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Results for “FOLIC ACID DEFICIENCY”

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PubMed1983

Folic acid deficiency in beta-thalassaemia heterozygotes.

Plasma and red cell folate mean contents have been found to be significantly lower in 41 symptom-free beta-thalassaemia heterozygotes than in 21 controls. Such decreases must be considered as effects of an increased folate utilization caused by the enhanced total, both effective and ineffective, erythropoiesis. Since no close correlation has been found between packed cell volume and plasma or red blood cell folate levels, it seems that in 'healthy' beta-thalassaemia subjects, the degree of anaemia is not influenced by folate body reserves. However, the frequent finding of reduced red cell folate contents suggests that further folate imbalance might lead to clinically significant degrees of folate deficiency.

Adolescent↗
PubMed1989

Folic acid deficiency, megaloblastic anemia and peripheral polyneuropathy due to oral contraceptives.

A 34-year-old woman developed megaloblastic anemia and peripheral polyneuropathy following the use of oral contraceptives for 4 years. Low levels of folic acid and vitamin B12 were found. Both the complete recovery after therapy with the vitamins, and the absence of other causes of vitamin B12 and folate deficiency, suggest that the vitamin deficiencies were caused by the oral contraceptives and resulted in the rare combination of megaloblastic anemia and polyneuropathy. The poor response to vitamin B12 alone, and the development of anemia and polyneuropathy 4 months after cessation of vitamin B12 therapy suggest that folate deficiency was the primary problem.

Adult↗
PubMed1993

[Folic acid deficiency in patients hospitalized with depression? A pilot study of clinical relevance].

Seventy-seven depressive inpatients were studied in a pilot study to determine their serum and red cell folate levels at admission. Only one depressive inpatient with a low serum folate value had a history of an illness-related lack of nutrition prior to admission, and the low value was only on day 1 of the study. Our results demonstrate that folate acid deficiency is not as common in depressive inpatients as reported, especially in British studies for two reasons: different eating habits and a methodological problem.

Adult↗
PubMed1990

[Folic acid deficiency can cause severe anemia and pancytopenia].

Pancytopenia is occasionally a consequence of folate deficiency. The most important differential diagnostic considerations are haematologic malignancies, aplastic anaemia and vitamin B12 deficiency. We discuss the problem as exemplified by three patients. Bone marrow examination and determination of blood concentrations of vitamin B12 and folate will give the correct diagnosis.

Adult↗
PubMed1997

[Folic acid deficiency with leukoencephalopathy and chronic axonal neuropathy of sensory predominance].

A 44-year-old, alcoholic, woman developed a prolonged folate deficiency with a chronic predominantly axonal sensory polyneuropathy. The cerebral CT and MRI revealed a diffuse, clinically asymptomatic, leukoencephalopathy. A partial improvement of the neurological symptoms was observed after two months of oral administration of folate. Neurological complications of folate deficiency are rare and similar to those observed in cobalamin deficiency. Both cobalamin and folate deficiencies may interfere with the synthesis of the central myelin. This case report illustrates the possibility to observe a leukoencephalopathy due to folate deficiency, in association with the classical polyneuropathies and/or subacute combined degenerations of the spinal cord.

Adult↗
PubMed2003

[Treatment with levodopa can affect latent vitamin B 12 and folic acid deficiency. Patients with Parkinson disease runt the risk of elevated homocysteine levels].

There is a well-known interaction between vitamin B12, folate, and homocysteine. More unknown is the fact that this interaction might be affected by long-term treatment with levo-dopa in patients with Parkinson's disease. An increase in homocysteine levels and tissue deficiency of vitamin B12 and folate may occur. The responsible doctor should be liberal in checking vitamin B12 and folate status and supplement with appropriate vitamins when needed.

Animals↗
PubMedDate not supplied

[Folic acid deficiency and increased concentrations of formate in serum and cerebrospinal fluid of patients with epidemic optical neuropathy].

We studied 62 patients aged 48 years as an average and diagnosed with bilateral optical neuropathy during an epidemics in Pinar del Río province. Of these patients, 42 showed the optical form whereas 20 had the mixed form of optical neuropathy. We researched into the levels of formate and folate in serum and cerebrospinal fluid samples and we found a marked deficiency of folates in more than 50% of samples and high formate concentration levels in almost 25% of samples. We concluded that nutritional shortages that lead to a reduction of folates, and the intake of small amounts of methanol in alcoholic drinks could lead to lacking energetic states which would facilitate that the optical nerve be affected and the epidemic optical neuropathy appear.

Alcohol Drinking↗
PubMed2004

Folic acid deficiency during late gestation decreases progenitor cell proliferation and increases apoptosis in fetal mouse brain.

In mice and rats, maternal dietary choline intake during late pregnancy modulates mitosis and apoptosis in progenitor cells of the fetal hippocampus and septum. Because choline and folate are interrelated metabolically, we investigated the effects of maternal dietary folate availability on progenitor cells in fetal mouse telencephalon. Timed-pregnant mice were fed a folate-supplemented (FS), control (FCT) or folate-deficient (FD) AIN-76 diet from d 11-17 of pregnancy. FD decreased the number of progenitor cells undergoing cell replication in the ventricular zones of the developing mouse brain septum (46.6% of FCT), caudate putamen (43.5%), and neocortex (54.4%) as assessed using phosphorylated histone H3 (a specific marker of mitotic phase) and confirmed by bromodeoxyuridine (BrdU) labeling of the S phase. In addition, 106.2% more apoptotic cells were found in FD than in FCT fetal septum. We observed 46.8% more calretinin-positive cells in the medial septal-diagonal band region of FD compared with pups from control dams. FS mice did not differ significantly from FCT mice in any of these measures. These results suggest that progenitor cells in fetal forebrain are sensitive to maternal dietary folate during late gestation.

Animals↗
PubMedDate not supplied

[Peripheral and optical myeloneuropathy in a folic acid deficient alcoholic patient].

INTRODUCTION: In Western countries, neurological disorders secondary to toxic nutritional problems usually present as isolated cases that are generally associated to identifiable causes (alcoholism, eating disorders, absorption disorders, use of medicines) that reduce the availability of basic nutrients, especially B group vitamins, but also folic acid (FA). The optic nerves and the peripheral axons are frequent target organs in this type of pathology, but leukoencephalopathy and spinal cord involvement may also appear, often in combination. CASE REPORT: We describe the case of a 38-year-old female smoker with a heavy alcohol habit, who developed a subacute clinical pattern of, predominantly axonal, sensitive peripheral polyneuropathy, with vegetative fibre involvement. She also presented involvement of the posterior spinal cord, which gave rise to an ataxic disorder in the gait, as well as a severe bilateral retrobulbar optic neuropathy. Likewise, she presented macrocytosis (MCV: 118) due to megaloblastosis. She was also found to have a FA deficit but a normal vitamin B12 metabolism. With the help of supplementary vitamins, stopping drinking and the regularisation of her diet, the patient presented progressive clinical improvement, and was able to walk without support at 3 months and almost completely recovered her sight, which was corroborated by an improvement in the studies of both visual and somatosensorial evoked potentials. CONCLUSIONS: In our community, alcoholism is a frequent cause of nutritional deficiencies, which lead to neurological problems. FA is one of the nutrients that become deficient in alcoholics. More and more descriptions are being reported of peripheral polyneuropathy, retrobulbular optic neuropathy, myelopathy or leukoencephalopathy associated to FA deficiency, above all in patients with a history of alcoholism.

Adult↗