Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of a female patient affected by Crohn's ileitis associated with small bowel angiodysplasia is reported. Despite a good clinical and laboratory response to steroid therapy the patient showed an unexplained hypochromic microcytic anemia. At laparotomy Crohn's ileitis as well as an angiodysplastic lesion were found. Both lesions were resected in continuity. During a 2-year follow-up the patient did not show anemia despite pregnancy. It is suggested that the angiodysplastic lesion was the possible cause of hypochromic anemia and that the patient should have been operated on before, based on her recurrent anemia.
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PMID:Small bowel angiodysplasia in association with Crohn's ileitis. A case report. 262 94

16 chronic haemodialysis patients (group I), with non-microcytic anaemia (mean haemoglobin 7.2 g/dl, SD 1.0, range 5.8-9.8), moderate aluminium overload (serum aluminium 44 micrograms/l, SD 16, range 21-74), and normal or high iron stores (ferritin 800 micrograms/l SD 464, range 34-2013) were treated with intravenous desferrioxamine 1 g at the end of each dialysis for six months. 8 patients with similar characteristics served as controls (group II). After six months group I showed a rise in haemoglobin to 9.1 (SD 2.5) g/dl and a decrease in blood transfusion requirements, both significant, whereas group II showed no changes. Other significant changes observed in group I, but not group II, were a rise in reticulocytes and in red cell creatine and a fall in red cell protoporphyrin and serum ferritin. Ferritin decreased more in the patients whose anaemia improved. Minor increases in serum aluminium in group I did not differ from those in the control group. Desferrioxamine may benefit the anaemia of chronic haemodialysis patients through improvement of erythropoiesis. The effect seems not to be related to chelation of a heavy aluminium overload.
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PMID:Improvement in the erythropoiesis of chronic haemodialysis patients with desferrioxamine. 289 66

Two groups of suckling rabbits were studied from the 15th to the 40th day after birth, one group receiving mothers milk only, the other having the choice of iron-containing food pellets from the 20th day. In the milk-only group, the plasma iron concentration (P-Fe), blood hemoglobin concentration (B-Hb), red blood cell count (B-RBC), and mean corpuscular volume (MCV) declined continuously, whereas the hemoglobin mass of the blood (Hb-mass) remained unchanged, and the blood platelet count (B-PLTS), plasma platelet count (P-PLTS), and the estimated platelet release to the blood (PLT-release) showed a continuous rise. The milk-pellet group showed the same pattern until the 25th-30th day; thereafter, P-Fe, B-Hb, and Hb-mass rose markedly, whereas B-PLTS and PLT-release declined. At the time of weaning, both groups showed bimodal erythrocyte volume distribution curves. Thereafter, the milk-only group developed a pure microcytemia, whereas the milk-pellet group got normovolemic erythrocytes only. In conclusion, the erythropoiesis in suckling rabbits is characterized by a balanced recycling of an essentially constant amount of available iron, preventing rise of Hb-mass. The anemia thus reflects a failure of the Hb-mass to keep up with the growth-related rise in plasma volume. A close relationship exists between postnatal iron deficient microcytic anemia and thrombocytosis.
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PMID:Postnatal anemia and thrombocytosis in suckling rabbits: influence of delayed weaning and iron supplies. 315 63

Neonatal rats from dams receiving 2 or 3 g NaNO2/liter in the drinking water through -gestation and lactation suffered severe microcytic anemia as well as growth retardation and high mortality. Lipemia, fatty liver damage, decreased erythropoiesis of spleen and bone marrow, and reduced plasma and tissue iron levels were noted in affected pups. These effects were all consistent with and characteristic of iron deficiency. Experiments presented here were designed to show that the maternally mediated toxicity of nitrite is actually an iron deficiency syndrome in the pups caused by inadequate iron transfer from dam to pup. It was found that administration of exogenous iron supplement to pups of treated mothers reversed the anemia and other effects of nitrite toxicity noted both in previous studies and in unsupplemented littermates. Mothers of affected pups were themselves anemic. Finally, we fully documented severe iron deficiency in pups of nitrite-treated mothers and showed that these mothers produced milk of reduced iron content. It appears then that nitrite-consuming dams have a reduced capacity to transfer iron to their pups. The nitrite-associated toxicities in the pups are actually a result of an iron deficiency.
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PMID:Nitrite-induced iron deficiency in the neonatal rat. 318 25

Microcytic anemia, long considered an effect of lead poisoning, may in fact result from coexisting iron deficiency. In this study, how RBC size, hemoglobin, and zinc protoporphyrin vary as a function of iron status in a group of children with high lead levels was examined. Charts of all children (N = 51) admitted to Cook County Hospital for treatment of lead poisoning in 1981 to 1983 were reviewed for data on age, blood lead level, hemoglobin concentration, MCV, transferrin saturation and zinc protoporphyrin level. The mean lead level was 86 micrograms/dL and the range was 63 to 190 micrograms/dL. Children with transferrin saturation values less than 7% had a mean MCV of 56 microL, hemoglobin of 8.9 g/dL, and zinc protoporphyrin of 693 micrograms/dL; for those with saturations of 7% to 16%, the values were 61 microL, 10.1 g/dL, and 581 micrograms/dL, respectively; the children with saturations greater than 16% had normal mean MCVs and hemoglobin concentrations (74 microL and 11.4 g/dL) and a mean zinc protoporphyrin value of 240 micrograms/dL (P less than .0005). Multiple linear regression was used to correct for effect of age, and transferrin saturation remained the most important predictor of MCV, hemoglobin, and zinc protoporphyrin levels; the addition of lead did not improve the models. Results of this study suggest that iron deficiency is strongly associated with some of the observed toxicities of lead. Also, lead poisoning can exist without producing microcytosis or anemia, and zinc protoporphyrin concentration may not be a sensitive indicator of lead level in the absence of iron deficiency.
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PMID:Interaction of iron deficiency and lead and the hematologic findings in children with severe lead poisoning. 327 57

Copper deficiency was found in an adult patient who had received excessive daily oral zinc for 10 mo. The deficiency was characterized by hypochromic-microcytic anemia, leukopenia, and neutropenia. Although initially thought to be caused by iron deficiency, the anemia did not respond to oral or intravenous iron. Cessation of zinc tablets and ingestion of an oral copper preparation daily for 2 mo failed to correct the anemia or leukopenia. It was not until shortly after intravenous administration of a cupric chloride solution during a 5-day period, at a total dose of 10 mg, that serum copper and ceruloplasmin levels increased and the anemia, leukopenia, and neutropenia resolved. These data suggest that the elimination of excess zinc is slow and that, until such elimination occurs, the intestinal absorption of copper is blocked.
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PMID:Zinc-induced copper deficiency. 333 23

The level of haemoglobin, serum iron, total iron binding capacity and ferritin were measured in patients with rheumatological conditions who were anaemic at the time of upper gastrointestinal endoscopy. These parameters were similar in patients with or without lesions of their upper gastrointestinal tract, and in patients with a positive or negative faecal occult blood result. Lesions of the upper gastrointestinal tract were not more frequent in patients with a microcytic anaemia when compared to those with a normocytic anaemia, nor were they found more frequently in patients with a positive faecal occult blood test. Lesions visible at upper gastrointestinal endoscopy are not an important cause of microcytic anaemia in patients with arthritis. The finding that patients with normocytic anaemia are more likely to proceed to lower bowel examination than patients with microcytic anaemia is a reflection of the difficulty in interpretation of these simple haematological tests and showed they were unhelpful in determining which patients warrant investigation of the lower bowel. The frequency of further investigation of the lower bowel was significantly reduced by a positive endoscopy report, irrespective of the nature of the lesion, but was not significantly increased by finding faecal occult blood. We suggest that patients with arthritis selected for investigation of possible gastrointestinal blood loss should follow an organized plan of investigation that includes examination of both upper and lower bowel, and which should proceed uninfluenced by pro tem results. Unfortunately the selection of patients for such further investigation is hampered by a lack of simple discriminatory tests.
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PMID:Anaemia in patients with arthritis: are simple investigations helpful? 291 44

A neurological theory was obtained and examination performed on 62 outpatient epileptics on anticonvulsant therapy. Blood counts, folate and B12 assays were performed on all patients and on a control group of 59 adult non-epileptic neurological outpatients. None of the anticonvulsant treated group had clinical peripheral neuropathy; there was one patient with microcytic anaemia and one with normochromic, normocytic anaemia. In 5 of this group the mean corpuscular volume (MCV) was slightly raised but there was no significant overall difference from the control group. In 17 patients serum folate was subnormal and in 7 the red cell folate was subnormal and this was significantly different to the control group (P less than 0.001). Vitamin B12 levels were normal in all subjects. It is concluded that despite subnormal measured folate levels, there is no increased incidence of clinical peripheral neuropathy or of significant macrocytosis. In view of this, we recommend that folate replacement should not be given to non anaemic asymptomatic patients, with subnormal folate levels, on anticonvulsant therapy.
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PMID:The clinical importance of subnormal folate levels in epileptic patients on anticonvulsant therapy. 344 45

The degrees of anaemia and microcytosis in 100 patients with juvenile chronic arthritis (JCA) were analysed according to the pattern of disease and its activity. Microcytosis was common (40% of patients had a mean corpuscular volume (MCV) of less than 75 fl), sometimes severe (MCV less than 65 fl in 14 patients), and closely correlated with the severity of the anaemia. The degrees of microcytosis and anaemia were both directly related to disease activity as measured by the ESR, and were most severe in cases with the systemic form of JCA. In 50 patients iron status was assessed. The serum iron concentration was directly related to the MCV, whereas the serum ferritin was inversely related to MCV and haemoglobin concentration and directly related to the ESR. Bone marrow iron stores were normal or increased in 6 patients with severe microcytic anaemia. These data suggest that the anaemia of JCA is typically microcytic, and that this microcytosis is associated with the disturbance of iron metabolism seen in the 'anaemia of chronic disorders' rather than overall depletion of body iron.
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PMID:Microcytic anaemia in juvenile chronic arthritis. 358 90

Reticulocyte iron and transferrin uptake was studied in hemoglobin deficit (gene symbol, hbd), an autosomal recessive trait in the mouse characterized by hypochromic microcytic anemia, reticulocytosis, hyperferremia, and increased red-cell-free protoporphyrin. Reticulocyte-rich red cells were incubated in vitro in a mixture of 125I-labeled diferric mouse transferrin and 59Fe-labeled iron-saturated mouse plasma. At 37 degrees C, the uptake of transferrin by reticulocytes from affected animals (15 ng/micrograms RNA) was the same as that of reticulocytes from control animals. However, the uptake of iron by affected reticulocytes (0.11 ng/micrograms RNA) was significantly lower than that by control reticulocytes (0.24). At 4 degrees C, transferrin binding by affected and control reticulocytes was again indistinguishable. The deficiency in the uptake of iron by affected reticulocytes was not observed on incubation at 4 degrees C. Scatchard analysis of transferrin receptors on hbd/hbd and control reticulocytes showed no difference in pKD and a slight elevation in number of receptors per reticulocyte for hbd/hbd animals. These findings suggest that hbd/hbd reticulocytes have a defect in iron acquisition that is distal to the binding of transferrin to the cell membrane receptor. This defect is similar to one already described in the anemia of the Belgrade laboratory rat.
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PMID:Diminished acquisition of iron by reticulocytes from mice with hemoglobin deficit. 359 66


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