The International Nutritional Anemia Consultative Group (INACG) has recommended routine iron supplementation in all pregnant women. This is because; the high physiological requirement for iron in pregnancy is difficult to meet with most diets. The recommended dose in those living in areas of prevalence of anemia < 40% is 60mg for 6 months during pregnancy.
For those living in area with prevalence more than 40%, the recommended dose is the same, but the duration recommended is 6 months during pregnancy and continuing to 3 months postpartum. Further, the group recommends that if 6 months duration cannot be achieved in pregnancy, supplementation must be continued during the postpartum period for 6 months, or the dose must be increased to 120 mg iron in pregnancy. The iron should be given along with 400mcg of folate (Stoltzfus & Dreyfuss, Iron Suppl. Guidelines).
According to the 1990 Institute of Medicine Committee and the 1991 Life Sciences Research Office Guidelines, nonanemic women should consume 30 mg iron per day beginning in the 12th week of pregnancy and anemic women with confirmed low plasma ferritin concentrations should take iron supplements of 120-180mg per day (Institute of Medicine, 1993, qtd in Beard, 2000). In 1993, the Institute of Medicine recommended that iron supplementation be initiated after assessing the initial iron status in the body ((Institute of Medicine, 1993, qtd in Beard, 2000).
Graves and Barger (2001) have also recommended a more conservative approach to supplementation of iron during pregnancy. This is because, unnecessary high doses of iron supplementation can lead to Fenton reaction resulting in free radicals and oxidative damage, thus initiating various pathogenic processes such as cardiovascular disease, neuropathologies, and cancer (Beard, 2000). Etiology Dietary Causes Iron is available to the body from various foods. The available iron is either in the form of heme or non-heme.
Heme is the iron-containing part of hemoglobin present in the blood of animals and humans. Heme-iron is found in animal foods such as meat, liver, poultry and fish. Non-heme iron is that form of iron we get from plant products such as cereals, fruits, vegetables and pulses (beans). Heme -iron is more easily absorbed and used by the body than non-heme iron. Its absorption is little influenced by the person’s iron status, whereas, the absorption of non-heme iron is greatly influenced by a person’s iron status and is more absorbed when people have low iron stores.
The absorption of iron in food depends not only on its iron content and the form it’s in, but more importantly on the presence of other foods that enhance or reduce its absorption. Vitamin C or ascorbic acid increases the amount of non-heme iron that can be absorbed from plant foods. The presence of heme iron from animal foods also enhances non-heme iron absorption. The presence of certain compounds such as tannin (in tea), phytates, oxalates, phosphates and carbonates reduce the “bioavailability” of iron (Conrad, 2006).
Some foods contain iron inhibitors or ligands that bind with iron and prevent it from passing through the intestinal wall into the bloodstream. Calcium also blocks iron absorption. In addition, certain foods can bind the non-heme iron in another food eaten at the same time. For instance, wheat and rice contain ligands that bind most of the non-heme iron in kidney beans. Thus iron deficiency can occur in those who consume pure vegeterian diet and have iron inhibitors or ligands in theirdiet preventing the absorption of iron.
Also, diet that is constantly low in fat, high in sugar and also high in fibre can lead to iron depletion. Diet that has low levels of folate, vitamin B12, or vitamin C, can also cause iron-deficiency anemia. Loss of iron Haemorrhage: Bleeding causes loss of iron through blood. Bleeding causes stimulation of bone marrow to synthesize blood cells. During this process, iron stores are depleted. Blood loss can be acute or chronic. Acute blood loss can occur in severe injuries, surgery and frequent blood drawing.
Chronic blood loss occurs in bleeding ulcer, polyp, colon cancer, hookworm infection and chronic abuse of non-steroidal anti-inflammatory drugs (NHLBI, 2008). In pregnant women, placenta previa and abruptio placenta can also lead to blood loss and iron depletion. In iron deficiency anemia due to blood loss, maximal changes in the red blood cell cellular indices occur in approximately 120 days. This is because; this is the time when all normal erythrocytes produced prior to the hemorrhage are replaced by microcytes (Conrad, 2006).
Loss of iron due to other conditions: Iron depletion and iron deficiency anemia can also occur in conditions like hemosiderinuria, hemoglobinuria, and pulmonary hemosiderosis. Malabsorption of Iron Though there is sufficient iron in the diet, certain malabsorption conditions in the stomach and intestine can lead to decreased absorption of iron. These include prolonged achlorhydria, starch and clay eating, untreated sprue or celiac syndrome and extensive surgical removal of the proximal small bowel (Conrad, 2006). Increased Physiological Need in Pregnancy
While the demand for everyday iron in a non-pregnant adult woman is about 0. 8 mg, in pregnancy, the demand increases to about 7. 5mg of absorbed iron per day (Beard, 2000). Thus, there is decline in iron stores during pregnancy leading to iron-deficient erythropoiesis and anemia. Though there is increased efficiency of absorption of dietary or supplemental iron during pregnancy, it is often difficult to maintain a neutral iron balance (Beard, 2000). A modest drop in hemoglobin concentration in pregnancy is actually a normal physiologic event.
The hemoglobin concentrations reach a nadir in the mid second trimester of pregnancy and then rise again in the third trimester (Beard, 2000). Pathophysiology Iron is one of the most important metals in the body. It is necessary for many metabolic processes like oxygen transport, DNA synthesis, and electron transport. Body tries to maintain equilibrium between iron intake and iron loss. When this equilibrium is lost, iron deficiency occurs. Iron is essential for the synthesis of heme, the prosthetic group present in hemoglobin.
Iron is an essential component of heme and depletion of iron leads to inappropriate production of heme molecules and thus decreased hemoglobin production. During iron deficiency, bone marrow produces erythrocytes which are microcytic and hypochromic. These cells cannot function properly. They have reduced oxygen carrying capacity and thus decrease oxygen delivery to the tissues. Regulation of Iron Transfer to Fetus Iron transfer from mother to fetus is regulated by placenta. Whenever there is decreased maternal iron status, the number of placental transferrin receptors increases so that more iron is taken up by the placenta.
When there is increased maternal iron, excessive iron transport to the fetus is prevented by placental synthesis of ferritin (Allen, 2000). Most iron transfer to the fetus occurs after week 30 of gestation (Allen, 2000). This is the time when there is maximum iron absorption noticed in the mother. The serum iron from the mother to the fetus is carried by serum transferring. Serum ferritin usually falls markedly between 12 and 25 wk of gestation. The cause of this is probably utilization of iron for expansion of the maternal red blood cell mass (Allen, 2000).