CHAPTER ONE
1.0 Introduction
1.1 Anaemia
1.1.1 Biochemistry
1.2 Iron therapy
1.3 Biosynthesis of Heme
CHAPTER TWO
2.0 Classification
2.1 Hyporegenerative
2.1.1 Aplastic
2.1.2 Pure red cell aplasia (PRCA)
2.1.3 related to the myelodysplastic syndrome
2.1.4 Deficiency
2.1.5 Bone marrow infiltration and fibrosis
2.1.6 chronic disease (ACD)
2.1.7 chronic renal failure
2.2 Regenerative
2.2.1 Immune haemolytic
2.2.2 Sickle cell
2.2.3 due to enzymopathies and red cell membrane defects
2.2.4 Haemorrhagic
CHAPTER THREE
3.0 Selected
3.1 Pure red cell aplasia
3.2 B12 deficiency
3.3 Immune haemolytic
3.3.1 Classification
3.3.2 Pathophysiology of immune haemolytic
3.3.3 Diagnosis of haemolytic
3.4 Non-immune haemolytic
3.4.1 Paroxysmal nocturnal haemoglobinuria (PNH)
3.4.2 Microangiopathic disorders
3.4.3 Haemolysis secondary to toxic agents and other causes
CHAPTER FOUR
4.0 Conclusion
References
CHAPTER ONE
1.0 INTRODUCTION
1.1 ANAEMIA
Anaemia is a condition in which the haemoglobin (Hb) content of blood is lower than normal as a result of a deficiency of one or more essential nutrients. Because anaemia is the most common indicator used to screen for iron deficiency, the terms anaemia, iron deficiency (ID), and iron deficiency anaemia are sometimes considered synonymous and used interchangeably (Beris and Tobler, 1997). However, there are cases where a person may not be anaemic but is mildly or moderately iron deficient and consequently may be functionally impaired. Iron deficiency anaemia (IDA) is the most common nutritional cause of anaemia and occurs when there is an inadequate amount of red blood cells caused by lack of iron. The prevalence of iron deficiency anaemia is, therefore, less frequent than iron deficiency.
Iron is involved in multiple critical body functions. The predominant use of iron is for the creation of haeme groups that are incorporated into haemoglobin and myoglobin. Iron is additionally involved in the production of cytochromes and other enzymes (Segel et al., 2002; Wu et al., 2002). Immediately, bioavailable iron is bound in the bloodstream to a specific carrier protein called transferrin. Iron in excess of immediate needs will be stored in the liver, spleen, and bone marrow as ferritin (Wu et al., 2002). The majority of iron can be conserved and reused; however, there are some finite losses through the gastrointestinal tract, skin, and urine that ultimately must be replenished.
Iron deficiency is often portrayed as a progressive condition that begins with normal body iron status, which becomes sub normal or depleted because of low dietary iron intake, inadequate intestinal iron absorption or increased iron losses. As this process continues, synthesis of iron containing proteins, such as Hb, is compromised. Finally, when Hb concentration falls below a specified cut-off value, the iron deficiency has progressed to IDA (Haas and Brownlie IV, 2001). Iron metabolism is unique in several aspects. The body is economical in its handling of iron in the body.
When a red cell dies, its iron is reutilised. Iron absorption is in some ways dictated by the requirements of the body. Extra iron can be stored by a specific protein (ferritin), which is utilised at the time of increased iron requirements. The highly reactive properties of iron are balanced by unique control and transport systems. In spite of these ingenious mechanisms, ID is the most common deficiency disorder in the world and also the main remaining deficiency in the industrialised, developed regions of the world (Hallberg, 2001).
Iron deficiency is one of the most prevalent nutrient deficiencies in the world, affecting an estimated two billion people (Stoltzfus and Dreyfuss 1998). Young children and pregnant and postpartum women are the most commonly and severely affected because of the high iron demands of infant growth and pregnancy. However, where diets are based mostly on staple foods with little meat intake, or people are exposed to infections that cause blood loss (primarily hookworms and urinary schistosomiasis), iron deficiency may occur throughout the life span. Current WHO/International Nutritional Anemia Consultative Group/United Nations Children’s fund/United Nations Children’s fund (WHO/INACG/UNICEF) guidelines recommend universal iron and folic acid supplementation of young children and pregnant women where anaemia is highly prevalent (Stoltzfus and Dreyfuss 1998).
Although much is known about iron metabolism, the health consequences of iron deficiency continue to be a subject of research and debate. This is partly because in many regions of the world iron supplements are the standard of care for individuals with anaemia. Most trials of iron supplementation have measured haemoglobin concentra tion as the primary outcome. There is a relatively small body of clinical trials of iron repletion to humans with functional iron deficiency (i.e. iron deficiency severe enough to affect erythropoiesis) with pregnancy outcomes or mortality as primary objectives. There is surprisingly little evidence to either support or refute a causal link between iron deficiency and these important adverse health outcomes. As processes like this comparative risk assessment (CRA) bring to light the overall weakness of evidence either supporting or refuting the relationship, new research priorities may emerge.