Acute Leukemias

Sample for Acute Leukemias

1. Blood in EDTA and a fresh blood smear are needed.
2. Bone marrow aspirate and biopsy are required.

Definition of acute leukemias

1. Leukemias are characterized by the uncontrolled (malignant) proliferation of the blood and bone marrow cells.
   1. In the case of a lymphocytic variety, there is the involvement of the lymph nodes.  OR
2. This is a malignant neoplasm of hematopoietic cells, particularly stem cells.  OR
3. There is diffuse infiltration of the bone marrow by these neoplastic cells. OR
4. Leukemias are a malignant disease of the hemopoietic tissue, characterized by replacing normal bone marrow elements with abnormal neoplastic blood cells.
5. These cells enter the blood and may infiltrate the liver, spleen, lymph nodes, and other organs.

Acute leukemias: Acute leukemias development from the stem cells and clinical presentations

Classification of Acute Leukemias

1. Based on the morphology, the leukemias  are divided into:
   1. Acute lymphocytic leukemia (ALL) involves the lymphocytes and their precursors.
   2. Acute myelocytic leukemia (AML) involves the granulocytes and their precursors.
   3. Acute monocytic leukemia involves the monocytes and their precursors.
   4. Acute plasmacytic leukemia involves the plasma cells and their precursors.
   5. Acute erythroblastic leukemia involves red blood cell precursors.
2. Acute leukemia develops from the stem cells and develops into myelocytic and lymphocytic varieties.

Pathophysiology of Acute Leukemias

1. The malignant transformation is at the level of pluripotential cells (stem cells), and these cells change into committed stem cells, and they are called stem cell disorders.
2. 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.

Acute Leukemias Criteria:

1. Acute leukemias are characterized by abnormal differentiation and proliferation of malignantly transformed hematopoietic blast cells.
2. These cells proliferate in the bone marrow and lead to the suppression of the normal cells.
3. These have little or no maturation and may see mainly blast cells.
4. Acute Leukemias are diagnosed on the percentage of blast cells in the bone marrow.
5. 30% or more blast cells are needed to classify the disorder as acute leukemia.
6. These leukemias are associated with varying degrees of anemia, neutropenia, thrombocytopenia, and infiltration of the tissues.
7. The most common infiltration site is lymph nodes, liver, spleen, CNS, and skin.

Epidemiology of acute leukemias:

1. ALL and AML can occur at any age. But the incidence increases with increasing age.
2. ALL predominate in children, while AML accounts for most of the cases in adults.
3. AML’s median age is around 60 years.
4. The peak age for ALL is between 3 to 5 years. These are morphologically different than adult cases.
5. Acute leukemias are more common in whites than blacks.
6. Acute leukemias are more common in the Jews than in the non-Jews.
7. Acute leukemias are more common in men than in women.

Etiological factors for acute leukemias (Risk factors):

1. The cause of acute leukemias is unknown; this may be hereditary or environmental factors.
2. The pathogenesis is very complex which may involve interaction between the host susceptibility and chromosomal damage secondary to physical or chemical agents.
3. Chromosomal abnormality:
   1. There are chromosomal abnormalities; examples are given below:
   2. Deletion:
      1. 5q –  = Myelodysplasia, preleukemia.
      2. Monosomy 7.
   3. Inversion:
      1. inv 16 = AML.
   4. Translocation:
      1. t18:14 = Burkitt’s lymphoma.
      2. t8:21 = AML.
      3. t4:11 = ALL.
      4. t9:22 = CML
4. Oncogenes:
   1. C-abl, C-sis = CML.
   2. C-myc = Burkitt’s lymphoma (L3).
5. Viruses:
   1. There are viruses known to give rise to leukemia in nonhuman species.
   2. The human role of viruses has been studied for a long time, but no conclusive data is available.
   3. Epstein-Barr virus is seen in the majority of Burkitt’s lymphoma.
   4. The Human T-leukemia virus  (HTLV-1) is associated with acute leukemia.
6. Inherited factors:
   1. The following examples favor the role of genetic abnormalities:
      1. Increased incidence of acute leukemia in families.
      2. Increased incidence of acute leukemia in monozygotic twins.
         1. If one twin has leukemia, the other is also at risk for leukemia, often before eight years of age.
         2. Leukemia starts in the next twin within a year of the first diagnosis.
   2. 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.
   3. There is an increased incidence of AML and ALL in Down’s syndrome, where there is trisomy 21.
      1. 5 to 10% of childhood AML occurs in Down’s syndrome.
   4. There is an increased incidence of Fanconi’s syndrome and Bloom’s syndrome.
      1. Both conditions are hereditary, and there is an increased chromosomal breakage.
   5. Ataxia-telangiectasia and congenital agammaglobulinemia have chromosomal abnormalities that are associated with acute leukemia.
7. Acquired factors:
   1. Drugs and Chemicals:
   2. Alkylating drugs like nitrogen mustard, chlorambucil, melphalan, cyclophosphamide, and procarbazine.
      1. Benzene compounds and pesticides.
   3. Exposure to melphalan or nitrogen mustard is associated with acute AML after 5 to 7 years of exposure.
      1. The patient will have pancytopenia, myelodysplasia, and cytogenetic abnormalities (a total loss or partial loss of chromosomes 5 and 7).
      2. Hodgkin’s lymphoma, Multiple myeloma, and ovarian cancer treatment complication of AML are well-known examples.
         1. Benzene complication of acute leukemia is well-known.
   4. Radiation: The leukemogenic potential of ionizing radiation has been recognized for a long time.
      1. Mostly myeloid leukemia takes its origins from radiation.
      2. Fetal exposure to radiation increases the risk of childhood leukemia.

Acute Leukemias signs and symptoms:

1. Appears suddenly.
2. Suspect leukemia in a patient who has pallor and purpura.
3. Patients may have nonspecific symptoms like breathlessness, malaise, and fever.
4. The patient may have weakness and fatigue.
5. The patient may have a low-grade fever.
6. There may be bruising and mild bleeding from the gums.
7. There is bone pain due to the expansion of the marrow.
8. Children may have bone pain.
9. Some patients are severely sick at the time of presentation. These patients may have sepsis and hemorrhage.

Clinical features of acute leukemias:

Diagnosis of Acute Leukemia:

1. These are more common in the younger age group.
   1. These are more frequent in children.
   2. Mostly seen before the age of 20 years.
2. Onset is an abrupt and fatal outcome.
   1. There is a fever.
3. There is a rapid development of anemia.
   1. There is normochromic and normocytic anemia.
   2. May see nucleated RBCs.
4. There is thrombocytopenia.
   1. May see petechiae and purpura in the skin and mucous membranes.
5. Leukocyte count is variable.
   1. Mostly leucocyte count is less than 100,000/cmm.
6. Diagnosis depends upon the microscopic examination of the blood and bone marrow.
7. Immunohistochemical staining.
8. Immunophenotyping by 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.
9. Cytogenetic studies can also be advised.
   1. Chromosomal abnormalities are seen in >50% of the cases

Difference between acute and chronic leukemias:

Treatment Goals for acute leukemias:

1. The main aim of the therapy is to restore bone marrow function and normality.
2. Complete remission when the patient fully recovered the peripheral blood smear and bone marrow showing <5% of the blast cells.
3. Induction therapy reduces the total body leukemia cell population roughly from 10¹² cells to below <10⁹.
4. The complication of the chemotherapy:
5. Cytotoxic drugs lead to:
   1. Tumor lysis syndrome and urate nephropathy.
   2. Hyperuricemia responds rapidly to rasburicase.
   3. Allopurinol, I/V therapy, and alkalinization of the urine reduce the chances of uric acid precipitation in the renal tubules.
6. Electrolyte imbalance like hyperkalemia, hypocalcemia, and hyperphosphatemia.
7. There may be gastrointestinal injury, diarrhea, and mucositis.
8. There may be thrombocytopenia, bleeding, and neutropenic infection.
9. Blood products are given to maintain the platelet count >10,000 µL in non-bleeding patients, and hematocrit to keep >25%.
10. Antibiotics are given if the body temperature is >38.5 °C.
11. In neutropenic patients, when TLC is <500 /µL, antifungal therapy is added to these febrile patients.

Acute Myeloid Leukemia (AML)

Pathogenesis of Acute myeloid leukemia:

1. There are primary AMLs that appear de novo.
2. Secondary AML develops from:
   1. The myelodysplasia.
   2. Other hematological diseases, such as myeloproliferative disorders.
   3. Or following previous treatment with chemotherapy.
3. Age: This is seen during the first month of life and in the latter age group.
   1. 10 to 15% of cases are found in children.
   2. Exposure to high-energy radiation in early childhood increases the risk of developing T-cell acute lymphoblastic leukemia.
4. Sex: More common in males than women.
   1. Male: female ratio is 3:2.

Signs and symptoms of Acute myeloid leukemia:

1. Mostly these patients present with a varying degree of bone marrow failure.
2. So clinical symptoms and signs are due to anemia, leukopenia, thrombocytopenia, and infections.
3. About 1/3 of the patient have bruises and hemorrhages.
4. About 1/4 of the patients have severe infections involving the lungs, soft tissue, or skin.
5. Splenomegaly and hepatomegaly are uncommon and are seen in<25% of the cases.
6. Lymphadenopathy is even less common.
7. Gingival hypertrophy or skin infiltration by the tumor occurs in 50% of the patients with monocytic leukemia.
8. Acute promyelocytic leukemias are more commonly seen with severe bleeding from the DIC.
9. Fever and fatigue are present in most of the patients.
10. Acute promyelocytic leukemia (M3) causes disseminated intravascular coagulopathy (DIC) and bleeding.
11. Acute myelomonocytic leukemia (M4) and acute monocytic leukemia (M5) cause gum hypertrophy.
12. 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.
13. These patients may have respiratory distress due to leukostasis within the pulmonary vasculature.
14. There may be retinal hemorrhage due to thrombocytopenia.

Classification of Acute myeloid leukemia (AML):

French-American-British (FAB) Classification of Acute Myelocytic Leukemia:

1. FAB has 85% concordance. This is based on morphology and cytochemistry.
2. Immunophenotyping and cytogenetics give additional information for the treatment.
3. WHO criteria for the AML is ≥20% blast cells.

FAB type	Characteristic features	Frequency
M0	Acute myeloblastic leukemia with minimal differentiation. Blast cells lake cytologic and cytochemical markers of the myeloid series cell. But express myeloid series lineage antigens. 2 to 3% of AML. Bone marrow contains ≥30% of the blast cells that don’t fulfill FAB criteria. Sudan black and myeloperoxidase stains are negative. Express CD13 and CD33 antigen-positive on the surface. These are not included in the current FAB classification. Immunologic markers or E/M are needed for the diagnosis.	2 to 3%
M1	Acute myeloblastic leukemia without differentiation. Its incidence is ≤20% of AML cases. Undifferentiated myeloblastic cells. >90% of the cells are blast cells, predominantly type 1. <10% of the cells are granulocytic series. No cytoplasmic granules; may see few. Only 3% of the cells are myeloperoxidase positive. Auer rods are common (another reference says few Auer rods). Acute myeloid leukemia (AML= M1)	20%
M2	Also called AML with maturation. Incidence is 25% to 30% of AML patients. Patients are younger, with a mean age of 28 years. There is splenomegaly in 28% of the cases. Chloromas, especially on the face, are seen in 20% of patients. Differentiated myeloblastic (30 to 89%) cells, sparse granules, and abundant cytoplasm. Myelocytes and promyelocytes are predominant. >30% blast cells Myeloblast with Auer rods is seen in 60% to 70% of cells. Monocytic cells are <20%. Eosinophils precursors are increased and contain Auer rods. Some of the cells are myeloperoxidase or Sudan black positive Cytogenetics show t(8;21)and (q22;22q). Frequent loss of sex chromosomes. It may be seen in Down syndrome (trisomy 21). Prognosis:  75% to 85%  of the cases go into complete remission after the chemotherapy. Median survival is 9.5 months duration on average. Acute myeloid leukemia (AML= M2)	25 to 30%
M3	Acute Promyelocytic Leukemia. These are 5% to 10% of the AML cases. The median age is 31 years. These patients present with bleeding episodes and ≤47% die of fatal hemorrhage. DIC is seen in ≤80% of the cases. Blast cells are <30% in most cases. Blast cells contain prominent granules; nuclei are bilobed or kidney-shaped. Granules are typical of promyelocytic morphology; these are azurophilic. Auer rods are many. These are strongly myeloperoxidase positive. Cytogenetics show t(15;17), t(11;17), and (q22;q11-12) are diagnostic for M3. M3v variant: These are micro granular types. 20% of the AML cases are this type. WBCs count is high, 50,000 to 200,000 µL, with small and difficult-to-see azurophilic granules. Acute myeloid leukemia (AML= M3)	5 to 10% (8 to 15%)
M4	Acute Myeloid Monoblastic Leukemia (Acute myelomonocytic leukemia). 20% to 25% of the AML cases are this type. The mixed population of myeloblastic (>30%) and monocytic (>20%) morphology. ≥30% of the cells are myelomonocytic blast cells. 2% to 8% are of myelocytic origin. 20% to 80% are of monocytic origin. The peripheral blood smear shows typical myelomonocytic blast cells. Auer rods may be seen. Nonspecific esterase and chloroacetate stains are often positive. Karyotype shows inversion or deletion of chromosome 16 [inv(16)(p13;q22)]. Cytochemistry is needed for the diagnosis of AML and M4. There is weak staining of nonspecific esterase. In 70% to 90% of cases, the prognosis is complete remission with a prolonged median survival of >18 months. >1/3 of cases come with a relapse of CNS involvement. Acute myeloid leukemia (AML= M4)	20 to 30% (20 to 25%)
M5	Acute Monoblastic Leukemia. These are 10% of AML patients. It involves mostly children and young adults. Pure monoblastic cells. Monoblast and promonocytes predominate>80%. These leukemic cells may infiltrate the skin or the gums and CNS. DIC is frequent in these cases. Serum lysozyme is often raised. There are poor survival and shorter remission. >30% of cells are blast cells, and >80% are monocytoid differentiation. Cytogenetics show t(9;11), (p22;q23), and t(11;q23). M-5a variant: This is called monoblastic leukemia. 4% are poorly differentiated  AML. >80% of the cells are monoblasts. M-5b variant: 6% of the AML cases. <80% of the cells are monoblasts. A karyotype is t(9;110)(p22;q23). Acute myeloid leukemia (AML= M5)	10%
M6	Acute Erythroleukemia. 4% to 5% of the AML patients. Predominantly immature erythroblast ≥50%, and can see multinucleated megaloblastoid erythroblast. There are megaloblasts, ringed sideroblast, and Howell-Jolly bodies that are common. Nucleated RBCs in the peripheral blood are common. Anemia is also common. Erythroblast cells are strongly PAS-positive. Myeloblasts are 30% or more. If <30%, then the diagnosis is a myelodysplastic syndrome. Acute myeloid leukemia (AML= M6)	5%
M7	Acute Megakaryoblastic leukemia. 1% to 2% of the AML cases. These cases are common in Down syndrome between infancy and 3 years. Megakaryocytic  Cells are small and large with shaggy borders that may show some budding. Megakaryoblasts are ≥30% of all cells. Blast cells are highly polymorphic and often labeled as undifferentiated cells. Mature megakaryocytes are also present. There is a high N/C ratio. There is myelofibrosis almost in all patients. 20% to 40% of cases, acute myelofibrosis is present, making blast cell counting difficult. Platelet peroxidase and platelet antibodies are often positive. Cytogenetics show t(1;22), and (p13;q13). Acute myeloid leukemia (AML= M7)	1 to 2% (1%)

Summary of the FAB classification of acute myelocytic leukemia:

Lab. findings of Acute myeloid leukemia (AML): 

1. WBC count is variable.
   1. 25% of the patient has >50,000/cmm.
   2. 25% has <5000/cmm, and 5% to 10% has count between 5000 to 10,000/cmm.
   3. A count>100,000/cmm is reported in <10% of the patients, but these patients have severe CNS or respiratory diseases due to leukostasis.
   4. In these patients, leukapheresis and chemotherapy may be life-saving.
2. WBC morphology. These are morphologically abnormal and immature cells.
   1. 20% or more of the blast cells in the bone marrow as diagnostic of AML.
   2. Ther blast cells of AML are larger than lymphoblast cells and have more significant heterogeneity in size and shape.
   3. AML blast cells are most abundant in the cytoplasm and often contain cytoplasmic granules.
   4. About 10% of the AML cases show Auer rods and azurophilic granules with Wright’s stain.
3. The peripheral blood smear may show blast cells in 85 to 90% of the cases.
4. FAB divides Acute myelocytic leukemia (AML) into:
   1. M1, M2, and M3 with granulocytic differentiation.
   2. M4, M5 with at least 20% monocytoid appearance.
   3. M6 with a high proportion of erythroblasts.
   4. M7 with predominantly megakaryoblasts.
   5. M0 with minimal myeloid differentiation. This needs immunohistochemical stains for the diagnosis. These cases have myeloid antigens on their surface and negative myeloperoxidase activity.
5. Biochemical tests:
   1. In 50% of the cases, uric acid is raised, which indicates increased cell turnover.
   2. Lactate dehydrogenase (LDH), about 50%, shows a raised level. This is not as common as in ALL.
6. Bone marrow shows >20% blast cells. Promyelocytes are numerous, particularly in M3.
   1. Auer rods can be seen in the cytoplasm.
   2. Cytochemical stains, peroxidase reaction, and Sudan black are positive.
7. Nucleated RBCs may be seen.
8. Platelet count may be low and may see a count between 30,000 to 100,000/cmm.
   1. In some cases may be <20,000/cmm.
9. Coagulation abnormalities are also seen. PT, PTT, and Thrombin time are prolonged.

Treatment of Acute myeloid leukemia (AML):

1. There is a supportive and specific treatment for AML.
2. Stem cell transplantation and autologous transplantation may be done. But because of the toxicity, overall no benefit.
3. The treatment of patients over 70 years of age with AML is poor because of primary disease resistance and poor tolerability of intensive treatment.
4. Death in older adults is usually from hemorrhage, infections, and failure of the heart, kidneys, or other organs compared to younger patients.

Prognosis of Acute myeloid leukemia (AML):

1. 50% of children and young adults may have a long-term cure.
2. Recently with the newer advanced chemotherapy, the prognosis in the 60 to 70 years is better.
3. Cytogenetics abnormalities and initial response to the treatment are the major predictors of the prognosis.
4. AML complete remission is 60 to 70%, and disease-free survival is 20 to 40%.
5. <60 years of complete remission is 70 to 80%, and disease-free survival is 40%.
6. >60 years of complete remission is 45 to 55%, and disease-free survival is 5 to 10%.

Acute myeloid leukemia (AML) prognostic factors:

 Acute Lymphoblastic Leukemia (ALL)

Age of Acute lymphoblastic leukemia (ALL):

1. ALL constitute 20% of adult leukemia, which is more common in children.
2. In adults, 80% of the ALL are B-cells, and 20% are T-lymphocytes origin.
3. This is most common in childhood.
   1. Mostly occur before the age of 4 years. The peak is between 2 to 10 years; it is also called childhood leukemia.
4. ALL comprises >80% of childhood leukemia.
5. 90% have chromosomal abnormalities.
6. Down syndrome has a 15x times higher incidence of ALL.
7. These are rare after the age of 30 years.
8. These are most common in children and young adults.
9. The second peak may be seen in the middle and old age groups.
10. L3 leukemia is most common in developing countries and may be associated with infection by the Epstein-Barr virus in the younger age group.
11. Children with trisomy 21 (Down’s syndrome) have an increased risk for childhood acute lymphocytic and acute myelocytic leukemias.
12. An increased incidence is seen in immunodeficiency diseases like ataxia-telangiectasia, osteogenesis imperfecta, siblings of ALL, and Poland syndrome.

Signs and symptoms of Acute lymphoblastic leukemia (ALL):

1. S/S of acute AML and ALL are similar, except the onset of ALL is strikingly acute.
2. The onset is sudden. There is no preleukemic stage.
3. Symptoms are present only for a few weeks before the diagnosis.
4. There are fatigue and fever. There is malaise, lethargy, and weight loss.
5. There may be bleeding and infections.
6. An enlargement of lymph nodes, spleen, and liver is more common than the AML, affecting 50% of adults.
7. There may be central nervous system (CNS) involvement in 5 to 10% of the cases.
8. This shows leukemic meningitis.
9. Cranial nerve palsy is more common in the 6th and 7th nerves.
10. There are headaches and papilledema due to meningeal involvement and the obstruction of the outflow of CSF.
11. CSF shows increased protein and leukemic cells.
12. Bone pain is due to the infiltration of the leukemic cells.
13. Retinal hemorrhage is due to thrombocytopenia.
14. Chest X-ray shows a thymic mass in 10 to 15% of the adults.

Classification of Acute lymphoblastic leukemia (ALL):

1. Classification of ALL is based on cytological features like:
   1. Cell size.
   2. Nuclear chromatin pattern.
   3. Nuclear shape.
   4. Presence of nucleoli.
   5. Amount of basophilia in the cytoplasm.
      1. 80% of the ALL are B-lymphocytes in origin.
      2. 15 to 20% of cases arise from T-lymphocytes. These cells will express CD2, CD5, and CD7.
         1. T- L ALL are lacking CD19 and CD20.
2. L1 – ALL accounts for >80% of the cases in children and consists of predominantly small, up to twice the size of small lymphocytes.
3. L2 – ALL are the majority of adult leukemia. The cells are larger than in the L1 and often heterogeneous in size.
4. L3 – ALL is the least common form of approximately 3 to 4% of children and adults. The cells are morphologically identical to the cells in Burkitt’s lymphoma.
5. FAB is no longer used.

FAB (French-American-British) classification of Acute Lymphocytic Leukemia:

L1	Lymphoblasts with uniform, round nuclei, and scant cytoplasm. Nucleoli are not prominent. ALL- L l
L2	More variable lymphoblast and cytoplasm are abundant. Nucleoli are large and may see one or more nucleoli. ALL- L2
L3	Lymphoblasts with fine nuclear chromatin and blue to deep blue cytoplasm contain vacuoles. Lymphoblast is large and has prominent nucleoli, and these are one or more than one. ALL-L3

Cytochemical classification of Acute lymphoblastic leukemia (ALL):

Lab. Findings of Acute lymphoblastic leukemia (ALL):

1. Lab diagnosis depends upon the following:
   1. Morphology.
   2. Cytochemistry.
   3. Immunophenotyping.
   4. Genetic analysis.
2. WBC count is variable from very high to low count.
3. There are anemia and thrombocytopenia.
4. Bone marrow: Very few leucocytes are seen.
   1. Difficult to find normal WBCs or RBCs in the bone marrow.
   2. Characteristically there are blast cells. >50% are lymphoblastic cells.
   3. Auer rods are absent.
5. Serum LDH, uric acid, and ESR are often raised.
6. Flow cytometry studies (differentiation of the antigens over the surface of these abnormal cells) provide rapid diagnosis.
   1. 80% of the ALL arises from the B-lymphocytes and will show CD molecules of CD19, CD20, or both.
   2. A few cases of ALL may show CALA (common ALL antigen), which is CD10.
   3. Roughly 20% of the CD10-positive cases may show cµ and are called pre-B – ALL.
7. Special stains for Acute lymphoblastic leukemia (ALL):
   1. Sudan’s black and peroxidase reactions must be negative to support the diagnosis of ALL.
   2. PAS stain shows clumpy positivity by glycogen in all ALL except the L3, which is negative.
   3. Cloroectate esterase and lysozyme stains were negative in all ALL.
   4. α-naphthyl acetate esterase may be positive in T-lymphoblast.
   5. All ALL cases contain the TdT (terminal deoxynucleotidyl transferase) enzyme, which is a fairly reliable marker of the ALL.
   6. ALL – L3 often stains with oil red O because of the presence of neutral lipids present in the vacuoles.
   7. Morphology of the cells:
      

      L1	Small uniform blast cells
      L2	Larger and more variable sizes 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 Acute lymphoblastic leukemia (ALL):

1. The aim is to restore the normal function of the bone marrow with multiple chemotherapy drugs.
2. Typically four drugs, e.g., vincristine, prednisone, daunorubicin, L-asparaginase, and cyclophosphamide, are used for induction and remission.
3. 80% to 90% of adult enters complete remission.
4. Around 30% to 50% will be alive and disease-free for three years.

Prognosis of Acute lymphoblastic leukemia (ALL):

1. Patients with a count >30,000/cmm have a shorter duration of remission than patients with a lower count.
2. Older age >60 years is not a good favorable factor.
3. Another factor that matters in the prognosis is:
   1. Circulating blast cells %.
   2. The degree of bone marrow involvement.
   3. The presence of splenomegaly, hepatomegaly, and lymphadenopathy.
   4. LDH level.
   5. Involvement of the CNS at the time of diagnosis.
   6. The time needed to get the remission for 4 to 6 weeks.
   7. Ph¹chromosome is present in ≤25% of adults and 3% of children. Its positivity shows poor prognostic signs.
4. Acute lymphoblastic leukemia (ALL) overall, 80 to 90% have complete remission, and disease-free survival is 30 to 40%.
   1. T-ALL 90% to 95% have complete remission, and disease-free survival is 60 to 65%.
   2. Precursor B-Cell ALL has 75% to 85% complete remission, and disease-free survival is 30 to 40%.
   3. ≥60 years of complete remission of 75% to 80%, and disease-free survival is 10 to 25%.
5. Poor prognostic signs are:
   1. Platelets count <50,000/cmm.
   2. WBCs count >100,000/cmm.
   3. Pre-B phenotype.
   4. Cytogenetic abnormalities.
   5. CD10 seronegative type.

Difference between Acute Myelocytic Leukemia and Acute Lymphocytic Leukemia

Prognosis of  Acute lymphoblastic leukemia (ALL) and Acute myeloid leukemia (AML):

Test value for the layman:

1. A blood examination is advised if the patient has a high TLC.
2. If the patient has anemia.
3. If the patient has enlarged lymph nodes.
4. In the case of patients has a fever and weakness.

Questions and answers: