PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “VITAMIN B 12 DEFICIENCY”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 19 recordsLinked to original sources
PubMed2004

Unusual neurological presentations of vitamin B(12) deficiency.

Vitamin B(12) deficiency (B(12)D) has a wide variety of neurological symptoms and signs. However, cerebellar dysfunction and cranial neuropathies other than optic neuropathy have been rarely reported. Herein, we describe two cases of unusual neurological manifestations of B(12)D. One patient showed prominent hoarseness with vocal cord paralysis, myelopathy, and peripheral neuropathy. The other had gait disturbance, lateral gaze limitation and cerebellar dysfunction in addition to the typical manifestations of subacute combined degeneration. Vitamin B(12) deficiency can rarely affect cerebellum and cranial nerves other than optic nerve.

Adult↗
PubMed1969

Methylmalonic acid and coenzyme A concentrations in the livers of pair-fed vitamin B 12-deficient and vitamin B 12-treated sheep.

The concentrations of CoA in the livers of severely vitamin B(12)-deficient ewes were about 2.6 times those in pair-fed animals treated with vitamin B(12). When the feeding rates of the pair-fed animals were closely similar, the concentrations of methylmalonic acid in deficient livers were about twice those in vitamin B(12)-sufficient livers. The molar concentrations of CoA present were more than three times those of methylmalonic acid in both deficient and treated animals, and it is concluded that the elevated concentrations of CoA in the deficient livers were not primarily due to accumulation of methylmalonyl-CoA.

Animals↗
PubMed1973

Vitamin B 12 and the macromolecular composition of Euglena. II. Recovery from unbalanced growth induced by Vitamin B 12 deficiency.

When vitamin B(12) is added to B(12)-deficient cultures of Euglena gracilis, the cells undergo two relatively synchronous cell divisions within a shorter than usual period of time, apparently as a result of a transitory shortening of the cell cycle. The first cell division pulse, occurring 4.5 h after addition of B(12), is preceded by the completion of DNA duplication, but appears to involve no net synthesis of RNA or protein. Before the second round of cell division at about 11 h, a significant amount of DNA synthesis is observed. This time it is accompanied by a minor increase in the RNA and protein content of the culture. The cellular contents of RNA and protein were observed to decrease steadily after the resumption of cell division in B(12)-depleted cultures receiving the vitamin. Ultimately all three macromolecules returned to their nondeficient, plateau stage levels; by this time, cell division had ceased.

Cell Division↗
PubMed1991

[Neuropsychological disorders in vitamin B 12 deficiency].

Vitamin B12 deficiency is often attended by neuropsychic disorders. In the geriatric population, the level of vitamin B12 is mostly reduced. However, the clinical manifestations and pathogenesis are not completely specified. The authors describe a female patients in whom vitamin B12 deficiency was coupled with manifest neuropsychic disorders. Provide a detailed depiction of the clinical status, the disease course and laboratory findings. Relate the most typical neuropsychic manifestations of vitamin B12 deficiency.

Ataxia↗
PubMed1985

Vitamin B 12 deficiency in the elderly.

Vitamin B 12 deficiency is usually a disease of older persons, and much controversy has surrounded the significance of the deficiency of this vitamin in these patients. This article explores the mechanism of action of vitamin B 12, the clinical and laboratory features of vitamin B 12 deficiency, and a rational treatment plan. Once vitamin B 12 deficiency is recognized and diagnosed, it can be easily treated, usually with gratifying results.

Aged↗
PubMed2004

[Helicobacter pylori can in rare cases be the cause of iron and vitamin B 12 deficiency. No increased risk of iron and vitamin B 12 deficiency due to proton pump inhibitors].

This article reviews iron and vitamin B12 malabsorption due to the use of proton pump inhibitors (PPI) and infection with Helicobacter pylori. The bacterium is in some studies associated with low serum values of both ferritin and cobalamin and has in several cases been shown to cause reversible deficiency of these nutrients. PPI depresses absorption of vitamin B12, but only one case of deficiency has been reported in standard reflux therapy. Case reports exist of PPI-related iron deficiency, but studies have not confirmed these risks. General substitution with iron or B12 supplements in PPI therapy can't be advocated. The safety of long-term use of PPI is well documented, but it is still unclear whether PPI accelerates the development of atrophic corpus gastritis in the presence of H pylori.

Anemia, Iron-Deficiency↗
PubMed2002

Gastric emptying in patients with vitamin B(12) deficiency.

The clinical presentation of patients with vitamin B(12) deficiency varies in a spectrum ranging from haematological disorders to neuropsychiatric diseases. In rare cases, orthostatic hypotension, impotence, constipation and urinary retention have been attributed to autonomic nervous system dysfunction due to vitamin B(12) deficiency. The aim of this study was to evaluate the effect of vitamin B(12) deficiency on autonomic nervous system function by studying gastric emptying times ( T(1/2)). Twenty patients with newly diagnosed vitamin B(12) deficiency and 12 control patients with gastritis and normal vitamin B(12) levels were enrolled in this study. Gastroduodenoscopy, endoscopic biopsy, histopathological evaluation of the biopsy specimens and radionuclide gastric emptying studies were performed. After vitamin B(12) replacement therapy for 3 months, radionuclide gastric emptying studies were repeated. Mean gastric emptying T(1/2) in patients before and after treatment and in controls were 103.83+/-48.80 min, 90.00+/-17.29 min and 74.55+/-8.52 min, respectively. The difference in mean gastric emptying T(1/2) between patients before treatment and controls was statistically significant ( P<0.01). The statistically significant difference persisted after vitamin B(12) treatment ( P<0.05), though mean gastric emptying T(1/2) was somewhat shorter. There were no positive or negative correlations between gastric emptying T(1/2) and the following parameters: haemoglobin, vitamin B(12) level and Helicobacter pylori positivity. In conclusion, gastric emptying T(1/2) was prolonged in patients with vitamin B(12) deficiency and this prolongation was not corrected after vitamin B(12) replacement therapy. Although autonomic nervous system dysfunction due to vitamin B(12) deficiency rarely gives rise to clinical manifestations, latent dysfunction demonstrated by laboratory tests seems to be a frequent phenomenon. The level of vitamin B(12) does not correlate with the degree of autonomic nervous system dysfunction measured by radionuclide gastric emptying studies.

Adult↗
PubMed1991

[Vitamin B 12 deficiency in strict vegetarian diet. Why do some people choose such a diet, and what will they do in case of vitamin B 12 deficiency].

Nine persons in the county of Troms, Norway, were interviewed on their strict vegetarian diet. Improved health was indicated as the main reason for their choice of diet, but religion was a contributing reason for some. Most of the study persons would increase the intake of vitamin B12 if a deficiency state were to occur. One person reported, however, that she would not regard vitamin B12 deficiency as a health problem. The interviews disclosed beliefs regarding human physiology that are very far removed from standard scientific knowledge. The article indicates that communication between patient and the health care system may be difficult in such circumstances. Problems of communication would probably be minimized if the patient had a thorough understanding of human physiology and the health worker a thorough understanding of the reasons for the patient's choice of diet.

Adult↗
PubMed1970

Factors affecting formiminoglutamic acid excretion in vitamin B 12 deficiency.

1. Formiminoglutamic acid, a product of the catabolism of histidine, is excreted in abnormally large amounts in the urines of vitamin B(12)-deficient rats and of vitamin B(12)-deficient sheep; the excretion is reduced to negligible amounts after administration of vitamin B(12). 2. After administration of certain methyl donors to vitamin B(12)-deficient rats or sheep urinary excretion of formiminoglutamic acid is temporarily decreased. 3. Irrespective of the pteroylglutamic acid status of the animals neither vitamin B(12)-deficient rats nor vitamin B(12)-deficient sheep have the ability to deal efficiently with histidine. 4. In sheep, urinary excretion of formiminoglutamic acid is increased after administration of aminopterin; treatment with pteroylglutamic acid restores the ability of the animal to deal with the catabolic products of histidine. 5. The possible functions of vitamin B(12) and methionine in relieving a virtual deficiency of pteroylglutamic acid are discussed.

Aminopterin↗
PubMed2006

Risk factors of vitamin B(12) deficiency in patients receiving metformin.

BACKGROUND: Identification of risk factors for metformin-related vitamin B(12) deficiency has major potential implications regarding the management of diabetes mellitus. METHODS: We conducted a nested case-control study from a database in which the source population consisted of subjects who had levels of both serum vitamin B(12) and hemoglobin A(1c) checked in a central laboratory. We identified 155 cases of diabetes mellitus and vitamin B(12) deficiency secondary to metformin treatment. Another 310 controls were selected from the cohort who did not have vitamin B(12) deficiency while taking metformin. RESULTS: A total of 155 patients with metformin-related vitamin B(12) deficiency (mean +/- SD serum vitamin B(12) concentration, 148.6 +/- 40.4 pg/mL [110 +/- 30 pmol/L]) were compared with 310 matched controls (466.1 +/- 330.4 pg/mL [344 +/- 244 pmol/L]). After adjusting for confounders, we found clinically important and statistically significant association of vitamin B(12) deficiency with dose and duration of metformin use. Each 1-g/d metformin dose increment conferred an odds ratio of 2.88 (95% confidence interval, 2.15-3.87) for developing vitamin B(12) deficiency (P<.001). Among those using metformin for 3 years or more, the adjusted odds ratio was 2.39 (95% confidence interval, 1.46-3.91) (P = .001) compared with those receiving metformin for less than 3 years. After exclusion of 113 subjects with borderline vitamin B(12) concentration, dose of metformin remained the strongest independent predictor of vitamin B(12) deficiency. CONCLUSIONS: Our results indicate an increased risk of vitamin B(12) deficiency associated with current dose and duration of metformin use despite adjustment for many potential confounders. The risk factors identified have implications for planning screening or prevention strategies in metformin-treated patients.

Age Factors↗
PubMed2000

Dementia associated with vitamin B(12) deficiency: presentation of two cases and review of the literature.

Vitamin B(12) deficiency has long been associated with a wide variety of hematological, neurological, and psychiatric disorders. The role of vitamin B(12) deficiency as one of the few treatable causes of dementia, however, is still controversial. The authors report on 2 elderly patients suffering from cognitive impairment and psychotic symptomatology probably related to cobalamin deficiency, who showed improvement after parenteral vitamin B(12) substitution. The literature concerning the pathophysiology and the diagnostic and therapeutic aspects of cobalamin deficiency is reviewed.

Aged↗
PubMed2004

The risk of folate and vitamin B(12) deficiencies associated with hyperhomocysteinemia among pregnant women.

The purpose of this study was to compare the folate and vitamin B (12) levels in pregnant and nonpregnant women to evaluate the risk for hyperhomocysteinemia and for folate and vitamin B (12) deficiencies during pregnancy. Healthy pregnant women (n = 92; 24 to 28 gestational weeks; 18 to 39 years old) and nonpregnant women (n = 176; 18 to 39 years old) were sampled for serum levels of folate, vitamin B (12), and homocysteine. Pregnant women were less likely to have folate deficiency (8.0% versus 12.0%) but much more likely to have vitamin B (12) deficiency (46.1% versus 0.6%) than nonpregnant women. Those with lower dietary vitamin intakes were more likely to have vitamin B (12) deficiency. Serum folate and vitamin B (12) were negatively correlated with homocysteine among pregnant women. Pregnant women with folate deficiency were more likely to have hyperhomocysteinemia than those without folate deficiency. The vitamin B (12) level associated with hyperhomocysteinemia was lower in pregnant subjects than in nonpregnant subjects in this study, indicating that pregnant women require vitamin B (12) supplementation.

Adolescent↗
PubMed2005

Coma and respiratory failure in a child with severe vitamin B(12) deficiency.

OBJECTIVE: Psychofunctional follow-up of severe vitamin B(12) deficit. DESIGN: Case report. SETTING: Pediatric intensive care unit. PATIENT: Ten-month-old boy. INTERVENTION: Follow-up at 3 yrs. MEASUREMENTS AND MAIN RESULTS: A 10-month-old boy was admitted to the pediatric intensive care unit with respiratory failure, muscular hypotonia, and involuntary movements. Although a central nervous system infection was excluded, computed tomography scan showed a diffuse cortical-subcortical atrophy. Vitamin B(12) deficiency was suspected because of a red-cell count of 1,350,000/mm(3) and a hemoglobin value 5.9 g/dL (MCV 116). The baby had been exclusively breast-fed, but his mother had been a strict vegan for 10 yrs. Chronic dietary vitamin B(12) deprivation was confirmed by blood and urinary samples. Treatment with vitamin B(12) led in 2 wks to rapid and complete hematological improvement and to partial regression of neurologic symptoms. During the following 3 yrs the boy had normal vitamin intake and underwent intensive rehabilitative treatment. The brain atrophy regressed, but linguistic and psychomotor delay persisted. CONCLUSIONS: Rapid clinical improvement after vitamin supply does not correlate with a complete recovery.

Breast Feeding↗