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Results for “Anemia, Megaloblastic”

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At least 19 recordsLinked to original sources
PubMed1983

The changing pattern of megaloblastic anemia: megaloblastic anemia in Israel.

The causes of megaloblastic anemia were studied in a survey of patients admitted to six Israeli hospitals over a period of 15 yr. Among the 203 patients identified, 69% had pernicious anemia, 12% had gastrointestinal disease, 9% had primary nutritional deficiency of whom only 1% were associated with pregnancy, and 7% had selective vitamin B12 malabsorption with albuminuria. Comparison with previously published surveys showed, that in contrast with earlier studies where primary nutritional deficiency was the cause of megaloblastic anemia in about 70% of cases and pernicious anemia in only 20%, in more recent studies the proportion of cases with primary nutritional anemia in general and those associated with pregnancy in particular was much lower. This is most probably the result of improved standards of living and a national program of preventive folate supplementation at maternity clinics. A potential hazard of such preventive programs is the aggravation of neurological complications in patients with undiagnosed vitamin B12 deficiency. Early recognition of pernicious anemia and other forms of selective B12 malabsorption is a new challenge created by the changing pattern of megaloblastic anemias.

Adolescent↗
PubMed1991

Diagnosis of megaloblastic anemia.

Megaloblastic anemia can be due to cobalamin deficiency, folate deficiency, or refractory forms of bone marrow disease. This essay reviews current thinking on the diagnostic procedures available to a physician considering these disorders. The questions to be answered are as follows: Is a megaloblastic anemia present? Is there a deficiency of cobalamin or folate? If a deficiency is present, what is its cause? Various diagnostic tests are discussed with regard to the differences in their sensitivity and metabolic implications. In particular, we consider the newest diagnostic tests for cobalamin deficiency, serum homocysteine, and methylmalonate, which appear to be highly sensitive predictors of clinical morbidity. Application of these tests suggests that many more patients are cobalamin-deficient than had been supposed.

Anemia, Megaloblastic↗
PubMed1999

[Pernicious anemia and other megaloblastic anemias].

OBJECTIVE: To describe the clinical and biological characteristics of a series of patients with megaloblastic anemia (MA) and to identify potential differences between patients with pernicious anemia (PA(+)) and patients with other MA (PA(-)). METHOD: Retrospective study of 50 patients with MA diagnosed in our service between 1993 and 1998. RESULTS: MA was diagnosed in 50 patients. The median age in the moment of diagnosis was 70.7 years. The causes of MA were: cobalamin deficiency (CD) in 40 cases (80%), folate deficiency (FD) in 7 cases (14%) and both deficiencies in 3 cases (6%). PA was diagnosed in 19 patients (38%). All cases showed hyper-segmented neutrophils and 41 cases (81%) macroovalocytosis. Hemoglobin level < 8 g/dl was present in 22 patients (44%). The median serum LDH level was 2.059 +/- 1.739 U/l. There was a lower frequency of female sex and a higher RDW in the group PA(+). There were no significant differences between both groups in the rest of studied features, except for the presence of antiparietal cell antibodies and anti-intrinsic factor antibodies in the group PA(+). CONCLUSIONS: CD was the most frequent cause of MA in our series. PA was the most frequent cause of CD. Most cases of MA corresponded to a severe macrocytic anemia with hyper-segmented neutrophils, macroovalocytosis and very high serum LDH level. We did not identify any clinical or biological characteristic, except for the presence of antiparietal cell antibodies and anti-intrinsic factor antibodies and a higher RDW in the group PA(+), to permit distinguish the groups PA(+) and PA(-).

Aged↗
PubMed2002

Linkage analysis of a large inbred family with congenital megaloblastic anemia.

OBJECTIVE: Megaloblastic anemia during infancy and early childhood often reflects a hereditary disorder of cobalamin's absorption, transport, or intracellular metabolism. There are 3 well defined autosomal recessive syndromes manifesting with megaloblastic anemia due to defects in cobalamin absorption or transport, namely congenital pernicious anemia, Imerslund-Grasbeck syndrome and Transcobalamin II deficiency. The genes responsible for the 3 disorders are gene intrinsic factor (GIF), MGA1 and TCN2, as well as the gene for Transcobalamin I, TCN1 are mapped or cloned, or both. METHODS: We describe the clinical picture of 7 patients from 3 sibships, belong to one large inbred family who presented with megaloblastic anemia during infancy. The mode of inheritance follows an autosomal recessive pattern and the syndrome was completely reversed by parentral vitamin B12 therapy. The ascertainment of the family was carried out in 1998 in the Princess Rhama Children's Hospital, which is affiliated with Jordan University of Science and Technology, Jordan. We performed linkage analysis in this family for genes or regions involved in the above mentioned disorders. RESULTS: The genes implicated in the etiology of the previously mentioned disorders were excluded from being responsible for the disorder in this family. CONCLUSION: The exclusion of the involvement of GIF, MGA1, TCN1 and TCN2 in this family suggests that another gene and its product, involved in cobalamin absorption or transport, remains to be identified. A genome-wide search of the gene implicated in this family may give some insight on that gene, and its function.

Anemia, Megaloblastic↗
PubMed1975

Intestinal iron absorption under the influence of available storage iron and erythroblastic hyperplasia. Comparative studies in children with hereditary spherocytosis, nonspherocytic enzymopenic hemolytic anemia, acquired hemolytic anemia, vitamin B12 deficiency induced megaloblastic anemia, erythroblastic hypoplasia and aplastic anemia.

A high negative correlation (coefficient similar to 0.9) between increased 59Fe absorption from a diagnostic 0.56 mg 59Fe2+ dose and the depletion of available storage iron was observed in menstruating and pregnant women, fullterm and premature infants, blood donors, patients with infections, inflammations, tumors, hepatic cirrhosis, gastric surgery, increased urogenital or gastrointestinal blood loss. The increased diagnostic 59Fe2+ absorption is a reliable and sensitive indicator of at least depleted iron stores or prelatent iron deficiency as caused by iron malnutrition or maldigestion, increased iron requirement in pregnancy, infancy, urogenital or gastrointestinal blood loss. Although the messenger system which signalyzes the depletion of iron stores to the iron absorbing enterocytes of the duodenal and jejunal mucosa is not yet known available storage iron seems to control intestinal iron absorption under normal and the great majority o pathological condition in humans. Anemia per se or high erythropoietin levels in blood do not influence iron absorption since patients with even severe erythroblastic hypoplasia, aplastic anemia and megaloblastic anemia due to vitamin B12 deficiency absorb iron according to their iron stores. An only mild hyperplasia of the erythropoietic system in the bone marrow does also not effect iron absorption which was still under the control of available storage iron in patients with hereditary spherocytosis, nonspherocytic congenital hemolytic anemia due to glucose-6-phosphate dehydrogenase deficiency, acquired hemolytic anemia and vitamin B12 deficiency induced megaloblastic anemia..

Adolescent↗