Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FOLIC ACID DEFICIENCY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed2002

Neurological signs are common in patients with urodynamically verified "idiopathic" bladder overactivity.

Overactive bladder dysfunction is an expression of defective neuromuscular control of the lower urinary tract. The causes and the way to classify this problem are currently under debate. In some patients the overactive bladder is one sign of a neurological disorder, in so called "idiopathic detrusor instability" the cause is less obvious. That an overactive bladder has a neurogenic cause is a reasonable hypothesis. We made a detailed neurological investigation in 45 patients with idiopathic overactive bladder. Cerebrospinal fluid (CSF) was examined and blood tests for vitamin B(12)and folic acid deficiency were checked, too. In 37 of the 45 patients (82%) pathological signs were observed in the neurological tests. The most common finding was central or peripheral paresis of the legs appearing in 24 patients (53%). Of the 45 patients, eight received a neurological diagnosis, definite or possible MS or dorsal column sensation neuropathy. The results of this study give an indication of the importance of the neurological examination and suggest that neuropathy might not be uncommon in patients with so-called idiopathic detrusor instability. This also invites to reconsideration of the current classification. It is possible that a new classification based on a functional view could provide a better fundament in the search of etiologic and pathogenetic factors and also guide in the selection of the treatment most optimal for the individual patient.

Adult↗
PubMed1994

Ki-S1 and PCNA expression in erythroid precursors and megakaryocytes--a comparative study on proliferative and endoreduplicative activity in reactive and neoplastic bone marrow lesions.

The monoclonal antibody Ki-S1 reacts with a cell proliferation-associated nuclear antigen which is expressed in the G1 through G2/M phases of the cell cycle and is resistant to formalin fixation. We have studied Ki-S1 and PCNA (PC10) immunostaining of erythroid precursors (proliferative activity) and megakaryocytes (endoreduplicative activity) in bone marrow trephine biopsies in a variety of reactive and neoplastic lesions using double immunohistochemistry to identify both cell lineages. A significant increase in Ki-S1 labelling compared with PCNA positivity was found in all conditions studied. In particular, specimens derived from secondary polycythaemia (SP), polycythaemia vera (P. vera), and primary osteomyelofibrosis (OMF), and from splenic tissue with myeloid metaplasia (MM), revealed a disproportionally high labelling index of erythropoiesis, which was not present in chronic myelogenous leukaemia (CML), AIDS, and autoimmune (idiopathic) thrombocytopenia (ITP). Enhancement of Ki-S1 (PCNA) staining in SP and P. vera is in keeping with the relevant increase in erythroid precursor proliferation, but in OMF and MM there is overexpression of both proliferation markers, possibly due to secondary folic acid deficiency, which is known to cause a block in the S-phase of the cell cycle. A significant correlation was observed between the sizes of megakaryocytes and their nuclei with Ki-S1 (and also PCNA) staining. Ki-S1 (and PCNA) labelling of predominantly smaller elements of this lineage supports a hypothesis that the phases of the cell cycle have different durations in the various steps of polyploidization, with a prolongation of G1/G2 at higher ploidy levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, Neoplasm↗
PubMed1986

Lipotropic factors and oncogenesis.

The lipotropes (choline, methionine, folate, and vitamin B12) have a rich history, with many fluctuations in scientific effort and popularity, covering the past 6 decades. A thin thread of common interest in 1-carbon metabolism and a small band of dedicated individuals have kept this area of biology alive. Today, the lipotropes are enjoying a resurgence of interest and effort with promise for significant contributions to some of our most serious chronic diseases. Between 1920, when Banting and Best initiated a work that led to the discovery of insulin, and 1982-83, when investigators working in 3 laboratories announced that lipotrope deficiency alone could result in liver cancer in rodents, many have used this model to study nutritional problems and, more recently, carcinogenesis. Lipotropes are important to lipid metabolism and to synthesis and maintenance of cellular membranes. When weanling rats were fed a diet low in lipotropes, within a few days the liver accumulated lipid, first in the centrilobular zone and later throughout the entire lobule and lobe. If the diet was continued for a longer period, the liver underwent fibrosis and cirrhosis with some rats ultimately developing hepatocellular carcinoma. Although lipotrope deficiency can result in liver cancer, all hepatocarcinogens tested thus far were enhanced in their activity by diets low in lipotropes. Important changes associated with lipotrope deficiency included membrane damage, decreased serum very low density lipoprotein and drug metabolizing enzymes, decreases in S-adenosylmethionine and in methylation of cytosine, increases in cellular peroxidation products and free radicals, decreased immunocompetence, and a markedly shortened lag time for chemical induction of liver cancer in animals. The overall effect of lipotrope deficiency is an increase in the susceptibility to cancer in animals; the exact mechanisms are unclear.

Animals↗
PubMed1977

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.

Adolescent↗
PubMed1991

Transient gyriform brightness on non-contrast enhanced computed tomography (CT) brain scan of seven infants.

Spontaneous gyriform brightness seen on CT scan is an unusual finding unless associated with arteriovenous malformations (AVM). There are sporadic case reports in the literature of its occurrence in association with herpex simplex virus encephalitis (HSVE), purulent meningitis, following chemotherapy for leukaemia, in a child with chronic renal failure, and in a child with folic acid deficiency. We present a series of seven cases exhibiting this phenomenon, none of whom have AVMs, who have been scanned at this hospital in the first 2 1/2 years following the installation of a CT scanner. Four of the cases had congenital heart disease requiring corrective surgery or cardiac catheterisation. The other three had probable meningo-encephalitis. In all cases the gyriform brightness followed an ischaemic insult to the child's brain. We hypothesise that this phenomenon is an ischaemic response in the immature brain and that its occurrence is not so rare as the literature may suggest.

Brain↗
PubMed2005

Scurvy in infantile tremor syndrome.

Infantile Tremor Syndrome is a distinct clinical entity most commonly seen in Indian Subcontinent. Syndrome consists of tremors, mental and developmental retardation, abnormal skin pigmentation and anemia in children between 6 months to 2 years. The etiology is still elusive. Amongst various theories, nutritional theory is the most accepted. So far there are no cases reported of vitamin C deficiency in ITS. In this article, three cases of ITS associated with vitamin C deficiency are reported.

Age Factors↗
PubMed1979

Histologic diagnosis of diseases of malabsorption.

The diagnoses which may be arrived at by examination of peroral small bowel mucosal biopsy specimens are presented. Celiac sprue, unclassified sprue (refractory sprue), infectious gastroenterititis, stasis syndrome and kwashiorkor have a severe mucosal lesion. Other clinical conditions are required to establish the diagnosis in these diseases. A number of diseases have specific diagnostic features. Included are Whipple's disease, abetalipoproteinemia, collagenous sprue, primary intestinal lymphoma, eosinophilic gastroenteritis, giardiasis, coccidiosis, strongyloidiasis, lymphangiectasis and the intestinal immunodeficiency diseases. Mucosal abnormalities may be present in other diseases but the diagnoses are usually made on other criteria than small bowel biopsy. These include vitamin B12 or folic acid deficiency, Crohn's disease, gastrinoma, acrodermatitis enteropathica, amyloidosis, chronic granulomatous disease, lipid storage diseases, histoplasmosis, capillariasis, cytomegalovirus infection, schistosomiasis and macroglobulinemia.

Biopsy↗
PubMed1982

Malabsorption secondary to Meckel's diverticulum.

This case report of a patient with a large Meckel's diverticulum with associated stagnation and bacterial proliferation demonstrates the resultant metabolic and nutritional alterations that have classically been described with the blind loop syndrome. A lesion as large as the one presented herein has rarely been reported with iron, vitamin B12, and folic acid deficiency anemias secondary to the contaminated small bowel (ileum) syndrome. A discussion of the pathophysiology, diagnosis, and treatment of this disorder and the multiple disease entities incorporated in the contaminated small bowel syndrome are included.

Adult↗
PubMed1986

Abnormalities of one-carbon metabolism in psychiatric disorders: study of methionine adenosyltransferase kinetics and lipid composition of erythrocyte membranes.

Two independent lines of inquiry have implicated some disturbance of one-carbon cycle metabolism in affective disorders. Folic acid deficiency commonly leads to depression, and S-adenosylmethionine has been reported to have antidepressant properties. Methionine adenosyltransferase has been reported to be underactive in depression and schizophrenia and overactive in mania. This study reports the effects on erythrocyte methionine adenosyltransferase (MAT) kinetics (Vmax) of a 2-week treatment in a population of patients housed on a psychiatric research ward. The drug-free schizophrenic patients and depressives had, upon admission, low Vmax values, and the drug-free manic patients had high Vmax values on admission. After 2 weeks of appropriate treatment, the values for all three patient samples showed significant normalization (i.e., the levels rose in schizophrenics and depressives and fell in manics). We have further shown that pretreatment low levels of erythrocyte membrane phosphatidylcholine in depressives and high levels in manics show statistically significant normalization following 2 weeks of pharmacotherapy. The significance of these results is discussed.

Bipolar Disorder↗
PubMed1991

Haematology and histopathology of seven-week-old broilers after early food restriction.

The haematology and histopathology of seven-week-old broilers were examined after periods of early food restriction, for six, 10 or 14 days from six days old. After several weeks on an ad libitum diet the birds failed to compensate for the weight lost during early food restriction. Immediately after the periods of food restriction, the birds demonstrated significantly increased heterophil/lymphocyte ratios, reduced eosinophils and slightly raised basophil counts. At seven weeks old, a significant reduction was seen in red and white blood cells and thrombocyte numbers together with significant increases in mean cell haemoglobin and mean cell volume. The haematological profile demonstrated a macrocytic normochromic anaemia caused possibly by a folic acid deficiency as a result of the food restriction. Histopathological lesions were seen in the heart, lungs and liver from birds on all diets but there were more lesions the longer the food had been restricted. Lung disease was more marked where there was inadequate ventilation. Cartilaginous and osseous lung nodules were significantly fewer after food restriction. It was postulated that the increase in pathological lesions in the food-restricted birds may be associated with a stress response.

Animals↗
PubMed1982

Diagnostic and prognostic significance of chromosome abnormalities in marrow and mitogen response of lymphocytes of acute nonlymphocytic leukemia.

Chromosomes of bone marrow from 28 patients with acute nonlymphocytic leukemia (ANLL) (26 with AML, 2 with AMMoL), 19 of whom had chromosome abnormalities, were studied; 11 cases exhibited previously unreported karyotypic abnormalities. The marrows of two cases had 8-21 translocations associated with an iso-X chromosome in the female patient and with 9q13- and a missing Y in the male patient. Usually, AML patients with a 8-21 translocation have been considered to have a good prognosis; however, our cases had rather short survival times. Therefore, the prognosis of AML with an 8-21 translocation but associated with other abnormalities is still not clear. Centromere spreading (CS), which was originally reported in marrow cells of megaloblastic anemia (B12 and folic acid deficiency), was detected in leukemic cells, disappeared during remission, and reappeared on relapse. These findings suggest that CS may be a new type of abnormality in AML. In two patients with atypical hypoplastic anemia and hemolytic anemia, chromosome abnormalities were detected at the anemic stage. One case with CS was associated with atypical hypoplastic anemia and developed AML after 1 year; the other with 48,XY,+i(1q),+3,/12 and -14 had hemolytic anemia and developed AMMoL 3 weeks later. Interestingly, identical clones were detected both before and after the clinical diagnosis of leukemia. These cases strongly support the concept that some chromosome abnormalities precede the clinical manifestations of leukemia. The present study also revealed that lymphocytes in ANLL respond poorly to PHA in the presence of high numbers of blasts but do respond well to mitogens during remission. Therefore, the response of lymphocytes to PHA may serve as one criterion for determining remission.

Adult↗
PubMed1992

Fibre in enteral formulae: effects of sugar-beet versus soy fibre on zinc and folic acid absorption in human subjects.

The present study was conducted to compare the effect of soypolysaccharide (Fibrem) and sugar-beet (Fibrex) on zinc and folic acid absorption when incorporated into enteral formulae. Following an overnight fast, 15 adults were challenged with an oral dose of zinc (60 mg) and folic acid (600 mug) given with enteral formula without fibre, or with 15g of dietary fibre from Fibrem or Fibrex. Serum concentrations of zinc and folic acid were measured at zero-time and at hourly intervals for up to 5h. Results showed that Fibrem caused a significant decrease in the concentrations of zinc and folic acid. However, Fibrex caused a slight increase in serum zinc concentration and a less pronounced decrease in serum folic acid concentration as compared to Fibrem. We conclude that for patients who are at risk of zinc or folic acid deficiency, the fibre source in enteral formulae should be selected carefully.

Journal Article↗
PubMed1996

[Celiac disease, cerebral calcifications and epilepsy syndrome].

The syndrome of coeliac disease, epilepsy and cerebral calcifications is a rare complication of coeliac disease. The pathological changes consist in a patchy pial angiomatosis and resemble those of Sturge-Weber syndrome, whose variant without port-wine angioma must be ruled out. Typical course includes three stages leading to a severe encephalopathy. However, the mental impairment is extremely variable. The pathogenetic process is so for unknown; main clues involve a chronic folic acid deficiency or a HLA-related autoimmune disorder. Treatment requires early gluten-free diet and anti-epileptic drug.

Adolescent↗
PubMed2004

Vitamin C or Vitamin B6 supplementation prevent the oxidative stress and decrease of prostacyclin generation in homocysteinemic rats.

We hypothesize that homocysteinemia causes oxidative stress, decreases the aortic ability to generate prostacyclin and that antioxidants have a protective role. Four groups of eight rats each were fed for 8 weeks the control diet (group A), control diet with folic acid omitted and excess methionine (Me) added to drinking water (group B), diet B + 500 mg/kg of Vitamin C (group C) or diet B + 60 mg/kg Vitamin B6 (group D). The three groups of rats fed folic acid deficient (FD) diets (groups B, C and D) were homocysteinemic as indicated by the significant increase in their serum homocysteine (HC) concentration. Rats fed diet B had oxidative stress as indicated by an increase in serum thiobarbituric acid reactive substances (TBARS) and advanced oxidation protein products (AOPP) and urinary isoprostanes and had a decreased ability of their aortas to generate prostacyclin. Homocysteinemic rats fed a FD diet + Vitamin C (group C) or Vitamin B6 (group D) also had high levels of serum homocysteine but the oxidative stress markers and the ability of their aortas to generate prostacyclin returned to normal. This indicates that the homocysteinemic effect is through an oxidative mechanism and that Vitamin C as a free radical scavenger prevents these effects. Serum Vitamin C and liver glutathione concentrations significantly increased in rats fed excess Vitamin B6 compared to the control or FD rats. This may explain why Vitamin B6 has an antioxidative effect.

Animals↗
PubMed2005

Coeliac disease, epilepsy and cerebral calcifications.

Coeliac disease, epilepsy and cerebral calcifications (CEC) syndrome is a rare clinical condition. One hundred and seventy-one patients have been reported in the literature. Patients are mostly from Italy, Spain, and Argentina, suggesting a geographically restricted condition. Epilepsy is more frequently characterized by occipital seizures. It may be benign or drug-resistant, sometime evolving into severe epileptic encephalopathy. Gluten free diet (GFD) efficacy seems to be inversely related to the duration of epilepsy and the young age of the patient. Patients with cerebral calcifications (CC) and coeliac disease (CD) without epilepsy are considered as having an incomplete form of CEC syndrome. Some patients with epilepsy and CC without CD are supposed to have a CEC syndrome with silent or latent CD. Whether CEC syndrome is a genetic condition, or whether epilepsy and/or CC are a consequence of an untreated CD is unknown yet. Since histopathological findings seem to be the expression of vascular calcified malformation, CEC syndrome may be considered a genetically determined entity, such as a type of Sturge-Weber-like phacomatosis. Moreover, CEC, as well as CD, is associated with HLA-DQ2 and HLA-DQ8 phenotype and genotype. The progressive growth and late occurrence of CC before beginning a GFD, the demonstration of anti-gliadin antibodies in the cerebro-spinal fluid and the association with HLA class II genes, suggest that an immune reaction originating from the jejunal mucosa, triggered by gliadin in gluten intolerance predisposed subjects (HLA phenotype) may be responsible for seizures and CC. Moreover, a long-lasting untreated CD folic acid deficiency may cause calcifications. Probably, CEC is considered a genetic, non-inherited, ethnically and geographically restricted syndrome associated with environmental factors.

Adolescent↗
PubMed2004

Thrombotic thrombocytopenic purpura due to alcohol binge drinking.

Binge alcohol drinking is a pattern of alcohol abuse that is common among young males worldwide. It has been found to be associated with an increased likelihood of injury as a cause of death. Chronic alcohol abuse is known to cause some common hematological manifestations such as macrocytosis, thrombocytopenia, sideroblastic anemia, global marrow suppression, and folic acid deficiency anemia. We present a rare case involving an unusual and severe hematological manifestation of binge alcohol drinking: thrombotic thrombocytopenic purpura (TTP). The patient we present had severe and prolonged TTP necessitating prolonged treatment with plasmapheresis and plasma exchange. We discuss the relevant medical literature and the possible physiopathology of this complication.

Journal Article↗
PubMed2006

Distinct effects of folate and choline deficiency on plasma kinetics of methionine and homocysteine in rats.

Both folate and betaine, a choline metabolite, play essential roles in the remethylation of homocysteine to methionine. We have studied the effects of folate and choline deficiency on the plasma kinetics of methionine, especially remethylation of homocysteine to methionine, by means of stable isotope methodology. After a bolus intravenous administration of [(2)H(7)]methionine (5 mg/kg body weight) into the rats fed with folate-, choline-, folate + choline-deficient or control diets, the plasma concentrations of [(2)H(7)]methionine, demethylated [(2)H(4)]homocysteine, and remethylated [(2)H(4)]methionine were determined simultaneously with endogenous methionine and homocysteine by gas chromatography-mass spectrometry-selected ion monitoring. The total plasma clearance of [(2)H(7)]methionine was not significantly different among groups, suggesting that the formation of [(2)H(4)]homocysteine from [(2)H(7)]methionine was not influenced by deficiencies of folate and choline. The area under concentration-time curve of [(2)H(4)]homocysteine significantly increased in the folate- and folate + choline-deficient group as compared with the control, but not in the choline-deficient group. The time profile of plasma concentrations of [(2)H(4)]methionine in the folate-deficient group was the same as the control group, whereas the appearance of [(2)H(4)]methionine in plasma was delayed in the choline- and folate + choline-deficient group. These results suggested plasma levels of remethylated methionine were influenced by choline deficiency rather than folate deficiency.

Animals↗
PubMed2006

Prevalence and etiology of anemia in renal transplant recipients.

We aimed to define the prevalence of anemia and possible causes for it in a group of renal transplant recipients. A total of 229 recipients (65 women; age 36.1 +/- 11.8 years; minimum posttransplant duration, 3 years) were included. Patients with iron, vitamin B(12), and folic acid deficiencies were excluded. Patients were grouped according to number of posttransplant years completed with functioning grafts (3, 5, or 10 years). Demographic data, donor information, HLA mismatches, acute rejection episodes, biochemical parameters, and medications received during the 3 months before transplant and at 3, 5, and 10 years posttransplant were collected retrospectively. The anemia threshold was 13 g/dL for men and 12 g/dL for women. Anemia prevalence was 41.5%, 35.3%, and 93.2% at 3, 5, and 10 years, respectively. Anemic patients had higher creatinine levels for all years. In the anemic patients, hemoglobin values were lower in the pretransplant period than at 3 and 5 years. Anemic patients had higher HLA mismatches for the same years. Three-year hemoglobin levels were positively correlated with pretransplant hemoglobin and negatively correlated with creatinine levels and HLA mismatches. Five-year hemoglobin levels were positively correlated with pretransplant hemoglobin and albumin levels. Ten-year hemoglobin levels were positively correlated with pretransplant hemoglobin and albumin values but negatively correlated with creatinine levels and HLA mismatches. The prevalence of anemia in renal transplant recipients increases in parallel with posttransplant duration. Hemoglobin levels in these patients are closely related with pretransplant hemoglobin, follow-up creatinine levels, and HLA mismatches.

Adult↗