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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lateral X-ray pictures of the skull in certain several and chronic disorders of the blood as thalassaemia, congenital haemolytic anaemia, sickle cell anaemia and iron deficiency disease show frequently changes of the outlines of the cranial bones. They consist of a double contour of the outer cranial border and on the interior side below the sagittal sutura of a band-like shadow or of multiple stripes and lines running parallel to the carnial vault. They concern the parietal bones and may extend from the bregma till to the lamda or occupy only a part of this distance. The roentgenological features are due to the enlargement of the crainal bones, the bulging out of both parietal bondes, the sometimes enlarged and deepened borders of the sulcus sagittalis superior and particularly to the furrow and depression on the skull above the sagittal suture caused by the protruding parietal bones on both sides. As these different abnormal structures must be passed by the picturing X-ray, effects of superposition and interference are produced. Longitudinal ridges or bony edges which could explain the roentgenological findings could not be established. Since the peculiar alterations of the cranial bones are mainly found in the mentioned blood disorders, where they are caused by the overgrowing red marrow, they also display the same roentgenological features. These features are, therefore, a characteristic sign of these diseases.
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PMID:[Double contours and companion shadows in the skull associated with anaemias (author's transl)]. 15 80

Five American black patients, ages 1 to 16 years, with the sickle cell anemia-alpha-thalassemia syndrome are described. Each patient had persistent microcytosis not explained by iron deficiency, and in each family the presence of alpha-thalassemia in combination with sickle cell trait was demonstrated in one of the parents. In one patient, in whom the diagnosis of sickle cell anemia was established at birth, an elevated level of Barts (gamma4) hemoglobin was also found. In these patients levels of alkali-resistant hemoglobin and reticulocyte counts were similar to those of sickle cell anemia patients of comparable age; however, stained smears of their peripheral blood rarely showed the presence of irreversibly sickled cells. No major ameliorative effect of the alpha-thalassemia on the clinical expression of the sickle cell disease of these patients was evident.
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PMID:Sickle cell syndromes. II. The sickle cell anemia-alpha-thalassemia syndrome. 63 12

Shear stress is a potential cause of erythrocyte fragmentation and hemolysis in flowing blood. In this study, the response of abnormal human erythrocytes to shear stress in virto was evaluated using a concentric cylinder viscometer. Compared to normal red cells, deoxygenated erythrocytes from persons with sicle cell anemia were particularly susceptible to fragmentation and hemolysis by shear stress. Oxygenation of sicke cell blood improved the resistance of those red cells to shear stress; they remain, however, more susceptible to shear stress than normal erythrocytes. Erythrocytes from patients with iron deficiency, thalassemia minor, and erythrocyte pyruvate kinase deficiency showed fragmentation and hemolysis at threshold shear stresses intermediate between those ovserved for blood from patients with sickle cell anemia and normal persons. Blood samples from patients with hereditary spherocytosis were more resistant to shear stress than normal blood. These results indicate that there are important differences in the response of various red cells to shear stress.
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PMID:Fragility of abnormal erythrocytes evaluated by response to shear stress. 114 31

Marrow aspiration in 22 pregnant women with haemoglobin S revealed a high incidence of iron deficiency. Eighteen patients showed depleted iron stores while depots were adequate in four patients. The practice of denying iron to pregnant women with haemoglobinopathies is not recommended; nor is the use of prophylactic iron in all patients with sickle cell disease or trait advised. It is suggested that it is better to diagnose and treat the iron deficiency specifically.
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PMID:Iron stores in pregnant patients with anaemia and haemoglobin S. 126 46

Between 1970-1990, the Laboratory tested 38,391 specimens for hemoglobinopathies, of which 7,935 were positive. The major abnormalities detected were beta thalassemia trait (4,688), alpha thalassemia trait (1,248) and sickle cell trait (847). Clinically significant hemoglobinopathies detected were Hemoglobin H disease (100), sickle cell disease (67) and sickle cell Hemoglobin C disease (79). Hemoglobinopathies are therefore common in the Hamilton area as a reflection of the cultural diversity of area citizens. Of the 49 patients with thalassemia without documented iron deficiency, 8 (16%) received iron therapy for a variable period of time and 3 were investigated for gastrointestinal blood loss. Hemoglobin abnormalities cause or have the potential to cause clinical disease and they can, if not detected, result in unnecessary iron therapy or gastrointestinal investigation.
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PMID:The clinical significance of hemoglobinopathies in the Hamilton region: a twenty-year review. 145 12

Iron deficiency anaemia was detected in 23% of cases with homozygous sickle cell disease. The aetiology of iron deficiency was similar to the other population in the community. High serum ferritin level was detected in 15.4% of the cases and was well correlated to the number of transfusions. Tissue haemosiderosis was not detected in any case. Patients with heterozygous sickle cell had either normal or low serum ferritin levels.
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PMID:Iron in sickle cell disease. 146 1

Generally, individuals who are heterozygous to haemoglobin S (Hb AS) are asymptomatic and do not present any haematological or clinical manifestations. However, other associated genetic abnormalities may influence the presentation in Hb AS cases. This study was conducted on twenty children heterozygous for HB S who presented clinical manifestations similar to those of sickle cell anaemia. All these children had anaemia associated with several red cell morphological abnormalities. The white blood cell counts were elevated in all patients and differential count studies showed a substantial increase in lymphocytes and polymorphonuclear leucocytes in the majority of the cases. Forty-five per cent of the patients had associated alpha-thalassaemia, 60 per cent had beta-thalassaemia, 30 per cent had G-6-PD deficiency and 10 per cent had partial glutathione reductase deficiency. Pyruvate kinase activity was normal in all cases. Riboflavin deficiency was encountered in 30 per cent of the patients and iron deficiency in 15 per cent of these Hb S heterozygotes. The major clinical findings were splenomegaly, hepatomegaly, and vaso-occlusive crisis. The majority of the patients had received blood transfusions. The hand and foot syndrome was identified in three (15 per cent) of the patients. The haematological and clinical findings in these twenty Hb S heterozygotes are presented in this paper and the possible causes for these abnormalities are discussed.
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PMID:Case studies on haemoglobin S heterozygotes with severe clinical manifestations. 228 93

Erythropoietin is produced mainly by the kidneys and stimulates erythropoiesis in the bone marrow. Chronic renal failure is characterized by anemia, which is principally caused by erythropoietin deficiency. Recombinant human erythropoietin (r-hEPO) corrects the anemia of chronic renal disease and improves patient well-being, exercise tolerance, and cognitive function. The clinical pharmacology, efficacy, safety, and tolerance of r-hEPO are presented. Four major studies attest to r-hEPO's efficacy in the treatment of anemia of chronic renal disease and document potential toxicities of hypertension, iron deficiency, thrombosis, and bone pain. Careful attention to the extent of correction of the hematocrit, increased heparinization during hemodialysis therapy, and compliance with dietary restrictions may minimize the incidence and severity of adverse reactions. Resistance to r-hEPO may be due to iron deficiency, aluminum toxicity, or inflammation, including infection. Potential future uses of r-hEPO include the treatment of various other anemias, such as those seen in sickle cell anemia, rheumatoid arthritis, and autologous blood donation. Controlled clinical studies in these areas have not been reported.
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PMID:Recombinant human erythropoietin. 266 69

The chemistry, pharmacology, pharmacokinetics, clinical uses and efficacy, adverse effects, drug interactions, dosage and administration, and formulary considerations of epoetin are described. Erythropoietin, a glycoprotein hormone primarily synthesized in the kidney, is the chief regulator of red blood cell production. Erythropoietin concentrations increase in response to a hypoxic state, resulting in increased red blood cell formation, accelerated hemoglobin production, and premature movement of reticulocytes into the circulation. The human gene responsible for the production of erythropoietin recently was cloned, and the recombinant product--epoetin--has been made available through mass production. The apparent volume of distribution of i.v. epoetin approximates the assumed plasma volume both in healthy volunteers and in patients with chronic renal failure. Little is known about the metabolism and route of elimination of epoetin and erythropoietin. Epoetin recently was approved by the FDA for treatment of anemia associated with chronic renal failure. Clinical trials in patients receiving hemodialysis or peritoneal dialysis and in predialysis patients with renal dysfunction demonstrate epoetin's efficacy. Other potential indications include augmentation of blood production in patients enrolled in autologous blood donation programs and treatment of anemias associated with rheumatoid arthritis, sickle cell disease, acquired immunodeficiency syndrome, cancer, and premature birth. The most frequent adverse effect associated with epoetin therapy is the worsening or development of hypertension. Other adverse effects include thrombocytosis, hyperkalemia, rise in serum urea concentration, iron deficiency, and flu-like symptoms. No drug interactions with epoetin have been reported in humans. The recommended starting epoetin dosage in patients with chronic renal failure is 50-100 IU/kg three times weekly. Epoetin is available only as an injection for i.v. or s.c. administration. Epoetin provides a new therapeutic approach to the treatment of anemia associated with chronic renal failure in hemodialysis, peritoneal dialysis, and predialysis patients. Benefits of epoetin therapy include reduced need for blood transfusions, the amelioration of anemic symptoms, and an improved quality of life.
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PMID:Epoetin: human recombinant erythropoietin. 268 Feb 41

Hemoglobin, mean corpuscular volume, erythrocyte count, and leukocyte count were measured, and hematocrit, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration were computed electronically for 7,739 healthy black persons. The study population comprised 3,393 males and 4,346 females 1-84 years of age, all from the Washington, DC, metropolitan area. Persons with sickle cell disease and elevated hemoglobin F were excluded from analysis, but those with traits for hemoglobin S, C, and thalassemia were not. Mean and percentile values are presented in tabular form. Hemoglobin, hematocrit, and mean corpuscular volumes were lower than those reported in surveys of white populations. Beginning with the 11-15-year age groups, black males had higher red cell values than black females. After age 30, mean hemoglobin levels for men gradually declined, while those in women rose, so that the sex difference diminished after 60 years of age. Leukocyte counts were higher in young children and in women, compared with men ages 21-50 years. After 60 years of age, the sex difference disappeared. Further large surveys that exclude data on persons with iron deficiency are needed in black populations.
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PMID:Age- and sex-related blood cell values in healthy black Americans. 310 82


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