eMedicine Specialties > Hematology > Red Blood Cells and Disorders

Macrocytosis

Wendy Brick, MD, Consulting Staff, Department of Internal Medicine, Division of Hematology and Oncology, Mecklenburg Medical Group
Russell Burgess, MD, Department of Internal Medicine, Division of Hematology/Oncology, East Carolina Internal Medicine

Updated: Aug 29, 2009

Introduction

Background

Macrocytosis is a term used to describe erythrocytes that are larger than normal, typically reported as mean cell volume (MCV) greater than 100 fL. The amount of hemoglobin in the cell increases proportionately, so the mean cell hemoglobin concentration (MCHC) remains within normal limits. Causes of macrocytosis are many and range from benign to malignant; thus, a complete workup to determine etiology is essential.¹

Pathophysiology

The most common cause of macrocytic anemia is megaloblastic anemia, which is the result of impaired DNA synthesis. Although DNA synthesis is impaired, RNA synthesis is unaffected, leading to a buildup of cytoplasmic components in a slowly dividing cell. This results in a larger-than-normal cell. The nuclear chromatin of these cells also has an altered appearance.²

Vitamin B-12 and folate coenzymes are required for thymidylate and purine synthesis; thus, their deficiency results in retarded DNA synthesis. In vitamin B-12 and folate deficiency, the defect in DNA synthesis affects other rapidly dividing cells as well, which may be manifested as glossitis, skin changes, and flattening of intestinal villi. The synthesis of DNA also may be delayed when certain chemotherapeutic agents are used. Examples of such agents include folate antagonists (methotrexate), purine antagonists (6-mercaptopurine), and pyrimidine antagonists (cytosine arabinoside [ara-C]).

Hydroxyurea, an agent now commonly used to decrease the number of vasoocclusive pain crises in patients with sickle cell disease, interferes with DNA synthesis, causing a macrocytosis by which compliance with therapy may be monitored. Patient compliance with zidovudine, an agent used in the treatment of patients with HIV, may be monitored in the same way.

Sternfeld et al assessed whether macrocytosis may be a marker of mitochondrial toxicity in antiretrovirally treated HIV-infected patients by using the¹³ C-methionine breath test to analyze the hepatic mitochondrial function in vivo in these HIV patients with macrocytosis.³  The investigators found a significantly negative correlation between mean corpuscular erythrocyte volume and the breath test results, concluding there is association between an increase of the mean corpuscular erythrocyte volume from treatment with nucleoside reverse transcriptase inhibitors and the hepatic mitochondrial function in vivo.³

Nonmegaloblastic macrocytic anemias are those in which no impairment of DNA synthesis occurs. Included in this category are disorders associated with increased membrane surface area, accelerated erythropoiesis, alcoholism, and chronic obstructive pulmonary disease (COPD).

Patients with hepatic disease and obstructive jaundice have a macrocytosis that is secondary to increased cholesterol and/or phospholipids deposited on the membranes of circulating RBCs. Similarly, in splenectomized patients, RBC membrane lipids that usually are removed during maturation in the spleen are not effectively removed, leading to a larger-than-normal cell.

In patients with hemolytic anemia or posthemorrhagic anemia, the reticulocyte count increases. The reticulocyte, an immature RBC, is approximately 20% larger than the more mature RBC. When released prematurely from the marrow, the volume of the reticulocyte is averaged with the volume of the more mature RBC, and the resultant MCV is increased.

Macrocytosis, sometimes without associated anemia, is often evident in persons with chronic alcoholism. Although the macrocytosis of alcoholism may be secondary to poor nutrition with a resulting folate or vitamin B-12 deficiency, it is more often due to a direct toxicity of the alcohol on the marrow. The macrocytosis of alcoholism usually reverses only after months of abstinence from alcohol.

The macrocytosis associated with COPD is attributed to excess cell water that is secondary to carbon dioxide retention.

Mortality/Morbidity

No complications are directly attributable to the increased size of the red cell. Complications are attributed to the condition causing the macrocytosis. Diagnosis of the etiology of macrocytosis is required before the morbidity and mortality can be determined.

Age

Macrocytosis may occur at any age, but it is more prevalent in older age groups because the causes of macrocytosis are more prevalent in older persons.⁴

Clinical

History

• Symptoms are attributable to the underlying condition causing the anemia or directly to the anemia. Symptoms may include the following:
  • Dyspnea
  • Headache
  • Fatigue
  • Sore tongue
  • Diarrhea or other gastrointestinal symptoms
  • Paresthesias
• A history of alcohol abuse may be an important clue as to the cause of the increased MCV.
• A thorough examination of the patient's medication regimen is also crucial in the workup of macrocytosis.
• Dyspnea is a consequence of anemia. In acute or severe anemia, the volume of hemoglobin in the blood is inadequate to provide appropriate oxygenation of the tissues.
• Fatigue may be attributed to underlying disease, if present, or to inadequate blood volume.
• Headache is a symptom of anemia due to decreased oxygenation of the tissues.
• A sore tongue may be glossitis or atrophy of the tongue, which are common findings in folate and vitamin B-12 deficiencies.
• Diarrhea or other gastrointestinal symptoms may be present in patients with tropical or celiac sprue. Sprue may cause folate or vitamin B-12 deficiencies.
• Long-term use of alcohol may have a direct toxic effect on the bone marrow, causing macrocytosis.
• A variety of medications may have an effect on the MCV.
• Paresthesia or gait disturbances suggest vitamin B-12 deficiency.
• Recent acute blood loss may signal that reticulocytosis is causing the MCV increase.

Physical

• Glossitis suggests that the macrocytosis stems from deficiency of vitamin B-12, folate, or both.
• Tachycardia is usually modest and is common in patients with severe anemia.
• Flow murmurs usually are noted only in patients with severe anemia.
• Splenomegaly may be quite remarkable when the macrocytosis is due to hemolysis, infiltrative disorders, or neoplasms.
• Jaundice suggests liver disease or hemolysis, both of which may lead to an increased MCV.
• Conjunctival pallor is evident in patients with severe anemia.
• Neurological disorders, such as ataxia, loss of posterior column sensations, loss of deep tendon reflexes (particularly ankle reflex), and confabulation, may suggest vitamin B-12 deficiency.

Causes

• Vitamin B-12 deficiency is a cause of macrocytosis. Because DNA synthesis requires cyanocobalamin (vitamin B-12) as a cofactor, a deficiency of the vitamin leads to decreased DNA synthesis in the erythrocyte, thus leading to macrocytosis. A dietary deficiency of vitamin B-12 is rare, although deficiency can result from the following:
  • Lack of intrinsic factor in patients with postgastrectomy status or who have pernicious anemia
  • Malabsorption of vitamin B-12 secondary to small bowel overgrowth, tapeworm, familial factors, drugs, ileal bypass, ileal enteritis, or sprue
• Folate also is needed as a cofactor in the synthesis of DNA. Folate deficiency may be caused by any of the following:
  • Dietary deficiency
  • Increased requirements of pregnancy
  • Congenital deficiency
  • Sprue
• Inherited disorders of DNA synthesis include the following:
  • Lesch-Nyhan syndrome
  • Deficient enzymes for folate metabolism
  • Homocystinuria
• Drug-induced macrocytosis is the most common cause in nonalcoholic patients. Usually, no associated anemia is present. The following categories of drugs are known to cause macrocytosis:
  • Folate antagonists (methotrexate)
  • Purine antagonists (6-mercaptopurine)
  • Pyrimidine antagonist (ara-C)
  • Alkylating agents (cyclophosphamide)
  • Azidothymidine (AZT)
  • Trimethoprim
  • Oral contraceptive pills (OCPs)
  • Dilantin
  • Arsenic
• Reticulocytosis may be due to posthemorrhagic blood loss or hemolysis. Reticulocytes are immature red cells released in response to decreased hematocrit levels.
• Long-term alcohol intake directly affects bone marrow. This effect is not related to the presence of liver disease or vitamin deficiency and resolves only after months of abstinence from alcohol.
• Refractory anemias
  • Myelodysplastic anemias
  • Myelophthisic anemias (marrow replacement by neoplasm, granuloma, or fibrosis)
  • Aplastic anemia
  • Acquired sideroblastic anemia
• Macrocytosis in patients with COPD is attributed to excess cell water secondary to carbon dioxide retention.
• Benign familial macrocytosis is an inherited syndrome in which patients have mild asymptomatic macrocytosis.
• Macrocytosis of liver disease is secondary to increased cholesterol and phospholipids deposited on membranes of circulating erythrocytes. This deposition effectively increases the surface area of the erythrocyte.
• Hypothyroidism
  • Hypothyroidism is a manifestation of hormone deficiency.
  • More commonly, hypothyroid patients exhibit a normocytic anemia.
  • Artifactually elevated MCVs must be considered in certain patients. This happens less frequently with newer counting machines.
  • Hyperglycemia and cold agglutinins may cause artificially elevated MCVs.

Differential Diagnoses

Alcoholism
Hemolytic Anemia
Hypothyroidism
Myelodysplastic Syndrome

Other Problems to Be Considered

Liver disease

Workup

Laboratory Studies

• Complete CBC with platelet count
  • The hemoglobin/hematocrit level may provide a guide to diagnosis, and it determines presence and severity of anemia.
  • WBC and platelet count may be decreased in primary marrow disturbances.
  • The MCV is a calculated average volume of the erythrocytes. An MCV greater than 100 fL is, by definition, macrocytosis. Because evaluation of the RBC size is key to the diagnosis of an anemia, the MCV is considered to be the most important of the RBC indices.
• Peripheral blood smear morphology may be helpful. Round macrocytes suggest liver or marrow infiltrative disease, whereas oval macrocytes tend to suggest a megaloblastic disorder.
  • This study provides clues to the etiology of macrocytosis.
  • Hypersegmented neutrophils and macro-ovalocytes strongly suggest megaloblastic anemia.
  • Nucleated RBCs, teardrop cells, decreased and/or large platelets, and immature WBCs are often present in myelophthisic disease and leukemias.
• Reticulocyte count
  • This study helps to determine if hemolysis is present; it also indicates malfunctioning bone marrow.
  • Expect marked reticulocytosis (>4) in hemolytic anemias.
  • Reticulocyte count less than 1% indicates inadequate marrow production.
  • Reticulocyte count must be corrected for degree of anemia.
• Coombs test
  • Perform this test if the reticulocyte count is elevated to aid in confirming the diagnosis of hemolysis.
  • Expect a positive direct Coombs test finding in autoimmune hemolytic anemias, hemolytic transfusion reactions, and some drug-induced anemias (eg, penicillin, methyldopa, some cephalosporins, sulfonamides).
• Lactate dehydrogenase (LDH) is elevated in both intravascular and extravascular hemolysis including the ineffective erythropoiesis that occurs in megaloblastic anemias.
• Because the haptoglobin binds free hemoglobin, a low or absent haptoglobin level indicates intravascular hemolysis.
• If macro-ovalocytes and hypersegmented neutrophils are noted on peripheral smear, the vitamin B-12 level may be low.
• RBC folate levels
  • If folate deficiency is the cause of the macrocytosis, the RBC folate level likely will be decreased.
  • As in vitamin B-12 deficiency, peripheral smear may reveal hypersegmented neutrophils and macro-ovalocytes.
• Homocysteine level: Serum total homocysteine levels almost always are elevated in patients with folate deficiency, because folate is required in the remethylation step converting homocysteine to methionine. Serum methylmalonic acid and homocysteine levels may be increased even in early vitamin B-12 deficiency.
• Serum unconjugated bilirubin is expected to be elevated in hemolysis.
• If vitamin B-12 deficiency is the cause of the macrocytosis, the serum vitamin B-12 level likely will be decreased. Serum methylmalonic acid and homocysteine levels are increased early in vitamin B-12 deficiency, even before hematologic manifestations or decreases in B-12 levels are noted.
• A Schilling test was previously considered the criterion standard to further investigate a low vitamin B-12 level. However, many institutions no longer offer the Schilling test. Alternative tests to the Schilling test are antibodies to parietal cells and intrinsic factor antibodies.
• A serum folate level may be obtained, although an RBC folate level is more reliable because it reflects the level over the lifespan of the RBC.

Procedures

• Bone marrow biopsy and aspirate
  • The bone marrow biopsy and aspirate determines if the marrow is functioning adequately and also may reveal replacement of marrow with tumor, granuloma, or fibrosis. Obtain the bone marrow prior to vitamin B-12 folate therapy or blood transfusion because megaloblastic changes may reverse rapidly.
  • The bone marrow in megaloblastic anemias is usually hypercellular with all cell lines proliferating. Marked erythroid hyperplasia may occur to the point at which the myeloid-erythroid ratio is reversed. Nuclear-chromatin dissociation with a young-appearing nucleus with abundant mature-appearing cytoplasm may occur. Granulocytic hyperplasia with giant metamyelocytes and bands often are noted.

Histologic Findings

• Blood: On peripheral smear, large RBCs are evident. Depending on the etiology of the macrocytosis, peripheral smear may reveal nucleated RBCs, target cells, RBC fragments, hypersegmentation of neutrophils, immature WBCs, large platelets, or pancytopenia.
• Marrow: Depending on the etiology of the macrocytosis, marrow may reveal hypercellularity, megaloblastic changes, fibrosis, infiltration by tumor or granulomatous disease, leukemic changes, or erythroid hyperplasia.

Treatment

Medical Care

• Evaluation usually can be performed on an outpatient basis.
• Medical treatment depends on the etiology of the macrocytosis, the presence and severity of an anemia, and the symptoms of the patient.
  • After the appropriate laboratory studies are obtained, the symptomatic anemic patient may be transfused with packed RBCs.
  • If a drug is thought to be the cause of the macrocytic anemia, especially if hemolysis is occurring, discontinue administration of the offending drug.
  • Patients deficient in vitamin B-12 or folate should receive replacement therapy.
  • Counsel patients suspected of abusing alcohol to abstain.
  • Treat malignancies, granulomatous diseases, and COPD according to standards for each.
• Hospitalization may be required to treat some causes of macrocytosis, especially acute leukemias.

Consultations

• Hematology
• Oncology

Diet

If folate or vitamin B-12 deficiency is the cause of the macrocytosis, modify the diet to include foods rich in these vitamins. Red meat is a good source of vitamin B-12, and green leafy vegetables are excellent sources of folate. Do not provide folate supplementation without vitamin B-12 replacement therapy in any patient with vitamin B-12 deficiency or with suspected vitamin B-12 deficiency, since this may precipitate subacute combined degeneration of the spinal cord.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Vitamins

In macrocytosis associated with vitamin deficiencies, the deficient vitamin is replaced.⁵

Folic acid (Folvite)

Important cofactor for enzymes used in production of RBCs.

Dosing

Adult

1 mg/d PO

Pediatric

Not established

Interactions

Increase in seizure frequency and a decrease in subtherapeutic levels of phenytoin reported when used concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

A - Safe in pregnancy

Precautions

Benzyl alcohol may be contained in some products as a preservative (associated with a fatal gasping syndrome in premature infants); resistance to treatment may occur in patients with alcoholism and deficiencies of other vitamins

Vitamin B-12 (Crystamine, Crysti 1000, Cyomin)

Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitamin B-12 in humans. Vitamin B-12 is synthesized by microbes but not by humans or plants. Vitamin B-12 deficiency may result from intrinsic factor deficiency (pernicious anemia), partial or total gastrectomy, or diseases of the distal ileum.

Dosing

Adult

100-1000 mcg IM qmo

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity; hereditary optic nerve atrophy

Precautions

Pregnancy

A - Safe in pregnancy

Precautions

Severe hypokalemia may result in vitamin B-12 megaloblastic anemia (may be fatal) because of increased cellular potassium requirements when anemia corrects

Multiple vitamins (M.V.I.-12, Cernevit-12)

Used as dietary supplement.

Dosing

Adult

M.V.I.-12: 10 mL/d IV
Cernevit: 5 mL/d IV

Pediatric

M.V.I.-12:
<12 years: 5 mL/d IV
>12 years: Administer as in adults
Cernevit:
<12 years: 2.5 mL/d IV
>12 years: Administer as in adults

Interactions

Hydralazine and isoniazid may decrease effect of pyridoxine; pyridoxine may decrease effect of levodopa

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in severe renal or liver failure; additional vitamin A may be required in pediatric patients

Follow-up

Further Outpatient Care

• Outpatient follow-up depends on the cause of the macrocytosis.

Inpatient & Outpatient Medications

• Folate 1 mg/d may be prescribed in patients with folate deficiency.
• Vitamin B-12 injections (100-1000 mcg IM per mo), continued indefinitely, may be prescribed.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose and treat the cause of the macrocytosis

References

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2. Rumsey SE, Hokin B, Magin PJ, Pond D. Macrocytosis--an Australian general practice perspective. Aust Fam Physician. Jul 2007;36(7):571-2. [Medline]. [Full Text].

3. Sternfeld T, Lorenz A, Schmid M, et al. Increased red cell corpuscular volume and hepatic mitochondrial function in NRTI-treated HIV infected patients. Curr HIV Res. May 2009;7(3):336-9. [Medline].

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5. Ganji V, Kafai MR. Hemoglobin and hematocrit values are higher and prevalence of anemia is lower in the post-folic acid fortification period than in the pre-folic acid fortification period in US adults. Am J Clin Nutr. Jan 2009;89(1):363-71. [Medline]. [Full Text].

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Keywords

macrocytosis, macrocytes, megaloblasts, anemia, megaloblastic anemia, myelodysplastic anemia, myelophthisic anemia, aplastic anemia, acquired sideroblastic anemia, vitamin B-12 deficiency, folate deficiency, chronic alcoholism, alcoholism, accelerated erythropoiesis, chronic obstructive pulmonary disease, COPD, Lesch-Nyhan syndrome, deficient enzymes for folate metabolism, homocystinuria, liver disease, hypothyroidism

Contributor Information and Disclosures

Author

Wendy Brick, MD, Consulting Staff, Department of Internal Medicine, Division of Hematology and Oncology, Mecklenburg Medical Group
Wendy Brick, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, and American Society of Hematology
Disclosure: Nothing to disclose.

Coauthor(s)

Russell Burgess, MD, Department of Internal Medicine, Division of Hematology/Oncology, East Carolina Internal Medicine
Russell Burgess, MD is a member of the following medical societies: American College of Physicians and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Paul Schick, MD, Emeritus Professor, Department of Internal Medicine, Thomas Jefferson University Medical College; Research Professor, Department of Internal Medicine, Drexel University College of Medicine; Adjunct Professor of Medicine, Lankenau Hospital, Wynnewood, PA
Paul Schick, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Hematology, International Society on Thrombosis and Haemostasis, and New York Academy of Sciences
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Ronald A Sacher, MB, BCh, MD, FRCPC, Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center
Ronald A Sacher, MB, BCh, MD, FRCPC is a member of the following medical societies: American Society of Hematology
Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership

CME Editor

Rajalaxmi McKenna, MD, FACP, Consulting Staff, Department of Medicine, Southwest Medical Consultants, SC, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Emmanuel C Besa, MD, Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, Thomas Jefferson University
Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Hematology, and New York Academy of Sciences
Disclosure: Nothing to disclose.

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National Guideline Clearinghouse

• Anemia in the long-term care setting. American Medical Directors Association - Professional Association. 2007. 28 pages. NGC:005655
• Folic acid for the prevention of neural tube defects: U.S. Preventive Services Task Force recommendation statement. United States Preventive Services Task Force - Independent Expert Panel. 1996 (revised 2009). 6 pages. NGC:007233  

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