Cases reported "Folic Acid Deficiency"

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1/91. 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. ( info)

2/91. phenytoin-folic acid interaction: a lesson to be learned.

    A case of a patient who developed symptomatic phenytoin-induced folic acid deficiency is reported. Folate supplementation of 5 mg/d was followed by a decrease of serum phenytoin concentration to a subtherapeutic level with a breakthrough seizure. Estimation of phenytoin's Km-Vmax Michaelis-Menten pharmacokinetic parameters in this patient demonstrated that folate supplements indeed caused a significant decrease in the Km value. This decrease correlates with a greater affinity of the metabolizing hepatic enzymes for the drug, and hence, with the resultant increase in phenytoin's metabolism and decrease of its serum concentration and anticonvulsive effect. In an era of increasing knowledge of folate's pivotal role in various diseases, we call attention to this drug-vitamin interaction, and to the previously suggested recommendation that folate supplementation should be initiated whenever phenytoin therapy commences. Because folic acid dosages as low as 1 mg/d may perturbate phenytoin's metabolism, smaller deficiency preventive doses may be the advisable allowance for phenytointreated patients with normal pretreatment folate levels. This suggestion must be confirmed by a prospective study in a large cohort of patients. ( info)

3/91. Nutritional deficiencies in a patient with glycogen storage disease type Ib.

    The current mainstay of treatment in glycogen storage disease type i (GSD I) is dietary management that includes providing a frequent source of glucose to prevent hypoglycaemia. To ensure compliance, routine follow-up by a health care team, including a dietitian, experienced in the treatment of GSD is necessary. We describe an adolescent patient with GSD Ib in good metabolic control who was admitted with a 3-month history of weakness, depression, vomiting, decreased appetite and a 11.4-kg weight loss. He had a recent onset of unsteady gait, inability to write, and sore mouth. After an extensive work-up, the patient was found to have vitamin B12, folate, iron and other nutritional deficiencies, which explained his symptoms. The patient improved within 72 h of initiation of total parenteral nutrition and therapeutic doses of deficient micronutrients, with a complete recovery in 2 months. Dietary restrictions, dependence on non-food products (e.g. cornstarch in GSD I), and social and developmental issues place individuals with metabolic disorders at a high risk for developing an array of nutritional deficiencies. This case highlights the importance of both close follow-up of the metabolic control and close monitoring of growth and nutritional intake in individuals with inborn errors of metabolism. This case also illustrates the importance of daily supplementation with appropriate multivitamins, calcium and other minerals needed to meet the Recommended Dietary Allowances (RDAs) in these patients. ( info)

4/91. Megaloblastic anemia due to folic acid deficiency after oral contraceptives.

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5/91. Pseudodementia in a twenty-one-year-old with bipolar disorder and vitamin B12 and folate deficiency.

    A twenty-one-year-old female known to suffer from bipolar type I disorder developed features of a pseudodementia. Following prompt initial response to treatment with antidepressants, there was an early recurrence of cognitive impairment. blood investigations confirmed a macrocytic anaemia and vitamin B12 and folate deficiencies. There was dramatic resolution of cognitive impairment after vitamin replacement. This suggested the occurrence of a reversible nutritional dementia and reinforced the need to rule out secondary organic causes of psychiatric symptoms even in patients previously diagnosed with a primary psychiatric disorder. ( info)

6/91. Recurrent cleft lip and palate in siblings of a patient with malabsorption syndrome, probably caused by hypovitaminosis a associated with folic acid and vitamin B(2) deficiencies.

    We present a woman with metabolic disorders secondary to malabsorption and renal disease who gave birth to a stillborn male fetus with left unilateral cleft lip and palate and a live born infant with left unilateral cleft lip and palate. We discuss potential cofactors that could be implicated in the abnormal embryonic process. ( info)

7/91. Reversible central nervous system dysfunction in folate deficiency.

    An epileptic patient on chronic anticonvulsant drug therapy is described, in whom anaemia and neurological abnormalities including progressive dementia, bilateral pyramidal tract signs, incontinence and ataxia developed. Vitamin B12 serum levels and absorption were normal, but serum folic acid levels were low. Both the neurological disturbances and anaemia resolved following oral folic acid administration. This sequence of events in our patient suggests a cause and effect relationship between the folate deficiency and the coexistent, transient neurological syndrome. ( info)

8/91. 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. ( info)

9/91. Severe folate deficiency masquerading as the syndrome of hemolysis, elevated liver enzymes, and low platelets.

    BACKGROUND: Although folate deficiency is common in pregnancy, progression to megaloblastosis is not. Hemolytic anemia, thrombocytopenia, and coagulopathy due to folate deficiency may mimic the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP). CASES: Two women presented in the second trimester with abdominal pain and severe thrombocytopenia. These symptoms were misinterpreted in the first woman as the hellp syndrome, leading to an emergency cesarean delivery. Subsequent investigation revealed folate deficiency; treatment resulted in rapid normalization of all abnormalities. In the second woman, folate deficiency was diagnosed antenatally. Treatment allowed continuation of the pregnancy to term. CONCLUSION: The serious complications of folate deficiency make a strong case for supplementation in pregnancy. Careful scrutiny of clinical and laboratory findings may help discriminate the hellp syndrome from its mimics, avoiding preterm delivery. ( info)

10/91. Mood disorder with mixed features due to vitamin B(12) and folate deficiency.

    Vitamin B(12) and folate deficiency is often associated with affective disorders mainly of the depressive type. We report a case of a 42-year-old woman with a mood disorder with mixed depressed/manic features that was due to vitamin B(12) and folate deficiency. The psychopathology developed over a five-year period without hematologic or other overt clinical characteristics of pernicious anemia. Replacement treatment with vitamin B(12) and folate was rapidly followed by full clinical remission, electroencephalographic normalization and neuropsychological improvement. At a one-year follow-up this condition was stable. Consequently, patients who respond poorly to psychopharmacologic treatment and/or present with atypical mood symptoms would warrant determination of vitamin B(12) and folate serum levels. ( info)
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