A sandwich-type radioimmunoassay for serum ferritin was developed using iron-rich human liver ferritin and evaluated for its clinical usefulness. In young healthy males and females, the mean serum ferritin concentrations were 44 ~g/L (range 7-158) and 16 p.g/L (range 4-56), respectively. In anemic patients lower serum ferritin concentrations were found, while in most patients with iron overload serum ferritin concentrations well above 1000 ~g/L were measured. Comparison of our method with a commercially available radioimmunoassay kit revealed a good correlation, except for sera with very low ferritin concentrations. Comparison with serum iron and transferrin parameters in patients with iron deficiency demonstrated that serum ferritin concentrations might be subnormal in a majority of patients with otherwise normal iron indices. Up to 70% of the ferritin in serum of normal subjects could bind to concanavalin A-Sepharose, indicating its glycoprotein nature. It is concluded that our serum ferritin radioimmunoassay gave reliable results and was useful in the laboratory diagnosis of latent iron-deficiency and in the analysis of the heterogeneity of serum ferritin.
We compared three serum ferritin radioimmunoassay kits and one noncommercial RIA for ferritin quantitation, with regression analysis of results for sera from 35 ostensibly healthy subjects. There was a good correlation (p less than 0.001) between these various RIAs, but the slope of the regression line varied widely, most probably because of lack of standardization of the serum ferritin assay. Determination of the ferritin content of purified samples of tissue ferritin revealed that the kits differ in specificity, differences for purified human spleen ferritin and human liver ferritin being larger than those for normal sera. Removing the iron from purified liver ferritin increased antiserum binding in two of the kits by twofold, but had no effect in two other kits. We conclude that commercial RIA methods for serum ferritin differ in specificity, and that this difference is related to the source of ferritin used in the production of the antibodies.
Four patients with idiopathic hemochromatosis were treated with intensive phlebotomy therapy. In 1 to 2 years, 8.8-16.7 g iron was removed. In three out of four patients hemoglobin levels fell at the end of therapy. Serum ferritin was continuously measured during therapy. The greatly elevated serum ferritin levels normalized or decreased to subnormal levels in all patients after therapy. Despite some fluctuations in the first phase of therapy, the fall in serum ferritin was regular with halving of the ferritin levels after about 50% of the excess iron was removed. The normalization of serum ferritin occurred in advance of the hemoglobin decrease at the end of therapy, indicating that in the later stages of therapy the normal iron stores are also depleted. It is emphasized that serum ferritin measurements are useful for monitoring of intensive phlebotomy therapy, and in particular to indicate the end of therapy before anemia develops.
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