Serum ferritin level

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... 

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. 

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. 

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). 

Biliary excretion As most entacapone excretion is via the bile, exercise caution when drugs known to interfere with biliary excretion, glucuronidation, and intestinal beta-glucuronidase are given concurrently with entacapone (see Drug Interactions). Lab test abnormalities Entacapone is an iron chelator. The impact of entacapone on the body s iron stores is unknown however, a tendency towards decreasing serum iron concentrations was noted in clinical trials. In a controlled clinical study, serum ferritin levels (as a marker of iron deficiency and subclinical anemia) were not P.764... 

Haemochomatosis should be treated with venesection, initially of 500 ml weekly and guided by serial serum ferritin levels and liver biopsy to assess residual iron stores. 

Ferritin is detectable in serum. Since the ferritin present in serum is in equilibrium with storage ferritin in reticuloendothelial tissues, the serum ferritin level can be used to estimate total body iron stores. 

A neurological examination is normal in patients with the primary form of RLS, but patients with late-onset RLS symptoms and secondary forms may show evidence of a peripheral neuropathy or radiculopathy [38], Apart from the established causes of secondary RLS, there are no known physical abnormalities associated with RLS. A low to normal serum ferritin level (45-50 mg/L) has been related to increased severity of RLS, and may be associated with an increased risk of the occurrence of RLS even in patients with normal hemoglobin levels [37,39], Therefore, evaluations of serum ferritin levels and percentage of iron saturation are highly recommended as part of the medical evaluation for RLS. 

There is an association between iron deficiency anemia and RLS thus patients should be screened with complete blood count indices and for serum ferritin level. The iron deficit will not be found using normal parameters such as a complete blood count and iron level. A serum ferritin level of <50 is associated with RLS. 

Wolff B, Volzke H, Ludermann J, et al. Association between high serum ferritin levels and carotid atherosclerosis in the study of health in Pomerania (SHIP). Stroke 2004 35(2) 453-457. 

The ferritin found in each tissue has a characteristic structure, and exists as isoferritin. Of special interest is the serum ferritin, which is considered to be different from any specific isoferritin. The serum ferritin level reflects the iron status of the body. 

The diagnosis of iron deficiency has its difficulties and ambiguities. Severe iron deficiency can be detected easily by the marked reduction in hemoglobin concentration, mean corpuscular hemoglobin and decreased serum iron concentration. However, in mild iron deficiency hemoglobin concentration, transferrin saturation, and serum ferritin levels are frequently normal in patients with depleted bone... 

Once an iron deficiency has been detected by low serum ferritin levels, the preceding three tests can be used to estimate its severity. 

Iron is rapidly mobilized from tissue stores (ferritin) during early pregnancy. This mobilization is reflected by decreases in serum ferritin levels. Ferritin levels may drop from a normal value of 60 ng/ml to about IS ng/ml during the first 2 months of pregnancy. The iron is being moMlized to expand the blood volume of the mother and to produce placental and fetal tissues. Apparently, the drop in serum ferritin in early pregnancy cannot be diminished by dietary iron supplements. 

Wjebu, M. S. (1980). Effect of iron therapy on serum ferritin levels in iron-deficiency anemia. Blood 56,138-140. 

ST12 McCarthy, M., Oeser, T.H., Kahn, S.E. and Bermes, E.W. (1985). Evaluation of the Stratus immunoassay system in the determination of serum ferritin levels. Clin. Chem. 31,924, Abstr. 111. 

Reference mtervals for serum ferritin levels are summarized in Table 31-5. However, considerable variation in reference values has been observed with different methods for serum ferritin assay. Consequently, reference intervals must be determined for each laboratory. 

Keep in mind that iron is a key element in the body s energy-producing system. If you lack energy, tire easily, or would like more energy, you should find out if your serum ferritin level is low. That s the best lab test for iron deficiency. Meanwhile, don t take any iron supplements over 20 milligrams. (You can find tablets or capsules with up to 300 milligrams of iron. That s a very dangerous dose.)... 

Measurement of serum ferritin levels has diagnostic utility. In iron deficiency anemia (discussed later), serum ferritin levels are low in iron storage disease, the levels are high. However, serum ferritin levels can also be elevated under many other circumstances, including liver diseases and chronic inflammatory diseases. 

Treatment of hereditary hemochromatosis is therapeutic phlebotomy (discussed earlier). This method is safe, effective, and life saving, and ideally should begin before symptoms develop. Serum ferritin levels are used as a surrogate marker for estimating total-body iron stores. Morphologic studies and quantitative determination of iron in liver tissue obtained by biopsy have been used in the assessment of early hereditary hemochromatosis and the degree of liver injury. 

The concentration of ferritin (storage iron) in the serum is proportional to total iron stores, and conseqnently is a reliable indicator of body iron stores. Ferritin levels indicate the amonnt of iron stored in the liver, spleen, and bone marrow cells. Therefore it is the best indicator of iron deficiency or iron overload. Low serum ferritin levels are virtually diagnostic of IDA, as they decrease only in association with IDA. In contrast, serum iron levels may decrease both in IDA and in ACD. Serum ferritin is an acnte phase reactant, so chronic infection or inflammation can raise its concentration independent of iron status, masking depleted tissne stores. This limits the specificity and the ntil-ity of the serum ferritin if it is normal or high in a chronically ill patient. 

Most patients tolerate EPO therapy well. Iron deficiency can occur in patients treated with EPO and close monitoring of iron levels is necessary. Oral iron supplementation should be given if transferrin saturation drops to 20% or the serum ferritin level drops below 100 ng/mL. Some patients develop functional iron deficiency, in which the iron stores are normal, but the supply of iron to the erythroid marrow is less than that necessary to support the demand for RBC production. Therefore many practitioners routinely supplement EPO therapy with oral iron therapy. The hypertension commonly seen in end-stage renal disease patients on EPO is far less common in AIDS patients. More common toxicities of EPO administration include nausea, headache, fever, bone pain, and fatigue. Other adverse effects to monitor include seizures, thrombotic events, and allergic reactions such as rash or local reactions at the injection site. 

Children with anemia as identified by labs are usually treated with further evaluation performed only if treatment response is inadeqnate. Therapeutic outcomes are assessed in children by checking Hgb, Hct, and RBC indices at 6 to 8 weeks after initiation of iron therapy. In premature infants, Hgb or Hct should be monitored weekly. Reticulocyte counts should be checked at 4 to 6 weeks after birth. Reticulocyte count, Hct, and absolute neutrophil counts are measured before and 1 to 2 weeks after starting EPO treatment. EPO is held for an absolnte neutrophil count of less than 1,000 units/L. Serum ferritin levels may help evaluate infants not responding. Use of EPO in premature infants is not associated with the side effects frequently seen in adults. 

Most patients who require dialysis have a normocytic normochronic anemia and a hypoproliferative bone marrow. As erythropoiesis decreases with advancing renal disease, iron shifts from circulating red cells to the reticuloendothelial system, leading to high serum ferritin levels. Repeated blood transfusion is also a common cause of iron overload and hyperferritinemia. Clearly the most important cause of the anemia of chronic renal failure is decreased erythropoietin production by the kidneys uremic patients have much lower plasma erythropoietin levels than comparably anemic patients with normal renal function (E8). Less important causes are shortened red cell survival, iron or folate deficiency, aluminum intoxication, and osteitis fibrosa cystica (E8). Uremic retention products such as methylguanidine (G10) and spermidine (R2) may also have an adverse effect on erythropoiesis. 

Recombinant erythropoietin, recently produced in large quantities by innoculat-ing the erythropoietin gene into the Chinese hamster ovary, has been used to treat the anemia of chronic renal failure with dramatic results (E6, E7, H5, L13, W8). Anemia is corrected in most patients, and there is a greater sense of well being and exercise tolerance (Mil). Iron overload from previous blood transfusions improves and serum ferritin levels fall as treatment with erythropoietin is continued. 

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