1. Non Hodgkin’s lymphoma
Rakesh Biswas
MD, Professor, Department of Medicine, People's College of Medical Sciences, Bhanpur, Bhopal, India

5. Staging
Stage I : Involvement of single LN region (I) or extra lymphatic site (IAE )
Stage II : Two or more LN regions involved (II) or an extra lymphatic site and lymph node regions on the same side of diaphragm
Stage III : Involvement of lymph node regions on both sides of diaphragm, with (IIIE) or without (III) localized extra lymphatic involvement or involvement of the spleen (IIS) or both (IISE)
Stage IV : Involvement outside LN areas (Liver, bone marrow)
A : Absence of ‘B’ symptoms
B : B symptoms present

7. Non Hodgkin’s lymphoma
Incidence is increasing
NHL>HD
Median age of presentation is yrs
M>F
More often clinically disseminated at diagnosis
B-cell-70% ; T-cell-30%

8. Clinical features Widely disseminated at presentation
Nodal involvement: Painless lymphadenopathy, often cervical region is the most common presentation
Hepatospleenomegaly
Extranodal : Intestinal lymphoma ( abdominal pain, anemia, dysphagia); CNS ( headache, cranial nerve palsies, spinal cord compression) ;
Skin, Testis; Thyroid; Lung Bone marrow (low grade): Pancytopenia

9. Clinical features contd
Systemic symptoms
Sweating, weight loss, itching
Metabolic complications: hyperuricemia, hypercalcemia, renal failure
Compression syndrome:
Gut obstruction
Ascites
SVC obstruction
S/C Compression

10. Classification REAL Clinical / Working Formulation Low grade
Intermediate grade
High grade

11. Classification Low grade Proliferation: Low Course: Indolent
Symptoms: ve
Treatment: Not curable
High grade
High
Rapid, fatal(un-Rx)
+ve
Potentially Curable

12. Etiology Cannot be attributed a single cause
Chromosomal translocations: t (14, 18)
Infection:
Virus:EBV, HTLV,HHV-8, HIV
Bacteria: H.Pylori - Gastric lymphoma
Immunology:
Congenital immunodeficiency,
Immunocompromised patients - HIV, organ transplantation

13. Management Low grade: Asymptomatic : No treatment ;
Radiotherapy for localised disease (Stage 1);
Chemotherapy: mainstay is Chlorambucil; Initial response good , but repeated relapses, median survival 6-10 yrs;
Newer: Fludarabine, 2-CdA (Chlorodeoxyadenosine)
Monoclonal antibody: Rituximab
SCT/BMT
All cells have protein markers on their surface, known as antigens. Monoclonal antibodies are designed in the laboratory to specifically recognise particular protein markers on the surface of some cancer cells. The monoclonal antibody then 'locks' onto this protein. This either triggers the cell to destroy itself or signals to the body's immune system to attack and kill the cancer cell.
For example, rituximab, the monoclonal antibody that is used in the treatment of non-Hodgkin's lymphoma, recognises a protein marker known as CD20. CD20 is found on the surface of the abnormal B cells that are found in some of the most common types of non-Hodgkin's lymphoma.
When rituximab locks onto CD20 on the surface of a B cell, the cell may be destroyed directly, but also the body's natural defences are alerted. Rituximab effectively targets the lymphoma cells for destruction by the body's immune system, which can now kill the cancer cells.
CD20 is also found on the surface of normal B cells, one of the types of white blood cells that circulate in the body. This means that these normal B cells, too, may be destroyed when rituximab is used. However, the stem cells in the bone marrow that develop into B cells do not have CD20 on their surface.
Stem cells are therefore not destroyed by rituximab and can go on to replenish the body with healthy B cells. Although the number of mature, normal B cells is temporarily reduced by the treatment, they return to previous levels after the treatment.

14. Aggressive ( high / intermediate grade):
Chemotherapy: mainstay CHOP every 3 weeks, at least 6 cycles Cyclophosphamide, Doxorubicin Hydrochloride, Vincristine, Prednisolone

15. High risk cases with poor prognostic factors or relapse : High dose chemotherapy combined with autologous BMT / SCT
Monoclonal antibody
With CNS involvement / leukemic relapse : Similar to ALL

16. Prognosis Low grade : Median survival –10 yrs High Grade:
Increasing age, advanced stage, concomitant disease, raised LDH,T- cell phenotype : Poor prognosis