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

Anemia is common among young women, and iron deficiency is one of the leading causes. In Europe and the US, the iron fortification of flour increased oral iron intake and decreased anemia prevalence from 30% to 10%. The National Nutrition Survey in Japan revealed that anemia prevalence among young Japanese women is increasing; however, no nationwide preventive policy has been aimed at iron deficiency anemia. The endpoint of this study was the estimation of anemia prevalence among healthy Japanese woman, based on a large sample size. We collected data from the consecutive check-up examination records of apparently healthy women (n = 13,147). We defined hemoglobin lower than 12 g/dL as anemia, hemoglobin lower than 10 g/dL as severe anemia, and a mean corpuscular volume lower than 80 fl as microcytic anemia. Of the 13,147 persons, anemia was identified in 2331 (17.3 %), and severe and microcytic anemia in 438 (3.3 %) and 700 (5.2 %), respectively. Among women younger than 50 years, anemia was identified in 22.3 %, and 25.2 % of them had severe anemia. In conclusion, the prevalence of anemia and severe anemia among young women is high in Japan. Some action needs to be considered to improve women's quality of life.
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PMID:Prevalence of anemia among healthy women in 2 metropolitan areas of Japan. 1705 Jan 94

Cerebral venous thrombosis (CVT) is rare and has a wide spectrum of symptoms, therefore it is difficult to diagnose. Thrombosis of the deep cerebral veins occurs very rarely: it has been reported that approximately 6% of patients with CVT have deep CVT, and the prognosis for patients with this condition is poor. CVT has been reported in association with dehydration, a hypercoagulable state, mastoiditis, tumour invasion of a venous sinus, use of oral contraceptives, pregnancy, puerperium, head trauma, vasculitis, and intracranial and systemic infections. However, in the literature, there are few reported cases of CVT in association with iron deficiency anaemia, especially in adults. We present here two patients with bilateral thalamic and basal ganglionic lesions due to thrombosis of the deep cerebral veins. Both of our patients had severe hypochromic microcytic anaemia due to iron deficiency, and both had a good prognosis after 2 months.
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PMID:Deep cerebral vein thrombosis associated with iron deficiency anaemia in adults. 1716 Dec 94

The iron deficiency is the first cause of anaemia. In healthy young adult, anemia is well tolerated because of its progressive installation. The most common symptoms of anemia are pallor, fatigue and dyspnea. In biological exams, anemia is classically associated with microcytosis and hypochromia. The origins of microcytic anemia are iron deficiency, inflammatory aetiologies, thalassemia and sideroblastic anaemia. The iron-deficiency diagnosis includes two explorations: biological and clinical. The biological exploration is based on interpretation of serum biologics tests as blood iron, ferritin, transferrin with saturation, total iron-binding capacity and its soluble receptors. This interpretation is simple if it is not associated with clinical disorders influencing the internal iron cycle. The clinical exploration must always be followed by a careful assessment of the underlying cause as blood loss. The most common causes in women of reproductive age are gynaecologic. In men and menopausal women, the gastrointestinal tract bleeding is source of anemia. Therapeutic management of anemia is oral iron therapy. Etiological diagnostic of microcytosis is essential before iron therapy. If not, the treatment could be inefficient or it could mask or delay the etiological diagnostic.
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PMID:[Iron deficiency anaemia: clinical presentation, biological diagnosis and management]. 1749 37

During chronic diseases, patients may develop a specific form of anaemia called "inflammatory anaemia" or anaemia of chronic disease. The objective of this study was to study the forms of anaemia during cirrhosis. The leading cause of cirrhosis in these 161 patients was chronic active (viral) hepatitis, accounting for 58.3% of cases. The overall prevalence of anaemia was 74.5%. All types of anaemia were observed. Normochromic normocytic anaemia was observed in 43.3%, combined with blood loss in 48%. These results show that the hypochromic microcytic anaemia observed in 20% of cases is not exclusively linked to blood loss or iron deficiency. They also emphasise the importance of the haemogram interpretation to avoid routine iron prescription.
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PMID:[Types of anaemia in patients with cirrhosis at the Yalgado Ouedraogo hospital centre of Ouagadougou (Burkina Faso)]. 1796 56

Reactive thrombocytosis (secondary thrombocytosis) is frequent and typically moderate. We report a case of extreme thrombocytosis and leukocytosis secondary to an iron deficiency anemia. A 21-year-old woman is admitted in emergency department for acute headache. Biological assessment reveals a severe microcytic anaemia (5.4 g/dL) with thrombocytosis (2500 giga/L) and leukocytosis (35 giga/L) leading to multiple diagnosis hypotheses. Finally, biological evaluation concludes to a diagnosis of iron deficiency anaemia related to insufficient oral intake and menorrhagia. Reactive hyperleukocytosis and thrombocytosis rapidly resolved with iron supplementation. This case is a reminder that iron deficiency-related thrombocytosis can sometimes be severe. However, the associated reactive leukocytosis is quite exceptional.
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PMID:[Severe thrombocytosis and leukocytosis associated with iron deficiency anaemia: a case-report]. 1830 30

Administration of an iron-deficient diet to Wistar rats resulted within 14 days in reduced serum iron concentrations, a microcytic hypochromic anemia, characteristic for impaired hemoglobin synthesis, and an increase of duodenal epithelial cell proliferation. After 5 weeks of iron deficiency, hypochromic microcytic anemia and a clear increase of duodenum weight but no pronounced effects on cell proliferation was observed. Increased duodenum weights corresponded to significant increases in mucosal area, indicating a diffuse, simple mucosal hyperplasia. The sequence of events following iron depletion thus appears to be: (1) reduced serum iron levels, (2) induction of hypochromic microcytic anemia, (3) increased duodenal epithelial cell proliferation, and (4) increased duodenal weight (increased mucosal area). Iron deficiency anemia was rapidly reversible after a 2-week recovery period. However, increased duodenum weights were still noted at that time. Intramuscular iron supplementation in animals fed with iron-deficient diet maintained body iron levels not below normal values, and neither anemia nor increased duodenum cell proliferation were detected after 14 days. A 5-week iron supplementation period resulted in slightly increased serum iron values, and slightly decreased duodenal epithelial cell proliferation. Thus, increased duodenum mucosal hyperplasia was shown to be secondary to depletion of body iron and anemia and reflects an attempt to increase iron absorption to counteract iron deficiency.
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PMID:Iron deficiency causes duodenum mucosal hyperplasia in male Wistar rats. 1835 45

Hepcidin, a liver-derived protein that restricts enteric iron absorption, is the key regulator of body iron content. Several proteins induce expression of the hepcidin-encoding gene Hamp in response to infection or high levels of iron. However, mechanism(s) of Hamp suppression during iron depletion are poorly understood. We describe mask: a recessive, chemically induced mutant mouse phenotype, characterized by progressive loss of body (but not facial) hair and microcytic anemia. The mask phenotype results from reduced absorption of dietary iron caused by high levels of hepcidin and is due to a splicing defect in the transmembrane serine protease 6 gene Tmprss6. Overexpression of normal TMPRSS6 protein suppresses activation of the Hamp promoter, and the TMPRSS6 cytoplasmic domain mediates Hamp suppression via proximal promoter element(s). TMPRSS6 is an essential component of a pathway that detects iron deficiency and blocks Hamp transcription, permitting enhanced dietary iron absorption.
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PMID:The serine protease TMPRSS6 is required to sense iron deficiency. 1845 Dec 67

Although its exact mechanism is unclear, anaemia is well recognised as a feature of hypopituitarism; and anaemia is associated with Sheehan's syndrome (SS). We aimed to evaluate the frequency and severity of anaemia and other haematological changes among patients with Sheehan's syndrome, in comparison with healthy controls. Sixty-five SS patients and 55 age-matched female healthy controls were included. Biochemical and hormonal assessments and haematological evaluations were carried out, and groups were compared. The mean number of red blood cells, as well as mean haemoglobin, iron and erythropoietin levels, total iron-binding capacity and transferrin saturation were all significantly lower in SS patients compared to controls. SS patients had significantly higher rates of anaemia (80.0% vs. 25.5%, p = 0.0001), iron deficiency (44.6% vs. 5.4%, p = 0.001), leukopenia (20.0% vs. 5.4%, p = 0.015), thrombocytopenia (9.2% vs. 0.0%, p = 0.028) and bicytopenia (21.5% vs. 1.8%, p = 0.001) compared to controls. Anaemic SS patients had normochromic-normocytic anaemia (55%) or hypochromic-microcytic anaemia (45%). Anaemia is frequently associated with Sheehan's syndrome and responds to appropriate replacement therapy. Hypopituitarism should be considered as a possible cause of anaemia, and a hormone examination should be undertaken promptly, particularly in patients with anaemia resistant to therapy and/or with a history suggestive of Sheehan's syndrome.
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PMID:Sheehan's syndrome as a rare cause of anaemia secondary to hypopituitarism. 1879 68

Microcytic anemia is the most commonly encountered anemia in general medical practice. Nutritional iron deficiency and beta thalassemia trait are the primary causes in pediatrics, whereas bleeding disorders and anemia of chronic disease are common in adulthood. Microcytic hypochromic anemia can result from a defect in globin genes, in heme synthesis, in iron availability or in iron acquisition by the erythroid precursors. These microcytic anemia can be sideroblastic or not, a trait which reflects the implications of different gene abnormalities. Iron is a trace element that may act as a redox component and therefore is integral to vital biological processes that require the transfer of electrons as in oxygen transport, oxidative phosphorylation, DNA biosynthesis and xenobiotic metabolism. However, it can also be pro-oxidant and to avoid its toxicity, iron metabolism is strictly controlled and failure of these control systems could induce iron overload or iron deficient anemia. During the past few years, several new discoveries mostly arising from human patients or mouse models have highlighted the implication of iron metabolism components in hereditary microcytic anemia, from intestinal absorption to its final inclusion into heme. In this paper we will review the new information available on the iron acquisition pathway by developing erythrocytes and its regulation, and we will consider only inherited microcytosis due to heme synthesis or to iron metabolism defects. This information could be useful in the diagnosis and classification of these microcytic anemias.
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PMID:Molecular basis of inherited microcytic anemia due to defects in iron acquisition or heme synthesis. 1918 81

We discuss the case of a 32 year-old male with severe microcytic anemia (hemoglobin 2,9 g/dl) and megaloblastic changes in the bone marrow. The patient reported of substantial dietary weight loss. The family history was positive for beta-thalassemia. Previous blood work showed iron deficiency with mild anemia. Further work-up verified beta-thalassemia minor and revealed severely decreased vitamin B12 levels with positive anti intrinsic-factor antibodies, pathognomonic for autoimmune pernicious anemia. The paradoxon therefore dissolved as a pernicious anemia with megaloblastic changes with microcytic erythrocytes due to beta-thalassemia.
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PMID:[Severe microcytic anemia with megaloblastic changes in the bone marrow. A hematological paradoxon?]. 1953 14


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