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Mean Corpuscular Volume as Alcohol Biomarker

MCV is printed in the report generated during complete blood count. The normal range is 82–95 fL. One of the most common causes of abnormal MCV is anemia. If MCV is below the normal range, then the anemia is considered as microcytic anemia, whereas if MCV is above the normal range, it is called macrocytic anemia. Anemia may also be present even if MCV is within the normal range (normocytic anemia). It may occur in an acute condition such as blood loss. MCV is also used as an alcohol biomarker because it increases in subjects with alcohol abuse (macrocytosis). As early as 1978, Whitehead et al. showed that consumption of 60 g (approximately four drinks) of alcohol daily increased MCV above the reference range in most individuals, with the highest MCV being 104 fL (range, 84–104 fL). The range of MCV was 84–100 fL for individuals who consumed up to three drinks daily and 84–98 fL for individuals who consumed only one drink daily [1]. With abstinence, MCV returns to normal values within 2–4 months. Alcoholism means.

Macrocytosis is usually defined as an MCV value greater than 100 fL, and alcohol dependence is one of the causes of macrocytosis other than anemia. In one study, the authors observed that approximately 3% of the general population had MCV values greater than 100 fL [2]. However, theoretically macrocytosis may be considered at an MCV value greater than 95 fL. In contrast, Rumsey et al. reported that 7% of the population they studied had an MCV greater than 96 fL, and approximately 1.7% had an MCV greater than 100 fL [3]. In another study, the authors observed that 138 of 3805 adult outpatients (3.7%) had an elevated MCV of greater than 98.5 fL (normal, 82–95 fL). The authors further evaluated 73 of these patients with a mean an MCV of 102.5 fL (another 55 patients were not evaluated further). Of these 73 patients, alcoholism was the cause of the elevated MCV in 47 patients [4]. Morgan et al. defined macrocytosis as an MCV value greater than 95 fL and studied 303 alcoholics with liver disease, 60 nonalcoholics with liver disease, and 35 control subjects. The authors observed that 70.3% of subjects with alcoholic liver disease showed macrocytosis, but macrocytosis was also found in 23.3% of subjects with nonalcoholic liver disease. An MCV value greater than 100 fL was observed in 49.5% of subjects with alcoholic liver disease but only in 3.3 subjects with nonalcoholic liver disease. Macrocytosis was more common in female alcoholics (86.3%) than in male alcoholics (63.0%). The authors concluded that an MCV greater than 100 fL in patients with liver disease is indicative of alcohol-related liver disease [5]. Koivisto et al. reported that an MCV up to 98 fL was observed in moderate drinkers (1–40 g alcohol per day); the reference interval of MCV calculated from mean and two standard deviations (mean ± 2SD) in these individuals was 82–98 fL, whereas the reference range calculated for abstainers was 82–96 fL. Use of 96 fL as the cutoff between alcoholics and nonalcoholics yielded a sensitivity of 44%, specificity of 98%, a positive predictive value of 96%, and a negative predictive value of 58% [6]. In general, MCV is less than 110 fL in chronic alcohol abusers [7]. However, in megaloblastic anemia, MCV can be greater than 110 fL, sometimes reaching 130 fL or higher.

6.2.1 Mechanism of Increased MCV in Alcoholics

The mechanism of increased MCV is probably related to hematotoxicity of both alcohol and its metabolite, acetaldehyde. Alcohol can permeate the cell membrane and alter lipid structures of the membrane. In addition, alcohol can alter erythrocyte metabolism, thus altering its stability [8]. Acetaldehyde, which is formed during alcohol metabolism by enzymatic reaction involving the alcohol dehydrogenase enzyme and nicotinamide adenine dinucleotide as a cofactor, is highly reactive and can form stable adducts with proteins and other constituents of the cell membrane. As a result, erythrocyte membrane structure may become more susceptible to damage such as hemolysis, thus shortening its half-life [9]. Patients who abuse alcohol and demonstrate macrocytosis often show the presence of circulating antibodies that recognize acetaldehyde-modified epitopes of protein, indicating that the acetaldehyde–protein adduct may play an important role in erythrocyte abnormalities seen in alcohol-dependent patients [6]. Studies of male Japanese alcoholics showed that patients with inactive aldehyde dehydrogenase 2 (ALDH-2) enzyme due to the presence of the ALDH2*1/2*2 genotype had higher MCV than patients with normal ALDH-2 enzyme activity. ALDH-2 is a key enzyme involved in the removal of the toxic acetaldehyde metabolite of alcohol. Therefore, patients with inactive ALDH-2 enzyme may have a higher acetaldehyde concentration, thus further indicating the role of acetaldehyde in increasing MCV. In addition, MCV of 106 fL or greater indicates a high risk of esophageal squamous cell carcinoma in Japanese alcoholic men [10]. Another study showed that in Japanese men with MCV greater than 99 fL but no flushing experience after alcohol use, the risk of esophageal cancer was 2.5 times greater compared to that for Japanese men with an MCV of less than 93 fL [11].

6.2.2 Other Causes of Macrocytosis

In addition to alcohol abuse, macrocytosis is observed in megaloblastic anemia, commonly caused by vitamin B

and folate deficiency. Vitamin B

deficiency alone may not cause megaloblastic anemia. In megaloblastic anemia, erythrogenic precursors are larger than mature red blood cells because folate and vitamin B

deficiencies result in defective RNA and DNA synthesis. A nonmegaloblastic process leads to round macrocytes or macroreticulocytes. Although increased MCV due to alcohol abuse is a nonmegaloblastic process, individuals who chronically abuse alcohol may be deficient in vitamin B

and folate [12]. Hypothyroidism and other diseases may also cause macrocytosis. Keenan commented that macrocytosis defined by an MCV greater than 100 fL should be considered as an indicator of human disease. In Keenan’s study, alcoholism was the main cause of macrocytosis. Anorexia nervosa may also cause macrocytosis [13]. Macrocytosis can be a manifestation of monoclonal gammopathy [14]. Unexplained macrocytosis may not be a benign finding and requires close follow-up because patients may develop worsening cytopenia or ultimately may be diagnosed with primary hematological malignancy [15]. Conditions that may cause macrocytosis other than alcohol abuse are summarized in Box 6.1. Various drugs may also cause increased MCV [16]. Common medications that may cause macrocytosis are listed in Table 6.1.

Red blood cell indices

The RBC indices consist of the mean cell volume (MCV), mean cell hemoglobin (MCH), and mean cell hemoglobin concentration (MCHC). These indices are used to differentiate the type of anemia and to assess patient response to replacement drug therapy.

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Mean corpuscular hemoglobin

MCH is the average RBC hemoglobin content. MCH is decreased in iron deficiency anemia and increased in folic acid and vitamin B

deficiencies and hemolytic anemia.

Mean corpuscular hemoglobin concentration

MCHC is the amount of hemoglobin per volume of RBCs.

Mean cell volume

MCV is the average volume of individual RBCs. MCV is decreased in iron deficiency anemia, thalassemia, and other chronic diseases (e.g., microcytic anemia). It is increased in folic acid and vitamin B

deficiencies (e.g., macrocytic anemia).

Macrocytic Anemia

Macrocytic anemias are characterized by red blood cells that have mean corpuscular volumes of greater than 100 fl. The three most common causes of macrocytic anemia are substance abuse, drug toxicity, and nutritional deficiency.

Substance abuse

Both alcohol and tobacco abuse can lead to a macrocytic anemia.

Drug toxicity

Drugs that commonly lead to macrocytic anemia are hydroxyurea, methotrexate, trimethoprim, and most cytotoxic chemotherapeutic agents.

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Nutritional deficiency

and folic acid deficiency are the two most common nutritional causes of macrocytosis. Folate deficiency is usually manifest by decreased folate levels in the serum or red blood cells. However, the most practical way to assess for folic acid deficiency is to measure serum homocysteine levels. Folic acid is required to convert homocysteine to methionine, and when it is deficient, homocysteine levels rise. High homocysteine levels can lead to more serious cardiovascular consequences.

deficiency is typically discovered by low serum B

levels. In the elderly, however, serum levels may be inaccurate. Measurement of the serum methylmalonic acid is a more accurate way to assess for B

is a required cofactor in the conversion of methylmalonyl coenzyme A to succinyl coenzyme A. Therefore, in true B

-deficient states, the levels of methylmalonyl coenzyme A would be expected to rise.

deficiency can result from an inadequate nutritional intake of vitamin B

or an inability to absorb vitamin B

from the GI tract. This is often caused by atrophic gastritis or the unavailability of the intrinsic factor that is required to absorb B

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from the gut, resulting in pernicious anemia.

deficiency can have a profound effect on DNA synthesis throughout the body, particularly in the central nervous system. In severe cases, permanent motor neuron injury and dementia (megaloblastic madness) can result. Thus, a comprehensive effort to establish the cause and implement correction of B

deficiency is warranted in any patient with macrocytic anemia.

Other causes of macrocytosis can be liver disease and hypothyroidism.

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