Ferritin, serum

Phuapradit W, Taeepanichskul S, Jetsawangsii T, Chaturachinda K, Khupulsup K, Kunakom M (1996) Serum ferritin levels in normal and HIV-1 infected pregnant women. Aust N Z J Obstet Gynaecol 36 24-26... 

A major contribution of the free-radical scavenging activity in blood plasma is attributable to the macro-molecular proteins (Wayner et al., 1985) of which albumin is a primary component and trapping agertt (Holt et al., 1984). Serum sulphydryl levels, primarily albumin-related, are decreased in subjects with rheumatoid complicated coalworkers pneumoconiosis, indicative of exacerbated inflammatory R.OM production (Thomas and Evans, 1975). Experimental asbestos inhalation in rats leads to an adaptive but evidendy insufficient response by an increase in endogenous antioxidant enzymes (Janssen etal., 1990). Protection of the vascular endothelium against iron-mediated ROM generation and injury is afforded by the iron sequestiant protein ferritin (Balia et al., 1992). 

Iron is, as part of several proteins, such as hemoglobin, essential for vertebrates. The element is not available as ion but mostly as the protein ligands transferrin (transport), lactoferrin (milk), and ferritin (storage), and cytochromes (electron transport) (Alexander 1994). Toxicity due to excessive iron absorption caused by genetic abnormalities exists. For the determination of serum Fe a spectrophoto-metric reference procedure exists. Urine Fe can be determined by graphite furnace (GF)-AAS, and tissue iron by GF-AAS and SS-AAS (Alexander 1994 Herber 1994a). Total Iron Binding Capacity is determined by fuUy saturated transferrin with Fe(III), but is nowadays mostly replaced by immunochemical determination of transferrin and ferritin. 

Decreased red blood cell (RBC) count, hemoglobin (Hgb) and hematocrit (Hct) iron metabolism may also be altered [iron level, total iron binding capacity (TIBC), serum ferritin level, and transferrin saturation (TSAT)]. Erythropoietin levels are not routinely monitored and are generally normal to low. Urine positive for albumin or protein. 

Decreased RBC count, Hgb, and Hct Decreased serum iron level, TIBC, serum ferritin, and TSAT Decreased erythropoietin levels relative to the degree of hypoxia that is present... 

Generally, treatment requires a combination of ESA and iron supplementation. The goal of treatment for anemia of CKD is to increase Hgb levels greater than 11 g/dL (6.8 mmol/L). The goal for iron supplementation is to maintain serum ferritin... 

Iron Supplementation Use of ESAs can lead to iron deficiency if iron stores are not adequately maintained. If serum ferritin and TSAT fall below the goal levels, iron supplementation is required. Oral iron supplements are less costly than IV supplements and are generally the first-line treatment for iron supplementation. When administering iron by the oral route, 200 mg of elemental iron should be delivered daily to maintain adequate iron stores. 

Shirley, NY) sodium ferric gluconate (Ferrlecit by Watson Pharmaceuticals, Inc., Corona, CA) and iron sucrose (Venofer by American Reagent, Inc., Shirley, NY). Initiation of IV iron should be based on evaluation of iron stores. A serum ferritin level less than 100 ng/mL in conjunction with a TSAT level less than 20% indicates absolute iron deficiency and is a clear indication for the need for iron replacement.31 When TSAT is less than 20% in conjunction with normal or elevated serum ferritin levels, treatment should be based on the clinical picture of the patient, as serum ferritin is an acute phase reactant, which may become elevated with inflammation and stress. Iron supplementation may be indicated if Hgb levels are below the goal level. 

Serum ferritin—the best indirect determinant of body iron stores. It is commonly decreased in patients with iron-deficiency anemia. 

Serum ferritin Less than 1 0-20 mcg/L (22-44 pmol/L) Ferritin is the protein-iron complex found in macrophages used for iron storage low in iron-deficiency anemia. 

Although EPO deficiency is the primary cause of CKD anemia, iron deficiency is often present, and it is essential to assess and monitor the CKD patient s iron status (NKF-K/DOQI guidelines). Iron stores in patients with CKD should be maintained so that transferrin saturation (TSAT) is greater than 20% and serum ferritin is greater than 100 ng/mL (100 mcg/L or 225 pmol/L). If iron stores are not maintained appropriately, epoetin or darbepoetin will not be effective, and most CKD patients will require iron supplementation. Oral iron therapy can be used, but it is often ineffective, particularly in CKD patients on dialysis. Therefore, intravenous iron therapy is used extensively in these patients. Details of the pharmacology, pharmacokinetics, adverse effects, interactions, dose, and administration of erythropoietin and iron products have been discussed previously. 

Serum ferritin A complex protein formed in the intestine, containing about 23% iron, the amount of ferritin found in serum is directly related to iron storage in the body. 

The aim of treatment of iron overload is to remove all potentially toxic iron from the body. In hereditary haemochromatosis this can be achieved by weekly phlebotomies of 500 ml until the desired serum ferritin concentration (mostly <50 gg/1) or a normal transferrin iron saturation is reached (Brissot et ah, 2000). 

The earliest and most sensitive laboratory change for iron-deficiency anemia is decreased serum ferritin (storage iron), which should be interpreted in conjunction with decreased transferrin saturation and increased total iron-binding capacity (TIBC). Hb, hematocrit, and RBC indices usually remain normal until later stages of iron-deficiency anemia. 

Diagnosis of anemia of chronic disease is usually one of exclusion, with consideration of coexisting iron and folate deficiencies. Serum iron is usually decreased but, unlike iron-deficiency anemia, serum ferritin is normal or increased and TIBC is decreased. The bone marrow reveals an abundance of iron the peripheral smear reveals normocytic anemia. 

In the same Beltsville study, no changes in clinical parameters or in serum ferritin levels were observed in the men nor in the women and children participating and consuming beef patties extended with the various soy products (54, 55). 

Once in the serum, aluminium can be transported bound to transferrin, and also to albumin and low-molecular ligands such as citrate. However, the transferrrin-aluminium complex will be able to enter cells via the transferrin-transferrin-receptor pathway (see Chapter 8). Within the acidic environment of the endosome, we assume that aluminium would be released from transferrin, but how it exits from this compartment remains unknown. Once in the cytosol of the cell, aluminium is unlikely to be readily incorporated into the iron storage protein ferritin, since this requires redox cycling between Fe2+ and Fe3+ (see Chapter 19). Studies of the subcellular distribution of aluminium in various cell lines and animal models have shown that the majority accumulates in the mitochondria, where it can interfere with calcium homeostasis. Once in the circulation, there seems little doubt that aluminium can cross the blood-brain barrier. 

Clearly this patient has both clinical and haematological symptoms of severe anaemia. The cause is too few red cells low RBC count and PCV but the erythrocytes which are present contain a higher than usual concentration of haemoglobin (MCHC result). Iron deficiency and vitamin B12 deficiency can be ruled out by the high serum ferritin and normal MCV results respectively. The negative HbS screen rules out sickle cell anaemia which is fairly common in Africans. 

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