How to know if you have thalassemia?

Most of the disease begins in infancy and manifests as anemia, weakness, intra-abdominal agglomeration, developmental retardation, etc. Severe cases often suffer from poor growth and development, and often die before adulthood. Patients with mild and intermediate forms generally can Live to adulthood and be able to participate in work. If you pay attention to labor saving and diet and daily life, complications can be reduced and symptoms improved. Insufficient endowment and weak kidney qi are the main reasons. The kidney is the foundation of innateness, and the kidney essence is insufficient. There is no source of biochemistry. "Children's labor is obtained from the mother's womb". It can be seen that "child's labor" is closely related to parents. Insufficient kidney essence also affects the acquired spleen and stomach function and growth and development. Over time, blood and qi will deteriorate. Symptoms such as jaundice and accumulation occur, resulting in this syndrome of mixed deficiency and excess.

Classification 1. α-thalassemia silent type: no clinical symptoms and signs, no anemia, normal red blood cell morphology; standard type: Mild anemia (hypochromic microcytic), red blood cell osmotic fragility may be slightly lower, some inclusion body formation tests are positive, and HbBarts reaches 5-15% at birth. HbH disease: mild or moderate anemia, hepatosplenomegaly, may If you have jaundice, hemolytic crisis often occurs due to taking oxidative drugs or infection. Pregnancy can aggravate the condition. HbH bands can be found on Hb electrophoresis, the inclusion body formation test is positive, and the osmotic fragility of red blood cells is reduced; HbBarts fetal edema: immediately after stillbirth or premature delivery Death, underweight, mild jaundice, obvious edema, hepatomegaly and spleen, uneven size and abnormal shape of red blood cells, HbBarts accounts for 80-90% of Hb.

2. β-thalassaemia static type: β+ thalassemia Anemic heterozygotes have no symptoms and no anemia. A few target-shaped red blood cells can be seen in the blood film. The osmotic fragility of red blood cells is slightly reduced and HbA2 (α2δ2) is slightly increased. Mild type: heterozygotes of β0 thalassemia, with mild to moderate symptoms. Anemia, mild spleen enlargement, anemia with microcytic hypochromia, visible target cells, reticulocytes up to 5%, reduced erythrocyte osmotic fragility, increased HbA2, half of cases have mildly increased HbF (α2γ2); severe : Homozygous, also known as Cooleys anemia, severe disease, often died in childhood, a few are mild, can live to adulthood, anemia gradually worsens within 1 year after birth, growth is retarded, liver and spleen are obviously enlarged, may be mild Jaundice, "Mongoloid" face, comb-shaped cranial plate X-ray, severe anemia, obvious microcytic hypochromia, red blood cells of varying sizes, target-shaped cells and basophilic stippling red blood cells are common, and immature red blood cells are present. Inclusion bodies can be seen, and HbF is often between 30-60%, or even up to 90%; intermediate type: a few symptoms are mild, mainly determined by the type of genetic variation.

3. Other HbLepore syndromes: A fusion gene β replaces the β chain; hereditary fetal hemoglobin (HbF) persistence syndrome