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Leukemia
Does leukemia cause fever?
Leukemia patients do experience fever, which can be categorized into two main types: infectious fever and tumor fever. Infectious fever occurs due to the compromised resistance and lowered immunity of leukemia patients, potentially leading to various types of infections such as pulmonary infections, skin and mucous membrane infections, digestive system infections, urinary system infections, etc. Tumor fever, on the other hand, occurs in the late stages of leukemia and is caused by the abnormal proliferation of leukemia cells, leading to tumor-related fever. Typically, the temperature in tumor fever does not exceed 38 degrees Celsius, with early-stage fevers responding well to treatment, but late-stage fevers showing poorer responsiveness.
How is leukemia diagnosed?
When a routine blood test suggests the possibility of leukemia, further diagnostic tests such as bone marrow aspiration, biopsy, and immunophenotyping are required to confirm the diagnosis. Leukemia can be divided into acute leukemia and chronic leukemia. Acute leukemia includes acute myeloid leukemia and acute lymphoblastic leukemia. Acute myeloid leukemia is further categorized into eight types, from M0 to M7. Acute lymphoblastic leukemia is divided into three subtypes: L1 to L3. Chronic leukemia can be divided into chronic myeloid leukemia and chronic lymphocytic leukemia.
The difference between chronic granulocytic leukemia and leukemia
Leukemia is divided into acute leukemia and chronic leukemia. Acute leukemia is further categorized into acute lymphocytic leukemia and acute myeloid leukemia, while chronic leukemia is divided into chronic lymphocytic leukemia and chronic myeloid leukemia. Chronic myeloid leukemia, also known as chronic granulocytic leukemia, generally has a better prognosis compared to acute leukemia, with a higher cure rate and longer survival. Among these, chronic granulocytic leukemia has targeted treatment drugs such as imatinib and dasatinib.
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.
Early symptoms of childhood leukemia
Generally speaking, leukemia can manifest symptoms related to a decrease in all three blood cell lines. Changes in these three lines typically include an increase or decrease in white blood cells, a decrease in red blood cells leading to symptoms of anemia, and a reduction in platelets, resulting in symptoms of bleeding. Children with leukemia often experience recurrent fevers and are prone to infections, as well as bleeding gums. There may also be enlargement of the liver, spleen, and lymph nodes, along with pallor of the face and lips, which appear pale and bloodless.
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.
The Difference Between Acute Leukemia and Chronic Leukemia
The difference between acute and chronic leukemia lies in the maturity stage of the leukemia cells. Acute leukemia is characterized by more immature leukemia cells, while chronic leukemia cells tend to be more mature. Acute leukemia is further divided into acute myeloid leukemia and acute lymphoblastic leukemia. Among them, acute myeloid leukemia is subdivided into eight types, from M0 to M7. Chronic leukemia is divided into two main categories: chronic lymphocytic leukemia and chronic myeloid leukemia. As the name suggests, acute leukemia has a rapid onset and a shorter survival period, whereas chronic leukemia develops more slowly and has a longer life expectancy.
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.
Is leukemia cancer?
Leukemia is a cancer of the blood system. Based on the maturity of the tumor cells, leukemia can be divided into acute leukemia and chronic leukemia. Acute leukemia is further divided into acute myeloid leukemia and acute lymphoblastic leukemia, while chronic leukemia is divided into chronic granulocytic leukemia and chronic lymphocytic leukemia. As the name suggests, acute leukemia has a rapid onset, a shorter survival period, and treatment is more challenging. Chronic leukemia, on the other hand, has a slower onset, a relatively longer survival period, and the treatment results are comparatively better.
Chronic Granulocytic Leukemia Classification
Chronic granulocytic leukemia is a myeloproliferative tumor originating from pluripotent stem cells, characterized by the presence of the Philadelphia chromosome or changes in the BCR/ABL fusion gene. Chronic granulocytic leukemia progresses through four stages: asymptomatic, chronic, accelerated, and blast crisis phases. Most patients are diagnosed after the onset of symptoms. Only a very few patients are diagnosed through routine physical examinations or other reasons when blood abnormalities are discovered. The earliest symptoms experienced during the chronic phase of the illness typically include fatigue, dizziness, and abdominal discomfort. The accelerated phase is a transitional stage before the blast crisis, marking a turning point where the disease worsens. It is often difficult to distinctly separate the accelerated phase from the blast crisis, and about 20%-25% of patients may enter the blast crisis phase directly without passing through the accelerated phase.