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Does Anemia Affect The Nervous System

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Does Anemia Affect The Nervous System

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Received: 8 March 2022 / Revised: 8 April 2022 / Accepted: 14 April 2022 / Published: 17 April 2022

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Pernicious anemia remains an overlooked problem in many clinical settings and is underdiagnosed in many patients. It is associated with pernicious anemia but is different from autoimmune gastritis. Pernicious anemia occurs in the later stages of autoimmune atrophic gastritis when there is a deficiency of gastric intrinsic factor and therefore vitamin B.

Can be reduced. The multifactorial nature of pernicious anemia is related to the important part of cobalamin, which, when lacking, can lead to many problems, and therefore, the clinical presentation of proteiniform anemia is dangerous. Indeed, pernicious anemia can cause serious long-term problems related to nutrient deficiencies and their effects on the development of colon cancer and type 1 gastric neuroendocrine tumors. . If not detected in time or if pernicious anemia is diagnosed late, these problems can be life-threatening and sometimes irreversible. The purpose of the present review is to focus on the epidemiology, pathogenesis, and clinical presentation of pernicious anemia in an effort to look beyond the boundaries of medical expertise. It aims to address micronutrient deficiencies in addition to the well-known B vitamins

Deficiency, diagnosis of pernicious anemia, its long-term complications and appropriate medical management, and endoscopic examination of patients with pernicious anemia.

Atrophic gastritis; autoimmune gastritis; Light blue image; cobalamin; the eye; colon cancer; stomach neuroendocrine tumor; intestinal metaplasia; iron deficiency anemia; narrow-screen endoscopy; Pernicious anemia

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Pernicious anemia (PA) is an autoimmune disease, probably the most frequently diagnosed at this time, which is still neglected in many clinical situations and is not properly diagnosed in many patients.

PA is associated with autoimmune gastritis (AAG), but PA and AAG are not confused, since PA appears in the later stage of AAG when internal factors in the stomach are lacking and therefore B vitamins.

Many types of PA are related to the important component of cobalamin, the lack of which can lead to many problems from hematopoiesis to neurological, mental and reproductive problems. The pathogenesis of PA has not been elucidated, but it may be associated with autoimmune destruction of the gastric gland by autoimmune T lymphocytes in genetically susceptible individuals. An early stage of Helicobacter pylori infection has been hypothesized but has not been conclusively proven as a cause of gastric immunity cannot be excluded.

Importantly, PA can cause serious long-term problems that can be linked to micronutrient deficiency and the development of gastrointestinal neoplasms, in particular, colon cancer and type 1 diabetes. – neuroendocrine tumors. If it is not recognized in time or if PA is detected late, these complications can be life-threatening and sometimes irreversible.

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The current review aims to focus on the epidemiology, pathogenesis, and clinical presentation of PA in an effort to look beyond the boundaries of clinical expertise. In addition, it aims to address micronutrient deficiencies and malabsorption in addition to the well-known B vitamins.

Finally, it aims to focus on the diagnostic process in PA, from biochemical tests to high-quality endoscopy and histopathology, as well as long-term complications and proper medical management and endoscopic examination of patients those with PA.

(cobalamin) malabsorption due to lack of endogenous factor [1]. In general, it takes 10-12 years to develop PA with clinical symptoms, so PA can start with subclinical vitamin B.

Reduction [2]. PA, the main pathogenetic mechanism is AAG, a disease related to the specific body, characterized by the loss of gastric parietal cells involved in the production of intrinsic factor and hydrochloric acid by the gastric proton pump [3] . The presence of antiparietal cell antibodies (PCAs) is directed towards the gastric proton pump (gastric H.

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ATPase) as well as antibodies against intrinsic factor (IF) (although in low percentages) are often associated with gastric corpus atrophy and intrinsic factor deficiency. Atrophic corpus gastritis is a chronic disease defined by the reduction or loss of the first gastric glands, pseudo-pyloric or intestinal metaplasia or fibrosis [4]. Gastric corpus atrophy is a necessary but not sufficient factor for the initiation of PA, as gastric corpus atrophy can occur without PA. PA is often confused with B vitamins

Due to decreased gastric atrophy and/or intrinsic factor deficiency) or distortion of the AAG factor of the disease. PA is considered a late stage of AAG.

Epidemiological studies have shown that PA affects 0.1% of the entire population and 2-3% of people aged > 65 (ratio of women: men ~ 2: 1) [3]. PA can affect people of all ages, but its incidence usually increases with age. In recent Italian and Turkish studies, the average age of men affected by PA was around 49-55 years, compared to 40-61 for women [4, 5]. Similarly, in a prospective study of cobalamin status in the elderly that included 729 individuals (≥60 years of age), the overall number of previously undiagnosed PA was approximately about 2%, higher in black (4.3%) and white women (4.0%) [6]. Similarly, although PA tends to affect older Northern European women, recent studies have shown a higher prevalence of PA in other ethnic groups (eg, Caucasians, Africans, Americans), with ts’ the first infection of the disease [7].

In addition, PA associated with common immunodeficiency, low serum immunoglobulin levels, selective IgA deficiency, or childhood PA should be distinguished from chronic PA by the onset of symptoms and non-union and gastric corpus atrophy. . In particular, childhood PE is characterized by genetic failure to produce endogenous factor or endogenous factor secretion that is ineffective [8]. However, these types are very rare.

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From a clinical point of view, the fact that PA is often asymptomatic reduces the true bias of PA diagnosis and complications. A recent study on upper gastrointestinal symptoms in AAG involving 379 participants with symptoms reported the presence of PA in 53.6% of cases [9]. A systematic review of PA complications highlighted a cancer incidence of 2.4% and a gastric cancer incidence of 0.3/100 years [10]. About Vitamin B

It is estimated that 2.9%, 10.6%, or 25.7%, respectively; However, this analysis is not limited to PA but extends to all causes of B vitamins

Population blood pressure. A lower increase in PA was observed in Africans (although there is a deficiency of vitamin B.

Due to insufficient food intake) and more so in the population of Northern Europe (due to the prevalence of independent diseases) [12].

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Regarding chronic atrophic gastritis, 23.9% using serological tests and 33.4% using biopsy have been reported in the general population worldwide [13]. Similarly, although serological tests show a prevalence of AAG of 8-20%, studies reporting histological findings have estimated the prevalence to be 0.5-4.5% [14]. Similarly, AAG is often asymptomatic in the early stages, so it may be underestimated by epidemiological studies.

Until now, it remains difficult to draw firm conclusions about the actual incidence, prevalence, prevalence, and characteristics of PA, due to the lack of available reports, several methodological differences, and the lack of agree on the results. Larger, high-quality studies are needed to obtain a global and more accurate assessment of the true frequency and characteristics associated with PA. Table 1 Summary of key epidemiological data.

In PA, the gastric oxyntic mucosa is damaged with loss of parietal cells, which causes a deficiency of IF and hydrochloric acid (HCl), thus hindering the absorption of B vitamins.

And other nutrients (see paragraph 3 below). In general, PA is associated with the presence of autoantibodies against IF (IFA) and parietal cells (PCA), thus contributing to

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