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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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Angina pectoris caused by pernicious anemia - Editorial
From CHEST, 3/1/94 by Panayiotis J. Asimacopoulos

Pernicious anemia, expressed as megaloblastic anemia, exists in individuals who fail to produce a glycoprotein, Castle's intrinsic factor (CIF). It is commonly thought that the parietal cells of the stomach do not secrete CIF due to autoantibodies, thus not allowing vitamin [B.sub.1,2] (cobalamin) to bond with CIF and so to be absorbed by the distal ileum. The failure of CIF secretion is associated with achlorhydria and gastric mucosa atrophy.[1] This acquired disease becomes symptomatic usually after the age of 50 and is most common in individuals of northern European descent, especially Scandinavians.[2] It is diagnosed with the Schilling test.

Anemia of any cause may result in increased cardiac output, especially when the hemoglobin level drops to 7 g/dl or less.[3] Tachycardia may not be present in chronic anemia, and the increased cardiac output at rest usually reflects an increased cardiac stroke volume.[4,5] The increased cardiac output is achieved at the cost of increased work of the left ventricle.[6] Right atrial, right ventricular, and pulmonary arterial pressures are usually normal unless cardiac decompensation develops.[4,7] Left ventricular end-diastolic pressure remains unchanged.[8]

Increased cardiac output in pernicious anemia and in other severe chronic anemias is of importance in maintaining an adequate oxygen supply to the tissues, and is facilitated by alterations in left ventricular afterload and myocardial contractility. Although ventricular end-diastolic volume, which is the preload of the left side of the heart, seems to be unchanged, myocardial contractility appears to increase.[6,9,10] Afterload and left ventricular wall stress, having as major determinants vascular resistance and blood viscosity, are reduced. Decrease in peripheral vascular resistance in severe pernicious anemia is of great importance in producing increased cardiac output.[11] Moreover, lowered blood viscosity associated with anemia complements the increased cardiac output. Effects of decreased viscosity with low hematocrit vaues can result in a fivefold increase in coronary perfusion.[12]

Maximum myocardial oxygen transport shows an inverted U-shaped relationship with the hematocrit value.[12] At extremely low or extremely high concentrations of red blood cells, myocardial oxygen transport may decrease due to decreased oxygen carrying capacity on the one hand and increased blood viscosity on the other. Thus, the peak of the above curve occurs at or slightly above the normal hematocrit level.[12] Compensatory mechanisms to counteract the low hematocrit level include alternations in peripheral vascular resistance in order to redistribute cardiac output to selective vascular beds, so that during anemia; the increasing blood flow is proportionally greater in the coronary bed than in the renal, mesenteric, or femoral beds.[13] This phenomenon is owed to vasoconstriction or vasodilation because of neurohumoral and/or local autoregulatory factors.[13] Also, in chronic anemia the red blood cells develop increased levels of 2,3-diphosphoglycerate, which facilitates release of oxygen from hemoglobin;[14] however, this mechanism may be of secondary importance in severe anemia since the arteriovenous difference is decreased 3 volumes per 100 ml of blood, compared with 4 to 5 volumes per 100 ml of blood in normal subjects.[11] Another important mechanism of increased oxygen delivery to the heart in pernicious anemia may be increased utilization of coronary collateral vessels.[15] Release of local vasodilators may help improve collateral blood flow after development of severe anemia.

If these adaptation mechanisms in severe anemia do not compensate adequately, angina pectoris may develop in these patients in spite of normal coronary arteries. Angina pectoris caused by severe anemia usually develops at very low hemoglobin levels, in the range of 3 to 4 g/dl. Coombs[16] noted an association between severe pernicious anemia and anginalike pain, especially on exertion. The true incidence of angina pectoris associated with pernicious anemia could not be determined accurately, since many of the patients reported did not have adequate studies of the coronary circulation to rule out associated coronary artery disease. Clinically, the incidence appears to be in the range of 2 to 3 percent.[17] Although severe anemia is not a common cause of angina, it should always be listed in the differential diagnosis of angina pectoris.

REFERENCES

[1] Jandl JH. Textbook of hematology. Boston: Little, Brown, 1987; 158-63

[2] Pedersen AB, Mosbech J. Morbidity of pernicious anemia. Acta Med Scand 1969; 185:449-52

[3] Brannon ES, Merrill AJ, Warren JV, Stead EA Jr. The cardiac output in patients with chronic anemia as measured by the technique of right atrial catheterization. J Clin Invest 1945; 24:332-36

[4] Bishop JM, Donald KW, Wade OL. Circulatory dynamics at rest and on exercise in the hyperkinetic states. Clin Sci 1955; 14:329-60

[5] Donald KW, Bishop JM, Cumming G, Wade OL. The effect of exercise on the cardiac output and circulatory dynamics of normal subjects. Clin Sci 1955; 14:37-73

[6] Graettinger JS, Parsons RL, Campell JA. A correlation of clinical and hemodynamic studies in patients with mild and severe anemia with and without congestive failure. Ann Intern Med 1963; 58:617-26

[7] Shubin H, Kaufman R, Shapiro M, Levinson DC. Cardiovascular findings in children with sickle cell anemia. Am J Cardiol 1960; 6:875-85

[8] Varat MA, Adolph RH, Fowler NO. Cardiovascular effects of anemia. Am Heart J 1972; 83:415-26

[9] Sharpey-Schafer EP. Cardiac output in severe anemia. Clin Sci 1944; 5:125-32

[10] Escobar E, Jones NL, Rapaport E, Murray JF. Ventricular performance in acute normovolemic anemia and effects of beta blockade. Am J Physiol 1966; 211:877-84

[11] Duke M, Abelmann WH. The hemodynamic response to chronic anemia. Circulation 1969; 39:503-15

[12] Baer WR, Vlahakes JG, Uhlig NP, Hoffman IEJ. Maximum myocardial oxygen transport during anemia and polycythemia in dogs. Am J Physiol 1987; 252(Heart Circ Physiol 21):H1086-95

[13] Fay FC, Chen ZYR, Schuessler GB, Chien S. Effects of hematocrit variations on regional hemodynamics and oxygen transport in the dog. Am J Physiol 1980; 238(Heart Circ Physiol 7):H545-52

[14] Benesch R, Benesch RE. The effect of organic phosphates from the human erythrocyte on the allosteric properties of hemoglobin. Biochem Biophys Res Commun 1967; 26:162

[15] Scheel KW, Williams SE. Hypertrophy and coronary and collateral vascularity in dogs with severe chronic anemia. Am J Physiol 1985; 249(Heart Circ Physiol 18):H1031-37

[16] Coombs CF. A note on the cardiac symptoms of pernicious anemia, with particular reference to cardiac pain. BMJ 1926; 2:185

[17] Willius FA, Giffin HZ. The anginal syndrome in pernicious anemia. Am J Med Sci 1927; 174:30-3

COPYRIGHT 1994 American College of Chest Physicians
COPYRIGHT 2004 Gale Group

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