Individuals all over the world are diagnosed with different diseases every day. The most common type of nutritional disorder worldwide is known as iron deficiency anemia. This disorder affects one-fifth of the world population and results from an insufficient dietary intake or absorption of iron, resulting in decreased incorporation of hemoglobin into red blood cells. Often times, individuals believe they are one of very few people suffering from a disease, when in reality there are many other people diagnosed with the same condition. It’s important to know the etiology, pathogenesis, clinical manifestations, laboratory diagnosis, and management of a particular disease if you have been diagnosed. Knowing this type of information is very useful and allows individuals to better manage the disorder.
It’s very important to understand the etiology of a disease. To prevent being diagnosed with iron deficiency anemia, it’s important to know what can cause it. It’s important to note that toddlers, adolescent girls, and women of childbearing age are most at risk for the development of iron deficiency anemia. However, the disease is also prevalent among individuals living in poverty, infants consuming cow’s milk, older individuals ingesting restricted diets, and teenagers eating poor diets with non-nutritional food. The daily requirement for iron consumption is 7-10 mg for adult men and 7-20 mg for adult women. It’s important to meet these requirements to prevent the onset of this disorder. Although these amounts of iron are consumed, only 10-15% of it are actually absorbed so it’s very important to meet the bare minimum requirement. There are many things that can cause individuals to develop this disease. The main causes include: dietary deficiency, impaired absorption, increased requirement, chronic blood loss, use of medications that cause gastrointestinal bleeding, surgical procedures that decrease stomach acidity, intestinal transit time and absorption, and eating disorders such as pica, where individuals crave and eat non-nutritional substances such as dirt, chalk, and paper. Overall, the clinical manifestations that result are mostly related to the reduction in adequate levels of hemoglobin.
An important thing to note is that women with excessive menstrual bleeding (menorrhagia) are primary candidates for this condition. Losing just 2-4 mL/day, 1-2 mg of iron is enough to cause iron deficiency anemia. This explains why this disease is most prevalent in females during their reproductive years and why it decreases following menopause. Some women have very heavy periods and can lose more than 2-4 mL/day of blood from them, putting them at a high risk for this condition. The opposite is true for males whose incidence rate peaks during childhood and adolescence and is lowest during young adulthood. Studies have also found that African American females living in urban poverty are at the highest risk and that overweight children, adolescents, women, and those undergoing bariatric surgery are more prone to being diagnosed. In developing countries, children can be affected by a chronic parasite manifestation that can cause intestinal blood and iron loss. Dietary intake of iron is outweighed by its losses. Upon treatment of such an infection, anemia, appetite, and growth will all show significant improvements. Although iron stores are depleted in the body or there is reduced absorption of it, there is an increased absorption of other elements, such as lead and cadmium.
Whether individuals have this disorder or are just looking to make themselves aware of its development, it’s important to note its pathogenesis. Iron deficiency anemia is a type of hypochromic-microcytic anemia. This type of anemia occurs when the body has low levels of red blood cells that are both smaller and paler than normal. Individuals will experience this disorder when their iron stores are depleted or there is decreased iron absorption. There are many metabolic disorders that can lead to an insufficient delivery of iron to bone marrow or an impaired iron use within the bone marrow. Although there may be a surplus of iron available, delivery can be inadequate to maintain heme synthesis, thus resulting in an iron deficiency. Iron is responsible for regulating immune effector mechanisms and acquired hypoferremia is part of the body’s response to the infection. After inflammation occurs to a sufficient degree, anemia can result as part of the nonspecific acute phase response. Evidently, many pathogens require iron to survive, so hypoferremia could prevent their growth.
The disease develops in three distinct stages. Progression of this disease begins when the iron stores in the body are depleted. At this point in time, erythropoiesis can proceed normally, with the hemoglobin content of the erythrocytes remaining normal. As the disease begins to progress, the transportation of iron in the bone marrow is diminished as a result of iron-deficient erythropoiesis. After the disease has had some time to develop, the small hemoglobin-deficient cells enter the circulation. There, they replace the normal aged erythrocytes and the normal red blood cells are removed from the circulation. Clinical manifestations do not occur until stage three of this disease, after iron stores are depleted and hemoglobin production is diminished.
It’s very important to be able to recognize clinical manifestations of this disease. The sooner that an individual realizes they have such a disease, the sooner that they can seek treatment. That is why it’s very important to know what to look for! It takes time for this disease to progress and symptoms begin gradually. It’s not until individuals’ hemoglobin levels fall to around 7-8 g/dL do they seek medical attention. Early symptoms are categorized by fatigue, weakness, shortness of breath, and pale earlobes, palms, and conjunctivae. As the disease progresses and becomes more severe, structural and functional changes begin to occur within the epithelial tissue. Individuals will begin to notice their fingernails becoming brittle, thin, coarsely ridged, and “spoon-shaped” or concave. This happens as a result of impaired capillary circulation. Often times individuals with iron deficiency anemia also experience an unexplained burning mouth syndrome. Their tongue papillae become sore, red, and often burn as atrophy occurs. Depending on how severe the iron deficiency is, determines the level of pain the individual will experience. Iron replacement therapy is given to these individuals and within 1-2 weeks, their symptoms will be relieved. Angular stomatitis is another possible symptom, where the epithelium at the corners of the mouth become both dry and sore. Individuals can have difficulty swallowing, which is associated with an esophageal “web.” This “web” is a thin, concentric, smooth extension of normal esophageal tissue consisting of mucosa and submucosa at the juncture between the hypopharynx and esophagus. Nonheme iron is a component in many enzymes throughout the body. Some of these enzymes include: cytochromes, myoglobin, catalases, and peroxidases. Deficiencies and abnormalities of these iron-dependent enzymes can account for many of the clinical manifestations listed for iron deficiency anemia. Individuals can also experience gastritis, neuromuscular changes, headache, numbness, irritability, vasomotor disturbances, and tingling. Elderly individuals diagnosed with this disease can exhibit mental confusion, memory loss, and disorientation. These symptoms are often ignored, as they are seen as part of old age. In younger children on the other hand, iron deficiency anemia can lead to cognitive impairment.
Individuals are diagnosed with this condition after an evaluation revealing clinical symptoms and decreased levels of hemoglobin and hematocrit. Although this type of anemia is known to prevail when iron stores are depleted, it’s also accompanied by lower than normal serum iron, ferritin, and transferrin saturation levels. To test an individual’s iron stores, bone marrow biopsy and iron staining can be directly measured or an indirect measurement can be conducted using laboratory exams for serum ferritin level, transferrin saturation, or total iron-binding capacity. For the past 25 years, serum ferritin has been the appropriate measurement for iron status. As a measurement, 1 mcg/L serum ferritin corresponds to 8-10 mg or 120 mcg of storage iron per kilogram body weight. One flaw with the measurement of serum ferritin levels is that they might be elevated from acute or chronic inflammation, liver disease, malignancy, or alcoholism. To measure heme synthesis, doctors look at the amount of free erythrocyte protoporphyrin (FEP) within erythrocytes. Determining the concentration of soluble fragment transferrin receptor can also allow doctors to differentiate between primary iron deficiency anemia and iron deficiency anemia as a result of a chronic disease. Doctors can also look at the serum transferrin receptor levels to determine individuals’ iron levels. Transferrin receptors are membrane glycoproteins that bind circulating transferrin for transport into cells. The ratio of serum levels of transferrin receptor to ferritin estimates body iron stores and differentiates primary iron deficiency anemia from a secondary chronic disease. A problem with this method however, is that there is a lack of proper standardization for the serum transferrin receptor assay.
The first step to manage iron deficiency anemia is to identify and eliminate any possible sources of blood loss. By doing so, less iron will be lost from the body. Individuals are offered iron replacement therapy beginning with doses of 150-200 mg/day of iron. Patients treated with this therapy should notice an increase in their hematocrit levels within the first 1-2 months. Measuring the serum ferritin level will provide a more accurate measurement when reevaluation of the individual’s total body stores of iron is required. Once the serum ferritin level reaches 50 mcg/L, the body is at an acceptable iron level. This will also decrease the symptom’s an individual is having from this disease such as fatigue, lethargy, etc. An individual will receive replacement therapy for around 6-12 months after the bleeding has stopped. Some individuals continue with it for as long as 24 months. As previously stated, menstruating females lose more blood than the average person, so they may need a daily oral iron replacement therapy of 325 mg/day until they have reached menopause and the bleeding has come to a halt. Parenteral iron replacement is another way to manage this disease, but it’s only used in instances of uncontrolled blood loss, intolerance to oral iron, intestinal malabsorption, or poor adherence to oral therapy. In the United States, iron dextran has been the only parenteral agent available for managing this disease. Additionally, intramuscular injection is recommended over intravenous administration. However, many individuals use the intravenous method because larger doses can be administered. Just recently, medications have been approved for parenteral therapy in treating iron deficiency anemia such as sodium ferric gluconate complex in sucrose (Ferrlecit) and iron sucrose injection (Venofer). The first choice by medical professionals is the iron dextran because it is cheaper and does not require as many infusions.
Individuals are diagnosed with new diseases each day. It’s important to stay aware of the symptoms that are prominent among certain disorders and to seek treatment for them. In this case, iron deficiency anemia is very common worldwide and its etiology, pathogenesis, clinical manifestations, laboratory diagnosis, and management should be noted.