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Pernicious Anemia Definition and History
From the moment of its discovery until nowadays, pernicious anemia has become and remains one of the most exciting topics in medicine. It was first described in 1855 by Dr. Thomas Addison whence it acquired the name Addison’s disease. Until the 1920s pernicious anemia remained lethal. Recognized as an incurable affliction, its treatment consisted primarily of blood transfusions which served the sole purpose of postponing inevitable death (Eppinger 783). However, in 1926, a group of three physiologists discovered liver therapy to celebrate one of the century’s great scientific breakthroughs and to share the 1934 Nobel Prize for medicine. Despite the magnitude of their success for the time, George Whipple, William Murphy, and George Manot only set the initial point for a long journey towards the exploration of the disease. Thanks to the efforts of such men present-day science have expanded substantially from the background of experience to provide a much more detailed picture of the true nature of pernicious anemia, its signs, causes, and symptoms. Once the problem has been clarified through an accurate diagnosis, possible treatment and monitoring can take place.
Pernicious anemia refers to the chronic condition of insufficient red blood cells and subsequently to the blood’s inability to carry enough oxygen throughout the body. A characteristic of pernicious anemia is the presence of enormously large (megaloblastic), immature erythrocytes. Although they are normochromic, containing hemoglobin within the standard range, they are insufficient in number (Hawley 52). Two reasons account for a drop in the number of red blood cells, either a decline in their production or an increase in their loss. The word ‘pernicious’ means harmful suggesting a usually subtle, long-term deleterious effect on the organism while ‘anemia’ is a general term linked with the shortage of erythrocytes in the body. The name ‘pernicious anemia’ denotes a specific case of anemia when the body can’t receive enough vitamin12 from the latter’s absorption in the gastrointestinal tract (Hawley 52).
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Pernicious anemia develops slowly and the first symptoms do not appear until the hemoglobin levels have fallen drastically (below 8g/dL). It is caused by the malabsorption of vitamin B12 hampering the process of erythropoiesis which defines the formation of red blood cells (Hawley 52). Inside the stomach, a protein called intrinsic factor binds to vitamin B12 so that the newly formed complex passes the intestinal wall and crosses into the bloodstream. In the case of pernicious anemia, this complex cannot form at all because the cells in the stomach responsible for the manufacture of intrinsic factors are damaged and hence unable to produce it. Consequently, vitamin B12 is no longer absorbed leading to deficiency and anemia. Most frequently this is the result of gastric atrophy. The latter is caused by either innate autoimmune disorder leading to the production of parietal cell antibodies or the continuous exercise of harmful habits such as smoking or excessive drinking.
It is a common mistake to associate symptoms of pernicious anemia with the shortage of red blood cells by itself. They should be rather regarded as the latter’s manifestation in disorders of the bone marrow, gastrointestinal tract, and central nervous system. The signs of pernicious anemia include pallor, weakness, breath shortness, fatigability. Indigestion, lack of appetite, and general stomach discomfort are other signs found in individuals suffering from pernicious anemia. They are consequences of the absence of hydrochloric acid. Moreover, vitamin B12 is crucial for healthy nerves and hence the involvement of the central nervous system adds features such as head tingling, numbness, walking difficulties, and occasionally, a loss of sphincter control. In rare instances, anemia is related to psychosis. If left untreated, pernicious anemia could potentially cause severe neurological disorders and death. An interesting symptom of anemia is the curious desire to chew non-food items such as ice, starch, paper, or clay. What triggers this kind of craving is unknown but if it appears, it is a sure sign of alert (Eppinger 783).
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