Cases reported "Folic Acid Deficiency"

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11/72. Severe folate deficiency mimicking hellp syndrome--report of two cases.

    Severe folate deficiency in pregnancy may mimick hellp syndrome as there are similar features in both. Proper diagnosis is important as far as the prognosis and management are concerned. Two cases of severe folate deficiency occuring in multigravid women mimicking hellp syndrome are reported below with review of literature.
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12/72. sarcoidosis: association with small bowel disease and folate deficiency.

    A 30 year old woman with recurrent anaemia due to folate deficiency had evidence of sarcoid granuloma on small bowel biopsy but was presumed to have Crohn's disease. The diagnosis of small bowel sarcoidosis was not seriously considered until she developed systemic manifestations of sarcoidosis (cutaneous and pulmonary lesions) over the following 20 years. sarcoidosis of the gastrointestinal tract, particularly the small bowel, is rare and this case is unusual because bowel pathology preceded more generalised lesions. As far as is known it is also the first case to be described presenting with malabsorption of folic acid.
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13/72. Potential association of thyrotoxicosis with vitamin B and folate deficiencies, resulting in risk for hyperhomocysteinemia and subsequent thromboembolic events.

    OBJECTIVE: To describe a patient with severe thyrotoxicosis attributable to Graves' disease who had a thrombotic cerebrovascular accident and hyperhomocysteinuria, which resolved on correction of the thyrotoxicosis, and to present findings in a pilot study undertaken to investigate the relationship among thyrotoxicosis, homocysteine, folate, and vitamin B(12). methods: We present a case report of the index case, with clinical and laboratory details. For the investigative analysis, 21 patients who were 18 to 50 years old and had newly diagnosed, untreated Graves' disease and 10 age-and sex-matched euthyroid control subjects were studied. Of the patients with Graves' disease, 11 underwent studies both at diagnosis and after treatment. fasting blood tests were performed for thyrotropin, free thyroxine, homocys-teine, vitamin B(12), folate, and methylmalonic acid, a marker of vitamin B(12) deficiency. RESULTS: Vitamin B(12), folate, homocysteine, and methylmalonic acid levels were not significantly different between the thyrotoxic and control or posttreatment groups. In patients with thyrotoxicosis, however, free thyroxine was positively correlated with both homocysteine (r = 0.67; P = 0.03) and methylmalonic acid (r = 0.89; P = 0.003). CONCLUSION: The positive correlation between free thyroxine levels and both homocysteine and methylmalonic acid suggests that thyrotoxicosis may be associated with functional vitamin B(12) deficiency. Such a deficiency may result in clinically important hyperhomocysteine-mia.
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14/72. RAEB-t in young adults--a rare entity.

    Refractory anemia with excess blasts in transformation (RAEB-t) in young adults is a rare entity. RAEB-t presenting with megaloblastic erythropoiesis should be differentiated from nutritional B12 and folic acid deficiency and from acute erythroleukemia. We report two cases in the present article.
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15/72. Destructive, granulating lesion in the temporal bone after elevated plasma homocysteine.

    OBJECTIVE: This is a presentation of a seemingly new otolaryngologic disease. SETTING: This study was conducted at a tertiary referral center. CASE REPORT: A 38-year-old healthy man developed left-sided sudden deafness with vertigo and temporary left facial palsy. A granulating and destructive lesion in the left temporal bone was discovered; repeated histologic examination only showed simple granulation tissue. After 6 months, a part of the bony cochlea was extruded. With approximately 8 months' delay and after the patient had had postoperative lung embolism, plasma homocysteine was found to be significantly elevated, a condition known as an independent risk factor for thromboembolic lesions. In the acquired form, it is most often caused by nutritional deficiency of vitamin B cofactors. Accordingly, the patient was treated with folic acid, which rapidly normalized plasma homocysteine. Subsequently, the granulation tissue in the temporal bone gradually disappeared, clinically and radiologically, and the lesion healed, obviously without cochlea function. CONCLUSIONS: Thromboembolic lesion in the left temporal bone, probably in the thin end artery a. labyrintina, i.e., an avascular osteonecrosis. During the latest years, an association between avascular osteonecrosis (most often in the hip) and conditions with increased risk of thrombosis such as hyperhomocystinemia has been established but, to the best of our knowledge, it is never with a lesion in the temporal bone.
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16/72. Megaloblastic anemia associated with psoriasis: case report and review of the literature.

    A 68-yr-old male with severe psoriasis developed megaloblastic anemia due to folate deficiency 3 months after the cessation of low-dose methotrexate therapy. The mechanism of megaloblastic anemia in this case was suggested to be multifactorial. The case report and a review of megaloblastic anemia associated with psoriasis are presented.
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17/72. Cerebral folate deficiency: life-changing supplementation with folinic acid.

    Cerebral folate deficiency is characterized by low cerebrospinal fluid (CSF) concentrations of 5-methyltetrahydrofolate and a broad spectrum of clinical signs and symptoms. A patient with progressive spasticity, gait disturbance, speech difficulties, initially diagnosed as a recessive spastic paraplegia recovered on folinic acid (15-30 mg/day) and her 5-methyltetrahydrofolate in CSF normalized. This report demonstrates the importance of CSF investigation in the diagnosis of cerebral folate deficiency and efficiency of folinic acid (5-formyltetrahydrofolate) supplementation.
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18/72. Cerebral folate deficiency with developmental delay, autism, and response to folinic acid.

    The authors describe a 6-year-old girl with developmental delay, psychomotor regression, seizures, mental retardation, and autistic features associated with low CSF levels of 5-methyltetrahydrofolate, the biologically active form of folates in CSF and blood. Folate and B12 levels were normal in peripheral tissues, suggesting cerebral folate deficiency. Treatment with folinic acid corrected CSF abnormalities and improved motor skills.
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19/72. Treatment of iron-deficiency anemia complicated by scurvy and folic acid deficiency.

    We present a case of a child with iron-deficiency anemia, folic acid deficiency, and scurvy. His anemia proved refractory to treatment with iron until he received both folic acid and vitamin C supplementation. This case illustrates the importance of the evaluation of ascorbic acid and folate status in treating iron-deficiency anemia initially refractory to iron supplementation, because multiple nutrient deficiencies may coexist.
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20/72. Cerebral folate deficiency and leukoencephalopathy caused by a mitochondrial dna deletion.

    OBJECTIVE: Our aim was to describe a child with an incomplete form of kearns-sayre syndrome who presented profound cerebrospinal fluid (CSF) folate deficiency and his response to folinic acid supplementation methods: CSF 5-methyltetrahydrofolate was analyzed by HPLC with fluorescence detection and mitochondrial dna deletions by southern blot hybridization. RESULTS: Cranial magnetic resonance imaging showed a leukoencephalopathy. Profound CSF 5-methyltetrahydrofolate deficiency was observed with normal blood folate values and decreased CSF/serum folate ratio, suggesting a transport defect across the blood-brain barrier. Folinic acid treatment was established, and after 1 year clinical response to folinic supplementation was remarkable, with almost normal white matter image. INTERPRETATION: The clinical response after folinic therapy highlights the need for the study of cerebral folate deficiency in patients with mitochondrial disorders and white matter lesions.
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