Chapter 11 Anemia and Its Effect on the Older Adult

excess supplementation should be stopped to avoid possible oversupplementation or negative side effects such as gastric upset. Anemia of chronic disease asso- ciated with end-stage renal disease and congestive heart failure may be treated effectively using endoge- nous erythropoietin (1).

Megaloblastic Anemia

Macrocytic anemias include megaloblastic anemia (folate deficiency) and pernicious anemia (vitamin B-12 deficiency). Both are normochromic and com- monly seen in older adults for a variety of different reasons.

Megaloblastic anemia is a folate deficiency most commonly seen in older adults. It has been associated with an increased risk for heart disease and end-stage renal disease because of the elevated homocysteine levels (18-20). Megaloblastic anemia occurs after approximately five months of folate depletion. It may be due to increased needs, a deficient diet, malabsorp- tion of folate, or a vitamin B-12 deficiency. In addition, some medications are folate antagonists and interfere with nucleic acid synthesis. Decreased folate levels are associated with megaloblas- tic anemia, hemolytic anemia, malnutrition, malabsorp- tion syndromes, liver disease, and celiac disease. A vitamin B-12 deficiency will eventually cause a folate deficiency because folate cannot be converted into an active form without vitamin B-12 (21-29). Megaloblastic anemia is categorized as a macro- cytic normochromic anemia. The initial clinical signs and symptoms of megaloblastic anemia are low levels of hemoglobin, hematocrit, and serum folate. However, elevated values are seen in serum iron, mean corpuscu- lar volume, ferritin, and homocysteine (5,11). Table 11.6 lists the laboratory values typically seen in mega- loblastic anemia.

The megaloblastic erythropoiesis is usually caused by impaired DNA, RNA, and/or protein syn- thesis. The result is abnormal cellular development and maturation. In this type of anemia, red blood cells are large and immature and their numbers are reduced, which results in a reduced oxygen-carrying capacity of the blood. The RBCs have shortened life spans and reduced capacity to carry hemoglobin. Iron is absorbed by the body and stored as serum iron or ferritin rather than in hemoglobin. Once the folate deficiency is addressed through pharmacolog- ical intervention, the iron stores from the serum iron and ferritin will shift back to the RBCs, and the hemoglobin and hematocrit will return to normal levels. Homocysteine levels may or may not return to normal levels with folate supplementation. Folate supplementation greater than 400 mcg daily is

Hemoglobin (g/dL) Hematocrit (%)

Mean corpuscular volume (mm3)

Mean corpuscular hemoglobin (pg/cell)

Mean corpuscular hemoglobin

concentration (g/dL) Serum iron (mg/dL) Ferritin (ng/mL) Transferrin

Total iron binding capacity (mg/dL)

Serum folate (mg/mL)

Serum vitamin B-12 (pg/mL)

Homocysteine (mmol/L)

TABLE 11.6 Laboratory Test Results for Megaloblastic Anemia

Laboratory Test

Folic Acid Deficiency

Macrocytic Megaloblastic

↓ ↓ ↑

↑ ↑ / ↔

↑ ↑

— —

↓ ↓ / ↔ ↑

considered a pharmacological dose. Taking 10,000 mcg/d, even for a number of years, did not produce significant side effects; however, intakes of 15,000 mcg resulted in insomnia, malaise, irritabil- ity, gastrointestinal problems, and decreased zinc status (30).

Pernicious Anemia

Pernicious anemia is a vitamin B-12 deficiency most commonly seen in older adults, but it is challenging to identify. It is associated with numbness of the hands and feet and with significant cognitive changes. Permanent nerve lining damage results from a B-12 deficiency. In some instances, the neurological signs of the deficiency develop before the person becomes

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