ANEMIE BIERMER PDF

Pernicious anemia (also known as Biermer’s disease) is an autoimmune atrophic gastritis, predominantly of the fundus, and is responsible for a. Aka: Vitamin B12 Deficiency, Pernicious Anemia, B12 Deficiency, Cobalamin .. pernicieuse addisonienne, Anémie de Biermer SAI, Anémie addisonienne. Anemia is a state that occurs when hemoglobin (an iron-protein compound in red blood cells that transports oxygen) is decreased and your body has too few red.

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Its prevalence is 0. Given its polymorphism and broad spectrum of clinical manifestations, pernicious anemia is a great pretender. Its diagnosis must therefore be evoked and considered in the presence of neurological and hematological manifestations of undetermined origin. Biologically, it is characterized by the presence of anti-intrinsic factor antibodies. Treatment is based on the administration of parenteral vitamin B12, although other routes of administration eg, oral are currently under study.

In the present update, these various aspects are discussed ahemie special emphasis on data of interest to the clinician. PA is an autoimmune atrophic gastritis that causes a deficiency in vitamin B12 due to its malabsorption.

In recent years, this disease has gained renewed interest both in regard to its pathogenesis and clinical features as well as to its diagnosis and treatment. In the present update, these aspects will be discussed with a special emphasis on data of interest to the clinician. Pathologically, PA is characterized by at least the anemid elements:.

PA-associated type A atrophic gastritis is restricted to the fundus and gastric body. Early lesions are characterized by chronic inflammation in the submucosa that extends into the lamina propria of the mucosa between gastric glands, with a loss of both gastric and zymogene cells.

The architecture of the gastric body and fundus is comparable to newsprint paper because of the dramatic biermerr or absence of gastric glands.

In particular, the parietal cells and zymogenic cells are absent from the gastric mucosa and are replaced by intestinal metaplasia. Experimental murine models have contributed significantly to the knowledge of the pathogenesis of autoimmune gastritis. The potential role bidrmer Helicobacter pylori in the pathogenesis of autoimmune gastritis and PA has been explored and postulated in recent years.

However, because of the wide prevalence of infection by H. This is especially true given that recent murine studies on the association between H. From a clinical standpoint, it should also be noted that serologic testing for H.

In the later stages of the disease, the incidence of anti-GPC antibodies decreases due to the progression of autoimmune gastritis and a loss of GPC mass, as a result of andmie decrease in antigenic rate. Anti-IF antibodies do not appear to have a clearly defined pathogenic role in the development of gastritis.

Two types of autoantibodies have been described:. Anemia is the most frequently encountered clinical sign during PA, together with accompanying functional manifestations, depending on their severity.

It should also be noted at this juncture that incipient PA may be associated in young women with a tendency for microcytosis due to iron deficiency linked to achlorhydria-induced iron malabsorption, menstrual bleeding, and a failure to ibermer the year reserves of vitamin B Neurological signs usually generate a clinical picture of combined sclerosis of the spinal cord.

Disorders are usually predominant in the lower limbs. However, neurological signs are inconsistent along with a highly variable clinical spectrum ranging from optic neuritis to manifestations of depression.

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It should also be kept in mind that neurological manifestations may only partially regress despite prolonged and high-dose vitamin B12 therapy, leading to — at times — irreversible sequelae. Lastly, Table 2 summarizes other clinical manifestations in addition to the biedmer manifestations of PA, eg, thromboembolic events, atherothrombosis with cardiac myocardial infarction and brain ischemic stroke impairments via hyperhomocysteinemia, fertility problems, and recurrent abortions.

Genetic bbiermer to Bifrmer appears to be genetically determined, although the mode of inheritance remains unknown. Evidence ansmie the role of genetic factors includes familial co-occurrence of PA and its association with other autoimmune diseases. With regard to susceptibility to PA, the role of the human leukocyte qnemie system has been demonstrated for certain loci such as human leukocyte antigen B8 DR3. Comprehensive studies are currently ongoing in an attempt to identify other susceptibility genes, notably within the context of familial PA.

The somewhat subtle progression from autoimmune gastritis to PA can take 20—30 years or even more, given that vitamin B12 stores can last 5—10 years depending on the individual.

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Thus, surveillance by upper endoscopy is recommended, quarterly during the first year in the presence of neoplastic lesions, and less frequently thereafter in the absence of macroscopic or histological recurrence. In the absence of such lesions, biannual endoscopic surveillance is suggested, with multiple biopsies.

This low-grade malignancy of PA-related gastric carcinoid tumors leads to conservative treatments, eg, limited resection, with three main decision criteria according to Cattan: The recent disappearance of Schilling tests and the difficulty in finding a laboratory able to assess the secretion of IF have led clinicians to develop alternative diagnostic strategies as illustrated in Figure 1. Thus, diagnostic criteria have changed in recently published studies. Other criteria commonly used to diagnose PA vary in specificity and sensitivity, routine availability, or invasiveness.

The primary differential diagnosis of vitamin B12 deficiency in adults is food-cobalamin malabsorption syndrome of nondissociation of vitamin B12 from its carrier proteinsan entity that is the primary etiology of vitamin B12 deficiency in elderly subjects Figure 1. Low vitamin B12 intake is uncommon in industrialized countries, aside from strict vegans and newborns of vegan women. Ultimately, one should bear in mind that PA is a great pretender due to the similarity of presentation with other clinical conditions that can result in vitamin B12 deficiency.

The diagnosis should be considered when faced with any hematological and neurological manifestations. In most countries, treatment of vitamin B12 deficiency related to PA is based on parenteral vitamin B12 administered intramuscularly under the form of cyanocobalamin, hydroxocobalamin, or methylcobalamin. Attitudes regarding the dosage and frequency of administration are very different from one group to another.

Currently, it is always recommended to use the parenteral route in severe neurological forms. Alternatively, the oral route could curtail or avoid the inconvenience related to discomfort of injections and of likely higher costs nursing care. On a final note, the authors would like to draw the attention of the field practitioner to the need for annual monitoring of these patients to ensure therapeutic adherence the vitamin has to be administered for life and to detect neoplastic complications of PA endoscopy at least twice yearly in the absence of detectable lesions as well as associations with other autoimmune disorders.

This latter surveillance can be done without the need for a systematic comprehensive assessment but rather by tracking all abnormal complaints or clinical signs. Professor Andres is a member of the National Commission of Pharmacovigilance. The data developed herein are solely his personal opinion.

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He is an expert consultant to several laboratories involved in hematology Amgen, Roche, Chugai, GSK, Vifor Pharma, Ferring, Genzyme, Actelion, Given Imaging and has participated in numerous international and national studies sponsored by these laboratories or to academic works.

Vitamin B12 deficiency anemia – Wikipedia

The authors report no conflicts of interest in this work. National Center for Biotechnology InformationU. Journal List J Blood Med v. Published online Sep Emmanuel Andres 1, 2 and Khalid Serraj 3.

Author information Copyright and License information Disclaimer. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited. This article has been cited by other articles in PMC. Elements of pathogenesis for the clinician Pathologically, PA is characterized by at least the following elements: Two types of autoantibodies have been described: They are found in one-third of cases and only in patients who already have anti-type I antibodies.

Clinical manifestations Anemia is the most frequently encountered clinical sign during PA, together with accompanying functional manifestations, depending on their severity. All stages of erythroid maturation are represented but the asynchrony of nucleocytoplasmic maturation is marked by immature nuclei and an already acidophilic cytoplasm.

Open in a separate window. Table 2 Main clinical manifestations of vitamin B12 deficiency. Association with other autoimmune diseases Genetic susceptibility to PA appears to be genetically determined, although the mode of inheritance remains unknown. Neoplastic complications The somewhat subtle progression from autoimmune gastritis to PA can take 20—30 years or even more, given that vitamin B12 stores can last 5—10 years depending on the individual.

Vitamin B12 metabolism, etiological implications, and elements of clinical course. IF, intrinsic factor; HCl, hydrogen chloride.

Differential diagnosis of vitamin B12 deficiency The primary differential diagnosis of vitamin B12 deficiency in adults is food-cobalamin malabsorption syndrome of nondissociation of vitamin B12 from its carrier proteinsan entity that is the primary etiology of vitamin B12 deficiency in elderly subjects Figure 1. Treatment of vitamin B12 deficiency and optimal management In most countries, treatment of vitamin B12 deficiency related to PA is based on parenteral vitamin B12 administered intramuscularly under the form of cyanocobalamin, hydroxocobalamin, or methylcobalamin.

Vitamin B12 cobalamin deficiency in elderly patients. Cobalamin deficiencies in adults: Update of pernicious anemia. A retrospective study of 49 cases. N Eng J Med. Toh BH, Alderuccio F. Gastritis and pernicious anemia.

Optimal management of pernicious anemia

Animal models of human disease: Is there a link between the food cobalamin malabsorption and the pernicious anemia? Ann Endocrinol Paris ; 65 2: Anticorps anti-estomac [Anti-stomach antibodies] Rev Franc Allergol.

Dosage des anticorps anti-facteur intrinseque: Lahner E, Annibale B. Update of clinical findings in cobalamin deficiency: Combined sclerosis of aenmie spinal cord revealing B12 deficiency: Neurological manifestations of vitamin B12 deficiency: Homocysteine, vitamin B12, wnemie and cognitive functions: Int J Clin Pract. Pernicious anemia — genetic insights.

Prevalence of pernicious anaemia in patients with type 1 diabetes mellitus and autoimmune thyroid disease.

A propos de 10 observations [Multiple autoimmune syndrome: Humbert P, Dupond JL. Ann Med Interne Paris ; 3: HLA antigen expression in autoimmune endocrinopathies. Malabsorption of food cobalamin.