What is a Megaloblast Anaemia Profile
Synonym: megaloblastic anemia
English: megaloblastic an (a) emia
Megaloblastic anemia is a collective term for forms of anemia in which the DNA synthesis of the blood-forming cells in the bone marrow is impaired. This leads to a developmental and maturation disorder of the erythrocytes. It is associated with the appearance of megaloblasts in the bone marrow and with an enlargement of the erythrocytes in the peripheral blood (megalocytes).
The megaloblasts are predominantly progenitor cells of erythropoiesis, which have an abnormal nuclear structure. In addition, other cell lines, such as the cells of granulopoiesis and megakaryocytes, can also be changed. Megaloblastic anemia shows up in the blood count as hyperchromic macrocytic anemia, i.e. MCH and MCV are increased. There are also oversegmented granulocytes with 6-7 segments. Pancytopenia is seen in the advanced stage.
The most common causes of megaloblastic anemia are folic acid deficiency (folic acid deficiency anemia) or vitamin B12 deficiency (vitamin B12 deficiency anemia). These two hypovitaminoses are discussed in detail in the corresponding articles.
3.1 Folic acid deficiency
Most folic acid deficiency patients have a nutritional reason, especially in old age or with alcoholism and psychiatric impairments. Folic acid malabsorption is particularly common in celiac disease. Furthermore, the deficiency can be based on an increased need or loss. This can have both physiological (pregnancy, breastfeeding, premature babies) and pathological causes (sickle cell anemia, autoimmune hemolytic anemia, chronic inflammation, long-term dialysis, heart failure, liver disease). In addition, drugs can cause a folic acid deficiency, especially folic acid antagonists (methotrexate, trimethoprim, co-trimoxazole) and anticonvulsants (phenytoin, primidone).
3.2 Vitamin B12 deficiency
A vitamin B12 deficiency can occur with strict veganism, if meat, fish, eggs, cheese and other animal products are avoided, as well as with inadequate nutrition due to poverty or psychiatric illnesses. Furthermore, malabsorption can lead to a deficiency which, however, is often not so pronounced and persistent as to cause megaloblastic anemia. The main causes of malabsorption include:
3.3 Other causes
Other causes of megaloblastic anemia can include:
All megaloblastic anemia is based on a defect in DNA synthesis, which particularly affects the hematopoietic cells in the bone marrow. The balance between the required synthesis rate and the availability of the purines (adenine, guanine) and pyrimidines (thymidine and cytosine) is disturbed. In the case of folic acid or vitamin B12 deficiency, deoxyuridine monophosphate (dUMP) cannot be converted to deoxythymidine monophosphate (dTMP). However, DTMP is required for the formation of deoxythymidine triphosphate (dTTP). In addition, deoxyuridine triphosphate (dUTP) accumulates so that uracil is incorporated into DNA.
Megaloblastic anemia due to vitamin B12 deficiency occurs with an incidence of about 9 cases per 100,000 population per year. The age of onset has a peak at around 60 years.
6.1 Symptoms related to anemia
Asymptomatic patients are discovered by chance during a blood test for an elevated MCV. In more severe cases, the typical symptoms of anemia are noticeable (fatigue, reduced performance, fatigue, headache, exertional dyspnea, tachycardia, dizziness). Other possible symptoms are:
Furthermore, thrombocytopenia can lead to hemorrhage, which occurs especially with simultaneous vitamin C deficiency or malnourished alcoholics. The anemia, low leukocytopenia and the reduced function of the phagocytes in the case of vitamin B12 deficiency predispose to infections of the respiratory and urogenital tracts.
6.2 Other symptoms
A deficiency in vitamin B12 or folic acid leads to a loss of fertility and can cause miscarriages and neural tube defects during pregnancy. In addition, a vitamin B12 deficiency causes neurological manifestations such as polyneuropathy or funicular myelosis.
In addition to megaloblastic anemia, diabetes mellitus, deafness and ring sideroblasts in the bone marrow can occur if the thiamine transport gene SLC19A2 is genetically defective.
7.2 Haematological changes
In the peripheral blood, oval macrocytes (ovalocytes) and pronounced anisocytosis and poikilocytosis are noticeable. The erythrocytes may show basophilic stippling. Occasionally, nucleated red precursor cells are found in the peripheral blood. The MCV is increased (except in the case of accompanying iron deficiency or thalassemia). Some neutrophils are hypersegmented (over 5 segments). Leukocytopenia is usually present due to a decrease in granulocytes and lymphocytes. The platelet count is only slightly reduced.
In severe anemia, the bone marrow becomes hypercellular and immature cells accumulate. A lot of iron can be detected in the iron dye. The erythroblasts have an immature nucleus with normal maturation of the cytoplasm (nuclear plasma maturation dissociation). The cells are larger than normoblasts (macroblasts) and many show an eccentric, lobulated cell nucleus as well as nuclear fragments. There are also giant metamyelocytes and enlarged megakaryocytes. In severe cases, immature cell accumulation can mimic AML.
Bone marrow cells and other proliferating body cells show chromosomal changes (e.g. chromosome breaks) in megaloblastic anemia. Furthermore, the death of erythrocyte bone marrow cells due to the ineffective erythropoiesis leads to the accumulation of unconjugated bilirubin in the plasma. Because of this, there is also an increased urobilinogen and decreased haptoglobin. Hemosiderin can be detected in the urine, while LDH increases slightly in the serum. A weakly positive Coombs test can misdiagnose autoimmune hemolytic anemia.
8.1 ... if there is a vitamin B12 deficiency
If causal therapy is not possible, cobalamin should be regularly substituted for life. Indications for substitution are megaloblastic anemia, other haematological abnormalities, or neuropathy. There are different strategies for substitution. In Germany, initially 1,000 µg / d hydroxycobalamin is usually injected intramuscularly over 5 days. This is used to replenish the body's stores. Then 500 µg intramuscularly is injected once a week until the blood count and the LDH normalize. Lifelong maintenance therapy is given with 500 µg intramuscularly every 6 months if causal therapy is not possible. In certain situations, e.g. in pernicious anemia, higher doses may also be necessary. In the United States, cyanocobalamin is mostly given orally.
8.2 ... if you have a folic acid deficiency
In the event of a folic acid deficiency, folic acid is usually administered orally in a dose of 5 mg / day in addition to eliminating the causal disorder. The duration of therapy is usually 4 months and should be continued until the blood count has normalized. Before folic acid substitution is started, a vitamin B12 deficiency must be excluded and corrected, as otherwise vitamin B12-induced neuropathy can develop despite the anemia responding to folic acid administration. If the cause cannot be remedied or there is a high probability that the deficiency will recur, folic acid can be substituted in the long term.
8.3 ... for other causes
Hereditary orotaciduria responds to uridine. If there is a genetic defect in the thiamine transprotgen SLC19A2, thiamine can be administered.
8.4 Supportive therapy
Blood transfusions are usually not necessary. If so, only 1 to 2 red cell concentrates should be given. Occasionally, severe thrombocytosis appears one to two weeks after the start of therapy. If the values are very high, ASA can be considered.
When methotrexate and other dihydrofolate reductase inhibitors (trimethoprim, co-trimoxazole) are administered, folinic acid (5-formyl-tetrahydrofolate) can be used to treat or prevent folic acid deficiency.
Folic acid prophylaxis is recommended for patients on chronic dialysis and on parenteral nutrition. Folic acid (400 µg / d) is also recommended before and during pregnancy to prevent megaloblastic anemia and reduce the incidence of neural tube defects. In women who have already given birth to a fetus with a neural tube defect, a substitution of 5 mg / day is carried out before and during the next pregnancy.
In premature infants with a birth weight of less than 1,500 g, folic acid is routinely given for the first 6 weeks of life. This also applies to premature babies who need an exchange transfusion, have difficulty feeding, and show signs of infection, vomiting, or diarrhea.
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