# Hodgkin Lymphoma Pathology

> Hodgkin lymphoma in MBBS Pathology: Reed-Sternberg cells CD30 CD15, subtypes, EBV association, Ann Arbor staging and ABVD treatment.

- Canonical URL: https://prepelephant.com/topics/mbbs/pathology/hodgkin-lymphoma-pathology
- Exam / course: MBBS · Subject: Pathology
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Hodgkin Lymphoma Pathology", PrepElephant, https://prepelephant.com/topics/mbbs/pathology/hodgkin-lymphoma-pathology

## Direct answer

Reed-Sternberg cells — large, binucleate or multinucleate B-lineage giants with owl-eye nucleoli sitting in a sea of reactive lymphocytes, eosinophils and plasma cells — define classical Hodgkin lymphoma, a bimodally distributed disease of young adults and the over-55s. The tumour cell population is tiny; the bulk of the mass is cytokine-attracted inflammatory tissue, which is why the pathology reads as much like an inflammation as a cancer. Immunophenotyping carries the diagnosis: CD30 and CD15 positive, CD20 weak or negative, CD45 negative, PAX5 characteristically dim. Nodular sclerosis dominates in young women with mediastinal masses; mixed cellularity, the most EBV-associated subtype, is the commonest form in Indian children; nodular lymphocyte-predominant disease stands apart with popcorn cells and a CD20-positive, CD30-negative profile.

## What you must remember

- **Reed-Sternberg immunophenotype:** CD30 strong, CD15 positive, CD45 negative, CD20 weak or absent, PAX5 dim but retained — the pattern that separates classical Hodgkin from every mimic.
- **The background teaches the biology:** eosinophils follow interleukin-5, fibrosis follows cytokine-driven fibroblast activation, and B symptoms reflect cytokine surge — the tumour is a minority in its own mass.
- **Subtype map:** nodular sclerosis (most common overall — young women, mediastinal disease, lacunar cells, collagen bands); mixed cellularity (older patients, strongest Epstein-Barr virus association, commonest in Indian children and in HIV); lymphocyte-rich (best prognosis among classical types); lymphocyte-depleted (worst, elderly and HIV).
- **Nodular lymphocyte-predominant Hodgkin lymphoma:** popcorn (L and H) cells, CD20 strongly positive, CD15 and CD30 negative, CD45 positive; indolent, treated like low-grade B-cell non-Hodgkin lymphoma, rarely B symptoms.
- **Epstein-Barr virus:** latent membrane protein-1 demonstrable in Reed-Sternberg cells in a large share of classical cases — more than half in Indian paediatric and mixed-cellularity series.
- **Contiguous spread:** Hodgkin lymphoma predictably involves adjacent lymph node groups, unlike the disparate-pattern spread of non-Hodgkin lymphoma — the biological basis of involved-field radiotherapy.
- **Staging and treatment:** Ann Arbor stages I-IV with A or B suffix (fever, drenching night sweats, over 10% weight loss in six months); ABVD (adriamycin, bleomycin, vinblastine, dacarbazine) cures most early-stage disease, with positron-emission tomography adapting intensity.

## A neck node that needs more than FNAC

A 23-year-old presents with a painless, rubbery left supraclavicular node and drenching night sweats. The first Indian error is repeating fine-needle aspirations: cytology may show Reed-Sternberg-like cells, but lymphoma diagnosis demands architecture — nodular sclerosis's collagen bands and the topography of tumour against background — so excision biopsy of the whole node is the standard. Immunohistochemistry follows: CD30 and CD15 positivity with dim PAX5 confirms classical Hodgkin lymphoma, nodular sclerosis type. Staging then anchors on the contiguous-spread rule: positron-emission tomography-computed tomography from neck to pelvis, with marrow biopsy now reserved for selected cases. Ann Arbor stage IIB with a mediastinal mass brings typically four to six cycles of ABVD with involved-field radiotherapy, and cure is the expectation — with late-effect counselling (bleomycin lung fibrosis, anthracycline cardiomyopathy, secondary malignancies after radiotherapy) that modern de-escalation trials chase. The lesson the case teaches is procedural: the biopsy, not the aspiration, makes this diagnosis.

## Markers that settle the cell

Vivas ask why Reed-Sternberg cells stain weakly for PAX5 yet lose every other B-cell marker: the cell is a crippled germinal-centre B cell that has downregulated its lineage transcription while retaining just enough PAX5 to betray origin. Reed-Sternberg-like cells appear in infectious mononucleosis, anaplastic large cell lymphoma and even carcinoma — only the full marker panel plus background converts a lookalike into a diagnosis. And in the CD30 era, brentuximab vedotin targets exactly the marker classical Hodgkin lymphoma cannot hide.

## Frequently asked questions

### What is the immunophenotype of the Reed-Sternberg cell?

CD30 strongly positive, CD15 positive, CD45 negative, CD20 weak or negative, with characteristically dim PAX5 — a B-cell origin betrayed by the weakest of stains.

### Which subtype is most common in young adults?

Nodular sclerosis classical Hodgkin lymphoma — young women, mediastinal bulk, lacunar cells and collagen banding.

### Which subtype carries the strongest Epstein-Barr virus association?

Mixed cellularity, the dominant subtype in Indian children and in HIV infection; latent membrane protein-1 is demonstrable in the tumour cells.

### What constitutes B symptoms in the Ann Arbor system?

Unexplained fever, drenching night sweats and loss of more than 10% body weight over six months — each worsens stage and steers treatment intensity.

### Why is excision biopsy preferred over fine-needle aspiration in suspected lymphoma?

Lymphoma diagnosis requires nodal architecture and full immunohistochemical context, both destroyed or absent in aspirated cytology — repeating FNAC only delays the tissue answer.