Chronic lymphocytic leukemia

Introduction to chronic lymphocytic leukemia Chronic lymphocytic leukemia (CLL) is a clonal proliferative neoplastic disease in which lymphocytes accumulate in bone marrow, lymph nodes, blood, spleen, liver and other organs. More than 95% of CLL is a clonal proliferation of B cells (ie, B-CLL), and less than 5% of cases are T cell phenotypes (ie, T-CLL). basic knowledge The proportion of illness: 0.001% - 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: Lung cancer Multiple myeloma Acute myeloid leukemia

Causes of chronic lymphocytic leukemia

(1) Causes of the disease

The cause of CLL is unknown. There is no evidence to suggest that retroviruses, ionizing radiation can cause this type of leukemia; however, several factors are found to be closely related to the disease: hereditary (racial and familial) and gender.

Genetic factors (30%):

In patients with a family history of CLL or other lymphatic malignancies, the incidence of immediate family members is three times higher than that of the general population, and the incidence of autoimmune diseases in relatives of CLL patients is also significantly increased.

Chromosomal abnormalities (50%):

About 50% of CLL patients have chromosomal abnormalities, often involving chromosomes 12 or 4, -8, i (7), i (2p), t (13; 21), 18, 6q-, 14q-, -X and other abnormalities. It has been reported that chromosomal abnormalities are related to the course of the disease. Early chromosomal abnormalities account for about 20% of cases, and advanced cases can reach 70%. CLL-affected chromosomes often involve immunoglobulin-encoding genes (such as the heavy chain gene of chromosome 14) or oncogenes. (eg c-ras-Harvey on chromosome 12 and c-ras-Kirsten on chromosome 11).

(two) pathogenesis

The exact pathogenesis of CLL is unknown, and environmental factors are not significantly related to the incidence of CLL. Factors that are closely related to other types of leukemia, such as ionizing radiation, chemical carcinogens, and insecticides, have been reported to be unrelated to the pathogenesis of CLL. Viral infections such as HCV (Hepatitis C virus), Epstein-Barr virus is also not associated with the incidence of CLL. Although there are more males than females in CLL patients, there is no correlation between sex hormones and CLL. The current research focuses on the pathogenesis and genetic factors of CLL, chromosomes, cells. The relationship between oncogenes and anticancer genes.

Genetic factor

The incidence of CLL is higher in Caucasians and blacks, and lower in Asian yellows. The incidence is not changed by ethnic migration, suggesting that certain genetic factors of different races are related to the pathogenesis of CLL. In addition, reports have been reported. In the same family, B-cell type CLL occurs in many people. The first-generation children of CLL have three times more risk of developing CLL or other malignant lymphoproliferative diseases than the average person, and most of them are younger, which also suggests genetic factors in the family. There is an important role in the pathogenesis of CLL, but there is no significant correlation between HLA single phenotype and CLL. At present, no genetic factors related to CLL have been found. Even in patients with single-oval twin CLL, no common genetic abnormalities have been found so far.

2. chromosome

The cytogenetic study of CLL is difficult because its lymphocytes are not easily stimulated by mitogens and proliferate, and it is difficult to obtain mitotic cells. In recent years, by improving the stimulation of CLL cell division technology, chromosome R banding and in situ hybridization (FISH) are applied. The method improved the success rate of CLL chromosome research. About 50% of CLL patients found cloned chromosomal abnormalities, while the remaining normal karyotype patients may be normal T cell karyotypes and no CLL abnormal karyotypes were detected.

(1) Chromosome 13 abnormality: Nearly 50% of CLL patients have long arm deletion of chromosome 13, and most of the missing sites are deleted in 13q12.3 and 13q14.3, 13q12.3, and the deletion site has breast cancer susceptibility gene (BRCA2). ), deleted at 13q14.3, the deletion site can affect the tumor suppressor gene RB-1 (retinal cell gene), DBM (related to preventing lymphocyte malignant transformation), LEV1, LEV2 and LEV5 (related to the pathogenesis of CLL).

(2) Chromosome 12 abnormality: The trisomy abnormality of chromosome 12 is rarely detected in CLL at the early stage, and CLL with chromosome 13 trisomy is found in CLL clinical progression or conversion to lymphoma (Richter syndrome). There are many complex changes in cells and atypical or young lymphocyte morphology, suggesting that trisomy 12 chromosomal abnormalities are associated with worsening CLL. The mechanism of trisomy 12 may be through some genes such as mdm gene located between 12q13 and 12q22. Reflected by the impact.

(3) Abnormal chromosome 11: Nearly 10% to 20% of CLL patients have chromosome 11 translocation or deletion, and those with abnormal chromosome 11 have a milder onset age (<55 years), and the course often shows invasiveness. Abnormal chromosome 11 may affect 11q13, and it has been recognized that this site includes the tumor suppressor gene - MEN-1 (multiple endocrine neoplasia type I). The most common chromosome 11 deletion is between 11q14-24, especially at 11q22. Between .3 and 23.1, there may be a tumor suppressor gene RDX (multiple neurofibromatosis type II tumor suppressor gene congener) and AIM (hereditary ataxia - hair cell vasodilator mutant gene). The function of the two genes is related to the activation of the tumor suppressor gene p53, which regulates the cell cycle and maintains the gene stabilizing effect. The expression product can arrest abnormal cells into the cell cycle and arrest them in the S1 phase, facilitating more abnormal cells. Time to perform DNA repair, such as cells can not repair damaged DNA by themselves, they will self-apoptosis.

(4) Chromosome 6 abnormality: including the short arm and long arm abnormality of chromosome 6, and the short arm abnormality of chromosome 6 has not been found to have corresponding specific gene function changes. The 6q21-q24 abnormal patient often shows the growth and invasion of young lymphocytes. Sexually ill, in addition, TNF- (tumor necrosis factor alpha), and LY- (lymph a) are located on the long arm of chromosome 6, which promotes proliferation of CLL cells and inhibits normal lymphocytes and bone marrow cells. Related to hyperplasia.

(5) Abnormal chromosome 14: often expressed as translocation, rare in CLL patients, more common in lymphoma patients t (11; 14) (q13; q32) translocation: rare in CLL, 14 q32 contains immunity Globulin a heavy chain isoform switch gene, and 11q13 has cyclin D1 gene (cyclic D1) t (11; 14), common in coat-type non-Hodgkin's lymphoma, t (14:18) CLL patients are rare, common For low-grade follicular lymphoma.

3. Special genetic changes

(1) p53 gene: p53 gene is an important tumor suppressor gene located at 17p13.1, encoding 53-kD nucleic acid phosphoprotein, its mutation or defect may be the cause of nearly half of tumor patients, short chromosome 17 The arm loss is only seen in 10% to 15% of CLL patients. In addition, 10% to 15% of CLL patients have p53 gene mutations, and patients with p53 gene mutations are mostly progressive, with high proliferation rate of leukemia cells and short survival time. The clinical features of first-line treatment drug resistance are found in half of Richter syndrome and B-cell lymphocyte leukemia, suggesting that p53 gene mutation may be acquired in some CLL patients.

(2) Multiple drug resistance gene (MDR): MDR-1 gene expression is increased in about 40% of CLL patients, MDR-1 is located in 7q21.1, encoding 170kD transmembrane glycoprotein, and MDR-1 expression in BLL patients B cells Increased but not increased in normal B cells, in addition to treatment or other factors can also induce increased MDR-1 gene expression, MDR gene abnormal expression is more to promote the progression of CLL patients rather than the primary cause of CLL.

(3) bcl-2: bcl-2 gene is located on chromosome 18q21. Most CLL patients have increased expression due to bcl-2 gene rearrangement. About 5% of CLL patients have bcl-2 gene rearrangement located at No. 2 and No. 8 The IGk or light chain gene on the chromosome is translocated with the bcl gene located on chromosome 18, but in addition to gene rearrangement, the increase in the expression of bcl-2 in CLL leukemia cells is related to the hypomethylation of its gene locus, and there may be some The genes involved are also involved in the action of making CLL cells resistant to apoptosis.

Cytokine

CLL cells have the ability to secrete a variety of cytokines, such as TNF-, TGF- (transfer growth factor ), IL-7 (interleukin-7), IL-5, IL-2, etc. These factors have direct or indirect It stimulates the proliferation of CLL leukemia cells or prevents the apoptosis of CLL cells, and inhibits the proliferation of normal lymphocytes and bone marrow hematopoietic cells. Therefore, cytokines are associated with the pathogenesis and disease progression of CLL patients.

Cellular dynamics studies showed that the number of 3H-labeled white blood cells in the peripheral blood of CLL patients was small, suggesting that most white blood cells were in the resting phase (G0 phase) without proliferation, and that almost all CLL leukocytes expressed high levels of anti-aging. The death protein bcl-2, and the low level of apoptotic protein bax, the imbalance of bcl-2/bax ratio, resulting in impaired apoptosis, consistent with the accumulation of a large number of mature small lymphocytes in clinical, constitute the main pathological basis of CLL.

Prevention of chronic lymphocytic leukemia

Preventive work begins with the details of life: 1. Maintain an optimistic and happy mood, balance the excitation and inhibition of the cerebral cortex, so you need to maintain a happy mood. 2, pay attention to rest, work and rest, life in an orderly manner, to maintain an optimistic, positive, upward attitude towards life has a great help to prevent disease. Do the regularity of tea and rice, live daily, not overworked, open-minded, and develop good habits. 3, reasonable diet can eat more high-fiber and fresh vegetables and fruits, balanced nutrition, including protein, sugar, fat, vitamins, trace elements and dietary fiber and other essential nutrients, meat and vegetables, diversified food varieties, Giving full play to the complementary role of nutrients in food is also helpful in preventing this disease.

Chronic lymphocytic leukemia Complications Lung cancer Multiple myeloma Acute myeloid leukemia

1. One of the main causes of death and deterioration of CLL patients is infection, which can affect about 40% of patients. Hypogammaglobulinemia is one of the main causes of infection and deterioration of the disease. In addition, there is neutropenia. T cell dysfunction, etc., the most common is bacterial infection, viral infection (especially herpes virus infection) accounts for about 15%, fungal infection is less common.

2. CLL patients with secondary tumors 9% to 20% can be secondary to the second tumor. The most common secondary tumors are soft tissue sarcoma, lung cancer, etc., the possibility of multiple myeloma in CLL patients is 10 times higher than that of ordinary people, but The two do not originate from the same malignant B cell clone, and the risk of CLL secondary acute myeloid leukemia does not increase.

Symptoms of Chronic Lymphocytic Leukemia Common Symptoms Bloating Skin Itching Skin Infiltration Diarrhea Herpes Skin Purpura Indigestion Immune Deficiency Weight Loss Night Sweat

1. General symptoms: About 1/4 of patients are asymptomatic, accidentally discovered by examination of blood routine, fatigue, physical activity decline and weakness are common symptoms, mostly in patients with anemia or lymph nodes, hepatosplenomegaly occurs before, other rare Symptoms include chronic rhinitis caused by infiltration of nasal mucosa in CLL cells, multiple neuropathy of sensorimotor nerves, allergies to mosquito bites, etc. During the progression of the disease, patients may have weight loss, repeated infections, bleeding or severe anemia symptoms. CLL patients are mostly elderly and can be associated with lung, heart and cerebrovascular disease.

2. Lymph node enlargement: 80% of CLL patients have painless lymphadenopathy at the time of diagnosis. The most common sites are the neck, supraclavicular and axillary lymph nodes. Typical CLL lymph nodes are not tender, but can be combined with infection. It is tender, high lymph node enlargement can cause local compression symptoms and affect organ function. For example, oropharyngeal lymph node enlargement can cause upper airway obstruction. Abdominal lymphadenopathy can cause urinary tract obstruction and hydronephrosis, and obstruction of bile duct is caused by obstruction. Astragalus, but the mediastinal lymphadenopathy in CLL patients rarely causes the superior vena cava syndrome. If this syndrome occurs, it is highly suspected to have a lung tumor.

3. Hepatosplenomegaly: About half of CLL patients have mild or moderate hepatosplenomegaly at the time of diagnosis, often accompanied by fullness and abdominal distension. In some patients, the splenomegaly can exceed the umbilical level and even extend to the pelvic cavity, and a few splenomegaly Can be associated with hypersplenism, resulting in anemia and thrombocytopenia, some CLL patients may have hepatomegaly, liver function abnormalities are mostly mild, mostly without jaundice, but if the abdominal lymph nodes enlarge the biliary tract can cause obstruction Sexual jaundice.

4. Extranodal involvement: In patients with CLL, autopsy is often found to have organ infiltration, but abnormal organ dysfunction is rare. For example, more than half of the patients found that the renal interstitial has leukemia cell infiltration, but rare renal failure, in a certain These organs and tissues can cause symptoms when infiltrated with leukemia cells, such as in the eyeball, pharynx, epidermis, prostate, gonads and lymphoid tissues. Leukemia cell infiltration can cause exophthalmos, upper airway obstruction, scalp nodules, urethral obstruction, etc. Corresponding symptoms, pulmonary interstitial infiltrates showed nodules or miliary changes, which can cause pulmonary dysfunction, pleural infiltration can produce bloody or chyle-like pleural effusion, leukemia cell infiltration can cause thickening of digestive tract mucosa, Produces ulcers, hemorrhage, malabsorption, CLL central nervous system infiltration is rare, can produce headache, meningitis, cranial nerve palsy, unresponsiveness, coma and other symptoms.

5. Rare clinical performance

(1) transformation into invasive lymphoma/leukemia: 10% to 15% of patients converted to invasive lymphoma/leukemia, the most common conversion to Richter syndrome, manifested as progressive liver, spleen, lymph node enlargement, fever, abdominal pain , weight loss, progressive anemia and thrombocytopenia, peripheral blood lymphocytes rapidly increase, lymph node biopsy pathology is large B cells or immunoblastic lymphoma, through immunophenotype, cytogenetics, immunoglobulin heavy chain gene rearrangement, DNA sequence analysis and other studies have shown that patients with 1/2 Richter syndrome have large lymphocytes derived from a single clone of CLL. Patients with Richter syndrome have poor response to systemic chemotherapy. The general survival period is 4 to 5 months, and CLL can also be transferred. For young lymphocytic leukemia, acute lymphocytic leukemia, plasma cell leukemia, multiple myeloma, Hodgkin's lymphoma and the like.

(2) autoimmune diseases: about 20% of CLL patients can be combined with Coombs test-positive autoimmune hemolytic anemia, half of them have obvious clinical manifestations, 2% of CLL patients with immune thrombocytopenia, CLL clinical severity It is not associated with immunological anemia and thrombocytopenia. Patients with autoimmune hemolysis and thrombocytopenia generally respond well to adrenocortical hormone. If the adrenal cortex hormone is ineffective, try a large dose of intravenous gamma globulin, splenectomy or spleen. District irradiation.

(3) pure red blood cell aplastic anemia: it has been reported that CLL combined with pure red blood cell aplastic anemia can be as high as 6%, the clinical manifestations are severe anemia, bone marrow erythrocytes and peripheral blood reticulocytes are reduced, but without granulocyte and thrombocytopenia Adrenal cortical hormone may have a transient effect. Most patients are effective for chemotherapy, which can increase the hemoglobin value, and the CLL condition is relieved. Cyclosporin A is also effective with or without adrenocortical hormone in CLL patients with pure red blood cell aplastic anemia. However, often only the amount of hemoglobin is elevated, and the condition of CLL is not improved.

6. Secondary malignant tumors CLL patients may be secondary malignant tumors due to autoimmune deficiency or chemotherapy, most commonly lung cancer and malignant melanoma, other tumors have Hodgkin's lymphoma, acute myeloid leukemia, chronic myeloid Leukemia, multiple myeloma, etc.

Examination of chronic lymphocytic leukemia

Peripheral blood

(1) Red blood cells: Anemia can occur in the late course of CLL. The most common cause is that the leukemia cells infiltrate the bone marrow and cause normal hematopoietic function inhibition. About 20% of patients in Europe and America have autoimmune hemolytic anemia, which is rare in China. Other reasons are Hypersplenism, anemia is mostly positive cells, positive pigmented anemia.

(2) Lymphocytes: The absolute count of peripheral blood lymphocytes of CLL is >5×109/L, and the typical patients are mostly between (10-200)×109/L, the highest can exceed 500×109/L, and the shape of lymphocytes is The mature small lymphocytes are the same, the cytoplasm is less, the chromatin of the nucleus is clot-like, and the cells are easily broken during the smear process, producing typical stain cells.

(3) granulocytes: the proportion of granulocytes decreased, often less than 40%, especially in the late stage, but the absolute count of early granulocytes was normal or increased.

(4) Platelets: Thrombocytopenia can be caused by bone marrow infiltration of leukemia cells, hypersplenism, and a small number of immune thrombocytopenia.

2. Bone marrow

Bone marrow examination is not necessary for CLL diagnosis, but it is beneficial for clinical stage prognosis. Active or extremely active hyperplasia, lymphocytes increase significantly, the number of nucleated cells is >40%, and the lymphocyte morphology is the same as blood, mostly mature small lymphocytes. There may also be a small amount of naive lymphocytes, which are especially common in the later stages of the disease.

3. The Coombs test is positive.

4. Bone marrow biopsy

Lymphocytes are infiltrated in different forms, and their invasive type is directly related to the prognosis of CLL patients:

1 Bone marrow interstitial infiltration: lymphocytic infiltration is banded, about 1/3 of patients showed the above performance, often early, the patient's prognosis is better;

2 nodular or nodular and interstitial mixed infiltration: 10% CLL patients with nodular shape, 25% of patients with nodular and interstitial infiltration mixed, the two forms of prognosis are also better;

3 diffuse infiltration: 25% of patients with diffuse infiltration of lymphocytes, bone marrow hematopoietic cells significantly reduced, this type of patients clinically progressive or invasive, poor prognosis.

5. Lymph node biopsy

It shows that the lymph nodes are diffusely infiltrated with the same small lymphocytes as peripheral blood, and histologically the same as small lymphocyte lymphoma. Therefore, lymph node biopsy has no diagnostic effect on CLL patients, but when the cause of lymphadenopathy is unknown, especially When CLL is suspected to be converted to Richter syndrome lymphoma, lymph node biopsy should be performed. At this time, the infiltrating lymphocytes are large B lymphocytes or immunoblasts.

6. Immunophenotype

The monoclonal antibody and flow cytometry can be used to determine the B or T cell differentiation antigen, surface immunoglobulin, kappa or lambda light chain on the surface of leukemia cells of CLL patients, which can not only identify CLL as T or B cell type, but also Other B-cell-derived leukemias that are easily confused with CLL, the B cell immunophenotypes of CLL are usually CD19, CD20, CD21, CD23 and CD24. Most CLLs have a cell phenotype of la, Fc receptor and mouse RBC rose. The flowering test is positive, but usually in the normal B cells, the marker transferrin receptor, CD22 is mostly negative, 95% B cell CLL is CD5, which is an important indicator for the diagnosis of CLL, CD5-type CLL may be its cell source and CD5 Different types, generally the cell immunophenotype CD22 is positive, cell surface IgM high level expression, CD23 weakly positive, and expressed myeloid markers CD11b and CD13, bone marrow diffuse infiltration, poor clinical prognosis, B-CLL and other B Cell-derived leukemia and lymphoma immunophenotypic characteristics.

According to clinical manifestations, symptoms, signs, you can choose to do CT, X-ray, B-ultrasound and other tests.

Diagnosis and diagnosis of chronic lymphocytic leukemia

Diagnostic criteria

1. Domestic diagnostic criteria: Comprehensive domestic reports for nearly 15 years and reference to foreign literature, the diagnostic criteria for CLL are summarized as follows.

(1) Clinical manifestations:

1 may have fatigue, physical strength, weight loss, low fever, anemia or bleeding.

2 may have lymph nodes (including head and neck, armpits, groin), liver, splenomegaly.

(2) Laboratory inspection:

1 peripheral blood leukocytes>10×109/L, lymphocyte ratio 50%, absolute value>5×109/L, the morphology is mainly mature lymphocytes, visible naive lymphocytes and atypical lymphocytes, the above abnormality lasts 3 month.

2 myeloproliferation is active or significantly active, lymphocytes 40%, mainly mature lymphocytes.

3 Immunophenotyping: B-CLL: CD5, CD19, CD20 positive; mouse rosette test positive; sIg weakly positive, showing or monoclonal light chain; CD10, CD22 negative, T-CLL: CD2, CD3 , CD8 and/or CD4 positive; sheep rosette test positive; CD5 negative.

(3) Exclude other diseases:

1 excluding lymphoma with leukemia and young lymphoblastic leukemia;

2 Exclude virus infection, tuberculosis, typhoid, infectious mononucleosis and other patients with lymphocytosis.

B-cell chronic lymphocytic leukemia (B-CLL) can be divided into three types according to the ratio of lymphocytes in peripheral blood and bone marrow, naive lymphocytes and atypical lymphocytes:

1 typical CLL: more than 90% are similar mature small lymphocytes;

2CLL with young lymphocytosis (CLL/PL): immature lymphocytes >10%, but <50%;

3 mixed type: there are different proportions of atypical lymphocytes, the cell volume is large, the nuclear/mass ratio is reduced, the cytoplasm is stained with different degrees of basophilic, with or without azurophilic particles.

2. International Diagnostic Criteria International CLL Working Conference (IWCLL) and National Cancer Institute (NCI) CLL Collaboration Group standards.

(1) The absolute value of peripheral blood lymphocytes increased by >5×109/L. After repeated examination, it lasted for at least 4 weeks (NCI), or 10×109/L, and persisted (IWCLL).

(2) Mainly mature small lymphocytes, morphological classification:

1 typical CLL: atypical lymphocytes 10%,

2LL/PL: Peripheral blood lymphocytes account for 11% to 54%,

3 atypical CLL: There are different proportions of atypical lymphocytes in peripheral blood, but young lymphocytes <10%.

(3) B-CLL immunophenotyping: SMIg+/-, showing kappa or lambda monoclonal light chain; CD5, CD19, CD20, CD23, FCM7+/-, CD22+/-.

(4) At least one bone marrow puncture and biopsy were performed. The smear showed active or significant hyperplasia, lymphocytes >30%; biopsy showed diffuse or non-diffuse infiltration.

Diagnostic evaluation:

Patient age is an important parameter for the diagnosis of CLL, because 95% of CLL occurs after the age of 50, the history of the neck and / or left upper abdomen painless mass has a suggestive value, according to which blood routine should be checked, such as showing the total number of white blood cells Increase, the absolute number of lymphocytes 5 × 109 / L, and persistence, should be highly suspected CLL, in addition to other causes of lymphocytosis can make a basic diagnosis, further blood smear microscopic review, such as mature Small lymphocytes account for more than 60% of the cases can be diagnosed, bone marrow smear is usually consistent with the results of blood smear, with an auxiliary diagnostic role, bone marrow pathological sections can understand the extent of the lesion, in the verification of the diagnosis, the choice of treatment options And prognosis judgment provides a reference basis, because B-CLL leukemia cells have a more specific immunophenotype, which is helpful for differential diagnosis in atypical cases. Various imaging examinations are mainly used to understand the extent of the disease, not the basis for diagnosis.

As can be seen from the above analysis, medical history and physical examination can provide diagnostic clues, while hematological tests have decisive value, and immunological examinations have an auxiliary effect.

Adult benign lymphocytosis is seen in several reasons:

1 virus infection: especially hepatitis virus, cytomegalovirus, EB virus infection, infectious mononucleosis, clinical manifestations of lymph nodes, mild swelling of the liver and spleen, through the corresponding virological examination, can be identified;

2 bacterial infection: brucellosis, typhoid, paratyphoid and other chronic infections, have their corresponding pathogenic diagnosis and corresponding clinical manifestations, can be identified;

3 autoimmune diseases, drugs and other allergic reactions;

4 hyperthyroidism and adrenal insufficiency;

5 after splenectomy.

2. The clinical manifestations of juvenile lymphocytic leukemia are obvious swelling. The cell body of young lymphocytes is larger than that of CLL cells, the cytoplasm is light blue, and there is a clear nucleolus. Under the electron microscope, the surface surface fluff is more than that of CLL cells, and cell surface immunity The level of globulin expression is high.

3. Hairy cell leukemia is mostly B cell source, T cell source is very rare, and CLL is two different diseases. Clinically, the spleen is highly swollen with typical hair cells in the blood, which contains acid phosphatase isoenzyme. 5, showing the positive characteristics of tartaric acid-resistant acid phosphatase staining.

4. Small lymphocytic lymphoma Small lymphocytic lymphoma and CLL are the closest in clinical and biological performance, and their prognosis and treatment are similar. Therefore, the latest clinical standards such as Real and WHO classify the two into one category. Lymph node pathology can not distinguish between the two, but small lymphocytic lymphoma does not necessarily infiltrate the bone marrow, the proportion of bone marrow lymphocytes <40%, even if there is bone marrow infiltration, nodular infiltration, and CLL is mostly diffuse.

5. Non-Hodgkin's lymphoma Leukemia during non-Hodgkin's lymphoma conversion to lymphoma leukemia, the cell body is large, the nucleus is folded, the cell surface is highly expressed immunoglobulin, CD5 is negative, all of these characteristics Easy to distinguish from CLL.

6. Skin T-cell lymphoma is often accompanied by extensive skin infiltration, and its nucleus is a cerebral gyrus, which is a non-Hodgkin's lymphoma derived from helper T cells (CD4).

7. Large-granulocyte lymphoblastic leukemia (LGL) Generally, lymphocytes are larger than CLL cells, and have abundant borders with clear translucent cytoplasm. There are cordier granules of different sizes, oval or irregular nuclei. The tissue is derived from NK/T cells, and the immunophenotypes derived from T suppressor cells (CD8) are CD3, CD4-, CD8, CD16, CD56-, CD57/-, with TCR gene rearrangement; from NK cells, CD3 -, CD4-, CD8-, CD16, CD56-, CD57 /-, no clonal gene abnormality, T cell LGL clinical condition is inert, chronic course, often accompanied by whole blood cell reduction and splenomegaly, NK cell LGL part of patients can be Acute fulminant onset, and some are chronic.

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