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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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Oral cobalamin for pernicious anemia
From Nutrition Research Newsletter, 4/1/91

VITAMINS AND HEALTH

ORAL COBALAMIN FOR

PERNICIOUS ANEMIA

In a commentary in the January 2, 1991 issue of JAMA, Frank Lederle of the University of Minnesota discusses the use of oral cobalamin in the treatment of pernicious anemia. He notes that a small but constant proportion of an oral dose of cyanocobalamin is absorbed even in the absence of intrinsic factor, and thus oral therapy can be effective if the dose is high enough (in the range of 1000 [microgram]g daily).

Lederle reports that oral cobalamin therapy (which ceased to be available in the US in the late 1950s but became available again in the early 1970s) is rarely prescribed in the US, although it is widely and successfully used in Sweden. The alternative--monthly cobalamin injections--has important disadvantages, including pain, cost of administering injections, and difficulty in reaching some individuals who are elderly or live alone.

Some medical texts have expressed concerns regarding "upredictable absorbancy, patient compliance and cost" of oral therapy, while acknowledging its effectiveness, particularly when injections are problematic. The author states that these concerns are based primarily on outdated data and need not be serious problems.

In a survey of 245 Minneapolis internists conducted by Lederle, it was revealed that none had used oral cobalamin to treat pernicious anemia, and only 1% had used it to treat dietary cobalamin deficiency. Over 90% believed that a sufficient amount of cobalamin could not be absorbed without intrinsic factor and 94% were unaware of an available effective oral cobalamin therapy. Most said they would welcome the option of oral therapy, stating that it would be their treatment of choice for the majority of their patients with cobalamin deficiency.

Lederle concludes that "it is clear from the Swedish experience and the survey results discussed herein that a wider appreciation of the effectiveness and availability of oral cobalamin therapy would be valuable to American physicians and their patients."

In a related editorial, John Hathcock and Gloria Troendle of the Food and Drug Administration agree that oral cobalamin therapy can be safe and effective but stress that patients must be closely monitored at least in the early months of therapy and cautioned not to consume large amounts of folate. They point out that 50% of the patients of the Minneapolis physicians preferred a monthly injection to a daily pill, and that this preference "may conflict with physicians' apparent willingness to accept oral therapy." Although high-dose oral cobalamin preparations are available over the counter, patients with pernicious anemia or others at risk of cobalamin deficiency should always be treated under the supervision of a physician.

COPYRIGHT 1991 Frost & Sullivan
COPYRIGHT 2004 Gale Group

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