Pediatric acute myeloid leukemia

Introduction to acute myeloid leukemia in children Acute myeloid leukemia (AML) is similar to adult (<50 years old) in molecular biology and chemotherapy response. AML in infants and young children is more prone to extramedullary leukemia than adults. The cure rate of AML in the past 20 years is about 40%, far less than that of children with ALL. After the first remission of AML, the results of sibling allogeneic BMT were slightly better than chemotherapy. Children with AML can occur at any age. The incidence rate of each age group is basically the same, slightly higher in adolescents, unlike ALL at 3 to 4 years old. There is no difference between men and women. The onset of AML is associated with certain hereditary diseases. For example, in the 21-trisomy, Fanconi anemia, the incidence of AML is higher. The likelihood of secondary AML after treatment for some malignant tumors is about 5%. AML occurs in association with certain medications (such as cyclophosphamide, podophyllotoxin) and radiation therapy. basic knowledge Sickness ratio: 0.0001% Susceptible people: children Mode of infection: non-infectious Complications: anemia, sepsis, optic disc edema, disturbance of consciousness

The cause of acute myeloid leukemia in children

(1) Causes of the disease

Possible pathogenic factors include the following aspects.

Factors that may cause childhood leukemia include genetic, environmental, viral infection, and immunodeficiency factors, but for each patient with leukemia, the cause of the individual is often undetermined.

(1) Environmental factors:

Radiation factors: The incidence of leukemia in people with X-ray diagnosis and treatment, 32P treatment, and atomic bombing is high. This was confirmed by the increase in the incidence of local leukemia after the atomic bombing in Japan during the Second World War. Exposure to therapeutic radiation also increases the incidence of leukemia.

Chemical factors: benzene, anti-tumor drugs such as alkylating agents and etoposide, and bis-morpholine for the treatment of silver diseases can cause leukemia. Other chemicals that may be associated with the onset of ALL include herbicides, insecticides, pregnant women, alcohol, contraceptives, tobacco, and chemical solvents, but the exact relationship between these factors and the onset of ALL is not yet certain.

(2) Infection factors:

The carcinogenic effects and leukemia effects of the virus in certain animals have been confirmed. Adult T-cell leukemia virus (HTLV) has been shown to cause adult T-lymphocytic leukemia in humans. In children with leukemia, no specific viral infection has been confirmed. Childhood Burkitt lymphoma is known to be associated with EB virus infection. In short, the cause of hematopoietic stem cell disorder in leukemia is multifactorial, with external causes and internal factors, internal and external factors. External factors such as physicochemical, viral, etc., internal factors such as chromosomal changes, abnormal DNA repair, immune imbalance. Although the incidence of leukemia is increased in congenital syndrome, most leukemias may be acquired. Regarding the exact cause of leukemia, people are constantly trying to explore the research.

(3) Congenital gene (genetic) factors:

It has been reported that the incidence of leukemia in children with leukemia (including ALL) is 2 to 4 times higher than that in the general population. After the occurrence of leukemia in one of the monozygotic twins, the chance of another leukemia is as high as 25%; the younger the age of onset, the higher the chance of another onset; when the age of onset is >7 years, the chance of another onset is significantly reduced. It shows that the occurrence of leukemia can be involved in congenital genetic factors, but the exact genetic factors are not yet clear. Chromosomal changes in ANLL are associated with many clinical features. ML: t (9; 22), inv (3). M2: t (8; 21), t (9; 22), t (6; 9), t/del (12). M3: t (15; 17). M4: t(8; 21), 5q inv(3), t/del(11). M4E0: inv (16), del (16). M5a: t (11q). M5b: t (3; 16). M6: t (3; 5). M7: inv (3). AML risk scores can be grouped according to the genetic characteristics of the diagnostic screening to facilitate the development of later treatment strategies. Refer to the NCCN (2010) recommended risk grouping: prognosis group, moderate prognosis group, and poor prognosis group.

Congenital diseases: such as Fanconi anemia, Downs syndrome, Bloom syndrome, etc., the incidence of leukemia is high.

(4) Other blood diseases:

Certain acquired diseases can be converted to AML. The most common is the conversion of myelodysplastic syndrome (MDS) to AML. In the past, MDS before transformation was called pre-leukemia. The majority of leukemias transformed by MDS are AML. Other myeloproliferative diseases such as polycythemia vera and primary myelofibrosis may be converted to AML in the later stages of the disease. A few atypical aplastic anemias and bursts Sexual sleep hemoglobinuria can also be converted to AML.

(two) pathogenesis

1. There are many studies on the pathogenesis of leukemia, including studies on molecular genetic changes, prognostic factors, molecular epidemiology and pharmacogenetics. It is speculated that there are two possibilities, that is, acquired genetic damage can activate the initial oncogene of the cell or inactivate the tumor suppressor gene (anti-cancer gene), both of which can lead to loss of tumor monitoring ability and uncontrolled proliferation of leukemia cells. These genetic changes can be point mutations, gene amplification, gene deletions or chromosomal translocations. Chromosomal translocations can be seen in many leukemias. Translocation can hide a gene into a new location, turning a new initial oncogene into a promoter or becoming an enhancer on other unique genes. For example, in the chromosomal translocation of t(8;14), the enhancer of the immunoglobulin heavy chain gene is a juxtaposed component close to the MYC gene, resulting in Burkitts lymphoma. Translocations can also occur within two genes, leading to gene rearrangements and chimeric proteins.

2. Activation of oncogenes In recent years, molecular genetic studies have confirmed that human tumors are closely related to oncogenes. Almost all leukemia patients have c-myc or Ha-ras gene expression. Increased expression of c-myc gene in acute leukemia and chronic catastrophe. The activity of N-ras in acute myeloid leukemia was significantly increased. The c-myc gene is amplified dozens of times when the promyelocytic and other acute myeloid leukemias recur. Oncogene activation is generally through three pathways, point mutations (proto-oncogenes are mutated at a specific position in the coding sequence, one nucleotide is mutated, causing a corresponding amino acid to change), amplification (some oncogenes replicate on the original chromosome) Multiple copies, resulting in increased gene product, leading to abnormal cell function) and translocation (oncogenes are transferred to other chromosomes in their normal position, making their resting proto-oncogenes become activated oncogenes).

3. Cytogenetic features and clinical significance of myeloid malignant tumors

According to WHO classification, myeloid malignancies include a series of malignant diseases involving myeloid myeloid cells including acute myeloid leukemia (AML), chronic myeloproliferative disease (MPD), and myelodysplastic syndrome (MDS). Because the cytogenetic features of myeloid malignancies are far more valuable in the diagnosis and prognosis assessment of diseases than in immunophenotyping and morphological classification, some specific types of diseases have been genetically based on current classification. The features are separated separately into an independent subtype. 79% to 85% of children with AML are associated with chromosomal abnormalities. 55% of AML cases only occurred as a single abnormality with the exception of additional abnormalities. Using high-resolution technology, the karyotype abnormality discovery rate is as high as 90% or more. Different from the change of ALL chromosome, the chromosomal abnormality of AML is changed to the main structure, up to 39 species. The quantitative aberration is relatively minor in terms of type and clinical significance.

Prevention of acute myeloid leukemia in children

1. Avoid contact with harmful factors to avoid exposure to harmful chemicals, ionizing radiation and other factors causing leukemia. Those engaged in radiation work should use benzene as a chemical raw material to do personal protection and strengthen preventive measures. Avoid environmental pollution, especially indoor environmental pollution; infants and pregnant women are more sensitive to radiation and vulnerable, women should avoid exposure to excessive radiation during pregnancy, otherwise the incidence of leukemia in the fetus is higher.

2. Vigorously carry out prevention and treatment of various infectious diseases, especially viral infectious diseases. Do a good job of vaccination. Pay attention to the rational use of drugs, use cytotoxic drugs with caution, etc., must be guided by a doctor, do not use or abuse for a long time.

3. Do a good job in eugenics to prevent certain congenital diseases, such as 21-trisomy, Fanconi anemia, etc.

4. Strengthen physical exercise, pay attention to food hygiene, maintain a comfortable mood, work and rest, and enhance the body's resistance. It is forbidden to take drugs that are harmful to bone marrow cells such as chloramphenicol and bisphedrine.

Complications of acute myeloid leukemia in children Complications, anemia, optic disc edema, consciousness

1. Anemia and hemorrhage: anemia is progressively aggravated, palpitations and tinnitus may occur; hemolysis and varying degrees of bleeding may occur; M3 type has a more serious bleeding tendency, and DIC is prone to occur before treatment and at the beginning of treatment; Subcutaneous hematoma, retinal hemorrhage in the fundus, leading to vision loss; increased intracranial pressure during intracranial hemorrhage, manifested as headache, vomiting, convulsions and coma; digestive tract and urinary tract bleeding; digestive tract and intracranial hemorrhage can cause death.

2. Infection: often complicated by infection, easy to spread to sepsis; common infection sites are respiratory system, skin bloated, intestinal inflammation, perianal inflammation, etc., can occur thrush, perianal fungal disease, fungal enteritis and deep fungus Infection, etc.

3. Leukemia cell infiltration: can be complicated by bone marrow failure and infiltration of whole body tissues and organs, liver and spleen, swollen lymph nodes; joint swelling and pain, hindering action; can be complicated by central nervous system leukemia, green tumor, manifested as increased intracranial pressure, Have headache, vomiting, blurred vision caused by optic disc edema, can also cause cranial nerve damage such as facial paralysis, and even epileptic seizures, disturbance of consciousness, etc.; parotid leukemia; testicular leukemia; obvious swelling of the kidney; skin, gastrointestinal tract, lung When the pleura and heart infiltrate, it causes symptoms of the corresponding organ dysfunction.

Symptoms of acute myeloid leukemia in children Common symptoms: Weakness, thrombocytopenia, neutropenia, bone pain, skin infiltration, splenomegaly, fever, hemorrhagic skin, mucous membrane, leukemia, cell infiltration

Children with AML begin to show varying degrees of paleness, fatigue, skin or mucous membrane bleeding or fever/infection (often ineffective for antibiotic treatment), these symptoms are due to anemia, thrombocytopenia and neutropenia, and blood changes are secondary to leukemia cell infiltration Bone marrow, normal blood cells, AML bone pain, joint pain is not as common as ALL, lymph nodes, liver, splenomegaly is not as obvious as ALL, huge liver, splenomegaly is only seen in small infants AML, M3 type often combined with severe bleeding and DIC M4 type, M5 type occurs more than small infants with high white blood cells, skin infiltration and with CNSL, M4 type, M5 type is more common in congenital leukemia, green tumor is more common in ML, M2 type, M6 type fetal hemoglobin (HbF) and hemoglobin H (HbH) increased, M7 can occur in infants under 3 years of age, especially with Down syndrome.

Examination of acute myeloid leukemia in children

Blood

Anemia and thrombocytopenia are extremely common (75% to 90%). The number of white blood cells in half AML patients is increased, mostly between 10×109 /L and 100×109 /L, and in 20% of cases, even >100×109 /L. In some patients, the number of white blood cells is normal, and the number of white blood cells in a small number of patients (often M3 or elderly) is < 4.0 × 109 / L. 80% of patients have lower hemoglobin than normal, and even severe anemia, reticulocytes often decrease. The number of platelets decreased in most patients, with a few normal or mildly elevated.

Bone marrow

Most patients are highly proliferating, and normal hematopoietic cells are replaced by leukemia cells; a small number of patients have low bone marrow hyperplasia, but the original cells are still more than 30%. If the Auer body is found in the cytoplasm, it is more helpful to rule out the diagnosis of AML.

Accurate diagnosis of leukemia is a prerequisite for the correct use of chemotherapy. At present, the internationally accepted are Morphology, Immunology, Cytogenetics and Molecular classification, which is what we often call the MICM classification. So if you consider leukemia, Need to do the above checks, one is to diagnose leukemia, the other is to determine the type of leukemia, choose a treatment plan and judge the prognosis.

1. Histochemical staining

The different cytochemical staining characteristics of different subtypes of AML are different, so the cytochemical staining of AML is very important for the diagnosis of this disease.

2. chromosome

79% to 85% of children with AML are associated with chromosomal abnormalities. About half of the AML cases were only caused by a single karyotype abnormality, and the others were accompanied by additional abnormalities. Using high-resolution technology, the karyotype abnormality discovery rate is as high as 90% or more. The chromosomal abnormalities of AML are structurally distorted, up to 39 species, and some special structural abnormalities, such as t(8;21)(q22;q22), t(15;17)(q22;q11-12) and Inv (16) (p13; q22) or t (16; 16) (p13; q11) is associated with a good prognosis. The value of karyotypic abnormalities in the diagnosis and prognostic significance of AML is far more important than immunophenotyping.

(1) Specific chromosome structure rearrangement:

t(8;21)(q22;q22) is one of the most common characteristic chromosomal abnormalities in AML. Children with poor efficacy and poor prognosis.

t(15;17)(q22;q21) and PML-RARA: seen in 70% of APL patients, molecular testing showed that 100% APL has t(15;17), since it has never been seen in other leukocyte subtypes and tumors, Therefore, it becomes a highly specific cytogenetic marker of APL. The patients in this group have a good overall effect and a long survival period.

t(9;11)(p22;q23): is the most common form of translocation in 11q23 anomalies. 75% is AML-M5 type, especially M5. The overall prognosis is good. However, the patient's age, white blood cell count, and presence or absence of central nervous system involvement also determine the patient's prognosis.

t(10;11)(p11-15;q23): mainly seen in patients with AML-M5 type, more common in children, 80% of patients <3 years old. Poor prognosis, 2-year disease-free survival rate of 50%. Translocation leads to the formation of the MLL-ELL fusion gene.

t(11;19)(q23;p13.3): can be found in ALL, AML-M4, M5, M1, M2, and is more common in infants younger than 1 year old. The median survival time was 17.6 months.

t(6;9)(p23;q34): 2% in AML, mainly M2, followed by M4. The initial description is characterized by normal basophilia in the bone marrow. 20% of patients have a history of previous MDS. Young patients (20 to 30 years old) have a poor prognosis.

Inv(3)(q21q26): including inv(3)(q21q26), t(3;3)(q21;q11q26), t(3;3)(q21;q26), inv(3)(q21;q26) , del (3) (q12q21), t (1; 3) (p36; q21) and other forms. This type accounts for about 1% AML. Young patients have a history of MDS and can be seen in M1, M4, M6, M7, etc.

t(3;5)(q21;q31): 1/4 of patients were M6. Unlike inv(3), there was no increase in platelets in patients, but there was a high risk of developing Sweet syndrome. Involved in the 5q34 NPM gene.

t(9;22)(q34;q11): a rare type with an incidence of less than 1%, mainly found in AML-M1 and a few in M2. The prognosis is poor.

Ht (7; 11) (p14; p15): a rare type, the vast majority of cases are morphologically diagnosed as AML-M2, and a few are M4. The clinically prominent feature is the three-line pathological hematopoiesis and the emergence of giant mature granulocytes with pseudo-pelger-huüt nuclear abnormalities.

t(8;16)(p11;p13): rare, characterized by phagocytosis of red blood cells by primitive cells, but without eosinophilia. Young patients are mostly, often with extramedullary infiltration. Poor prognosis.

t(1;22)(p13;q13): only found in children M7, 28% of children M7 and 67% of infants M7.

t(16;21)(p11;q22): Young patients (MA 22 years old), all of the FAB subtypes, with poor prognosis (MS 16 months).

t(16;21)(q24;q22): The fusion gene AML1-MTG16 product function is similar to AML1/MTG8 of t(8;21)(q22;q22), which may be a variation of t(8;21).

Del(20)(q11, 2q13.3) can be seen in 2% to 3% of AML patients with poor prognosis.

t(1;7)(p10;p10) usually has a pre-white history.

(2) Abnormal number of chromosomes:

A. Trisomy 8: Trisomy 8 is the most common number of abnormalities in AML. It can be seen in 20% of cases, as an isolated abnormality, 8 often occurring in AML-M5, M4, M1, and rarely in M3. Being an additional exception can be seen in various types. 8 abnormal AML has a moderate prognosis.

B. Trisomy 4: A rare type, more common in AML-M4, and some reports suggest that the occurrence of this translocation is related to the history of contact with previous distortion agents. Most merge with additional chromosomal abnormalities, such as 8. The patient has a poor prognosis.

C. Other trisomy: 21-trisomy is commonly found in AML-M2 as an isolated abnormality with poor prognosis. 9, 22, 11, 13, 19, 6 have also been reported.

D.-7: The detection frequency is second only to trisomy 8, and patients with monomer 7 may be related to exposure to chemical or other toxic substances. Familial leukemia can be seen in monomer 7. Childhood 7 syndrome manifests as a pre-leukemia diagnosis and then gradually evolves to AML with a poor prognosis, often accompanied by infection.

E.-5/5q-: Not as common as MDS, often accompanied by 1L-4, 1L-5 gene deletion.

3. Immunological typing

The main basis of FAB typing is cell morphology and histochemistry. Due to human factors, the diagnostic agreement rate is quite different. The immunophenotype can indicate the differentiation and differentiation stages of leukemia cells, and the discrimination rate is as high as 98%. Therefore, for some AMLs that are difficult to form by morphologically, such as M0, ML, M7, acute undifferentiated leukemia (AUL), acute heterozygosis leukemia (AHL), etc., immunization The type checking is very important. However, immunophenotyping has little value in the prognosis of AML.

Other auxiliary inspections:

(1) uric acid hyperuricemia is common in patients with increased white blood cell count and induction chemotherapy, and is associated with tumor lysis, but the incidence of hyperuricemia in AML is lower than ALL;

(2) thrombocytopenia may occur when DIC occurs, thrombocytopenia, prothrombin and partial thromboplastin time prolonged, plasma fibrinogen decreases fibrin degradation products and clotting factors VVII, VIII, X and so on.

(3) serum enzyme

1 serum lactate dehydrogenase (LDH) can be elevated, especially M4, M5 subtype, the degree of increase is generally lighter than ALL;

2 serum lysozyme (lysozyme) increased also M4, M5 type more common.

Diagnosis and diagnosis of acute myeloid leukemia in children

diagnosis

It is not difficult to diagnose AML based on typical clinical findings and laboratory tests.

1.AML ML-M7 7 subtypes diagnosis

In 1986, the Tianjin Leukemia Classification and Classification Symposium synthesized new developments on leukemia typing at home and abroad. Several modifications were made to the recommendations of the 1980s, and AML was divided into ML-M7 7 subtypes:

(1) Undifferentiated type of acute myeloid leukemia (ML): Myeloblasts (I II type) in bone marrow 90% (non-erythroid cells), few promyelocytic cells, neutral neutrophils are not seen in the following stages or rare.

(2) Partially differentiated type of acute myeloid leukemia (M2): divided into two subtypes:

1M2a: Myeloblasts in the bone marrow (type I II) >30% to <90%, monocytes <20%, and promyelocytic cells >10%,

2M2b: The original and promyelocytes in the bone marrow increased significantly, with abnormal neutral mesangial cell proliferation. The nucleus often had nucleoli and obvious nucleoplasmic development imbalance. Such cells were >30%.

(3) Promyelocytic leukemia (M3) with increased acute granules: abnormally promyelocytic hyperplasia with increased particle size in the bone marrow, >30%, with different nucleus sizes and different sizes in the cytoplasm Particles can be divided into 2 subtypes:

1 coarse particle type (M3a): aniline blue particles are coarse, dense or even fused,

2 Fine particle type (M3b): The azuramide blue particles are dense and small.

(4) Acute granulocyte-monocytic leukemia (M4): Depending on the morphology of the granulosa and monocyte lines, the following four subtypes may be included:

1M4a: primary and promyelocytic hyperplasia, primary, juvenile and monocyte >20%,

2M4b: primary, progenitor mononuclear cell proliferation, primary and promyelocytes >20%,

3M4c: primordial cells with both granulocyte and mononuclear cell line morphology >30%,

4M4ED: In addition to the above characteristics, there are large and round eosinophils with darker coloration of eosinophils, accounting for 5% to 30%.

(5) Acute monocytic leukemia (M5): divided into 2 subtypes:

1 undifferentiated (M5a): primary monocytes in the bone marrow (type I II) I> 80%,

2 partially differentiated (M5b): primary and naive cells in the bone marrow >30%; proto-mononuclear cells (type I II) <80%.

(6) erythroleukemia (M6): erythrocyte lineage in the bone marrow >50%, and often morphological abnormalities, bone marrow non-erythroid blasts (or primordial mononuclear cells) I II type >30%; Granules (type I II) (or original) cells > 5%, myelocytes (or primordial mononuclear cells) in bone marrow non-erythroid cells > 20%.

(7) megakaryocyte leukemia (M7): peripheral megakaryocytes (small megakaryocytes); megakaryocytes in bone marrow 30%, protoplasts confirmed by histochemical or monoclonal antibodies; bone marrow hematopoietic cells are few, often dry Pumping, biopsy has increased primordial and megakaryocytes, and reticular fibers increase.

2. FAB-M0 type (undifferentiated type) diagnostic criteria

In recent years, FAB-M0 type (undifferentiated type) has been identified. The original granulocytes cannot be distinguished under light microscope. The characteristics of the myeloid system need to be confirmed by electron microscopy POX to confirm positive particles or immunological methods to detect myeloid monoclonal antibodies. In October 1990, the London meeting proposed the following diagnostic criteria for M0:

1 Morphologically, it is characterized by primitive cells: most of the cytoplasm is translucent or moderately alkalophilic, no azurophilic particles and Auer bodies, and the nucleolus is obvious, similar to the acute lymphoblastic L2 type.

2 cytochemistry: myeloperoxidase and Sudan black B staining <3%.

3 Immunology: the myeloid marker CD33 and/or CD13 can be positive; the lymphoid antigen is negative, respectively, CD7, TdT.

4 electron microscopy: myeloperoxidase positive, M0 type abnormal chromosome expression: -5 or del (5), -7 or del (7), M0 type is rare in children, AML histochemical staining characteristics are shown in Table 9.

Differential diagnosis

1. Identification of AML and ALL

(1) can be identified according to immunological classification: the principle of immunophenotyping is based on the differentiation of leukemia formation theory, that is, leukemia cell gene abnormality, differentiation is blocked at a certain stage to form different subtypes of leukemia, this group of cells are filled with bone marrow, antigen There is no significant difference between the expression and the corresponding series/stage of blood cells. The research on the immunophenotyping of AML is slower than ALL, mainly used for the difference between AML and ALL. Myeloperoxidase (MPO) is the myeloid cell line-acute non-lymphocyte. It is unique to leukemia. There is no acute lymphoblastic leukemia. During the differentiation of myeloid cells, CD34 appears in the granulocyte-macrophage progenitor cell (CFU-GM) and disappears into the granulocyte stage. CD33, CDL3 are found in the whole process of myeloid differentiation. HLA-DR is present in CFU-GM and various monocytes, naive and mature granules, CDL1b appears on the surface of monocytes, CDL5 is expressed in granules, and about 90% of AML The cells express CDL17, CDL4, CD64, which are markers of monocytes. They are found in M4 or M5. CD71 and glycophorin A are erythroid markers, which are found in M6 type CD41a (GpIIb/IIIa), CD61 (GpIIIa), CD41b (II). b), CD41b (Ib), CD42c (Ib) is a marker of megakaryocytes, found in M7 type, platelet peroxidase (PPO) is also an important marker for the identification of M7, but must be observed under an electron microscope, see the immune markers of AML Table 10, in general, the immunological typing of AML is not significantly related to FAB typing, but a few types are related, such as M4/M5 expressing CDL4, M3 lacking HLA-DR antigen, Bene MC, etc. FAB typing and membrane The relationship of the signs is summarized as follows:

(2) Identification of MIC classification: In September 1986, the 2nd International MIC Research Collaboration Group developed the MIC classification criteria for AML. First, AML and ALL were distinguished according to cell morphology, cytochemical staining and immunological markers.

Specific chromosomal changes in AML are more common than ALL, often with independent prognostic value, and specific chromosomal abnormalities associated with morphology and AML.

2. Reaction with leukemia and differentiation of neuroblastoma

In the recovery phase of granulocyte deficiency in children, leukemia-like reactions caused by certain infections and neuroblastoma often have clinical manifestations similar to those of AML, which need to be carefully identified.

(1) Infectious mononucleosis: an acute mononuclear-macrophage system proliferative disease caused by Epstein-Barr virus (EBV), the course of which is often self-limiting, clinically irregular fever, angina , liver, spleen and lymph node enlargement, the total number of peripheral white blood cells increased to varying degrees, with a large number of abnormal lymphocytosis, serum lymphoagglutination test and Epstein-Barr virus antibody can be positive, the above clinical manifestations and laboratory tests can be AML phase identification.

(2) Leukemia-like reactions: Leukemia-like reactions are a leukemia-like hematological change caused by certain factors such as infection, poisoning, malignant tumor bone marrow metastasis, acute blood loss, hemolysis, etc., such as peripheral blood. The total number of leukemias is increased, and the immature cells can be seen in the classification. Some cases can be accompanied by anemia and thrombocytopenia, but they are not true leukemia. The medical history is carefully diagnosed and the corresponding laboratory tests are easy to identify.

(3) Neuroblastoma: Children with neuroblastoma often use the infiltration of the orbital bone as the first manifestation, which needs to be differentiated from the green tumor of AML.

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