Disappearance of cerebral cortical atrophy following replacement therapy with vitamin B12 in an infant

Abstract During the Centers for Disease Control and Prevention’s Zika Virus Response, birth defects surveillance programs adapted to monitor birth defects potentially related to Zika virus (ZIKV) infection during pregnancy. Pregnancy outcomes occurring during January 2016-June 2017 in 22 U.S. states and territories were used to estimate the prevalence of those brain and eye defects potentially related to ZIKV. Jurisdictions were divided into three groups: areas with widespread ZIKV transmission, areas with limited local ZIKV transmission, and areas without local ZIKV transmission. Prevalence estimates for selected brain and eye defects and microcephaly per 10,000 live births were estimated. Prevalence ratios (PRs) and 95% confidence intervals (CIs) were estimated using Poisson regression for areas with widespread and limited ZIKV transmission compared to areas without local ZIKV transmission. Defects with significantly higher prevalence in areas of widespread transmission were pooled, and PRs were calculated by quarter, comparing subsequent quarters to the first quarter (January – March 2016). Nine defects had significantly higher prevalence in areas of widespread transmission. The highest PRs were seen in intracranial calcifications (PR=12.6, 95% CI [7.4, 21.3]), chorioretinal abnormalities (12.5 [7.1, 22.3]), brainstem abnormalities (9.3, [4.7, 18.4]), and cerebral/cortical atrophy (6.7, [4.2, 10.8]). The PR of the nine pooled defects was significantly higher in three quarters in areas with widespread transmission. The largest difference in prevalence was observed for defects consistently reported in infants with congenital ZIKV infection. Birth defects surveillance programs could consider monitoring a subset of birth defects potentially related to ZIKV in pregnancy.

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

10.36502/2021/asjpch.6168 ◽

2021 ◽

Vol 3 (2) ◽

pp. 48-51

Author(s):

Akhrif M ◽

Saghir S ◽

Kmari M ◽

Ourrai A ◽

Hassani A ◽

...

Keyword(s):

Vitamin B12 ◽

Clinical Signs ◽

Vitamin B12 Deficiency ◽

Vegan Diet ◽

Cortical Atrophy ◽

Neurological Damage ◽

Delay In Diagnosis ◽

Raising Awareness ◽

B12 Deficiency ◽

High Level

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.

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