Amount Of Stainable Iron Research Articles

A Single Center Study Comparing the Stainable Iron Depositions in 1000 Explanted Cirrhotic Livers of Different Causes.

Background:There have been very few studies evaluating the close association between excess iron and cirrhosis; however, cirrhosis could be regarded as an iron-loading disorder.Objectives:In this study, the goal was to show the levels of the iron content in the liver tissue in certain types of cirrhosis.Patients and Methods:In this 7 year study (2008 - 2014), in 1000 explanted livers, the amount of iron was scored and compared according to the cause of the cirrhosis. The amount of iron in the liver was determined via the histochemical staining of the liver tissue, using Prussian-blue staining. Additionally, in each patient, the serum iron was determined and compared according to the cause of cirrhosis.Results:The highest content of iron has been found in cirrhosis caused by chronic hepatitis (i.e. hepatitis B, C, and autoimmune hepatitis), as well as in alcoholic cirrhosis. The least amount of stainable iron has been shown in biliary cirrhosis.Conclusions:The presence of high stainable iron in patients with cirrhosis, secondary to chronic viral hepatitis, autoimmune hepatitis, and alcoholic hepatitis, should not be considered indicative of the presence of hereditary hemochromatosis; however, in those patients with biliary cirrhosis, a high iron content is rare, and can be a sign of the presence of the high iron Fe (HFE) gene mutation, or another type of hereditary hemochromatosis.

The Effect of Decalcifying Solutions on Hemosiderin Staining

To determine whether routine decalcification may reduce the amount of stainable iron that is visible on tissue sections, samples of liver and lung tissue with excessive iron stores were placed in three standard decalcifying solutions (i) formic acid [33%], formaldehyde [4%], and NaCl [0.85%]; (ii) formic acid [30%], formaldehyde [4%], and water; and (iii) nitric acid [5%] for 24, 48, 72, and 96 h. After exposure to the decalcifying solutions, the tissues were stained with Perls stain. The slides were examined blind and the intensity of iron staining was scored semiquantitatively from 0 to 3+. The trend in all samples over the course of the experiment (96 h) was for reduction in the intensity of hemosiderin staining. As the amount of stainable hemosiderin in tissues may be significantly altered by decalcification, the absence of hemosiderin in tissues adjacent to a fracture site does not necessarily indicate that the injury was acute.

Severe anaemia in an 11-month-old girl

An 11-month-old girl came to Chikwawa District Hospital Malawi in March 2003 with a 7-day history of fever. She had been treated at a rural health center with sulfadoxine-pyrimethamine for suspected malaria without improvement. The child was pale here weight was 7.6 kg (90% weight for height) temperature 38.6°C pulse rate 160 per min and respiratory rate 28 per min. There were no signs of jaundice or bleeding. Her chest was clear liver 3 cm enlarged and her spleen was not palpable. Initial laboratory tests showed haemoglobin (Hb) of 35 g/L and negative malaria microscopy. After obtaining consent from her parents a bone-marrow aspirate was taken as part of a severe anaemia protocol. Blood transfusion was commenced and broad-spectrum antibiotics started. At discharge after two days she was afebrile with Hb of 81 g/L. Additional laboratory results showed platelets 172X10(12)/L; mean cell volume 92.5 fl reticulocytes 1(2% leucocytes 22.1X10(9)/L (neutrophils 36% lymphocytes 47%); folic acid 14.8 ng/mL (normal 3-17) and vitamin B(12) 131.1 pg/mL (200-950); HIV serology and blood culture were negative. Bone-marrow microscopy showed megaloblastic changes and a minimal amount of stainable iron (2% sideroblast no iron particles in macrophages). Flow cytometry showed a high expression of CD71 (transferrin receptor) on the red progenitor cells in accordance with an increased iron need. Because of constipation she could not provide a stool sample at admission but one was collected 4 days after discharge. (excerpt)

Visceral lesions caused by Yersinia pseudotuberculosis, serotype II, in different species of bird

The size and distribution of histological lesions was studied in 14 cases of avian pseudotuberculosis using a combination of serotype-specific immunohistochemistry and image analysis. The material was derived from recent and archival cases in six canaries (Serinus canaria), two zebra finches (Poephila guttata), three psittaciformes (a kaka, Nestor meriondalis, one rainbow lorikeet, Trichoglossus mollucanus, and one budgerigar, Melopsittacus undulatus), and three New Zealand wood pigeons (Hemiphaga novaeseelandiae). The disease observed in the passerine species appeared to have an acute clinical course and the bacterial lesions were predominately enteric. In the pigeons and the psittaciformes examined, the clinical course of the disease was more chronic in nature and involved the liver and spleen. A correlation was found between the amount of stainable iron in the liver of affected birds and the area of bacterial lesions. All of the 11 strains of Yersinia pseudotuberculosis isolated from fresh necropsy material were serotype II, as determined using a standard serum agglutination test. Immunohistochemistry indicated the presence of antigen(s) common to serotype II in histological material from confirmed cases and in another three cases where the organism had been cultured but the serotype not specified. The in vitro virulence characteristics and plasmid profiles of Y. pseudotuberculosis isolates were also determined.

Intrahepatic Iron Variation May Greatly Affect the Hepatic Iron Index

The quantitative hepatic iron index is considered the gold standard for the diagnosis of primary hemochromatosis. While intrahepatic variability in the amount of stainable iron in histologic sections of liver is well known, the quantitative variability has not been addressed. Eight native livers removed at transplantation for cirrhosis associated with hepatitis C were studied. Iron-stained sections from multiple different areas of each liver were examined, and small areas were graded for iron content on a scale of 0 to 4. The fragments of liver corresponding to these were then cut out of the corresponding section of the paraffin block and sent for iron quantitation. We found that marked quantitative heterogeneity in iron content (>260%) can exist in a given liver, leading, in two cases, to false positive results for the diagnosis of hemochromatosis. In addition, it was found that quantitative iron content did indeed linearly correlate with histologic grading. Thus, intrahepatic variation in iron content in a given liver is yet another reason to interpret the hepatic iron index with caution.

The effect of decalcification and choice of fixative on histiocytic iron in bone marrow core biopsies.

IRon stains are often used for bone marrow core biopsies obtained by needle biopsy of the iliac crest. Because bone must be decalcified by brief treatment with acid, it is possible that an undetermined amount of stainable histiocytic iron may be lost. A study was carried out to determine whether decalcification results in loss of histiocytic iron and the effects of fixatives and the recovery of histiocytic iron in decalcified bone marrow tissue. Aspirates of bone marrow were stained for iron with Prussian blue. Because aspirate material does not require decalcification, it served as a control for the study. One hundred bone marrow biopsies and accompanying aspirates from 100 adult subjects were evaluated. Fifty bone marrow biopsies were fixed using a fixative containing mercuric chloride (B-5) and the remaining 50 were fixed in zinc-formalin. Histiocytic iron was graded as minimal, moderate or marked depending on whether less than 5, 6-10, or more than 10 iron positive histiocytes, respectively, were observed. When histiocytic iron was markedly present in aspirate material, at least moderate amounts of stainable iron were found in 22 of 25 B-5 fixed and 21 of 25 zinc-formalin fixed decalcified bone marrow. When aspirate histiocytic iron was minimal or moderate, 14 of 25 B-5 fixed and 7 of 25 zinc-formalin fixed decalcified bone marrow specimens revealed histiocytic iron. Decalcification results in decreased recovery of stainable iron, and where histiocytic iron is minimally or moderately present, B-5 fixation results in greater postdecalcification recovery. There was no significant difference in recovery when larger quantities of histiocytic iron were present prior to the decalcification step.

Elevated serum iron predicts poor response to interferon treatment in patients with chronic HCV infection.

To date, there are no firm clinical, demographic, biochemical, serologic, or histologic features predicting which patients with chronic hepatitis C are more likely to respond to therapy with interferon-alpha. Serum iron, total iron-binding capacity, transferrin saturation, and ferritin were measured in the fasting state. The amount of stainable iron in liver biopsy specimens was evaluated histochemically as well. All patients received subcutaneous recombinant human IFN-alpha 2a three million units thrice weekly by self-administration. Eleven of 13 (84%) responders had low to normal serum iron levels as compared to one of 26 (4%) nonresponders (P < 0.001). The serum transferrin was similar in both groups, but iron saturation was significantly lower in responders (30 +/- 10%) than in nonresponders (53 +/- 12%) (P< 0.001). Serum ferritin and hepatic iron content were higher in nonresponders (NS). It is suggested that increased serum iron and transferrin saturation blunt the action of interferon, as they have opposite effects on the immune system. Iron overload can thus lead to a poor response to interferon. It remains to be seen whether reducing iron overload will improve the response to interferon therapy.

Limited value of serum ferritin in evaluating iron status in children with protein-energy malnutrition.

26 of 46 Nigerian children with protein-energy malnutrition (PEM) had elevated S-Ferritin levels; the geometric mean value in the entire group of children with PEM was 146 micrograms/l and the observed range 11-7000 micrograms/l. There was no statistically significant correlation between the logarithm of the S-Ferritin level and the amount of stainable iron in marrow fragments (r = 0.23; p greater than 0.2). A stepwise multiple linear regression analysis in which the logarithm of the S-Ferritin level was used as the dependent variable and a total of 17 clinical, biochemical and haematological parameters were used as the independent variables showed that 34.8% of the variability in S-Ferritin could be accounted for by variations in the percentage of lymphocytes in the bone marrow. We speculate that the latter parameter may be an index of previous infection and that the elevated S-Ferritin levels may, therefore, be at least partly caused by infections. Increased serum aspartate transaminase activities were also encountered in PEM, suggesting that hepatocellular damage may contribute to the high S-Ferritin levels in this condition. Our data indicate that S-Ferritin has a limited value as an indicator of iron status in subjects with PEM, presumably because of the frequency of infections and of hepatocellular damage in such subjects.

Comparison of stainable iron in bone marrow smears and needle marrow biopsies

In 111 patients, the amount of stainable iron was compared in bone marrow smears and marrow needle biopsies. The correlation between the two methods was good (r = 0,73, p &lt; 0,001), but with a higher frequency of false negative results in the marrow biopsies (5,4%) than the marrow smears (1,8%). As both methods may occasionally fail, it may be desirable to perform iron staining in both smears and biopsies. If it is necessary to choose one of the methods, we would recommend bone marrow smears for the routine determination of stainable marrow iron stores.

Iron absorption and serum ferritin in chronic inflammatory bowel disease.

Iron absorption and serum ferritin concentration were studied in 44 patients with chronic inflammatory bowel disease (CIBD) (31 with Crohn's disease (CD) and 13 with ulcerative colitis (UC)), in 11 control subjects and in 3 patients with simple iron-deficiency anaemia. Iron absorption was determined from both whole body counting and red cell 59Fe incorporation following oral administration of 59FeCl3 with a small carrier dose (0.5 mg Fe). Serum ferritin was measured by a two-site immunoradiometric assay. Iron stores were estimated from the amount of stainable iron in sternal marrow. Normal range of iron absorption was 7–86%. In patients with CD and UC no correlation was present between iron absorption and disease activity, site of lesion, intestinal resection (no patient with severe short-bowel syndrome was studied), serum iron, transferrin, albumin or haemoglobin. In contrast, a significant and inverse correlation was found between iron absorption and serum ferritin, and a significantly positive correlation was found between serum ferritin and the iron content of sternal marrow. Following intravenous supply of 1 g iron (as iron-dextran) in 8 patients with CIBD, iron absorption decreased and serum ferritin increased, both on a statistically significant level. It is concluded that: (1) The ability to absorb iron is well preserved in CIBD, even in severe cases. (2) A decreased serum iron concentration does not imply an iron-deficiency state in CIBD. (3) Serum ferritin determination is a sensitive and little invasive way to assess whether a patient with CIBD is iron-deficient or not. (4) Parenteral supply of iron is in practice superior to oral iron medication in iron-deficient patients with CIBD.

Stainable iron in aspirated and needle-biopsy specimens of marrow: a source of error.

Marrow iron was assessed in needle biopsy sections and in simultaneously obtained aspirated smears and aspirated clot sections from 251 patients. Significantly different amounts of stainable iron were observed in needle biopsy sections and aspirated smears in 15% of the specimens. The usual difference consisted of significantly less stainable iron in needle biopsy sections as compared to the aspirated smears (13%). Of clinical importance was the finding of absent stainable iron in 8% of the needle biopsy sections, in contrast to the definite deposits observed in the corresponding aspirated smear. Of similar interest was the observation that 6% of the needle biopsy sections had significantly less stainable iron than corresponding hemosiderotic smears. The amounts of stainable iron in needle biopsy sections were similar to the amounts observed in the corresponding aspirated clot sections. Evaluation of marrow iron using needle biopsy sections as well as aspirated clot sections differs from results observed in aspirated smears and could be a source of significant error in the assessment of iron stores.

Iron Metabolism, Sickle Cell Disease, and Response to Cyanate

Abstract In an attempt to understand the variability of the hematologic response to oral sodium cyanate, iron metabolism was studied in a group of 39 patients with sickel cell disease. Eleven of the 39 patients were found to have no stainable iron in the marrow despite the fact that patients with sickle cell disease are generally considered to have hemosiderosis. The mean per cent saturation and total iron-binding capacity were in the low-normal range in sickle cell patients whether or not stainable iron was present in the bone marrow aspirate. Serum ferritin concentrations, on the other hand, were found to be high in both groups (greater than 500 mu g/liter) when compared to controls (60 mu g/liter). The high serum ferritin levels denoted significant total- body iron deposition which may be unavailable for normal metabolic processes. One patient with no stainable iron in the bone marrow aspirate did respond to iron therapy alone with an increase in hemoglobin concentration. Serum ceruloplasmin levels were also found to be high in sickle cell disease patients. The ability to respond to oral cyanate therapy was correlated with the amount of stainable iron in the bone marrow aspirate. These studies emphasize the necessity of a reevaluation of iron metabolism in the pathophysiology and treatment of sickle cell disease.

Iron metabolism, sickle cell disease, and response to cyanate

In an attempt to understand the variability of the hematologic response to oral sodium cyanate, iron metabolism was studied in a group of 39 patients with sickel cell disease. Eleven of the 39 patients were found to have no stainable iron in the marrow despite the fact that patients with sickle cell disease are generally considered to have hemosiderosis. The mean per cent saturation and total iron-binding capacity were in the low-normal range in sickle cell patients whether or not stainable iron was present in the bone marrow aspirate. Serum ferritin concentrations, on the other hand, were found to be high in both groups (greater than 500 mu g/liter) when compared to controls (60 mu g/liter). The high serum ferritin levels denoted significant total-body iron deposition which may be unavailable for normal metabolic processes. One patient with no stainable iron in the bone marrow aspirate did respond to iron therapy alone with an increase in hemoglobin concentration. Serum ceruloplasmin levels were also found to be high in sickle cell disease patients. The ability to respond to oral cyanate therapy was correlated with the amount of stainable iron in the bone marrow aspirate. These studies emphasize the necessity of a reevaluation of iron metabolism in the pathophysiology and treatment of sickle cell disease.

Iron deficiency anaemia and "normal" bone marrow haemosiderin.

During a survey of patients with epithelial symptoms, pica and restless legs an apparently normal amount of stainable iron was found in the bone marrow of four women with chronic iron deficiency anaemia. They all had previously been treated with different parenteral iron preparations. No massive iron dextran infusion had been given. The diagnosis of iron deficiency was confirmed by a positive response to iron therapy. There was no indication that these iron complexes which were slowly utilized (if at all) had any harmful effects. The finding is primarily important from a diagnostic point of view.