Pernicious anemia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pernicious anemia (also known as Biermer’s anaemia or Addison’s anaemia or Addison-Biermer anaemia) is a form of megaloblastic anaemia due to vitamin B₁₂ deficiency dependent on impaired absorption of vitamin B₁₂ in the setting of atrophic gastritis, and more specifically of loss of gastric parietal cells. While the term “pernicious anaemia” is sometimes also incorrectly used to indicate megaloblastic anaemia due to any cause of vitamin B₁₂ deficiency, its proper usage refers to that caused by atrophic gastritis and parietal cell loss only.

Pernicious anemia is a decrease in red blood cells that occurs when the body cannot properly absorb vitamin B12 from the gastrointestinal tract. Vitamin B12 is necessary for the proper development of red blood cells.

Pernicious anemia is a type of megaloblastic anemia.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The treatment for pernicious anemia was first devised by George Whipple who bled dogs to make them anemic and then fed them various substances to see what (if anything) would make them healthy again. He discovered that ingesting large amounts of liver seemed to cure the disease. George Minot and William Murphy then set about to chemically isolate the curative substance and ultimately were able to isolate the vitamin BTemplate:Ssub from the liver. For this, all three shared the 1934 Nobel Prize in Medicine. As a result, pernicious anemia is now treated with either vitamin B12 injections, or large oral doses of vitamin B12, typically between 2 and 4 mg daily.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Vitamin B₁₂ cannot be produced by the human body, and must therefore be obtained from diet. Normally, dietary vitamin B₁₂ can only be absorbed by the ileum when it is bound by the intrinsic factor produced by parietal cells of the gastric mucosa. In pernicious anaemia, this process is impaired because of loss of parietal cells, resulting in insufficient absorption of the vitamin, which over a prolonged period of time ultimately leads to vitamin B₁₂ deficiency and thus megaloblastic anaemia.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Most commonly, the cause for impaired binding of vitamin B₁₂ by intrinsic factor is autoimmune atrophic gastritis, in which autoantibodies are directed against parietal cells (resulting in their loss) as well as against the intrinsic factor itself (rendering it unable to bind vitamin B₁₂). Less frequently, loss of parietal cells may simply be part of a widespread atrophic gastritis of non-autoimmune origin, such as that frequently occurring in elderly people affected with long-standing chronic gastritis of any cause (including Helicobacter pylori infection). Note that forms of vitamin B₁₂ deficiency other than pernicious anaemia must be considered in the differential diagnosis of megaloblastic anaemia.

• The body needs vitamin B12 to make red blood cells. To provide vitamin B12 to your blood cells, you need to eat enough foods containing vitamin B12, such as meat, poultry, shellfish, eggs, and dairy products. To absorb vitamin B12, your body uses a special protein called intrinsic factor, which is released by cells in the stomach. The combination of vitamin B12 bound to intrinsic factor is absorbed in the last part of the small intestine.

When the stomach does not make enough intrinsic factor, the intestine cannot properly absorb vitamin B12.

• Very rarely, infants and children are born without the ability to produce enough intrinsic factor, or the ability to absorb the combination of intrinsic factor and vitamin B12 in the small intestine. Pernicious anemia that occurs at birth (congenital) is inherited. You need the defective gene from each parent to get it.

• Common causes of pernicious anemia include:

• Atrophic Gastritis(weakened stomach wall)
• Autoimmunity against gastric parietal cells(The body’s immune system attacking the cells that make intrinsic factor or intrinsic factor itself)

• The disease begins slowly and may take decades to fully establish. Although the congenital form occurs in children, pernicious anemia usually does not appear before age 30 in adults. The average age at diagnosis is 60.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Risk factors include:

• Family history of the disease
• History of autoimmune endocrine disorders, including:

• Addison’s disease
• Chronic thyroiditis
• Graves disease
• Hypoparathyroidism
• Hypopituitarism
• Myasthenia gravis
• Secondary amenorrhea
• Type 1 diabetes
• Testicular dysfunction
• Vitiligo
• Scandinavian or Northern European descent

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

• People with pernicious anemia may have gastric polyps, and they are at increased risk for gastric cancer and gastric carcinoid tumors.

• Brain and nervous system (neurological) problems may continue if treatment is delayed.

• The outcome is usually excellent with treatment.

• Any damage to nerves may be permanent, especially if treatment is not started within 6 months of when symptoms began.

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