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The iron is there, it is only held back — so the ferritin is normal, and the transferrin saturation is the value that separates the two anaemias.
Also known as: anemia of chronic disease · inflammatory anemia
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With lasting inflammation the body switches its iron housekeeping. Through a messenger from the liver, iron is held in the store and less is taken up from the gut — originally a sensible protection, since bacteria need iron to grow. If the state persists, the marrow lacks material and an anaemia develops although there is enough iron in the body. It is typical in rheumatic disease, chronic bowel inflammation, kidney disease, heart failure, recurring infections and cancer. The anaemia is usually mild to moderate and the red cells are of normal size — unlike in iron deficiency, where they grow smaller. This distinction is the whole point of the dossier, because it decides the treatment: in true deficiency the ferritin is low, here it is normal or high, since it is also an inflammation value. What is low in both cases is the transferrin saturation — so that is the value that helps. Giving iron where none is missing achieves little. The effective lever is treating whatever keeps the inflammation going. Often, though, both are present together, and then iron is very much worthwhile.
Ferritin alone is not enough with inflammation. Only with the saturation beside it can one say whether real iron is missing as well — and exactly that decides whether iron helps.
If the underlying illness settles, the haemoglobin rises by itself. That is the lever with the greatest effect and it is often overlooked behind the iron question.
With a raised CRP a higher threshold applies. A ferritin that looks unremarkable in the report can here still mean a true deficiency.
With declining kidney function there is also too little of the messenger that drives blood formation. That is a separate, treatable cause.
Having a chronic illness does not stop someone bleeding — through painkillers, an ulcer or a finding in the bowel. The low saturation is the door opener here.
With a full store, iron achieves little and often causes stomach trouble and constipation. Two blood values beforehand save months with a supplement that cannot work.
A worm that entered through the skin takes small amounts of blood daily. With anaemia and no visible source and a matching travel history the stool sample is worthwhile.
After a stay in a malaria area the pallor can come from red cells breaking down, not from a deficiency. Fever with it is an emergency the same day.
Iron often does not work here, although the iron value looks low: with lasting inflammation the body deliberately holds iron back in the stores — a messenger called hepcidin locks uptake. So haemoglobin barely rises on tablets, while iron given into the vein gets past that lock. What really lifts the value is treating the underlying illness; that takes months and comes before the blood count.
After iron deficiency it is the second most common anaemia. Haemoglobin usually lies between 90 and 120 g/l and rarely falls below 80. Ferritin is normal or raised while transferrin saturation is low — that combination is exactly what separates it from iron deficiency, where both are low. With inflammation, a ferritin under 100 no longer counts as sufficient, because it rises as an acute phase protein. It improves with the underlying illness, over weeks to months.
The combination by which this anaemia is recognised. In pure iron deficiency both are low.
Rheumatic disease, Crohn or colitis, kidney disease, heart failure, recurring infections. The anaemia here is a measure of the activity in the background.
If an iron supplement changes nothing over weeks, that is itself a piece of information. It speaks for the access to the store being the problem, not the store.
The haemoglobin usually stays only a little below normal, and stays there. A rapid fall does not fit and belongs clarified differently.
A new anaemia is never simply age. It needs an explanation, even when a chronic illness is known.
What a deficiency makes visible on the body — skin, nails, tongue, eyes and nerves. The signs are unspecific: they show where to look, they prove nothing.
The value that helps when the ferritin is distorted by inflammation. If it is very low, real iron is missing as well — and then iron is worthwhile here too.
A double role: iron store and inflammation value at once. With a raised CRP a higher lower limit applies, otherwise a real iron deficiency is missed.
Shows whether inflammation is running at all. Without a raised CRP or ESR this explanation is unlikely, and the search goes on.
Here the red cells usually stay normal in size. If they grow smaller, that speaks for an additional true iron deficiency.
Here the iron is present but locked away: with ongoing inflammation hepcidin holds it in the stores, and tablets barely arrive. This is why ferritin is often normal or high although the blood is poor — transferrin saturation shows it more clearly.
Two deficiencies at once can hide each other in the blood count — small cells from iron, large from B12, average unremarkable. This is why both are measured rather than inferred from cell size.
With ongoing inflammation EPO is dampened and the marrow answers it less well. Together with the locked-away iron that gives an anaemia which barely responds to iron tablets.
An underactive thyroid itself causes a mild anaemia that recovers with treatment. It is among the values checked before an anaemia is classed as “chronic”.
In anaemia of chronic disease there is enough iron in the body, it is just held back. Extra iron therefore usually does not work — the underlying disease is treated. Ferritin is not informative here, as it rises with inflammation.
Here there is enough iron in the body, it is merely held back. Extra iron therefore usually does not work — and ferritin misleads, because it rises with inflammation anyway. The underlying disease is treated.