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Results for “FOLIC ACID DEFICIENCY”

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At least 469 records · Page 26Linked to original sources
PubMed1991

Vitamin B12 and folic acid deficiency in chronic pancreatitis: a relevant disorder?

Vitamin B12 malabsorption was reported earlier to occur in patients with exocrine pancreatic insufficiency, and pancreatic extracts were shown to improve the absorption of vitamin B12. We investigated serum levels of vitamin B12 and serum folate in patients with chronic pancreatitis and different degrees of pancreatic insufficiency. 137 patients (84 males, 53 females, age 34-72 years) with chronic pancreatitis (C.P.) were included in the study. 123 of 137 (89.8%) patients had a pathologic pancreatic function test result, classified into mild (n = 24), moderate (n = 61) or severe (n = 38) insufficiency. The normal range of serum vitamin B12 and folic acid was established in 58 healthy controls and was found to be 190-1020 pg/ml for serum vitamin B12 and 2.4-16.1 ng/ml for folic acid. 7 patients (5.7%) with C.P. had vitamin B12 serum levels below 190 pg/ml; 4 of these had severe and 3 had mild or moderate exocrine pancreatic insufficiency. However there was no overall correlation between the degree of pancreatic insufficiency and vitamin B12 values. Serum levels of Vitamin B12 were 512 +/- 48 pg/ml in mild, 493 +/- 52 pg/ml in moderate and 428 +/- 45 pg/ml in severe exocrine insufficiency. Serum folic acid below 2.4 ng/ml were present in 5 patients (3.6%). Folic acid serum levels were 8.34 +/- 0.76 ng/ml in mild, 6.34 +/- 0.52 ng/ml in moderate and 7.45 +/- 0.53 ng/ml in severe exocrine insufficiency. We conclude that vitamin B12 deficiency is a rare finding in chronic pancreatitis and does not strictly depend on the degree of exocrine pancreatic insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Obesity Surgery in Children.

BACKGROUND: There have been few articles about bariatric surgery for morbidly obese children. Nevertheless, children who suffer clinically severe obesity also suffer poor social acceptance and an inability to participate in sports or other life activities. Since 1983 the author has performed vertical banded gastroplasty (VBG), Roux-en-Y gastric bypass (RYGBP), or biliopancreatic diversion (BPD) on 22 children, ages 8 - 18 years. METHODS: This was a retrospective review of 22 children, 11 with sleep apnea and 11 without sleep apnea. There were nine males and 13 females. The procedures were VBG-5; RYGBP-14; and BPD-4. RESULTS: There were no operative deaths, infections, or other serious immediate complications. Body mass index (BMI) in those with sleep apnea decreased from a mean of 67.8 preoperatively to 46.5 kg/m(2) at an average follow-up of 32 months. Likewise, for those without sleep apnea, BMI decreased from 56.4 preoperatively to 35.5 kg/m(2) at an average follow-up of 50 months. All patients with sleep apnea had this condition resolve with adequate weight loss. Furthermore, these patients have been able to stay awake in school and have made better grades. Postoperative complications included protein deficiency in three BPD patients, and Vitamin A and D deficiency, folic acid deficiency, gallstones, kidney stones, postoperative laryngeal edema, and incisional hernia in one patient each. There were two late deaths; one at 15 months and one at 3.5 years postoperatively. CONCLUSIONS: Clinically severely obese children can safely undergo bariatric operations usually offered to adults. Furthermore, most patients have sustained significant weight loss. Those patients with sleep apnea have had resolution of their sleep apnea. Complications can be minimized with adequate vitamin, mineral, and trace element supplementation. Long-term results are not yet known.

Journal Article↗
PubMed1972

Idiopathic hypoparathyroidism with impaired vitamin B 12 absorption and neuropathy.

A 68-year-old man presenting with chronic intermittent diarrhea and progressive ataxia was found to have idiopathic hypoparathyroidism. Intrinsic factor-resistant vitamin B(12) malabsorption was demonstrated. Both the diarrhea and vitamin malabsorption were reversed by correction of hypocalcemia.His neurological profile was a combination of peripheral nerve, posterior column and cerebellar deficits. He had calcifications in the dentate nuclei of the cerebellum. Possible etiological factors such as vitamin B(12) deficiency, folic acid deficiency and steatorrhea have been excluded. Posterior column and cerebellar abnormalities improved with treatment. It is postulated that hypocalcemia causes functional, reversible spinal cord and cerebellar dysfunction.

Aged↗
PubMed1994

Whole-body autoradiographic disposition and plasma pharmacokinetics of 5,10-dideazatetrahydrofolic acid in mice fed folic acid-deficient or regular diets.

The effect of folic acid depletion on the tissue distribution and plasma pharmacokinetics of the oncolytic agent 5,10-dideazatetrahydrofolic acid (DDATHF) was evaluated in mice fed either folic acid-deficient or regular diets. Mice were maintained on diets for 2 weeks prior to receiving a single i.v. 30 mg/kg dose of [14C]DDATHF (tissue distribution) or DDATHF (plasma pharmacokinetics). Whole-body autoradiographic evaluation and plasma analysis for DDATHF were conducted in mice at 5 min and 6, 24, 48, 96, 120, and 168 h postdose. Radiocarbon associated with [14C]DDATHF was readily distributed to all tissues in both diet groups at the early time points and was rapidly cleared from most tissues at 24 h postdose. At the later time points, substantial amounts of radioactivity remained in liver from mice fed either diet. However, levels of radiocarbon in liver from mice fed the folic acid-deficient diet were approximately 2.5-4.2-fold the radiocarbon levels in liver from mice fed the regular diet. Similarly, plasma pharmacokinetics indicated that mice fed the folic acid-deficient diet had sustained plasma concentrations of DDATHF compared to plasma concentrations in mice fed the regular diet. These data indicated that a deficiency in dietary folic acid in mice caused increased hepatic retention of radioactivity and sustained plasma concentrations of DDATHF which are probably responsible for the observed toxicity of DDATHF in mice.

Animals↗
PubMed1975

Trypanosoma rhodesiense: folate levels in sera and tissues of normal and folic acid-deficient rats.

An experimental model composed of the folic acid deficient Sprague-Dawley rat and Trypanosoma rhodesiense was used to study folate levels in sera and tissues. Serum folate levels in well fed rats inoculated on day 21 averaged 21 plus or minus ng/ml; well fed normal rats averaged 18 plus or minus 4 ng/ml. In rats given the pair-fed control diet, serum folate levels averaged 17.2 plus or minus 4 ng/ml for trypanosome-free animals and 20.2 plus or minus 3 ng/ml for infected ones. In rats given the folic acid-deficient diet, serum folate levels averaged 8.6 plus or minus 2 ng/ml for noninfected control animals and 9.3 plus or minus 2 ng/ml for trypanosome-infected ones. Regardless of diet, the infected animals inoculated on day 56 had higher serum folate levels over the controls on the last day of observation (day 5 of infection). Livers from rats fed complete and pair-fed diets and inoculated on day 21 showed no significant differences in folate content when compared to control animals. However, livers of rats on a deficient diet showed significantly more folate when compared with uninfected controls, reaching a maximum of 362% of day 25. Liver folate levels of rats (regardless of the dietary regimen) inoculated on day 56 showed significantly higher values than the controls on day 60. Irrespective of the time of inoculation or diet, brain and spinal cord of T. rhodesiense-infected rats had significantly higher folate values than their controls on day 5 of infection. The folate level of the brain and spinal cord, at this time, ranged up to 58 and 107% respectively.

Animals↗
PubMed2002

Investigation of the effects of folate deficiency on embryonic development through the establishment of a folate deficient mouse model.

BACKGROUND: Folic acid (FA) has been shown to reduce the incidence of neural tube, craniofacial, and cardiovascular defects and low birth weight. The mechanism(s) by which the vitamin is effective, however, has not been determined. Therefore, a folic acid deficient mouse model was developed. METHODS: To create a folic acid deficiency, ICR female mice were placed on a diet containing no FA and including 1% succinyl sulfathiazole (SS) for 4 weeks before mating. Control mice were fed diets with either: 1) FA and 1% SS [+SS only diet]; 2) FA [normal diet]; or 3) a breeding diet. Dams and fetuses were examined during various days of gestation. RESULTS: Blood analysis showed that by gestational day 18, plasma folate concentrations in the -FA+SS fed dams decreased to 1.13 ng/ml, a concentration approximately 3% of that in breeding diet fed dams (33.24 ng/ml) and 8% of that in +SS only/normal fed dams (13.59 ng/ml). RBC folate levels showed a similar decrease, whereas homocysteine concentrations increased. Reproductive outcome in the -FA+SS fed dams was poor with increased fetal deaths, decreased fetal weight, and delays in palate and heart development. CONCLUSIONS: Female mice fed a folic acid deficient diet and 1% succinyl sulfathiazole exhibited many of the characteristics common to human folic acid deficiency, including decreased plasma and RBC folate, increased plasma homocysteine, and poor reproductive outcomes. Thus, an excellent model has been created to investigate the mechanism(s) underlying the origin of birth defects related to folic acid deficiency.

Animals↗
PubMed1979

Studies on folate metabolism in folic acid-deficient rats.

The distribution in liver of pteroylpolyglutamates and urinary excretion of folate metabolites was studied in folic acid deficient rats after injection of the vitamin, in order to evaluate the effect of folic acid deficiency on the conversion of the vitamin into actual coenzymic forms. Any significant difference neither in total activity nor in pteroylpolyglutamates of liver does not appear between deficient supplemented and unsupplemented animals. Also the urinary amounts of reduced metabolites in deficient rats do not increase after injection of folic acid. Therefore the inability of deficient rat liver to synthesize polyglutamates may be ascribed to the lower availability of tetrahydrofolates as they are the preferred substrates of pteroylpolyglutamate synthetase.

Animals↗