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Chronic Lymphocytic Leukemia

Chapter 112 | Harrison's 22e · Part 4 – Oncology: Hematologic Malignancies · Chapter 112


Key Clinical Points

  1. CLL is defined by an absolute lymphocyte count ≥5 × 10⁹/L with monoclonal B-cell proliferation.
  2. Median age at diagnosis is 71 years; incidence rate is 4.6/100,000 in the US.
  3. Prevalence has increased due to improved therapies and an aging population (survival rates rose from 70% in 1980 to 92% in 2015).
  4. NOTCH1 mutations (10–13%) correlate with poor response to CD20 therapy and risk of Richter's transformation.
  5. SF3B1 mutations (8–14%) affect RNA splicing and are linked to specific cytogenetic abnormalities.
  6. ATM mutations (8–11%) can lead to resistance to venetoclax; TP53 mutations are associated with poor response to DNA-damaging therapy.
  7. Targeted therapies include BTK inhibitors (ibrutinib, acalabrutinib), BCL-2 inhibitors (venetoclax), and PI3K inhibitors (idelalisib).
  8. MRD negativity after treatment is a key predictor of improved survival outcomes.

1. DEFINITION & OVERVIEW

Definition: Chronic lymphocytic leukemia (CLL) is a monoclonal proliferation of mature B lymphocytes defined by an absolute lymphocyte count ≥5 × 10⁹/L.

Precursor State: Monoclonal B-cell expansion without cytopenias or organomegaly (MBL).

Clinical Course: Highly variable, ranging from asymptomatic indolent forms to aggressive transformations.

Progression Risk: 1–2% annual progression risk from MBL.


2. EPIDEMIOLOGY

Demographics: Primarily a disease of older adults. ◦ Median age at diagnosis: 71 years. ◦ Male-to-female ratio: 2:1 (equal after age 80).

Incidence & Prevalence: ◦ Age-adjusted incidence: 4.6/100,000 in the US. ◦ Survival rates increased from 70% (1980) to 92% (2015).

Ethnicity: ◦ Most common in Caucasians. ◦ Less frequent in Hispanics and African Americans. ◦ Rare in Asians.

Environmental Factors: ◦ No definitive links to radiation exposure. ◦ Agent Orange exposure associated with service-connected status.


3. ETIOLOGY & PATHOPHYSIOLOGY

Molecular Heterogeneity: Influences prognosis and treatment response.

Recurrent Mutations (Table 112-1): ◦ SF3B1: 8–14% frequency; affects RNA splicing, linked to specific cytogenetic abnormalities. ◦ NOTCH1: 10–13% frequency; mutations in the PEST domain cause constitutive signaling and are associated with Richter's transformation. ◦ ATM: 8–11% frequency; mutations can lead to resistance to venetoclax. ◦ XPO1, POT1, EGR2: <5% frequency each.

Genetic Impact (Figure 112-2): ◦ TP53 mutations: Associated with poor response to DNA-damaging therapy. ◦ SF3B1 mutations: Linked to specific cytogenetic abnormalities.


4. CLINICAL MANIFESTATIONS

Presentation: ◦ Asymptomatic: 20–30% of cases at diagnosis. ◦ Symptomatic manifestations (70–80% will eventually require treatment): ◦ Fatigue (most common). ◦ Lymphadenopathy (70–80%). ◦ Splenomegaly (50–60%). ◦ Autoimmune phenomena: e.g., hemolytic anemia, thrombocytopenia.

Natural History: ◦ 10–20% of patients never require therapy. ◦ Median survival: 10 years with modern therapies.


5. DIAGNOSTIC APPROACH

  1. Initial Diagnosis: • Confirm absolute lymphocyte count ≥5 × 10⁹/L. • Identify monoclonal B-cell population (Table 112-2: CD5+, CD19+, CD20+ [dim], CD23+). • Exclude other lymphoproliferative disorders.

  2. Staging (Table 112-3): • Rai System: ◦ Stage 0 (Low risk): Lymphocytosis only. ◦ Stage I/II (Intermediate risk): Lymphocytosis with lymphadenopathy, with or without splenomegaly or hepatomegaly. ◦ Stage III/IV (High risk): Lymphocytosis with anemia or thrombocytopenia due to bone marrow involvement. • Binet System: Categorized as A, B, or C.

  3. Risk Stratification (Table 112-4): • Calculate International Prognostic Index (IPI) based on: ◦ TP53 status: Deleted or mutated → 4 points. ◦ β-Microglobulin concentration: >3.5 mg/L → 2 points. ◦ Age: >65 years → 1 point. • Interpretation of Risk Score: ◦ 0–1: Low risk (93.2% 5-year survival). ◦ 4–6: High risk (63.3% 5-year survival).

  4. Decision to Initiate Therapy (Table 112-5): Identify triggers for treatment initiation: • Marrow Failure: worsening of anemia or thrombocytopenia not due to autoimmune destruction. • Splenomegaly: Massive (≥6 cm below costal margin), progressive, or symptomatic. • Lymphadenopathy: Massive (≥10 cm), progressive, or symptomatic. • Rapid Progression: Lymphocytosis increase ≥50% over a 2-month period OR lymphocyte doubling time <6 months. • Autoimmune Issues: Anemia or thrombocytopenia not responsive to standard therapy. • Extranodal Involvement: Symptomatic or functional involvement. • Constitutional Symptoms: One or more of the following: ◦ Unintentional weight loss ≥10% over 6 months. ◦ Significant fatigue. ◦ Fevers ≥100.5°F for 2+ weeks without infection. ◦ Night sweats for >1 month without infection.


6. MANAGEMENT & TREATMENT

  1. Initial Strategy: • Watchful waiting for asymptomatic patients with low-risk features.

  2. First-line Therapies: • BTK inhibitors: ibrutinib, acalabrutinib. • BCL-2 inhibitors: venetoclax. • PI3K inhibitors: idelalisib.

  3. Advanced/High-Risk Options: • CAR-T cell therapy: for high-risk relapsed/refractory disease. • Bispecific antibodies: blinatumomab.

  4. Response Assessment (Table 112-6):Complete Response (CR) Criteria: ◦ Lymphocyte count: <4000/μL. ◦ Lymph nodes: None >1.5 cm. ◦ Spleen/Liver size: Not palpable. ◦ Bone marrow: Normocellular, <30% lymphocytes, no B lymphoid nodules. ◦ Peripheral blood counts: ◦ Platelet count >100,000/μL. ◦ Hemoglobin >11 g/dL. ◦ Neutrophils >1500/μL. • Partial Response (PR) / Stable Disease (SD): ◦ Defined by ≥50% decrease from baseline in lymphocyte count, lymph node size, or spleen/liver size. • Progression (PD): ◦ Increase ≥50% from baseline in any of the above metrics.


7. KEY PEARLS & HIGH-YIELD POINTS

Morphology: Smudge cells (basket cells) are a hallmark of CLL due to fragile cell membranes.

Immunophenotype Comparison (Table 112-2): ◦ CLL: CD5+, CD19+, CD20+ (dim), CD23+. ◦ Mantle Cell Lymphoma: CD5+, CD19+, CD20+ (mod/bright), Cyclin D1+.

Prognostic Cytogenetics: ◦ 17p deletion: Worst prognosis. ◦ 13q deletion: Best prognosis.

Treatment Goal: Achieving MRD negativity after treatment correlates with improved survival outcomes.


Reference Tables

TABLE 112-1 Recurrent Mutations in

Harrison's 22e, p.851

GENE FREQUENCY OF MUTATIONS (%
SF3B1 8–14
NOTCH1 10–13
ATM 8–11
XPO1 <5
POT1 <5
EGR2 <5

TABLE 112-2 Typical Immunophenotype of CLL Compared with Other B-Cell Malignancies

Harrison's 22e, p.852

DISEASE CD5 CD10 CD19 CD20 CD23 CYCLIN D1 SURFACE IG
CLL + + + (dim) + + (dim)
+ + + (mod/bright) +
Marginal zone lymphoma −/+ + + (mod/bright) −/+ + (mod/bright)
+ + + +

TABLE 112-4 CLL International Prognostic Index Risk Score VARIABLE TP53 status IGHV mutational status β -Microglobulin…

Harrison's 22e, p.854

Risk Score
VARIABLE ADVERSE FACTOR RISK SCORE
TP53 status Deleted or mutated 4
Unmutated
β-Microglobulin
2
concentration
>3.5 mg/L 2
Rai I–IV or Binet B–C
Age >65 years 1
Implications of Risk Score
RISK SCORE RISK CLASSIFICATION 5-YEAR SURVIVAL
(TRAINING SET DATA)
0-1 Low 93.2%
Intermediate
4-6 High 63.3%
Very high

TABLE 112-5 Criteria for the Initiation of Therapy Symptoms Indicating Need for Therapy in CLL Evidence of progressive…

Harrison's 22e, p.854

  • Symptoms Indicating Need for Therapy in CLL
  • Evidence of progressive marrow failure (worsening of anemia or
    thrombocytopenia not due to autoimmune destruction)
  • Massive (≥6 cm below costal margin), progressive, or symptomatic splenomegaly
  • Massive (≥10 cm), progressive, or symptomatic lymphadenopathy
    Progressive lymphocytosis with an increase of ≥50% over a 2-month period or
    lymphocyte doubling time <6 months
  • Autoimmune anemia or thrombocytopenia not responsive to standard therapy
    Symptomatic or functional extranodal involvement
  • Constitutional symptoms (one or more of the following: unintentional weight loss
    ≥10% over 6 months, significant fatigue, fevers ≥100.5°F for 2+ weeks without
    infection, night sweats for >1 month without infection)

TABLE 112-3 Staging of CLL Rai Staging System Low risk (stage 0) Intermediate risk (stage I/II) High risk (stage…

Harrison's 22e, p.854

Rai Staging System
Low risk (stage 0) Lymphocytosis only
Intermediate risk (stage I/II) Lymphocytosis with lymphadenopathy, with or
without splenomegaly or hepatomegaly
High risk (stage III/IV) Lymphocytosis with anemia or thrombocytopenia
due to bone marrow involvement
Binet Staging System

TABLE 112-6 Response Criteria in CLL CR

Harrison's 22e, p.856

LYMPHOCYTE
COUNT
LYMPH NODESa SPLEEN/LIVER SIZEb BONE MARROWc PERIPHERAL BLOOD COUNTS
CR <4000/μL None >1.5 cm Not palpable Normocellular, <30%
lymphocytes, no B
lymphoid nodules
• Platelet count >100,000/μL
• Hemoglobin >11 g/dL
• Neutrophils >1500/μL
Decrease ≥50%
from baseline
Decrease ≥50% from
baseline
Decrease ≥50% from
baseline
Infiltrate ≤50% of baseline
Stable disease Not meeting CR/
PR/PD criteria
Not meeting CR/PR/
PD criteria
Not meeting CR/PR/PD
criteria
Not meeting CR/PR/PD
criteria
Not meeting CR/PR/PD criteria
Increase ≥50% Increase ≥50% Increase ≥50%