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Acute Leukemia in Children Journal of Pharmacy and Pharmacology 4 (2016) 457-471 doi: 10.17265/2328-2150/2016.09.001 D DAVID PUBLISHING Acute Leukemia in Children Amanda Jensen Einungbrekke and Lukàš Plank Jessenius Faculty of Medicine Faculty of Medicine in Martin, Comenius University in Bratislava, Martin 03601, Slovakia Abstract: Acute leukemia is the most common childhood cancer and accounts for 31% of all cancers in children. There are two main types of acute leukemia. The most common is ALL (acute lymphoblastic leukemia) affecting the lymphoid lineage, and the more rare AML (acute myeloid leukemia) affecting the myeloid linage. The intention of this thesis is to follow the course of treatment from the admission to the hospital until the last check up and also see how a child will react to the treatment and side effects in later life. We studied literature and my own case records from the period when I was treated for ALL. From the literature and my case records, we can see that children tolerate treatment quite well. Due to rapid diagnostics and the possibility to give high doses chemotherapy, the overall prognosis appears to be very good. Today, acute leukemias of paediatric patients have a really favourable prognosis. The overall survival rate for ALL is higher than 80% and for AML 65%. So the results are good, but there is still a long way to go before we can be satisfied. To date we do not have a contingency program for children treated for acute leukemia after 18 years of age (neither in Norway or Slovakia) so perhaps this should be a focus point in the future. It could be extended to follow up patients in adulthood in order to monitor late effects that may occur in later life after many years of treatment. Key words: Acute leukemia, ALL, AML. Abbreviations HR High risk group HSV Herpes simplex virus ACTH Adrenocorticotropic hormone IgA Immunoglobulin A ALAT Alanine aminotransferase IgG Immuoglobulin G ALL Acute lymphoblastic leukemia IgM Immunoglobulin M AML Acute myeloid leukemia IR Intermediate risk group ASAT Aspartate aminotransferase LD Lactate dehydrogenase BBB Blood brain barrier MRD Minimal residual disease BM Bone marrow MTX Methotrexate BNP Brain type natriuretic peptide PCR Polymerase chain reaction CMV Cytomegolavirus PTSD post traumatic stress disorder CNS Central nervous system RBC Red blood cell count CRP C-reactive protein SR Standard Risk group CT Computertomography TBC Thrombocytes CVC Central vein catheter VZV Varicella zoster virus FAB French American British WBC White blood cell FCA Flow cytometric analysis WHO World Health Organization FISH Fluorescence in situ hybridisation Nordic Society of Paediatric Hematology and NOPHO Gamma GT Gamma glutamyl transpeptidase Oncology GIT Gastrointestinal tract GP General practitioner 1. Introduction GFR Glomerular filtration rate 1.1 History GVHD Graft versus host disease Hb Hemoglobin Acute leukemia, the most common form of Hct Hematocrit paediatric cancer has become one of the success stories HE Haematoxylin and eosin stain in the field of oncology. This once fatal disease is now Corresponding author: Amanda Jensen Einungbrekke, curable in the majority of paediatric patients who M.D., research fields: pathology, pediatrics and oncology. 458 Acute Leukemia in Children receive fast and appropriate treatment [1, 2]. In the treatment protocol and differentiate ALL into three 1970 era, approximately 10% of all children diagnosed groups: standard risk, intermediate risk and high risk. with any type of paediatric cancer survived. Since then, Allocating each child to a risk group is dependent on there has been a tremendous development, and today cell type, leukocyte count, cytogenetics and how he/she 80% survive [3]. responds to the given treatment [1, 4]. AML is a malignant clonal disorder of myeloid cells. 1.2 Definition It is a heterogeneous, clonal disturbance in the Acute leukemia is a malignant clonal disorder in one hematopoietic cells. They loose their capability to or more cell-lines in the hematopoietic system. It is the differentiate normally and to respond to normal most common form of childhood leukemia, and regulatory mechanisms in proliferation. According to comprises 1/3 of all paediatric cancers (Fig. 1). There FAB classification, there must be a presence of at least are two main types of acute leukemia found in children. 30% blasts in the BM. WHO classification has lowered The most common is ALL (acute lymphoblastic the criteria to at least 20%. AML accounts for leukemia) (Fig. 2), and the more rare AML (acute approximately 15 % of leukemias in children, and is myeloid leukemia). In Norway, there are 30~40 cases rare. It can affect all age groups, and is more common per year in children from 0~14 years [1, 4]. in adults. Paediatric AML is more difficult to treat than ALL is a malignant clonal disorder that affects the ALL. And in comparison to ALL where it is more lymphoid line in the hematopoietic blood system. It is a common to use WHO classification, we use FAB high count of immature lymphocytes, called lymphoblasts. classification in AML. We have eight groups M0-M7. The diagnosis can be confirmed when there are more M3, also called “acute promyelocytic leukemia”, has a than 25% lymphoblasts in the bone marrow picture. special translocation t(15; 17). This type of leukemia is The cancer cells can arrive either from B or T cells, treated with a special protocol. Also M7 called where immature precursors of B are most common “megakaryocytic leukemia” is extremely rare and very (90%). In Norway and Slovakia, they follow NOPHO difficult to treat [1, 4, 5]. Distribution of Childhood Cancer NOPHO 1985-2004 1% 1% 3% 3% Acute leukemia 4% CNS tumours 4% 31% Lymphomas 5% Kidney cancer Neuroblastoma 6% Sof tissue sarcoma Germinal cell tumour 6% Bone sarcoma Retinoblastoma 7% Carcinomas 29% Liver cancer Other Fig. 1 Distribution of paediatric cancer [1]. Acute Leukemia in Children 459 Total Norway Slovakia 18 16 14 12 10 8 6 Incidence per 100,000 4 2 0 Fig. 2 Age specific incidence according to Norway and Slovakia. 2. Theoretical Part This is a widely-used classification which can be found on many publications, such as the articles from 2.1 Classification Vardiman et al. [7] and Mautes et al. [8]. Classification is the language of medicine: Diseases AML and related precursor neoplasms; must be described, defined and named before they can AML with recurrent genetic abnormalities: be diagnosed, treated and studied, from WHO. (1) AML with t(8; 21) (q22; q22); There are two classifications used in the definition of RUNX1-RUNX1T1; acute leukemias: FAB (French American British (2) AML with inv (16) (p13.1; q22); classidfication) and WHO (World Health CBFB-MYH11; Organisation). The difference between the two (3) Acute promyelocytic leukemia with t(15; 17) classifications is mostly related to the number of blasts (q22; q12); PML-RARA; in the BM. According the FAB criteria, number of (4) AML with t(9; 11) (p22; q23); MLLT3-MLL; blasts in the bone marrow should be more than 30%. (5) AML with t(6; 9) (p23; q34); DEK-NUP214; WHO has a criterion of 20%. FAB classification is (6) AML with inv (3) (q21; q26.2) or t(3; 3) (q21; mostly based on morohology and cytochemistry. WHO q26.2); RPN1-EVI1; on the other hand is based on clinical, cytogenetic and (7) AML (megakaryoblastic) with t(1; 22) (p13; molecular abnormalities. WHO is the newest q13); RBM15-MKL1; classification, and is widely used for leukemia, (8) AML with mutated NPM1; especially ALL. (9) AML with mutated CEBPA; AML with myelodysplasia-related changes; 2.2 WHO Classification Therapy related myeloid neoplasms; In 2007, WHO updated their classification of Acute myeloid leukemia, NOS: tumours of haematopoietic and lymphoid tissues [6]. (1) AML with minimal differentiation; 460 Acute Leukemia in Children (2) AML without maturation; 19) (q23; p13.3); E2A-PBX1 (TCF3- PBX1). (3) Acute myelomonocytic leukemia; 2.3 FAB Classification (4) Acute monoblastic and monocytic leukemia; (5) Acute erythroid leukemia; French American British classification is a much (6) Acute megakaryoblastic leukemia; older classification, but still widely used today [9]. It is (7) Acute basophilic leukemia; a much easier classification and mostly used in the (8) Acute panmyelosis with myelofibrosis; diagnosis of AML. Myeloid sarcoma; FAB classification divide AML into eight subtypes Myeloid proliferations related to down syndrome: M0-M7: (1) Transient abnormal myelopoiesis; M0—Minimally differentiated AML; (2) Myeloid leukemia associated with Down M1—AML without maturation; syndrome; M2—AML with maturation; Blastic plasmacytoid dendritic cell neoplasm; M3—Acute promyelocytic leukemia; Acute leukemias of ambiguous lineage: M4—Acute myelomonocytic leukemia; (1) Acute undifferentiated leukemia; M5—Acute monocytic leukemia; (2) Mixed phenotype acute leukemia with t(9; 22) M6—Acute erythroleukemia; (q34; q11.2); BCR-ABL1; M7—Acute megakaryocytic leukemia. (3) Mixed phenotype acute leukemia with FAB classification divide ALL into three subtypes: t(v11q23); MLL rearranged; L1—Childhood-ALL (B-ALL, and T-ALL); (4) Mixed phenotype acute leukemia, B/myeloid, L2—Adult ALL (mostly T-ALL); NOS; L3—Burkitt type ALL (B-ALL). (5) Mixed phenotype acute leukemia, T/myeloid, 2.4 Feature AML and ALL NOS; Precursor lymphoid neoplasms; Both AML and ALL have many of the same clinical B lymphoblastic leukemia/lymphoma: features, and it is not possible to distinguish them only (1) B lymphoblastic leukemia/lymphoma, NOS; on clinical signs [10]. The importance of morphology, (2) B lymphoblastic leukemia/lymphoma with cytogenetic and immunophenotyping is invaluable recurrent genetic abnormalities; when talking about diagnosis of acute leukemia. (3) B lymphoblastic leukemia/lymphoma with t(9; Table 1 shows the most contrasting features of AML 22) (q34; q11.2); BCR-ABL1; and ALL (taken directly from Ref. [10]). (4) B lymphoblastic leukemia/lymphoma with 2.5 Etiology t(v11q23); MLL rearranged; (5) B lymphoblastic leukemia/lymphoma with t(12; There is no exact etiology which positively defines 21) (p13; q22); TEL-AML1 (ETV6- RUNX1); leukemia.
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