Acute Leukemias and their Diagnosis, Acute Myelocytic and Acute Lymphocytic Leukemia
Acute Leukemias
Sample
- Blood in EDTA and fresh blood smear are needed.
- Bone marrow aspirate and biopsy are required.
Definition of acute leukemia
- Leukemias are characterized by the uncontrolled (malignant) proliferation of the blood and bone marrow cells.
- In the case of a lymphocytic variety, there is the involvement of the lymph nodes. OR
- This is a malignant neoplasm of hematopoietic cells, particularly stem cells. OR
- There is diffuse infiltration of the bone marrow by these neoplastic cells. OR
- Leukemias are a malignant disease of the hemopoietic tissue, characterized by replacing normal bone marrow elements with abnormal neoplastic blood cells.
- These cells enter the blood and may infiltrate the liver, spleen, lymph nodes, and other organs.
Classification of Acute Leukemias
- Based on the morphology, the leukemias are divided into:
- Acute lymphocytic leukemia (ALL) involves the lymphocytes and their precursors.
- Acute myelocytic leukemia (AML) involves the granulocytes and their precursors.
- Acute monocytic leukemia involves the monocytes and their precursors.
- Acute plasmacytic leukemia involves the plasma cells and their precursors.
- Acute erythroblastic leukemia involves the red blood cell precursors.
- Acute leukemia develops from the stem cells and develops into myelocytic and lymphocytic varieties.
Pathophysiology of Acute Leukemias
- The malignant transformation is at the level of pluripotential cells (stem cells), and these cells change into committed stem cells and they called stem cell disorders.
- There is abnormal proliferation, monoclonal expansion, and decreased apoptosis of these cells leads to the replacement of normal bone marrow cells with these malignant cells or immature cells.
Clinical features of acute leukemias are:
Acute Leukemias Criteria:
- Acute leukemias are characterized by abnormal differentiation and proliferation of malignantly transformed hematopoietic blast cells.
- These cells proliferate in the bone marrow and lead to the suppression of the normal cells.
- These have little or no maturation and may see mainly blast cells.
- Acute Leukemias are diagnosed on the percentage of blast cells in the bone marrow.
- 30% or more blast cells are needed to classify the disorder as acute leukemia.
- These leukemias are associated with varying degrees of anemia, neutropenia, thrombocytopenia, and infiltration of the tissues.
- The most common infiltration site is lymph nodes, liver, spleen, CNS, and skin.
Epidemiology of acute leukemias:
- ALL and AML can occur at any age. But the incidence increases with the increasing age.
- ALL predominates in the children, while AML accounts for most of the cases in adults.
- AML’s median age is around 60 years.
- The peak age for ALL is between 3 to 5 years. These are morphologically different than adult cases.
- Acute leukemias are more common in whites than blacks.
- Acute leukemias are more common in the Jews than in the non-Jews.
- Acute leukemias are more common in men than in women.
Etiological factors for acute leukemias (Risk factors):
- The cause of acute leukemias is unknown; this may be hereditary or environmental factors.
- The pathogenesis is very complex, and this may involve interaction between the host susceptibility and chromosomal damage secondary to physical or chemical agents.
- Chromosomal abnormality:
- There are chromosomal abnormalities; examples are given below:
- Deletion:
- 5q – = Myelodysplasia, preleukemia.
- Monosomy 7.
- Inversion:
- inv 16 = AML.
- Translocation:
- t18:14 = Burkitt’s lymphoma.
- t8:21 = AML.
- t4:11 = ALL.
- t9:22 = CML
- Oncogenes:
- C-abl, C-sis = CML.
- C-myc = Burkitt’s lymphoma (L3).
- Viruses:
- There are viruses known to give rise to leukemia in nonhuman species.
- The human role of viruses has been studied for a long time, but no conclusive data is available.
- Epstein-Barr virus is seen in the majority of Burkitt’s lymphoma.
- The Human T-leukemia virus (HTLV-1) is associated with acute leukemia.
- Inherited factors:
- The following examples favor the role of genetic abnormalities:
- Increased incidence of acute leukemia in families.
- Increased incidence of acute leukemia in monozygotic twins.
- If one twin has leukemia, the other is also at risk for leukemia, often before eight years of age.
- Leukemia starts in the next twin within a year of the first diagnosis.
- Increased incidence of acute leukemias in members of a certain family with high susceptibility, the high increased frequency of leukemia in monozygotic twins, and an association of acute leukemias with genetic disorders, all these factors have established that hereditary abnormalities play a role in the development of acute leukemia.
- There is an increased incidence of AML and ALL in Down’s syndrome where there is trisomy 21.
- 5 to 10% of childhood AML occurs in Down’s syndrome.
- There is an increased incidence of Fanconi’s syndrome and Bloom’s syndrome.
- Both conditions are hereditary, and there is an increased chromosomal breakage.
- Ataxia-telangiectasia and congenital agammaglobulinemia have chromosomal abnormalities that are associated with acute leukemia.
- The following examples favor the role of genetic abnormalities:
- Acquired factors:
- Drugs and Chemicals:
- Alkylating drugs like nitrogen mustard, chlorambucil, melphalan, cyclophosphamide, and procarbazine.
- Benzene compounds and pesticides.
- Exposure to melphalan or nitrogen mustard is associated with acute AML after 5 to 7 years of exposure.
- The patient will have pancytopenia, myelodysplasia, and cytogenetic abnormalities (a total loss or partial loss of chromosomes 5 and 7).
- Hodgkin’s lymphoma, Multiple myeloma, and ovarian cancer treatment complication of AML are well-known examples.
- Benzene complication of acute leukemia is well-known.
- Alkylating drugs like nitrogen mustard, chlorambucil, melphalan, cyclophosphamide, and procarbazine.
- Radiation: The leukemogenic potential of ionizing radiation has been recognized for a long time.
- Mostly myeloid leukemia takes its origins from the radiation.
- Fetal exposure to radiation increases the risk of childhood leukemia.
- Drugs and Chemicals:
Type of cells | % of the cases | FAB subtype |
Pre B- cells ALL | 75 | L1 and L2 |
B-cell ALL | 5 | L3 |
T – cell ALL | 20 | LI and L2 |
Acute Leukemias signs and symptoms
- Appears suddenly.
- The patient may have weakness and fatigue.
- The patient may have a low-grade fever.
- There may be bruising and mild bleeding from the gums.
- There is bone pain due to the expansion of the marrow.
Clinical features of acute leukemias are due to:
Pathology | Signs and symptoms |
Bone marrow failure leads to: | |
Anemia | This will cause:
|
Thrombocytopenia | This will leads to:
|
Leucopenia | This will leads to:
|
Metastasis or infiltration of the other organs: | |
Bone marrow involvement | There is bone or joint pain |
Involvement of spleen | There is splenomegaly |
Infiltration of the liver | There is hepatomegaly |
Infiltration of the lymph nodes | There is lymphadenopathy |
Involvement of gum and mouth |
|
Involvement of the central nervous system (CNS) | There are neurologic symptoms |
Diagnosis of Acute Leukemia
Clinical features:
- These are more common in the younger age group.
- These are more frequent in children.
- Mostly seen before the age of 20 years.
- Onset is an abrupt and fatal outcome.
- There is a fever.
- There is a rapid development of anemia.
- There is normochromic and normocytic anemia.
- May see nucleated RBCs.
- There is thrombocytopenia.
- May see petechiae and purpura in the skin and mucous membranes.
- Leukocyte count is variable.
- Mostly leucocyte count is less than 100,000/cmm.
- Diagnosis depends upon the microscopic examination of the blood and bone marrow.
- Immunohistochemical staining.
- Immunophenotyping by the flow cytometry to distinguish T-cell, B-cell, and non-T, non-B cells type of ALL. This is very important because of the response of all these three types of leukemias.
- Cytogenetic studies can also be advised.
- Chromosomal abnormalities are seen in >50% of the cases
Difference between acute and chronic leukemias:
Clinical features | Acute leukemia | Chronic leukemia |
Age incidence | All ages | Mainly seen in adults |
The onset of the disease | There is sudden onset | There is an insidious onset |
The course of the disease | <6 months | It usually takes 2 to 6 years |
Type of the leukemic cells | Mainly immature cells (blast cells) | Mainly mature cells |
The severity of the anemia | This is mild to severe | This is usually mild |
Platelets status | Mild to severe thrombocytopenia | Mild thrombocytopenia |
WBCs count | It is variable | It is usually increased |
Involvement of the organs | This is mild | This is quite prominent |
Treatment Goals
- The main aim of the therapy is to the restorative bone marrow function and normality.
- Complete remission when the patient fully recovered the peripheral blood smear and bone marrow showing <5% of the blast cells.
- Induction therapy reduces the total body leukemia cell population roughly from 1012 cells to below <109.
- The complication of the chemotherapy:
- Cytotoxic drugs lead to:
- Tumor lysis syndrome and urate nephropathy.
- Hyperuricemia responds rapidly to rasburicase.
- Allopurinol, I/V therapy, and alkalinization of the urine reduce the chances of uric acid precipitation in the renal tubules.
- Electrolyte imbalance like hyperkalemia, hypocalcemia, and hyperphosphatemia.
- There may be a gastrointestinal injury, diarrhea, and mucositis.
- There may be thrombocytopenia, bleeding, and neutropenic infection.
- Blood products are given to maintain the platelet count >10,000 µL in non-bleeding patients, and hematocrit to keep >25%.
- Antibiotics are given if the body temperature is >38.5 °C.
- In neutropenic patients, when TLC is <500 /µL, antifungal therapy is added to these febrile patients.
- Tumor lysis syndrome and urate nephropathy.
- Cytotoxic drugs lead to:
Acute Myeloid Leukemia (AML)
Pathogenesis:
- There are primary AMLs that appear de novo.
- Secondary AML develops from:
- The myelodysplasia.
- Other hematological diseases such as myeloproliferative disorders.
- Or following previous treatment with chemotherapy.
- Age: This is seen during the first month of life and in the latter age group.
- 10 to 15% of cases are found in children.
- Exposure to high-energy radiation in early childhood life has an increased risk of developing T-cell acute lymphoblastic leukemia.
- Sex: More common in males than women. Male: female ratio is 3:2.
Signs and symptoms:
- Mostly these patients present with a varying degree of bone marrow failure.
- So clinical symptoms and signs are due to anemia, leukopenia, thrombocytopenia, and infections.
- About 1/3 of the patient have bruises and hemorrhages.
- About 1/4 of the patients have severe infections involving the lungs, soft tissue, or skin.
- Splenomegaly and hepatomegaly are not common and are seen in<25% of the cases.
- Lymphadenopathy is even less common.
- Gingival hypertrophy or skin infiltration by the tumor occurs in 50% of the patients with monocytic leukemia.
- Acute promyelocytic leukemias are more commonly seen with severe bleeding from the DIC.
- Fever and fatigue are present in most of the patients.
- Acute promyelocytic leukemia (M3) causes disseminated intravascular coagulopathy (DIC) and bleeding.
- Acute myelomonocytic leukemia (M4) and acute monocytic leukemia (M5) cause gum hypertrophy.
- There may be a tumor infiltration of AML called granulocytic sarcoma (Chloroma), skin, and the bone, particularly the sternum, ribs, and orbit, are common sites. Myeloid sarcomas may involve many organs.
- These patients may have respiratory distress due to leukostasis within the pulmonary vasculature.
- There may be retinal hemorrhage due to thrombocytopenia.
Classification of AML:
French-American-British (FAB) Classification of Acute Myelocytic Leukemia:
- FAB has 85% concordance. This is based on morphology and cytochemistry. Immunophenotyping and cytogenetics give additional information for the treatment.
- WHO criteria for the AML is ≥20% blast cells.
FAB type | Characteristic features | Frequency |
M0 | Acute myeloblastic leukemia with minimal differentiation.
|
2 to 3% |
M1 | Acute myeloblastic leukemia without differentiation.
|
20% |
M2 | Also called AML with maturation.
|
25 to 30% |
M3 | Acute Promyelocytic Leukemia.
|
5 to 10% (8 to 15%) |
M4 | Acute Myeloid Monoblastic Leukemia (Acute myelomonocytic leukemia).
|
20 to 30% (20 to 25%) |
M5 | Acute Monoblastic Leukemia.
|
10% |
M6 | Acute Erythroleukemia.
|
5% |
M7 | Acute Megakaryoblastic leukemia.
|
1 to 2% (1%) |
Summary of the FAB classification of acute myelocytic leukemia:
Abbreviation of FAB | Differentiating features of AML cells | Type of leukemia |
M1 | There are undifferentiated myeloblastic calls | AML-M1 (AML I= Acute myeloblastic leukemia) |
M2 | There are early signs of myeloblastic cells differentiation | AML-M2 (AML II =Acute myeloblastic leukemia) |
M3 |
|
AML-M3 (AML III =Acute promyelocytic leukemia) |
M3 (var) |
|
AML-M3 (var) (AML III (var) = Variant of Acute promyelocytic leukemia) |
M4 |
|
AML-M4 (AMML=Acute myelomonocytic leukemia) |
M4-Eo | There are abnormal eosinophils | AML-M4 (AMML-Eo=Acute myelomonocytic leukemia with abnormal eosinophils) |
M5 | There are differentiated and undifferentiated monoblastic cells | AML-M5 (AMoL= Acute monoblastic-monocytic leukemia) |
M6 |
|
AML-M6 (AEL= Acute erythroleukemia) |
M7 | There are megakaryoblastic cells | AML-M7 (AMegL= Acute megakaryoblastic leukemia) |
- Lab. findings of AML:
- WBC count is variable. 25% of the patient has >50,000/cmm, 25% has <5000/cmm and 5 to 10% has count between 5000 to 10,000/cmm.
- A count>100,000/cmm is reported in <10% of the patients, but these patients have severe CNS or respiratory diseases due to leukostasis.
- In these patients, leukapheresis and chemotherapy may be life-saving.
- WBC morphology. These are morphologically abnormal and immature cells.
- 20% or more of the blast cells in the bone marrow as diagnostic of AML.
- Ther blast cells of AML are larger than lymphoblast cells and have more significant heterogeneity in size and shape.
- AML blast cells are most abundant in the cytoplasm and often contain cytoplasmic granules.
- About 10% of the AML cases show Auer rods and azurophilic granules with Wright’s stain.
- The peripheral blood smear may show blast cells in 85 to 90% of the cases.
- FAB divides AML into:
- M1, M2, and M3 with granulocytic differentiation.
- M4, M5 with at least 20% monocytoid appearance.
- M6 with a high proportion of erythroblasts.
- M7 with predominantly megakaryoblasts.
- M0 with minimal myeloid differentiation. This needs immunohistochemical stains for the diagnosis. These cases have myeloid antigens on their surface and negative myeloperoxidase activity.
- 20% or more of the blast cells in the bone marrow as diagnostic of AML.
- In 50% of the cases, uric acid is raised, which indicates increased cell turnover.
- Lactate dehydrogenase (LDH), about 50%, shows a raised level. This is not as common as in ALL.
- Bone marrow shows >20% blast cells. Promyelocytes are numerous, particularly in M3.
- Auer rods can be seen in the cytoplasm.
- Cytochemical stains, peroxidase reaction, and Sudan black are positive.
- Nucleated RBCs may be seen.
- Platelet count may be low and may see a count between 30,000 to 100,000/cmm. In some cases may be <20,000/cmm.
- Coagulation abnormalities are also seen. PT, PTT, and Thrombin time are prolonged.
- WBC count is variable. 25% of the patient has >50,000/cmm, 25% has <5000/cmm and 5 to 10% has count between 5000 to 10,000/cmm.
- Treatment of AML: There is a supportive and specific treatment for AML.
- Stem cell transplantation and autologous transplantation may be done. But because of the toxicity, overall no benefit.
- The treatment of patients over 70 years of age with AML is poor because of primary disease resistance and poor tolerability of intensive treatment.
- Death in older adults is usually from hemorrhage, infections, and failure of the heart, kidneys, or other organs compared to the younger patients.
- Prognosis of AML:
- 50% of children and young adults may have a long-term cure.
- Recently with the newer advanced chemotherapy, the prognosis in the 60 to 70 years is better.
- Cytogenetics abnormalities and initial response to the treatment are the major predictors of the prognosis.
- AML complete remission is 60 to 70%, and disease-free survival is 20 to 40%.
- <60 years of complete remission is 70 to 80%, and disease-free survival is 40%.
- >60 years of complete remission is 45 to 55%, and disease-free survival is 5 to 10%.
- AML and prognostic factors:
Clinical parameters Good prognosis Poor prognosis Age <60 years >60 years Onset of AML Primary Secondary BM response to remission induction <5% blast cells after one course of chemotherapy 20% blast cells after the first course of chemotherapy Cytogenetics t(15;17), t(8;21), inv(16), NPM mutation t(6;9), 11q23, abn(3q), deletion of chromosome 5 or 7
Acute Lymphoblastic Leukemia (ALL)
- Age: ALL constitute 20% of adult leukemia, which is more common in children.
- In adults, 80% of the ALL are B-cells, and 20% are T-lymphocytes origin.
- This is most common in childhood. Mostly occur before the age of 4 years. The peak is between 2 to 10 years; it is also called childhood leukemia.
- ALL comprises >80% of childhood leukemia.
- 90% have chromosomal abnormalities.
- Down syndrome has a 15x times higher incidence of ALL.
- These are rare after the age of 30 years.
- These are most common in children and young adults.
- The second peak may be seen in the middle and old age groups.
- L3 leukemia is most common in developing countries and may be associated with infection by the Epstein-Barr virus in the younger age group.
- Children with trisomy 21 (Down’s syndrome) have an increased risk for childhood acute lymphocytic and acute myelocytic leukemias.
- An increased incidence is seen in immunodeficiency diseases like ataxia-telangiectasia, osteogenesis imperfecta, siblings of ALL, and Poland syndrome.
- Signs and symptoms:
- S/S of acute AML and ALL are similar, except the onset of ALL is strikingly acute.
- The onset is sudden. There is no preleukemic stage.
- Symptoms are present only for a few weeks before the diagnosis.
- There are fatigue and fever. There is malaise, lethargy, and weight loss.
- There may be bleeding and infections.
- An enlargement of lymph nodes, spleen, and liver is more common than the AML affecting 50% of the adults.
- There may be central nervous system (CNS) involvement in 5 to 10% of the cases.
- This shows leukemic meningitis.
- Cranial nerve palsy is more common in the 6th and 7th nerves.
- There are headaches and papilledema due to meningeal involvement and the obstruction of the outflow of CSF.
- CSF shows increased protein and leukemic cells.
- Bone pain is due to the infiltration of the leukemic cells.
- Retinal hemorrhage is due to thrombocytopenia.
- Chest X-ray shows a thymic mass in 10 to 15% of the adults.
Classification of ALL:
- Classification of ALL is based on cytological features like:
- Cell size.
- Nuclear chromatin pattern.
- Nuclear shape.
- Presence of nucleoli.
- Amount of basophilia in the cytoplasm.
- 80% of the ALL are B-lymphocytes origin.
- 15 to 20% of cases arise from T-lymphocytes. These cells will express CD2, CD5, and CD7.
- T- L ALL are lacking CD19 and CD20.
- L1 – ALL accounts for >80% of the cases in children and consists of predominantly small, up to twice the size of small lymphocytes.
- L2 – ALL are the majority of adult leukemia. The cells are larger than in the L1 and often heterogeneous in size.
- L3 – ALL is the least common form of approximately 3 to 4% of the children and the adults. The cells are morphologically identical to the cells in Burkitt’s lymphoma.
- FAB is no longer used.
FAB (French-American-British) classification of Acute Lymphocytic Leukemia:
L1 |
|
L2 |
|
L3 |
|
Cytochemical classification of Acute lymphoblastic leukemia (ALL):
Type of leukemia | Periodic acid-Schiff reaction (PAS) | Acid phosphatase reaction (AP) | Terminal deoxynucleotidyl transferase reaction (TdT) |
c-ALL (common ALL) | >70% coarse, lumpy, granular (++) | Negative (rare cases +) | Positive (+) |
T-ALL (L1 and L2) | <40%, granular (+) | >80%focal (++) | Positive (+) |
B-ALL (L3) | Negative to positive (- to +) | Granular (+) | Negative (-) |
B-ALL (AUL- lymphocytic origin) | Negative to positive(- to +) | Negative to positive (- to +) | Positive (+) |
Lab. Findings of ALL:
- Lab diagnosis depends upon:
- Morphology.
- Cytochemistry.
- Immunophenotyping.
- Genetic analysis.
- WBC count is variable from very high to low count.
- There are anemia and thrombocytopenia.
- Bone marrow: Very few leucocytes are seen.
- Difficult to find normal WBCs or RBCs in the bone marrow.
- Characteristically there are blast cells. >50% are lymphoblastic cells.
- Auer rods are absent.
- Serum LDH, uric acid, and ESR are often raised.
- Flow cytometry studies (differentiation of the antigens over the surface of these abnormal cells) provide rapid diagnosis.
- 80% of the ALL arises from the B-lymphocytes and will show CD molecules of CD19, CD20, or both.
- Few cases of the ALL may show CALA (common ALL antigen), which is CD10.
- Roughly 20% of the CD10-positive cases may show cµ and are called pre-B – ALL.
- Special stains for ALL:
- Sudan’s black and peroxidase reactions must be negative to support the diagnosis of ALL.
- PAS stain shows clumpy positivity by glycogen in all ALL except the L3, which is negative.
- Cloroectate esterase and lysozyme stains were negative in all ALL.
- α-naphthyl acetate esterase may be positive in T-lymphoblast.
- All ALL cases contain the TdT (terminal deoxynucleotidyl transferase) enzyme, which is a fairly reliable marker of the ALL.
- ALL – L3 often stains with oil red O because of the presence of neutral lipids present in the vacuoles.
- Morphology of the cells:
L1 Small uniform blast cells L2 Larger and more variable size of the cells L3 1. Uniform cells with basophilic and sometimes vacuolated cytoplasm, typical of Burkitt’s lymphoma.
2. Philadelphia chromosomes-positive in acute lymphoblastic leukemia and t(8;14) found.
- Treatment of ALL:
- The aim is to restore the normal function of the bone marrow with multiple chemotherapy drugs.
- Typically four drugs, e.g., vincristine, prednisone, daunorubicin, L-asparaginase, and cyclophosphamide, are used for induction and remission.
- 80 to 90% of the adult enters complete remission.
- Around 30 to 50% will be alive free of disease for three years.
- Prognosis of ALL:
- Patients with a count >30,000/cmm have a shorter duration of remission than patients with a lower count.
- Older age >60 years is not a good favorable factor.
- Another factor that matters in the prognosis is:
- Circulating blast cells %.
- The degree of bone marrow involvement.
- The presence of splenomegaly, hepatomegaly, and lymphadenopathy.
- LDH level.
- Involvement of the CNS at the time of diagnosis.
- The time needed to get the remission for 4 to 6 weeks.
- Ph1chromosome is present in ≤25% of adults and 3% in children. Its positivity shows poor prognostic signs.
- ALL overall, 80 to 90% have complete remission, and disease-free survival is 30 to 40%.
- T-ALL 90 to 95% have complete remission, and disease-free survival is 60 to 65%.
- Precursor B-Cell ALL has 75 to 85% complete remission, and disease-free survival is 30 to 40%.
- ≥60 years of complete remission of 75 to 80% and disease-free survival is 10 to 25%.
- Poor prognostic signs are:
- Platelets count <50,000/cmm.
- WBCs count >100,000/cmm.
- Pre-B phenotype.
- Cytogenetic abnormalities.
- CD10 seronegative type.
Difference between Acute Myelocytic Leukemia and Acute Lymphocytic Leukemia
Characteristic Features | Acute Myelocytic Leukemia | Acute Lymphocytic Leukemia |
Origin of the cells | Myeloid series cells | Lymphoid series cells |
Features of Blast cells | Large in size, | Small in size |
Cytoplasm is moderate | Cytoplasm is scanty | |
Chromatin is fine and lacy. | Chromatin is dense | |
Nucleoli are prominent and >2 | Nucleoli are indistinct and <2 | |
Auer rods | Present | Absent |
Sudan black and peroxidase | Positive | Negative |
Bone marrow | A mixed population of myeloid cells and blast cells | Mainly blast cells and very few WBCs or RBCs |
Leukocyte Alkaline phosphatase (ALP) | Positive (differentiate CML from the leukemoid reaction. | Negative |
Periodic Acid-Schiff (PAS) | Positive in Erythroblast in M6 leukemia |
Positive (block patterns) in L1 and L2 Negative in L3 |
Prognosis of the ALLand AML:
Type of leukemia | Complete remission | Disease-free survival |
ALL |
||
ALL (overall types) | 80 to 90% | 30 to 40% |
Precursor B cell ALL | 75 to 85% | 30 to 40% |
Ph1+ ALL | 70 to75% | 0 to 10% |
Burkitt’s lymphoma | 75% | 70% |
≥60 years | 75 to80% | 10 to 25% |
AML | ||
AML (overall types) |
60 to 70% | 20 to40% |
Acute promyelocytic leukemia |
90% | 70 to 75% |
<60 years |
70 to 80% | 40% |
≥60 years | 45 to 55% | 5 to 10% |
Test value for the layman:
- A blood examination is advised if the patient has a high TLC.
- If the patient has anemia.
- If the patient has enlarged lymph nodes.
- In the case of patients has a fever and weakness.
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