A low reading on the Mean Corpuscular Volume (MCV), a calculation that forms part of a routine Complete Blood Count (CBC), is a common finding that signals an underlying issue with red blood cell production. When this value is low, it means the red blood cells circulating in the bloodstream are smaller than the average size. This laboratory result is not a diagnosis in itself, but rather indicates that further investigation is necessary to determine the cause of the cell size reduction.
Understanding MCV and Microcytosis
The Mean Corpuscular Volume measures the average volume of the red blood cells, which transport oxygen throughout the body. These cells contain the protein hemoglobin, which binds to oxygen in the lungs and releases it to the body’s tissues. The MCV is measured in femtoliters (fL), and the normal range for adults is approximately 80 to 100 fL, though this can vary slightly between laboratories.
A reading below this threshold, typically under 80 fL, is referred to medically as microcytosis, meaning the red blood cells are abnormally small. The size of the red blood cell is closely linked to the amount of hemoglobin it contains. When the cell-making process in the bone marrow is hindered, particularly in producing sufficient hemoglobin, the resulting cells are smaller and paler.
This reduction in size and hemoglobin content can directly impact the efficiency of oxygen delivery to organs and tissues. Consequently, microcytosis is frequently associated with anemia, a condition characterized by a reduced ability of the blood to carry oxygen. Identifying the reason for the small cell size is the next step in management.
Primary Medical Conditions Linked to Low MCV
The appearance of microcytosis points toward underlying conditions that interfere with hemoglobin synthesis. The most common cause worldwide is iron deficiency, where iron forms the central component of the heme group within the hemoglobin molecule. Without adequate iron stores, the body cannot construct enough hemoglobin, causing red blood cell precursors to undergo extra divisions, ultimately leading to smaller mature cells.
Iron deficiency often stems from chronic blood loss (such as heavy menstrual bleeding or slow gastrointestinal bleeding), insufficient dietary intake, or impaired absorption. This condition, known as Iron Deficiency Anemia (IDA), represents a true shortage of the raw material needed for hemoglobin synthesis. Replenishing iron stores is necessary to correct this type of microcytosis.
Another significant cause involves genetic conditions called thalassemias, which are inherited disorders affecting the production rate of the globin protein chains that make up hemoglobin. Unlike IDA, thalassemias involve a quantitative defect in hemoglobin synthesis rather than an iron shortage. The resulting imbalance of globin chains leads to the premature destruction of red blood cell precursors and the production of small, fragile red blood cells, even if the iron supply is normal.
Thalassemia minor, or thalassemia trait, is a mild form that often causes only asymptomatic microcytosis and is frequently an incidental finding. Because this condition is genetic, it is permanent and does not respond to iron supplementation. Ethnic background, such as Mediterranean, African, or Southeast Asian ancestry, can increase the likelihood of this diagnosis.
A third condition that may present with microcytosis is the Anemia of Chronic Disease (ACD), usually associated with long-term inflammatory states like autoimmune disorders, chronic infections, or cancer, which triggers the release of signaling molecules, most notably the hormone hepcidin. Hepcidin effectively locks iron away within storage cells, such as macrophages, and reduces its absorption from the gut. This creates a “functional iron deficiency” where iron exists in the body but is inaccessible to developing red blood cells. Although ACD more commonly results in red blood cells of normal size, it can lead to microcytosis.
Navigating Diagnosis and Treatment
A low MCV result triggers a process of differential diagnosis, requiring a healthcare provider to use additional laboratory tests to pinpoint the cause. The first and often most informative follow-up test is the serum ferritin level, which directly measures the amount of iron stored in the body. A low ferritin level is highly indicative of Iron Deficiency Anemia, confirming the need for iron repletion.
However, because ferritin is an acute phase reactant, its levels can be artificially elevated by inflammation, complicating the diagnosis in cases of Anemia of Chronic Disease. In such instances, a full iron panel is often ordered, which includes measurements for serum iron, Total Iron Binding Capacity (TIBC), and Transferrin Saturation. The pattern of these results helps distinguish between the absolute iron deficit of IDA and the functional iron restriction of ACD.
If iron studies are inconclusive or if the patient has a relevant family history or ethnic background, hemoglobin electrophoresis may be performed. This specialized test separates and measures the different types of hemoglobin present in the blood, which is the definitive method for identifying thalassemias.
Treatment is entirely dependent on the confirmed cause of the microcytosis. If Iron Deficiency Anemia is diagnosed, management involves oral iron supplementation to rebuild iron stores and identifying the source of chronic blood loss, which may require an endoscopic evaluation. For those with thalassemia trait, no treatment is usually necessary, although genetic counseling may be offered. When Anemia of Chronic Disease is the cause, the focus shifts to treating the underlying inflammatory condition, as iron therapy alone is often ineffective.