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

Causes of anaemia in 101 adult Melanesian patients admitted to Port Moresby General Hospital over a 3-year period with haemoglobin levels of 4.0 gms per 100 ml or less were studied retrospectively. Cases of anaemia due to acute haemmorrage were excluded. Iron deficiency was found in 80, haemolysis in 39, megloblastosis in 26 and anaemia of chronic diseases in 5 patients. Anaemia was secondary to multiple causes in 56 and to a single cause in 45 patients. In the group with multiple causes, a combination of iron deficiency and haemolysis was found in 28, iron deficiency and megaloblastosis in 18, iron deficiency, haemolysis and megaloblastosis in 6 and haemolysis and megaloblastosis in 5 patients. In the group with a single cause, iron deficiency was found in 34, anaemia of chronic diseases in 5, haemolysis in 4 and megaloblastosis in 2 patients. Hookworm infestation and malaria appeared to be the major underlying causes of anaemia in the majority of these patients. Three of 45 patients who had received blood transfusions shortly after admission to the hospital died, while there was only one death in the nontransfused group. It is concluded that: i) severe anaemia in Papua New Guinea is commonly secondary to multiple causes; ii) administration of iron and folic acid as well as treatment for malaria and hookworm is a responsible approach when these patients can not be investigated; and iii) blood transfusion does not appear to be necessary in this group of patients despite a very low haemoglobin level.
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PMID:Severe anaemia in Port Moresby. A review of 101 adult Melanesian patients with haemoglobin level of 4G/100 ml or less. 29 26

Nutritional anaemia, due chiefly to iron deficiency, is widely prevalent in many parts of the world. There is increasing evidence that even mild anaemia affects health and reduces productivity and that a high prevalence of anaemia has profound socioeconomic consequences. The pathogenesis of nutritional anaemia is now reasonably well understood. Measures avilable for combating it include: therapeutic supplementation for accessible population groups with a high prevalence of anaemia, such as pregnant women and schoolchildren; iron fortification of one or more widely consumed foodstuffs; management of those conditions, such as hookworm infestation, that increase requirements for haemopoietic nutrients; and education of the public, and of all categories of health personnel, regarding the importance of anaemia and the ways of controlling it. Experience has shown that there is no simple solution to the problem and in each area where iron deficiency anaemia is prevalent it will probably be necessary to develop and combine many or all of these measures. In each community it will be necessary to introduce these measures so that their effectiveness can first be studied in a pilot trial. When this has been successfully completed it should be followed by a field trial under realistic conditions, and only when this has proved successful should a regional or national programme be introduced. However, the problem is complex and it is only by sustained effort of all concerned that it will prove possible to develop adequate public health control of nutritional anaemia.
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PMID:Nutritional anaemia--a major controllable public health problem. 31 Jul 14

Treatment of severe iron deficiency with iron-poly(sorbitol-gluconic acid) complex (Ferastral) intramuscular 10 ml (iron 500 mg) on alternate days has been shown highly effective and well tolerated. In order to see whether the time of treatment could be shortened, 20 Nigerians with severe iron deficiency (mostly from hookworm infection) were treated with daily intramuscular Ferastral 10 ml until their calculated total requirement of iron was met. The total iron deficit was 877-2763 mg (mean 1875 mg). Supportive treatment included antimalarials, folic acid and anthelmintics. No patient complained of undue pain at injection sites or of any other undesirable side-effects. There was no evidence of hepatic or renal toxicity in any patient, including eight who were followed at intervals up to eight weeks from the start of treatment. The initial haemoglobin (Hb) level was 2.2-7.8 g/dl (mean 4.6 g/dl). Daily regeneration of Hb in the first 14 days was 0.12-0.49 g/dl (mean 0.30 g/dl), and haematological indices were generally normal by eight weeks. Recovery was slow or incomplete in six patients, all of whom had complications other than iron deficiency. Serum iron was measured in five patients, rose to around 8000 micrograms/dl on about day 4, and fell to physiological levels by day 14. The serum unsaturated iron binding capacity fell to nil in five out of six patients on around day 3, and reappeared between days 7 and 10. Five patients who had persistent blood loss from continued hookworm infestation received a further single dose of Ferastral (iron 1000 mg) 10 ml into each buttock after four weeks, and one patient after two weeks. This large dose was also acceptable to patients if given slowly; it was followed by an accelerated Hb regeneration, but no toxicity. Daily intramuscular Ferastral 10 ml until the calculated iron requirements are met (usually in less than five days) is recommended for the treatment of severe iron deficiency. Patients with continued blood loss or Hb less than 10 g/dl after four weeks without other cause of anaemia, may receive a boost of one intramuscular injection of Ferastral 20 ml (10 ml into each buttock).
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PMID:Treatment of iron deficiency in Nigerians with daily intramuscular Ferastral. 49 69

Porotic hyperostosis was observed in 34 percent of 539 crania excavated from sites in Arizona and New Mexico. Common causes of this cranial pathology in the Old World (thalassemia, sickel cell anemia, and malargia) do not explain its occurrence in the American Southwest, as malaria and hemoglobinopathies are not known to have existed in the New World prior to European contact. Iron deficiency anemia which may also be assoicated with porotic hyperostosis occurs on a mass level only with hookworm infestation or nutritionally-related iron deficiency. Since hookworm infestation is rare in the American southwest and has not been reported in prehistoric southwestern American Indians, the hypothesis of nutritional anemia was examined. In canyon bottom sites where the diet was heavily dependent on maize, which is low in iron and also contains an inhibitor of iron absorption, significantly more crania had porotic hyperostosis than in sage plain sites, where the diet included ample animal protein rich in easily absorbable iron (p less than .001). Furthermore, canyon bottom children, who were more susceptible to iron deficiency anemia, had a higher incidence of porotic hyperostosis lesions than adults (p less than .0001).
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PMID:The paleoepidemiology of porotic hyperostosis in the American Southwest: Radiological and ecological considerations. 110 84

Trichuriasis may be asymptomatic or, in heavy infection, lead to profuse, bloody diarrhea and rectal prolapse. Diagnosis is made by finding the distinctive barrel shaped eggs in the stool or in the heavily infested patient, by anoscopy and identification of worms attached to reddened and ulcerated rectal mucosa. Mebendazole is the drug of choice in treatment. Capillariasis, a parasitic infection encountered mainly in the Philippine Islands, is of interest in that the eggs may be confused with the eggs of trichuris. Hookworm disease is generally asymptomatic, but in heavy infection, leads to iron deficiency and hypochromic, microcytic anemia. Diagnosis is made by finding the characteristic hookworm eggs on a examination of a direct fecal film. Accidental invasion of humans by dog and cat hookworm leads to cutaneous larva migrans, also known as "creeping eruption." Human hookworm is treated most effectively with mebendazole, while the rash produced by creeping eruption responds to topical thiabendazole. Strongyloides is fairly common in rural areas of the southeastern United States and may be seen in the urban setting among inmates of mental institutions, prisons, and in immigrants who formerly resided in endemic tropical regions. Because of its remarkable capacity for dissemination of larvae throughout the body, this parasite is now recognized as a serious problem for the patient who is immunocompromised. Diagnosis is made by finding larvae in the stool or by the Enterotest. All infected patients should be treated with thiabendazole. I consider the issue on Drugs For Parasitic Infections, published annually or biannually by The Medical Letter on Drugs and Therapeutics, to be the single best source of information on the treatment of parasitic diseases for primary care physicians.
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PMID:Parasitic diseases. Other roundworms. Trichuris, hookworm, and Strongyloides. 201 42

The aetiology of severe anaemia (haemoglobin less than 7.0 g dl-1) has been studied in 37 pregnant Zambians. Aetiology was usually multiple; 31 (84%) had Plasmodium falciparum malaria, 23 (62%) were folate deficient, 13 (35%) were iron deficient, one had sickle-cell anaemia and one had the acquired immunodeficiency syndrome (AIDS). Folate deficiency was most often secondary to malarial haemolysis: iron deficiency was nutritional, but hookworm was contributory in about one-third of patients. The anaemia of malaria and folate deficiency was both more common and more severe than anaemia due to iron deficiency; it was seen in younger women although primigravidae were not over-represented, it occurred earlier in pregnancy, and was associated with low birthweight. AIDS must now be included in the differential diagnosis of anaemia in pregnancy. Vigorous antimalarial treatment and prophylaxis are essential in the management and prevention of anaemia in pregnancy. Total dose iron infusion is indicated only when severe iron deficiency anaemia has been proven, and must be accompanied by antimalarial therapy and folic acid supplements. Because of the risk of transmission of human immunodeficiency virus, it is more important than ever to prevent anaemia and malaria in pregnancy, and to give blood transfusion only as a life-saving treatment.
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PMID:The aetiology of severe anaemia in pregnancy in Ndola, Zambia. 268 77

Iron is an essential trace element. In its heme-form as well as in its non heme-form it is a part of enzymes and hemoproteins. For a safe and adequate dietary intake 10-18 mg of iron are recommended daily. Frequently, this quantity is not available: approximately 20% of the world population is iron-deficient. In this state the enteral transfer capacity for toxic metals, e.g., Cd and Pb, is increased and the adaptation to physical strain as well as the immunological responses are depressed. Alterations of body iron-stores are almost exclusively balanced by adequate adaptation of the enteral iron-transfer capacity. The mechanism of this adaptation process can neither be satisfactorily explained by the "mucosal block hypothesis", nor by the "mucosal transferrin hypothesis". When the time-course of iron storage and its relation to intestinal iron transfer was investigated after i.v. iron administration to iron-deficient rats, the results indicated that the process of adaptation is located in the intestinal mucosa. Intestinal iron loading is decreased in iron deficiency, whereas the iron transfer into the organism is increased. Further investigation is necessary to find out by which mechanism the iron manages to bypass existing mucosal storage capacity in this situation. The geographical distribution of iron deficiency is influenced by a variety of local factors. Still, the paramount causes of iron-deficiency are unbalanced iron losses and the lack of bioavailable iron in the diet. The bioavailability of non heme iron is influenced by the composition of the diet. The effect of promotors of iron absorption, such as meat, amino acids, polycarbonic acids and ascorbate is opposed by the influence of inhibitors, such as bran, soya products, vegetables and egg-dishes. Iron losses are mainly due to blood losses. Thus, the wide distribution of hookworm diseases in tropical areas contributes significantly to the endemic iron-deficiency in these regions. A more physiological loss of iron is caused by menstruation and pregnancy. In small infants the iron-demand of the organism is increased by rapid growth, which in turn increases the intestinal iron transfer. An increased iron-demand can be balanced by an iron-supplemented diet or by pharmaceutical iron compounds. Acute intoxications can be caused by an overdose of such preparations. The pathophysiology and symptoms of acute iron intoxication are summarized. Their frequency has markedly decreased since "childproof" packaging has been introduced for iron-preparations. To meet the increased iron demand of young children, commercial infant formulas are frequently fortified with iron, preferentially with heme-iron.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The role of iron as a deficient element]. 269 40

Iron status, folacin status, haemoglobinopathies, malarial infection and intestinal parasitosis frequencies were assessed in a representative sample of 586 subjects living in a rural district of South Benin. Anaemia according to WHO reference values for haemoglobin was observed in 42 per cent of subjects. The prevalence was higher in children and menstruating women. Iron deficiency, defined by two or more abnormal values in the four independent indicators of iron status used (transferrin saturation, erythrocyte protoporphyrin, serum ferritin, and mean corpuscular volume) was present in 30 per cent of subjects. Half of the anaemias were associated with iron deficiency. Folate deficiency was associated with anaemia in 20 per cent of subjects. Anaemia, iron and folacin status were not significantly related to the degree of malarial infection nor to the type of haemoglobin. Although hookworm infection was very common, there was no significant relationship between egg count and haemoglobin level or haematological parameters of iron and folacin status. The lack of correlation can be explained by the low wormload observed.
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PMID:Relationship between anaemia, iron and folacin deficiency, haemoglobinopathies and parasitic infection. 353 63

104 patients with positive stool for hookworm ova were studied in detail with regard to anemia, iron and protein deficiency, and their relation to hookworm ova load. A variable degree of anemia was seen in 80 of 104 patients. Hypochromia was noticed in 66 (64%). In 48 (46%), morphological changes due to vitamin B12 and/or folic acid deficiency were recorded. Iron deficiency was most common in anemic patients. Less than 15% saturation of transferrin was the most sensitive biochemical index of iron deficiency in these patients. Severity of anemia was significantly associated with iron deficiency. Hypoalbuminemia (serum albumin less than 3.25 g%) was found in 33 (32.6%) of the patients. Anemia and hypoalbuminemia were both significantly associated with the hookworm load. However, the association of hookworm load was seen with severe anemia (hemoglobin less than 5 g%) and hypoalbuminemia (serum albumin less than 2.75 g%). It has been suggested that besides parasitic factors, nutritional deficiencies of vitamin B12 and/or folic acid and protein are contributory factors in the pathogenesis of anemia and hypoalbuminemia respectively found in these patients.
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PMID:A study of iron and protein deficiency in hookworm infestation. 550 9

The iron status in children with sickle cell anaemia has been studied in 45 patients. The mean haemoglobin level was 7.4 g/dl (s.d. 1.7) and the white cell count more than 11 X 10(9)/l in 35 (78%). Bone marrow examination showed depletion of iron stores of 21 (47%). The total iron binding capacity was elevated in most of the children and serum iron was below the normal mean level for age in 14 (31%) children. The possible causes of iron deficiency in some of these children include dietary deficiency, infections, malabsorption, blood loss through hookworm infestation and growth spurt. In the management of a child with sickle cell disease, iron administration is not recommended unless there is evidence of coexisting iron deficiency.
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PMID:Iron deficiency in sickle cell anaemia in Nigerian children. 618 85


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