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The patient with acute gastrointestinal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Rebecca Maindonald, Adrian Jugdoyal
Vitamin B12, ingested mainly through dietary protein, is an essential component to maintain normal red blood cell function. Vitamin B12 cannot be absorbed without intrinsic factor, secreted by parietal cells. Conditions resulting in an absence of intrinsic factor will lead to Vitamin B12 deficiency, resulting in a condition known as pernicious anaemia. This anaemia occurs when the body’s own immune system mistakenly attacks parietal cells, or a portion of the stomach is removed.
Immunopathology
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Pernicious anemia is a syndrome of gastric mucosal dysfunction and atrophy combined with a megaloblastic anemia and neurologic symptoms. A cellular immune reaction to gastric mucosal cells is responsible for gastric atrophy. Two major targets of autoantibodies are the a and β subunits of the gastric hydrogen-potassium ATPase. Symptoms also result from production of antibodies binding intrinsic factor. This is a secretory product of neck cells in the gastric glands, and is required for absorption of vitamin B12, a cofactor essential to a number of biochemical pathways. Antibodies binding intrinsic factor inhibit B12 uptake; deficiency of B12 leads to anemia and mixed neuropathy.
Megaloblastic Anemias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Pernicious anemia is the most common cause of decreased absorption of vitamin B12. Several other potential causes of defective absorption exist (Table 1), but are encountered in clinical practice only rarely. In fact, pernicious anemia is the most common cause of vitamin B12 deficiency in the United States. The fundamental defect in pernicious anemia is severe gastric atrophy, with loss of all gastric secretions including intrinsic factor, the presence of which is necessary for absorption of vitamin B12. Pernicious anemia is a disease of insidious onset that usually begins in middle age or later. It is rare under age 30, although children can be affected (juvenile pernicious anemia). It is found in all ethnic groups. Pernicious anemia is currently believed to result from immunologically mediated destruction of gastric mucosa. There is a significant association of pernicious anemia with other autoimmune disorders such as Grave’s disease, Hashimoto thyroditis, and vitiligo.
Vitamin B12, homocysteine, and folic acid in patients suffering from bipolar disorders: Relationship with suicide
Published in The World Journal of Biological Psychiatry, 2023
Paola Mangiapane, Manuel Glauco Carbone, Alessandro Arone, Lucia Massa, Stefania Palermo, Walter Flamini, Elisabetta Parra, Benedetto Morana, Florinda Morana, Giovanni Bertini, Donatella Marazziti
Vitamin B12, also known as cobalamin, is a group-B vitamin regulating a variety of functions and requires dietary intake, as the human body cannot synthesise it (Watanabe and Bito 2018). Its sources include meat, eggs, legumes, some cheeses and others that influence its bioavailability (Allen 2010; Doets et al. 2013). Once ingested, B12 is released from animal proteins through the action of gastric factors, such as HCl and pepsin, and it is bound to a protein known as haptocorrin that is then destroyed in the intestine, thus allowing B12 to bind to a key glycoprotein, the intrinsic factor (IF) (Nielsen et al. 2012). The next step is the bonding of the B12-IF complex to the cubulin receptor in the ileum and then B12 gets transported to the plasma (Nielsen et al. 2012), where it is bound to transcobalamin and, to a greater extent, to haptocorrin, being then driven to cells or, alternatively, being stored in the liver (Carmel 2008; Stabler 2013; Miller and Green 2014).
Efficacy of B-vitamins and vitamin D therapy in improving depressive and anxiety disorders: a systematic review of randomized controlled trials
Published in Nutritional Neuroscience, 2023
Jaqueline G. Borges-Vieira, Camila K. Souza Cardoso
Second, absorption of vitamin B12 occurs through an active process in the distal ileum, first requiring intrinsic factor (IF) to form a complex before binding to receptors in the intestine and, after absorption, being converted to the coenzymes methylcobalamin and 5'-deoxyadenosylcobalamin. In IF deficiency, B12 absorption is compromised, as in autoimmune atrophic gastritis and gastrectomies, resulting in a lack of B12 absorption [38]. Celiac disease can also affect vitamin absorption, and B vitamins supplementation may be recommended to normalize plasma Hcy levels [104]. In addition, there is a need to investigate drug-nutrient interactions in psychiatric patients. For example, proton pump inhibitors and long-term use of metformin contribute to the risk of vitamin B12 depletion through inhibition of absorption [105,106]. Therefore, clinical conditions of malabsorption and long-term pharmacotherapy that affect B vitamins metabolism may lead to consequences on the Hcy regulation cycle generating hyperhomocysteinemia that has been consistently associated with depressive symptoms [36,107].
Clinical, immunological, and genetic features in 938 patients with autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED): a systematic review
Published in Expert Review of Clinical Immunology, 2021
Niusha Sharifinejad, Majid Zaki-Dizaji, Shafi Tebyanian, Hamed Zainaldain, Mahnaz Jamee, Fatema Sadaat Rizvi, Soheila Hosseinzadeh, Farimah Fayyaz, Haleh Hamedifar, Araz Sabzevari, Mojdeh Matloubi, Edyta Heropolitańska-Pliszka, Fatemeh Aghamahdi, Hassan Abolhassani, Gholamreza Azizi
We further analyzed the frequency of tissue-specific AAbs in patients with specific organ involvements, based on prior studies and available data. In patients presenting ADI compared to cases without this manifestation, 21-OHAb (40% vs. 14.5%, p < 0.001), 17-OHAb (17.9% vs. 1.8%, p = 0.003), SCCAb (24.6% vs. 1.8%, p < 0.001), and ACAb (11.3% vs. 5.5%, p = 0.200) were more frequent. Patients with HP had NALP5Ab (10.1% vs. 0%, p = 0.01) prevalently, in comparison to patients without HP. Previous AAbs were compared in presence and absence of gonadal failure, 21-OHAb (32.5% vs. 43%, p = 0.159), 17-OHAb (20.8% vs. 12.9%, p = 0.168), SCCAb (29.9% vs. 16.1%, p = 0.032), ACAb (10.4% vs. 9.7%, p = 0.878), and NALP5 (15.6% vs. 4.3%, p = 0.012). Hepatitis correlated with lower CYPAAb (15.8% vs. 17.9%, p = 0.736) and higher AADCAb (26.3% vs. 22.3%, p = 0.564) presence. Thyroid disorders associate with TPOAb (35.5% vs. 9%, p < 0.001) and TGAb (27.1% vs. 7.5%, p < 0.001). Vitiligo positively correlates with AADCAb (46.9% vs. 24.3%, p = 0.008) but not Tyrosine Hydroxylase Ab (0% vs. 6%, p = 0.155). Type 1 diabetes revealed significant connection with GADAb (62.5% vs. 17.3%, p < 0.001) and not Islet cell Ab (8.3% vs. 3.8%, p = 0.266). As reported, pernicious anemia is the main hematologic manifestation related to higher intrinsic factor (IF) presence (13.3% vs. 2.6%, p = 0.015).