Cases reported "Folic Acid Deficiency"

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1/10. Folate and Vitamin B(12) deficiency presenting as pancytopenia in pregnancy: a case report and review of the literature.

    We present a case of extreme pancytopenia in a 27-year-old pregnant woman. The initial picture was compatible with a severe hematological problem in the category of aplastic anemia, paroxysmal nocturnal hemoglobinuria or even acute leukemia. The further biochemical investigations revealed, however, a folate deficiency.Nowadays this is a very rare cause of pancytopenia. Next to this she also had a Vitamin B(12) deficiency due to intrinsic factor failure. The recent literature is discussed.
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2/10. Sulphasalazine associated pancytopenia may be caused by acute folate deficiency.

    agranulocytosis and aplastic anaemia associated with sulphasalazine are well recognised, but pancytopenia caused by acute megaloblastic arrest of haemopoiesis while taking sulphasalazine has not previously been described. We report three patients who, after taking sulphasalazine for over two years, suddenly developed severe pancytopenia with gross megaloblastic changes in the marrow. In two patients there was a good response to high dose oral folic acid but the third required folinic acid. The mechanism appears to be acute folate deficiency, and the requirement for folinic acid in one case suggests that the known inhibition of folate metabolism by sulphasalazine also contributes. The syndrome appears to be associated with high dosage and slow acetylator status. The drug has been successfully restarted at reduced dosage with folate supplements in two patients both of whom were slow acetylators. In the third case, whose acetylator status is not known, progression of her disease led to colectomy.
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3/10. pancytopenia--a rare manifestation of folic acid deficiency.

    In the western world folic acid deficiency is a relatively rare cause of anaemia in the elderly population. A 79-year-old woman presented with pancytopenia (haemoglobin 3.4 mmol l-1, leucocytes 1.2.10(9)l-1, thrombocytes 22.10(9)l-1) due to folic acid deficiency. The deficiency was caused by an extremely low dietary intake. The case was complicated with infection and haemorrhagic manifestations. Administration of folic acid increased the number of erythrocytes, leucocytes and thrombocytes markedly. Beside vitamin B12 deficiency folic acid deficiency must be borne in mind in megaloblastic anaemias complicated with leucopenia and/or thrombocytopenia. Since the body stores of folic acid are low, rapid diagnosis and treatment are important.
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4/10. pancytopenia and folate deficiency in alcoholics.

    Three alcoholic patients are reported who presented with pancytopenia and macrocytosis due to acute folate deficiency. While folate deficiency is a common finding in alcohol abusers due to abnormalities in diet, intestinal absorption, internal metabolism and excretion, this life-threatening complication has not been well documented.
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5/10. Folate deficiency presenting as pancytopenia in pregnancy.

    Folate deficiency is a well-known complication of pregnancy. We present a case of folate deficiency with profound pancytopenia. Although this is a well-known consequence of folate deficiency, we wish to reemphasize this dramatic complication of pregnancy.
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6/10. Folate deficiency during intravenous hyperalimentation.

    Two alcoholic patients were supported with hyperalimentation therapy during the management of complicated surgical problems. Folate deficiency was documented after ten and two weeks of intravenous feeding. One patient developed severe pancytopenia. Folic acid treatment resulted in hematologic recovery in both cases. Early development of folate deficiency in these patients seems to be related to multiple factors, viz., poor folate stores related to chronic alcoholism, poor dietary intake before and during the hospitalization, infection, prolonged gastric suction, and lack of folate in the intravenous hyperalimentation fluids. Rationale for the supplementation of folates in such patients is discussed.
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7/10. Acute folate deficiency in surgical patients on aminoacid/ethanol intravenous nutrition.

    Acute folate deficiency with pancytopenia and megaloblastic haemopoiesis developed in four patients after abdominal operations; all four responded to folic acid over 3-9 days. Three of them had been given intravenous nutrition with amino-acid/ethanol before the blood changes developed. A prospective study of twenty-five surgical patients with gastrointestinal diseases revealed a high frequency of acutely developing negative folate balance. Megaloblastic haemopoiesis and consequent blood changes were found in five patients. Treatment with intravenous nutrition correlated strongly with a fall in serum-folate and megaloblastic haemopoiesis. Some surgical patients develop acute folate deficiency which may proceed to megaloblastic arrest of haemopoiesis. patients receiving intravenous nutrition containing ethanol are especially prone to this complication, which may be life-threatening if untreated. It is not yet known whether other forms of intravenous nutrition carry a similar risk.
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8/10. Folate-induced remission in aplastic anemia with familial defect of cellular folate uptake.

    Severe aplastic anemia developed in a young man with an extensive family history of leukemia, pancytopenia, and neutropenia. Megaloblastic changes became evident, and treatment with high doses of folic acid resulted in striking clinical improvement. However, red-cell folate levels remained persistently low despite high serum folate levels. A defect in cellular folate uptake was suspected, and, indeed, uptake of 5-14CH3-H4-folate by stimulated lymphocytes and by bone-marrow cells from the patient was significantly reduced (P less than 0.05 as compared to normal cells. Further characterization of folate metabolism showed that intestinal absorption of the vitamin, membrane transport of 5-14CH3-H4-folate by mature red cells, folate utilization in the conversion of deoxyuridylate to thymidylate and polyglutamate formation were all normal. At least five other family members manifest decreased uptake of 5-14CH3-H4-folate by stimulated lymphocytes. These studies suggest that a genetically induced abnormality of folate uptake contributed to this patient's severe, but reversible, aplasia.
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9/10. Acute pancytopenia due to megaloblastic arrest in association with co-trimoxazole.

    Three patients who were taking co-trimoxazole developed acute pancytopenia due to megaloblastic arrest, and two of the three died while pancytopenic. One patient had a pre-existing megaloblastic anaemia. In the other two patients, there was no macrocytosis or neutrophil hypersegmentation despite the severe megaloblastosis. Because specific treatment is needed urgently, it is important to distinguish megaloblastic arrest from drug-induced hypoplasia.
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10/10. Phagocyte dysfunction in common variable immune deficiency.

    The history of a 13-year old boy is reported who suffered from frequent bacterial, enteroviral, and protozoal infections since late infancy. A decrease in the serum levels of IgG2, IgG3, IgA, a neutrophil dysfunction, and a partial cellular immune deficiency could be demonstrated. A deficiency of folic acid produced a pancytopenia which enhanced the patient's susceptibility to infections. The combined substitution of gammaglobulins and folic acid only was able to break this vicious cycle.
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