Valores literarios de la obra de Henry Bäx “El Pergamino Perdido”

ANEMIA 3

Iron deficiency anemia is the most common nutritional deficiency in the world. In order to understand the symptoms, etiology and treatment of this anemia, it is necessary to review normal iron and heme metabolism.

Iron Metabolism

The total body iron content of the normal adult varies from 3 to 5 g depending on the sex and weight of the individual. It is great in males than in females, and it increases roughly in proportion to body weight.

Hemoglobin iron constitutes approximately 60-70% of the total body iron.

The absolute amount is varying from 1.5 to 3 grams. At the end of their life span, the aged red cells are phagocytosed by cells of the RES. Nearly all the iron derived from the breakdown of hemoglobin is released into the circulation bound to the iron binding protein, transferrin, and is re-utilised by marrow erythroblasts for hemoglobin synthesis.

Storage

The amount of storage iron has been estimated to be about 1000-2000 mg in the healthy adult male, and less in the female. Storage irons occur in two forms- ferritin and hemosiderin. Ferritin is normally predominant.

In the normal person, storage iron is divided about equally between the reticuloendothelial cells (mainly in spleen, liver and bone marrow), hepatic parenchyma cells and skeletal muscle. Hemosiderin, the main storage form in reticuloendothelial cells, is more stable and less readily mobilized for hemoglobin formation than ferritin, which predominates in hepatocytes. In states of iron overload, hemosidern increases to a great degree than ferritin and became the dominant storage form.

Plasma (transport) Iron

Between 3 and 4 mg iron are present in the plasma, where it is bound to a specific protein, transferrin, a B-globulin of molecular weight 88000 that is synthesized in the liver. Each molecule of transferrin binds one or two atoms of ferric iron.

The function of transferrin is the transport of iron. It is the means by which iron absorbed from the alimentary tract is transported to the tissue stores, from tissue stores to bone marrow erythroblasts, and from one storage site to another. When transferrin reaches the storage sites or the bone marrow, it attaches to specific receptors on the cells and liberates its ferric ions, which pass into the cell to be stored or utilized. The total amount of transferrin in the plasma is about 8 g in the extracellular fluid. The level of serum iron in normal subjects averages about 20 mol (men > women).

Transferrin is a glycoprotein present in the serum in concentration, which enables it to combine with 44-80 mol of iron per litre. This value is known as the total iron binding capacity of the serum.

Serum ferritin concentration in adult’s range between 15-300 g/l and the mean level in men and women are 123 g/l and 56 g/l. In iron deficiency, concentration is less than 12 g/l. In iron overload, levels are very high.

Serum ferritin increased in: infections, inflammations, malignancy (lymphomas, leukemias) and liver diseases.

Absorption

The small intestine is highly sensitive to repletion of iron stores and rapidly corrects imbalance by decreasing or increasing absorption. The daily intake of a normal adult on a mixed western type diet contains 10-20 mg iron of which 10% or somewhat less is absorbed. Absorption is greater requirement due to menstrual loss and childbearing.

The chief dietary sources are meats (liver, kidney) egg yolk, green vegetables and fruit milk.

Heme iron present in the hemoglobin and myoglobin of meat is well absorbed.

Non-heme iron is released from food as ferric or ferrous ions by the action of acid in the stomach. It is absorbed only in the ionic state and almost exclusively as the ferrous form. Ferric ions are soluble at low PH. Ferrous ions are more soluble under these conditions.

Absorption of iron is most efficient in the duodenum and proximal jejunum, following entry into the cell, depending on the body requirement for iron; a proportion is rapidly transferred across the cell and on to the portal circulation for distribution to tissue iron stores. Most of the remaining iron in the mucosal cell combines with apoferritin to form ferritin. The ferritin containing cells are exfoliated from the mucosal surface at the end of their 2-3 lifespan, and the iron is lost in the faeces.

Excretion

The amount of iron lost from the body per day is between 0.5 and 1.0 mg under physiological conditions. The rate of loss is relatively constant and independent of intake.

Iron Imbalance

Under normal circumstances, iron absorption exceeds iron excretion. The diet normally contains 10-20 mg of iron, of which 10% is absorbed.

Uptake varies from 1-2 mg per day. Basal loss ranged from 0.5 to 1 mg per day. Menstrual iron loss is monthly 15-25 mg that mean between 0.5 and 1 mg per day. (28 days). The daily absorption necessary to compensate for daily loss is 0.5 to 1mg in males and about twice this amount i.e. 1-2 mg in female during the reproductive period of life.

The daily iron requirement for hemoglobin synthesis is 20-25 mg. It has been pointed out that the body conserves its iron stores by reutilising the iron derived from the breakdown of the hemoglobin from aged red cells. In normal individual red cell destruction and formation take place at almost identical rates. Normal males are a state of positive iron balance. Female of childbearing age, the positive balance is only very slender, because of the

additional loss by menstruation. Thus, a moderate increase in menstrual loss, especially if associated with impaired intake, can easily induce negative iron balance.

Causes

1. Increased physiological requirements;

a. Growth: IDA is more common in children between age of 6 month and 2 years, and froom11 to 16 years due to spurts of growth during these periods.

b. Menstruation: Anemia common in adult menstruating females.

c. Pregnancy: During pregnancy anemia is almost universal.

2. Pathological blood loss:

a. Menorrhagia- Antepartum and postpartum bleeding.

b. Gastrointestinal tract:

Bleeding piles

Drugs: Aspirin, Indomethacin, Butazolidin and Corticosteroids Peptic ulcer

Intestinal infestations and infections: Ankylostoma, whipworm, chronic colitis

due to amoebic or bacillary infections and giardiasis,

Miscellaneous: Cirrhosis of liver, hiatus hernia, diverticulosis of colon, TB bowels,

Crohn's disease, ulcerative colitis and malignancy of bowels.

c. Malabsorption: Coeliac disease, postgastrectomy and atrophic gastritis.

d. Urinary Tract: Recurrent hematuria and hemoglobinuria d. Others

 Regular blood donation

 Recurrent epistaxis

 Recurrent hemoptysis.

 Pulmonary hemosiderosis

 Hereditary telangiectasis 3. Nutritional defect

 Low iron intake

 Inhibitors in diet 4. Excess iron loss

Exfoliative dermatitis, PNH, gastritis, GI infection and intravascular hemolysis.

Pathophysiology

Iron deficiency develops in sequential stages over a period of negative balance (loss exceeds absorption).

Since Fe is absorbed with difficulty, most people barely meet their daily requirements added losses due to menstruation (mean 0.5 mg/day), pregnancy (0.5 to 0.8 mg/day), lactation (0.4 mg/day) and blood loss due to disease or accident readily lead to Fe deficiency. Fe depletion results in sequential changes or stages.

Stage I (Depletion of iron stores): Fe loss exceeds intake: with this negative Fe balance, storage Fe (represented by bone marrow Fe content) is progressively depleted. Although the Hb and serum Fe remain normal, the serum ferritin concentration falls to <20 ng/ml. As storage Fe decreases,

there is a compensatory increase in absorption of dietary Fe and in the concentration of transferrin (represented by a rise in Fe-binding capacity.

Stage II (Impaired erythropoiesis: Exhausted Fe stores cannot meet the needs of the erythroid marrow, while the plasma-transferrin level increases, the serum-Fe concentration declines, leading to a progressive decrease in Fe available for RBC formation. When serum falls to < 50 g/dl, and transferrin saturation to <16%, erythropoisis is impaired. The serum ferritin receptor concentration rises (>8.5mg/l)

Stage III (Anemic stage): The anemia with normal appearing RBCs and