Vitamin B12 Deficiency In Infants Research Articles

Biochemical, Nutritional, and Clinical Parameters of Vitamin B12 Deficiency in Infants: A Systematic Review and Analysis of 292 Cases Published between 1962 and 2022

Pooled data from published reports on infants with clinically diagnosed vitamin B12 (B12) deficiency were analyzed with the purpose of describing the presentation, diagnostic approaches, and risk factors for the condition to inform prevention strategies. An electronic (PubMed database) and manual literature search following the PRISMA approach was conducted (preregistration with the Open Science Framework, accessed on 15 February 2023). Data were described and analyzed using correlation analyses, Chi-square tests, ANOVAs, and regression analyses, and 102 publications (292 cases) were analyzed. The mean age at first symptoms (anemia, various neurological symptoms) was four months; the mean time to diagnosis was 2.6 months. Maternal B12 at diagnosis, exclusive breastfeeding, and a maternal diet low in B12 predicted infant B12, methylmalonic acid, and total homocysteine. Infant B12 deficiency is still not easily diagnosed. Methylmalonic acid and total homocysteine are useful diagnostic parameters in addition to B12 levels. Since maternal B12 status predicts infant B12 status, it would probably be advantageous to target women in early pregnancy or even preconceptionally to prevent infant B12 deficiency, rather than to rely on newborn screening that often does not reliably identify high-risk children.

Nitrous oxide in labour predicted newborn screening total homocysteine and is a potential risk factor for infant vitamin B12 deficiency.

Risk factors for vitamin B12 deficiency in infants are not fully understood. The aim of the study was to assess predictors of total homocysteine and methylmalonic acid analysed in newborn screening dried blood spots. In a Norwegian case control study, we analysed total homocysteine and methylmalonic acid in newborn screening dried blood spots of 86 infants clinically diagnosed with vitamin B12 deficiency during 2012-2018. Results were compared to 252 healthy infants and 400 dried blood spot controls. Medical records were reviewed, and mothers completed questionnaires. Both total homocysteine and methylmalonic acid were significantly higher on newborn screening dried blood spots in infants later clinically diagnosed with vitamin B12 deficiency than controls. Multiple regression analysis showed that the dose of nitrous oxide during labour was the strongest predictor for total homocysteine level in newborn screening dried blood spots for all infants, with larger effect in infants later clinically diagnosed with vitamin B12 deficiency than controls. Nitrous oxide dose during labour was a predictor for total homocysteine and may impact the interpretation of total homocysteine analysis in newborn screening. Nitrous oxide is suggested as a contributing risk factor for infants prone to develop vitamin B12 deficiency.

The prevalence and clinical relevance of hyperhomocysteinemia suggesting vitamin B12 deficiency in presumed healthy infants.

Previous studies have demonstrated a high prevalence of biochemical vitamin B12 deficiency in infants in Norway. Increased total homocysteine (tHcy) is the most important marker of B12 deficiency in infants. There is a need to evaluate its clinical relevance. To investigate the prevalence of hyperhomocysteinemia (S-tHcy > 8μmol/L) suggestive of suboptimal B12 status and the prevalence of clinically relevant hyperhomocysteinemia in presumed healthy infants in Norway. Further, to evaluate risk factors, presence of symptoms and psychomotor development in these children. In a prospective study we clinically examined 252 infants aged 3-7 months using standardized neurological and psychomotor tests prior to analyzing biochemical B12 deficiency markers in 250 infants. Twenty-five of 250 (10%) infants had hyperhomocysteinemia combined with clinically relevant symptoms suggestive of B12 deficiency. Hyperhomocysteinemia was associated with tremor, excessive sleep, and sub-normal scores in the fine motor section of the Ages and Stages Questionnaire. One-hundred and fourteen of 250 (46%) infants had hyperhomocysteinemia. Multiple regression analysis showed months of infant formula use as the strongest negative predictor for hyperhomocysteinemia. We have demonstrated associations between symptoms suggestive of infant B12 deficiency and increased levels of tHcy in presumed healthy infants The combination of hyperhomocysteinemia and associated relevant symptoms suggestive of B12 deficiency was a common finding, albeit most infants with hyperhomocysteinemia did not show symptoms.

Efficiency of the sublingual route in treating B12 deficiency in infants.

Objective: To evaluate the efficiency of the sublingual route for the treatment of vitamin B12 deficiency in infants. Background: Vitamin B12 deficiency is common in children. In breastfed infants, the main reason is maternal B12 deficiency. Parenteral administration is commonly prescribed. However, patient compliance is not satisfactory due to repeated painful parenteral applications. It is also known that the oral route is efficient in high doses. In recent years, the sublingual route has been tried. This route stands out due to its easy applicability and low cost. However, there are few efficacy studies in infants for the sublingual route. Materials and methods: The study included 49 infants aged 6-12 months. All infants with marginal or deficient B12 levels (<300 pg/mL) were incidentally detected and treated with sublingual methylcobalamin. Each dose was 1000 μg and administered once a day in the first week, every other day in the second week, twice a week in the third week, and once a week in the last week. Serum vitamin B12 levels were measured before and after the treatment. Paired Sample T-Test was used to compare variables. Results: All infants had normal physical development and had no hematological or neurological issues. It was learned from the parents that the infants tolerated treatment well, and no side effects related to the treatment, such as vomiting or rash, were observed. Before and after the treatment, the mean vitamin B12 levels were 199±57 pg/mL and 684±336 pg/ml, respectively. The difference between the means was statistically significant (p<0.001). Conclusion: According to the study, it seems possible to treat vitamin B12 deficiency via a sublingual route in infants. In addition, methylcobalamin can be an alternative to the commonly used cyanocobalamin.

A Preventable Cause of Hypotonia in Infants: Case Report of Two Infants with Vitamin B12 Deficiency

Introduction: Innate deficits in the metabolism or transport of vitamin B12 are exceptional. The main cause of vitamin B12 deficiency in infants is secondary to maternal deficiency. Maternal deficiency can have a vegan diet, low socio-economic level (developing countries) and a high level of development with a poor diet) or digestive pathologies responsible for a lack of absorption. The clinical signs are not very specific (developmental delay, pallor, hypotonia, vomiting and diarrhoea), which explains the frequent delay in diagnosis. The pathophysiology of the neurological damage, which is still uncertain, is thought to be secondary to a defect in myelination with altered nerve conduction and cortical atrophy. The aim of this work is to underline the importance of raising awareness of vitamin B12 deficiency in order to avoid its profound neurological repercussions, especially as substitution treatment allows an improvement or a reversibility of the neurological damage and raises the question of the possibility of screening new-borns. Materials and Methods: We report the case of two infants aged 6 months and 10 months with hypotonia and psychomotor regression from an early age, whose biological examination revealed pancytopenia with a collapsed vitamin B12 level in both infants and both mothers.

Assessment of Vitamin B12 Deficiency and Risk Factors in Healthy Infants.

To study vitamin B12 deficiency in apparently healthy infants and their mothers and assess the risk factors. A hospital-based, cross-sectional, observational study was conducted from July 2016 through December 2017. Consecutive healthy and normally developing infants were enrolled. Red blood cell folate, plasma vitamin B12, homocysteine and methylmalonic acid levels of mothers and infants were assessed. Seventy-four healthy infants were enrolled. Male-to-female ratio was 1.5:1. Anemia in 66.2% (n = 49), low plasma B12 in 17.6% (n = 13), hyperhomocysteinemia in 48.6% (n = 36), plasma methylmalonic acid in 100% (n = 74) and 'confirmed' B12 deficiency in 38% (n = 28) infants were noted. The proportion of hyperhomocysteinemia increased to 75.7% (n = 56) infants using a lower cut-off of >10μmol/L. In mothers, low B12 in 19%, hyperhomocysteinemia in 57% and elevated plasma methylmalonic acid in 100% were noted. Median plasma B12 level was 314pg/ml (IQR 221-421), median plasma homocysteine 15.4μmol/L (IQR 11.3-21.7) and median plasma methylmalonic acid was 8.28μmol/L (IQR 4.4-13.1) in mothers. Folate deficiency was noted in 9.4% infants and 12% of mothers. Overall, 63.5% mothers were vegetarian and, 64% of the mothers of infants with confirmed vitamin B12 deficiency were pure vegetarians. Odds of developing vitamin B12 deficiency increased by more than 5 times in those whose mothers' serum vitamin B12 levels were low as compared to normal maternal vitamin B12 levels (OR 5.42; 95% CI:1.96-16.6; p 0.002). There is a high prevalence of vitamin B12 deficiency in infants and their mothers. There is urgent need to supplement our population with vitamin B12.

Особенности клинических проявлений витамин В12-дефицитной анемии у детей разного возраста

Vitamin B12 deficiency affects not only the bone marrow, but also the nervous system. Usually, B12 hypovitaminosis develops slowly during several years, although infants may also have this disorder. Patients and methods. We performed a retrospective analysis of clinical symptoms and results of routine laboratory testing in patients with vitamin B12 deficiency anemia. Our sample included 19 children of 3–24 month age (Group 1) and 9 adolescents (Group 2). All patients were treated in Krasnoyarsk Regional Clinical Center for Maternal and Child Health in 2012–2019. All participants had serum levels of vitamin B12 below 83 pg/mL. Results. All patients from Group 1 were found to have nervous system disorders, including muscular hypotonia (100%), hypo- or adynamia and retardation of motor skills (63%), and hyporeflexia (42%). More than two-thirds of adolescents (67%) had pancytopenia. One-third of children of 3–24 month age (32%) developed involuntary movements during treatment with cyanocobalamin. Conclusion. Vitamin B12 deficiency in infants may manifest itself with neurological disorders that do not correlate with the severity of anemia. Children with muscular hypotonia and delayed psychomotor development should be tested for their serum level of vitamin B12 if all other potential causes of these disorders have been excluded. It is also important to perform differential diagnosis with paroxysmal conditions, including those induced by cobalamin therapy. Key words: anemia, vitamin B12, involuntary movements, hypodynamia, hyporeflexia, hypotonia, pancytopenia, cyanocobalamin

Does Vitamin B12 Deficiency in Infants Cause Severe Clinical Symptoms Necessitating Intensive Care?

Does Vitamin B12 Deficiency in Infants Cause Severe Clinical Symptoms Necessitating Intensive Care?

Vitamin B12 status and neurodevelopmental delay in Indian infants: a hospital-based cross-sectional study

ABSTRACTBackground: Vitamin B12 deficiency owing to a vegetarian diet is common in India and is associated with neurodevelopmental disorders.Objective: To investigate the prevalence of vitamin B12 deficiency in infants aged 1–12 months and to correlate the results with neurodevelopment.Methods: A cross-sectional study of 200 infants aged 1–12 months presenting to the emergency department or ward and requiring blood sampling or intravenous cannulation was undertaken in a tertiary-care centre of Northern India. Patients’ serum vitamin B12 levels were correlated with Denver development screening test II (DDST II).Results: Of 200 infants recruited, 43 (22%) were vitamin B12-deficient (<211 pg/ml). After excluding 16 (8%) infants who were unsuitable for DDST screening, 21/39 (54%) and 22/145 (15%) were DDST-suspect in the vitamin B12-deficient and sufficient groups, respectively (p = 0.0001). There was a statistically significant correlation between B12 deficiency and an abnormal DDST (p < 0.0001).Conclusion: In India, vitamin B12 deficiency is prevalent in infancy and is associated with neurodevelopmental delay.

Dermatologic findings of vitamin B12 deficiency in infants.

Vitamin B12 deficiency in infants is uncommonly reported from developed countries and generally lacks dermatologic manifestations. On the contrary, infantile vitamin B12 deficiency is common in India and cutaneous manifestations are a constant feature, although often overshadowed by neurologic and hematological manifestations. The aim of this study was to describe the skin changes of vitamin B12 deficiency in infants. A retrospective chart review of vitamin B12 deficient infants for clinical and laboratory parameters was performed and data analyzed. Forty-three infants, 30 boys and 13 girls, aged 4 to 27months, with vitamin B12 deficiency were identified. Skin hyperpigmentation was present in 41 infants; it was localized to the dorsa of hands and feet in 26. Fifteen infants had generalized hyperpigmentation; 10 had a reticulate pattern, and 5 had a homogeneous pattern. Brown and sparse scalp hair were present in all. Glossitis was seen in 5 infants and cheilitis in 3. Of the 32 infants who underwent laboratory investigations, 28 had anemia and 21 macrocytosis. Serum vitamin B12 was measured in 30 infants; it was low in 19. Of the 11 with normal serum vitamin B12 , 9 had received vitamin B12 before referral but had macrocytosis and low maternal serum vitamin B12 . The infants were treated with vitamin B12 . Skin pigmentation and mucosal changes resolved completely by 3-4weeks, but hair changes were slower to reverse. Cutaneous findings are a common feature of vitamin B12 deficiency in Indian infants and resolve with treatment.

Persistent diarrhea, hemolytic anemia, and splenohepatomegaly due to Vitamin B12 deficiency in an infant

Vitamin B12 is essential for DNA and RNA synthesis. Vitamin B12 deficiency usually occurs in infants who are exclusively breastfed born to Vitamin B12-deficient mothers. Even though macrocytic anemia is the classic feature, the spectrum of hematological findings due to Vitamin B12 deficiency ranges from simple macrocytosis to life-threatening hemolytic anemia. Other manifestations of Vitamin B12 deficiency in infants include delay in growth and development, anorexia, diarrhea, sparse hair, failure to thrive, abnormal pigmentation, hypotonia, and enlarged liver and spleen. Herewith, we are presenting a 6-month-old child with growth retardation, persistent diarrhea, anorexia, irritability, anemia, and splenohepatomegaly due to Vitamin B12 deficiency who responded to Vitamin B12 therapy.

Vitamin B12 status in pregnant women and their infants in South India

Vitamin B12 deficiency during pregnancy has been associated with increased risk of adverse perinatal outcomes. However, few studies have investigated the burden and determinants of vitamin B12 status in young infants. This study was conducted to determine the associations between maternal and infant vitamin B12 status. Pregnant women participating in a vitamin B12 supplementation trial in Bangalore, India, were randomized to receive vitamin B12 (50 μg) or placebo supplementation daily during pregnancy through 6 weeks postpartum. All women received 60 mg of iron and 500 μg of folic acid daily during pregnancy, as per standard of care. This prospective analysis was conducted to determine the associations between maternal vitamin B12 biomarkers (that is, plasma vitamin B12, methylmalonic acid (MMA) and tHcy) during each trimester with infant vitamin B12 status (n=77) at 6 weeks of age. At baseline (⩽14 weeks of gestation), 51% of mothers were vitamin B12 deficient (vitamin B12<150 pmol/l) and 43% had impaired vitamin B12 status (vitamin B12<150 pmol/l and MMA>0.26 μmol/l); 44% of infants were vitamin B12 deficient at 6 weeks of age. After adjusting for vitamin B12 supplementation, higher vitamin B12 concentrations in each trimester were associated with increased infant vitamin B12 concentrations and lower risk of vitamin B12 deficiency in infants (P<0.05). After adjusting for vitamin B12 supplementation, infants born to women with vitamin B12 deficiency had a twofold greater risk of vitamin B12 deficiency (P<0.01). Higher maternal folate concentrations also predicted lower risk of vitamin B12 deficiency in infants (P<0.05). Impaired maternal vitamin B12 status, which combined both circulating and functional biomarkers, was the single best predictor of infant vitamin B12 status. Impaired maternal vitamin B12 status throughout pregnancy predicted higher risk of vitamin B12 deficiency in infants, after adjusting for vitamin B12 supplementation. Future interventions are needed to improve vitamin B12 status periconceptionally, and to ensure optimal vitamin B12 status and health outcomes in pregnant women and their children.

B12 deficiency is common in infants and is accompanied by serious neurological symptoms

Adverse neurological symptoms have been linked to vitamin B12 deficiency in infants. This explorative study described the clinical presentation associated with vitamin B12 deficiency in this age group. The study comprised infants who were born between 2004 and 2012 and were tested for vitamin B12 levels after they were admitted to a hospital with neurological symptoms at less than one year of age. Vitamin B12 deficiency was defined as low cobalamin in serum and/or increased homocysteine and/or increased methylmalonate. It was diagnosed according to the applicable International Classification of Diseases, 10th revision, and recorded as vitamin B12 deficiency in the medical records. All information was retrieved from medical records and compared to symptomatic infants with normal levels. Of the 121 infants tested, 35 had vitamin B12 deficiency and 86 had normal levels. Vitamin B12 deficiency was diagnosed at an average age of 1.7 months and was more common among boys. Seizures and apparent life-threatening events were the most common symptoms among infants with B12 deficiency compared to infants with normal levels. Vitamin B12 deficiency was more common in infants than we expected and presented with severe symptoms, such as seizures and apparent life-threatening events.

West syndrome due to vitamin B12 deficiency

Vitamin B12 is one of the essential vitamins affecting various systems of the body. Vitamin B12 deficiency in infants often produces haematological and neurological deficits including macrocyticanaemia, neurodevelopmental delay or regression, irritability, weakness, hypotonia, ataxia, apathy, tremor andseizures. In this article, we report the case of a six-month-old male patient diagnosed with West syndrome associated with vitamin B12 deficiency. Although the patient had no evidence of macrocytic anemia in complete blood count, we measured the level of vitamin B12 because the patient had hypotonicity and found it to be low. No other problem was found in the other investigations directed to the etiology of West syndrome. He was being exclusively breast-fed and vitamin B12 deficiency was related with nutritional inadequacy of his mother. Vitamin B12 deficiency should be considered in the differential diagnosis of patients presenting with different neurological findings. In addition, vitamin B12 deficiency should be considered as a rare cause in West syndrome which has a heterogeneous etiology.

Vitamin B12 Deficiency in Infants.

To determine different clinical presentations of vitamin B12 deficiency in infants. Infants at the age of 1-20 mo admitted to infancy clinic of authors' hospital between January 2011-2013 with various clinical presentations due to vitamin B12 deficiency were included in the study. Hospital records of all the patients were evaluated by means of history, physical, laboratory, imaging examinations and treatment. The diagnosis was based on a nutritional history of mothers and infants, clinical findings, hematological evaluation, and low level of serum vitamin B12. A total of 20 patients with a mean age of 6.65 ± 4.5 mo were included in the study. The weight and height were below the third percentile in four patients. The most common symptoms of the patients were; infections in 30 %, pallor in 25 %, hypotonia and neuro-developmental delay in 25 %, refusal to solid food or to suck in 20 %, failure to thrive in 15 %, fatigue in 10 %. Twenty-five percent of patients had neurologic signs and symptoms. Anemia was found in 16/20 (80 %) patients. Three (15 %) patients had leukopenia, 7 (35 %) had neutropenia, 2 (10 %) patients had thrombocytopenia. All of the mothers had vitamin B12 deficiency. All of the patients were fed with breast milk. Cyanocobalamin was administered to all the patients and mothers. After the treatment, clinical and laboratory findings of all the patients improved. Vitamin B12 deficiency should be considered in the differential diagnosis of some hematological, neurological, and gastrointestinal disturbances of infants.

Frequency of hematological findings associated with severe plasma vitamin B12 deficiency in infants and adolescents.

The aim of this study was to determine the hematological status of severe vitamin B12 deficiency in infants and adolescents. This study involved 95 infants and 117 adolescents with severe plasma vitamin B12 deficiency (< 120 pg/ mL) and normal plasma folate and ferritin. Infants were aged between one and 24 months. Adolescents were aged between 11 and 17 years. Macrocytic anemia was associated with nine (9.5%) out of 95 infants with severe vitamin B12 deficiency. Neutropenia was found in 16 (16.8%) out of 95 infants with severe vitamin B12 deficiency. Thrombocytopenia was not found in 95 infants with severe vitamin B12 deficiency. Macrocytic anemia was found in two (1.7%) out of 117 adolescents with a severe vitamin B12 deficiency. Neutropenia was associated in one (0.8%) out of 117 adolescents with severe vitamin B12 deficiency. Thrombocytopenia was not found in 117 adolescents with severe vitamin B12 deficiency. Low clinical or hematological findings for B12 deficiency in infants and adolescents living in regions at risk, such as those with low consumption of meat and other animal products warrant the measurement of vitamin B12 level.

Severe vitamin B12 deficiency in an exclusively breastfed 5-month-old Italian infant born to a mother receiving multivitamin supplementation during pregnancy

BackgroundIn infants, vitamin B12 deficiency may be due to an inborn error of absorption and metabolism, or nutritional problems.Case presentationAn exclusively breastfed 5-month-old Italian male infant, who was born after a normal full-term pregnancy to a vegan mother who was apparently daily treated with a multivitamin oral preparation during the second and third trimester, was hospitalised because of poor weight gain, feeding difficulties, severe pallor, muscle hypotonia and somnolence. Upon admission, his weight, length and head circumference were below the third percentile, he had an enlarged liver and spleen, and showed a significant delay in developmental milestones and communicative reactions. He had a hemoglobin level of 4.7 g/dL with an MCV of 84.2 fL, a white blood cell count of 4,680/mm3, and a platelet count of 45,000/mm3. His serum vitamin B12 level was 57 pg/mL (normal value 180–500 pg/mL) and serum folate level 12.8 ng/mL (normal value >3 ng/mL). The results of metabolic examinations excluded a cobalamin C disorder, whereas nutritional screening showed a serum iron concentration of 9 μg/dL and serum ferritin of 4 ng/mL. Magnetic resonance imaging of the brain showed mild dilatation of the lateral ventricles with diffuse delayed myelination. The child was diagnosed as having vitamin B12 and iron deficiency due to nutritional inadequacy and was immediately treated with packed red blood cells, intramuscular vitamin B12 injections, and iron supplementation. A few days after the start of therapy, his hemoglobin levels and other hematological parameters rapidly improved, and a clinical improvement was observed within few weeks. There was an increase in his achievement of developmental milestones, but his development was still retarded seven months after the start of therapy.ConclusionThis case underlines the importance of adequately controlling maternal vitamin B12 intake during pregnancy by means of supplementation which, in the case of vegan mothers, should be significantly greater than that usually given. Moreover, the supplementation should be continued during lactation in order to avoid the development of signs of deficiency that may be associated with persistent neurological problems in infants. The case also highlights the need to consider vitamin B12 deficiency in infants with severe anemia even if their hematological parameters do not indicate megaloblastic anemia because the concomitant presence of substantial iron deficiency may modify the characteristics of the anemia.

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.

Nutritional B12 Deficiency in Infants of Vitamin B12-Deficient Mothers

Nutritional vitamin B₁₂ deficiency in infants may occur because the maternal diet contains inadequate animal products. Clinical presentations of the infants who had nutritional vitamin B₁₂ deficiency were analyzed in this study. Patients with nutritional vitamin B₁₂ deficiency were enrolled in the study between 2003 and 2010. The diagnosis was based on a nutritional history of mothers and infants, clinical findings, hematological evaluation, and low level of serum vitamin B₁₂. Thirty children aged 1 - 21 months constituted the study group. Poverty was the main cause of inadequate consumption of animal products of the mothers. All infants had predominantly breastfed. The most common symptoms were developmental delay, paleness, apathy, lethargy, anorexia, and failure to thrive. Hematological findings were megaloblastic anemia (83.3 %), thrombocytopenia (30 %), and severe anemia (13.3 %). All of the mothers had low serum B₁₂ levels; eight of them had megaloblastic anemia. The unusual clinical manifestations of vitamin B₁₂ deficiency may also be seen apart from neurological and hematological findings. Nutritional vitamin B₁₂ deficiency due to maternal deficiency might be a serious health problem in infants. Therefore, screening and supplementation of pregnant and lactating women to prevent infantile vitamin B₁₂ deficiency should be considered.

Serum Vitamin B12 Concentrations among Mothers and Newborns and Follow-up Study to Assess Implication on the Growth Velocity and the Urinary Methylmalonic Acid Excretion

Cobalamin (B(12)) deficiency has been reported in infants born to mothers with low cobalamin intake. Early diagnosis of vitamin B(12) deficiency in infants is critical for the prevention of neurobehavioral disorders. We investigated the relationship between serum vitamin B(12) level in newborns and in their healthy mothers who consumed an omnivorous diet. Anthropometry was studied longitudinally to assess the growth velocity of the infants. Urinary methylmalonic acid (MMA) excretion of 6-month old infants was compared retrospectively as the biomarker correlated with the initial serum vitamin B(12) concentrations. Serum cobalamin and blood hemoglobin were determined in 84 pairs of newborns and their mothers. Urinary MMA excretion was measured in the same subjects during the first 6 months of the post partum period. At birth, median serum cobalamin levels were 152.0 pmol/L in the mothers and 296.6 pmol/L in the newborns. Maternal and neonatal serum cobalamin levels had no effect on growth velocity during the first six months of postnatal life. Serum maternal and neonatal cobalamin levels were inversely associated with urinary MMA excretion. Early diagnosis of vitamin B(12) status in neonates and infants is crucial, particularly in nutritionally deprived areas. Biochemical measurement of plasma cobalamin or its metabolic marker MMA is highly recommended. Urinary MMA measurement in cobalamin diagnostics provides an advantage in that blood sampling is not required. A vitamin B(12) taskforce should be created to alleviate vitamin deficiency and its negative consequences.