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A New Look at Vitaminb A new look at vitaminB 18 The Nurse Practitioner • Vol. 34, No. 11 www.tnpj.com 2.5 CONTACT HOURS 12 deficiency By Sandra M. Nettina, APRN-BC, ANP, MSN ona Abraham is a 78-year-old widow who sees you for refill of her arthritis and antihypertensive med- M ications. She recently relocated from another state to be closer to her daughter, although she lives in her own “se- nior” apartment. Through history taking, you learn that she has a long history of osteoarthritis, mild hypertension requir- ing medication for the past 5 years, and occasional gastroe- sophageal reflux. Surgical history includes appendectomy as a teenager, a ventral hernia repair after her last child was born, and right knee arthroscopy about 5 years ago. Her medications include triamterene/hydrochlorthiazide 37.5/25 mg daily, acetaminophen 650 mg (2) twice daily , cal- cium citrate 600 mg/vitamin D 400 international units twice daily, omeprazole 20 mg daily p.r.n for heartburn, and hy- drocodone/acetaminophen 5/325 mg every 6h p.r.n. for severe pain. You perform a physical exam, discuss healthy diet and physical activity, order serum electrolytes and creatinine, refill her prescriptions, and advise her to schedule a follow-up ap- pointment in 3 months for preventative screening. You are about to conclude the visit and leave the room when Mrs. Abra- ham asks if she can get a vitamin B12 shot now. You question her about her need for B12 and Mrs. Abraham states she never knew how her previous primary care provider knew she had a vitamin B12 deficiency, but monthly shots have helped boost her energy over the past year. ■ Introduction Vitamin B12 (cobalamin) is the largest and most complex of the B vitamins. It is required for synthesis of DNA used for red blood cells (RBCs), myelin, and other tissues. Deficiency www.tnpj.com The Nurse Practitioner • November 2009 19 A new look at vitamin B12 deficiency occurs in approximately 5% to 20% of the elderly.1,2 Vita- with the patient’s age.3 Although no gold standard exists min B12 is defined as serum cobalamin less than 200 pg/mL for determining a precise serum concentration that defines (150 pmol/L) on two separate occasions, or one instance of B12 deficiency, additional metabolites have been identified, decreased cobalamin with either elevated homocysteine or namely MMA and homocysteine, that can help identify methylmalonic acid (MMA) in the absence of renal failure deficiency in cases where serum B12 levels are borderline 2 or folate or B6 deficiency. It may take many years to develop or normal. Additionally, studies have shown that oral B12 and may be subclinical or mildly symptomatic, affecting the therapy is as effective as I.M. injection in many cases.4 hematologic, neurologic, and gastrointestinal (GI) systems. ■ The most common cause is food malabsorption, in which Overview of vitamin B12 absorption enough vitamin B12 is consumed in the diet but not released Vitamin B12 and folic acid are required for the synthesis of from carrier proteins and thus not absorbed. Food malab- DNA in many tissues, primarily RBCs. Although deficiency sorption accounts for 60% to 70% of cases, and pernicious because of dietary deficiency is rare, it often occurs because anemia, the second most common cause, occurs in 15% to of inadequate absorption. Multiple steps at multiple loca- 20% of cases.2 Other causes of malabsorption also occur to tions in the gut are needed for adequate absorption. Vita- a lesser extent, and dietary deficiency of vitamin B12 is rare min B12 is derived from animal products (meat or dairy). because of the prevalence of B12 in the diet and availability Following ingestion, vitamin B12/animal protein bonds are of fortified foods and supplements. severed in the presence of gastric secretions (see Absorption Many people believe that supplementation of vitamin of vitamin B12 ). B12 with or without evidence of deficiency will result in The vitamin B12 combines with R proteins from salivary increased energy, improved cognitive status, improved mood, and gastric sections. Intrinsic factor is secreted by parietal and even weight loss. There are many claims like these on the cells in the gastric fundus but binding to B12 is weak in the Internet, and supplements, even injections that can be bought presence of B12/R protein complexes. Intrinsic factor and online. The likelihood that a clinician will prescribe vita- B12/R protein complexes travel to the duodenum and are min B12 injections without assessing for deficiency rises joined by biliary B12/R protein complexes. Both types of B12 complexes are now easily degraded by pancreatic enzymes, releasing free cobalamin. Here instrinsic factor binds with Absorption of vitamin B12 cobalamin and these complexes travel to the distal ileum for absorption. Absorption occurs through attachment to mucosal cell receptors and binding to transport proteins Dietary vitamin B12 known as transcobalamin I, II, and III.5 Vitamin B12 deficiency can develop from decreased intake or absorption (see Causes of vitamin B12 deficiency). Decreased intake may result from strict vegetarian diet, very Stomach B12 limited oral intake, or chronic malnutrition. Decreased ab- sorption may result from lack of unbinding of vitamin B12 from protein in food sources; lack of intrinsic factor from the stomach as in cases of total or partial gastrectomy, gas- Parietal cell tric bypass surgery, or autoimmune gastric atrophy, known Intrinsic factor (IF) as pernicious anemia. Decreased absorption also results from surgery or disease of the ileum such as Crohn’s disease. Cer- tain drugs can also interfere with unbinding and absorption. B /IF Ileum Portal Fortunately, B stores in the liver are significant; therefore, 12 vein 12 complexes manifestations of deficiency may not become apparent for Epithelial cell 5 to 10 years.2 with IF receptor RBCs formed in a state of B12 or folic acid deficiency are structurally abnormal. Increased numbers of myeloid B 12 / transcobalamin II precursor cells are produced in the bone marrow, but they complex are large and bizarre in appearance. Many become trapped Source: Porth CM, Matfin, G. Pathophysiology Concepts of Altered Health in the bone marrow and are destroyed, so there are actually States. 8th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams fewer mature cells that enter the blood stream from the & Wilkins, 2009:291. myeloid line (RBC, platelet, nonlymphoid white blood 20 The Nurse Practitioner • Vol. 34, No. 11 www.tnpj.com A new look at vitamin B12 deficiency cells). Pancytopenia may occur, and be- cause the RBCs are large, megaloblastic Causes of vitamin B12 deficiency anemia is the prominent feature. Since RBCs have flimsy membranes and are Pathophysiology Condition oddly shaped, their life span is short. Folic Nutritional deficiency of B • Malnutrition acid deficiency also causes megaloblas- 12 • Alcohol abuse tic anemia, and it develops much more • Institutionalization quickly than with B12 deficiency, because • Strict vegan diet the body stores very little folic acid. Lack of intrinsic factor • Pernicious anemia (autoimmune gastric atrophy) ■ Manifestations of B12 deficiency • Total and partial gastrectomy Megaloblastic anemia is the most com- Food-bound B12 malabsorption • Atrophic gastritis of aging or chronic mon feature of vitamin B12 deficiency. alcohol abuse Signs of anemia may develop slowly • Chronic Helicobacter pylori infection depending on the body’s ability to com- • Long-term use of metformin pensate. Signs and symptoms include • Reduced acid environment through listlessness, fatigue, dyspnea, and pallor. long-term use of histamine-2 receptor antagonists and proton pump inhibitors Prominent lab features are elevated mean corpuscular volume (MCV) of 110 mm3 Pancreatic exocrine failure • Chronic pancreatitis, pancreatectomy or greater, reflecting the large RBCs, and Small intestinal malabsorption • Crohn’s disease, lymphoma, through damage to last 80 cm tuberculosis, amyloidosis, varying size and shape of RBCs (aniso - of ileum scleroderma, Whipple’s disease, celiac poikilocytosis). Hypersegmented neu- disease, chronic ingestion of colchicine trophils (mature neutrophils with more or cholestyramine, ileal resection than five distinct lobes) may be seen on Genetic deficiency of transport • Imerslund-Grasbeck syndrome peripheral blood smear. Folic acid defi- proteins • Transcobalamin II deficiency ciency causes the same findings, but does not cause the additional neurologic and GI manifestations and vitamin B12 is also deficient, anemia may improve but seen in vitamin B12 deficiency. Neurologic manifestations irreversible neurologic symptoms may develop. Reference seen with B12 deficiency may be prominent and irreversible. ranges for vitamin B12 vary by lab with ranges of 200 to Abnormal synthesis of myelin protein causes demyelination 220 pg/mL identified as the lower limit. A recent study of the dorsal and lateral columns of the spinal cord. Signs using recommendations from the National Committee and symptoms include confusion, numbness and paresthe- for Clinical Laboratory Standards and International Feder- sias of the lower extremities, disequilibrium, and loss of po- ation of Clinical Chemistry found the central 95% reference sition and vibratory sense. GI manifestations seen with B12 interval to be 101 to 666 pg/mL for women and 100 to deficiency are smooth, sore, red tongue, and mild diarrhea. 699 pg/mL for men.6 Symptoms may wax and wane for many years, with partial A more sensitive early indicator of B12 deficiency is remission occurring when any vitamin B12 is replaced, determination of MMA. Increased MMA indicates de- but in severe cases death due to heart failure secondary to creased tissue B12. A patient with neurologic symptoms anemia is possible. indicative of deficiency, but normal hematologic studies and serum B12 level, may show significantly increased level of ■ 7 Identifying deficiency MMA, indicating B12 deficiency. Homocysteine levels Vitamin B12 deficiency is often identified through mega- may also be increased due to a deficiency of B12, folate, loblastic anemia with decreased RBC count, hematocrit, and or vitamin B6 because of their role in its metabolism.
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