One hormone. Behind all of it.
Hepcidin is the master regulator of iron metabolism. High hepcidin closes the gut door — oral iron cannot enter the bloodstream.
Ferritin, the test clinicians rely on, rises with inflammation regardless of iron stores. A patient with ferritin of 200 ng/mL can be functionally iron-deficient.
One hormone. Behind all of it.
- 01
Inflammation signals
Malaria, HIV, TB, cancer, CKD — any inflammatory signal drives IL-6 release. Iron stores are irrelevant.
- 02
The liver secretes hepcidin
Hepcidin-25 enters circulation and targets ferroportin, the body's only cellular iron exporter.
- 03
The gut door closes
Ferroportin is internalised. Iron is trapped in the enterocyte and excreted. Nothing reaches the patient.
- 04
We measure it in 15 minutes
One finger-prick before prescription tells the clinician whether the pathway is open or blocked.
Ferritin lies. Hepcidin does not.
Ferritin, the test clinicians rely on, rises with inflammation regardless of iron stores. A patient with ferritin of 200 ng/mL can be functionally iron-deficient.
Finger-prick to decision.
Finger-prick
20–30 µL capillary blood. No venipuncture. Any health worker can collect it.
Lateral flow
Proprietary antibody detects hepcidin-25. Room temperature, 15 minutes.
Two lines
One line, the pathway is open. Two lines, oral iron is blocked. No training needed.
Decision
Paired with haemoglobin, the result directs treatment before the patient leaves.
Step 01 — Finger-prick
Playing
Three anaemias that look identical today.
Oral iron will work.
Stores are depleted and the absorption pathway is open.
Ferrous sulphate / iron polymaltose
Oral iron will not absorb.
Iron is sequestered, not absent. Inflammation has closed the pathway.
IV iron + treat the infection
Iron is not the problem.
Supplementation risks overload. The underlying condition drives the anaemia.
Treat the underlying condition