Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was carried on 60 male patients, 20 have simple intestinal mansoniasis, 20 have simple urinary bilharziasis and 20 have hepatosplenic mansoniasis. Latent iron deficiency anaemia, defined as those having normal Hb content (greater than 13 g/dl) and low serum ferritin (less than 15 ng/mL). Such latent anaemia was found in 35% of cases with simple mansoniasis, 20% of cases with simple urinary bilharziasis but not in any case with hepatosplenic mansoniasis. Also it was associated with mild intensity of infection.
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PMID:Latent iron deficiency anaemia in schistosomiasis. 249 81

Iron status was assessed using a combination of several biochemical indicators (serum ferritin, erythrocyte protoporphyrin, serum iron, MCV, hemoglobin) in 3,676 apparently healthy children. Children who were 10 months, 2 years and 4 years of age were selected from the population undergoing a free medical check up in a Paris Child Health Center. The prevalence of iron deficiency in children of parents from continental France was 29% in the 10 month olds, 13% in the 2 year olds and 7% in those who were 4 years of age. Corresponding figures in children born of immigrant parents were 50%, 44% and 15% respectively. Iron deficiency anemia was found in 8% of 10 month olds from continental France versus 23% in the other group. Children born of parents from the South Sahara were found to be at high risk for iron deficiency.
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PMID:[Iron status in presumably healthy children 10 months, 2 years and 4 years of age]. 259 46

Plasma ferritin (PF), erythrocyte protoporphyrin (EP) and hemoglobin (Hb) were used to assess the iron status of 158 Filipino pregnant women included as subjects in the third national nutrition survey conducted by the Food and Nutrition Research Institute in 1987. The prevalence of iron depletion was 39.9% based on PF (less than 12 ng/ml). Iron deficient erythropoiesis was present in 36.1% based on EP of greater than 28 micrograms/dl whole blood and 40.5% based on EP/Hb ratio of greater than 2.4. When the criterion of iron deficiency was that both PF and EP were abnormal, the prevalence of deficiency was lower and only 16.4%. Iron deficiency anemia was present in 14.6% based on Hb less than 11 g/dl in addition to abnormal PF and EP. Significantly lower mean values for PF were obtained in women on the 2nd and 3rd trimesters of pregnancy indicating decreasing iron stores and the need for iron therapy to prevent anemia during those periods. The iron status of 38 women who reported taking iron supplements was not significantly different from those who did not take supplements.
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PMID:Assessment of iron status of Filipino pregnant women. 263 54

Haemoglobin (Hb), free erythrocyte protoporphyrin (FEP), ratio of FEP and Hb (FEP/Hb), serum ferritin (SF) packed red cell volume (PCV), serum iron (SI), total iron binding capacity (TIBC), transferrin saturation (TS) were evaluated in 170 healthy pregnant women and their full-term babies. The pregnant women were devided into normal and iron deficient groups. The status of iron nutrition of babies of normal mothers and mothers with iron deficiency anemia (IDA) was compared. It showed that the decreased value of PCV in late pregnancy was mainly related to IDA. While the values of SF, FEP/Hb and Hb were more sensitive for detecting pregnancy associated IDA, the values of FEP, FEP/Hb and Hb in babies of IDA mothers were significantly higher than those in babies of normal mothers. Maternal iron status bore no significant correlation with the iron store of their babies. However, Hb less than 11 g/L, FEP/Hb greater than 4.5 micrograms/g, FEP greater than 0.92 mumol/L or SF less than 50 micrograms/L in early pregnancy were indications for iron supplementation.
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PMID:[Status of iron nutrition in term pregnant women and their newborns]. 275 10

Red cell volume distribution width (RDW-CV) was examined as a means of diagnosing iron deficiency. Iron deficiency was classified as iron deficiency anaemia, prelatent or latent iron deficiency in 1648 students. MCV and RDW-CV (mean +/- ISD) in each group were 89 +/- 4 ft, 12.7 +/- 0.7% in normal individuals, 89 +/- 4 fl, 13.2 +/- 0.8% in prelatent deficiency, 86 +/- 6 fl, 14.0 +/- 1.5% in latent deficiency, and 79 +/- 7 fl, 15.6 +/- 1.7% in iron deficiency anaemia, respectively. Although microcytosis was evident only in iron deficiency anaemia, RDW-CV showed larger values concomitant with the development of iron deficiency. The sensitivity of RDW-CV for the diagnosis of iron deficiency anaemia was 77.1%, and for iron deficiency anaemia and latent deficiency 49.2%, the specificity being 90.6%. In countries with a high prevalence of iron deficiency and low thalassaemia, iron deficiency should be screened by RDW-CV determination without serum iron or ferritin measurements.
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PMID:Change in red blood cell distribution width with iron deficiency. 276 69

Plasma ferritin was measured in 420 apparently healthy active elderly subjects living in the community. Mean values were comparable to other published results for elderly subjects. Higher values were obtained in men and in diabetic subjects. Mean values for men and women after exclusion of subjects with diabetes and other diseases were not significantly lower. It is concluded that a) the age-related rise in plasma ferritin observed in other studies represents a physiologic change, with pathologic processes only playing a small part in contributing to the increase, b) reference intervals appropriate to the elderly should be used, and c) plasma ferritin may not be a useful screening test for iron deficiency anemia or hemochromatosis in the elderly.
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PMID:Plasma ferritin in an elderly population living in the community. 276 82

The paper covers present-day methods of diagnosis, treatment, primary and secondary prophylaxis of iron deficiency anemia. Serum ferritin determination useful for evaluating total iron deposits in the body is thought to allow early diagnosis. Oral administration of iron preparations is recommended as more advantageous. It is emphasized that the disease treatment should not be discontinued after recovery of normal hemoglobin values. The next therapeutic measures are to provide normal levels of serum iron and ferritin.
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PMID:[Treatment and prevention of iron deficiency anemia]. 281 Dec 30

Serum ferritin levels were determined by radioimmunoassay (RIA) method and then analysed in 240 normal full-term pregnant women. Their hemoglobin concentrations were found to be normal in the first trimester. None of them had received any hematonic during their whole pregnancy period. Their mean age was 27.7 years and the mean pregnancy duration was 39.5 weeks. Mean hemoglobin concentration in these normal pregnant women was 12.6 g%. Mean serum ferritin was 23.1 ng/ml. It was significantly lower than the mean value of the normal non-pregnant women of the same age. In this study, we found that even normal pregnant women, 15.42% (37 out of the 240) had subclinical iron deficiency and 12.92% (31 out of the 240) of the previously normal pregnant women had clinical anemia during their term of pregnancy. Multiparity was found to be a factor in the prevalence of iron deficiency but age and gravida number played no role in the occurrence of iron deficiency anemia.
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PMID:Serum ferritin levels and their significance in normal full-term pregnant women. 288 63

Patients with Hb SC disease were found to have microcytic and hyperchromic red cell indices despite mild reticulocytosis. Iron deficiency anemia was ruled out by the finding of normal serum ferritin levels. In order to determine whether the microcytosis was due to coexistent alpha-thalassemia, restriction endonuclease mapping was performed on genomic DNA extracted from peripheral blood leukocytes. Patients with Hb SC disease had microcytic indices despite the presence of a full complement of four alpha-genes (alpha alpha/alpha alpha), suggesting that the microcytosis may be due to cellular dehydration (or xerocytosis), since the mean corpuscular hemoglobin concentration in Hb SC disease patients was significantly higher than in controls. This possibility was investigated further by the determination of RBC cation content. RBC Na levels were similar in SC and normal red cells. Hb SC RBCs, however, had significantly reduced K levels. These findings show that RBC cation content, and thus cell water, is decreased in Hb SC disease. The decreased RBC K level in the presence of normal cellular Na concentration suggests selective K loss that is not due to inhibition of the Na K pump. Ouabain-insensitive K+ efflux was increased to four times normal in SC cells. Cell dehydration was confirmed by the demonstration of increased high-density RBCs on discontinuous Stractan density gradients and by osmotic gradient ektacytometry. Cellular dehydration and its sequelae were worse in CC erythrocytes and milder in AC cells than in Hb SC red cells. Taken together, these data indicate that in Hb SC disease the RBCs are severely dehydrated and typically microcytic and hyperchromic. Hb SC RBCs seem to be dehydrated due to selective K loss. These findings suggest a functional interrelationship between Hb SC, the red cell membrane, and cation regulation.
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PMID:The xerocytosis of Hb SC disease. 294 42

Myeloperoxidase (MPO) activity was studied in adults with iron deficiency anemia (IDA) or anemia of chronic disorders (ACD). MPO activity (biochemical quantitation) was found to be decreased in IDA when compared to the control group (p less than 0.05); ACD subjects also had lower values although the difference was not significant (p less than 0.05). MPO scores (MPO staining) were significantly lower in IDA and ACD subjects than in the healthy control group (p less than 0.05). A significant positive correlation was noted between ferritin (R = 0.40) and percent transferrin saturation (R = 0.37) and MPO activity (p less than 0.001) in IDA and for the healthy controls.
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PMID:Myeloperoxidase activity of polymorphonuclear leukocytes in iron deficiency anemia and anemia of chronic disorders. 300 16


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