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Pernicious anemia which doctors have also referred to as Biermer’s anemia or Addison’s anemia is generally a decrease in red blood cells. It occurs as a result of small intestines not properly absorbing vitamin B12. This deficiency is one of the types of anemias that belong to a larger family known as megaloblastic anemias. The disease was first described in 1849 by a British doctor, Thomas Addison. It is from him that the disease acquired the name Addison’s anemia. In the beginning of the twentieth century, a research showed that patients with pernicious anemia had an average survival of one to three years. The disease remained fatal during this time up to twenties but with a lot of researches on progress.
A research conducted by Dr. William Castle demonstrated that the gastric juice contained intrinsic factor which was a major step in finding the cure. Additionally, Dr. George Whipple suggested that taking raw liver was the appropriate treatment for patients with pernicious anemia. He arrived at this conclusion after conducting a research that involved bleeding dogs, just enough to make them anemic and then feeding them with different foods while observing their rate of recovery. Though this research proved liver to be a cure for anemia out of blood loss and not pernicious anemia, he proved tremendous improvement on patients with pernicious anemia after feeding on large amounts of liver. In 1926, it was discovered that it is iron that cured anemic dogs and not the soluble factor contained in liver juice. However, coincidentally, it was the soluble liver juice factor that cured anemia.
It was not until 1948 when two chemists isolated and named the curative factor in liver juice as vitamin B12. It was then that pernicious anemia’s treatment was declared as either injection of vitamin B12 or oral dosage of the same vitamin. This disease is now clearly understood and scientists have explained it to be caused by loss of gastric parietal cells that contribute to the secretion of intrinsic factor. Intrinsic factor is a protein essential for the absorption of the vital vitamin B12 in the small intestines. The gastric parietal cells are seen to be destroyed in an autoimmune process and, therefore, the level of intrinsic factor reduces making absorption of vitamin B12 from normal diets impossible as it depends on intrinsic factor.
Though there are other causes of vitamin B12 deficiency, the loss of the ability to absorb it in the small intestines is the most common cause. The immune system of the patients of pernicious anemia mistakenly fights the intrinsic factor and parietal cells resulting into insufficient absorption of vitamin B12. The effects are not abruptly detected as the body stores lots of vitamin B12 in the liver. It could take up to approximately five years before it is depleted and then resulting into anemia. Research has shown that people with a weakened stomach lining, a disease referred to as atrophic gastritis are prone to the pernicious anemia. In rare occasions pernicious anemia has been inherited down through families in which case it is referred to as congenital pernicious anemia. Adults mostly show signs of pernicious anemia after attaining the age 30. However, in average, the age of diagnosis is 60. Other diseases that have proved to increase the risk of getting pernicious anemia include Graves disease, chronic thyroiditis, Addison’s disease, hypoparathyriodism, secondary amenorrhea etc. This anemia has also proved to be more prevalent to Northern Europeans as well as Scandinavians.
Pernicious anemia like any other anemia means that a patient does not have enough healthy red blood cells which carry oxygen to all the body parts. This makes you feel tired and weak even without doing anything. This comes about as a result of the body tissues not getting enough oxygen. The heart is forced to pump blood at a faster rate to supply oxygen which may result into heart problems after some time. The stress caused to heart leads to heart murmurs which are unusual sound the heart produces during heartbeat. Eventually, the heart experiences speedy and irregular heartbeats, growing in size of the heart and even heart failure in the worst cases.
Vitamin B12 which is also referred to as folic acid or folate helps in keeping the level of homocysteine chemical down. Its deficiency results into subsequent buildup of the chemical which increases the buildup of fatty deposits in the blood vessels causing strokes and heart attacks. Lack of vitamin B12 has also shown to cause damage to the nerve cells. Patients would experience frequent numbness and tingling feelings when touching both hands and feet coupled with balance problems. Other senses like taste and smell eventually become impaired and finally the patients start experiencing memory loss and confusion. These problems result from advanced pernicious anemia which has probably not been treated. Failure to treat vitamin B12 deficiency also leads to problems of the digestive tract. In most cases the surface of the tongue changes and the stomach lining becomes thinner. These patients become more susceptible to cancer infection due to the shrinking of the stomach lining (Kass, 1976).
The nature of this disease makes diagnosis delayed but when a patient’s blood smear indicates large, immature and fragile erythrocytes should be further examined as it may be as a result of pernicious anemia. Doctors would then look for intrinsic factor antibodies which are found in all anemia patients. Anti-parietal cell antibodies could also be present. Before the advent of the modern tests, doctors used the schilling test to diagnose pernicious anemia. To diagnose pernicious anemia, doctors first check megaloblastic anemia which calls for a full blood count. The full blood count examines the mean corpuscular volume (MCV) and the mean corpuscular hemoglobin concentration (MCHC) where pernicious patients demonstrate a high MCV and a normal MCHC (Miederer, 1977). Doctors have also diagnosed pernicious anemia through the examination of its direct cause, the vitamin B12 deficiency. Detection of the vitamins malabsorption would directly indicate that the patient could be suffering from pernicious anemia. Further tests should, however, be conducted to prove the condition.
The treatment adopted on pernicious anemia varies from place to place but the bottom line is that there is no permanent cure of disease. However, replenishing vitamin B12 heals the symptoms and results in improvement of the neurological system in cases where it had been badly affected. The patients need to keep supplementing their vitamin B12 to remain healthy. This could be done in a variety of ways. Some patients with low vitamin B12 seem to absorb sufficient amounts after ingesting large amounts while others require injections which are usually given once in a month. Patients could be taught on how to administer the injections from home or visit the nearby clinics. The injection of cyanocobalamin to the muscle tissue is usually administered in countries like Canada, United States, and majority of European countries. However, Australia and United Kingdom use hydroxocobalamin. Other methods of administering vitamin B12 include sprays in the nose and behind the ear patch (William, 1974). These methods are, however, under further investigations. This condition can only be prevented from by ensuring presence of the vitamin in your diet but not with certainty.
Patients of pernicious anemia may be forced to stay under the treatment for the rest of their lives. This disease could be fatal if not treated or diagnosed at a very advanced stage. Patients who suspect to be suffering from the disease should enquire about the family history as it has proved to run in families (Antony, 2011). The patients should also share this information with siblings and children to ease the diagnosis at early stages in case they inherit the disease.