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The article deals with the case of a patient who had a partial gastrectomy and developed a vitamin B12 deficiency syndrome with anemia, myelopathy and complete loss of the senses of taste and smell. Regression of the symptoms followed liberal dosing with vitamin B12.
Haemoglobin, serum vitamin B(12), and serum and red cell folate levels have been measured in 322 pregnant immigrant women in London at their first booking and in a proportion at 34 weeks of gestation and postnatally. The Indian, East-African Indian, and Pakistani and Bangladeshi patients showed significantly lower initial mean serum vitamin B(12) levels than the European group, the levels being lower in Hindu and Sikh patients than in Moslems. The patients of West Indian, Indian, and East-African Indian origin showed significantly lower initial mean haemoglobin levels than the immigrants from European countries. Though there was no overall correlation between haemoglobin and serum vitamin B(12) level the incidence of hypersegmented polymorphs and macrocytosis in the peripheral blood was highest in the Indian and East-African Indian patients, and both these features were particularly frequent in patients with subnormal serum vitamin B(12) levels. Only one patient, however, had overt megaloblastic anaemia due to vitamin B(12) deficiency. The Indian patients whose red cell folate levels were less than 200 ng/ml also had a lower mean serum vitamin B(12) level than those with red cell folate levels greater than 200 ng/ml. The Indian patients had smaller babies than the Europeans but this was not related to the differences in vitamin B(12) status between the two groups. However, out of 39 babies of the Indian group 5 (13%) showed subnormal serum vitamin B(12) levels in the first 10 days of life, the lowest level being 120 pg/ml.Though there was an overall statistically significant fall in serum vitamin B(12) between first booking and 34 weeks of pregnancy there was no significant fall in serum vitamin B(12) in those who initially had subnormal levels. Thus many Indian women are vitamin B(12) deficient in pregnancy, and this is associated with morphological blood abnormalities in many cases, but megaloblastic anaemia due to this deficiency is relatively infrequent.
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Vitamin B(12) stores at birth are adequate for infants until the end of the first year of life even if it 's concentration in maternal breast milk is low. However, there are some situations in which infants have depleted vitamin B(12) stores and in addition have a low dietary intake of cobalamin. Vitamin B(12) depletion occurs in infants who are exclusively breastfed by mothers who have unrecognized pernicious anemia or are strict vegetarians for many years. In those infants symptoms of bone marrow disfunction and impaired development of the central nervous system appear already in the first months of life. Unrecognized cobalamin deficiency may lead to serious neurologic consequences, and even to the death of the child. The authors present a case of a 7.5 month old girl admitted to the Department of Paediatrics, Haematology, Oncology and Endocrinology. Gdańsk Medical University suspected of acute leukaemia. Based on a detailed diagnostic procedure a final diagnosis of vitamin B(12) deficiency anaemia was established. The child was exclusively breast-fed. Results of investigations into the reason for cobalamin deficiency in the patient s organism. Led to the diagnosis of pernicious anaemia in the mother. Such a suspicion had been made during pregnancy, but no continuation of investigations nor appropriate treatment were implemented. After treatment with vitamin B(12) supplements and modification of the diet the patient improved quickly and remarkably. A few months follow-up was enough to observe remarkable improvement of psychomotor development of this child.
Low serum vitamin B(12) concentrations in pregnancy may not indicate true megaloblastic anaemia. In the present study we compared biochemical indices of vitamin B(12) deficiency (serum homocysteine and urine methylmalonic acid) in non-anaemic pregnant women with and without low serum vitamin B(12) concentrations. The groups were matched for age, parity and gestational age. No differences were found, and all values were within normal range. These results suggest that the measurement of low serum B(12) concentrations in pregnant women should be followed by analysis at the biochemical level before vitamin B(12) injections are started.
Imerslund-Gräsbeck syndrome (IGS) or selective vitamin B(12) (cobalamin) malabsorption with proteinuria is a rare autosomal recessive disorder characterized by vitamin B(12) deficiency commonly resulting in megaloblastic anemia, which is responsive to parenteral vitamin B(12) therapy and appears in childhood. Other manifestations include failure to thrive and grow, infections and neurological damage. Mild proteinuria (with no signs of kidney disease) is present in about half of the patients. Anatomical anomalies in the urinary tract were observed in some Norwegian patients. Vitamin B(12) absorption tests show low absorption, not corrected by administration of intrinsic factor. The symptoms appear from 4 months (not immediately after birth as in transcobalamin deficiency) up to several years after birth. The syndrome was first described in Finland and Norway where the prevalence is about 1:200,000. The cause is a defect in the receptor of the vitamin B(12)-intrinsic factor complex of the ileal enterocyte. In most cases, the molecular basis of the selective malabsorption and proteinuria involves a mutation in one of two genes, cubilin (CUBN) on chromosome 10 or amnionless (AMN) on chromosome 14. Both proteins are components of the intestinal receptor for the vitamin B(12)-intrinsic factor complex and the receptor mediating the tubular reabsorption of protein from the primary urine. Management includes life-long vitamin B(12) injections, and with this regimen, the patients stay healthy for decades. However, the proteinuria persists. In diagnosing this disease, it is important to be aware that cobalamin deficiency affects enterocyte function; therefore, all tests suggesting general and cobalamin malabsorption should be repeated after abolishment of the deficiency.
To clarify the effects of microwave heating on the loss of vitamin B(12) in foods, raw beef, pork, and milk were treated by microwave heating and then their vitamin B(12) contents were determined according to a chemiluminescent vitamin B(12) assay with hog intrinsic factor. Appreciable loss ( approximately 30-40%) of vitamin B(12) occurred in the foods during microwave heating due to the degradation of vitamin B(12) molecule by microwave heating. When hydroxo vitamin B(12), which predominates in foods, was treated by microwave heating and then analyzed by silica gel 60 thin layer chromatography, two vitamin B(12) degradation products were found. One of the compounds with a R(f)() of 0.16 was purified and partially characterized. The vitamin B(12) degradation product did not show any biological activity in the growth of a vitamin B(12) requiring microorganism, Euglena gracilis Z, and was not bound to hog intrinsic factor, a mammalian vitamin B(12) binding protein. Intravenous administration of the compound (1 µg/day) for 7 days to rats showed that the compound neither has toxicity nor acts as a vitamin B(12) antagonist in mammals. These results indicate that the conversion of vitamin B(12) to the inactive vitamin B(12) degradation products occurs in foods during microwave heating.
BACKGROUND: Elevated plasma levels of total homocysteine (tHcy) before and after an oral methionine load (PML) are associated with an elevated risk of deep-vein thrombosis (DVT). We investigated whether plasma levels of B vitamins that are involved in Hcy metabolism are associated with an elevated risk of DVT. METHODS AND RESULTS: We compared 397 cases with previous DVT with 585 matched healthy controls. The plasma levels of folate, vitamin B(12), vitamin B(6,), and fasting and PML tHcy were measured. The ORs for DVT associated with high (>95th percentile) fasting levels and PML increases of tHcy were 2.1 (95% CI, 1.2 to 3.4) and 2.4 (95% CI, 1.5 to 3.9) after adjustment for established risk factors for DVT. Fasting plasma levels and PML increases in tHcy correlated negatively with vitamin levels. The crude OR for folate levels in the lowest quartile compared with the highest was 1.5 (95% CI, 1.1 to 2.1), and that for B(6) levels in the lowest and second quartiles compared with the highest was 1.5 (95% CI, 1.0 to 2.1). However, after adjustment for established risk factors and fasting and PML tHcy, the ORs for B(6) levels in the lowest and second quartiles only remained statistically significant (lowest quartile: OR, 1.8; 95% CI, 1.2 to 2.8; second quartile, OR, 1.9; 95% CI, 1.3 to 2.9). CONCLUSIONS: High fasting and PML tHcy and low vitamin B(6) plasma levels are associated with an elevated risk for DVT independently of established risk factors for DVT. The association of low vitamin B(6) levels with the risk for DVT is independent of fasting and PML tHcy levels.
The effect of low protein choline-deficient diet on total vitamin B12 content and individual cobalamin level in the blood serum and liver of rats was determined. Moreover the total and non-protein SH-group content and glutathione transferase activity in the liver of rats were studied. Total cobalamin content increased in the blood serum, but it did not change in the liver of rats fed choline-deficient low protein diet. Total and non-protein SH-group level as well as glutathione transferase activity in the liver decreased significantly. The causes of changes revealed are discussed. Methylcobalamin (but not adenosylcobalamin) administration normalized individual cobalamin level in the blood serum. Administration of both methylcobalamin and adenosyl-cobalamin resulted in total SH-group content restoration whereas non-protein SH-group level and glutathione transferase activity were restored only in methylcobalamin-treated rats.
OBJECTIVES: Vitamin B(12) deficiency is an important long-term problem after urinary diversion using an intestinal segment. In this study, we examined serum vitamin B(12) concentrations in patients with neobladders constructed from various intestinal segments to determine the anatomic factors important for avoiding vitamin B(12) deficiency. METHODS: Twenty-two patients (19 men and 3 women) had an ileal neobladder (modified Studer type); 9 men had an ascending colonic neobladder (Goldwasser type); 30 patients (24 men and 6 women) had a sigmoid neobladder (modified Reddy type); and 18 (15 men and 3 women) had an ileocolic neobladder (Mainz type). The postoperative follow-up ranged from 3 months to 11 years (mean +/- SD, 3.4 +/- 2.8 years). The serum vitamin B(12) concentration was determined at several points after surgery. RESULTS: No patient with a neobladder fashioned from ascending or sigmoid colon developed a low vitamin B(12) concentration. Of the 18 patients with an ileocolic neobladder, 3 (16.6%) developed decreased serum vitamin B(12) concentrations after 5 to 6 years. Of the 22 patients with an ileal neobladder, 3 (13.6%) developed a low serum concentration of vitamin B(12) between 9 months and 3 years after surgery. No patient developed megaloblastic anemia or neurologic symptoms. CONCLUSIONS: Preservation of the terminal 15 cm of ileum is not sufficient to ensure adequate vitamin B(12) absorption, and thus, preserving the ileal length is important. Use of colonic segments to construct neobladders appears to be preferable to ileal segments to preserve vitamin B(12) absorption.
Report on a case of severe megaloblastic anemia in a vegetarian, associated with marked erythroleukemic blood findings probably caused by infections (bronchopneumonia, asthmatic bronchitis, urinary tract infection) and severe heart failure. Successful treatment of the above mentioned complications resulted in almost complete disappearance of pathologic cells from the blood even before vitamin B12 treatment was started. With this therapy complete recovery was achieved and the signs suspect for erythroleukemia in blood and bone marrow disappeared definitively. The case also fulfilled all the criteria of pernicious anemia (Schilling's test and determination of intrinsic factor were not done).
Absorption of radioactive vitamin B(12) was measured by the Schilling procedure in 14 patients who had had a partial gastrectomy. Injection of carbachol (250 mug) before the administration of the test dose increased absorption to a much smaller degree than the ingestion of a light meal containing a minimal quantity of the natural vitamin. The results support the belief that food may improve absorption of vitamin B(12) after partial gastrectomy by stimulating the secretion of a small residual amount of intrinsic factor.
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.
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.
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.
Vitamin B(12) levels in erythrocytes were low in untreated hypochromic anaemia, rose to abnormally high levels during therapy with iron alone, and finally slowly fell to normal. These changes were similar to those previously found in pernicious anaemia in response to vitamin B(12) therapy and in folate-deficiency anaemia in response to folic acid, thus changes in erythrocyte B(12) levels are not always due directly to changes in B(12) metabolism but may be secondary to changes in the levels of other haematinic factors.
INTRODUCTION: Cobalamin deficiency is common in the elderly. However, most of the patients are asymptomatic or present with few symptoms. A subacute combined degeneration of the spinal cord accounts for only 10% of the neurological complications. Revealing forms of this myelopathy are exceptional, and were rarely documented by magnetic resonance imaging (MRI) study. EXEGESIS: We report a case of subacute combined degeneration of spinal cord in an 81-year-old woman evaluated by a spinal cord MRI. We discuss the role of the spinal cord radiographic study in the diagnosis, the etiopathogeny of cobalamin deficiency and the benefit of vitamin supplementation even at a late stage of the disease in geriatrics patients. CONCLUSION: The spinal cord MRI is useful in the diagnosis of late-form combined spinal cord degeneration. The high frequency of atrophic gastritis in elderly prevents the identification of a deficiency of the cobalamin etiology. The treatment relies on vitamin therapy even in the late stages. The severe disability of cobalamin deficiency neurological complications must encourage an earlier diagnosis in elderly patients.
White rats kept on the B12-deficient diet for 9 weeks developed hyperchromic anemia, manifested the reduced content of cobalamines in the blood, kidneys, liver, myocardium and urine, the increased excretion of methylmalonic acid (MMA) and the intensified activity of CoA and its precursors participating in the reaction of acetylation in the liver, kidneys and myocardium. There was a decrease in the content of cobalamine-protein complexes that break down to the greatest extent at 80 degrees C. Ten-fold administration of cyanocobalamine (0.5 microgram/kg), calcium pantothenate (3.3 mg/kg) or of both the preparations concurrently removed the aforesaid disorders of cobalamine metabolism, with the most complete therapeutic effect being attained upon combined use of the vitamin preparations. Administration of pantothenate increased the content of cobalamines and cobalamine-protein complexes in the liver and myocardium, normalizing methylmalonylaciduria.