Iron deficiency interferes with hemoglobin synthesis that will cause microcytic and hypochromic corpuscles. While B12 or folate defeciency interfere with DNA synthesis that delays the maturation of the corpuscles (macrocytic).
First of all, you must obtain a reticulocyte count. If the patient has reticulocytosis, you may have an increased MCV because of retics are larger than normocytes. This may happen in three instances: hemorrhage, hemolysis or during recovery from aplasia. Only if you have a low reticulocyte count you may classify anemias in micro-, normo- or macrocytic. In such instances (hyporigenerative anemias), please refer to what dr. Saadeldin has already stated.
This may happen more often than one might think. The MCV may be normal or slightly reduced or slightly increased, whichever deficiency prevails, or is of longer duration. The clinician should be astute to diagnose this condition, by evaluating multiple CBC along time.
The cause of most of the anemias can be determined through assessment of the mean corpuscular volume (MCV), reticulocyte count, and peripheral smear. MCV refers to the average volume of RBCs and reflects RBC size. A low MCV suggests small RBCs, a condition known as microcytosis, which occurs from insufficient hemoglobin synthesis. Red cell distribution width (RDW) is a derived measure of RBC size variation. In the normal child, RBC size is usually uniform and the RDW is 11.5%-14.5% of RBC volume divided by the MCV. Though highly sensitive, it has low specificity as a test, which limits its use as an independent clinical marker. However, in conjunction with MCV it may clarify the diagnosis of microcytosis. For example, the ratio of MCV to RBCs, also known as Mentzer's Index, differentiates anemias with uniformly small RBCs from those producing variably sized cells. Iron deficiency anemia creates a low MCV due to production of microcytic RBCs. However, the RDW is increased due to variation in RBC size and shape. In iron deficiency anemia the Mentzer index will be elevated, greater than 13. The reticulocyte count measures circulating immature erythrocytes. Expressed as either a percentage or absolute count, an elevation suggests premature release of immature RBCs into the circulation to replace losses, as can occur with active hemolysis. Conversely, a low reticulocyte count reflects insufficient bone marrow release of RBCs. The normal range of reticulocytes is 0.5%-1.5% of RBC populations. Iron deficiency anemia is notable for a decreased reticulocyte count, indicating inadequate RBC production.
Analysis of the peripheral blood smear allows interpretation of multiple visible characteristics of the RBC, including shape, size, uniformity, and pigmentation. RBC shape (bicon-cave disk or abnormal forms), size (microcytic, normocytic, or macrocytic) and color intensity (hypochromic, normochromic, or hyperchromic) are visible RBC features that may provide diagnostic clues to the origin of anemia. Iron deficiency anemia due to iron deficient erythropoiesis is notable for microcytosis and hypochromia, which will be evident on the smear as small, hypopigmented RBCs.
Also in countries with high prevalence of Thalessemia minor, a low MCV may not be helpful in the differential diagnosis and commonly misdiagnosed as Iron deficiency anemia. In that case look at the RDW. High RDW can be in favor of iron def. anemia.
You go into a semantic problem. The type of anemia to my understanding governs the size of the red cell and not the other way round. But your question is relevant anyway - I'm following the discussion with interest
The statement of Hamdi about the RDW and iron deficiency anemia is nicely explained in Anil's answer, so thank you both for clarifying this.
and whether the same mechanism applies to lymphocytes is still vague to me as I could not download the full text of Urs's link. So, if any one can post this, it would be fantastic.
Thanks a million Islam for the paper. I finally got the picture and I quote from the paper:"Cobalamin deficiency leads to impaired DNA synthesis, whereas RNA synthesis remains intact. This impairment leads to a buildup of cytoplasmatic components and consecutive cell growth in slowly dividing cells, which morphologically can be recognized as macrocytosis, not only in red blood cells."
I am intrigued though to know the anonymous reference from which the authors got this explanation; it was written in NEJM in 1967. The same anonymous reference explained that :"the size of a variety of cells is influenced by cobalamin deficiency". Perhaps iron deficiency doesn't have the same influence because of its effect on hemoglobin per se.