Search

The article focuses on the relationship between the use of metformin, a commonly prescribed medication for type 2 diabetes, and vitamin B12 deficiency among diabetic patients, highlighting the potential health implications. It discusses the mechanism behind vitamin B12 absorption, emphasizing how deficiency can impact metabolic and neurological health.

Vitamin B12 deficiency in early childhood is an important cause of neurodevelopmental delay and regression. Most of these cases occur in exclusively breast-fed infants of deficient mothers. Symptoms and signs of vitamin B12 deficiency appear between the ages of 2 to 12 months and include vomiting, lethargy, failure to thrive, hypotonia, and arrest or regression of developmental skills. Approximately one half of this cases exhibit abnormal movements, variously described as tremors, twitches, chorea, or myoclonus. Urinary concentrations of methylmalonic acid and homocysteine are characteristically elevated in vitamin B12 deficiency. Hyperglycinuria is sometimes present. The early diagnosis and treatment of vitamin B12 deficiency is crucial for significant neurological impairment and long-term prognosis. Treatment with vitamin B12 corrects these metabolic abnormalities very rapidly (within a few days). Vitamin B12 supplementation of pregnant women may prevent neurological and neuroradiological findings of the infants. Because of the importance of vitamin B12 in the development of the foetal and neonatal brain, vegetarian and vegan mothers should be aware of the severe and not fully-reversible damages caused by insufficient nutritional intake of vitamin B12 during pregnancy and lactation. Therefore, efforts should be directed to prevent its deficiency in pregnant and breastfeeding women on vegan diets and their infants. It is also important to take the nutritional history of both infants and their mothers for the early prevention and treatment. Here an interesting case of vitamin B12 deficiency in a 10-month-old boy presented with psychomotor regression, hypotonia and lethargy.

Vitamin B12 deficiency may present with gastrointestinal, haematologic, dermatologic and neuropsychiatric signs and symptoms. Skin hyperpigmentation is a dermatologic manifestation which may mimic the features seen in Addison´s disease. We report a case of a 33-year-old non-vegan man who presented with progressive darkening of his palms, knuckles and feet which was associated with anaemia. Low serum vitamin B12 levels coupled with characteristic morphology of peripheral blood smear and bone marrow aspirate were identified. An extensive work up to establish the cause of Vitamin B12 deficiency revealed Helicobacter pyloriassociated gastritis as the likely aetiology. The patient had significant reversibility of hyperpigmentation and normalisation of the haematological indices following parenteral vitamin B12 supplementation. This case highlights the need for a high index of suspicion when clinicians are faced with a case of hyperpigmentation, so that the appropriate treatment can be promptly instituted and the late irreversible complications of vitamin B12 deficiency prevented.

La carence en vitamine B12 demeure un trouble fréquent et potentiellement grave, notamment chez les sujets âgés de plus de 65 ans. Patients et méthodes : étude rétrospective, incluant tous les patients âgés de plus de 65 ans carencés en vitamine B12 et hospitalisés dans le service de gériatrie du centre hospitalier universitaire de Reims sur une période de cinq mois. Résultats : 23 patients inclus, sex-ratio de 1:1 (12 femmes et 11 hommes), l'âge moyen était de 83,9 ans (71-94), le taux moyen de cobalamine de 148,3 pg/mL. Une anémie était observée chez 61 % des patients, une macrocytose chez 26 % et une anémie macrocytaire chez 17 %. On notait 61 % de syndrome de non-dissociation de vitamine B12 de ses protéines porteuses, 13 % de dénutrition, 4 % de maladie de Biermer, et 22 % d'étiologie indéterminée. Cliniquement, aucun signe imputable à une carence en vitamine B12 n'a été observé. Conclusion : la carence en vitamine B12 reste donc un trouble difficile à gérer, en raison de sa pauvreté en termes de symptomatologie et de ses multiples étiologies. [ABSTRACT FROM AUTHOR]

A vitamin B12 deficiency in infants is rare, but may sometimes be seen in breastfed babies of strict vegetarian mothers. Vitamin B12, also known as cobalamin, is only found in meat and other animal products. Most babies have a sufficient supply as long as the mother was not deficient herself. Symptoms and signs of vitamin B12 deficiency appear between the ages of 2 to 12 months and include vomiting, lethargy, failure to thrive, hypotonia, and arrest or regression of developmental skills. Urinary concentrations of methylmalonic acid and homocystine are characteristically elevated in vitamin B12 deficiency. Early treatment for a vitamin B12 deficiency in an infant involves immediate administration of vitamin B12 to the baby and the breastfeeding mother. The infant and mother will each receive an injection of vitamin B12 containing 1,000 mcg or more of the vitamin, and the mother will continue to receive injections every month to raise her own stores. After the initial injection, the baby will often receive future vitamin B12 through food sources. We present a case of vitamin B12 deficiency in a 9-month-old girl presented with psychomotor regression, hypotonia and lethargy. The child was exclusively breast-fed from birth by a mother who was on strict vegetarian diet and belong to a low socio-economic status. Laboratory data revealed bicytopenia with macrocytic anemia and methylmalonic acid in the urine, consistent with vitamin B12 deficient anemia. The Brain CT revealed a cerebral atrophy and delayed myelination. Vitamin B12 supply was effective on anaemia and psychomotor delay. This case figures out the importance of an early diagnosis in front of psychomoteur regression and hypotonia, given the risk of incomplete neurologic recovery due to vitamin B12 deficiency mainly in the setting of maternal nutritional deficiency.

Aim: To study the epidemiological, clinical, paraclinical and therapeutic aspects of Biermer's disease in the hematology service of campus teaching hospital of Lomé. Method: This retrospective study was conducted in the laboratory service of the University Hospital campus in which there is a unit of clinical hematology. This study took place over a period of twelve years and has identified 13 patients (5 men, 8women). Patients were selected on the basis of clinical, paraclinical (blood cells count, bone marrow, dosage of vitamin B12 and the intrinsic factor antibody) and the therapeutic test. Results: The mean age was 53 years ranging from 32 to 68 years. There was a female predominance with a sex ratio of 0.6. Clinically, there was conjonctival palor and asthenia (92% each) followed by paresthesia (62%). The blood cell count essentially showed profound anemia (7g/dl on average), macrocytic (84,6%), normocytic (15,3%), bicytopenia (61,5%) and pancytopenia (23%). In all patients, the bone marrow study showed megaloblasts, the dosage of the vitamin showed a collapse of vitamin B12 (76,9%), and intrinsic factor antibody was positive (92,3%). The fibroscopy showed atrophic gastritis (76,9%), intestinal metaplasia (69,2%) and an absence of Helicobacter pylori. The evolution was favorable with parenteral B12 vitamin therapy for all patients. Conclusion: We recommend looking for iron deficiency during the follow-up and gastric biopsy even if no macroscopic lesions are found. [ABSTRACT FROM AUTHOR]

La maladie de Biermer est une gastrite atrophique auto-immune à l'origine d'une carence en vitamine B12. Une association avec des maladies auto-immunes est souvent observée dont l'hypothyroïdie est la plus fréquente. L'association d'une anémie de Biermer aux rhumatismes inflammatoires chroniques est néanmoins beaucoup plus rare. Nous rapportons un cas d'une association de la maladie de Biermer à une polyarthrite rhumatoïde (PR). [ABSTRACT FROM AUTHOR]

Introduction: MetforminHydrochloride is an antidiabetic used for many years, currently; it considered the first choice in treatment of type 2 diabetes (T2D). It decreases insulin resistance, does not induce hypoglycaemia, increases glucose utilization in the liver and skeletal muscle, and decreases hepatic glucose production. Its adverse effects (AE) are gastrointestinal, decrease in vitamin B12 absorption, abnormalities of hemogram and rarely skin reactions. The objective of this study was to report the type and frequency of AEs of Metformin Hydrochloride used in the therapeutic management of T2D patients admitted to the medical center and the diabetes home of Sidi Bel-Abbès in Algeria., Materials and Methods: A cross-sectional descriptive study was carried out over a period of four months, from January 1st, 2017 to April 30th, 2017, involving 130 patients treated with Metformin Hydrochloride consulting at Mimoun City Diabetes Home and Gambetta Diabetes Center in the town of Sidi Bel-Abbès. The primary outcome measure was the determination of the type and frequency of AEs related to normal dosages or overdose use of Metformin Hydrochloride in T2D. Data were collected from patient records, using a questionnaire, and analyzed using Statistical Package for the Social Sciences, version 20 software., Results: 130 patients were included, including 82 women, with a mean age of 51.08±8.85 years (30-66). One hundred and ninety-eight (198) AEs were reported, an average of 1.52 AEs per patient. Among them, 95 (47.98%) AEs are digestive disorders (30.77% of patients suffered from diarrhea, 10.77% had nausea and vomiting, 8.46% suffered from abdominal pain and bloating, 3.85% lost their taste, 7.69% complained of epigastric cramps and 11.54% of anorexia), 29 (14.65%) AEs are hypoglycaemia, 73 (36.87%) AEs are other symptoms and 1 (0.50%) EI is vitamin B12 deficiency and no cases of lactic acidosis or allergic reaction were reported. Five (3.85%) patients had a total and lasting intolerance to Metformin Hydrochloride leading to its discontinuation following persistent diarrhoea., Conclusion: AEs of Metformin Hydrochloride used in the management of T2D patients consulting at the medical center and the Diabetes home of Sidi Bel-Abbès are frequent. Digestive disorders were the most frequent, diarrhea was very frequent and led to discontinuation of treatment in 3.85% of T2D patients, followed by nausea and vomiting, then abdominal pain, bloating and epigastric cramps, and rarely taste metallic. Hypoglycaemia was frequent following its association with insulin, the onset of headaches and fatigue were frequent, but no case of lactic acidosis or allergic reaction was reported. Due to a lack of means, the dosage of homocysteine and methylmalonic acid had not been carried out to confirm the vitamin B12 deficiency in the patient whose level was less than 200ng/mL. A precise assessment of the imputability of reported AEs is necessary., (Copyright © 2022 Académie Nationale de Pharmacie. Published by Elsevier Masson SAS. All rights reserved.)

Résumé: Introduction: Le protoxyde d’azote est largement utilisé en anesthésie. Il est réputé inoffensif mais peut avoir des effets indésirables lorsqu’il est utilisé au long cours ou de manière répétée. Nous rapportons ici une observation de sclérose combinée de la moelle iatrogène liée à une carence en vitamine B12. Observation: Un jeune homme drépanocytaire homozygote SS de 20 ans, régulièrement hospitalisé pour des crises vaso-occlusives sévères, présentait des signes déficitaires sensitivomoteurs ascendants, secondairement associés à des troubles sphinctériens. Il était initialement traité comme un syndrome de Guillain-Barré. Des symptômes neurologiques persistants permettaient de diagnostiquer une sclérose combinée de la moelle, secondaire à une carence en vitamine B12 induite par l’usage répété de protoxyde d’azote lors d’accès douloureux. Conclusion: L’utilisation large du protoxyde d’azote dans la prise en charge des crises vaso-occlusives drépanocytaires ne doit pas faire méconnaître ses risques potentiels notamment neurologiques. [ABSTRACT FROM AUTHOR]

Copyright of Bulletin de la Société de Pathologie Exotique is the property of John Libbey Eurotext Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of IBS, Immuno-analyse & Biologie Specialisee is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Summary: Vitamin B12, or cobalamin, deficiency is often unrecognized because the clinical manifestations are subtle; they are also potentially serious. We report a case of pseudothrombotic microangiopathy related to cobalamin deficiency. Vitamin B12 deficiency, which is more commonly recognized in the context of malnutrition, should be considered in the context of microangiopathy. [ABSTRACT FROM AUTHOR]

Abstract: Purpose: The high incidence of cobalamin (vitamin B12) deficiency results in frequent dosages of this vitamin in a department of internal medicine may reveal paradoxically high blood levels of cobalamin. The objective of the study was to estimate underlying diseases and potential diagnostic relevance of high cobalamin blood levels in internal medicine. Methods: A retrospective study was conducted, including in-patients from December 2005 to July 2006 presenting high cobalamin blood levels, as determined with our laboratory normal values (200–950pg/mL). Results: High cobalamin blood level is not unusual (18.5% of all dosages) and, most of time, it is associated with one or several diseases, among which acute and chronic liver diseases (often of alcoholic origin), various neoplasias, malignant hemopathies (myelodysplasia, myeloproliferative diseases, multiple myeloma), renal insufficiency and transient hematologic abnormalities (neutrophilic hyperleucocytosis, hypereosinophilia). Vitamin B12 supplementation and chronic myeloid leukemia represent less than 5% of all hypervitaminemia. There is no correlation between the level of cobalamin blood level and the number of underlying diseases for each patients. However, very high cobalamin blood levels (>1275pg/mL) are significantly associated to malignant hemopathies (p <0.05). It is noteworthy that most of diagnosed neoplasia were unknown and at a non-metastatic stage. Conclusion: Very high cobalamin blood levels are significantly associated to malignant hemopathies among the population of a department of internal medecine. Referent laboratory should actively advertise the numerous diseases involved with high cobalamin blood levels. [Copyright &y& Elsevier]

Abstract: The newborn’s vitamin B12 storage exclusively comes from placenta transfer, later from animal food.We relate 3 observations of infants (3-11-13 months) with failure to thrive, anorexia, vomiting and for the two olders refusal of weaning, associated with psychomotricity regression and hypotony. Blood cell count showed a macrocytosis without anemia (case 2-3) and a severe microcytic anemia for the first case caused by a mild α-thalassemia, with megaloblastic bone marrow. Vitamin B12 levels were very low associated with increased methylmalonic acid and homocysteine serum levels wich confirm the diagnostic . Cerebral imaging showed diffuse cortical atrophy. Cobalamin deficiency was caused by strict vegetarian diets mothers of breastfed infants (cases 2-3) and for younger by mother’s unrecognized pernicious anemia. 3 mothers had no anemia and normal B12 ‘s levels at diagnosis. Vitamin B12 supply lead to a rapid clinical and hematologic improvement. In two cases, neurologic recovery was incomplet. About one hundred case of B12 deficiency ‘s infant are reported, 2/3 are breast-fed by vegetarian mothers, and 1/4 have mothers with pernicious anemia. The failure to thrive is due to anorexia, refusal of weaning and partial villous atrophy. Neurologic manifestations are secondary to cerebral disorders, sometimes revealed by an exposure to anesthetic nitrous oxyd. The macrocytic anemia is inconstant. The etiologic research of developmental delay in an infant may include vitamin B12’s deficiency, even if there is no haematologic signs, especially if breast-fedding ‘s mothers is vegetarian. [Copyright &y& Elsevier]

Abstract: Purpose: During last decades, several progresses have been made in the diagnosis of cobalamin (vitamin B12) deficiency. Routine used of cobalamin standardized assays have potentially modified the frequency and the type of hematologic abnormalities. Current knowledge and key points: Current studies on cobalamin deficiency, including more precise definitions and the description of new etiologies of cobalamin deficiency in adults, as the food-cobalamin malabsorption syndrome, show that hematological abnormalities are generally incomplete compared to historical descriptions of megaloblastic anemia. Nevertheless, they include severe manifestations in 10% of the patients: pancytopenia, severe anemia (hemoglobin < 6 g/dl) or hemolytic anemia and pseudo thrombotic microangiopathy related to cobalamin deficiency. These studies also show the efficacy of new treatment modalities including oral cobalamin administration. Prospects and projects: Future studies will confirm these data with the routine use of the new cobalamin assay: holotranscobalamine and validate the usefulness of oral cobalamin therapy. [Copyright &y& Elsevier]

Abstract: Purpose. – Neurological symptoms of B12 vitamin deficiency are polymorph. Causes are dominated by Biermer''s disease and B12 vitamin non dissociation that is frequent in the elderly. Methods. – We realized a retrospective study during 11 years. Patients with neurological symptoms associated to megaloblastosis were included. Treatment with B12 vitamin lead to haematological manifestation regression. Results. – 26 cases were analyzed. Mean age was 50±14.5 years and there were 11 women and 15 men. Neurological signs included combined medullar sclerosis (N =10), peripheral neuropathy (N =10), isolated paresthesia (N =5) and inferior limb pyramidal syndrome (N =1). Neurological signs revealed vitamin B12 deficiency in 4 cases. Mean haemoglobin rate was 6.2±2.6 g/dl, mean MCV was 109±56 fl. Eight patients had macrocytic anaemia, nine bicytopenia and eight deep pancytopenia. Electromyography (N =8) confirmed neuropathy and medullar MRI (N =2) showed antero-posterior cordonal demyelisation of cervico-dorsal medulla. Causes of B12 vitamin deficiency were Biermer''s disease (N =11), non dissociation of B12 vitamin''s syndrome (N =8) and partial gastrectomy (N =1). In 6 patients, no aetiology was found. Treatment with parenteral vitamin B12 induced neurological symptoms regression in 14 cases. Patient with neurological disorder had significantly higher platelet count and haemoglobin level as compared with patients without neurological disorder. Reticulocyte crisis was more precocious in patients with neurological disorders. Conclusion. – Neurological symptoms in vitamin B12 deficiency are frequent. We insist on isolated forms, inaugural forms and on the interest of medullar MRI for early diagnosis. [Copyright &y& Elsevier]

Abstract: Purpose. – Update of the adult cobalamin deficiencies. Current knowledge and key points. – More precise definitions establish the true cobalamin deficiencies and determine their real epidemiology. The current clinical data suggest the concept of food-cobalamin malabsorption as the leading etiology of cobalamin deficiency. The new features of cobalamin deficiency include neurological, gynecological and vascular manifestations. Current treatment modalities include nasal, sublingual and oral cobalamin administration. Prospects and projects. – Studies are in the way to establish the relevance of the new clinical manifestations and to validate the usefulness of oral cobalamin therapy. [Copyright &y& Elsevier]

Abstract: Objective. – To describe an electroclinical presentation of a peripheral neuropathy in a patient who suffered from vitamin B12 deficiency. Patient and methods. – We report the case of a 56-year-old man who, 17 years after a subtotal gastrectomy, presented with a diffuse sensory-motor demyelinating peripheral neuropathy with multifocal alteration of conduction confirmed by electromyography. Its causal relationship with vitamin B12 deficiency was biologically demonstrated. This neuropathy improved within a few days after intramuscular hydroxocobalamin treatment. Both clinical and electrophysiological signs had totally disappeared 3 months later on. Conclusion. – This observation demonstrates that, in spite of its poor outcome reported by several authors, peripheral neuropathy induced by vitamin B12 deficiency can recover completely with substitutive treatment. [Copyright &y& Elsevier]

Purpose. – Approximately 15% of people over 60 years old have a cobalamin (Cbl) deficiency in relation with a food-cobalamin malabsorption (FCM). But to date, only case reports or small series have been reported. The aim of this study was to describe the clinical characteristics of the FCM in old subjects.Methods. – Sixty patients, at least 65 years old, presenting a Cbl deficiency related to FCM, were extracted from a cohort study of the Hoˆpitaux universitaires de Strasbourg, France (n = 169). All these patients had an established diagnosis of Cbl deficiency and met the Carmel's criteria of FCM. Their clinical data were retrospectively analysed.Results. – The median age of the 60 patients was 75 years and the female/male ratio was 2.3. The principal clinical symptoms were peripheral neuropathy (35%), confusion and dementia (30%) and anemia-related manifestations such as asthenia and edemas of the legs (20%). Average hemoglobin was 10.7 ± 2.5 g/dl and average mean erythrocyte cell volume was 95.5 ± 13.8 fl. There was an anemia, a leucopenia, a thrombocytopenia and a pancytopenia in respectively 27%, 18%, 15% and 8% of the cases. Average serum vitamin B12 and homocystein levels were with 138 ± 42 pg/ml and 22.5 ± 15.2 μmol/l. No patient had anti-intrinsic factor antibody and the Schilling's test was normal in all patients. Main disorders associated with FCM were atrophic gastritis (59%), long-term metformin or antiacid intake (17%), chronic alcohol intake (8%) and idiopathic FCM (n = 10). Sixteen patients have been successfully treated with oral crystalline cyanocobalamin (500 ± 280 μg/d).Conclusions. – This study shows that: firstly, the Cbl deficiency related to FCM may be responsible of severe neurological and hematologic manifestations in approximately 20% of the elderly patients; secondly, the disorders associated with the FCM are multiple in old age, with mainly atrophic gastritis; and thirdly, in clinical practice, oral cyanoCbl treatment may be successful. [Copyright &y& Elsevier]

Introduction. – Cobalamin deficiency is common in the elderly. However, most of the patients are asymptomatic or present with few symptoms. A subacute combined degeneration of the spinal cord accounts for only 10% of the neurological complications. Revealing forms of this myelopathy are exceptional, and were rarely documented by magnetic resonance imaging (MRI) study.Exegesis. – We report a case of subacute combined degeneration of spinal cord in an 81-year-old woman evaluated by a spinal cord MRI. We discuss the role of the spinal cord radiographic study in the diagnosis, the etiopathogeny of cobalamin deficiency and the benefit of vitamin supplementation even at a late stage of the disease in geriatrics patients.Conclusion. – The spinal cord MRI is useful in the diagnosis of late-form combined spinal cord degeneration. The high frequency of atrophic gastritis in elderly prevents the identification of a deficiency of the cobalamin etiology. The treatment relies on vitamin therapy even in the late stages. The severe disability of cobalamin deficiency neurological complications must encourage an earlier diagnosis in elderly patients. [ABSTRACT FROM AUTHOR]

Résumé La carence en vitamine B12 reste une anomalie biologique fréquente chez le sujet âgé. Elle relève de divers mécanismes, dont l’infection à Helicobacter pylori . Nous rapportons le cas d’une patiente de 85 ans chez laquelle une carence en vitamine B12 était diagnostiquée, sans retentissement clinique et biologique (absence d’anémie, absence de macrocytose). Le bilan étiologique utilisant la sérologie objectivait une infection à H . pylori . Un traitement séquentiel par inhibiteurs de la pompe à protons et antibiothérapie était prescrit, associé à un apport en vitamine B12 per os. La sérologie est un moyen simple, peu coûteux et non invasif pour diagnostiquer une infection à H . pylori . Il est essentiel chez les sujets âgés fragiles. Cet examen est adapté au bilan étiologique d’une carence en vitamine B12 inexpliquée. Les recommandations actuelles soutiennent l’idée qu’une quadrithérapie est plus efficace que la trithérapie actuelle. Vitamin B12 deficiency is a common abnormality in the elderly under various mechanisms, including infection with Helicobacter pylori . Thus, we report the case of an 85-year-old patient to whom a vitamin B12 deficiency was diagnosed without clinical and biological impact (no anemia, no macrocytosis). The etiological assessment objectified H . pylori infection, through the use of serology. A sequential treatment, combining inhibitors of proton pump and antibiotics, this combined with an intake of vitamin B12 orally, was prescribed. Diagnostic methods are varied, including serology, which is very simple to perform, inexpensive and non-invasive, and essential in the frail elderly. Moreover, it is suitable in relation to etiological unexplained vitamin B12 deficiency. Current recommendations support the idea of a more efficient quadruple therapy than the current triple therapy, actually used. [ABSTRACT FROM AUTHOR]

Abstract: Imerslund-Gräsbeck disease is an autosomic recessive disease characterised by a megaloblastic anemia due to a vitamin B12 deficiency and by a moderate proteinuria without kidney failure. It is caused by the malabsorption of Cobalamin-intrinsic factor complex bringing into play cubulin and other proteins (megaline, amnioless), some mutations of which are described at present. We report herein the observation of a child whose diagnosis was made belatedly during an acute decompensation with biological hemophagocytic syndrome. Its evolution was marked by the appearance of neurological disorders at the beginning of the vitamin B12 substitution treatment. These disorder regressed as the dosage was increase. The purpose of this observation is to recapitulate the main characteristics of this disease and to review the current data. [Copyright &y& Elsevier]

L’intérêt c’est de souligner l’importance du dosage de la vitamine B12 en cas d’anémie associée à d’autres signes notamment neurologiques chez l’enfant. Nous rapportons l’observation d’un nourrisson âgé de 4 mois allaité exclusivement au sein, admis pour vomissements chroniques installés depuis l’âge de 3 mois avec stagnation pondérale. L’examen clinique a révélé une hypotonie, un retard pondéral -2DS et une pâleur cutanéomuqueuse. L’hémogramme a objectivé une pancytopénie. Un médullogramme réalisé a montré une mégaloblastose. Les dosages de la vitamine B12 chez le nourrisson ainsi que chez la mère ont révélé des taux très effondrés. On a conclu à un déficit carentiel. Le nourrisson est mis sous traitement substitutif et la maman est adressée en médecine interne pour bilan étiologique de son déficit vitaminique. Conclusion: À partir de cette observation, nous mettons le point sur cette cause rare d’anémie carentielle chez le nourrisson et nous insistons sur le dosage de la vitamine B12 devant tout retard, stagnation ou régression du développement avec des signes neurologiques inexpliqués. [ABSTRACT FROM AUTHOR]

Aims: To study the epidemiological, clinical, paraclinical and therapeutic aspects of Biermer's disease in the hematology service of campus teaching hospital of Lomé., Method: This retrospective study was conducted in the laboratory service of the University Hospital campus in which there is a unit of clinical hematology. This study took place over a period of twelve years and has identified 13 patients (5 men, 8women). Patients were selected on the basis of clinical, paraclinical (blood cells count, bone marrow, dosage of vitamin B12 and the intrinsic factor antibody) and the therapeutic test., Results: The mean age was 53 years ranging from 32 to 68 years. There was a female predominance with a sex ratio of 0.6. Clinically, there was conjonctival palor and asthenia (92% each) followed by paresthesia (62%). The blood cell count essentially showed profound anemia (7g/dl on average), macrocytic (84,6%), normocytic (15,3%), bicytopenia (61,5%) and pancytopenia (23% ). In all patients, the bone marrow study showed megaloblasts, the dosage of the vitamin showed a collapse of vitamin B12 (76,9%), and intrinsic factor antibody was positive (92,3%). The fibroscopy showed atrophic gastritis (76,9%), intestinal metaplasia (69,2%) and an absence of Helicobacter pylori. The evolution was favorable with parenteral B12 vitamin therapy for all patients., Conclusion: We recommend looking for iron deficiency during the follow-up and gastric biopsy even if no macroscopic lesions are found., (Le comitée de rédaction se réserve le droit de revoyer aux auteurs avant toute soumission à l'avis des lecteurs les manuscrits qui ne seraient pas conformes à ces modalités de présentation. En outre il leur conseille de sonserver un examplaire du manuscrit, des figures et des tableaux.)

A 58 year old woman presents with a progressive fatigue and dyspnea associated with paresthesia. Laboratory tests show pancytopenia with hypersegmented neutrophiles, macrocytic hyporegenerative anemia and arguments for hemolysis, in particular highly increased LDH. This constellation strongly suggests vitamin B12 deficiency, which was confirmed with an undetectable cobalamine concentration in the blood of our patient. The etiologic work up shows the presence of anti-parietal cells antibodies at a titer of 1/640, diagnostic of Biermer anemia.

Introduction: Le traitement des patients diabétique de type 2 (DT2) par metformine augmente le risque de carence en vitamine B12 (Vit B12), déficit susceptible d’entraîner des taux plus élevés d’homocystéine plasmatique. Les conséquences cliniques n’ont jamais été évaluées. Patients et méthodes: Dans cette étude transversale, nous avons regardé si la carence en Vit B12 et l’hyperhomocystéinémie observées chez des patients DT2 traités par metformine avaient un impact sur la prévalence de l’ischémie myocardique silencieuse (IMS). Résultats: Notre population comporte 645 patients DT2 (266 femmes/379 hommes, âge 62,5 ± 9,2 ans, ancienneté du diabète 12,9 ± 9,2 ans, IMC 30,4 ± 5,5 kg/m2, HbA1c 8,2 ± 1,5%), avec > = 1 facteur de risque associé, ayant bénéficié d’un dépistage d’IMS par scintigraphie myocardique sensibilisée par épreuve d’effort et dipyridamole. Les patients traités par metformine (64,2%, N = 414) présentaient plus fréquemment une carence en Vit B12 définie par une valeur < 150 pmol/l (12,9% vs 5,6% p < 0.01). Ce risque persistait après ajustement sur sexe, tabac, IMC, âge, ancienneté du diabète, fonction rénale et rapport ASAT/ALAT (OR = 2,76, IC95% = 1,25 ; 6,09). La carence en Vit B12 chez les patients traités par metformine était associée à une hyperhomocystéinémie (18,0 vs 13,8 μmol/L, p < 0,001) mais pas à une augmentation du risque d’IMS (7,8 vs 14,4%, OR = 0,43, IC95% = 0,17 ; 1,13, p = 0,08). La carence en Vit B12 n’était pas non plus associée à un risque d’anémie (26% vs 22% p = 0,50) ni de macrocytose (4% vs 2% p = 0,36). Conclusion: Dans ce travail, nous confirmons l’association entre traitement par metformine, carence en Vit B12 et hyperhomocystéinémie. L’absence d’association avec l’IMS et l’anémie rassurent sur le risque cardiovasculaire potentiellement lié à ces perturbations biologiques. [Copyright &y& Elsevier]

Objectif: Mettre le point sur une cause rare de pan cytopénie chez l’enfant. Observation: II s’agit d’une fille âgée de 12 ans, sans antécédents notables, hospitalisée pour une pan cytopénie découverte sur un hémogramme pratiqué devant une pâleur et un ictère. Le bilan d’admission montrait une anémie sévère à 2,9g/dl, une leucopénie à 2700/mm3 et une thrombopénie à 78 000/mm3. Le myélogramme montrait une moelle moyennement riche avec érythroblastose macrocytaire, des signes d’asynchronisation de maturation nucléo cytoplasmique, des corps de Joly et des mitoses anormales. L’ensemble évoquait une pan cytopénie carentielle. Le dosage vitaminique a mis en évidence une baisse du taux de vitamine B12 avec un taux normal des folates. L’évolution sous suplémentation en vitamine B12 était favorable avec un recul de 8 mois. Conclusion: La responsabilité d’une carence en vitamine B12 doit être systématiquement évoquée devant une pan cytopénie. Les dosages vitaminiques et le traitement d’épreuve sont d’un grand apport pour le diagnostic. [ABSTRACT FROM AUTHOR]