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

The pattern of HLA antigens was studied in 127 patients with Addisonian pernicious anaemia. The pattern in the whole group of patients differed significantly from that in 586 controls. But different subgroups of the patients had different HLA antigens. Among 27 patients with anaemia associated with endocrine disease there was an increased frequency of HLA-B8, B18, and BW15. The remaining 100 patients, who did not have endocrine disease, showed increased frequencies of HLA-B7 and B12. The positive association with HLA-B12 among this subgroup was confined to 62 patients with severly impaired vitamin B12 absorption, including 13 patients with vitamin B12 neuromyelopathy, who had the highest frequencies of HLA-B7 and B12. The significant heterogeneity in HLA patterns in different clinical subgroups of these patients indicates genetic heterogeneity in pernicious anaemia and explains previous discrepancies in the associations between HLA antigens and pernicious anaemia.
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PMID:HLA patterns in pernicious anaemia. 85 85

Serum C3 and C4 levels have been determined in patients with Addisonian pernicious anaemia (PA) and megaloblastic anaemia due to vitamin B12 deficiency from other causes, before and after treatment, in order to study the interaction between vitamin B12 deficiency and complement and the role of complement in the pathogenesis of the gastric lesion of PA. C3 levels are significantly reduced in vitamin B12 deficiency and return to normal on treatment; C3 levels correlate with the degree of anaemia but not with serum vitamin B12 levels at diagnosis. C4 levels are normal. These observations suggest that the observed C3 hypocomplementaemia is not a consequence of immune mechanisms, but may be due to altered synthesis of C3 complement component.
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PMID:Reversible C3 hypocomplementaemia in megaloblastic anaemia due to vitamin B12 deficiency. 87 22

The pathogenesis of anemia in 84 patients with valvular protheses of the heart was investigated. A secondary deficiency of serum iron and folate, caused by chronic hemolysis, was found. There was no indication of vitamin-B12-deficiency.
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PMID:[Anemia in patients with artificial heart valves (author's transl)]. 89 64

A series of patients with primary hyperparathyroidism showed a high incidence of anemia. Red cell morphology and indices, iron, folate and B12 were generally normal and reticulocyte counts inappropriately low. Focal fibrosis of the marrow space was observed in marrow biopsies from two patients, but no patient showed overt signs of a myelophthisic process. Anemia tended to occur in those with more severe hyperparathyroidism (higher serum calcium level or radiographic osteitis fibrosa cystica). Since severe hyperparathyroidism frequently compromises renal function, it is not always clear whether the anemia should be attributed to renal failure or to the metabolic disease. In nine of the 24 anemic patients, however, renal function was normal. Hyperparathyroidism may cause a hyporegenerative anemia, the mechanisms for which have not been elucidated.
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PMID:Hyporegenerative anemia in primary hyperparathyroidism. 91 Jan 74

Red cell anisocytosis as assessed using the Coulter Channelyzer C-1000 showed an increase with progressive anaemia in 25 patients with macrocytosis due to B12 and/or folate deficiency. In deficiency of a single factor, the degree of anisocytosis increased with progressive anaemia. In five cases with B12 and folate deficiency combined, anisocytosis was markedly increased out of proportion to the degree of anaemia present. Iron stores were also reduced in four of these cases. It is suggested that objective measurement of anisocytosis is of early diagnostic value in the assessment of multiple haematinic factor deficiency, for example, in macrocytic anaemia associated with malabsorption states and unexpected multiple deficiency states.
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PMID:Anisocytosis and the C-1000 Channelyzer in macrocytic anaemia. 95 53

The anemia observed in patients with partial gastric resection results from a complex interrelationship of deficiencies of these three important hematemics-iron, vitamin B12, and folic acid. Reliance upon morphological evidence of anemia in the peripheral blood smear may be difficult and confusing since deficiency of one hematemic may mask the coexisting deficiency of another. It is common for deficiencies of more than one hematemic to occur in these patients. A number of studies have demonstrated the masking effect of iron deficiency on concurrent vitamin B12 or folic acid deficiency. In addition, the morphologic hallmarks of iron deficiency may be modified by the presence of deficiencies of either vitamin B12 or folate or both. Full hematologic recovery may not occur until more than one hematemic is given to the patient. It is our policy at the University of Florida to rely on serum levels of these three hematemics, especially vitamin B12 and iron, to detect the cause of the anemia in a patient with partial gastric resection. Less reliance is placed upon the appearance of the peripheral smear because of the masking effect described above. If either the serum iron level or vitamin B12 level is decreased, we treat the patient with a preparation such as ferrous sulfate (300 mg. orally three times a day) and vitamin B12 (100 mug. intramuscularly once a month). We are less concerned with folic acid deficiency because of its relatively infrequent occurrence in this setting and because a good diet will usually suffice as adequate therapy for the folic acid deficiency when present. In patients who have had partial gastric resection but who are not anemic, we assess vitamin B12 absorption by the conventional vitamin B12 urinary excretion test (Schilling test) on a yearly basis since deficiency of this hematemic may lead to serious hematologic and neurologic sequelae. If the patient manifests decreased vitamin B12 absorption uncorrected by the administration of pancreatic extract or antibiotics, this patient is also treated with 100 mug. of vitamin B12 intramuscularly on a monthly basis. We have not evaluated the absorption of food B12 as suggested by Doscherholmen. Perhaps more attention should be paid to this aspect of vitamin B12 absorption in these patients. Indeed, because of the serious complications of vitamin B12 deficiency and the observations that deficiencies of this vitamin may occur even when the absorption of crystalline vitamin B12 is normal in the fasting state (the conventional Schilling test), some authors, such as Rygvold, have suggested that prophylactic vitamin B12 be administered to all patients with partial gastric resection.
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PMID:Hematologic abnormalities following gastric resection. 95 76

Several haematological findings (especially the values of serum LDH and its isoenzymes) were compared with changes in the gastrin level in pernicious anaemia. While vitamin B12 substitution therapy led to normalization of the anaemia and of the enzyme levels, gastric atrophy and, hence, the elevation in serum gastrin levels remained unchanged. Determination of serum gastrin, therefore, provides a valuable tool for the verification of the diagnosis of pernicious anaemia in treated cases.
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PMID:[LDH isoenzymes and gastrin in achlorhydri (author's transl)]. 96 Jul 4

Alterations in reticulocyte size occur 2-3 days after the onset of iron deficient or megaloblastic erythropoiesis and precede, by several weeks, changes in mean corpuscular volume (MCV). Iron-deficiency anemia induced in a normal subject by repeated phlebotomies was characterized by the initial development of larger than normal reticulocytes followed by an abrupt decrease in reticulocyte size. Microreticulocytes appeared 3 days after the fall in per cent iron saturation and antedated the decrease in MCV to below normal by 6 wk. Mean reticulocyte size was disproportionately smaller than normal in patients presenting with iron deficiency. In contrast, reticulocyte size increased abruptly in a patient (and rats) 2-3 days after administration of methotrexate. Mean reticulocyte size was disproportionately larger than normal in patients presenting with folate or vitamin B12 deficiency. Specific replacement therapy with iron, folate, or vitamin B12 was quickly followed by normalization of reticulocyte size.
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PMID:Reticulocyte size in nutritional anemias. 97 64

Thymidine kinase has been measured in phytohaemagglutinin (PHA)-stimulated lymphocytes from 13 normal subjects and eight patients with megaloblastic anaemia. The levels in normal subjects ranged from 0.20 to 2.10 units/mg protein (mean 0.903 units/mg protein) and in megaloblastic anaemia from 2.99 to 9.97 units/mg protein). All the patients showed raised levels of the enzyme which were partly but not completely reduced to normal by addition of folic acid in vitro. Vitamin B12 in vitro had a lowering effect in the five vitamin-B12-deficient patients and two patients with combined deficiencies but not in one 'pure' folate-deficient patient. Thymidine kinase activity was highest in the cells of the least anaemic patients, suggesting that the degree of anaemia in megaloblastic anaemia may be determined in part by the ability of the cells to utilize thymidine by the 'salvage' pathway when the de novo pathway of thymidylate synthesis is failing. The rise in thymidine kinase activity in megaloblastic anaemia is presumably due to induction of the enzyme. Addition of methotrexate or 5-fluorouracil, drugs known to inhibit de novo thymidylate synthesis, caused an increase in thymidine kinase activity in normal PHA-stimulated lymphocytes after 24 h (but not after 1 h) which could be completely blocked by addition of puromycin. Thymidine mono- and di-phosphate kinases were also measured in normal PHA-stimulated lymphocytes. The activities were substantially higher than that of thymidine kinase and their activities were unaffected by methotrexate addition.
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PMID:Thymidine kinase in megaloblastic anaemia. 100 25

Cobalt deficiency was produced in goats by feeding them rhode grass hay. The deficient animals excreted increased amounts of methyl malonic acid in their urine, indicating a lack of vitamin B12. Erythrocyte reduced glutathione levels increased with the onset of anemia. There was a concomitant increase in the levels of erythrocyte glutathione reductase (GSSG NADPH Reductase) and glutathione peroxidase (GSH:H2O2 peroxidase)during deficiency. These results are compared with similar observations reported for vitamin B12 deficiency in humans.
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PMID:Erythrocyte glutathione metabolism in cobalt-deficient goats. 103 28


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