�ݺ�ߣ

MALIGNANT
LYMPHOMAS
Dr. S. Ocheni MB;BS (Ibadan), FMCPath.
Dr. Nwabueze MBBS{Nig} ]

INTRODUCTION
• Lymphomas are a heterogenous group of tumors arising in
the reticuloendothelial and lymphatic system.
• Lymphomas - heterogenous grp of malignant neoplasms of
the immune system arising from cells of the lymphoid
series, mononuclear phagocytes, and reticular cells which
make up the lymphatic system

THE LYMPHATIC
SYSTEM
• The Lymphatic system helps filter out bacteria and is
important in fighting disease
• The lymph vessels often widen into lymph nodes
• Because there is lymph tissue in many parts of the body,
lymphomas can start in almost any organ of the body
• Clusters of lymph nodes connected to each other and to the
spleen, thymus, and parts of the tonsils, stomach and small
intestine by a network of vessels.

CELLS IN THE
LYMPHATIC SYSTEM
• Lymphocytes
• Histiocytes
• Reticular cells

TYPES OF LYMPHOMAS
• Lymphoma is differentiated by
• The Cell type [the type of cell that multiplies] and
• Presentation. [how the cancer presents itself.]
• Broadly classified into
•Hodgkin lymphoma and
•Non-Hodgkin’s lymphoma (NHL)
based on the histological presence of Reed-Sternberg
(RS) cells in Hodgkin lymphoma.

DIFFERENCES BWN HL AND NHL
Parameter HL NHL
1 Reed – Stenberg giant cells Present Absent
2 Age Bimodal - 1st Peak 15-40yrs, 2nd peak > 60yrs >50yrs
3 Sex (M : F) 1.4:1 [5:1 in children] 1.7:1
4 Stage at presentation Early [1&11] Late [III & IV]
5 Symptoms & Signs 25-40% have B symptoms and signs 15% have B symptoms and signs
6 Site of Origin 90% Nodal 80% Nodal, 20% Extra-Nodal
7 Nodal Involvement Localized to a specific group of nodes Usually deiminated among >1 nodal group
8 Lymph node consistency Firm and Robbery Soft and Not Robbery
9 Spread Predictable to contigous lymph nodes Random spread
10 Hematogenous Spread Rare Common
11 Mediastinal Mass 50% 20%
12 Waldeyer’s ring and
Mesenteric Nodes
Usually does not involve Commonly affects Mesenteric nodes.
May affect Waldeyer’s ring
13 Extra nodal involvement Infrequent [CNS, BM, GIT, Liver involvement] Frequent
14 Leukemic Phase Rare Very common
15 Superior vena cava obstruction Rare Common
15 Histology Class in Children Usually one with favorable prognosis Usually aggressive

DIFFERENCES BWN HL AND NHL
S/No Parameter HL NHL
7 Leukaemic phase Rare Very common
8 Site(s) of origin >95% primarily nodal
in origin
80% nodal
20% extranodal
9 Haematogenous spread Rare Common
10 Trochlear, Mesenteric or pharyngeal
lymph nodes
Rare Very Common
11 Mediastinal involvement 50% 20%
12 CNS Disease Rare Common

DIFFERENCES BWN HD AND NHL
S/No Parameter HL NHL
13 Bone Marrow
involvement
<10% 70%
14 GIT and Liver
involvement
Rare Common
15 Consistency of lymph
nodes
Firm and Rubbery Soft and not rubbery
16 Superior vena cava
obstruction
Rare Common
17 Curability by
chemotherapy
Yes Some eg Burkitt’s
lymphoma

Hodgkin lymphoma
• Hodgkin lymphoma is a localized or disseminated
proliferation of cells o f the lymphoreticular system
primarily involving the lymph nodes, spleen, liver
and bone marrow.
• 1st
of the lymphomas to be recognized
• 1832: 1st
described by Thomas Hodgkin
• 1856: Samuel Wilks 1st
used the term HD
• Sternberg in 1898 and Reed in 1902 described the distinctive
histologic features of HD, in particular: the Reed-Sternberg
giant cell.

THE REEDSTERNBERG GIANT CELL
• The Reedsternberg giant cell is the morphologic diagnostic hall
mark of HL, required for the diag. of HL
• diameter ≈14-40 microns
• Normal B cell diameter 8-10 microns
• Plasma cell diameter – 14-20 microns
• irregular in shape
• multi-lobed nucleus
• clumped chromatin pattern in the nucleus with large nucleoli
• Abundant acidophilic cytoplasm
• Believed to be of B-cell origin

EPIDEMIOLOGYOF HL
• 1% of cancer registrations per annum.
• Annual incidence ≈ 3 per 100,000 in Europe and USA
• Higher incidence in males
• 1.4:1 – Adult
• 5:1 - Children
• Almost always nodal in origin
• Centripetal (axial) contiguous nodal spread.
• Nodular Sclerosing HD is most common subtype in young
adults
• Bimodal age incidence
 1st peak 15-40 yrs
 2nd peak > 60yrs

AETIOLOGY & PATHOGENESIS OF HL
Predisposing Factors:
 Male sex
 Genetic susceptibility
 Family History
 Certain HLA types
 Jewish race – suggesting genetic susceptibility
 Occupational exposure
 Wood dust
 Benzene
 Nitrous Oxide
 Immunosuppression
 Post transplant taking Immunosuppressant
 Congenital immunodeficiency
 Klinifelters
 Ataxia telangiectasia
 Chediak Higashi Syndrome
 Wiskott-Aldrich
 Infections
 Ebstein Barr Virus (EBV)
 Mycobacterium TB
 Herpesvirus 6
 HIV
 Certain Autoimmune disorders
 RA, SLE,
 Celiac disease
 Sjogren syndrome
• Most patients develop a slowly
progressive defect in cell mediated
immunity [T-Cell function] that in
advanced disease contribute to
common bacterial and unusual fungal,
viral and protozoal infections.
• Humoral Immunity is depressed in
advanced disease.
• Death can result from infection or
progressive disease.

CLINICAL FEATURES OF HL
 Painless supradiaphragmatic lymph node swelling - most common presentation
 Painless cervical or axillary lymphadenopathy
 Pain rarely may occur immediately after alcoholic beverages.
 [Alcohol induced lymph node pain (most probably as a result of vasodilatation
 May be solitary and rubbery
 Lymphadenopathy may wax and wane (decreasing and increasing in size spontaneously)
 Contiguous centripetal spread through RES
 Intense Pruritus [Not amenable to usual therapies]
 Constitutional or B Symptoms
 Fever
 Occasionally Pel Epstein type [Few days of high fever alternating with a few days to several weeks of normal or subnormal temperature
 Night sweats
 Anorexia, Malaise
 Weight loss [>10% of BW in 6months], Suggestive of Internal lymph node involvement.
 Cachexia – Advanced disease.
 Spleen involved in 50% of cases[Splenomegaly], Liver involvement less frequent.
 Abdominal lymphadenopathy is unusual without splenic involvement
 Bone involvement
 Common - Asymptomatic, Vertebral osteoblastic lesions [ivory vertebrae]
 Rare – Pain with osteolytic lesions and compression vertebral fractures

CLINICAL FEATURES OF HL
 Waldeyer’s ring involvement is rare and suggests a diagnosis of NHL
 Local compression symptoms
 Jaundice – Intrahepatic or extrahepatic bile duct obstruction
 Leg edema – (lymphedema) – Pelvic lymp hnode obstruction
 Severe dyspnea and Wheezing – Tracheobronchial compression due to mediastinal disease
 Lung cavitation or Mass – Infiltration of lung parenchyma. May result in Lobar consolidation
or bronchopneumonia.
 Pleural effusion or superior vena cava obstruction.
 Paraplegia – Cord compression following epidural invasion have been reported.
 Horner’s syndrome – Cervical sympathetic compression
 Laryngeal paralysis 0 Recurrent laryngeal nerve compression
 Neuralgic pain – Nerve root compression.

Subtype Incidence/Epidemiology Sites Prognosis
NLPHL 3% CD15-
CD30-
CD20+
EMA+
Nodular.
Few
Neoplastic
cells.
Many B
M:F (3:1), unimodal peak in
4th
decade, also occurs in
children
Peripheral LN; single node
rather than group of nodes
Good response to Rx,
slow progression,
frequent relapses, may
‘progress’ to THRBCL
or DLBCL
LRCHL 3% CD15+
CD30+
CD20-
Few RS
Many B
M:F (2:1) Peripheral LN Usually low stage, good
prognosis, infrequent
relapses
MCCHL 25% CD15+
CD30+
CD20-
Mod RS
Mod B
Infiltrates
M:F (2:1), Developing
countries, young children
and older adults, HIV, B-
symptoms
Peripheral LN, spleen,
advanced stage
Prognosis intermediate
between LRHL and
LDHL
LDCHL Rare CD15+
CD30+
CD20-
Many RS
Few B
M:F (4:1), Rare, HIV,
Developing countries, B-
symptoms
Retroperitoneal and abdominal
Advanced stage
Aggressive course
NSCHL 67% CD15+
CD30+
CD20-
Dense
fibrous
tissue
obscuring
lymph node
architecture
M:F (1:1), Most common
subtype in West,
adolescents and young
adults, B-symptoms
Cervical, axillary and
mediastinal
Prognosis intermediate
between LRHL and
LDHL
Salient Clinical Features of Hodgkin lymphoma

Diagnosis & histological
classification of HL
• A. Confirm Diagnosis
 Tissue Biopsy
 Morphology: Presence of RS giant cells,
identified as large, often, binucleated
cells with prominent nucleoli. Two mirror-
image nuclei (owl eyes)
 CD 30 + RS giant cells
 heterogeneous population of leucocytes
and variable fibrosis

MALIGNANT LYMPHOMAS by Ocheni and Nwabueze

The classical RS cell is binucleate, each nucleus contains
a prominent eosinophilic nucleolus with perinucleolar
halos giving the cell an “owl-eye” appearance (H&E).
Mani H. Clin Lymphoma Myeloma. 2009
June; 9(3):206216.

The LP cell, the neoplastic cell in NLPHL, has a
multilobate/folded nucleus with smaller basophilic nucleoli
giving the cell a “popcorn” appearance (H&E).
Mani H. Clin Lymphoma Myeloma. 2009 June;
9(3):206216.

Diagnosis & histological classification of
HL
HL is subdivided into:
Classical HL and Nodular Lymphocyte Predominant
HL (NLPHL).
Classical HL (CHL) further subtyped as:
Nodular sclerosis (NSCHL
Lymphocyte rich (LRCHL)
Mixed cellularity (MCCHL)
Lymphocyte depletion (LDCHL)

• B. Document extent of nodal
involvement by clinical
examination
CXR, Computerised
Tomography(CT) of Chest,
abdomen, pelvis, abdominal
ultrasound scan
• Document bone marrow(BM)
status by BM trephine biopsy

C. OTHER INVESTIGATIONS
FBC-
 normochronic, normocytic
anaemia,
 Reactive leucocytosis,
 neutrophiliaa,
 eosinophilia
 ± reactive thromobocytosis.
 PCV↓
ESR↓
Uric acid ↑
LDH depends on tumor load

Staging of Hodgkin lymphoma
ANN ARBOR STAGING, 1971
I. Lymph node involvement in one
anatomical region
II. Involvement of 2 or more lymph
node regions on the same side of
the diaghragm either above or
below
III. Involvement of lymph node
regions on both sides of the
diaphragm.
IV. Disseminated (Multifocal)
involvement of 1 or more
extralymphatic organs.

Staging of Hodgkin lymphoma
COTSWOLD’S STAGING, 1984
-a modification of Ann Arbor Staging
-Subdividing III into
III 1. - Involvement of splenic, celiac or
portal nodes
III 2.- Involvement of para –aortic,
iliac or mesenteric nodes
• Definition of bulk:
Mediastinal mass greater than 0ne third
the maximum diameter of the chest
Nodal mass > 10cm

Staging of HL
• Presence or absence of
constitutional symptoms
A- asymptomatic
B- symptomatic
Night sweats (Drenching)
Unexplained weight loss of > 10% of
body wt in the preceding 6 months.
Unexplained fever with temp. > 38ºC

MANAGEMENT
• Radiotherapy
• Chemotherapy
• Combination of both
Stages IA & IIA- Radiotherapy
Types of Radiotherapy
 Inverted Y technique – to irradiate the
lymph nodes below the diaphragm
including the para-aortic and the inguinal
lymph nodes
 Mantle technique to irradiate the lymph
nodes in the neck and above the
diaphragm
Stages III and IV- Chemotherapy
Bulky Dx: Combined chemoradiotherapy

Combination chemotherapy
• ABVD (Adriamycin, Bleomycin,
Vinblastine and Dacarbazine).
First Line, Less infertility
• MOPP: (Mustine hydrochloride,
oncovin or vincristine,
procarbazine and Prednisolone).
• COPP: C = cyclophosphamide

Outcomes of Trt
• stages I & II: > 80% achieve 10 yr
survival
• stags III & IV: ≈ 70% achieve 10 yr
survival
SALVAGE THERAPY
For relapsed cases, treat with other
regimens or give high dose
chemotherapy with autologous
peripheral/bone marrow stem cell
transplantation

Prognostic Factors
1.Histologic Subtype
Lymphocyte predominant – Best
prognosis
Lymphocyte depleted - Worse
prognosis
2. Staging
1A – Best prognosis
Stages I & II better than III & IV
3. B Symptoms – Bad prognosis
4. Disseminated disease (eg
with liver, bone marrow or lung
involvement): bad prognosis

Prognostic Factors
Other bad prognostic factors
5. Male sex
6. Age > 45yrs
7. Hb < 10.5g/dl
8. WBC > 15,000/mm3
9. lymphocyte count less than
800/mm3
10. Albumin less than 4g/dl

LATE COMPLICATIONS OF
TREATMENT
Secondary malignancies eg AML
Myelodysplastic syndrome
(MDS)
Infertility
Intestinal complications
Myocardial infarction
Pulmonary complications.

NON HODGKIN’S
LYMPHOMAS (NHLs)
• NHLs : Reed- Sternberg (RS) giant cells
are absent.
• EPIDEMIOLOGY OF NHL
 World wide, with rising incidence
 Among top 5 causes of cancer mortality
in young adults.
 More than 50,000 new cases per year
diagnosed in US.
 Incidence has increased in each of the
last 5 decades
 Incidence increases with age.

Aetiological factors of NHL
1.Immunosuppression
 Inherited eg ataxia telangiectasia, Wiskott-
Aldrich syndrome
 Acquired eg AIDS, Organ transplants
2. Autoimmune diseases e.g. Hashimoto
thyroiditis, systemic lupus
Erythematosis, Rheumatoid arthritis
3. Infectious agents eg EBV, HTLV,
Helicobacter pylori, Hepatitis C, Human
Herpes Virus-8,Human Herpes Virus-6

4. Male gender
5. Increasing age
6. Family history of NHL
7. Drug history –phenytoin,
Immunosuppressive agents
8. Occupational history, Exposure
to herbicides, pesticides, wood
dust, organic solvents

Other possible etiologic factors
Hair dye use
Sunlight exposure
History of allergies
Ionizing radiation
Inherited disorders affecting DNA
damage/ repair eg Fanconi’s
anaemia.

CLINICAL FEATURES OF NHL
• A spectrum from low grade NHL
which may follow an indolent course
to high grade NHL with short history
of localized, rapidly enlarging
lymphadenopathy with/without
constitutional symptoms.
• Superficial lymphadenopathy is the
most common presenting feature of
NHL

CLINICAL FEATURES OF NHL
Other possible presenting features of NHL
• Oropharyngeal involvement (5-10%)
• Auto Immune cytopaenias
• GIT involvement ~ 15%.
• CNS involvement 5-10%
• Skin involvement especially in T-cell
lymphomas such as mycosis fungoides
and sezary syndrome
• Constitutional Symptoms:
fever, night sweats and weight loss occur
less frequently than in Hodgkin’s disease
and their presence is usually associated
with disseminated disease

DIAGNOSIS AND HISTOLOGICAL
CLASSIFICATION OF NHLs
Lymph node biopsy
• Routine Histology /morphology
• Immunoperoxidase staining
• Immunophenotyping/ Flow Cytometry
• cytogenetic analysis
• Molecular biology methods (PCR)
• Electron microsopy.

DIAGNOSIS AND HISTOLOGICAL
CLASSIFICATION OF NHLs
Various classification systems:
Rappaport Classification –1966
Modified Rappaport classification- 1974
Luke’s and Collin’s classification-1974
Kiel’s Classification-1975
Working Formulation classification-1982
---most clinically user friendly
REAL (Revised European American
Lymphoma ) 1994
WHO Classification – a modification of
REAL

Working Formulation
Classification
 1. Low Grade NHL eg CLL
≈ 40% of NHL
Most common in middle /old age,
median age 55yrs
Generally indolent, presents with
stage III or IV disease in 2/3 of
patients
Bone marrow frequently involved at
diagnosis
Median survival ≈8yrs

Low Grade NHL
May present with
• painless lymphadenopathy at > 1
site
• effects of BM infiltration
• constitutional symptoms.

2. Intermediate Grade NHL e.g
large cell follicular NHL
moderately aggressive disease
50% of cases of NHL.
Usually presents with stg I or II dx
in 50% of pts
Disseminated extranodal
involvement can occur
1/3 of patients have constitutional
symptoms
Median survival ≈ 3 years

3. High Grade NHL
Eg immunoblastic NHL,
lymphoblastic NHL
Burkitt’s and non Burkitt’s small
non- cleaved NHLs
Often seen in younger patients
Aggressive tumors requiring immediate
treatment
Blood and CNS involvements are common
Blood and CNS involvements are common

INVESTIGATIONS AND
STAGING IN NHL
• Investigations are similar to those
of HL
• Staging system in NHL uses the
Ann Arbor staging scheme except
in Burkitt’s lymphoma

Staging system for BL
• Stage A- Single extra abdominal
site
• Stage B- Multiple extra- abdominal
sites
• Stage C- Intra- abdominal tumor
• Stage D- Intra- abdominal tumor
with multiple extra-abdominal
sites.
• Stage AR- Stage C disease with >
90% of tumor surgically removed.

MANAGEMENT OF NHLs
• Supportive
Counseling
IV fluids
Blood products
Antibiotics, antimalarials etc
• Curative
Stages I – IIA: Radiotherapy
Stages IIB –IIIB: Radiotherapy +
Chemotherapy
Stage IV: Chemotherapy

Trt modalities for NHL
• Low Grade NHL
Watch and wait
Chlorambucil or Cyclophosphamide
± Prednisoline
Combination chemotherapy e.g CVP
(cyclophosphamide, Vincristine,
prednisolone), CHOP(Hydroxydaunorubicin)
Radiotherapy for treatment of local
problems of cord compression
Total body Irradiation (TBI) or total
lymphoid irradiation

INTERMEDIATE GRADE NHL
Age < 65 yrs
1st line – COPP as for HD
2nd line-- CHOP
Age > 65 yrs
Chlorambucil or
Cyclophosphamide
• Localized diffuse large cell NHL:
Radiotherapy may be curative
with stage 1
• Advanced stage NHL- CHOP

HIGH GRADE NHL 1
• ALL – like therapy
Eg COAP + CNS Prophylaxis
• High dose therapy with
autologous or allogeneic
peripheral blood/Bone Marrow
Transplantation (BMT)
• Burkitt’s lymphoma
COMP or COAP with CNS
prophylaxis

HIGH GRADE NHL 2
• SALVAGE THERAPY
Pts failing to achieve remission
with initial therapy have poor
prognosis. Almost all will die of
progressive lymphoma without
effective second line (salvage)
therapy.
• RELAPSE IN NHL
High dose therapy and Auto/Allo
SCT

Prognostic Factors for NHL
No Parameter Good Prog. Bad Prog
1 Age <60yrs >60yrs
2 Performance
status
O or 1 > 2
3 Ann Arbor Stage I or II III or IV
4 Number of extra-
nodal sites
0 or 1 >2
5 Serum LDH Normal Raised

Prognostic Factors for NHL
• Patients are assigned a number for
each risk factor they have
• 0-1 factor - low risk
• 2 factors - low intermediate risk
• 3 factors - high intermediate risk
• 4-5 factors - High risk

BURKITT’S LYMPHOMA (BL)
• an aggressive childhood B- Cell NHL
• first described by Dennis Burkitt, a
British surgeon practicing in Uganda in
1950
• fastest growing tumour known to man
• doubling time of ≈ 24 hours.

Epidemiology of Burkitt’s
lymphoma
• Commonest childhood tumor in Tropical
Africa.
• Most affected age grp: 4 - 9 years
Rare < 2 years and > 15 years
• Males >> females (M:F = 2:1)
• Occurs in areas with humid climate and
malaria endemicity (malarial holoendemic
areas)

Epidemiology of Burkitt’s
lymphoma
• Tropical rain forest of Africa,
Latitudes 10-15º North and South of
the Equator and other parts of the
world with similar climatic
conditions such as Papua New
Guinea.
• Common in children from low
socioeconomic clan.
• Uncommon in children from high
socio-economic class, living in
endemic areas.

AETIOLOGY OF BL
• Epstein Barr virus infection
especially African BL. Chronic
exposure of infants to malaria
results in immunosuppression
which permits the proliferation of
EBV- transformed cell.
• Clonal chromosomal abnormalities
involving translocations between
chromosomes 8 and 14.

Types of Burkitt’s Lymphoma
• 1. Endemic (African ) BL
Seen in areas with chronic malaria
exposure and is associated with EBV
infection
• 2. Sporadic BL
May occur anywhere in the world and is
not associated with EBV infection

DIFFERENCES BETWEEN
ENDEMIC AND SPORADIC BL
Characteristics Endemic/
African
Sporadic
1 EBV Causation Positive Nil
2 Malaria Positive Nil
3 Age (peak) ≈ 7 yrs ≈11yrs
4 Presentation Facial Abdominal
5 Lymph Node
involvement
Rare Present
6 Response to
Cyclophosphamide
Excellent involvepoor
ment

Clinical Features of Burkitt’s
Lymphoma
• Rapidly growing tumor
• presentation within 2-6 weeks of
illness.
• African/Endemic BL: Jaw swelling
with loosening of the teeth and
distortion of dental anatomy
• sporadic BL: abdominal tumors ±
ascites, abdominal swelling,
symptoms of bowel obstruction

Clinical Features of Burkitt’s
Lymphoma
• CNS disease
 cranial / nerve palsies
 Paraplegia
 Ocular disease, associated with proptosis ±
blindness
• Bone marrow disease
• lung involvement
• Skin nodules
• long bones
• Peripheral lymphadenopathy is uncommon
except in sporadic BL
• Very rarely – fever, anaemia, bleeding and
peripheral lymphadenopathy similar to ALL

Burkitt’s Lymphoma
Differential Diag. of BL
• Neuroblastoma
• Nephroblastoma
• Ameloblastoma

Burkitt’s Lymphoma
DIAGNOSIS OF Burkitt’s Lymphomas
(A) FNAC (Fine Needle Aspiration
Cytology)
 Leishmann’s Stain shows
large monomorphic lymphoblasts
containing distinct nucleoli,
abundant deeply basophilic and
vacuolated cytoplasm.
 With methyl- green pyronin stain,
the cytoplasm stains red with
multiple vacuoles containing
neutral fat.

DIAGNOSIS OF Burkitt’s
Lymphomas
B. Histologic examination:
homogenous sheets of lymphoblasts,
with round to oval nuclei, slightly
coarse chromatin, multiple nucleoli,
and intensely basophilic vacuolated
cytoplasm that contains neutral fat.
The homogenous appearance is
interspersed with scattered
macrophages, containing necrotic
debris, giving a starry- sky
appearance

DIAGNOSIS OF Burkitt’s
Lymphomas
C. Cytogenetic analysis
t(8;14) and c-myc gene
rearrangement in the presence
of A and / or B above, confirms
the diagnosis of BL

GENERAL INVESTIGATIONS IN
BL
 FBC with differentials
 E & U, creatinine, calcium, uric acid,
phosphates
 LFTs
 Bone Marrow Aspiration (BMA)/Biopsy
 CSF tap for cytology
 Radiological studies
 Plain X Rays:
Chest (lung metastasis and Mediastinal
involvement)
Jaw (to confirm the destruction of
dental lamina dura)
 CT scan or MRI of chest, abdomen
 Abdominal USS

STAGING OF Burkitt’s Lymphoma
• Stage A – Single extra – abdominal mass
• Stage B- Multiple extra abdominal masses
• Stage C- Intra- abdominal mass
• Stage D- Intra- abdominal and extra-
abdominal masses
• AR – Stage C Disease with >90% of tumor
surgically removed .

Management of BL
A:Supportive care
• Counselling
• Adequate fluids to prevent tumor lysis
syndrome
• Hyperkalaemia
• Hyperuricaemia
• Hyperphosphataemia
• Allopurinol
• Antimicrobial agents as indicated
• Blood and Blood products as indicated

Management of BL
B: CHEMOTHERAPY
 COM + Intrathecal (IT) drugs
(Cyclophosphamide, Oncovin or
Vincristine, and Methothrexate)
 IT Drugs: Methotrexate, Cytosar,
Hydrocortisone
C: SURGERY– To reduce tumor load

PROGNOSIS IN BL
• Highly chemosensitive & Curable.
• Patients with Bone marrow and CNS
involvement have a poor prognosis
• Adult patients with advanced stage
disease do more poorly than
children.
• Overall survival in Nigeria is still
very poor, because of inability of
most patients to buy drugs and high
default rates.

�ݺ�ߣ

MALIGNANT LYMPHOMAS by Ocheni and Nwabueze

More Related Content

MALIGNANT LYMPHOMAS by Ocheni and Nwabueze

Editor's Notes