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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since macrocytosis was observed in a high percentage of our renal transplant patients, a follow-up study was carried out on 36 patients with determination of the mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH) and haemoglobin concentration (MCHC). These parameters were determined monthly for periods of up to two years (16 cases) following transplantation. There was a rise in both MCV and MCH within one month. Macrooperative MCHC, however, remained normal. Anaemia was absent or mild. The bone marrow showed striking megaloblastic changes with nuclear-cytoplasmatic dissociation in both red and white cell precursors. Vitamin B 12 absorption tests were normal in all 8 patients investigated. Macrocytosis was not detectable in two patients with a low serum iron concentration. Macrocytosis disappeared in 4 patients with chronic rejection when progressive renal failure developed. It is concluded that azathioprine therapy induces macrocytosis in renal transplant patients provided renal function is satisfactory.
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PMID:[Macrocytosis in renal transplant patients (author's transl)]. 79 85

We treated a 29-year-old male patient with pseudohypoparathyroidism type I, who showed a slight increase in serum indirect bilirubin without any signs of liver dysfunction. Serum levels of total, direct and indirect bilirubins were 2.4, 0.7 and 1.7mg/dl, respectively (normal ranges: 0.2-0.8, 0-0.2 and 0.2-0.6mg/dl, respectively). The cause of the increases in serum bilirubin levels was not clear; however, hemolytic anemia, hereditary unconjugated hyperbilirubinemia or ineffective erythropoiesis were ruled out as causes for the increase, since 1) his serum level of haptoglobin was normal, 2) increase in serum level of indirect bilirubin 120 minutes after the infusion of 50mg nicotinic acid was within the normal range, and 3) severe anemia was not observed. Osmotic fragility of his circulating red blood cells was also within normal range. Three other patients with pseudohypoparathyroidism visiting our clinic also showed slightly high levels of serum indirect bilirubin, although four outpatients with idiopathic hypoparathyroidism showed no such abnormality. Abnormality in the responsiveness to parathyroid hormone and/or to that in the cyclic AMP productivity in this disease may cause the increase in the circulating unconjugated bilirubin.
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PMID:[Case report of a patient with pseudohypoparathyroidism associated with slight increase in serum level of unconjugated bilirubin]. 196 49

The morbidity pattern and nutritional profile was evaluated of school children who resided around Mosaboni Copper Mines and in surrounding villages of Ghatsila subdivision in Singhbhum district of Bihar State, India. A total of 1424 school children (816 boys and 608 girls) between 5-17 years old were studied. Children were examined on school premises with the assistance of teachers and health visitors. Body weight and height, nutritional deficiency signs, common infective conditions, and cardiac murmurs were recorded. Evidence of morbidity was found in 52.8% boys and 67.4% girls. 11.9% boys and 12.2% girls had 2 or more conditions existing together. The average number of children per family was 5.13; it was 4.77 in families with no child illness; 5.03 with 1 illness and 6.94 if 2 or more morbid conditions were found in a child. Approximately 2% girls over 12 years old had dysmenorrhea and polymenorrhea. Only 15.4% of boys and 19% of girls weighed above 80% of the 50th percentile of the Harvard Standard. 76.4% of boys and 71.7% of girls weighed between 61% and 80%, while 8.1% of boys and 9.l% of girls weighed less than 60%. 20% of boys and girls showed features of stunting. Deficiencies of Vitamin B-complex and Vitamin A as well as clinical anemia were common while rickets and scurvy were rare. The prevalence of worm infestation, lymphadenopathy as well as skin and respiratory infections were lower than in some other studies. Dental caries was observed in 21% of cases, but the prevalence of periodontal disease and malocclusion was higher than reported by others. Convulsive disorders and myopia were less common than in urban school children. Prevalence of congenital cardiac lesions was higher than in urban studies probably due to heredity. Nutritional supplementation in schools, regular medical checkups of school children, and health education of the community with emphasis on small family norms could improve the overall health status of rural children.
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PMID:Health status of rural school children. 258 10

Food, supplements, and fortified foods can all be appropriate sources of nutrients. It is the responsibility of nutrition educators to help consumers use those nutrient sources appropriately. Consumers should consider at least six factors when they select foods, supplements, and fortified foods: flavor, convenience, cost, nutrient content, toxic factors, and bioavailability of nutrients. Consumers are often less concerned about the latter two factors than they should be. For example, many case histories have been published on the symptoms caused by overconsumption of vitamins A, B-6, C, and D and nicotinic acid. Generally those toxic symptoms were caused by the ingestion of supplements, not foods. Current widespread use of supplements containing one or two nutrients may not only cause overt toxicity symptoms but also adversely affect the bioavailability of other nutrients. For example, ingestion of excessive amounts of vitamin C appears to interfere with copper metabolism in human subjects; ingestion of high levels of zinc impairs immune function, depresses copper absorption, and induces anemia; consumption of supplemental calcium as calcium phosphate dibasic is associated with renal calcification in rats; and ingestion of supplemental magnesium depresses the apparent absorption of calcium and retention of calcium in bone by rats.
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PMID:Food, supplements, and fortified foods: scientific evaluations in regard to toxicology and nutrient bioavailability. 365 65

Vitamin B(12) levels in erythrocytes were low in untreated hypochromic anaemia, rose to abnormally high levels during therapy with iron alone, and finally slowly fell to normal. These changes were similar to those previously found in pernicious anaemia in response to vitamin B(12) therapy and in folate-deficiency anaemia in response to folic acid, thus changes in erythrocyte B(12) levels are not always due directly to changes in B(12) metabolism but may be secondary to changes in the levels of other haematinic factors.
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PMID:Vitamin B 12 levels in erythrocytes in hypochromic anaemia. 513 May 36

Several vitamins have been demonstrated to interfere with the pathogenesis of some metabolic diseases, mainly by three different mechanisms: 1) vitamin malabsorption, 2) errors in vitamin metabolism, 3) vitamin dependent syndromes. The latter is due to a deficiency of the apoenzyme whose coenzyme is the vitamin itself. In this case pharmacological, instead of nutritional doses of the vitamin may be needed. The vitamins which interfere with inborn metabolic errors are reviewed; for each vitamin the corresponding diseases which may be treated are indicated. The vitamins are: 1) thiamine (leucinosis); b) nicotinic acid (hyperlipoproteinemia); c) biotin (beta-methyl-crotonyl-glycinuria, propionic aciduria); d) pyridoxine (infantile convulsions, familial pyridoxine responsive anemia, homocystinuria, cystathioninuria, xanthurenicaciduria); e) cobalamins (congenital intrinsic factor deficiency, cobalamin malabsorption, transcobalamin deficiency, methylmalonic aciduria) f) folic acid (congenital folic acid malabsorption, formimino-transferase deficiency, methylenetetrahydrofolic reductase deficiency, Lesch-Nyhan syndrome); g) vitamin D (phosphatic diabetes, Prader's type rickets, Albright's syndrome; essential hereditary hypophosphatemia, etc). It is noteworthy that the vitamin therapy of these diseases, not only corrects the metabolic errors, but can also promote the healing or the amelioration of the psycho-physical growth, of central nervous system alterations and of other lesions.
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PMID:[Vitamins in metabolic diseases]. 702 68

To determine the prevalence and causes of anemia in rural Mexico, blood samples and longitudinal dietary data were collected from 187 women, some pregnant and then lactating, and from 72 men. Blood was used to measure anemia, mean cell volume, and plasma ferritin, folate and vitamin B-12. Anemia was found in 33% of the men, 54% of nonpregnant, nonlactating women, 35% of pregnant women and 41% of lactating women, and varied by season. Low iron stores (ferritin) accompanied anemia in only 8% of men compared with 38-67% of women. Low meat intake and poor dietary iron bioavailability were associated with anemia in women. There were no cases of low plasma folate. Low plasma vitamin B-12 was common in all groups, and the incidence increased from 15% at 7 mo of pregnancy to 30% at 7 mo of lactation. Vitamin B-12 was lower in the plasma and milk of anemic lactating women than in plasma and milk of non-anemic lactating women and was classified as deficient in 62% of breast milk samples.
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PMID:Iron, vitamin B-12 and folate status in Mexico: associated factors in men and women and during pregnancy and lactation. 806 68

A niacin-deficient purified amino acid diet that contained adequate (40 mg/kg) or deficient (10 or 15 mg/kg) iron was used to assess the growth promoting efficacy of tryptophan as a niacin precursor. Basal diets contained 1400 mg/kg tryptophan, a level that was established as meeting the requirement for tryptophan per se in diets containing excess nicotinic acid. Chicks fed the iron-deficient diets had markedly lower hemoglobin concentrations than those fed the iron-adequate diets. Regardless of iron level, chicks exhibited linear growth responses to either nicotinic acid or tryptophan supplementation. Using multiple-linear regression of weight gain on supplemental tryptophan or nicotinic acid intake, the efficiency (wt:wt) of tryptophan conversion to niacin activity (i.e., tryptophan slope divided by nicotinic acid slope) was a mean of 1.77% (56:1) for chicks fed the iron-deficient diet. This was significantly (P < 0.05) lower than the 2.39% (42:1) efficiency calculated for chicks fed the iron-adequate diet. Thus, iron deficiency reduced tryptophan utilization (for NAD synthesis) but had no effect on nicotinic acid utilization. The results suggest that pellagra in populations having endemic anemia and protein-energy malnutrition may be due not only to inadequate intakes of bioavailable niacin but also to inadequate intakes of bioavailable iron.
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PMID:Iron deficiency reduces the efficacy of tryptophan as a niacin precursor. 812 Jun 64

The diets and growth of children reared on vegetarian diets are reviewed. Excessive bulk combined with low energy density can be a problem for children aged < or = 5 y and can lead to imparied growth. Diets that have a high content of phytate and other modifiers of mineral absorption are associated with an increased prevalence of rickets and iron-deficiency anemia. Vitamin B-12 deficiency is a real hazard in unsupplemented or unfortified vegan and vegetarian diets. It is suggested that vegans and vegetarians should use oils with a low ratio of linoleic to linolenic acid in view of the recently recognized role of docosahexaenoic acid in visual functioning. If known pitfalls are avoided, the growth and development of children reared on both vegan and vegetarian diets appears normal.
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PMID:Vegetarian diets and children. 817 20

Deficiency of any of the vitamins and minerals essential for normal erythropoiesis (haematinics), including iron, copper, cobalt, vitamins A, B12, B6, C, E, folic acid, riboflavin and nicotinic acid, may be associated with defective erythropoiesis and anaemia. Iron, vitamin B12 and folate are the haematinics for which deficiency states manifest most often clinically and are the focus of this review. The normal absorption of these haematinics and gastrointestinal causes of their deficiency are described. Investigations, including the use of homocysteine metabolite levels and new techniques such as serum transferrin receptor assays, and treatment of haematinic deficiency are discussed in detail.
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PMID:Review article: the diagnosis and treatment of haematinic deficiency in gastrointestinal disease. 1021 44


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