Acute Lymphoblastic Leukemia (ALL)

Acute lymphoblastic leukemia (ALL) is a neoplasm of B- or T-lineage lymphoid progenitors; blasts abnormally proliferate/accumulate in marrow and suppress normal hematopoiesis, causing anemia, thrombocytopenia, and neutropenia; blasts also infiltrate extramedullary tissues (meninges, gonads, thymus, liver, spleen, lymph nodes) causing corresponding lesions.

Common Symptoms

Splenomegaly; intracranial hemorrhage; vaginal bleeding; gingival bleeding; hepatomegaly; epistaxis

Causes and Pathogenesis

(1) Etiology: malignant transformation of hematopoietic progenitors/stem cells. (a) Genetic/familial: 5% of ALL; Down syndrome = 10-30x risk (B-cell precursor ALL); Fanconi anemia. Twin with leukemia: co-twin 20% within 1y; if <1y, almost certain. Non-identical sibling risk 2-4x. Mechanism: gene-stability/DNA-repair defects. (b) Environmental: ionizing radiation; in-utero X-ray exposure; insecticides/active/passive smoking in children; trichloroethylene-contaminated water; >60y smokers. Benzene/alkylating agents; virus (HTLV-1 discovered 1980s from adult T-cell leukemia line). (c) Acquired gene changes: 2/3 non-random numeric/structural changes (translocations most common; inversions/deletions/point mutations/duplications). (2) Mechanism: oncogene activation + tumor-suppressor inactivation (p53, INK4a/p16/p19ARF); p15/p16 deletion in 20-30% B-ALL / 60-80% T-ALL; relapses often have p15/p16 loss. Pathologic changes: marrow (diffuse leukemic infiltrate, maturation arrest; vertebral/sternal/pelvic/rib most affected), nodes (~70% generalized; early: focal infiltration/widened cords/narrow sinuses/atrophic follicles; late: structure destroyed), spleen (white-pulp infiltrate → red pulp/sinuses), liver (portal tracts), tonsils/thymus (78.5%, T-ALL → mediastinal mass). CNS: meningeal/parenchymal infiltrate, hemorrhage/hematoma/transverse myelitis; cranial-nerve palsy (VII>VI>III>IV); spinal/peripheral nerve rare. Genitourinary: testis painless enlargement (children), priapism, renal subcapsular nodules. Other: lung (peribronchial nodes/pleural effusion), oropharynx (infection), heart (myocardial/epicardial/endocardial → effusion/conduction failure), GI (nodes/ulcers/necrosis/perforation), skin (perivascular/follicular nodules). Clonal evidence: Ig/TCR rearrangement; identical cytogenetics/G6PD/immunophenotype; relapse clone reproduces diagnostic genotype. Growth factors/CSF/IL-2R drive proliferation; suppress normal CFU-C.

Treatment

Drug, supportive, surgery, chemotherapy

Preventive Measures

(1) Avoid excessive X-rays/radiation (medical X-rays low-dose are safe). (2) Don't abuse chloramphenicol/cytotoxic/immunosuppressants. (3) Reduce benzene exposure (workplace protection). (4) Prevent/treat complications.

Department to Visit

It is recommended to visit the Hematology department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.