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Hodgkin’s
lymphoma

 Dr.Prashant kumbhaj
 SMS Medical College
        Jaipur
Lymphoma
 Clonalmalignant disorders that are derived
 from lymphoid cells: either precursor or
 mature T-cell or B-cell

 Majority   are of B- cell origin

 Dividedinto 2 main types :
1. Hodgkin’s lymphoma
2. Non - Hodgkin’s lymphoma
Hodgkin’s             Disease
 Histologically
               & clinically a distinct
  malignant disease
 Predominantly, B-cell disease
 Course of the disease is variable,
           but the prognosis has improved
  with modern treatment
Etiology


   Infection – EBV,HIV

 Higher   social class,advanced education



   Environmental factors
WHO Classification
 Classic:(CD   15+,CD30+)
   Nodular Sclerosis-70%,Adolesent and young
    adults,mediastinal mass
   Lymhocyte rich-10%
   Mixed Cellularity-20%,young children,
   Lymhocyte depleted-<5%,mostly in AIDS,B
    symptoms ,worst prognosis

 Non-Classic
   NodularLymphocyte predominant
   Best OS,B Symptoms <10%
HISTOLOGY
 Diagnosis   of HL depends on RS
  cells(reedsternberg cells )
 Bulk of lymphatic tissue is not composed
  of malignent cells but rather a vareity of
  normal appearing lymphocytes ,plasma
  cells ,eosinophils ,neutrophils,histiocytes.
 Importent varient of reedsternberg cells
  includes L&H(lymphocyte and
  histiocyte)cells,lacunar cells,RS like cells.
 Reed  sternberg cells are giant cells with
  binucleate and large cytoplasmic
  eosinophilic inclusions
 CD 15+, CD30+
Clinical features
 Bimodal    age distribution :
     young adults ( 20-30 yrs) & elderly (> 50yrs)
      May occur at any age
M  >F
 Lymphadenopathy:
   most  often cervical region
   asymmetrical, discrete
   painless, non-tender
   elastic character on palpation ( rubbery)
   not adherent to skin
   fluctuate in size
MODE OF SPREAD
 HL  always almost originate in a lymph
  node
 It spreads in orderly fashion through
  lymphatic system by contiguity
 Axial lymphatic system is always involved
  whereas distal sites (epitrochiliar
  ,popliteal) rarely involved.
 Hematogenous involvement occurs late
  and is common in LD type .
 Contiguous  spread via the lymphatic chain
  eg.involvement of abdominal & thoracic
  LNs
 Extra nodal disease - rare
 Hepatospleenomegaly
Sites of involvment
 Peripheral lymph node-Cervical or
  Supraclavicular lymphadenopathy occurs
  in >70% of cases .axillary and inguinal
  lymph nodes are less frequently involved .
 Generalized lymphadenopathy is atypical
  of HL
 Spleen ,splenic hilar nodes,and celiac
  nodes are the earliest abdominal sites of
  invovlement in infradiaphragmatic HL.
  Mesentric lymph nodes are rarely involved
Thorax
 Ant   mediastinum is primary location for NS
  HL
 Lung involvement may occur by direct
  contiguity with hilar involvement as well as
  hematogenous invovlement .
 Plural effusion may occur by lymphatic
  compression
 SVC is more common in NHL
Abdominal
 Spleen  ,splenic hilar nodes ,celiac nodes
 are the earliest sites of invovment in
 abdomen
 Mesentric lymph nodes are rarely
 involved.
 Liver involvement is uncommon at
 diagnosis and is always almost associated
 with infiltration of the spleen.
 Retero  peritoneal lymph node involvement
  occurs late in the course of
  supradiagphramatic HL and after
  spleen,splenic hilar nodes and celiac
  nodal involvement .
 Bone marrow- rarely involved at the time
  of diagnosis ,pt with advanced stage and
  systemic symptoms ,LD,MC are common
  types of bone marrow involvement .
 Constitutional  symptoms ( B symptoms )
   Night sweats,
   sustained fever > 38 degree celsius,
   loss of weight >10% of body weight in 6
    months
 Fever sometimes cyclical (‘Pel-Ebstein fever’)
 Pain at the site of disease after drinking
  alcohol
 Pallor
 Pruritis
 Symptoms of Bulky (>10 cm) disease
Extranodal
 Liverand skin involvement is rare
 CNS involvement uncommon
 No involvement of meninges ,brain
  ,waldeyars ring.
Investigations
 CBC  :
  Anemia ( normochromic / normocytic), eosinophilia,
  neutrophilia, lymphopenia
 ESR -raised
 LFT- (liver infil / obs at porta hepatis)
 RFT- prior to treatment
 Urate , Ca,
 LDH - adverse prognosis
 CXR- mediastinal mass
 CT thorax / abdomen / pelvis-for staging
 Other: Gallium scan, PET, Lymphangiography ,
  Laporotomy
 LN   FNAC / biopsy :

   Malignant REED-STERNBERG ( RS) Cell: Bi-
   nucleate cell with a prominent nucleolus. Derived
   from B cell, at an early stage of differentiation

   Reactive
           background of eosinophils,
   lymphocytes, plasma cells

   Fibrous   tissue
REED-STERNBERG ( RS ) Cell
REED-STERNBERG ( RS) Cell
>10 cm




Bulky disease
An Arbor 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
Adverse prognostic factors
 Male sex
 Age >45yrs
 Stage IV
 Hemoglobin<10.5g/dl
 WBC count >15,000/ul
 Lymphocyte count <600/ul
 Serum albumin <4g/dl
Treatment

 RT
 Chemo
 BMT   / SCT

 Supportive
Treatment - Guidelines
 Indicationsfor RT:
   Stage I disease
   Stage II disease with 3 or lesser areas involved
   For Bulky disease
   For pressure problems


 Indications for CT
   All with B symptoms
   Stage II disease with >3 areas involved
   Stage III and IV disease
Treatment
 Stage   IA , Stage IIA with 3 or < 3 areas involved:
 ABVD X 4 CYCLES WITH IFRT(CLASSICAL HL)
 NLPHL – IFRT ALONE ,OBSERVATION(IF PT
 CANNOT TOLERATE RT)


 Stage   IB, Stage II A with > 3 areas , Stage IIB:

 ChemotherapyABVD every 3-4 weeks, 6
 cycles; either alone, or in combination with
 radiotherapy

 Stage
     III & IV :
 Chemotherapy + Radiotherapy ( for bulky
Irradiation fields used in Hodgkin’s Lymphoma
Chemotherapy
 MOPP     :
                            Nitrogen Mustard,
 Vincristine (Oncovin),
 Procarbazine,
           Prednisolone


 ABVD:
      Adriamycin,
                         Bleomycin,
                                Vinblastine,
                                  Dacarbazine

 Higher   dose for relapse or younger pts with poor
Prognosis

 Overall   10 yr survival – 80%

 In   long term survivors there is a risk of
   secondary  malignancy: (leukemia , NHL), Solid
                           (
    tumors- Lung, breast
   Infections
   Cardiac, pulmonary, endocrinal abnormalities
Side effects of treatment

 HYPOTHYROIDISM
 STERLILITY
 LUNG DAMAGE
 BLEOMYCIN PULMONARY TOXICITY
 CARDIAC DAMAGE
 ASEPTIC NECROSISOF FEMORAL
  HEADS
 DEPRESSED CELLULAR IMMUNITY
 SECONDARY   NEOPLASM –
  AML,NHL,EPITHELIAL TUMORS
  ,SARCOMAS ,
 NEUROLOGIC COMPLICATIONS
 RETROPERITONEAL FIBROSIS
 NEPHROTIC SYNDROME
 ICHTHYOSIS

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Hodgkin lymphoma

  • 1. Hodgkin’s lymphoma Dr.Prashant kumbhaj SMS Medical College Jaipur
  • 2. Lymphoma  Clonalmalignant disorders that are derived from lymphoid cells: either precursor or mature T-cell or B-cell  Majority are of B- cell origin  Dividedinto 2 main types : 1. Hodgkin’s lymphoma 2. Non - Hodgkin’s lymphoma
  • 3. Hodgkin’s Disease  Histologically & clinically a distinct malignant disease  Predominantly, B-cell disease  Course of the disease is variable, but the prognosis has improved with modern treatment
  • 4. Etiology  Infection – EBV,HIV  Higher social class,advanced education  Environmental factors
  • 5. WHO Classification  Classic:(CD 15+,CD30+)  Nodular Sclerosis-70%,Adolesent and young adults,mediastinal mass  Lymhocyte rich-10%  Mixed Cellularity-20%,young children,  Lymhocyte depleted-<5%,mostly in AIDS,B symptoms ,worst prognosis  Non-Classic  NodularLymphocyte predominant  Best OS,B Symptoms <10%
  • 6. HISTOLOGY  Diagnosis of HL depends on RS cells(reedsternberg cells )  Bulk of lymphatic tissue is not composed of malignent cells but rather a vareity of normal appearing lymphocytes ,plasma cells ,eosinophils ,neutrophils,histiocytes.  Importent varient of reedsternberg cells includes L&H(lymphocyte and histiocyte)cells,lacunar cells,RS like cells.
  • 7.  Reed sternberg cells are giant cells with binucleate and large cytoplasmic eosinophilic inclusions  CD 15+, CD30+
  • 8. Clinical features  Bimodal age distribution :  young adults ( 20-30 yrs) & elderly (> 50yrs) May occur at any age M >F  Lymphadenopathy:  most often cervical region  asymmetrical, discrete  painless, non-tender  elastic character on palpation ( rubbery)  not adherent to skin  fluctuate in size
  • 9. MODE OF SPREAD  HL always almost originate in a lymph node  It spreads in orderly fashion through lymphatic system by contiguity  Axial lymphatic system is always involved whereas distal sites (epitrochiliar ,popliteal) rarely involved.  Hematogenous involvement occurs late and is common in LD type .
  • 10.  Contiguous spread via the lymphatic chain eg.involvement of abdominal & thoracic LNs  Extra nodal disease - rare  Hepatospleenomegaly
  • 11. Sites of involvment  Peripheral lymph node-Cervical or Supraclavicular lymphadenopathy occurs in >70% of cases .axillary and inguinal lymph nodes are less frequently involved .  Generalized lymphadenopathy is atypical of HL  Spleen ,splenic hilar nodes,and celiac nodes are the earliest abdominal sites of invovlement in infradiaphragmatic HL. Mesentric lymph nodes are rarely involved
  • 12. Thorax  Ant mediastinum is primary location for NS HL  Lung involvement may occur by direct contiguity with hilar involvement as well as hematogenous invovlement .  Plural effusion may occur by lymphatic compression  SVC is more common in NHL
  • 13. Abdominal  Spleen ,splenic hilar nodes ,celiac nodes are the earliest sites of invovment in abdomen  Mesentric lymph nodes are rarely involved.  Liver involvement is uncommon at diagnosis and is always almost associated with infiltration of the spleen.
  • 14.  Retero peritoneal lymph node involvement occurs late in the course of supradiagphramatic HL and after spleen,splenic hilar nodes and celiac nodal involvement .  Bone marrow- rarely involved at the time of diagnosis ,pt with advanced stage and systemic symptoms ,LD,MC are common types of bone marrow involvement .
  • 15.  Constitutional symptoms ( B symptoms ) Night sweats, sustained fever > 38 degree celsius, loss of weight >10% of body weight in 6 months  Fever sometimes cyclical (‘Pel-Ebstein fever’)  Pain at the site of disease after drinking alcohol  Pallor  Pruritis  Symptoms of Bulky (>10 cm) disease
  • 16. Extranodal  Liverand skin involvement is rare  CNS involvement uncommon  No involvement of meninges ,brain ,waldeyars ring.
  • 17. Investigations  CBC : Anemia ( normochromic / normocytic), eosinophilia, neutrophilia, lymphopenia  ESR -raised  LFT- (liver infil / obs at porta hepatis)  RFT- prior to treatment  Urate , Ca,  LDH - adverse prognosis  CXR- mediastinal mass  CT thorax / abdomen / pelvis-for staging  Other: Gallium scan, PET, Lymphangiography , Laporotomy
  • 18.  LN FNAC / biopsy :  Malignant REED-STERNBERG ( RS) Cell: Bi- nucleate cell with a prominent nucleolus. Derived from B cell, at an early stage of differentiation  Reactive background of eosinophils, lymphocytes, plasma cells  Fibrous tissue
  • 21.
  • 23. An Arbor 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
  • 24.
  • 25. Adverse prognostic factors  Male sex  Age >45yrs  Stage IV  Hemoglobin<10.5g/dl  WBC count >15,000/ul  Lymphocyte count <600/ul  Serum albumin <4g/dl
  • 26. Treatment  RT  Chemo  BMT / SCT  Supportive
  • 27. Treatment - Guidelines  Indicationsfor RT:  Stage I disease  Stage II disease with 3 or lesser areas involved  For Bulky disease  For pressure problems  Indications for CT  All with B symptoms  Stage II disease with >3 areas involved  Stage III and IV disease
  • 28. Treatment  Stage IA , Stage IIA with 3 or < 3 areas involved: ABVD X 4 CYCLES WITH IFRT(CLASSICAL HL)  NLPHL – IFRT ALONE ,OBSERVATION(IF PT CANNOT TOLERATE RT)  Stage IB, Stage II A with > 3 areas , Stage IIB: ChemotherapyABVD every 3-4 weeks, 6 cycles; either alone, or in combination with radiotherapy  Stage III & IV : Chemotherapy + Radiotherapy ( for bulky
  • 29. Irradiation fields used in Hodgkin’s Lymphoma
  • 30. Chemotherapy  MOPP : Nitrogen Mustard, Vincristine (Oncovin), Procarbazine, Prednisolone  ABVD: Adriamycin, Bleomycin, Vinblastine, Dacarbazine  Higher dose for relapse or younger pts with poor
  • 31. Prognosis  Overall 10 yr survival – 80%  In long term survivors there is a risk of  secondary malignancy: (leukemia , NHL), Solid ( tumors- Lung, breast  Infections  Cardiac, pulmonary, endocrinal abnormalities
  • 32. Side effects of treatment  HYPOTHYROIDISM  STERLILITY  LUNG DAMAGE  BLEOMYCIN PULMONARY TOXICITY  CARDIAC DAMAGE  ASEPTIC NECROSISOF FEMORAL HEADS  DEPRESSED CELLULAR IMMUNITY
  • 33.  SECONDARY NEOPLASM – AML,NHL,EPITHELIAL TUMORS ,SARCOMAS ,  NEUROLOGIC COMPLICATIONS  RETROPERITONEAL FIBROSIS  NEPHROTIC SYNDROME  ICHTHYOSIS