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      Les troubles neurologiques secondaires à une carence en vitamine B12: analyse de 29 cas Translated title: Neurological disorders secondary to vitamin B12 deficiency: about 29 cases

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          Abstract

          Les troubles neurologiques secondaires à une carence en vitamine B12 sont polymorphes et variés. Peu de travaux se sont intéressés à leur analyse aussi bien dans la population marocaine qu'africaine. L'objectif de notre étude est donc de décrire les aspects cliniques, paracliniques et évolutifs des manifestations neurologiques des patients atteints d'une carence en vitamine B12, au sein du Service de Neurologie de l'Hôpital Militaire Moulay Ismail de Meknès sur une durée de 18 ans (1999-2017). Il s'agissait de 06 femmes et 23 hommes âgés en moyenne de 57 ans. Le délai du diagnostic était de 3 mois. L'atteinte neurologique était révélatrice de la carence en vitamine B12 dans 100% des cas. Le taux moyen de l'hémoglobine était de 10g/dl, le volume globulaire moyen de 115 fl. Une mégaloblastose médullaire et une gastrite atrophique étaient présentes dans respectivement 95% et 90% des cas. La réalisation systématique d'électroencéphalographie (EEG), électromyogramme (EMG) et potentiel evoqué visuel (PEV), a retrouvé chez nos patients des neuropathies périphériques et optiques infracliniques. Sur le plan étiologique, il s'agissait d'une anémie de Biermer dans 20 cas. Sous vitamine B12 parentérale, l'évolution était favorable chez tous nos patients. A la lumière de ces résultats, nous insistons sur l'intérêt du diagnostic précoce en raison de la gravité potentielle de certains tableaux neuropsychiatriques et le traitement substitutif qui doit être rapide car il est le seul garant d'une évolution favorable de ces atteintes.

          Translated abstract

          Neurological disorders secondary to vitamin B12 deficiency are polymorphic and diverse. There have been very few studies conducted in the Moroccan as well as in the African population. This study aims to describe the clinical, paraclinical, evolutionary features of neurological manifestations in patients with vitamin B12 deficiency within the Department of Neurology at the Moulay Ismail Military Hospital, Meknes over a period of 18 years (1999-2017). The study involved 06 women and 23 men, with an average age of 57 years. The mean time between symptom onset and diagnosis was 3 months. Neurological manifestation was indicative of vitamin B12 deficiency in 100% of cases. The average hemoglobin level was 10 g/dl, the mean corpuscular volume was 115 fl. Medullary megaloblastosis and atrophic gastritis were found in 95% and 90% of cases respectively. Regular electromyography (EMG), electroencephalography (EEG) and visual evoked potentials (VEP) showed subclinical peripheral and optic neuropathies. In 20 cases they were caused by Biermer’s anemia. All the patients received parenteral Vitamin B12 with good outcome. These results demonstrate the importance of early diagnosis in patients with a potentially serious neuropsychiatric condition as well as of rapid substitution treatment which is the only therapeutic option to secure a good outcome.

          Most cited references12

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          Vitamin B12 deficiency.

          Vitamin B12 (cobalamin) deficiency is a common cause of macrocytic anemia and has been implicated in a spectrum of neuropsychiatric disorders. The role of B12 deficiency in hyperhomocysteinemia and the promotion of atherosclerosis is only now being explored. Diagnosis of vitamin B12 deficiency is typically based on measurement of serum vitamin B12 levels; however, about 50 percent of patients with subclinical disease have normal B12 levels. A more sensitive method of screening for vitamin B12 deficiency is measurement of serum methylmalonic acid and homocysteine levels, which are increased early in vitamin B12 deficiency. Use of the Schilling test for detection of pernicious anemia has been supplanted for the most part by serologic testing for parietal cell and intrinsic factor antibodies. Contrary to prevailing medical practice, studies show that supplementation with oral vitamin B12 is a safe and effective treatment for the B12 deficiency state. Even when intrinsic factor is not present to aid in the absorption of vitamin B12 (pernicious anemia) or in other diseases that affect the usual absorption sites in the terminal ileum, oral therapy remains effective.
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            Challenges in the identification of cobalamin-deficiency polyneuropathy.

            Diagnosing cobalamin (Cbl) deficiency as a cause of polyneuropathy (PN) is problematic, as the frequency of both disorders increases with age, and serum Cbl levels can be difficult to interpret. To identify unique clinical or laboratory features among PN patients with Cbl deficiency and to examine the role of testing of serum metabolite levels in the identification of Cbl deficiency. Cohort survey comparing patients with Cbl deficiency and cryptogenic PN identified during a 2-year period. Cobalamin deficiency was diagnosed using low serum Cbl levels or elevated serum methylmalonic acid or homocysteine levels. Academic neuromuscular clinic. Of 324 PN patients, 27 were diagnosed as having Cbl deficiency. Twelve had Cbl levels within the normal range, but elevated serum metabolite levels. Compared with patients with cryptogenic sensory/sensorimotor PN, those with Cbl deficiency were more likely to have concomitant involvement of the upper and lower extremities and experience symptom onset in the hands and a sudden onset of symptoms (P<.005). These differences were seen regardless of whether Cbl deficiency was defined using low Cbl levels or elevated serum metabolite levels. Autoimmune pernicious anemia was identified in 6 (50%) of 12 Cbl-deficient patients with normal serum Cbl levels. The patients with PN and Cbl deficiency showed little objective improvement after parenteral replacement therapy; however, progression occurred less often in these patients compared with those with cryptogenic sensory/sensorimotor PN (P =.02). This study highlights the challenges of proving that Cbl deficiency is the cause for PN and identifies clinical features that suggest Cbl-deficiency PN. Testing of serum metabolite levels may identify Cbl deficiency in some patients with normal serum Cbl levels.
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              Visual Evoked Responses in Pernicious Anemia

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                Author and article information

                Journal
                Pan Afr Med J
                Pan Afr Med J
                PAMJ
                The Pan African Medical Journal
                The African Field Epidemiology Network
                1937-8688
                08 March 2019
                2019
                : 32
                : 108
                Affiliations
                [1 ]Service de Neurologie, Hôpital Militaire Moulay Ismaïl, Meknès, Maroc
                Author notes
                [& ]Auteur correspondant: Maha Ait Berri, Service de Neurologie, Hôpital Militaire Moulay Ismaïl, Meknès, Maroc
                Article
                PAMJ-32-108
                10.11604/pamj.2019.32.108.17609
                6560986
                2a48ce63-c571-44fb-ad2e-62970b3dbfb4
                © Maha Ait Berri et al.

                The Pan African Medical Journal - ISSN 1937-8688. This is an Open Access article distributed under the terms of the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 14 November 2018
                : 16 February 2019
                Categories
                Case Series

                Medicine
                vitamin b 12 deficiency,biermer’s disease,neurological disorders,carence en vitamine b 12,maladie de biermer,troubles neurologiques

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