Serum ferritin and bone marrow iron stores. I. Correlation with absence of iron in biopsy specimens.
ABSTRACT Serum iron, total iron-binding capacity, and percentage saturation of transferrin have classically been used to demonstrate a hypoferremic state; however, these tests may not discriminate between depleted iron stores and conditions associated with defective reticuloendothelial release of iron. Estimation of stainable iron in the bone marrow biopsy specimen is then the most practical way to assess body iron stores. With the availability of a radioimmunoassay procedure for serum ferritin, we undertook a prospective study to determine whether serum ferritin concentrations might replace assessment of the marrow biopsy iron stores as an indicator of hypoferremia. Iron stores were absent from bone marrow biopsy specimens from 104 patients. A good correlation between low serum ferritin levels and absence of iron stores in biopsy specimens was found for 91 patients (87.5%). Thirteen (12.5%) had normal serum ferritin concentrations with absence of biopsy iron. These individuals had hematopoietic malignancies or active hepatic disease, or were receiving iron therapy. In this group, a bone marrow biopsy would still be necessary for evaluation of a hypoferremic state, even though the serum ferritin concentration might be normal.
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ABSTRACT: In veterinary medicine, hyperferritinemia is often observed in dogs with various diseases (e.g., histiocytic sarcoma and immune-mediated hemolytic anemia) without evidence of iron overload. The mechanism underlying hyperferritinemia development is not well understood. Anemia caused by inflammation is termed as anemia of chronic disease (ACD), and experimentally induced ACD is known to cause slight hyperferritinemia. However, almost all these studies were based on short-term acute inflammation. Hepcidin, a protein mainly produced by hepatocytes, is thought to be a key regulator in iron release from reticuloendothelial cells (RECs), and its expression is related to ACD. We hypothesized that in the case of long-term ACD, iron deposition in RECs increases through hepcidin, causing a diachronic increase in serum ferritin levels. In the present study, we used a canine model with repeated subcutaneous administration of turpentine oil every 3 days over a period of 42 days (15 injections) and induced long-term inflammatory conditions; furthermore, we evaluated the change in serum ferritin concentration. Hypoproliferative anemia, bone marrow iron deposition and hypoferremia, which are characteristic of ACD, were observed on administering the turpentine injections. Hepatic iron content, hepatic hepcidin mRNA expression and serum ferritin concentration increased during the early period after turpentine injection, but returned to normal levels later. These results show that experimentally induced long-term ACD caused hypoproliferative anemia without sustained increase in hepcidin expression and did not cause systemic iron overload. Thus, chronic inflammation may not contribute greatly to increase in hyperferritinemia.Journal of Veterinary Medical Science 06/2013; · 0.88 Impact Factor
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ABSTRACT: Serum ferritin concentration increases in dogs in association with various diseases. In this study, we measured serum ferritin levels in dogs with splenic masses, using a sandwich ELISA assay. Eleven dogs with hemangiosarcoma (HSA), six with hematoma, one with hemangioma and three with lymphoma, were enrolled. All dogs with HSA had serum ferritin concentrations above the normal limit (1,357 ng/ml, mean + 2× standard deviation of normal). Increased serum ferritin concentrations have also been observed in few cases of hematoma, hemangioma and lymphoma. Therefore, hyperferritinemia is not specific for splenic HSA, but may have clinical usefulness as a sensitive test for the disease. Further evaluation of serum ferritin concentrations in dogs with splenic HSA is needed.Journal of Veterinary Medical Science 06/2013; · 0.88 Impact Factor
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ABSTRACT: Isolated hepatic tuberculosis is an uncommon manifestation of one of the most common infections worldwide, caused by Mycobacterium tuberculosis. Extremely high serum ferritin, which is regarded as a marker of adult onset Still's disease, has not been observed in patients with tuberculosis of the liver. We report a case of hepatic tuberculosis who presented with clinical criteria of adult-onset Still's disease and extreme hyperferritinemia, which posed a diagnostic confusion. Our patient was a 48-year-old Sri Lankan man who presented with fever, polyarthralgia and a generalized skin rash of three months duration. He had marked constitutional symptoms, oral ulcers, hair loss, anemia and hepatomegaly. Laboratory investigations disclosed an inflammatory syndrome, evidence of hepatic dysfunction, bone marrow suppression and a raised serum ferritin level of 34,674 ng/ml. A rapidly deteriorating course of illness prompted treatment based on a presumptive diagnosis of adult-onset Still's disease until liver histology was available. The patient died of sepsis followed by multi-organ dysfunction. Later, the liver histology revealed tuberculosis. Extrapulmonary tuberculosis, although well known to present with peculiar manifestations, has not been reported to be associated with extremely high levels of serum ferritin in immunocompetent individuals. Isolated hepatic tuberculosis presenting with clinical criteria of adult-onset Still's disease is remarkable. Since tuberculosis remains a potentially curable disease, an awareness of its' protean manifestations is essential.Journal of Medical Case Reports 07/2012; 6(1):195.