CHAPTER 13 | Anemia and Its Effects on the Older Adult 203
Folate-Related Anemia and Megaloblastic Anemia
The primary clinical sign of folate or vitamin B12 deficiency is megaloblastic anemia, which is char- acterized by large, abnormally nucleated, irregularly shaped erythrocytes. Vitamin B12 and folate deficien- cies are associated with macrocytic erythrocytes. A very high MCV (> 130 fL) almost always indicates a vitamin B12 or folate deficiency. Elevated homocys- teine levels associated with megaloblastic anemia are of particular concern, owing to their association with an increased risk of heart disease, Alzheimer disease, and dementia.29
Previous studies reported that vita-
min B12 and folate supplements lower homocysteine levels but not cardiovascular disease risk.18 Folate deficiency occurs when folate intake is inadequate, absorption is impaired, or requirements or losses are increased. Older adults with alcohol use disorder, malabsorptive disorders (celiac dis- ease, tropical sprue, or inflammatory bowel disease), diminished gastric acid secretion (atrophic gastritis, gastric surgery), and methylenetetrahydrofolate reductase (MTHFR) genetic variation are at particu- lar risk of folate deficiency. In addition, older adults taking antiseizure drugs (which reduce serum folate levels; conversely, folate may reduce serum levels of these medications), methotrexate (a folate antag- onist), and sulfasalazine (which inhibits intestinal absorption of folate) also have an increased risk of folate deficiency.5,29 Vitamin B12 deficiency eventually leads to folate
deficiency because folate cannot be converted into its active form without vitamin B12. Folate deficiency usually appears first because normal body folate stores are depleted within 2 to 4 months, whereas it takes several years for vitamin B12 to deplete.30
Biochemical Indicators
Elevated MCV is not the most sensitive indicator of vitamin B12 deficiency because coexisting condi- tions, such as iron deficiency, chronic infection, or genetic hemoglobin disorders, can mask macrocyto- sis. A peripheral blood smear may be more helpful. Abnormal cellular development and maturation is caused by impaired DNA, RNA, or protein synthesis.
Findings of macro-ovalocytosis, teardrop-shaped RBCs, and hypersegmented neutrophils are notable for folate or B12 deficiency.16 Serum folate concentrations are commonly used
to assess folate status. Concentrations greater than 3 ng/ mL indicate adequate levels but are affected by recent dietary intake. Erythrocyte folate concentra- tions provide a longer-term measure, and levels below 140 ng/mL indicate folate deficiency.29,30
Elevated
plasma homocysteine (≥ 16 mcmol/L) is another indi- cator of folate deficiency. However, serum B12 and methylmalonic acid levels should also be obtained because homocysteine levels can be elevated with a vitamin B12 deficiency.16
Homocysteine levels can also
be influenced by other factors, including kidney dys- function and deficiencies of other micronutrients.29
Nutrition Focused Physical Examination
Common signs and symptoms of folate deficiency include weakness, fatigue, difficulty concentrating, irritability, headache, heart palpitations, shortness of breath, gastrointestinal symptoms (eg, diarrhea or soreness of and shallow ulcerations on the tongue and oral mucosa), anorexia, and weight loss. Changes in skin, hair, or fingernail pigmentation may also be observed.29,30
ciated with depression.29
Low folate status has also been asso- The association between
alcohol use disorder and folate deficiency is discussed later in regard to anemia and special populations.
Vitamin B12–Related Anemia and Pernicious Anemia
Vitamin B12 is bound to protein in food and must be freed before absorption. When food is mixed with saliva in the mouth, vitamin B12 binds with hapto- corrin, a cobalamin-binding protein. During diges- tion, gastric acid and gastric protease further aid in the release of vitamin B12 from protein. (Vitamin B12 added to fortified foods and dietary supplements is already in a freed form and does not need to be sepa- rated.) In the duodenum, freed vitamin B12 combines with intrinsic factor (IF), a glycoprotein secreted by the stomach’s parietal cells. The resulting complex is then absorbed in the distal ileum. Vitamin B12 cannot be properly absorbed if IF is not available.18,30
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