**2.1 Iron-deficiency anemia**

In case of iron deficiency anemia, the blood lacks an adequate number of normal red blood cells for carrying oxygen to the body tissues. Iron is one of the most plentiful elements on the surface of the earth. It participates in redox reactions which are crucial for numerous elementary organic processes such as cellular respiration and digestion. Therefore, it is not starling that iron contributes an important role in nearly all animal's lives. In *Homo sapien* iron is assimilated into proteins as an important constituent of heme (e.g., globin's, proteins, oxidases, and synthetases). These iron-containing proteins are essential for carrying out vital cellular and organismal functions including oxygen transport, mitochondrial respiration, nucleic acid replication and repair, host defense, and cell signaling. About 4 grams of iron is present in an adult human body. More than 75% of total body iron is correlated with hemoglobin, which is accountable for transporting oxygen (**Figure 1**). Deficiency of iron in the body decreases the production of the iron-containing heme group, which is a prosthetic group of hemoglobin protein that in turn limits the production of hemoglobin and decreases the synthesis of red blood cells (RBCs) from stem cells in the bone marrow which results in anemic conditions [6].

Pregnancy is one of the major reasons for iron-deficiency anemia because during the 2nd and 3rd trimester of pregnancy the iron demands of the body increase incredibly. The other major causes of iron deficiency anemia are heavy menstrual periods, pregnancy, bleeding from the gut, bleeding from the kidney, lack of certain

**Figure 1.** *Hemoglobin in RBC'S carrying oxygen from lungs.*

#### *Anemia during Pregnancy and Its Prevalence DOI: http://dx.doi.org/10.5772/intechopen.99521*

vitamins, and problems with bone marrow [7]. Apathy, inactiveness, feeling feeble, faded and weak, panting, becoming exhausted and puffed easily, asymmetrical and disorderly heartbeats, fatigue and weariness, taste disturbances, smarting mouth are some common symptoms of iron-deficiency anemia.

Besides this, anemia during pregnancy can increase the risk of premature delivery and premature babies suffering from other health issues including low birth weight and neural tube defects to death. In developing countries, this premature birth is one of the main causes of death of an infant before his or her first birthday and this risk can be reduced by taking iron supplements during pregnancy [8].

#### *2.1.1 Treatment*

Due to the astounding effect of iodine deficiency anemia on maternal and fetal wellbeing, iron treatment is emphatically suggested. The adequacy of iron enhancement for the treatment of iron insufficiency is recorded by clinical preliminaries including pregnant ladies. The utilization of liposomal iron may address a promising technique of oral iron treatment in pregnant ladies with IDA. This compound shows high gastrointestinal retention and bioavailability and a low rate of results. Hence, liposomal iron presents great bearableness and favors preferable consistency over iron salts [9].

During pregnancy, a continuous elective treatment to oral iron, when it is not demonstrated, is IV iron. The new details of IV iron treatment advance a higher, just as quicker, increment of Hb focus and SF levels than oral iron supplementation, as was at that point appeared in changed studies in contrast with oral iron, ICM ensures a faster rectification of frailty and an apparent improvement of value existence with a slower pace of side effects like weariness and sorrow. It likewise presents higher bearableness and, thusly, more noteworthy consistency than oral iron. As the carb moiety ties the essential iron all the more firmly, high dosages of FCM (around 1000 mg in a solitary organization with a short implantation time) are permitted, in this way ensuring an improvement in consistency and a decrease of expenses because of rehashed organizations [10].

#### **2.2 Pernicious anemia**

Pernicious Anemia is an autoimmune disorder that affects the gastric mucosa of the stomach causing the lower and inadequate absorption of dietary Cobalamin or vitamin B12. It is essential for the proper functioning and forming of red blood cells. Vitamin B12 is also essential for the proper and normal functioning of the central nervous system and peripheral nervous system. The food or products which are enrich with protein such as beef, mutton, chicken, pork, fish, (dried fish, tilapia, halibut, tuna, salmon, carps, and shrimps), cereal, milk, yogurt, cheese, egg white, and other dairy products are major sources of vitamin B12 [11].

Vitamin B12 is separated from the proteins in the stomach through the action of hydrochloric acid. After this separation, vitamin B12 become incorporated with a protein called intrinsic factor in parietal cells of the stomach and is absorbed through villi which is present on the inner wall of the small intestine through which it is either computed into the blood circulation for the formation of red blood cells or stored in the liver (**Figure 2**). In the stomach, the parietal cell synthesizes intrinsic factor (IF) and secretes it, as well as hydrochloric acid into the gastric cavity of the stomach. The inability of parietal cells to secrete the intrinsic factor leads to failure of efficient vitamin B12 absorption into the blood. This inability is due to autoimmune antibody-mediated devastation of parietal cells of the gastric lumen which critically reduces the amount of intrinsic factor secreted in the

**Figure 2.** *Metabolic pathway for vitamin B12 absorption.*

stomach. The antibodies attack and block the active site on intrinsic factors where vitamin B12 binds. This blockage of IF and inhibition of vitamin B12 binding will inhibit the formation of intrinsic factor-vitamin B12 complex. Without the formation of this complex, blood circulation cannot take up vitamin B12 and this will lead to the decrease in the level of red blood cells because vitamin B12 is an essential component in the synthesis of RBC'S. These blocking antibodies have been found in blood-serum or gastrointestinal fluid of 90% of patients suffering from pernicious anemia [12].

The major causes of pernicious Anemia are either the deficiency of vitamin B12 in diet or the inability of the stomach to absorb vitamin B12 from the diet. Vitamin B12 is also stored in the body. This stored vitamin B12 can last for years. When this is eventually depleted, pernicious anemia begins to develop. The amount of vitamin B12 required to fulfill the demands of a body depends on age [13]. The most serious outcome of B12 deficiency is diminished development and function of neurological processes throughout the lifecycle. Low maternal plasma vitamin B12 may result in pregnancies affected by anencephaly that is a type of neural tube defect (NTDs) [14].

Hypotonic muscles, failure to thrive, cerebral atrophy, and developmental regression are general outcomes of deficiency of vitamin B12. Folic acid supplemented pregnant women with negative B12 balance have increased risk for adverse maternal and infant outcomes (e.g., increased cardiometabolic disease risk) while pregnant women with Low B12 and a normal-to-high range of folate have high insulin resistance and adiposity in the offspring at 5 years of age [15].
