gastroenterology. Pages 102962. Oct 30, 2026. Epub Oct 30, 2026.

Abstract

Phlebotomy is the cornerstone of treatment for patients with hereditary hemochromatosis (HH) (C282Y/C282Y). Its role in patients with hyperferritinaemia (HF) and moderate iron overload remains controversial. In recent years, HF due to metabolic syndrome and obesity has increased significantly.
To study the causes and indications for bloodletting in patients undergoing treatment at our hospital's Gastroenterology Department and to determine the prevalence of HH and compare iron profiles between patients with confirmed HH and patients with other causes of HF.
A total of 179 patients were included. There were 48 women and 131 men. The median age was 55. In the homozygous C282Y group, it was 49.5, and in the rest, it was 60 (p: 0.0019), requiring earlier treatment in the HH group. The indication for bloodletting was correct (HH with significant hepatic iron overload) in 48% of cases. HFE mutations: C282Y/C282Y 70 (39.55%), C282Y/H63D 50 (28.25%). Patients with metabolic syndrome and hyperferritinaemia (33%) were placed on a bloodletting programme. Obesity (BMI>30) was present in 37.76% of patients. A significant alcohol consumption was present in 38.22% of patients. In the MRI study, only 25.50% of patients had elevated iron overload (>80 mmol/g), with 47.65% having moderate overload (>36<80). LIC was significantly higher in C282Y/C282Y patients (101.22 vs 51.98) (p: 0.0000). Laboratory: Serum ferritin (p:0.0268), IST (p:0.0000) and Fe (p:0.0000) values were significantly higher in patients with HH (C282Y/C282Y).
We must re-evaluate patients undergoing chronic bloodletting, as a high percentage do not benefit from it.

PMID:
42962819
Bibliographic data and abstract were imported from PubMed on 31 Oct 2026.

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