TextbookHaematologyHodgkin Lymphoma

Hodgkin Lymphoma

Lymphoid neoplasm characterised by Reed-Sternberg cells in a reactive inflammatory background. Highly curable with chemotherapy ± radiotherapy. Bimodal age distribution with peaks at 20–30 and >60 years.

Key Facts

Reed-Sternberg cells: large binucleated cells ('owl-eye' appearance) — pathognomonic; CD15+ and CD30+ Bimodal age distribution: peak 20–30 years and >60 years Painless cervical/supraclavicular lymphadenopathy: most common presentation (~70% cervical) B symptoms: fever >38°C, drenching night sweats, weight loss >10% in 6 months (important for staging and prognosis) Contiguous spread: spreads to adjacent lymph node groups (unlike NHL which is non-contiguous) Treatment: ABVD (doxorubicin, bleomycin, vinblastine, dacarbazine) ± radiotherapy; ~85–90% cure rate overall PET-CT: essential for staging (Ann Arbor + Lugano) and response assessment (interim PET guides therapy) Alcohol-induced lymph node pain: rare but classic symptom; mechanism unclear

Overview

Key Facts

Hodgkin lymphoma (HL) is a lymphoid neoplasm characterised by the presence of Reed-Sternberg cells within a reactive inflammatory background. It is one of the most curable cancers.

Epidemiology

  • ~2,000 new cases/year in the UK
  • Bimodal: peak 20–30 years, second peak >60 years
  • Slight male predominance
  • EBV-associated in ~40% of classical HL

Aetiology

  • EBV: detected in ~40% of HL (higher in mixed cellularity subtype)
  • Immunosuppression: HIV, post-transplant
  • Genetic: slightly increased risk in siblings

Pathophysiology

  • Reed-Sternberg cells are derived from germinal centre B cells
  • RS cells secrete cytokines → recruit reactive inflammatory infiltrate (T cells, eosinophils, histiocytes)
  • RS cells constitute <1% of tumour mass; the rest is reactive
  • Classical HL (95%): nodular sclerosis (most common), mixed cellularity, lymphocyte-rich, lymphocyte-depleted
  • Nodular lymphocyte-predominant HL (5%): LP cells ('popcorn cells'), CD20+, indolent

Clinical Presentation

Typical Presentation

  • Painless lymphadenopathy: cervical (~70%), mediastinal, axillary
  • Nodes: rubbery, non-tender
  • Mediastinal mass (bulky): especially nodular sclerosis subtype

B Symptoms (~30–40%)

  • Fever >38°C (Pel-Ebstein fever: cyclical, rare but classic)
  • Drenching night sweats
  • Weight loss >10% in 6 months

Other

  • Alcohol-induced lymph node pain (rare but specific)
  • Pruritus (sometimes severe)
  • Fatigue

Red Flags

  • Mediastinal mass with SVC obstruction
  • Progressive lymphadenopathy with B symptoms
  • Young adult with unexplained lymphadenopathy >2 weeks

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
NHLNon-contiguous spread, various subtypes, may be extranodalExcision biopsy, flow cytometry
Reactive lymphadenopathyTender, often cervical, associated infectionClinical, biopsy if persistent
TB lymphadenitisCaseating granulomata, matted nodes, systemic featuresAFB, culture, biopsy
SarcoidosisBHL, non-caseating granulomata, hypercalcaemiaACE, biopsy
Metastatic carcinomaHard, fixed nodes, primary tumourBiopsy, CT

Diagnosis / Investigation

Bloods

  • FBC: may be normal; eosinophilia, lymphopenia
  • ESR: elevated (prognostic; >30 mm/hr is adverse)
  • LDH: prognostic marker
  • Albumin: low = adverse
  • LFTs, U&Es: baseline
  • HIV: screen

Biopsy

  • Excision lymph node biopsy: ESSENTIAL (core biopsy may be inadequate)
  • Reed-Sternberg cells: CD15+, CD30+, CD20-/weak, CD45-
  • Nodular lymphocyte-predominant: LP cells, CD20+, CD15-, CD30-

Staging (Ann Arbor/Lugano)

  • PET-CT: gold standard for staging
    • Stage I: single lymph node region
    • Stage II: ≥2 regions, same side of diaphragm
    • Stage III: both sides of diaphragm
    • Stage IV: diffuse extranodal involvement (liver, bone marrow)
    • Add 'A' (no B symptoms) or 'B' (B symptoms present)
    • 'X' or 'bulky' if >10cm mass

Fertility

  • Semen cryopreservation / oocyte preservation BEFORE chemotherapy

Management

Early Stage (I/II) — Favourable

  • ABVD × 2–4 cycles + involved-field radiotherapy (IFRT)
  • ~95% cure rate

Early Stage — Unfavourable

  • ABVD × 4–6 cycles ± IFRT

Advanced Stage (III/IV)

  • ABVD × 6 cycles (standard)
  • Escalated BEACOPP × 6: more intensive; higher response but more toxicity (used in some centres for high-risk)
  • PET-adapted: interim PET after 2 cycles guides therapy (if PET-negative, may omit bleomycin — RATHL trial)

Relapsed/Refractory

  • Salvage chemotherapy (DHAP, ICE, GDP) → autologous SCT (~50% cure in relapse)
  • Brentuximab vedotin (anti-CD30 ADC): post-ASCT consolidation or relapsed HL (NICE TA524)
  • Pembrolizumab/nivolumab (anti-PD-1): relapsed after ASCT + brentuximab (NICE TA540)

Supportive

  • Fertility preservation before treatment
  • Bleomycin lung toxicity monitoring (PFTs)
  • Long-term follow-up: second cancers, cardiac disease, thyroid dysfunction

Referral Criteria

  • Haematology/oncology: urgent for suspected lymphoma
  • 2-week-wait referral: unexplained lymphadenopathy

Prognosis

  • Overall cure rate: ~85–90%
  • Early stage favourable: >95% cure
  • Advanced stage: ~75–85% cure with ABVD
  • Relapsed after ASCT: ~50% salvage with brentuximab/checkpoint inhibitors
  • Late effects in survivors: secondary malignancy (breast, lung — 10–20 years), cardiac disease (anthracycline, radiotherapy), hypothyroidism, infertility
  • Long-term survival: requires lifelong surveillance for late complications

Other Relevant Information

IPS-7 (International Prognostic Score for Advanced HL)

Factor (1 point each)Adverse
Age >45Adverse
Male sexAdverse
Stage IVAdverse
Hb <105 g/LAdverse
Albumin <40 g/LAdverse
WCC ≥15 × 10⁹/LAdverse
Lymphocytes <0.6 × 10⁹/L or <8%Adverse
Score 0–1: ~90% 5-year PFS; Score ≥4: ~60% 5-year PFS