Nutritional Vitamin B12 Deficiency in a Breastfed Infant Following Maternal Gastric Bypass

Breasfed infants of women who have had gastric or intestinal bypass procedures may develop nutritional deficiencies. We describe a 10-month-old exclusively breastfed white male infant who presented with vomiting, failure to thrive, and megaloblastic anemia. He was found to have vitamin B₁₂ deficiency. His mother had undergone a gastric bypass procedure for morbid obesity 2 years Prior to her pregnancy with this child. She had subclinical vitamin B₁₂ deficiency, with an abnormal Schilling test that corrected with the addition of intrinsic factor. Therefore, we believe that the mother's gastric bypass had caused a decrease in available intrinsic factor, resulting in subclinical vitamin B₁₂ deficiency and decreased breast milk B₁₂. Although she was asymptomatic, her breastfed infant developed symptomatic B₁₂ deficiency. This is the first reported case of a maternal gastric bypass resulting in vitamin B₁₂ deficiency in an infant. These mothers should receive vitamin supplements, including vitamin B₁₂ during and after pregnancy, and my require parenterally administered vitamin B₁₂.     

Nutritional Vitamin B12 Deficiency in Infancy: Three Case Reports and a Review of the Literature

Three cases of vitamin B₁₂ deficiency that occurred during infancy are presented. These cases appeared to be the result of pre-existing maternal deficiency. All three infants demonstrated evidence of neurodevelopmental delay at presentation, and one had sustained loss of milestones and developed involuntary motor movements. Prior to the initiation of therapy, all three infants were anemic: one was thrombocytopenic and one pancytopenic. In all three cases the hematologic and neurologic abnormalities were corrected with vitamin B₁₂ therapy. The literature is reviewed and discussed with respect to the mechanism of the infants' vitamin B₁₂ deficiency and neurodevelopmental manifestations.     

Vitamin D Deficiency Rickets and Vitamin B12 Deficiency in Vegetarian Children

ABSTRACT. During the years 1978-83 four vegetarian children have been admitted to the pediatric departments of Ullevaal and Aker Hospitals in Oslo and Haukeland Hospital, Bergen, with the diagnosis of vitamin D deficiency rickets. One had vitamin B₁₂ deficiency as well. All had been fed a vegetarian diet with some cows'milk, but without vitamin supplementation. All had marked hypocalcemia, and three had tetany or convulsions. All responded well to conventional doses of vitamin D therapy. Two of the mothers had vitamin D deficiency, and one of them also had vitamin B₁₂ deficiency. This report describes the case histories of these children, and also discusses predisposing factors of vegetarian diets for the development of nutritional rickets     

Vitamin B12 Deficiency in Infancy: The Case for Screening

The classic principles put forth by Wilson and Jungner are often applied to determine the suitability of a condition for universal newborn screening. The three cases described here portray the harmful effects of vitamin B₁₂ deficiency in infancy. The challenges and opportunities of early recognition and treatment are highlighted. Screening newborns would allow early detection and prevention of severe neurological damage in vitamin B₁₂‐deficient infants and enable diagnosis of unrecognized maternal pernicious anemia in asymptomatic mothers. However, lack of standardized methodology and screening cutoffs present challenges to the use of current tandem mass spectrometry technologies for screening.     

Nutritional vitamin B12 deficiency in hospitalized young children

The authors sought to determine prevalence, social, economic, and dietary patterns of young children (n = 20) identified as having vitamin B₁₂ deficiency anemia after admission to their hospital in the last 3 years. The diagnosis of vitamin B₁₂ deficiency was based on symptoms and clinical findings, findings on peripheral blood films and bone marrow aspirates, and serum levels of vitamin B₁₂. The children had been exclusively breast-fed without any animal food supplementation. Serum vitamin B₁₂ levels were also measured in the sera of mothers and found to be low. The authors concluded that vitamin B₁₂ deficiency might be an important health problem among children of mothers who do not consume animal foods adequately.     

Vitamin B12 treatment reduces mononuclear DNA damage

Background: DNA damage effects of vitamin B₁₂ deficiency were performed in vitro and in adults. Methods: The study group included 32 children (13 girls, 19 boys) with vitamin B₁₂ deficiency (mean age 44 ± 58 months) and their 27 mothers (mean age 30.4 ± 5.3 years). The control group contained 30 healthy children and 25 mothers. DNA strand breaks in peripheral blood mononuclear leukocytes were assayed by single‐cell alkaline gel electrophoresis (comet assay) before and 8 days after the first injection of vitamin B₁₂. Results: Mean DNA damage scores in children with vitamin B₁₂ deficiency and their mothers were significantly higher before treatment than those after treatment. The DNA damage scores of children after treatment were still significantly higher than controls. There were significant negative correlations between the children and their mothers in terms of vitamin B₁₂ levels and DNA damage scores (r = 0.3, P= 0.02; r = 0.58, P= 0.002, respectively). There were correlations between the children's and their mothers' DNA damage and the severity of vitamin B₁₂ deficiency, suggesting that the children and their mothers may play a role in the scarcity of nutritional vitamin B₁₂. Conclusion: DNA damage is increased in children with vitamin B₁₂ deficiency and in their mothers. DNA damage scores were significantly improved through vitamin B₁₂ therapy 8 days after the first injection, however, they were still significantly higher than those of controls.     

Maternal vitamin B12 deficiency affects spermatogenesis at the embryonic and immature stages in rats

To evaluate the role of cobalamin (Cbl) on spermatogenesis, the effect of dietary vitamin B(12) deficiency on early spermatogenesis was histologically investigated in male fetuses and newborns in the first filial generation (F(1) males) of rats. There was no difference in the number of gonocytes and supporting cells of Sertoli in the gonad in male fetuses on day 16 of gestation and in the testes in F(1) males at 0 days of age between vitamin B(12)-deficient (VB12-D) and vitamin B(12)-supplemented (VB12-S) groups. However, at 21 days of age, a decreased number of spermatogonia and no spermatocytes were observed in the VB12-D group. Numerous TUNEL positive cells were located among spermatocytes of the spermatogenic epithelium. The ultrastructural features examined using transmission electron microscopy were considered to be indicative of apoptosis. The incidence of seminiferous tubules having apoptotic cells was 51.5% in the VB12-D group. At 60 days of age, aplasia of the spermatids and spermatozoa was detected in the VB12-D group. In the connective tissue between the seminiferous tubules, many interstitial Leydig cells and blood vessels were observed in the VB12-D group, as compared with the VB12-S group. These changes produced by vitamin B(12) deficiency can be reversed by providing a VB12-S diet after weaning at 21 days of age. From these findings, such a vitamin B(12) deficiency during gestation and lactation could affect the germ cells and especially damage spermatocytes in F(1) male rats, which indicates that Cbl may be an essential constituent in the meiosis of spermatogenesis.     

Elevated Serum Vitamin B12 in Cystic Fibrosis

ABSTRACT. In 62 patients with cystic fibrosis the serum vitamin B12 concentration ranged from 160–2 600 pmol/l with a mean of 1105 pmol/l. Both vitamin B12-binding proteins in the serum, transcobalamin II and R-binders, carried increased amounts of vitamin B12, but showed relatively normal levels of unsaturated vitamin B12-binding capacity. This combination is rather typical for hepatic dysfunction, although the recurrent pulmonary infections might exert an upward effect on plasma R-binder concentration through increased turnover of myeloid cells. A significant positive correlation between transcobalamin II-vitamin B12 and serum alkaline phosphatase suggests that transcobalamin H-bound vitamin B12 might be an early indicator of focal biliary cirrhosis, which is known to occur in these patients.     

Vitamin B12 Absorption in Cystic Fibrosis

Vitamin B12 absorption was measured in 30 patients with cystic fibrosis by means of the urinary excretion method and found to be impaired, i.e. less than 10%, in 25. The mean urinary excretion amounted to 4.7 ± 0.8 %. In all patients vitamin B12 absorption improved by the addition of trypsin (18.9 ± 2.1 %). Addition of the vitamin B12 analogue cobinamide, which prevents vitamin B12-binding by R-binders, raised the vitamin B12 absorption to 15.0 ± 2.2 %. A further improvement was obtained by the simultaneous addition of cobinamide and trypsin, 18.2 ± 2.6 %, the same value as with trypsin alone. Assuming that cobinamide addition was effective in suppressing all R-binder activity, the additional effect of trypsin suggests a second, stimulatory function of trypsin on vitamin B12 absorption, separate from R-binder-inactivation. In 5 patients only marginal improvement of vitamin B12 absorption was gained by the addition of either trypsin or cobinamide. The deficient serum vitamin B12 (110 pmol/I) in one of them indicates that the normal pancreas-substitution therapy not always implies sufficient restoration of vitamin B12 absorption.     

NEONATAL ACIDOSIS ASSOCIATED WITH TRANSIENT METHYLMALONICACIDURIA AND VITAMIN B12 DEFICIENCY

Abstract Investigation of a neonate presenting with a metabolic acidosis, vomiting and an apnoeic attack revealed abnormal urinary excretion of methylmalonic acid (MMA) associated with a low serum vitamin B12. Restriction of dietary protein was followed by normalisation of acid-base balance. Reintroduction of normal daily protein intake did not precipitate further acidosis or increased excretion of MMA. The transient methylmalonicaciduria was probably due to deficiency of vitamin B12.     

A pediatric patient with recurrent pseudotumor cerebri and vitamin B12 deficiency

Pseudotumor cerebri is a syndrome of increased intracranial pressure, normal cerebrospinal fluid values, and a normal cerebral ventricles on brain imaging studies. A patient with a diagnosis of pseudotumor cerebri was admitted to the authors' hospital twice within a 2.5-year interval and treated with vitamin B₁₂ (vit-B₁₂). At the second admission she also presented with a cerebral venous thrombosis that might have been explained by vit-B₁₂ deficiency, homocysteinemia, and an increased level of lipoprotein-a.     

Acute Vitamin D Toxicity in an Infant

We report vitamin D toxicity in an infant following consecutive administration use of a large dose of vitamin D, causing symptomatic hypercalcemia, which was successfully managed with injectable calcitonin. However, the child developed bilateral medullary nephrocalcinosis which persisted 42 mon after the initial episode.     

Serum vitamin B12-binding proteins in a case of eosinophilic leukemia

A patient with subacute eosinophilic leukemia is presented, with full recognition of the controversy surrounding that entity. Serum vitamin B₁₂ and B₁₂ -binding protein studies and simultaneous complete blood counts were done before and during 6 months of high-dose, intermittent combination chemotherapy. The patient presented with extremely high levels of serum vitamin B₁₂, unsaturated B₁₂-binding capacity, and transcobalamin I, all of which resembled the highest values seen in chronic myelogenous leukemia. Serial studies, during and after remission induction, showed a precipitous fall of serum vitamin B₁₂ and unsaturated B₁₂-binding capacity to normal levels. The data show that transcobalamin I levels, which eventually reached low-normal range, correlate best with the level of circulating and bone marrow eosinophils. Transcobalamin II and serum third binder appeared to be normal throughout the patient's course. The B₁₂-binding protein abnormalities are not considered diagnostic of eosinophilic leukemia.     

Neglect‐induced pseudo‐thrombotic thrombocytopenic purpura due to vitamin B12 deficiency

Although thrombotic thrombocytopenic purpura (TTP) is rare, early diagnosis and treatment are important for decreasing the mortality rate. Acquired vitamin B12 deficiency is frequently overlooked because of its rarity in developed countries, particularly in children and adolescents. The hematological changes in vitamin B12 deficiency present as megaloblastic anemia, increased lactate dehydrogenase, vasoconstriction, increased platelet aggregation, and abnormal activation of the coagulation followed by microangiopathy as well as neutropenia and thrombocytopenia. We report herein the case of a 15‐year‐old girl who had been neglected, which might have caused pseudo‐TTP through malnutrition, particularly vitamin B12 deficiency. When we encounter cases of TTP in children, clinicians must be aware of the possibility of malnutrition, particularly with vitamin B12 deficiency, even in developed countries, and investigate the cause of malnutrition including neglect.