Macrocytosis is defined as having the mean corpuscular volume (MCV) ≥ 100 fL. This study assessed hematinic deficiencies and pernicious anemia (PA) in oral mucosal disease patients with macrocytosis.Macrocytosis is a blood condition in which erythrocytes are larger than normal. It has been defined as having the mean corpuscular volume (MCV) ≥ 100 fL. Patients with macrocytosis may or may not have anemia. In fact, erythrocytes of newborns, infants, and women during pregnancy tend to be larger than normal adult erythrocytes. Macrocytosis with associated anemia (macrocytic anemia) can be divided into megaloblastic and nonmegaloblastic anemia, based on the examination of the bone marrow. The etiologies of macrocytic anemia include nutritional deficiencies (vitamin B12 and folic acid), drugs (e.g., chemotherapeutic, antiretroviral, and antimicrobial agents), primary bone marrow disorders (e.g., myelodysplasia and leukemia), and other chronic illness (such as alcoholism and hypothyroidism). As multiple causes are involved in macrocytosis, it is important to determine the pivotal cause of macrocytosis for giving each macrocytosis patient an appropriate treatment. Folic acid deficiency results from poor nutritional intake, malabsorption, hepatobiliary dysfunction, increased folate catabolism, and medication (e.g., methotrexate, 5-fluoro-uracil, phenytoin, etc.). Causes of vitamin B12 deficiency include inadequate intake (especially for strict vegetarians), food-bound vitamin B12 malabsorption (for those with prolonged use of proton pump inhibitors or histamine H2 receptor blockers), lack of intrinsic factor or parietal cells (for patients with pernicious anemia, atrophic gastritis, or gastrectomy), ileal malabsorption (for patients with enteritis or ileal resection), biologic competition (including bacterial overgrowth and tapeworm infestation), and defective transport (such as transcobalamin II deficiency). 

The intrinsic factor, which is produced by the parietal cells of the stomach lining, can avidly bind dietary vitamin B12. The vitamin B12-intrinsic factor complex is carried to the terminal ileum, where it is absorbed after binding to intrinsic factor receptors on the luminal membranes of ileal cells. Vitamin B12 deficiency may lead to pernicious anemia (PA). In PA patients, there are two mechanisms that cause the intrinsic factor deficiency or inactivation: (1), ∼85% of PA patients possess the gastric parietal cell antibodies (GPCA) that induce destruction of parietal cells and in turn result in failure of intrinsic factor production;5, 6 (2) 40–80% of PA patients have intrinsic factor antibodies that bind to the vitamin B12-binding site of intrinsic factor and subsequently inactivate the vitamin B12 absorption-aiding function of intrinsic factor.

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Journal of  Autoimmune Disorders