Demographic:

• Most common in people aged 15-40 and >55 bimodal peak.
• Higher incidence in males

Aetiology

EBV is the common culprit in classical (not in Lymp.pred.HL)

Pathophysiology

• Random, unknown mutations in cells of lymphatic tissue and germinal centre B lymphocytes → generation of Reed-Sternberg Cells → RS cells accumulate within lymphoid tissue and secrete cytokines → Cytokines attract other reactive WBCs to form bulk of lymph node tumour → Lymph nodes enlarge → node capsule responds by laying down more connective tissue around the mass (rubbery, fixed, painless nodes)
• Reactive WBCs further support RS cell accumulation → progress by continuity to nearby LN.
• no metastasis

<aside> 💡 Only reed-Sternberg cells are malignant (more RS = more malignant)

• Contiguous spread – Staging is Important </aside>

Risk Factors

• Previous EBV infection
• HIV infection
• Higher socioeconomic status
• Autoimmune disease
• Male gender