Severe deficiency of either folate or vitamin B12 leads to megaloblastic anemia which clinically manifests as fatigue, weakness, and shortness of breath owing to a low red blood cell count. Hematologically, megaloblastic anemia is characterized by the presence of large, immature, nucleated cells (megaloblasts) in the bone marrow and macrocytes in the peripheral blood. Folate deficiency typically arises when folate requirement is increased (e.g., in pregnancy) and/or when folate availability is reduced as a result of low dietary intakes or malabsorption (e.g., in celiac disease). Pernicious anemia, the clinical condition of severe deficiency of vitamin B12, arises from an autoimmune gastritis characterized by B12 malabsorption owing to loss of intrinsic factor. A more subtle depletion of vitamin B12 status can however arise from mild atrophic gastritis leading to reduced gastric acid production, thereby diminishing B12 absorption from food. Apart from folate and B12, riboflavin deficiency can also lead to nutritional anemia. There are consequences of B-vitamin deficiency throughout the lifecycle, adversely affecting metabolic functioning and contributing substantially to the global burden of disease. This chapter will consider the causes, detection, and consequences of B-vitamin deficiency, ranging from the anemia of clinical deficiency to other manifestations associated with less severe deficiency, and the potential for prevention through effective public health measures.
|Title of host publication||Nutritional Anemia|
|Editors||Crystal Karakochuk, Klaus Kraemer, Diego Moretti, Michael Zimmermann|
|Publisher||Springer International Publishing|
|Number of pages||13|
|Publication status||Published online - 16 Dec 2022|