Immunofluorescence staining<unk> ttern of gastric<unk> rietal cell antibodies on a stomach section<unk>  is thought mainly to be an autoimmune disorder that attacks the gastric<unk> rietal cells that produce intrinsic factor resulting in impaired absorption of B12. However,<unk>  may also have a genetic component, potentially running in families.<unk>  may be suspected when a blood smear shows large, brittle, immature, erythrocytes, known as megaloblasts. To make a diagnosis a full blood count, and blood smear, with the following tests included is needed: * A complete blood count and blood smear evaluates the mean corpuscular volume (MCV) and the mean corpuscular hemoglobin concentration (MCHC) to demonstrate megaloblastic<unk> .<unk>  is identified with a high MCV (macrocytic<unk>  and a normal MCHC (normochromic<unk> . Ovalocytes are also typically seen on the blood smear, and a<unk> thognomonic feature of megaloblastic<unk> s (which include<unk>  and others) is hypersegmented neutrophils. * Vitamin B12 serum levels are used to detect its deficiency, but do not distinguish its causes. Vitamin B12 levels can be falsely high or low and data for sensitivity and specificity vary widely. Normal serum levels may be found in cases of deficiency where myeloproliferative disorders, liver disease, transcobalamin II deficiency, or small intestinal bacterial overgrowth are present. * Intrinsic factor and<unk> rietal cell antibodies – the blood is checked for antibodies against IF and<unk> rietal cells in the stomach. The presence of antibodies to gastric<unk> rietal cells and IF is common in<unk> .<unk> rietal cell antibodies are found in other autoimmune disorders and also in up to 10% of healthy individuals. However, around 85% of<unk> <unk> tients have<unk> rietal cell antibodies, which means they are a sensitive marker for the disease. Intrinsic factor antibodies are much less sensitive than<unk> rietal cell antibodies, but they are much more specific. They are found in about half of<unk> <unk> tients and are very rarely found in other disorders. These antibody tests can distinguish between<unk>  and food-B12 malabsorption. * Methylmalonic acid and/or homocysteine – vitamin B12 plays an important role in metabolic processes and cellular functions. Therefore, its deficiency leads to the accumulation of some metabolic products. Methylmalonic acid and/or homocysteine is one of the metabolic products that can be measured in the blood. as the increase in the levels of both helps differentiate between vitamin B12 deficiency and folic acid deficiency, because homocysteine alone increases in the latter. Elevated gastrin levels can be found in around 80–90% of<unk>  cases, but they may also be found in other forms of gastritis. Decreased pepsinogen I levels or a decreased pepsinogen I to pepsinogen II ratio may also be found, although these findings are less specific to<unk>  and can be found in food-B12 malabsorption and other forms of gastritis. The diagnosis of atrophic gastritis type A should be confirmed by gastroscopy and stepwise biopsy. About 90% of individuals with<unk>  have antibodies for<unk> rietal cells; however, only 50% of all individuals in the general population with these antibodies have<unk> . Forms of vitamin B12 deficiency other than<unk>  must be considered in the differential diagnosis of megaloblastic<unk> . For example, a B12-deficient state which causes megaloblastic<unk>  and which may be mistaken for classical<unk>  may be caused by infection with the tapeworm Diphyllobothrium latum, possibly due to the<unk> rasite's competition with host for vitamin B12. The classic test for<unk> , the Schilling test, is no longer widely used, as more efficient methods are available. This historic test consisted, in its first step, of taking an oral dose of radiolabelled vitamin B12, followed by quantitation of the vitamin in the<unk> tient's urine over a 24-hour period via measurement of the radioactivity. A second step of the test repeats the regimen and procedure of the first step, with the addition of oral intrinsic factor. A<unk> tient with<unk>  presents lower than normal amounts of intrinsic factor; hence, addition of intrinsic factor in the second step results in an increase in vitamin B12 absorption (over the baseline established in the first). The Schilling test distinguished<unk>  from other forms of B12 deficiency, specifically, from Imerslund–Gräsbeck syndrome, a B12-deficiency caused by mutations in CUBN that codes for cubilin the cobalamin receptor.
Pernicious anemia
Zinc deficiency
Iron poisoning
Zinc toxicity
Hookworm infection
Fruit allergy
Pinworm infection
African iron overload