Serious hematological, metabolic and neurological complications owing to the nutritional deficiency of vitamin B12 may occur in infants of mothers on a strict vegetarian diet.
The mother of the first child was a strict vegetarian. She had an elevated urinary methylmalonic acid level and a low concentration of serum vitamin B12. Her 13-month-old daughter was exclusively breast-fed until the age of 9 month and then she was fed only vegetables. Physical examination revealed psychomotoric retardation, apathy, muscular hypotonia, abnormal movements and failure to thrive. Laboratory analysis showed a megaloblastic anaemia, a low level of vitamin B12 and methylmalonic aciduria. MRI of the brain revealed diffuse frontotemporoparietal atrophy and retardation of myelination. After treatment with vitamin B12 supplements, abnormal movements disappeared and development improved, but a mild generalised hypotonia continued. A cranial MRI 9 months after treatment still showed signs of retardation of myelination. The second patient, an 8 month-old male, son of a strict vegetarian mother too, was referred for investigation of psychomotoric retardation, hypotonia, dyskinesia, failure to thrive and microcephaly. He was breast-fed and from 6 month of age he had also received fruit juices. Laboratory analysis revealed megaloblastic anaemia, high methylmalonic aciduria and homocystinuria. The patient's and his mother's serum level of vitamin B12 were low. After treatment with vitamin B12 supplements, biochemical and metabolic markers of disease were normal but there continued a generalised hypotonia, microcephaly and language delay.
Our observations emphasize the health complications of nutritional cobalamine deficiency and a requirement of clinical, biochemical and metabolic monitoring in infants within strict vegetarian families.
[Show abstract][Hide abstract] ABSTRACT: It has been known for many years that vitamin B12 deficiency can cause neurologic problems. One of these problems is involuntary movements that can appear both before and after the initiation of vitamin B12 treatment. Here, we report 3 infants who developed movement disorder during vitamin B12 administration. The movement disorder consisted of a combination of tremor and myoclonus affecting face, tongue, and limbs. Because of the severity of the symptoms, they all needed symptomatic treatment. In 2 of them, the involuntary movements resolved with clonazepam. The involuntary movements in the other patient were successfully treated with piracetam.
[Show abstract][Hide abstract] ABSTRACT: Vitamin B 12 deficiency is an uncommon disorder in infancy. Most cases are because of maternal deficiency resulting from insufficient storage and/or reduced intake and are generally seen in exclusively breast-fed infants. Accentuation of the hemolytic process has never been described in association with Varicella Zoster Virus (VZV) infections.
We describe a 9-months-old breast-fed infant with megaloblastic anemia secondary to maternal vitamin B 12 deficiency. He presented severe pancytopenia and regression of motor functions and developed hemolytic crisis during a VZV infection.
Nutritional cobalamin deficiency should be considered in anemic infants with a history of prolonged exclusive breastfeeding and delayed developmental milestones. VZV infection can trigger a hemolytic process in infants with severe megaloblastic anemia secondary to B12 deficiency. A normal mean corpuscular volume does not rule out megaloblastic anemia, when the condition is combined with severe hemolysis.
[Show abstract][Hide abstract] ABSTRACT: Megaloblastic anemia (MA), in most instances in developing countries, results from deficiency of vitamin B(12) or folic acid. Over the last two to three decades, incidence of MA seems to be increasing. Of the two micronutrients, folic acid deficiency contributed to MA in a large majority of cases. Now deficiency of B(12) is far more common. In addition to anemia, occurrence of neutropenia and/or thrombocytopenia is increasingly being reported. Among cases presenting with pancytopenia, MA stands out as an important (commonest cause in some series) cause. This article focuses on these and certain other aspects of MA. Possible causes of increasing incidence of MA are discussed. Observations on other clinical features like neurocognitive dysfunction, associated hyperhomocysteinemeia and occurrence of tremors and thrombocytosis during treatment are highlighted.
The Indian Journal of Pediatrics 07/2010; 77(7):795-9. DOI:10.1007/s12098-010-0121-2 · 0.87 Impact Factor
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