Hyperferritinemia

I often write about Iron Deficiency (absolute) identified with Hypoferritinemia, which in fact is the biggest medical deficit and the most worsened, undervalued, and mistreated medical problem (everyone tries, but with almost 100% failure). But today I will write about the opposite, Hyperferritinemia, the increase in blood ferritin levels. It is common (not as much as iron deficiency), but it is just as poorly managed and treated. To evaluate, they evaluate, everyone is afraid.

The problem starts with the term: ferritin is an intracellular protein (mostly in hepatocytes, the liver cells), that ensures the storage of iron in a non-toxic form. In blood tests, it is written “ferritin”, in fact, it should be written “ferritinemia”; as they do with the term glycemia (we measure glucose in the blood = glycemia, we do not measure stored glucose (glycogen, glycolipids).

Ferritinemia is the ferritin (a very small amount compared to what is stored, represents approximately 1/10 of the iron stores respectively 600 mg of iron in females and 1,200 mg in males) that circulates in the blood and that we measure in the laboratory. We do not measure ferritin in the liver, etc., but ferritinemia (circulating ferritin). The normal minimum value for females is 20 ng/ml, for males 40 ng/ml (twice as much) and the optimal value for females is about 60 ng/ml and for males about 120 ng/ml.

Lowered ferritinemia (< 20 ng/ml in females and < 40 ng/ml in males) = absolute lack of iron.

But increased ferritinemia (not ferritin) is not only an indicator of absolute iron overload, it is also an indicator of inflammation. So not every hyperferritinemia is equal to iron overload, thus with the risk of organ damage from iron deposition (liver, heart, pancreas, skin). Patients are scared of the ferritin increase and doctors quickly tell them to do bloodletting!! (and when there is true iron deposition the damages are gradual). Ferritinemia 417 ng/ml, phlebotomy recommended!!

Ferritinemia is considered increased when it is > 500 ng/ml. Up to 1,000 ng/ml, it is considered a mild increase. We do not expect any complaints from the patient. As soon as hyperferritinemia is assessed, Transferrin Saturation should be done = the Sideremia /TIBC ratio x 100.

If this ratio is 50% or more in males and 45% or more in females, it is considered Hyperferritinemia with Iron Overload and only in this case and when ferritinemia is > 1,000 ng/ml does the deposition in organs (liver, heart, pancreas, skin) and the gradual damage to them begin. Only in these cases are iron chelators, bloodletting used and they are performed in specific centers, by qualified doctors. Here a diet low in iron might be useful (red meat is the richest in iron; it's practically impossible not to intake iron, at least to hinder the absorption of iron - milk, yogurt, tea). Hereditary Hemochromatosis and Thalassemia Major are two diseases with increased iron absorption. But in Thalassemia Major phlebotomy cannot be done, there is anemia, only iron chelators work and if possible, iron absorption should be reduced.

If this ratio is 20-50% in males and 15-45% in females, it is considered Hyperferritinemia without iron overload. No matter the ferritin value (not ferritin), there is no possibility of deposition in organs. It is of inflammatory origin, it is not a hematological pathology. Non-alcoholic fatty liver disease, certainly alcoholic and the use of alcohol itself, increased cholesterol, triglycerides, obesity, rheumatologic diseases, tumors, etc. are evaluated. The cause is treated (dyslipidemia, rheumatologic disease, obesity, alcohol removal, etc.), but not hyperferritinemia. It makes no sense to maintain a diet low in iron.

If this ratio is < 20% in males and < 15% in females = Absolute Lack of Iron, the patient should take iron medication, regardless of the ferritinemia value. Note that inflammation increases ferritinemia, but decreases sideremia.

And one last piece of information, one of the common follies we hear; when iron is taken orally, no more iron is absorbed than necessary and the liver is never damaged. The only exceptions are two diseases: Hereditary Hemochromatosis and Thalassemia Major.