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 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.     

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.     

Brain atrophy caused by vitamin B12-deficient anemia in an infant

Vitamin B12 deficiency in infants often presents with nonspecific hematological, gastrointestinal, and neurological manifestations. It is usually caused by inadequate intake, abnormal absorption, or congenital disorders of vitamin B12 metabolism, including transport disorders. We describe a vitamin B12-deficient infant with severe anemia who was breastfed. His mother had undiagnosed vitamin B12 deficiency having undergone total gastrectomy 18 years earlier. The infant developed normally after taking vitamin B12. It is important to suspect vitamin B12 deficiency in mothers who have undergone gastrectomy. Early diagnosis and treatment of vitamin B12 deficiency in infants is important and will help improve long-term prognosis.     

Solid food refusal as the presenting sign of vitamin B<Subscript>12</Subscript> deficiency in a breastfed infant

Dietary vitamin B₁₂ (vitB₁₂) deficiency, although common in the elderly, is rare in childhood. We report on an exclusively breastfed 8-month-old infant, presenting with persistent refusal of solid foods. Three months later, developmental regression and failure to thrive led to the diagnosis of vitB₁₂ deficiency, as a consequence of a subclinical pernicious anaemia with vitB₁₂ deficiency in the mother. Treating the infant with parenteral vitB₁₂ induced prompt recovery including acceptance of weaning food. Conclusion: This case illustrates refusal of complementary foods as a presenting symptom of vitB₁₂ deficiency in a breastfed infant. Symptoms, diagnostic tests and treatment of vitamin B₁₂ deficiency are reviewed. Early diagnosis and treatment are important to prevent irreversible neurological damage.     

Gastric bypass: a risk factor for neural tube defects? Case report

Gastric bypass surgery has become a safe and acceptable surgical weight loss treatment for individuals who suffer from morbid obesity. Patients who undergo this procedure are subject to vitamin deficiencies due to an iatrogenic malabsorptive state. Folate, a vitamin known for its role in the prevention of neural tube defects (NTDs), can be part of the deficiency spectrum resulting from this procedure. The authors describe the case of a woman who was nonadherent to multivitamin treatment after undergoing gastric bypass surgery. Her lack of understanding and appreciation of the relationship between gastric bypass surgery, folate deficiency, and NTDs may have contributed to her noncompliance with daily multivitamin consumption. As a result, her potential problems with folate absorption could have contributed to her subsequently giving birth to a child with a myelomeningocele. Thus, patient awareness and counseling along with aggressive vitamin supplementation among this particular population may help prevent the occurrence of NTDs after gastric bypass surgery.     

Vitamin K status of lactating mothers and their infants

Vitamin K deficiency remains a world-wide problem in the newborn. Vitamin K traverses the placenta from mother to infant very poorly and is present only in very low concentrations in human milk. Thus, it is not surprising that the newborn infant has undetectable vitamin K serum levels with abnormal amounts of the coagulation proteins and undercarboxylated prothrombin. Hemorrhagic disease of the newborn, secondary to vitamin K deficiency, remains largely a disease of breastfed infants. Lactating mothers easily achieve the recommended dietary allowance for vitamin K (1 μg kg⁻¹ d⁻¹) and the breast milk concentration is readily increased by increasing maternal vitamin K intake. Breastfed infants do not receive the recommended vitamin K intake via human milk. To prevent vitamin K deficiency in the newborn, intramuscular or oral vitamin K prophylaxis is necessary.     

The effects of dietary vitamin B12 deficiency on sperm maturation in developing and growing male rats

ABSTRACT  To evaluate the role of vitamin B₁₂ on spermatogenesis, the effects of dietary vitamin B₁₂ deficiency on sperm maturation in developing rat fetuses and young growing rats were examined. The vitamin B₁₂-defi-cient diet was given to all the animals for three different periods: whole period (gestation to mature), gestation period (gestation to weaning), or immature period (3–12 weeks postnatal). Sperm examination revealed that the sperm count was markedly lower in male progeny (F1) that were vitamin B₁₂-deficient during the whole period. In addition, a significantly higher number of abnormal sperm, such as tailless and amorphous sperm, was observed. In male rats that were vitamin B₁₂-deficient during the immature period, the incidence of abnormal sperms was 14.4% and 4.8% for tailless and short tail, respectively. The motion rates, such as path velocity and straight line velocity, were decreased to 20–40% of the control value in rats that were vitamin B₁₂-deficient both during the whole and gestation periods. However, no effects of vitamin B₁₂ deficiency on sperm motility were observed during the immature and mature periods. From these findings, we suggest that dietary vitamin B₁₂ deficiency during pregnancy may induce irreversible damage in the germ cells of embryos and affect the maturation of spermatozoa.     

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     

Congenital intrinsic factor deficiency. Apropos of 3 cases in a sibship

Three familial cases of congenital intrinsic factor deficiency are reported: the stress is put on the interest of gastric investigations and especially of the quantity of intrinsic factor in the gastric juice when investigating megaloblastic anemia due to vitamin B12 deficiency. The study of the level of intrinsic factor in the gastric juice is proposed as a test for identifying carriers.     

Recurrent urinary tract infections and genitourinary tract abnormalities in the Imerslund-Gräsbeck syndrome

Two Imerslund-Grasbeck patients who presented with recurrent urinary tract infections and genitourinary abnormalities are described. The patients were evaluated with abdominal ultrasounds, voiding cystourethrograms, and Schilling tests. Each patient had large postvoid residual urine secondary to a motor-neurogenic bladder. One had a duplication of the distal urethra manifesting as two meatal openings. There was lack of urinary excretion of radioactive vitamin B₁₂ on Schilling tests in both patients. Patients with Imerslund-Grasbeck syndrome may be predisposed to urinary tract infections because of incomplete bladder emptying. Complete physical and radiological examinations of the genitourinary tract should be performed.     

Alpha1-antitrypsin deficiency with fatal intracranial hemorrhage in a newborn.

A 4-week-old boy had a fatal intracranial hemorrhage resulting from vitamin K deficiency. The infant had received no vitamin K prophylaxis and was exclusively breastfed. At autopsy, examination of the liver showed cholestasis and fibrosis. DNA was isolated from a blood spot on a Gutherie sample card obtained from the infant for routine metabolic screening. This DNA was used for alpha1-antitrypsin genotyping studies. Genotyping studies identified homozygosity for the point mutation 9989G-->A, confirming a diagnosis of alpha1-antitrypsin deficiency (ZZ phenotype), and resulted in appropriate screening of siblings born after this child's death. Alpha1-antitrypsin deficiency should be considered in the differential diagnosis of infants with late hemorrhagic disease of the newborn. Use of blood from the metabolic screening card as a source of DNA allowed confirmation of this diagnosis after the infant's death.     

Late onset haemorrhagic disease in premature infants who received intravenous vitamin K1

Abstract: The clinical details are reported of two premature infants who developed late onset haemorrhagic disease after receiving their initial doses of vitamin K₁ prophylaxis intravenously. Both reported infants had received two doses of intravenous vitamin K₁, 0.1 mg, in the 1st week of life, and a further oral dose, 1.0 mg, at 4 weeks. Bleeding due to vitamin K deficiency occurred on days 74 and 84, respectively. Vitamin K deficiency bleeding is rare in low birthweight infants, probably because it has been routine practice to give such infants intramuscular vitamin K₁. One of the reported infants had cytomegalovirus hepatitis, the other did not have liver disease. These findings could be explained if intramuscular vitamin K₁ were to have a longer duration of effect than intravenous vitamin K₁. This may be because intramuscular vitamin K₁ acts as a depot preparation. The findings suggest that intravenous vitamin K₁ is less effective than intramuscular for long-term prophylaxis against late onset haemorrhagic disease. Intravenous vitamin K₁ should not be used for long-term prophylaxis in the prevention of late onset haemorrhagic disease.     

Non-spherocytic Haemolytic Anaemia in Mother and New-born Infant

Summary
A case is described of non-spherocytic haemolytic anaemia in a woman. The condition was aggravated during her two pregnancies, and exhibited some megaloblastic features. The first child was healthy, but the second developed anaemia with reticulocyte response first to folic acid, then to a liver preparation, and finally to cortisone and blood transfusion. Haemolytic anaemia was undoubtedly present, but the child also had folic-acid and vitamin B₁₂ deficiency.     

Clinical manifestations of infants with nutritional vitamin B deficiency due to maternal dietary deficiency

Aim: In developing countries, nutritional vitamin B₁₂ deficiency in infants due to maternal diet without adequate protein of animal origin has some characteristic clinical features. In this study, haematological, neurological and gastrointestinal characteristics of nutritional vitamin B₁₂ deficiency are presented.
Methods: Hospital records of 27 infants diagnosed in a paediatric haematology unit between 2000 and 2008 were evaluated retrospectively.
Results: The median age at diagnosis was 10.5 months (3–24 months). All the infants were exclusively breast fed and they presented with severe nonspecific manifestations, such as weakness, failure to thrive, refusal to wean, vomiting, developmental delay, irritability and tremor in addition to megaloblastic anaemia. The diagnosis was confirmed by complete blood counts, blood and marrow smears and serum vitamin B₁₂ and folic acid levels. The median haemoglobin level was 6.4 g/dL (3.1–10.6) and mean corpuscular volume (MCV) was 96.8 fL (73–112.3). Some patients also had thrombocytopaenia and neutropaenia. All the infants showed clinical and haematological improvement with vitamin B₁₂ administration. Patients with severe anaemia causing heart failure received packed red blood cell transfusions as the initial therapy.
Conclusion: Paediatricians must consider nutritional vitamin B₁₂ deficiency due to maternal dietary deficiency in the differential diagnosis of some gastrointestinal, haematological, developmental and neurological disorders of infants with poor socioeconomic status. Delay in diagnosis may cause irreversible neurological damage.     

Morbidity in children born to women infected with human immunodeficiency virus in South Africa: does mode of feeding matter?

Aim: To examine infant morbidity risks associated with refraining from breastfeeding where it is used in an attempt to prevent mother-to-child transmission (MTCT) of human immunodeficiency virus (HIV). Methods: The population consisted of infants born to HIV-infected women in South Africa who were participating in a vitamin A intervention trial to prevent MTCT of HIV. Women chose to breastfeed or formula feed their infants according to UNAIDS guidelines. Actual feeding practices and morbidity were recorded at clinic follow-up visits at 1 wk, 6 wk, 3 mo and every 3 mo thereafter until 15 mo of age or cessation of breastfeeding. The infant's HIV status was assessed according to a predetermined algorithm. Results: HIV-infected infants who were never breastfed had a poorer outcome than those who were breastfed; 9 (60%) of those who were never breastfed had 3 or more morbidity episodes compared with 15 (32%) of breastfed children [odds ratio (OR) 4.05, 95% confidence interval (95% CI) 0.91-20.63, p = 0.05]. During the first 2 mo of life, never-breastfed infants (regardless of HIV status) were nearly twice as likely to have had an illness episode than breastfed infants (OR 1.91, 95% CI 1.17-3.13, p = 0.006).

Conclusion: The significant extra morbidity experienced in the first few months by all never-breastfed infants and at all times by HIV-infected infants who are not breastfed needs to be considered in all decisions by mothers, health workers and policy makers so as not to offset any gains achieved by decreasing HIV transmission through avoiding breastfeeding.     

Vitamin K in human milk--still not enough

The breastfed infant has limited sources of vitamin K, as it is transmitted poorly across the placenta and is present in very low concentrations in human milk. The author of this paper reports a concentration of vitamin K in human milk (0.517 ± 1.521 μg/dl) that is about twice the average of earlier reports (0.25 μg/dl). About half of the increased concentration (0.235 ± 0.144 μg/dl) is accounted for by vitamin K ₂ (menaquinone) rather than vitamin K ₁ (phylloquinone); the latter generally thought to be more important in human nutrition. The significance of these findings is discussed.     

Prevention of vitamin K deficiency in infancy by weekly administration of vitamin K

Vitamin K prophylaxis has been developed to prevent classic haemorrhagic disease of the newborn. Single vitamin K administration after birth has been reported to fail, resulting in late haemorrhagic disease of the newborn. The preventive effect of oral administration of vitamin K₁ 1 mg, repeated weekly during the first three months of life, was studied in 48 healthy breast-fed infants, by determination of thrombotest, PIVKA-II and vitamin K₁ concentrations at the age of 4, 8 and 12 weeks. All infants showed normal thrombotcst values and PIVKA-II was not detectable. Vitamin K₁ concentrations were negatively correlated with the number of days elapsed since the most recent vitamin K administration. Six to seven days after the latest application, mean levels were 1223,927 and 748 pg/ml at ages 4, 8 and 12 weeks, respectively. In conclusion, weekly administration of vitamin K₁ 1 mg offers complete protection against vitamin K deficiency and does not result in an accumulation of vitamin K₁ in the blood.     

Prevention of vitamin K deficiency in infancy by weekly administration of vitamin K

Vitamin K prophylaxis has been developed to prevent classic haemorrhagic disease of the newborn. Single vitamin K administration after birth has been reported to fail, resulting in late haemorrhagic disease of the newborn. The preventive effect of oral administration of vitamin K₁ 1 mg, repeated weekly during the first three months of life, was studied in 48 healthy breast-fed infants, by determination of thrombotest, PIVKA-II and vitamin K₁ concentrations at the age of 4, 8 and 12 weeks. All infants showed normal thrombotcst values and PIVKA-II was not detectable. Vitamin K₁ concentrations were negatively correlated with the number of days elapsed since the most recent vitamin K administration. Six to seven days after the latest application, mean levels were 1223,927 and 748 pg/ml at ages 4, 8 and 12 weeks, respectively. In conclusion, weekly administration of vitamin K₁ 1 mg offers complete protection against vitamin K deficiency and does not result in an accumulation of vitamin K₁ in the blood.