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Antipernicious Anemia Factor

Pernicious (per-nish-uhs) anemia, one of the causes of vitamin B12 deficiency, is an autoimmune condition that prevents your body from absorbing vitamin B12. Without adequate vitamin B12, you have fewer red blood cells carrying oxygen throughout your body. You can have pernicious anemia for several years before noticing changes in your body. Left untreated, pernicious anemia can cause serious medical issues, including irreversible damage to your nervous system. Healthcare providers treat pernicious anemia by prescribing vitamin B12 supplements.

antipernicious anemia factor


Yes. Normally, your body stores vitamin B12 that it gets from what you eat. Your body stores vitamin B 12, slowly using it over time. It can take three to five years for your body to use up your vitamin B12 reserves. After that, it can be several more years before you develop pernicious anemia symptoms.

Pernicious anemia symptoms can take years to surface. You may be surprised to learn you have a condition that can cause serious medical problems. Here are some questions you may want to ask your healthcare provider:

Pernicious anemia is a disease in which not enough red blood cells are produced due to a deficiency of vitamin B12.[5] Those affected often have a gradual onset.[5] The most common initial symptoms are feeling tired and weak.[4] Other symptoms of anemia may include shortness of breath, lightheadedness, headaches, sore red tongue, cold hands and feet, pale or yellow skin, chest pain, and an irregular heartbeat.[4] The digestive tract may also be disturbed giving symptoms that can include nausea and vomiting, heartburn, upset stomach and loss of appetite.[4] Symptoms of vitamin B12 deficiency may include decreased ability to think, numbness in the hands and feet, memory problems, blurred vision, trouble walking, poor balance, muscle weakness, decreased smell and taste, poor reflexes, clumsiness, depression, and confusion.[4] Without treatment, some of these problems may become permanent.[5]

Pernicious anemia refers to a type of vitamin B12 deficiency anemia that results from lack of intrinsic factor.[5] Lack of intrinsic factor is most commonly due to an autoimmune attack on the cells that create it in the stomach.[9] It can also occur following the surgical removal of all or part of the stomach or small intestine; from an inherited disorder or illnesses that damage the stomach lining.[9] When suspected, diagnosis is made by blood tests initially a complete blood count, and occasionally, bone marrow tests.[6] Blood tests may show fewer but larger red blood cells, low numbers of young red blood cells, low levels of vitamin B12, and antibodies to intrinsic factor.[6]

Because pernicious anemia is due to a lack of intrinsic factor, it is not preventable.[10] Pernicious anemia can be treated with injections or pills of vitamin B12.[7] If the symptoms are serious, injections are typically recommended initially.[7] For those who have trouble swallowing pills, a nasal spray is available.[7] Often, treatment may needed for life.[11]

Pernicious anemia due to autoimmune problems occurs in about one per 1000 people in the US. Among those over the age of 60, about 2% have the condition.[8] It more commonly affects people of northern European descent.[2] Women are more commonly affected than men.[12] With proper treatment, most people live normal lives.[5] Due to a higher risk of stomach cancer, those with pernicious anemia should be checked regularly for this.[11] The first clear description was by Thomas Addison in 1849.[13][14] The term "pernicious" means "deadly", and this term came into use because, before the availability of treatment, the disease was often fatal.[5][15]

Pernicious anemia often presents slowly, and can cause harm insidiously and unnoticeably. Untreated, it can lead to neurological complications, and in serious cases, death.[16] It can take several years for pernicious anemia to appear, and the disease often goes unrecognized, as the body becomes used to feeling unwell.[17]The onset may be vague and slow, as the same symptoms are often also present with anemia; in 81.1% of cases of cobalamin deficiency, pernicious anemia is not observed.[18] Pernicious anemia may be present without a person experiencing symptoms at first, over time, feeling tired and weak, lightheadedness, dizziness, headaches, rapid or irregular heartbeat, breathlessness, glossitis (a sore red tongue), poor ability to exercise, low blood pressure, cold hands and feet, pale or yellow skin, easy bruising and bleeding, low-grade fevers, tremor, cold sensitivity, chest pain, upset stomach, nausea, loss of appetite, heartburn, weight loss, diarrhea, constipation, severe joint pain, feeling abnormal sensations including tingling or numbness to the fingers and toes (pins and needles), and tinnitus, may occur.[19][20][21][22][23] Anemia may present with a number of further common symptoms,[19][24] including hair thinning and loss, early greying of the hair, mouth ulcers, bleeding gums,[20] angular cheilitis, a look of exhaustion with pale and dehydrated or cracked lips and dark circles around the eyes, as well as brittle nails.[21]

In more severe or prolonged cases of pernicious anemia, nerve cell damage may occur,[17] which can lead to more severe symptoms, including sense loss, difficulty in proprioception, neuropathic pain, difficulty walking, poor balance, loss of sensation in the feet, muscle weakness, blurred vision (either due to retinopathy[25] or optic neuropathy[26]), impaired urination, fertility problems, decreased sense of taste and smell, decreased level of consciousness, changes in reflexes, memory loss, mood swings, depression, irritability, cognitive impairment, trouble talking, confusion, anxiety, clumsiness, psychosis, and, in more severe cases, dementia.[19][20][21][22][23][27][28] Anemia may also lead to cardiac murmurs[22][21] and/or altered blood pressure (low or high). The deficiency may also present with thyroid disorders.[19] In severe cases, the anemia may cause congestive heart failure.[24] A complication of severe chronic PA is subacute combined degeneration of spinal cord, which leads to distal sensory loss (posterior column), absent ankle reflex, increased knee reflex response, and extensor plantar response.[29] Other than anemia, hematological symptoms may include cytopenias, intramedullary hemolysis, and pseudothrombotic microangiopathy.[1] Vitamin B12 deficiency, which is reversible, is occasionally confused with acute myeloid leukemia, which is an irreversible autoimmune condition presenting with some of the same hematological symptoms, including hypercellular bone marrow with blastic differentiation and hypersegmented neutrophils.[30] Pernicious anemia can cause osteoporosis and may lead to bone fractures.[31] Pernicious anemia can contribute to a delay in physical growth in children, and may also be a cause for delay in puberty for adolescents.[5]

Vitamin B12 cannot be produced by the human body, and must be obtained from the diet. When foods containing B12 are eaten, the vitamin is usually bound to protein and is released by proteases released by the pancreas into the small bowel. Following its release, most B12 is absorbed by the body in the small bowel (ileum) after binding to a protein known as intrinsic factor. Intrinsic factor is produced by parietal cells of the gastric mucosa (stomach lining) and the intrinsic factor-B12-complex is absorbed by enterocytes in the ileum's cubam receptors.[32][33] PA is characterised by B12 deficiency caused by the absence of intrinsic factor.[34] Other disorders that can disrupt the absorption of vitamin B12 in the small intestine include celiac disease, surgical removal of crohn's disease, and HIV.[35]

PA may be considered as an end stage of autoimmune atrophic gastritis, a disease characterised by stomach atrophy and the presence of antibodies to parietal cells and intrinsic factor.[36][37] Autoimmune atrophic gastritis, is localised to the body of the stomach, where parietal cells are located.[34] Antibodies to intrinsic factor and parietal cells cause the destruction of the oxyntic gastric mucosa, in which the parietal cells are located, leading to the subsequent loss of intrinsic factor synthesis. Without intrinsic factor, the ileum can no longer absorb the B12.[38] Atrophic gastritis is often a precursor to gastric cancer.[37]

Although the exact role of Helicobacter pylori infection in PA remains controversial, evidence indicates H. pylori is involved in the pathogenesis of the disease. A long-standing H. pylori infection may cause gastric autoimmunity by a mechanism known as molecular mimicry. Antibodies produced by the immune system can be cross-reactive and may bind to both H. pylori antigens and those found in the gastric mucosa. The antibodies are produced by activated B cells that recognise both pathogen and self-derived peptides. The autoantigens believed to cause the autoreactivity are the alpha and beta subunits of the sodium-potassium pump.[38][39] In a study, B12 deficiency caused by Helicobacter pylori was positively correlated with CagA positivity and gastric inflammatory activity, rather than gastric atrophy.[40] Less commonly, H. pylori and Zollinger-Ellison syndrome may cause a form of nonautoimmune gastritis that can lead to pernicious anemia.[41]

Impaired B12 absorption can also occur following gastric removal (gastrectomy) or gastric bypass surgery. In these surgeries, either the parts of the stomach that produce gastric secretions are removed or they are bypassed. This means intrinsic factor, as well as other factors required for B12 absorption, are not available. However, B12 deficiency after gastric surgery does not usually become a clinical issue. This is probably because the body stores many years' worth of B12 in the liver and gastric surgery patients are adequately supplemented with the vitamin.[42][43]

Although no specific PA susceptibility genes have been identified, a genetic factor likely is involved in the disease. Pernicious anemia is often found in conjunction with other autoimmune disorders, suggesting common autoimmune susceptibility genes may be a causative factor.[34] In spite of that, previous family studies and case reports focusing on PA have suggested that there is a tendency of genetic heritance of PA in particular, and close relatives of the PA patients seem to have higher incidence of PA and associated PA conditions.[44][45][46] Moreover, it was further indicated that the formation of antibodies to gastric cells was autosomal dominant gene determined, and the presence of antibodies to the gastric cells might not be necessarily related to the occurrence of atrophic gastritis related to PA.[44][46] 041b061a72


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