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Anemia, Pernicious

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.

Maurice Beddow Bayly, an anti-vaccinationist and anti-vivisectionist, campaigned against the use of liver therapy, having failed to recognise the nature of the disease (despite reciting the necessary information) .

Symptoms

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

Treatment

Treatment is with vitamin B12 (hydroxycobalamin or cyanocobalamin) injected intramuscularly. Body stores (in the liver) are refilled with half a dozen injections in the first couple of weeks and then maintenance with monthly to quarterly injections throughout the life of the patient.

B12 has traditionaly been given parenterally to ensure absorption. Alternatively, since it has become appreciated that when B12 given orally in sufficient quantity is absorbed regardless of intrinsic factor or the ileum, oral replacement has emerged as an accepted route. Generally 1000 to 2000 mcg daily is required . By contrast, the typical Western diet contains 5-7 mcg of B12.

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Folic acid, pernicious anemia, and neural tube defects - adapted from the British Medical Journal, April 22, 1995
From Nutrition Research Newsletter, 6/1/95

Authorities in the US and other countries have proposed fortifying foods with folic acid in order to reduce the incidence of neural tube defects. The safety of such fortification has been questioned, however, on the grounds that increased folic acid intake might mask the anemia of vitamin B12 deficiency, thereby delaying the diagnosis of this disorder, with possible permanent neurologic damage.

Two recent articles by British authors dispute the idea that folic acid fortification would be harmful to patients with B12 deficiency. In one commentary, Dr CJ Dickinson of St. Bartholomew's Medical College, London, reviews the early literature on folic acid and pernicious anemia and finds no convincing evidence that the speed of neurological deterioration is faster in [B.sub.12] deficient patients treated with folic acid than in untreated patients.

Dr. Dickinson acknowledges that folic acid can correct the anemia of [B.sub.12] deficiency. "Thus it could mask the underlying disease, and allow the development or progression of neurological deterioration, if diagnosis depended on the presence of anemia symptoms. This possibility can readily be overcome by adequate education of doctors, so that a macrocytic anemia is not regarded as a necessary accompanying sign of the neurological disorder. The hypothetical and avoidable side-effects of food fortification with folic acid have to be balanced against the certain benefit of preventing neural tube defects in unplanned pregnancies, and also against the probability that adults may be spared the neuropsychiatric and other ill-effects which result from inadequate dietary folic acid."

Similarly, in an editorial in the British Medical Journal, Dr Nicholas J Wald and Dr Carol Bower, also of St. Bartholomew's Medical College, argue that a selective approach to prevention of neural tube defects (in which only women planning a pregnancy would take extra folic acid) is unlikely to be successful. In general, selective approaches to public health problems have been less effective than population-based approaches. Also, a selective policy would fail to prevent neural tube defects in unplanned pregnancies.

Dr Wald and Dr Bower contend that the problem of folic acid masking the anemia of vitamin [B.sub.12] deficiency can be solved by educating physicians. They also argue that possible interference by folic acid with anticonvulsant therapy can be solved by increasing the doses of anticonvulsant drugs.

"The solution, then, is to fortify food with folic acid," according to these editorial writers. "A public health initiative is urgently needed; the tragedy of a pregnancy in which the fetus has a neural tube defect is even greater when it can be so easily prevented .... If this opportunity is missed, the costs - the needless suffering of seriously disabled children, unnecessary terminations of pregnancy carried out because of an antenatal diagnosis of a neural tube defect, and wasted financial resources - will be great."

CJ Dickinson, Does Folic Acid Harm People with Vitamin [B.sub.12] Deficiency? Medicine Medicine88(5):357-364 (May 1995) [Correspondence: Professor CJ Dickinson, Wolfson Institute of Preventive Medicine, Medical College of St Bartholomew's Hospital, Charterhouse Square, London EC1M 6BQ, UK]

Nicholas J Wald and Carol Bower, Folic Acid and the Prevention of Neural Tube Defects, BMJ 310(6986); 1019-1020 (22Apr 1995) [Correspondence: Professor Nicholas J Wald, Department of Environmental and Preventive Medicine, Wolfson Institute of Preventive Medicine, Medical College of St Bartholomew's Hospital, London EC1M 6BQ, UK]

COPYRIGHT 1995 Frost & Sullivan
COPYRIGHT 2004 Gale Group

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