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Pernicious anemia

Pernicious anemia refers to a type of autoimmune anemia. Antibodies are directed against intrinsic factor or parietal cells which produce intrinsic factor. Intrinsic factor is required for vitamin B12 absorption, so impaired absorption of vitamin B12 can result. more...

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The term pernicious anemia is sometimes used more loosely to include non-autoimmune causes of vitamin B12 deficiency.

Diagnosis

Blood testing typically shows a macrocytic anemia, and low levels of serum vitamin B12. A Schilling test can then be used to distinguish between pernicious anemia, vitamin B12 malabsorption, and vitamin B12 deficiency. Approximately 90% of individuals with pernicious anemia have antibodies for parietal cells, however only 50% of individuals with these antibodies have the disease.

History

The treatment for pernicious anemia was first devised by William Murphy 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 George Whipple then set about to chemically isolate the curative substance and ultimately were able to isolate the vitamin B12 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 (hydroxocobalamin or cyanocobalamin), or large oral doses of vitamin B12, typically between 2 and 4 mg daily.

Symptoms

Pernicious anemia may cause inflammation of the tongue (glossitis). Perncious anemia is also associated with premature greying, blue eyes, vitiligo, and blood group A.

Treatment

Treatment usually consists of an initial two week course of B12 injections every other day to cause B12 to be stored in the liver, or a longer course if the patient's B12 level is seriously low in the view of the doctor; then booster shots performed at regular intervals, usually once a month, throughout the life of the patient. Injections usually contain a reddish liquid called hydroxycobalamin or cyanocobalamin. They are given directly into the muscle, usually in the arms, to avoid going through the ileum and being destroyed.

Alternatively, B12, when given in sufficient quantity, can be absorbed orally in a pathway that does not require intrinsic factor or an ileum. Usually, this requires a dose of around 1000 to 2000 mcg. By contrast, the typical Western diet contains 5-7 mcg of B12.

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Folic acid, pernicious anemia, and prevention of neural tube defects
From Nutrition Research Newsletter, 2/1/94

Both the United Kingdom and the United States have planned programs of folic acid fortification of staple foods in an effort to ensure that women of childbearing age receive enough of this vitamin to minimize the occurrence of neural tube defects. Concerns have been expressed, however, about the possibility that individuals with vitamin [B.sub.12] deficiency might consume enough of the fortified foods to mask the anemia associated with this deficiency, leading to delayed diagnosis and the possibility of permanent neurologic damage.

In a commentary published in The Lancet, Nicholas J Wald and Carol Bower of the Wolfson Institute of Preventive Medicine at St Bartholomew's Hospital, London, contend that this concern is misplaced. They state, "We believe that it is a mistake to regard this effect--the correction of the blood abnormality in pernicious anaemia by folic acid--as a masking of the disease or as a toxic effect of the vitamin. Currently about 12% of patients with pernicious anaemia present with neuropathy alone. An increase in dietary folic acid might increase this percentage while reducing the proportion of patients presenting with anaemia....It is not necessary to 'preserve' the anaemia to achieve an earlier diagnosis. Moreover, it is unreasonable to encourage extra haematological morbidity to help make the diagnosis, which in any case should be based on assessment of [B.sub.12] status."

Concerns about the possibility of masking the anemia of vitamin [B.sub.12] deficiency have prompted authorities to recommend relatively low levels of folic acid fortification--levels which may not be adequate to provide all women of childbearing potential with sufficient folic acid. The authors criticize this decision, stating, "Concern over the presence or absence of an accompanying macrocytosis or anaemia [in patients with neurologic symptoms attributable to vitamin [B.sub.12] deficiency] is misplaced; and, to the extent that this might limit public health measures designed to prevent neural tube defects, it represents an error of judgment. The haematological effect of folic acid in pernicious anaemia should not be used as a reason for failure to implement adequate folic acid fortification for prevention of neural tube defects." Nicholas J Wald and Carol Bower, Folic Acid, Pernicious Anaemia, and Prevention of Neural Tube Defects [Commentary], Lancet 343(8893):307 (5 Feb 1994)

COPYRIGHT 1994 Frost & Sullivan
COPYRIGHT 2004 Gale Group

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