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PubMed1976

[The effect of mesterolone in panmyelopathic anemia and anemia of renal failure].

A controlled randomized multicenter trial was carried out to examine the therapeutic value of the androgen mesterolone in aplastic anemia and anemia of renal failure. the drug was given in a dose of 2 mg/kg orally for 6 months. Control patients received no androgens but were otherwise similarily treated. 31 patients with aplastic anemia could be evaluated. No significant difference was found between androgen treated control cases in respect to bone marrow cellularity, improvement of peripheral blood cell counts or survival. In a group of 14 patients not being hemodialyzed with anemia from renal failure, 3 of the androgen treated and none of the control patients showed progressive and significant improvement of erythropoiesis; however, this was not a statistically significant difference when the both groups of patients were compared. The results do not suggest that the androgen mesterolone is of therapeutic value in the majority of adult patients with aplastic anemia. Possible reasons of the discrepancy to positive results reported in the literature are discussed.

Adolescent↗
PubMed1983

Rate of repair of iron deficiency anemia and blood loss anemia in young and mature rats.

The purpose of this study was to evaluate the effect of age on the rate of recovery from iron deficiency and red cell loss anemia in the rat. Iron-deficient diets and exchange transfusions with plasma were used to decrease the hematocrit by about 40% below the control value. The results showed progressively slower reversal of the anemia of red cell loss with increasing age. Hematocrit reached control values after 5, 10, and 14 days, at 50, 100, and 360 days of age, respectively. In contrast, iron-deficiency anemia was reversed at similar rates after intravenous treatment with iron dextran; control hematocrit values were reached after 4 and 5 days in the 50-and 100-day-old rats, respectively. The results indicate that the rate of reversal of the anemia of red cell loss is more age-dependent than the rate of reversal of iron-deficiency anemia in the male rat.

Aging↗
PubMed2005

Anemia, iron deficiency, and iron deficiency anemia in 12-36-mo-old children from low-income families.

BACKGROUND: Iron deficiency (ID) is the most common nutritional deficiency in the world and remains relatively common in at-risk groups in the United States. The actual prevalence of anemia, ID, and iron deficiency anemia (IDA) in California remains unclear. OBJECTIVE: The objective was to determine the prevalence of anemia, low iron stores, ID, and IDA in children participating in the Special Supplemental Nutrition Program for Women, Infants and Children (WIC) population, and to assess the value of using hemoglobin to predict ID. DESIGN: This was a cross-sectional study of a convenience sample of 12-36-mo-old children from WIC clinics in 2 California counties. RESULTS: The prevalence of anemia was 11.1% (hemoglobin <110 g/L at 12-24 mo or <111 g/L at 24-36 mo). Study- and literature-determined abnormal values for iron measures were as follows: serum ferritin or=8.4 or >10.0 microg/mL, and transferrin saturation or=2 abnormal iron measures) were 16.2% and 8.8%, and of IDA (ID with low hemoglobin) were 3.4% and 3.2% on the basis of study- and literature-determined cutoffs, respectively. Hemoglobin concentration was used to predict study- and literature-determined ID on the basis of receiver operating characteristic curves. The sensitivity of low hemoglobin in predicting study- and literature-determined ID was low (23.2% and 40.0%, respectively). CONCLUSIONS: Anemia and ID were prevalent in this WIC sample, but IDA was uncommon. Low hemoglobin is a poor predictor of ID.

Anemia↗
PubMedDate not supplied

Asplenia in a patient with Fanconi's anemia-like congenital aplastic anemia.

Fanconi's anemia (FA) is an autosomal recessive disease manifested by pancytopenia resulting from bone marrow failure, variable physical anomalies and cancer susceptibility. A seven-year-old girl with Fanconi's anemia-like congenital aplastic anemia and concurrent asplenia without the congenital heart defects or the abdominal heterotaxia is reported. Asplenia was indicated using denatured red cells labelled with 51Cr, abdominal ultrasonography and computerized tomography. Immunological studies showed immunoglobulins (IgG, IgA, IgM), C3 and C4 levels within normal limits and the percentage of CD3, and C4 cells and the CD4/CD8 ratio decreased. The patient had not been exposed to recurrent pneumococcal infections. We think that isolated asplenia may occur in patients with Fanconi's anemia-like congenital aplastic anemia without the congenital heart diseases or abdominal heterotaxia.

Anemia, Aplastic↗
PubMed1992

Serum transferrin receptor distinguishes the anemia of chronic disease from iron deficiency anemia.

Recent studies have shown that the serum transferrin receptor is a sensitive, quantitative measure of tissue iron deficiency. This study was undertaken to determine the serum transferrin receptor's ability to distinguish iron-deficiency anemia from the anemia of chronic inflammation and to identify iron deficiency in patients with liver disease. The mean transferrin receptor level in 17 normal controls was 5.36 +/- 0.82 mg/L compared with 13.91 +/- 4.63 mg/L in 17 patients with iron-deficiency anemia (p less than 0.001). The mean serum receptor level was normal in all 20 patients with acute infection, including five with acute hepatitis, and was also normal in 8 of 10 anemic patients with chronic liver disease. Receptor levels were in the normal range in all but 4 of 41 patients with anemia of chronic disease. We conclude that unlike serum ferritin levels, which are disproportionately elevated in relation to iron stores in patients with inflammation or liver disease, the serum transferrin receptor level is not affected by these disorders and is therefore a reliable laboratory index of iron deficiency anemia.

Anemia↗
PubMed1993

Pathologic features associated with decreased longevity of mutant sphha/sphha mice with chronic hemolytic anemia: similarities to sequelae of sickle cell anemia in humans.

A colony of sphha/sphha mice with congenital hemolytic anemia and an abnormality in erythrocyte spectrin assembly was screened to determine the cause of premature death. Sphha/sphha mice have decreased life span, with 50% of animals dying by 6 months of age. The phenotype of these mutant mice includes moderate anemia (hematocrit: 21 to 28%), reticulocytosis, leukocytosis, lymphocytosis, extensive extramedullary hematopoiesis in spleen and liver, lymph node hyperplasia and membranoproliferative glomerulonephritis. With increased surveillance of this mouse colony, 20 clinically sick anemic mice were evaluated (complete blood counts and cultures of blood), euthanized and necropsied. Compared with anemic mice without clinical signs of disease, sick anemic mice had significantly higher white blood cell counts with only 4 (20%) of 20 animals being severely anemic (hematocrit: 4 to 8%). Blood from 11 (45%) of 20 animals was culture-positive for Pasteurella pneumotropica, Enterococcus, and/or Escherichia coli. In addition to the usual lesions in sphha/sphha mice, sick anemic mice had pneumonitis (95%) with thrombosis and infarction (80%) of one or more organs (spleen, myocardium, pancreas, liver, or bone marrow). The thrombotic tendency that accompanies the chronic hemolytic anemia in sphha/sphha mice, as well as the other clinicopathologic changes in these mutant mice, bears a striking resemblance to some poorly understood sequelae in human patients with sickle cell anemia. This mouse model may be useful in studying the pathophysiology of complications associated with sickle cell anemia in humans.

Anemia, Hemolytic↗
PubMed1998

Effect of androgen therapy and anemia on serum erythropoietin levels in patients with aplastic anemia and myelodysplastic syndromes.

Immunoreactive serum erythropoietin (EPO) was measured in anemic and non-anemic patients with acquired non-severe aplastic anemia (AA; n = 22) and myelodysplastic syndromes (MDS; n = 31) receiving or not androgens to examine the effect of androgen therapy and anemia on EPO levels in these disorders. Soluble transferrin receptor (TfR) and absolute reticulocyte count (ARC) were also assayed in order to evaluate erythropoietic activity. AA and MDS patients were stratified for anemia and androgen treatment as follows: 12 untreated anemic patients; 17 anemic patients during androgen therapy; 14 non-anemic patients without any treatment (> 1 year); and 10 non-anemic patients on androgen therapy. Although EPO levels in non-anemic patients were significantly higher than in healthy controls (n = 29) no statistically significant differences in Hb and EPO values were found between non-anemic patients receiving or not androgen therapy. In the linear regression analysis between Hb and log EPO concentration, no statistically significant differences in the slopes between untreated and androgen-treated anemic groups nor between both groups and patients with iron deficiency anemia (n = 23) were observed. However, the y intercept (log EPO) of regression line was significantly higher in androgen-treated anemic patients than in the androgen therapy-free anemic group. Serum TfR levels were higher in treated than in untreated anemic patients, whereas ARC was not different between both groups. These data seemingly indicate that (1) androgens at pharmacological doses do not increase serum EPO levels in non-anemic AA and MDS patients, and (2) in patients with AA and MDS, androgen-driven EPO stimulation is appreciably enhanced by anemia.

Adult↗
PubMed1990

Improvement of anemia by recombinant erythropoietin in patients with myelodysplastic syndromes and aplastic anemia.

Eight patients with myelodysplastic syndromes (MDS) and four patients with aplastic anemia (AA) were treated with recombinant erythropoietin (rEpo) to investigate its effect on the anemia of these patients. rEpo was administered by i.v. injection three times a week for at least four weeks. The doses were 3,000, 6,000, or 12,000 U/day. Despite an elevated "endogenous" Epo level, a greater than 1.5 g/dl increase in hemoglobin (Hb) concentration was observed in one patient with refractory anemia (RA), one patient with refractory anemia with excess of blasts (RAEB), and one patient with AA. A greater than 50% decrease in red cell transfusion requirement was observed in one patient with RA and one patient with AA. One RA patient and one AA patient have received rEpo as maintenance therapy for more than 64 and 100 weeks, respectively. They no longer need red cell transfusions and have had a normal Hb concentration and normal ferrokinetics. No side effect was seen. These results indicate that rEpo may benefit some patients with MDS and AA who are dependent on red cell transfusions while further studies will be necessary to elucidate the mechanism by which rEpo stimulates erythropoiesis and improves anemia in patients with these diseases.

Adult↗
PubMed2004

[Normocytic anemia in the elderly. Should the cause of anemia systematically investigated independently of hemoglobin concentration?].

UNLABELLED: In clinical practice the will to find out the cause of normocytic anemia (NA) in elderly patients is preferentially based on individual physician's background rather than on objective data such as their hemoglobin level. However, it could be postulate that this clinical performance depends on this "cut off" of hemoglobin (more this value is decreased more it could be easy to find the cause of anemia). The aim of this study was to investigate the relationship between the number of cases with defined cause of NA (after a standardized procedure) and the level of hemoglobin. METHODS: In this prospective study 211 inpatients aged 70 years or more with NA disclosed on admission or during hospitalization have been selected. In 162 of them finally included, a standardized procedure with complementary explorations was performed. RESULTS: In 134 patients, the cause of NA was established amongst inflammatory diseases and chronic renal failure was the most frequently identified. In 20%, anemia was multifactorial. Despite investigations anemia remained unexplained in 17.3% of studied patients. For a decrease of at least 10% below the normal range of hemoglobin level, sensitivity of diagnosis was 70% and specificity 60%. Positive predictive value to make the diagnosis when hemoglobin level was below 20% from normal value was 100%. CONCLUSION: The cause of NA in elderly patients after basic explorations may be assessed in up to 80% of cases. We found a significant relationship between the value of hemoglobin level and the number of anemia with confirmed diagnosis. More hemoglobin level is decreased better is clinical performance.

Aged↗
PubMed1992

Microcytic anemia. Differential diagnosis and management of iron deficiency anemia.

Microcytic anemia is defined as the presence of small, often hypochromic, red blood cells in a peripheral blood smear and is usually characterized by a low MCV (less than 83 micron 3). Iron deficiency is the most common cause of microcytic anemia. The absence of iron stores in the bone marrow remains the most definitive test for differentiating iron deficiency from the other microcytic states, ie, anemia of chronic disease, thalassemia, and sideroblastic anemia. However, measurement of serum ferritin, iron concentration, transferrin saturation and iron-binding capacity, and, more recently, serum transferrin receptors may obviate proceeding to bone marrow evaluation. The human body maintains iron homeostasis by recycling the majority of its stores. Disruptions in this balance are commonly seen during menstruation, pregnancy, and gastrointestinal bleeding. Although the iron-absorptive capacity is able to increase upon feedback regarding total body iron stores or erythropoietic activity, this physiologic response is minimal. Significant iron loss requires replacement with iron supplements. The vast majority of patients respond effectively to inexpensive and usually well-tolerated oral iron preparations. In the rare circumstances of malabsorption, losses exceeding maximal oral replacement, or true intolerance, parenteral iron dextran is effective. In either form of treatment, it is necessary to replete iron stores in addition to correcting the anemia.

Anemia, Hypochromic↗
PubMed1994

Anemia and iron-deficiency anemia: compilation of data on pregnancy outcome.

Anemia diagnosed early in pregnancy is associated with increased risks of low birth weight and preterm delivery. In several studies, the association between anemia and outcomes reversed direction during the third trimester; maternal anemia was no longer a risk factor for poor pregnancy outcomes. Camden study data were used to examine the probable cause of this observation. Maternal iron-deficiency anemia, diagnosed at entry to prenatal care, was associated with low dietary energy and iron, inadequate gestational gain, and twofold or greater increases in the risks of preterm delivery and low birth weight. During the third trimester, these associations (except with inadequate gestational gain) were no longer present. This reversal of risk status may be attributable to the poor predictive value of anemia and iron deficiency tests during the third trimester. However, the relationship between poor diet (with inadequate iron intake) and increased likelihood of preterm delivery persisted during the third trimester.

Anemia, Hypochromic↗
PubMed2004

Low dose daily iron supplementation improves iron status and appetite but not anemia, whereas quarterly anthelminthic treatment improves growth, appetite and anemia in Zanzibari preschool children.

Iron deficiency and helminth infections are two common conditions of children in developing countries. The consequences of helminth infection in young children are not well described, and the efficacy of low dose iron supplementation is not well documented in malaria-endemic settings. A 12-mo randomized, placebo controlled, double-blind trial of 10 mg daily iron and/or mebendazole (500 mg) every 3 mo was conducted in a community-based sample of 459 Zanzibari children age 6-71 mo with hemoglobin > 70 g/L at baseline. The trial was designed to examine treatment effects on growth, anemia and appetite in two age subgroups. Iron did not affect growth retardation, hemoglobin concentration or mild or moderate anemia (hemoglobin < 110 g/L or < 90 g/L, respectively), but iron significantly improved serum ferritin and erythrocyte protoporphyrin. Mebendazole significantly reduced wasting malnutrition. but only in children <30 mo old. The adjusted odds ratios (AORs) for mebendazole in this age group were 0.38 (95% CI: 0.16, 0.90) for weight-for-height less than -1 Z-score and 0.29 (0.09, 0.91) for small arm circumference. In children <24 mo old, mebendazole also reduced moderate anemia (AOR: 0.41, 0.18, 0.94). Both iron and mebendazole improved children's appetite, according to mothers' report. In this study, iron's effect on anemia was limited, likely constrained by infection, inflammation and perhaps other nutrient deficiencies. Mebendazole treatment caused unexpected and significant reductions in wasting malnutrition and anemia in very young children with light infections. We hypothesize that incident helminth infections may stimulate inflammatory immune responses in young children, with deleterious effects on protein metabolism and erythropoiesis.

Anemia, Iron-Deficiency↗
PubMedDate not supplied

Anemia and iron target realization in 1998: clinical management of anemia in 1,639 patients on hemodialysis.

Anemia management in hemodialysis patients continues to evolve, and recently, greater emphasis has been placed on the wider use of intravenous iron to maintain adequate iron levels. This survey provides scarcely available yet potentially useful information on the clinical treatment of anemia in a large cohort of hemodialysis patients. The erythropoietin and iron administration details and pertinent laboratory measurements from 1,639 patients were analyzed for the month of December, 1998. A standardized protocol had been used in that erythropoietin was begun at a total weekly dose of 150 U/kg IV or 100 U/kg subcutaneously and was then adjusted to maintain a hematocrit (Hct) of 33-36%. Iron supplements, oral, IV, or both, were administered to maintain percent transferrin saturation (TSAT) at 20-30% and/or a serum ferritin of 100-500 ng/ml. No intravenous iron was administered if the ferritin was more than 500 ng/ml. Although 82% of patients were on iron supplementation and, among them, 58% were on IV iron, the percentage of patients with TSAT >20, i.e., bioavailable iron, was only 51%. The serum ferritin was high at 498 +/- 10 ng/ml (mean +/- SEM) and 88% and 10% of patients had serum ferritin >100 and >1,000 ng/ml, respectively, suggestive of sequestration of part of the infused iron. Erythropoietin was administered to 96% of patients, 99.5% by IV route. The latter was consistent with the US dialysis population at large but in variance with DOQI preference for the subcutaneous route. The target Hct range of 33-36 was found in 33%, with a mean Hct of 34.0 +/- 0.12. When the data were reanalyzed by excluding patients who had not been receiving erythropoietin and had not been on dialysis for at least 3 months, the percentage of patients achieving the target Hct increased to 37%. Paired analysis of 875 patients present in 1996 and 1998 showed that, although there was a marked increase in the use of IV iron, the improvement in anemia was modest, and there was evidence for increased iron accumulation. In summary, this 1998 survey on the clinical practice of anemia management in a large hemodialysis population indicates that there is a marked increase in need-based IV iron usage that was associated with modest improvement in anemia and evidence for increased iron storage. A maintenance iron dosing protocol with smaller doses of iron, such as 25 mg of iron dextran per hemodialysis, may make bioavailable iron continuously present for erythropoiesis, yet may reduce the chance for iron catalyzed lipid peroxidation and tissue iron deposition.

Anemia↗
PubMed1996

Hydroxyurea and sickle cell anemia. Clinical utility of a myelosuppressive "switching" agent. The Multicenter Study of Hydroxyurea in Sickle Cell Anemia.

Painful crises in patients with sickle cell anemia are caused by vaso-occlusion and infarction. Occlusion of blood vessels depends on (at least) their diameter, the deformability of red cells, and the adhesion of blood cells to endothelium. Deoxygenated sickle cells are rigid because they contain linear polymers of hemoglobin S (Hb S); polymerization is highly concentration dependent, and dilution of Hb S by a nonsickling hemoglobin such as fetal hemoglobin (Hb F) would be expected to lead ultimately to a decrease in the frequency of painful crises. It might also be expected to decrease the severity of anemia, although the pathogenesis of anemia in sickle cell anemia (SS disease) is not clearly understood. Reversion to production of fetal rather than adult hemoglobin became practical with the discovery that HU was an orally effective and relatively safe "switching agent." Preliminary dose-ranging studies led to a double-blind randomized controlled clinical trial, the Multicenter Study of Hydroxyurea in Sickle Cell Anemia (MSH), designed to test whether patients treated with HU would have fewer crises than patients treated with placebo. The MSH was not designed to assess the mechanism(s) by which a beneficial effect might be achieved, but it was hoped that observations made during the study might illuminate that question. The 2 MSH treatment groups were similar to each other and were representative of African-American patients with relatively severe disease. The trial was closed earlier than expected, after demonstration that median crisis rate was reduced by almost 50% (2.5 versus 4.5 crises per year) in patients assigned to HU therapy. Hospitalizations, episodes of chest syndrome, and numbers of transfusions were also lower in patients treated with HU. Eight patients died during the trial, and treatment was stopped in 53. There were no instances of alarming toxicity. Patients varied widely in their maximum tolerated doses, but it was not clear that all were taking their prescribed treatments. When crisis frequency was compared with various clinical and laboratory measurements, pretreatment crisis rate and treatment with HU were clearly related to crisis rate during treatment. Pretreatment laboratory measurements were not associated with crisis rates during the study in either treatment group. It was not clear that clinical improvement was associated with an increase in Hb F. Crisis rates of the 2 treatment groups became different within 3 months. Mean corpuscular volumes (MCVs) and the proportion of Hb F containing red cells (F cells) rose, and neutrophil and reticulocyte counts fell, within 7 weeks. When patients were compared on the basis of 2-year crisis rates, those with lower crisis rates had higher F-cell counts and MCVs and lower neutrophil counts. Neutrophil, monocyte, reticulocyte, and platelet counts were directly associated, and F cells and MCV were inversely associated, with crisis rates in 3-month periods. In multivariable analyses, there was strong evidence of independent association of lower neutrophil counts with lower crisis rates. F-cell counts were associated with crisis rate only in the first 3 months of treatment; MCV showed an association over longer periods of time. Overall, the evidence that decreased neutrophil counts played a role in reducing crisis rates was strong. Increased F cells or MCV and evidence of cytoreduction by HU were also associated with decreased crisis rates, but no definitive statement can be made regarding the mechanism of action of HU because the study was not designed to address that question. Future studies should be designed to explore the mechanism of action of HU, to identify the optimal dosage regimen, and to study the effect of HU when combined with other antisickling agents.

Adolescent↗
PubMed2004

The interaction between heart failure, renal failure and anemia - the cardio-renal anemia syndrome.

BACKGROUND: Many patients with congestive heart failure (CHF) have chronic kidney insufficiency (CKI) and anemia. AIMS: The purpose of this review is to clarify the relationship between these three factors and to study the effect of correction of anemia in CHF and CKI. FINDINGS: Anemia, CHF and CKI are each capable of causing or worsening each other. Thus they form a vicious circle which can result in progressive CHF, CKI and anemia. Aggressive therapy of CHF, CKI and control of the associated anemia with erythropoietin and i.v. iron can prevent the progression of CHF and CKI, reduce hospitalization, and improve quality of life. CONCLUSION: CHF patients are a major source of end-stage renal failure patients and deserve special attention. If treated well and early, progressive heart failure and renal failure can be prevented. Cooperation between nephrologists, cardiologists, and other internists will improve the care of all three conditions and prevent their progression.

Anemia↗