Pediatric acute non-lymphocytic leukemia

Introduction to acute non-lymphocytic 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 prone to extramedullary leukemia. basic knowledge The proportion of illness: 0.005% Susceptible people: children Mode of infection: non-infectious Complications: anemia, sepsis, green tumor, headache

The cause of acute non-lymphocytic leukemia in children

(1) Causes of the disease

Cause

The etiology of childhood leukemia is still unclear, and the possible pathogenic factors include the following aspects.

(1) Physical and chemical factors: So far, although there are a large number of studies on the relationship between environmental factors and leukemia, only the relevant factors identified are ionizing radiation. For example, the exposure of benzene and ionizing radiation is related to the pathogenesis of AML, but it can be clearly The disease factor only accounts for a very small part of the number of cases. A study of survivors of the atomic bombing area in Hiroshima, Japan, found that the incidence of leukemia increased after 5 to 15 years of atomic bombing, and the incidence of AML increased by 20 times. The risk of leukemia is related to the dose of radiation received 6 to 8 years after receiving radiation, and the follow-up study of the nuclear accidents in Sanli and Chernobyl has not been found to be associated with the onset of childhood leukemia, and smoking during pregnancy has also increased. The incidence of AML, in the second tumor, AML is a more common type, mainly related to the exposure of previous alkylating agents such as cyclophosphamide, nitrogen mustard, busulfan, etc., often occurs in the first tumor 4 ~ 5 After the year, it can be expressed as myelodysplastic syndrome (MDS) and then developed into AML, but after 10 to 12 years, the chance of AML is reduced. In addition, the episodes of scorpion toxin VP-16 It is related to the pathogenesis of second tumor AML, and its onset time is often earlier than that induced by alkylating agents. It was reported in the 1950s that X-ray irradiation in pregnant women's uterus increased the risk of leukemia in children, but now this view is still Controversy, there are also studies that believe that low-level radiation exposure before pregnancy can increase the risk of infant leukemia. Multi-center studies have shown that mothers are exposed to pesticides, herbicides, fungicides, etc. before pregnancy, during pregnancy and during fatherhood. The incidence of childhood leukemia is related.

The correlation between electromagnetic fields and the pathogenesis of leukemia has been reported as early as the 1970s, and subsequent large series of studies have not confirmed the hypothesis that low-intensity electromagnetic fields are associated with childhood leukemia and other childhood cancers. Research results from the United States, Canada and the United Kingdom in recent years. It is believed that exposure to high-intensity magnetic fields (>0.4T) may increase the risk of acute leukemia, while low-intensity magnetic fields have little effect on the body.

Recent studies have also shown that domestic organic solvents are associated with the development of childhood acute leukemia.

Occupational exposure to benzene is closely related to the occurrence of adult acute leukemia. Although childhood ALL is unlikely to be caused by occupational exposure, the increasing concentration of benzene in the environment may be one of the causes of childhood ALL. Studies have reported that living in traffic routes or refueling Children near the station (within 100m) have an increased risk of leukemia. This result is based on ecological studies. The exact correlation needs further research. The results of more than 1,000 children with leukemia in China show that 46% of families are The child has undergone internal decoration within 6 months before diagnosis. The possible mechanism of benzene leading to childhood leukemia is strong with children's individual susceptibility. Children's toxic metabolic enzymes such as cytochrome p4502E1, myeloperoxidase (MPO), glutathione Genetic polymorphisms such as peptide thiotransferases (GSTs) and genetic defects inherent in children are related.

(2) Virus: A virus associated with the onset of AML has not been confirmed.

(3) Genetic factors: To date, the participation of genetic factors has not been confirmed in most children with AML. Occasionally reports of sibling or familial morbidity, children with Down syndrome have a 14 times higher chance of developing AML than the normal population. In the same twins, if one child develops before the age of 6, the chance of another child is about 20%; in the case of a child before the age of one, the chance of another child is greatly increased; and one child is after 6 years old. In the case of the disease, the chance of developing another child is significantly lower than that of the 6-year-old. The chance of developing AML in some congenital bone marrow diseases is also increased. Some hereditary syndromes, such as 21-trisomy syndrome, have been proved. Down syndrome and Fanconi anemia are closely related to the susceptibility of leukemia. Studies in the United Kingdom and the United States have shown that 2.3% to 2.6% of children with acute leukemia are associated with genetic factors.

The investigation of siblings, parents and offspring of all types of leukemia patients did not reveal a high incidence of tumors. Although there were reports of leukemia in siblings, the incidence was extremely low, and the probability of leukemia in identical twins was greater than that of fraternal twins. Grandfather, parents, and hereditary defects among siblings are associated with the onset of multiple types of ALL, including musculoskeletal disorders, gastrointestinal disorders, allergic diseases, hereditary heart disease, and lung disease.

Because there have been many long-lived cases in recent years, some scholars have investigated the risk of leukemia in the offspring of long-lived patients. The results showed that the risk of leukemia increased in this population, and the children with healthy leukemia were also healthy. In the examination of chromosomal stability, no increase in chromosomal instability was observed in either the control group or the bleomycin-induced aberration group. A controlled study with healthy people found no increase in congenital malformations in the offspring of children with long-lived ALL. .

Genetic and environmental factors interact in the development of childhood ALL. Histocompatibility leukocyte antigen (HLA) is considered to be one of the genetic risk factors for leukemia susceptibility, and its correlation is expressed as the most common allele in men. The expression of HLA-DR53, HLA-DRB104 was enhanced, and the homozygous gene of HLA-DRB104 was found in ALL patients, which specifically enhanced the specificity of HLA-DR53, and the homozygous gene of HLA-DRB104 and ALL. Correlation is particularly prominent in male patients. The cross-reactivity between HLA-DR53 and H-2Ek broadly mimics the HLA-DR53 immunodominant antigenic determinant by some oncogenic viruses, and an additional number of DNA proofs adjacent to the HLA-DRB4 gene HLA-DRB104 may be one of the genetic factors of childhood ALL. In 60 children with ALL and 78 neonatal DQA1 and DQB1 allele control studies, male patients DQA10101/0104 and DQB10501 were found to be normal. The incidence of control was high, and this result suggests a male-related susceptible HLA line in ALL patients.

The role of transferase and cytochrome P-450 genes in childhood tumors has been studied. Both enzymes are involved in carcinogen metabolism and constitute a high risk factor for many cancers in adults, and N-acetyltransferase encoded by NAT1 and NAT2. Participate in the biotransformation of aromatic amines in cigarettes, the environment and foods. These fast and slow acetylation alleles are modified in a variety of adult solid tumors, low folate uptake or as methylenetetrahydrofolate reduction Changes in folate metabolism caused by methylene tetrahydrofolate reductase (MTHFR) polymorphism are associated with neural tube defects and some cancers. Changes in MTHFR polymorphism lead to increased thymidine pools and high-quality DNA synthesis. The occurrence of protection provides protection, especially in relation to leukemia where chromosomal translocation occurs.

Wiemels et al. reported the association of MTHFR polymorphism with MLL gene rearrangement in infant leukemia and TEL-AML1-positive or hyperdiploid childhood leukemia. These findings suggest that different molecular biology subtypes of childhood leukemia may have different causes. The evidence also suggests the role of folate in the development of childhood leukemia. Krajinovic et al found that GSTML naked genotype and CYP1A1 genotype can meaningfully predict the risk of ALL. When NAT2 is slowly acetylated, it is usually considered Combined with other high-risk genotypes such as GSTML naked genotype and CYP1A2A genotype, increasing the risk of developing leukemia, Davies et al found that GSTML naked genotype is for children with AML (especially M3 and M4 in FAB typing) Predicting genotypes of significance, these findings suggest a possible role for the interaction of genes with environmental factors in the pathogenesis of childhood leukemia.

Nearly 80% of infant leukemias have genetic abnormalities on the 11q23 chromosome, forming MLL fusion genes, and 11q23 is also common in secondary leukemia (AML) caused by topoisomerase II inhibitors. Therefore, Ross and other scholars speculate Infant leukemia may be associated with topoisomerase inhibitors (including caffeine, variants of fruits and vegetables) exposed to the natural state, and a multicenter study was conducted. No results were found for topoisomerase II inhibitors. Correlation of various types of ALL, but the increase in topoisomerase II inhibitor food supplementation has a significant correlation with the pathogenesis of AML. Recent in vivo studies have shown that bioflavonoids and food additives naturally present in foods The same can cause site-specific DNA cleavage in the MLL gene breakpoint region. These results suggest that maternal intake of bioflavonoids can induce MLL gene breaks and may lead to chromosomal translocation in the uterus, leading to the occurrence of infantile leukemia, smoking, Drinking alcohol, taking certain Chinese medicines and drugs that cause DNA damage, exposure to pesticides can increase the urgency associated with MLL gene changes. Leukemia cancer risk.

2. Past medical history

2117 cases of ALL and 650 cases of AML found that Down syndrome, congenital heart disease, gastrointestinal malformation is more common in children with ALL; Down syndrome, mental retardation, congenital heart disease is more common in AML .

3. Biological characteristics

AML has a mechanism to escape the regulation of sequential death, and some cells are immortalized. In M3, it has been confirmed that PML/RARa fusion is caused by t(15;17), which blocks the regulation of normal differentiation of cells, and is easy to produce in AML treatment. Drug resistance, involving a variety of drug resistance mechanisms, including P glycoprotein, which is encoded by MDR in the multidrug resistance gene family, the main function is to actively pump a variety of drugs into the cell to make tumor cells resistant Calcium channel blockers and cyclosporine A can block the function of P glycoprotein. The common characteristic chromosomal abnormalities of AML are M2 t(8;21) and t(3;21), M3 t(15). ;17) and t(11;17), M4Eo's inv(16).

4. Morphological classification

According to the more accepted law, the English and American (FAB) morphological classification, AML is divided into seven types of M1 to M7.

(two) pathogenesis

1. Cell oncogene and viral oncogene

How viruses, ionizing radiation, chemicals, etc. cause leukemia, the mechanism is not fully understood, cell proliferation, differentiation and aging death are determined by genes, obviously the malignant transformation of cells must also be associated with some change in genes, now It is known that animal and human cells, as well as certain kinds of virus strains, have tumor genes that can induce malignant transformation of normal cells and obtain new biological characteristics. The former is called cell oncogene or protooncogene, the latter. Known as a virus oncogene, a cell oncogene is a member of a normal gene that acts during a certain period of cell proliferation, differentiation, and aging death, and is regulated and controlled by internal mechanisms when these genes are abnormally activated. When converted to a tumor gene, it has carcinogenic activity. Studies have shown that the viral oncogene is not inherent to the virus itself, but is inserted into the viral genome by recombinant DNA fragments of the host cell during repeated infections of the host.

2. Oncogene activation

Abnormal activation of cell oncogenes is converted into oncogenes, which are obtained through changes in genetic DNA structure and regulation disorders, including:

(1) Point mutation: one to several nucleotide sequences on the DNA strand of the gene are changed as point mutations, for example, the oncogene ras is derived from the ras mutation of the cell oncogene;

(2) Chromosome rearrangement: Due to changes in chromosomal translocations, inversions, deletions, etc., DNA structure and sequence changes in genes or their regulatory regions are a common way of oncogene activation. A typical example is the formation of Ph chromosomes, which is t ( 9;22) (q34;q11) translocation formation, that is, the cell oncogene c-ABL translocation on chromosome 9 is translocated to the break on chromosome 22 and forms a BCR/ABL fusion gene to activate;

(3) Gene amplification: These genes can be replicated into multiple sets of copies, some of which are separated from the chromosome to form a double microsome, and some can be integrated into the chromosome again, so the protein product increases and may cause malignant transformation of the cell.

3. About tumor suppressor genes

In recent years, it has been found that there are genes that inhibit tumor formation in human cells, called tumor suppressor genes. The human tumor suppressor genes reported so far have nearly ten kinds of RB, P53, P16, WTI, etc. due to gene mutation. The deletion can cause abnormal inactivation of the tumor suppressor gene, and the result is that the cell oncogene is over-expressed and the cell is transformed. We have used PCR-SSCP (single stranded conformational polymorphism) analysis and Southern blot hybridization to detect 31 children with acute lymphoid cells. P16 tumor suppressor gene deletion and point mutation in children with cell leukemia, the results showed that the P16 gene deletion rate (including point mutation) was 25.8%, of which homozygous deletion: B-ALL was 16%, T-ALL was 33%, point Mutations in 1 case of each type indicate that P16 gene inactivation due to gene deletion and point mutation has a high incidence in acute lymphoblastic leukemia, suggesting a close relationship with disease occurrence, development and prognosis.

4. Carcinogenic mechanism of viral oncogene

The viruses that induce animal and adult T-cell leukemia are almost all C-type retroviruses. After infecting host cells, the double-stranded proviral DNA is synthesized by reverse transcriptase and DNA polymerase using viral RNA as a template. Integrating into the DNA of the host cell, the viral oncogene can be activated and expressed to induce malignant transformation of the cell after integration into the host cell, or can be in a stationary phase by the genetic regulation of the host cell, when activated by radiation or chemicals. Inducing tumors, the newly proposed trans-regulatory effect of viral gene products explains the carcinogenic effects of HTLV-1 viruses on the other hand, that is, certain genes of such viruses can encode a special protein factor, which can not only increase The replication of the virus and the selective initiation of certain genes in the host cell, for example, induce an increase in the synthesis of interleukin 2 (IL-2) and its receptor, thereby promoting T cell malignancy.

5. About apoptosis

Apoptosis is a gene-directed process of cell self-destruction. It is a normal pathway for normal embryogenesis and cell clearance during adult tissue and organ development. When the apoptotic pathway is inhibited or blocked, cells can be made. Immortalization and malignant transformation, apoptosis involves a series of gene regulation, genes that promote apoptosis include Fas, Bax, ICE, P53, etc., genes that inhibit apoptosis include Bcl-2, Bcl-XL, etc. It not only opens up new fields for leukemia etiology and pathogenesis research, but also provides new ideas for the treatment and drug resistance of leukemia. Many drugs for treating leukemia such as doxorubicin, cisplatin, etoposide, and release line are known. Mycorrhizin D, methotrexate, and cytarabine can induce apoptosis in leukemia cells. Our department has studied the apoptosis of HL-60 leukemia cells induced by homoharringtonine, and found that the drug is mainly passed. Activation of Fas protein, down-regulation of Bel-2 protein, and initiation of apoptosis program, many drug resistance studies indicate that leukemia cells are sensitive to apoptosis-inducing drugs and intracellular Bcl-2 gene expression levels , Bcl-2 expression levels worse the higher the sensitivity, the detection level of expression of Bcl-2 leukemia cell chemosensitivity can be measured and the estimated prognosis.

Prevention of acute non-lymphocytic leukemia in children

1. Avoid contact with harmful factors to avoid exposure to harmful chemicals, ionizing radiation and other factors causing leukemia. When exposed to poisons or radioactive materials, various protective measures should be strengthened; avoid environmental pollution, especially indoor environmental pollution; pay attention to rational use of drugs, use with caution Cytotoxic drugs, etc.

2. Vigorously carry out prevention and treatment of various infectious diseases, especially viral infectious diseases, and do a good job of vaccination.

3. Do a good job in eugenics, prevent certain congenital diseases, such as 21-three-body, Fanconi anemia, etc., strengthen physical exercise, pay attention to food hygiene, maintain a comfortable mood, work and rest, and enhance the body's resistance.

Acute non-lymphocytic leukemia complications in children Complications anemia sepsis green tumor headache

Anemia and bleeding

Anemia is progressively aggravated, palpitations, tinnitus, hemolysis and varying degrees of bleeding may occur. M3 type clinically has a more severe bleeding tendency. It is prone to DIC before and immediately after treatment, and subcutaneous hematoma may occur, and retinal hemorrhage may occur. Vision loss, digestive tract and urinary tract bleeding, intracranial hemorrhage, increased intracranial pressure, manifested as headache, vomiting, convulsions and coma, etc., 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 swelling, intestinal inflammation, perianal inflammation, etc., can occur thrush, perianal fungal disease, fungal enteritis and deep fungal infections.

3. Leukemia cell infiltration

Can be complicated by bone marrow failure and systemic organs are infiltrated, with green tumor, liver and spleen, lymphadenopathy; superior vena cava syndrome; joint swelling and pain, hindering action; central nervous system infiltration can be complicated by central nervous system leukemia, It is characterized by increased intracranial pressure, 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.; no painful enlargement of both parotid glands; testicular leukemia The kidneys are obviously swollen; when the skin, gastrointestinal tract, lungs, pleura, and heart are infiltrated, symptoms of the corresponding organ dysfunction are caused.

Symptoms of acute non-lymphocytic leukemia in children Common symptoms Hemorrhagic tendency Lymph node enlargement Hepatosplenomegaly pale pale eyeball

The clinical manifestations of childhood acute leukemia are common, mainly manifested as anemia, skin mucosa or visceral bleeding tendency, fever and various types of infection. Unlike ALL, M3 type clinically has a more serious bleeding tendency, before treatment and just beginning treatment. DIC is prone to occur, and M5 type gingival infiltration is more common. Except for M4 and M5, other AMLs have less chance of infiltrating the central nervous system than ALL.

Physical examination except for varying degrees of pale, bleeding, purpura, more than half of the patients have liver, spleen, lymph nodes with different degrees of swelling; skin, subcutaneous tissue infiltration when the sputum and nodules, eyelid infiltration can have eyeballs, these infiltration The cut surface of the tumor (tumor part) can be converted into green by the action of myeloperoxidase contained in the tumor cells, so it is called "green tumor".

Examination of acute non-lymphocytic leukemia in children

Blood picture

Peripheral blood examination showed red blood cells, hemoglobin (Hb) decreased to varying degrees; white blood cell count (WBC) was increased by more than half, and the rest could be normal or decreased. At this time, it was also called hypoproliferative leukemia, and white blood cells were elevated in peripheral blood. Seeing leukemia cells is a strong evidence for the diagnosis of leukemia. Leukemia cells are not easily seen in the blood of leukopenia, also known as aleukemic leukemia. The blood picture of 1024 children with ALL is reported as follows: 1 white blood cells <10 ×109/L accounted for 34%, (10~24)×109/L accounted for 25%, (25~49)×109/L accounted for 22%, >50×109/L accounted for 19%, and 2Hb level <70g /L accounted for 44%, 70-110g/L accounted for 43%, >110g/L accounted for 14%, 3BPC20×109/L accounted for 29%, (2049)×109/L accounted for 23%, (50 99) × 109 / L accounted for 20%, 100 × 109 / L accounted for 29%.

2. Bone marrow

Most of the bone marrow in the newly diagnosed acutely ill children are obviously active or extremely active. In a few cases, the proliferative hypoplasia is called hypoproliferative leukemia, and the latter has a better prognosis. So far, the bone marrow is still the most accurate basis for the diagnosis of acute whiteness. The ratio of the original plus naive cells is 30% to diagnose, and the ANLL also removes the erythroid and then calculates the ratio. Due to the differentiation and maturation of normal hematopoietic cells in the bone marrow, a large number of leukemias that are arrested at a certain stage are replaced. Cells, due to the absence of one or more stages in the process of maturation, are called "cracks". In AML, especially in promyelocytic cells, rod-shaped Auer bodies are often seen, which are certain in the identification of ALL. In recent years, it has been found that rod-shaped or spindle-shaped phi bodies can be found in AML cells stained with 3,3-diylbenzidine, and more than 50% of the acute particles can be detected, which is helpful for differential diagnosis.

3. Other

The immunology, cytochemistry, and cytogenetic examination of leukemia have been described before, and the use of transmission electron microscopy can help diagnose M7 and acute undifferentiated leukemia. Terminal deoxynucleotidyl transferase (TdT) is in B- Significantly decreased in ALL and AML, and significantly increased in T-ALL and C-ALL Pre-B-ALL, so it has certain discriminative significance.

1. X-ray of chest X-ray examination is mostly non-specific. Chest radiographs often have hilar lymphadenopathy. Leukemia infiltrates the lungs with plaque shadows. T-ALL often has mediastinal masses.

2. Bone X-ray examination often shows osteoporosis and decalcification, sometimes with focal osteolytic and lamellar periosteal reaction signs, and the transverse strip with reduced density at the end of long bones is called leukemia line.

Diagnosis and diagnosis of acute non-lymphocytic leukemia in children

diagnosis

1. The following conditions should consider the diagnosis of this disease

(1) The diagnosis of this disease should be considered for an unexplained anemia, bleeding, fever, fever that cannot be fully explained by infection, and symptoms of multiple organ infiltration.

(2) An anemia, liver, spleen, and swollen lymph nodes that are inconsistent with the degree of bleeding are found in the physical examination, especially those with parotid gland, testicular and soft tissue infiltration, and those with bone and joint pain should be considered. Diagnosis of the disease.

(3) Peripheral blood found 2 series of abnormalities or seeing immature cells should consider the possibility of this disease, further for bone marrow smear examination.

2. Leukemia diagnosis

The following three aspects of cell morphology, immunophenotype and cytogenetics should be included, and genotype analysis should be included as the development progresses.

(1) Morphology of bone marrow cells: When clinically suspected leukemia, bone marrow smear must be used for morphology, and histochemical staining can confirm the diagnosis. Bone marrow smears often show hyperplasia, immature cells 30%, at 30%-100 %, about 4/5 patients can make a clear morphological diagnosis after morphological and histochemical staining, and 1/5 patients need immunophenotypic and cytogenetic analysis to further identify AML and ALL, AML The chemical staining characteristics of the middle tissues are shown in Table 1.

(2) Immunophenotype: When bone marrow hematopoietic stem cells gradually differentiate and mature, they can express the immunophenotype associated with specific cell lines and differentiation stages. Immunophenotype plays an important role in diagnosis when cell morphology and histochemical staining results are inconsistent. At least one of CD33, CD13, CD15, CD11b and CD36 is expressed in 90% of AML patients, and some myeloid antigens are also expressed on immature lymphocytes, so it cannot be diagnosed based only on immunophenotype, 4%-25 % ALL can express at least 1 myeloid antigen, 11% to 28% of AML, and simultaneously express lymphoid antigen.

(3) cytogenetics: characteristic and characteristic chromosomal abnormalities in AML are t(8;21), t(3;21), common in M2; t(15;17), t(11;17) , common in M3; inv (16) is common in M4Eo.

Clinical diagnosis of ITP, aplastic anemia, neutropenia, infectious mononucleosis, various arthritis, leukemia-like reactions should be thought of this disease, when it is not certain that leukemia is excluded, it should be timely bone marrow puncture The film further confirms the diagnosis.

Differential diagnosis

Leukemia-like reaction

Peripheral leukocytosis, a significant increase and / or emergence of immature white blood cells called leukemia-like reactions, usually infection, poisoning, tumors, blood loss, hemolysis, drugs, etc., granule, monocytic leukemia reaction often has a significant increase in white blood cells There are also immature white blood cells in the peripheral blood, but the former neutrophil alkaline phosphatase score is significantly increased, lymphocytic peripheral blood leukocytes can be slightly increased, but naive lymphocytes appear, in general, remove the cause of leukemia The reaction can return to normal, and usually the leukemia and platelets in the peripheral blood of the leukemia-like reaction are not affected, the leukemia has no leukemia-like changes, and the leukemia reaction in occasional cases is difficult to distinguish from leukemia. At this time, it should be closely observed and supplemented with immunity. , genetic and other methods carefully distinguish.

2. Aplastic anemia

The disease has anemia, hemorrhage, fever, and reduction of whole blood, which is easy to be confused with hypoproliferative leukemia. However, the liver, spleen and lymph nodes of the disease are not swollen, the bone marrow hyperplasia is low and there is no original, and the proportion of naive cells is increased.

3. Malignant histiocytosis

The disease is a malignant proliferative disease of the mononuclear-macrophage system. Clinically, fever, anemia, hemorrhage, liver, spleen and lymphadenopathy can be seen, as well as extensive invasive lesions of the whole body. It is difficult to distinguish from leukemia, and peripheral blood is also Similar to leukemia, Hb and BPc decrease, more than half of white blood cells are reduced, and immature red blood cells and immature granulocytes can be found. However, if malignant tissue cells are found, the disease is highly suggestive, bone marrow hyperplasia is active or decreased, and reticular cells are increased. How many tissue cells can be divided into general abnormal tissue cells, mononuclear tissue cells, lymphoid tissue cells, multinuclear giant tissue cells and phagocytic tissue cells according to morphology, if a large number of phagocytic tissue cells are seen and appear Abnormal tissue cells support the diagnosis of this disease, malignant histiocytosis lacks specific diagnostic methods, bone marrow support and clinical non-conformity can not be diagnosed, and vice versa, clinical support and bone marrow incompatibility can not rule out the diagnosis, so the disease relies on comprehensive Analytical diagnosis, sometimes biopsy such as bone marrow and lymph nodes can be used for children's blood and tumor diseases Provide some evidence.

4. Infectious mononucleosis

This disease is caused by EB (Epstein-Barr) virus infection, clinical fever, rash, angina, liver, spleen, lymph node enlargement; blood leukocyte increase is mainly lymphocyte elevation, and variant lymphocytes often reach 10 More than %, clinical manifestations and blood is easy to be confused with acute white, but the disease recovers quickly, the bone marrow appears as no proto-lymphocytes, and EBV-specific antibodies such as EBV-VCA-IgM can be diagnosed.

5. myelo dysplastic syndrome (MDS)

It is a group of hematopoietic and dysfunctional diseases caused by hematopoietic stem cell damage. The disease is mainly characterized by anemia, which may be accompanied by different degrees of hemorrhage, hepatosplenomegaly, and bone pain in a few cases. MDS not only It should be differentiated from acute leukemia, and 20% to 30% of the cases will eventually turn into acute leukemia. The bone marrow of this disease presents pathological hematopoiesis of the three or two lines or any line, and the red line is too high (>60%). Or too low (<5%), red blood cells, nuclear lobulation, fragmentation or multinuclear red blood cells appear in the nucleus, large nuclear nucleus, small nuclear meganucleus, multi-nuclear megakaryocytes, etc. Granule-mononuclear cells can be seen in primary or young mononuclear cells and morphological changes, but the proportion of primordial cells (or original single) is <30%, so it can not be diagnosed as acute leukemia.

It has been suggested in foreign countries that the diagnostic procedure for ANLL can be clinically considered according to Figure 1, including differential diagnosis with MDS.

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