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Results for “Folic Acid Deficiency”

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PubMed1977

Structural and functional abnormalities of the small intestine due to nutritional folic acid deficiency in infancy.

Structural abnormalities and disaccharidase deficiency were demonstrated in biopsies of duodenal mucosa from four infants who had symptoms of failure to thrive and chronic diarrhea associated with a megaloblastic anemia. Goat's milk was the main dietary constituent for each infant for six to eight months prior to presentation. The structural abnormalities consisted of villous blunting, crypt hypertrophy, megaloblastic changes in epithelial cells, and nuclear enlargement. All changes reverted to normal with the addition of folic acid to the diet. This study provides evidence that nutritional folic acid deficiency can cause structural and functional alterations of the small intestine in infants.

Anemia, Megaloblastic↗
PubMed1976

Intracranial calcification mimicking the Sturge-Weber syndrome: a consequence of cerebral folic acid deficiency?

Cerebral cortical calcification identical to that of the Sturge-Weber syndrome was observed in two children. In one child the calcification appeared after intrathecal administration of methotrexate and skull irradiation because of leukemia involving the central nervous system. In the other child, who had coeliac disease and epilepsy, the calcification appeared after treatment with anticonvulsants. This treatment was also contributing to the development of profound megaloblastic anemia. The unspecificity of the Sturge-Weber calcification is stressed and the hypothesis is put forward that the calcification may be secondary to folic acid deficiency interfering with the matabolism in the central nervous system.

Angiomatosis↗
PubMed1979

Severe thrombocytopenia probably due to acute folic acid deficiency.

Thirteen patients with significant hemorrhage, severe thrombocytopenia, and megaloblastic bone marrows are described. Unusual features of this problem included its acute onset, frequent absence of the typical peripheral blood changes of megaloblastic anemia, normal serum B12 levels, and serum folates which were often not clearly abnormal. Most patients were critically ill and common clinical features included reduced dietary intake, renal failure, renal dialysis, the postoperative state, and sepsis. These clinical features, the laboratory findings, and a platelet increase in most patients after folate therapy lead to the conclusion that this problem is probably due to acute folic acid deficiency. Possible explanations for the atypical laboratory findings include the acuteness of onset, recent blood transfusion therapy, and impaired folate utilization. This problem may be relatively common. Because of its potential clinical importance, rapid onset, and attendent diagnostic difficulties, prophylactic folic acid is recommended in the clinical setting described.

Acute Disease↗
PubMed1977

Neutrophilic hypersegmentation as an indicator of incipient folic acid deficiency.

The authors have identified a group of subjects with neutrophilic hypersegmentation who are normal or near-normal with respect to other hematologic indices (hemoglobin, mean corpuscular volume). In a high proportion of these subjects, serum folate levels are abnormally low. In this group and a non-hypersegmented-neutrophil control group there was a significant negative correlation between average numbers of neutrophilic lobes and serum folate levels. In the subjects with hypersegmented neutrophils the predominant alteration is a shift from three-lobed to five-lobed neutrophils. It is believed that neutrophilic hypersegmentation can be a valuable adjunct in documenting and/or uncovering incipient folate deficiency.

Erythrocytes↗