What can pernicious anemia cause swelling

Pernicious anemia

The pernicious anemia, also called Biermer's disease, is a special form of vitamin B12 deficiency anemia. The cause is the lack of or reduced absorption of the vital vitamin.

What is pernicious anemia?

Pernicious anemia is megaloblastic, hypochromic anemia (anemia). Due to a disturbance in the gastric mucosa, the vitamin B12 cannot be absorbed in the small intestine. Since the liver can store large amounts of vitamin B12, pernicious anemia often only becomes noticeable years after the onset of the uptake disorder.


Vitamin B12 is an essential vitamin that plays an important role in many processes in the body. It is necessary for DNA synthesis, cell division and the formation of hormones. It also performs important tasks in the nervous system. The vitamin is mainly found in meat, especially in liver, but also in milk and eggs. Vitamin B12 is bound to proteins in these foods.

These compounds are dissolved by the stomach acid. The parietal cells of the gastric mucosa in turn produce another protein, the so-called intrinsic factor. Only when vitamin B12 is bound to this intrinsic factor can it be absorbed by the mucous membrane of the small intestine and thus get into the blood. A deficiency in intrinsic factor inevitably leads to a deficiency in vitamin B12.

The most common cause of an intrinsic factor deficiency is chronic type A gastritis. Type A gastritis is an autoimmune disease in which the body produces autoantibodies against the parietal cells, i.e. the cells that produce the intrinsic factor.

Another cause of intrinsic factor deficiency is gastric resection. Without a stomach, of course, no intrinsic factor production is possible. The daily requirement for vitamin B12 is around 3 µg. The liver can store up to 3mg of B12. Thus, even if no more vitamin B12 can be absorbed, symptoms of anemia will only occur 4-5 years later.

Symptoms and course

Typical symptoms of pernicious anemia:

  • neurological complaints

As mentioned at the beginning, vitamin B12 plays a role in DNA synthesis, cell division, blood formation and in protecting the nerve cords of the spinal cord and the brain. Vitamin B12 is also involved in the breakdown of homocysteine. Homocysteine ​​is a toxic intermediate product of protein metabolism, which is suspected to be involved in vascular calcification, heart attack or stroke.

A deficiency in vitamin B12 has many consequences. Pale skin, tiredness and poor concentration are typical symptoms.

As diverse as the functions of vitamin B12 are, the symptoms that show up in pernicious anemia are just as varied. A deficiency in vitamin B12 leads to a delay in the division of stem cells in the formation of red blood cells. Fewer erythrocytes (red blood cells) are produced than normal. These are also larger than normal and are therefore sorted out by the spleen at an early stage.

The result is anemia with typical symptoms such as paleness of the skin and mucous membranes, fatigue, poor performance, susceptibility to infections and an accelerated heartbeat. The increased breakdown of red blood cells can lead to a slight yellowing of the skin (jaundice). Swelling of the spleen and itching are also signs of this increased breakdown.

The disorders in the nervous system cause neurological complaints such as abnormal sensations, pins and needles, tingling, unsteady gait, nerve pain, muscle tremors or a disturbed vibration sensation.

Further consequences of the vitamin deficiency are particularly evident on the mucous membranes. Typical of pernicious anemia is the so-called glossitis Hunter, an inflammation of the tongue that manifests itself as a burning sensation and a strong reddening of the tongue. Torn corners of the mouth and difficulty swallowing can also be an indication of pernicious anemia.

If the pernicious anemia is based on type A gastritis, symptoms of this underlying disease will of course also appear. Above all, these include nausea and indigestion. If left untreated, pernicious anemia can lead to the most severe disorders such as paralysis, cerebral infarction or heart attack and is fatal.


A first suspected diagnosis of pernicious anemia can be made based on the symptoms of the underlying disease and the symptoms of vitamin B12 deficiency. The blood count shows a decreased vitamin B12 level. The red blood cells are enlarged and their number also decreased. The increased breakdown of erythrocytes increases indirect and direct bilirubin in the blood serum.

If pernicious anemia is suspected, the Schilling test is carried out. The patient is given an oral dose of radioactively labeled vitamin B12. The excretion in the urine is then checked. In pernicious anemia, excretion in the urine is reduced because the vitamin cannot be absorbed in the small intestine and consequently does not get into the blood and thus, in turn, does not get into the urine.

If it is suspected that the cause of the pernicious anomaly is type A gastritis, the determination of autoantibodies in the blood can also provide diagnostic reliability. In pernicious anemia, over 90% of those affected have parietal cell autoantibodies, i.e. antibodies against the intrinsic factor-producing cells.

Treatment and therapy

In most cases, the treatment of choice for pernicious anemia is lifelong parenteral substitution of vitamin B12. Parenteral literally means "past the intestine", which means that vitamin B12 is injected directly into the bloodstream.

Since around 1% of vitamin B12 can be absorbed in the small intestine without intrinsic factor, oral therapy is also possible. However, a minimum dose of 1000 µg per day is necessary here. It is also possible to supply intrinsic factor so that the B12 taken up through food can be absorbed in the small intestine.

In the case of chronic gastritis, cortisone can also be used to alleviate the inflammation of the gastric mucosa so that the parietal cells can recover and produce intrinsic factor. In the case of long-term inflammations, however, this is not particularly promising.

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Pernicious anemia can only be prevented by early detection of the underlying disease and rapid substitution of vitamin B12.


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  • Herold, G .: Internal Medicine. Self-published, Cologne 2013
  • Hahn, J.-M .: Checklist internal medicine. Thieme, Stuttgart
  • Siegenthaler, W. (Ed.): Siegenthaler's differential diagnosis internal diseases - from symptom to diagnosis. Thieme, Stuttgart 2005
  • Arastéh, K., et al .: Dual series. Internal Medicine. Thieme, Stuttgart 2013
This article has been written using the latest medical literature and sound scientific sources.
Quality assurance by: Dr. med. Nunmaker
Last updated on: October 30, 2018
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