What Is The Most Common Cause Of Microcytic Anemia – Microcytic anemia describes the presence of decreased hemoglobin concentration and decreased mean corpuscular volume (MCV).

The normal concentration of hemoglobin (Hb) in red blood cells is approximately 130–175 g/l in men and 120–155 g/l in women. Hb levels below this level are considered anemia.

What Is The Most Common Cause Of Microcytic Anemia

MCV describes the average volume of red blood cells and is measured in femtoliters (fL). The standard range for red blood cells is 82-99 fL. Levels <82 fL are considered microcytic.

Hypochromic Microcytic Anaemia Hi Res Stock Photography And Images

IDA is commonly observed in women of reproductive age and children worldwide. Premenopausal women are at particular risk due to iron loss during menstruation and pregnancy.

It is estimated that 2–5% of adult men and postmenopausal women suffer from IDA in developed countries.

Dietary iron deficiency is rare in developed countries due to adequate access to dietary components such as meat. Where meat is not a staple diet, the incidence of IDA is 6-8 times higher.

Etiology and pathophysiology Iron is a molecule essential for living organisms; it is essential for many cellular processes, including oxygen transport and DNA synthesis.

Microcytic Anemias • The Blood Project

The absorption of iron from enterocytes in the gastrointestinal tract is tightly regulated to match the loss of iron from the body each day. When the rate of iron absorption does not keep up with the rate of iron loss, it will lead to depletion of the body’s iron stores and ultimately IDA.

Chronic hemorrhage (e.g., increased iron loss) is one of the most common causes of IDA in developed countries. It is usually caused by excessive amenorrhea in premenopausal women, but may suggest an underlying gastrointestinal pathology.

Due to the chronicity of IDA, symptoms usually appear with low hemoglobin levels (e.g. < 80 g/l). These include fatigue, shortness of breath, dizziness, headache, nausea, intestinal disturbances and possible exacerbation of underlying cardiovascular diseases causing angina, palpitations and intermittent claudication.

Interestingly, some children with IDA may develop a peculiar dietary appetite (pica) for materials such as earth, clay or chalk. It is not fully understood whether this is a cause or a consequence of IDA.

Evaluation Of Microcytosis

FBC is useful in the diagnosis of microcytic anemia (e.g., low Hb and low MCV), but further testing is needed to determine the cause.

FBC also provides mean cellular hemoglobin concentration (MCHC). Low MCHC levels are reflected in the blood film as small, pale red blood cells that may show some shape changes (e.g., pencil-shaped cells).

Serum iron and ferritin levels are usually low, suggesting depletion of iron stores. On the other hand, transferrin levels are normal or increased, reflecting an increase in total iron-binding capacity (i.e., no binding of iron to transferrin, which increases its binding potential). Due to the reduction in iron binding to transferrin, transferrin saturation decreases.

Postmenopausal men and women with unexplained IDA should be evaluated for suspected GI malignancy (or indeed benign GI pathology). The upper gastrointestinal tract is more often the site of pathology than the lower gastrointestinal tract.

Microcytic Anemia Notes: Diagrams & Illustrations

A common pharmacotherapy is oral iron replacement in the form of ferrous fumarate or ferrous sulfate. Follow-up blood tests should always be performed to assess response to treatment, and patients should be warned about side effects. These may include constipation, black stools, diarrhea, nausea and indigestion/upper abdominal discomfort. For those who cannot tolerate oral iron, an iron infusion can be arranged. Treatment should be continued for 3 months to ensure adequate replacement of supplies.

Iron replacement should usually be offered once daily. If side effects occur, this can be limited to alternative days. Importantly, if limited red blood cell transfusion is required for severe, symptomatic anemia, iron supplementation is still necessary after treatment.

Anemia of chronic disease (ACD) is a complex and multifactorial condition resulting from a chronic inflammatory process resulting from infection, malignancy, or systemic disease.

ACD is the second most common cause of anemia worldwide and is common among hospitalized patients. ACD is essentially a functional iron deficiency (FID) in which the supply of iron for erythropoiesis (i.e. the production of new red blood cells) is inadequate despite abnormal cellular iron stores.

Classification Of Anemia For Gastroenterologists

Etiology and pathophysiology ACD is classically described as normocytic, normochromic anemia secondary to systemic disease, infection, or malignancy.

The pathophysiology of ACD is complex and a number of mechanisms have been proposed, including altered hepcidin regulation, inhibition of erythropoiesis, low erythropoietin levels, and increased phagocytosis of erythroid cells. ACD or FID is often seen in patients with chronic kidney disease (CKD) and chronic heart failure (CHF).

Hepcidin is a normal regulator of iron absorption from enterocytes and iron distribution in tissues. It is an acute phase protein that usually acts to reduce the availability of iron from infecting microorganisms.

Chronic IL-6-mediated inflammation may lead to hepcidin-induced blockade of iron absorption and release from macrophages. This reduction in iron availability for red blood cell production through erythropoiesis may lead to microcytic anemia. However, this phenomenon occurs only in 25% of cases.

Investigation Of Anaemia

Clinical manifestations The clinical presentation of ACD is usually a reflection of the underlying disease and unless the hemoglobin concentration is significantly reduced, patients may be asymptomatic.

If present, the clinical symptoms are typical of all anemias, including fatigue, headache, and dizziness. If symptoms are severe, patients may experience palpitations, angina or shortness of breath.

FBC may show normocytic normochromic anemia (approx. 75%) or the development of microcytic anemia (approx. 25%). In ACD, MCV rarely falls below 70 fL.

Ferritin, like hepcidin, is an acute phase reactant, which means its levels usually increase with chronic inflammation. Therefore, in ACD, ferritin levels may be normal or elevated.

Iron Deficiency And Other Types Of Anemia In Infants And Children

Serum transferrin and iron levels are usually decreased. Normal or decreased transferrin levels are a differentiating factor from IDA.

Another differentiating factor is iron reserves in the marrow (assessed by biopsy). In IDA, iron stores are absent, while in ACD they are normal or increased.

As mentioned, ACD is a multifactorial disease with many treatment options depending on the degree of anemia, severity of symptoms, and diagnosis.

In general, treatment should include treatment of the underlying disease and proper management of any factors causing complications, including iron, B

Pdf) Inherited Microcytic Anemias

Other treatment options for ACD may include erythropoietin, parenteral iron, and transfusions, as indicated. Patients should be diagnosed with ACD or FID because they respond poorly to oral iron replacement therapy.

Beta-thalassemias are a heterogeneous group of diseases resulting from reduced production of beta-globin chains or its absence.

The prevalence of beta-thalassemia varies greatly among ethnic populations. Beta-thalassemia is more commonly seen in African, Mediterranean, and Southeast Asian populations.

Beta-thalassemias result from genetic mutations in the beta-globin genes, which are located on the short arm of chromosome 11.

A General Pediatrician’s Approach To Anemia In Childhood

Which lead to the development of thalassemia. Generally, mutations can lead to no production (beta thalassemia 0) or reduced production (beta thalassemia +) of the beta-globin chain.

Patients with two abnormal alleles (homozygous) are considered to have severe beta-thalassemia and are characterized by absent or significantly reduced production of beta-globin chains.

Patients with one abnormal allele (heterozygous) are said to have beta-thalassemia minor or “trait” and have a mild reduction in beta-globin chain production.

Reduced/absent production leads to excess alpha-globin chains. These excess alpha-globin chains precipitate in cells because they are unstable and unable to form normal tetramers. The degree of excess alpha-globin chain determines the severity of the clinical picture.

Anemia Classification, Diagnosis, And Routine Workup

Clinical manifestations In patients with severe beta-thalassemia, symptoms usually appear in the first year of life when the production of fetal hemoglobin (HbF: two alpha chains/two gamma chains) is replaced by defective adult hemoglobin.

Clinical symptoms usually reflect the severity of beta-thalassemia. Patients with severe beta-thalassemia usually have significant extramedullary hematopoiesis and complications secondary to iron overload from repeated transfusions.

Patients with low/trait beta-thalassemia are usually asymptomatic and routine testing reveals microcytic anemia.

Hb electrophoresis shows decreased or absent HbA levels and the presence of increased HbF and HbA2 levels. The latter consists of two alpha chains and two delta chains. Importantly, HbA1c may be present in patients who have recently received a blood transfusion.

Pdf) Red Blood Cell Microcytosis And Hypochromia In The Differential Diagnosis Of Iron Deficiency And Β Thalassemia Trait

Other laboratory tests are important in the diagnosis of beta-thalassemia and include FBC, blood smear, iron tests, hematics, LDH, bilirubin (as part of LFT), and haptoglobin.

The dominant symptom is profound microcytic anemia (MCV < 75 fL) with features of microcytic, hypochromic erythrocytes in the blood smear and normal iron tests.

Patients with severe beta-thalassemia will require early and frequent blood transfusions. Other treatment options include splenectomy and hematopoietic stem cell transplantation. Patients receiving repeated transfusions may suffer from iron overload and require iron chelation therapy.

Sideroblastic anemia may be congenital (X-linked recessive) or acquired. This results in the incorporation of a perinuclear ring of thick iron-containing granules (“sideroblast ring”) into erythrocyte progenitors.

Microcytic Anemia: Causes, Symptoms, And Treatment

Acquired causes may be seen in myelodysplastic syndromes or with medications such as isoniazid or chloramphenicol.

Lead poisoning is a rare cause of microcytic anemia, which can cause decreased heme synthesis and shortened erythrocyte lifespan.

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