Hepcidin

Anemia

Report in 192Hrs

At Home

No Fasting Required

Details

Iron regulatory hormone.

₹2,398₹3,425

30% OFF

Hepcidin Test Information Guide

Why is it done?
- Hepcidin is a hormone produced by the liver that regulates iron absorption and iron metabolism throughout the body. The test measures serum hepcidin levels to assess iron homeostasis and diagnose iron-related disorders.
- Primary indications include: • Suspected hemochromatosis (iron overload disorder) • Iron deficiency anemia evaluation and differentiation • Anemia of chronic disease assessment • Chronic kidney disease with anemia management • Monitoring iron metabolism in patients with hereditary iron disorders • Evaluation of abnormal iron studies (ferritin, transferrin saturation, serum iron) • Assessment of erythropoietin resistance in dialysis patients
- Typical timing: • Performed during initial evaluation of iron metabolism disorders • Ordered alongside iron studies (serum iron, ferritin, TIBC, transferrin saturation) • Can be performed at any time; no specific time-of-day requirements • May be repeated to monitor response to treatment for iron disorders
Normal Range
- Reference ranges vary by laboratory but typical values are: • Normal hepcidin levels: 29-254 ng/mL (nanograms per milliliter) or 3.2-28.1 pmol/L (picomoles per liter), depending on assay method used • Range may vary between 15-200 ng/mL depending on laboratory and measurement technique
- Interpretation of results: • Normal hepcidin: Indicates appropriate iron regulation and normal iron metabolism • Low/suppressed hepcidin: Suggests iron deficiency or increased iron absorption • High/elevated hepcidin: Indicates iron overload, chronic inflammation, or anemia of chronic disease • Disproportionately low hepcidin with elevated iron: Characteristic of hereditary hemochromatosis
- Units of measurement: • Primary unit: ng/mL (nanograms per milliliter) • Alternative unit: pmol/L (picomoles per liter) • Conversion factor: 1 ng/mL ≈ 0.111 pmol/L
- Normal vs abnormal interpretation: • Normal: Hepcidin within laboratory reference range indicates balanced iron homeostasis • Abnormal low: Suggests iron deficiency, iron-refractory anemia, or hereditary hemochromatosis • Abnormal high: May indicate iron overload, secondary hemochromatosis, or chronic disease • Clinical correlation with iron panel results is essential for accurate interpretation
Interpretation
- Detailed interpretation of result values: • Markedly low hepcidin (<10 ng/mL): Characteristic of hereditary hemochromatosis, iron deficiency anemia, or iron-refractory anemia of chronic disease (IRIDA) • Low-normal hepcidin (10-29 ng/mL): Suggests iron deficiency or inadequate hepcidin suppression • Normal hepcidin (29-254 ng/mL): Indicates appropriate iron regulation • Elevated hepcidin (>254 ng/mL): Suggests iron overload, secondary hemochromatosis, inflammation, or anemia of chronic disease
- Clinical significance of different patterns: • Low hepcidin + high ferritin + high transferrin saturation: Indicates hemochromatosis (primary or secondary) • Low hepcidin + low ferritin: Confirms iron deficiency anemia • Normal hepcidin + elevated ferritin: Suggests anemia of chronic disease or inflammation • Disproportionately low hepcidin + elevated iron stores: Highly specific for hereditary hemochromatosis genotypes (HFE mutations)
- Factors affecting hepcidin levels: • Iron stores: Directly proportional relationship • Inflammatory markers (IL-6, CRP): Elevate hepcidin levels • Erythropoietic activity: Suppresses hepcidin levels • Hypoxia: Suppresses hepcidin production • Medications: Some therapies may affect hepcidin regulation • Kidney function: Hepcidin metabolism may be altered in renal disease • Age and gender: Minor variations may exist • Blood transfusions: Increase hepcidin indirectly through iron load
- Clinical applications: • Differentiating iron deficiency anemia from anemia of chronic disease • Early detection of hereditary hemochromatosis before iron accumulation • Monitoring response to iron chelation therapy • Assessing iron metabolism in dialysis patients • Evaluating iron-refractory anemia of chronic disease (IRIDA) • Predicting response to erythropoiesis-stimulating agents (ESAs)
Associated Organs
- Primary organ systems involved: • Liver: Primary site of hepcidin production and regulation; essential for iron metabolism control • Small intestine: Iron absorption site; regulated by hepcidin • Bone marrow: Iron utilization for erythropoiesis; signals hepcidin regulation • Kidneys: Metabolize hepcidin; involved in erythropoietin regulation • Spleen: Contains iron from aged red blood cells; iron recycling • Pancreas: Iron accumulation can occur; contributes to complications
- Medical conditions associated with abnormal results: • Hereditary hemochromatosis (HFE, HFE2, HFE3 mutations): Most common genetic iron disorder • Secondary hemochromatosis: From multiple transfusions, chronic liver disease, or thalassemia • Iron deficiency anemia: Various etiologies including bleeding, malabsorption • Anemia of chronic disease: Associated with chronic infections, malignancies, inflammation • Iron-refractory anemia of chronic disease (IRIDA): Due to TMPRSS6 mutations • Chronic kidney disease: Altered iron metabolism and hepcidin clearance • Type 2 diabetes: Associated with hemochromatosis risk • Chronic viral hepatitis: Especially hepatitis C
- Diseases this test helps diagnose or monitor: • Hemochromatosis (primary and secondary): Iron overload disorder • Iron deficiency anemia: Most common anemia worldwide • Anemia of chronic disease: Common in chronic illness populations • Polycythemia vera: May show altered iron metabolism • Hereditary persistence of fetal hemoglobin: Related iron disorders • Atransferrinemia: Rare iron transport disorder
- Potential complications from abnormal results: • Iron overload complications: Cirrhosis, hepatocellular carcinoma, cardiac arrhythmias, cardiomyopathy • Organ damage: Liver fibrosis/cirrhosis, pancreatic damage leading to diabetes, cardiac dysfunction • Iron deficiency complications: Severe anemia, cognitive impairment, heart failure • Chronic disease progression: In patients with anemia of chronic disease • Increased infection risk: Related to immune system effects of iron imbalance • Arthropathy: Joint involvement in hemochromatosis • Hypogonadism: From iron deposition in pituitary and gonads
Follow-up Tests
- Recommended follow-up tests based on hepcidin results: • Iron panel (serum iron, TIBC, transferrin saturation): Essential complementary testing • Ferritin: Assess iron stores; evaluate for iron overload or deficiency • Complete blood count (CBC): Assess hemoglobin, hematocrit, red blood cell indices • Liver function tests (AST, ALT, bilirubin, albumin): Evaluate hepatic function • HFE gene mutation testing: If hemochromatosis is suspected • TMPRSS6 gene testing: For iron-refractory anemia of chronic disease evaluation
- Further investigations that might be needed: • Liver biopsy or elastography: Assess for cirrhosis in hemochromatosis patients • Cardiac MRI: Evaluate cardiac iron deposition • Glucose tolerance test: Screen for diabetes in iron overload • Pituitary hormone testing: If hypogonadism suspected • Colonoscopy: Screen for colorectal cancer in hemochromatosis • Abdominal ultrasound: Assess liver, spleen, and pancreas
- Monitoring frequency for ongoing conditions: • Hemochromatosis on phlebotomy therapy: Hepcidin every 3-6 months initially, then annually • Iron deficiency anemia treatment: Iron panel and hepcidin at 6-8 weeks after starting therapy • Anemia of chronic disease: Every 3-6 months based on clinical stability • Chronic kidney disease patients: Every 1-3 months if receiving ESA therapy • Post-treatment follow-up: At 6 weeks, 3 months, 6 months, then annually
- Related tests providing complementary information: • Transferrin receptor (sTfR): More sensitive marker of iron deficiency than ferritin • sTfR/ferritin ratio: Differentiates iron deficiency from anemia of chronic disease • Soluble transferrin receptor-ferritin index: Assesses iron status • Hemoglobin A1c: In patients with diabetes or glucose intolerance • Inflammatory markers (CRP, IL-6): Affect hepcidin regulation in chronic disease • Reticulocyte count: Assess bone marrow response to therapy • Peripheral blood smear: Evaluate red blood cell morphology
Fasting Required?
- Fasting requirement: No • Hepcidin testing does not require fasting • The test can be performed at any time of day • Food intake does not significantly affect hepcidin measurement • Patients may eat and drink normally before the test
- Special instructions for sample collection: • A simple blood draw is required, typically 2-5 mL of blood • Blood is usually collected in a serum separator tube or EDTA tube (verify with lab) • Sample should be refrigerated or kept on ice after collection • Transport to laboratory promptly for analysis • Delayed sample processing may affect result accuracy
- Medications to avoid: • Generally, no specific medications need to be avoided before hepcidin testing • However, certain medications may affect hepcidin levels and should be noted: - Iron supplements: May affect interpretation of results - Erythropoiesis-stimulating agents (ESAs): Affect hepcidin regulation - Corticosteroids: May affect inflammation and hepcidin levels • Inform healthcare provider of all current medications • Do not discontinue medications without medical guidance
- Other patient preparation requirements: • Arrive well-hydrated; adequate hydration ensures good vein access • Wear loose-fitting, short-sleeved clothing for easy blood draw access • Inform phlebotomist of any bleeding disorders or anticoagulant use • If testing is part of an iron panel, note timing of last blood transfusion (if applicable) • Stress reduction recommended as stress may affect some test results • Consistent timing of blood draw may be important for follow-up testing • No specific dietary restrictions necessary

How our test process works!