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He Li Fang
Hematology
About me
Loudi Central Hospital, Department of Hematology, Attending Physician.
Proficient in diseases
Specializes in the diagnosis and treatment of common diseases in hematology.
Voices
What department should I go to for iron deficiency anemia?
Anemia refers to a condition in which the total volume of red blood cells in the circulating blood is reduced below normal levels, resulting in anemia. Iron deficiency anemia is a type of anemia caused by a lack of hematopoietic raw materials. Iron deficiency anemia occurs when the body's stored iron is depleted and cannot meet the needs for normal red blood cell production. As the most common type of red blood cell disease, iron deficiency anemia falls within the category of hematology. Therefore, patients with iron deficiency anemia should seek specialized consultation in the department of hematology. Furthermore, we recommend seeking medical advice as early as possible since moderate to severe iron deficiency anemia can lead to a series of circulatory disorders, thereby exacerbating the condition.
Is leukemia treatment free?
Leukemia is a type of malignant tumor originating from hematopoietic stem cells and progenitor cells in the myeloid hematopoietic system. Leukemia cells differentiate and organize at the early stages of different myeloid developments, exhibiting the morphological and immunophenotypic characteristics of myeloid development. The incidence of acute myeloid leukemia in the population is 2-4/100,000, with the median age of onset being sixty-four to seventy years, making it a disease of the elderly. The incidence increases with age, accounting for 70% of acute leukemias, and representing 55%-70% of infant, 17%-20% of childhood, and 80%-90% of adult acute leukemias. Regarding the medical insurance situation in China, some leukemia conditions are eligible for major illness assistance. All leukemia treatments can be reimbursed at a certain ratio under the national health insurance, although there is no free treatment for leukemia at present, unless one participates in relevant clinical trials, which could offer some compensation, and certain treatment drugs are provided free of charge.
Causes of Chronic Myeloid Leukemia
Chronic granulocytic leukemia, also known as chronic myeloid leukemia, is a myeloproliferative tumor originating from pluripotent stem cells. It is characterized by a specific chromosomal alteration, commonly referred to as the Philadelphia chromosome, which is formed by the translocation of chromosomes 9 and 22, resulting in the formation of the BCR-ABL fusion gene at the molecular level. Chronic granulocytic leukemia is a clonal disease originating from pluripotent stem cells. Due to a significant expansion of the progenitor cell pool, there is excessive proliferation of myeloid cells and increased granulocyte production. The slow clearance of granulocytes leads to the accumulation of granulocytes in the body, which is the main cause of the disease.
Is Mediterranean anemia leukemia?
Thalassemia, formerly known as Mediterranean anemia or oceanic anemia, is a hereditary hemolytic anemia caused by mutations or deletions in globin genes, leading to insufficient synthesis of globin peptide chains. Those who lack beta chains are referred to as having beta-thalassemia, and those who lack alpha chains are known as having alpha-thalassemia. Clinically, it is classified into mild, intermediate, and severe forms based on the severity of anemia. The disease is widespread in many regions of the world, including the Mediterranean, the Middle East, Africa, Southeast Asia, and southern China. In China, it is more commonly found in Guangxi, Guangdong, Sichuan, Hong Kong, northern Taiwan, Yunnan, Guizhou, Hainan, Fujian, Hunan, and Hubei, and less commonly in the north. Thalassemia is fundamentally defined not as leukemia, but as a genetic disease.
Can a fetus with thalassemia be kept?
Thalassemia, commonly referred to as "Mediterranean anemia," is a hereditary hemolytic anemia caused by mutations or deletions in globin genes, leading to insufficient synthesis of globin peptide chains. Cases with a deficiency in the globin chain are called thalassemia. Regarding whether a thalassemia fetus should be carried to term, one must first consider the maternal family history, including any history of stillbirths, occurrences of hydrops fetalis (swelling in infants), or cases of severe thalassemia in children, as well as instances where both parents are carriers, marking a high-risk pregnancy. In such cases, strict prenatal diagnosis is required. Prenatal diagnosis includes taking samples of fetal chorion, amniotic fluid, and umbilical cord blood for genetic analysis. If severe thalassemia or Hemoglobin Barts Hydrops Fetalis Syndrome is detected in the fetus, the pregnancy should be terminated immediately. Therefore, it is recommended to terminate pregnancies where the fetus is found to have severe thalassemia or Hemoglobin Barts Hydrops Fetalis Syndrome.
Treatment of Iron Deficiency Anemia
The treatment principles for iron deficiency anemia mainly involve two aspects. One is to identify the cause of the iron deficiency anemia. Once the cause is confirmed, fundamental treatment of the cause should be conducted to restore the body's normal iron stores. The second aspect is iron supplementation, which is recommended to be administered orally. The daily supplemental iron dose is approximately 150 to 200 milligrams, typically using ferrous preparations such as ferrous succinate, ferrous fumarate, ferrous gluconate, and iron dextran. It is suggested that iron supplements be taken with meals or after meals to reduce gastrointestinal irritation caused by the medication. Additionally, it is advised to avoid consuming tea, coffee, and other substances that could interfere with iron absorption during the treatment period.
The causes of iron deficiency anemia
The causes of iron deficiency anemia primarily refer to the disruption of the normal dynamic balance between iron absorption and excretion, leading to the consumption of stored iron as well as an increased need for iron and insufficient iron intake, especially in cases of chronic blood loss, resulting in a long-term negative iron balance. The causes of iron deficiency can be divided into two main aspects: insufficient iron intake and excessive iron loss. In the first aspect, decreased iron intake includes dietary insufficiency, meaning inadequate food intake, and reduced absorption, which includes decreased absorption due to lack of stomach acid and reduced absorption following gastric surgery. Excessive iron loss includes the following eight aspects: 1) gastrointestinal bleeding, which includes bleeding caused by tumors, gastrointestinal ulcers, gastritis, as well as bleeding due to parasites and hookworm infections. It also includes bleeding caused by hemorrhoids in men and arteriovenous malformations; 2) excessive menstrual bleeding; 3) frequent blood donations; 4) multiple pregnancies in women; 5) chronic intravascular hemolysis causing hemoglobinuria; 6) hereditary hemorrhagic telangiectasia; 7) primary pulmonary hemosiderosis; and 8) coagulation disorders or the use of anticoagulants leading to iron deficiency. These eight categories all result from excessive loss of iron, causing iron deficiency which leads to iron deficiency anemia.
Chronic granulocytic leukemia etiology
Chronic granulocytic leukemia is a myeloproliferative tumor originating from multipotent stem cells. It is characterized by the translocation of chromosomes 9 and 22 forming the BCR/ABL fusion gene. The Philadelphia chromosome is a characteristic change in chronic granulocytic leukemia, first discovered and named in Philadelphia in 1960. Initially, it was observed as a deletion of the long arm of the primary chromosome in dividing blood cells of patients with this leukemia. Currently, studies have shown that abnormalities in the interaction between hematopoietic progenitor cells and the stroma might be central to treating the disease. Abnormal adhesion and anchoring characteristics of progenitor cells lead to disrupted cell maturation and proliferation. Chronic granulocytic cells do not adhere to stromal cells as normal cells do, particularly lacking integrin-mediated adhesion. Additionally, the expression of the adhesion molecule lymphocyte function-associated antigen 3 is also reduced in these cells. Therefore, the progression of the disease results from clonal changes. During the transformation of chronic granulocytic leukemia to acute myeloid leukemia, there is an increased rate of genetic mutations. Changes in gene expression during the progression involve various aspects, including nucleosome sugar metabolism, bone marrow myeloid differentiation, genomic instability of cell apoptosis genes, and processes related to DNA damage repair.
How is iron deficiency anemia diagnosed?
The diagnosis of iron deficiency anemia includes two aspects: one is to establish whether there is anemia caused by iron deficiency, and the other is to clarify the cause of the iron deficiency. First, we need to carefully inquire and analyze the medical history, combined with the patient's physical examination, which can provide a series of clues for diagnosing iron deficiency anemia. A definitive diagnosis also requires laboratory evidence. Clinically, we can divide iron deficiency and iron deficiency anemia into three stages: iron deficiency, iron-deficient erythropoiesis, and iron deficiency anemia. The following describes the diagnostic criteria for iron deficiency anemia specifically. Iron deficiency anemia is characterized by a significant reduction in hemoglobin in red blood cells, presenting as microcytic hypochromic anemia. Its diagnostic basis includes three aspects: first, conforming to the diagnosis of iron deficiency and iron-deficient erythropoiesis; second, having microcytic hypochromic anemia; and third, effective treatment with iron supplements. These three factors together can confirm the diagnosis of this disease.
What tests are for thalassemia?
Thalassemia firstly requires genetic diagnosis through a series of techniques such as DNA restriction endonuclease map PCR, which identify the genotype of thalassemia. Secondly, hemoglobin electrophoresis needs to be completed. Through complete hemoglobin electrophoresis, it can discriminate between silent gene carriers and those with thalassemia, hemoglobin H disease, and hemoglobin Bart's hydrops fetalis syndrome. Additionally, a significant increase in hemoglobin A2 in overt thalassemia also has certain specificity. Thirdly, a complete bone marrow picture is necessary, which will match the bone marrow picture of hemolytic anemia. There is pronounced erythroid hyperplasia, positive iron staining, and an increase in sideroblastic erythroblasts. Fourthly, a complete blood count is needed. Different types of blood counts show different levels of hemoglobin reduction. In mild thalassemia and thalassemia traits, hemoglobin is mostly normal or mildly decreased. In severe thalassemia, hemoglobin is generally below 50 grams per liter, indicating a severe anemic state. Blood smears might show anisocytosis, poikilocytosis, and target cells. It is common to see nucleated erythrocytes and reticulocytes significantly increased, which matches the signs of hemolytic anemia. Fifth, iron metabolism testing needs to be completed. By improving iron metabolism testing, it serves as a discriminant for silent gene carriers, as well as those with thalassemia traits and patients with mild thalassemia based on serum iron, iron saturation, and serum ferritin concentration. Sixth, X-ray examination needs to be completed. Severe thalassemia features typical hair-on-end changes, visible as vertical striations between the trabeculae of the cortical bone in the skull X-rays, resembling upright hair and rays of sunlight.