Anemia

Pernicious anemia

Anemia
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Pernicious anemia
foto de Ignacio Antépara Ercoreca Ph.D.
Written by

Ignacio Antépara Ercoreca Ph.D.
Medically reviewed by our Medical staff

Last update: 31-08-2021

How else can it be called?

  • Biermer's disease

  • Megaloblastic anemia due to vitamin B12 deficiency

  • CIE-9: 281.0

  • CIE-10: D51.0

What is pernicious anemia?

Pernicious anemia is a disorder caused by the lack of vitamin B12 due to the absence of intrinsic factor in the stomach. The absence of intrinsic factor prevents the absorption of vitamin B12.

Anemia is a condition caused by a low level of hemoglobin in the bloodstream. Hemoglobin is an essential component of red blood cells (RBCs), whose deficit prevents the correct supply of oxygen to cells and tissues of the body.

Vitamin B12 (also known as cobalamin) is necessary for the synthesis and production of blood cells in the bone marrow. Because stem cells in the bone marrow must quickly multiply to produce red blood cells, a lack of vitamin B12 can lead to anemia.

Vitamin B12 will bind to a specific protein, called intrinsic factor (or Castle's intrinsic factor), before being absorbed in the intestine. Intrinsic factor is secreted by the parietal cells of the stomach. When the stomach does not produce enough intrinsic factor, for example in case of gastric mucosa atrophy, the intestine cannot properly absorb vitamin B12 and it leads to pernicious anemia.

Pernicious anemia can be classified as a type of macrocytic anemia and also as a specific type of megaloblastic anemia.

What causes pernicious anemia?

In more than 90% of cases, the absence of intrinsic factor (or Castle's intrinsic factor) is caused by an autoimmune reaction.

The body produces antibodies that attack and destroy the parietal cells of the stomach. Once destroyed, these cells cannot secrete enough intrinsic factor for the absorption of vitamin B12.

Pernicious anemia may also be due to a genetic disorder.

The most common reasons that may result in a lack of vitamin B12 are:

  • Poor diet, especially vegetarian diets that lack vitamin B12.
  • Gastric bypass, which may decrease the production of hydrochloric acid, also necessary for the absorption of vitamin B12.
  • Stomach cancer (gastric cancer) or gastritis.
  • Bulimia or anorexia nervosa.

The incidence of autoimmune reaction is higher in adults between 50 and 60 years old.

Pernicious anemia due to a genetic disorder is more common in Northern Europe, while rare in black and Asian people.

What are the main symptoms of pernicious anemia?

The most common symptoms of pernicious anemia are:

  • Anemia symptoms such as weakness, fatigue or headache.
  • Pale skin.
  • Tongue disorders: glossitis, redness at the tip and edges of the tongue, etc.
  • Loss of appetite and loss of weight.
  • Tingling and numbness in hands and feet (paresthesia).
  • Neurological disorders (dementia, ataxia, gait abnormalities, etc.).

How can it be detected?

A blood test is needed to determine levels of vitamin B12.

Another test frequently used for diagnosis is the Schilling test with radioactive vitamin B12 to assess the absorption of vitamin B12.

A bone marrow test can also be used for diagnosis.

What is the recommended treatment?

There is no cure for pernicious anemia, but the symptoms may be relieved with a lifelong vitamin B12 supplementation.

Vitamin B12 supplement is given by intramuscular injection. The frequency of the injections will depend on the severity of the disease.

Once the disorder is diagnosed, the common frequency has been a daily injection for 7 days, then a weekly injection for a month, and finally a monthly injection for the rest of the life.

Pernicious anemia increases the risk of suffering stomach cancer, heart failure, and male impotence.

Medically reviewed by our Medical staff on 31-08-2021

Bibliography

  • Hematology and Oncology (3rd Ed) 2017, Dan L. Longo, ISBN: 978-1-25-983582-7, Pag. 103.
  • Oxford Handbook of Clinical Immunology and Allergy (3rd Ed) 2013, Gavin P Spickett, ISBN: 978–0–19–960324–4 Pag. 182.

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