Cervical lymph adenopathy

Cervical lymphadenopathy
TB/HL/NHL
DR SUMER YADAV
MCh- plastic surgeon
sumeryadav2004@gmail.com

Lymph Nodes
• Anatomy
– Collection of lymphoid cells attached to both vascular and
lymphatic systems
– Over 600 lymph nodes in the body

Anatomy
• Are small bean-shaped
organs
• Each node has fibrous
capsule & and has a
hilum at one side.
• It receives many afferent
vessels & gives efferent
vessel from its hilum.

• The lymph node is divided into an outer cortex and an inner medulla.
• Fibrous trabeculae extend from the deep surface of the capsule into
the cortex to divide it into compartments.
• Fibrous trabeculae in the medulla are irregular & called medullary
Cords.
• Lymphoid follicles form continuous row in the cortex and are absent
in the medulla.

Lymph
• Fluid similar in composition to blood plasma.
• Derived from blood plasma by filtration
through capillary walls at the arterial end.
• As soon as the interstitial fluid enters the
lymph capillaries, it is called lymph.
• Returning the fluid to the blood helps to
maintain normal blood volume and pressure.

Function
• To provide optimal sites for the concentration of free or cell-
associated antigens and recirculating lymphocytes –
“sensitization of the immune response”
• To allow contact between B-cells, T-cells and macrophages
• Lymph nodes and other lymphatic organs filter the lymph to
remove & destroy microorganisms and other foreign particles
• It returns excess interstitial fluid to the blood to maintain
blood volume and blood pressure .
• Absorption of fat and fat-soluble vitamins from the digestive
system by special lymph capillaries, called lacteals The lymph
in the lacteals has a milky appearance due to its high fat
content and is called chyle.

• CLASSIFICATION
1. Upper horizontal chain of nodes
(a) Submental
(b) Submandibular
(c) Parotid
(d) Postauricular
(e) Occipital
(f) Facial

• 2. Lateral cervical nodes. They include nodes,
superficial and deep to sternocleidomastoid
muscle and in the posterior triangle.
(a) Superficial external jugular group
(b) Deep group
(i) Internal jugular chain
(upper, middle and lower
groups)
(ii) Spinal accessory chain
(iii) Transverse cervical chain

• 3. Anterior cervical nodes
(a) Anterior jugular chain
(b) Juxtavisceral chain
• (i) Prelaryngeal
• (ii) Pretracheal
• (iii) Paratracheal

• They lie on the mylohyoid muscle in
the submental triangle, 2–8 in number.
Afferents come from the chin, middle part of lower lip, anterior
gums, anterior floor of mouth and tip of tongue.
Efferents go to submandibular nodes and internal jugular
chain.

• They lie in submandibular triangle in
relation to submandibular gland and
facial artery.
Afferents come from lateral part of
the lower lip, upper lip,cheek, nasal
vestibule and anterior part of nasal
cavity, gums,teeth, medial canthus,
soft palate, anterior pillar, anterior
part of tongue, submandibular and
sublingual salivary glands
and floor of mouth.
Efferents go to internal jugular chain.

• Parotid nodes
• They lie in relation to the parotid salivary
gland and are extraglandular and
intraglandular. Preauricular and
infraauricular nodes are part of the
extraglandular group.
• Afferents come from the scalp, pinna,
external auditory canal, face, buccal
mucosa.
• Efferents go to internal jugular or
external jugular chain.
• Postauricular nodes (mastoid nodes)
• They lie behindthe pinna over the
mastoid.
• Afferents come from the scalp, posterior
surface of pinna and skin of mastoid.
• Efferents drain into infra-auricular nodes
and into internal jugular chain.

• Occipital nodes.
 They lie both superficial and deep to
splenius capitus at the apex of the
posterior triangle.
 Afferents come from scalp, skin of upper
neck.
 Efferents drain into upper accessory
chain of nodes.
• Facial nodes.
 They lie along facial vessels and are
grouped
according to their location. They are
midmandibular, buccinator, infraorbital
and malar (near outer canthus) nodes.
 Afferents come from upper and lower
lids, nose, lips and cheek.
 Efferents drain into submandibular nodes.

LATERAL CERVICAL NODES
• Lateral Cervical Nodes
a) Superficial group – it lies
along external jugular vein
and drains into internal
jugular and transverse
cervical nodes.

b.Deep Group
• It consists of three chains,
1. the internal jugular chain
2. spinal accessory and
3. Transverse cervical
• Internal jugular chain
Lymph nodes of internal jugular chain lie anterior, lateral and
posterior to internal jugular vein.
Upper group (jugulodigastric node) – drains oral cavity, orpharynx,
nasopharynx, hypopharynx, larynx and parotid.
Middle group drains hypopharynx, larynx, throid, oral cavity,
oropharynx.
Lower jugular group drains larynx, thyroid and cervical oesophagus.

• Spinal accessory chain
Lies along the spinal
accessory nerve. Spinal
accessory chain drains
the scalp, skin of the
neck, the nasopharynx,
occipital and
postauricular nodes.
Efferents from this chain
drain into transverse
cervical chain

• Transverse cervical chain
(supraclavicular nodes)
It lies horizontally, along the
trasverse cervical vessels, in the
lower part of the posterior
triangle. The medial nodes of
the group called scalene nodes.
Afferents to those nodes come
from the accessory chain and
also infraclavicular structures,
e.d. breast, lung, stomach,
colon, ovary and testis.

Anterior Cervical Nodes
Anterior Cervical Nodes
They lie between the two carotids
and below the level of hyoid bone
and
consist of two chains:
(a) Anterior jugular chian - It lies
along anterior
jugular vein and drains the skin of
anterior neck.
(b) Juxtavisceral chain – It consists of
• prelaryngeal
• pretracheal
• and paratracheal nodes

(i) Prelaryngeal node (Delphian node)
lies on cricothyroid membrane and drains subgottic
region of larynx and pyriform sinuses.
(ii) Pretracheal nodes
lie in front of the trachea, and drain
thyroid gland and the trachea. Efferents from these
nodes go to paratracheal, lower internal jugular and
anterior mediastinal nodes.
(iii) Paratracheal Nodes
drain the thyroid lobes, subglottic
larynx, tracha and cervical oesophagus

• Post cervical: scalp, neck skin of arms thorax cervical and axillary nodes (lymphoma, head/neck ca)

AJCC(American Joint Committee on
Cancer) classification
• Level 1 –submental+ submandibular
• Level 2 –upper deep cervical nodes
• Level 3 –middle deep cervical nodes
• Level 4 –lower deep cervical nodes
• Level 5 –spinal accessory + transverse cervical
• Level 6 –pretracheal, prelaryngeal, paratacheal
• Level 7 –upper mediastinal nodes

What is lymphadenopathy
• Lymph nodes that are abnormal in size > 1cm,
consistency or number
• Localized – one area involved
• Generalized – two or more non-contiguous
areas

Why do lymph nodes enlarge?
• Increase in the number of benign lymphocytes
and macrophages in response to antigens
• Infiltration of inflammatory cells in infection
(lymphadenitis)
• In situ proliferation of malignant lymphocytes
or macrophages
• Infiltration by metastatic malignant cells
• Infiltration of lymph nodes by metabolite
laden macrophages (lipid storage diseases)

Epidemiology
• 0.6% annual incidence of unexplained
adenopathy in the general population
• 10% were referred to a subspecialist and 3.2 %
required a biopsy and 1.1% had a malignancy

When to worry?
• Age
• Characteristics of the node
• Location of the node
• Clinical setting associated with
lymphadenopathy

Age
• Children/young adults – more likely to
respond to minor stimuli with lymphoid
hyperplasia
– Lymph nodes in patients less than the age of 30
are clinically benign in 80% of cases whereas in
patients over the age of 50 only 40% are benign
– Biopsies done in patients less than 25 yrs have a
incidence of malignancy of <20% vs the over-50
age group has an incidence of malignancy of 55-
80%

Clinical examination
• Localized adenopathy should prompt a search
for an adjacent precipitating lesion and an
examination of other nodal areas to rule out
generalized lymphadenopathy. In general,
lymph nodes greater than 1 cm in diameter
are considered to be abnormal.
Supraclavicular nodes are the most worrisome
for malignancy. A three- to four-week period
of observation is prudent in patients with
localized nodes and a benign clinical picture.

• The body has approximately 600 lymph nodes,
but only those in the submandibular, axillary
or inguinal regions may normally be palpable
in healthy people.1 Lymphadenopathy refers
to nodes that are abnormal in either size,
consistency or number. There are various
classifications of lymphadenopathy, but a
simple and clinically useful system is to classify
lymphadenopathy as “generalized” if lymph
nodes are enlarged in two or more
noncontiguous areas or “localized” if only one
area is involved.

Characteristics of the node
• Nodes lasting less than 2 weeks or greater
than one year with no progression of size have
a low likelihood of being neoplastic – excludes
low grade lymphoma
• Cervical nodes – up to 56% of young adults
have adenopathy on clinical exam
• Inguinal adenopathy is common – up to 1-2
cm in size and often benign reactive nodes

Characteristics of the node
i. Consistency – Hard/Firm vs Soft/Shotty; Fluctuant
ii. Mobile vs Fixed/Matted
iii. Tender vs Painless
iv. Clearly demarcated
v. Size
i. When to worry – 1.5-2cm in size
ii. Epitroclear nodes over 0.5cm; Inguinal over 1.5cm
vi. Duration and Rate of Growth
vii. Mobile vs fixed
viii. Symmetrical vs asymmetrical

Consistency
• Stony hard: typical of cancer usually metastatic
• Firm rubbery: can suggest lymphoma
• Soft: infection or inflammation
• Fluctuant : Suppurated nodes.
• Matting : . A group of nodes that feels connected
and seems to move as a unit is said to be “matted.”
Nodes that are matted can be either
 benign (e.g., tuberculosis, sarcoidosis or
lymphogranuloma venereum)
 or malignant (e.g., metastatic carcinoma or
lymphomas).

Pain/Tenderness
• When a lymph node rapidly increases in size,
its capsule stretches and causes pain. Pain is
usually the result of an inflammatory process
or suppuration, but pain may also result from
hemorrhage into the necrotic center of a
malignant node. The presence or absence of
tenderness does not reliably differentiate
benign from malignant nodes

size
• in one series of 213 adults with unexplained
lymphadenopathy,
 no patient with a lymph node smaller than 1 cm2 (1
cm × 1 cm) had cancer,
 while cancer was present in 8 percent of those with
nodes from 1 cm2 to 2.25 cm2 (1 cm × 1 cm to 1.5 cm
× 1.5 cm) in size, and
 in 38 percent of those with nodes larger than 2.25
cm2 (1.5 cm × 1.5 cm).
• In children, lymph nodes larger than 2 cm in diameter
(along with an abnormal chest radiograph and the absence
of ear, nose and throat symptoms) were predictive of
granulomatous diseases (i.e., tuberculosis, cat-scratch
disease or sarcoidosis) or cancer (predominantly
lymphomas).

Location of the node
• The anatomic location of localized adenopathy
will sometimes be helpful in narrowing the
differential diagnosis. For example, cat-scratch
disease typically causes cervical or axillary
adenopathy, infectious mononucleosis causes
cervical adenopathy and a number of sexually
transmitted diseases are associated with
inguinal adenopathy .

Location of the node
• Supraclavicular lymphadenopathy
 Highest risk of malignancy – estimated as 90% in
patients older than 40 years vs 25% in those
younger than 40 yrs
 Right sided node – cancer in mediastinum, lungs,
esophagus
 Left sided node (Virchow’s) – testes, ovaries,
kidneys, pancreas, stomach, gallbladder or
prostate
• Paraumbilical node (Sister mary Joseph’s)
– Abdominal or pelvic neoplasm

Generalized Lymphadenopathy
CHICAGO
• C- Cancer- HL/NHL/MM/Leukemia/ secondaries
• H- hypersensitivity- drugs, serum sickness
• I – infection – bacterial, viral
• C – connective tissue disorders- SLE/RA
• A- atypical – castlemans , wegeners dis
• G- Granulomatous dis- TB, Histoplasma,
cryptococcus, silicosis
• O- OTHERS- Kikuchi (histiocytic necrotizing
lymphadenitis ( non-cancerous enlargement
of the lymph nodes)

Unexplained Generalized
lymphadenopathy
• Always requires an evaluation
• Start with CXR and CBC
• Review Medications
• PPD (TB test), RPR(Rapid plasma reagin , a
blood test for syphilis) , Hepatitis screen, ANA,
HIV
• No yield on above test: Biopsy from most
abnormal node.

History
• Identifiable cause for the lymphadenopathy?
– Localizing symptoms or signs to suggest
infection/neoplasm/trauma at a particular site
• URTI, pharyngitis, periodontal disease, conjunctivitis, insect bites,
recent immunization etc
• Constitutional symptoms(fever, night sweats, weight
loss, Fatigue, Pruritis)
• Epidemiological clues
– Occupational exposures, recent travel, high-risk behaviour
• Medications – serum-sickness syndrome

Physical Exam
• Full nodal examination – nodal characteristics
• Organomegaly
• Localized – examine area drained by the nodes
for evidence of infection, skin lesions or
tumours

Radiographic Investigation of the Head
and Neck Masses
• MRI – Magnetic Resonance Imaging can clearly highlight soft tissue
pathologies better than the C.T. Scan.
– It uses a magnetic field rather than x-rays (radiation).
• CT SCAN – Computed tomography is less accurate than M.R.I for the
soft tissue examination, but is very useful to locate bony tumors
and their dimensions and extensions.
– C.T with contrast is used to enhance the visibility of abnormal tissue
during examination.
• PET (Positron Emission Tomography) and SPECT (Single Photon
Emission Tomography) are useful after diagnosis to help determine
the grade of a tumor or to distinguish between cancerous and dead
or scar tissue.
– They involve injection with a radioactive tracer.
• Gallium scanning

Fine Needle Aspirate
• Safe Convenient, less invasive, quicker turn-around time
• especially beneficial for verification of lymphoid
origin of the enlarged growth and in differentiating
between metastatic, infectious, reactive and
lymphomatous causes of lymphadenopathy. It also
helps in the determination of the extent of tumor;
detection of recurrence; monitoring of the course of
disease; obtaining of material for special studies such
as microbiological cultures, immunological or genetic
studies as well as electron microscopy. Furthermore
• Most patients with a benign diagnosis on FNA biopsy do
not undergo a surgical biopsy
• overall sensitivity was 92.7%, specificity 98.5%

• If the LN are
not palpable, endoscopic ultrasound-guided fine
needle aspiration (EUS-FNA) has been shown to
accurately diagnose mediastinal lymph node
pathology with diagnostic accuracy of 84%
• endobronchial ultrasound guided transbronchial
needle aspiration (EBUS-TBNA) have been shown
to
be highly sensitive and specific in the diagnosis of
mediastinal and hilar lesions

• Limitations of FNA:
– the lack of proper
tissue sample to run special studies including
cytogenetics, flow cytometry, electron microscopy,
– the potential risk of
seeding a tract with malignancy as a result of FNA

BIOPSY
• Can be done by bedside, open surgery, mediastinoscopy FNA
cannot distinguish between lymphomas (nodal architecture needs
to be intact) The preservation of nodal architecture is critical to the
proper diagnosis of lymphadenopathy, particularly when
differentiating lymphoma from benign reactive hyperplasia
• Biopsy should be avoided in patients with probable viral illness
because lymph node pathology in these patients may sometimes
simulate lymphoma and lead to a false-positive diagnosis of
malignancy.
• The diagnostic yield of the biopsy can be maximized by obtaining an
excisional biopsy of the largest and most abnormal node (which is
not necessarily the most accessible node). If possible, the physician
should not select inguinal and axillary nodes for biopsy, since they
frequently show only reactive hyperplasia.
• Patients should be cautioned to remain alert for the reappearance
of the nodes because lymphomatous nodes have been known to
temporarily regress.

Management
• Identify underlying cause and treat as
appropriate – confirmatory tests
• Generalized adenopathy – usually has
identifiable cause
• Localized adenopathy
– 3-4 week observation period for resolution if not
high clinical suspicion for malignancy
– Biopsy if risk for malignancy - excisional

Tubercular lymphadenopathy

Microbiology
• M. tuberculosis is the usual cause of tuberculous
lymphadenitis.
• Other infectious causes of chronic lymphadenitis
include :
– Nontuberculous mycobacteria (including M.
scrofulaceum, M. avium, and M. haemophilum)
– Pseudomonas pseudomallei
– Toxoplasma species
– Bartonella species
– Fungi.

Tuberculous granuloma
•

Symptomatology
• Patients do not generally report significant pain at
presentation.
• Node tenderness during examination is noted in
only 10%–35% of cases.
• A draining sinus may be present in 4%–11% of
cases.
• Unilateral involvement of 1–3 nodes has been
noted in 85% of cases.
• Cervical chain involvement is most common
(45%–70%) with 12%–26% in the supraclavicular
region; 20% of cases are bilateral.

Stage I
Enlarged firm
mobile discrete
nodes
(Lymphoid
hyperplasia
with formation
of tubercles &
granuloma)
Stage II
Large rubbery
nodes fixed to
surrounding
tissue due to
periadenitis
(Caseation
starts)
Stage III
Central
softening due to
abscess
formation
(progressive
Caseation
necrosis)
Stage IV
Collar stud
abscess
formation. skin
over is inflamed
(Rupture of
caseous
material)
Stage V
Sinus tract
formation

TB abscess
Treatment should be
started following the
national TB
Guidelines.

Mx
• Good FNAC / needle biopsy / ZN staining / MT
test & ESR make diagnosis in almost all cases.
• Optimal management of comorbid conditions.
• LNTB enlarge during ATT or appear afresh will
eventually respond to treatment.
• Development of fluctuation requires immediate
attention - Early surgical intervention.
• Residual LN at end of ATT should be closely
monitored.

Hodgkin lymphoma

Hematopoietic Malignancies
Lymphoma is a general term used for proliferations that
arise as discrete tissue masses.
Leukemia is used for neoplasms that present with
widespread involvement of the bone marrow and
the peripheral blood(usually).

WHAT IS LYMPHOMA?
LYMPHOMA
is the term applied to a heterogeneous
collection of diseases characterised by the
presence of malignant lymphoid cells.
i.e.
Cancer of the Lymphatic System

Haemopoiesis
erythroid myeloid megakaryocytic
B lymphoid T lymphoid
AML
Lymphoma/
CLL
ALL

How does lymphoma present?
• Patient notices lumps in
neck, under arms, in groin
(lymphadenopathy)
• Lymphadenopathy noted
during examination for
other reason eg. check up
Abnormal blood findings unusual
(cf. leukaemia)

Clinical features
• Most common presentation is asymptomatic lymphnode enlargement,
typically in the neck.
• Cervical lymphnodes are involved in 80% cases.
• Mediastinal involvement is seen in about 50% cases. They produce
symptoms like chest pain, cough and dyspnoea.
• Infradiaphrgamatic involvement is seen in 5% cases and usually seen with
older patients.
• Other less common symptoms are :
Pruritis, alcohol induced pain over involved lymphnodes, nephrotic syndrome,
erythema nodosum, cerebellar degeneration, immune hemolytic
anaemia, thrombocytopenia, hypercalcemia.

B symptoms
• About 33 % present with B symptoms overall
• Only 15-20% of stage I-III have B symptoms like
1. Fever(>38^C)
• May first present as fever of unknown origin
• Fever persists for days to weeks followed by afebrile intervals and then
recurrence.
• This pattern is called Pel Ebstein fever.
2. Drenching night sweats
3. Weight loss (>10% in 6 months)

Ann Arbor Staging System
• Stage I: Single lymph node region (I) or single extralymphatic organ or
site (IE)
• Stage II: > 2 lymph node regions on same side of diaphragm (II) or with
limited, contiguous extra lymphatic tissue involvement (IIE)
• Stage III: both sides of diaphragm involved, may include spleen (IIIS) or
local tissue involvement (IIIE)
• Stage IV: multiple/disseminated foci involved with > 1 extralymphatic
organs (i.e. bone marrow)
(A) or (B) designates absence/presence of “B” symptoms
*(E) Localized, solitary involvement of extralymphatic tissue, excluding liver
and bone marrow sumeryadav2004@gmail.com

Stage I Stage II Stage III Stage IV
Staging of lymphoma
A: absence of B symptoms
B: fever, night sweats, weight loss

Risk Factors
• No clear risk factors, several implicated
• EBV (pathogen or passenger)
• HIV
• woodworking, farming
• rare familial aggregations
• First degree relatives have five fold increase in risk for Hodgkin lymphoma.
• Associated with EBV infection mainly with mixed cellularity type.
• High socio economic status.
• Prolonged use of of human growth hormone.
• men > women
• whites > blacks > Asians

Diagnostic workup

2008 WHO Classification of Hodgkin Lymphoma

Reed Sternberg cell
Common feature of ALL Hodgkin Lymphomas.
• Large cells ( >45um in diameter) with classically binucleate or bilobed
central nucleus each with a large acidophilic central nucleoli surrounded
by a clear halo. “owl’s eye appearance”
• Variants: mononuclear (Hodgkin’s cell), mummified cell, lacunar cell, L/H
cell.
• Requirement of Reed-Sternberg cell for initial diagnosis is “absolute”(less
strict for LPHL or recurrent disease)
• Classic Reed-Sternberg cell:
+ CD15, CD30, CD25
– CD45, pan-B, S-100, keratin, EMA
• Most current studies indicate the RS cells of HL are lymphocytic in nature
and, in the great majority of cases, are of B-cell origin.

Reed-Sternberg cell

Lymphocyte predominant Hodgkin
lymphoma
• <5% of Hodgkin lymphoma
• Mainly involves cervical, axillary or mediastinal
• L&H cells or Popcorn cells are seen
• Positive for CD20, 45, CD79a, Bcl-6, J-chain, and PAX-5. EMA positive
in 50% cases.
• Negative for CD15, 30.
• Differential Diagnosis: Well differentiated lymphocytic lymphoma,
mononucleosis, malignant melanoma,, progressive transformation of
germinal centers

Classical Hodgkin Lymphoma

1. Nodular Sclerosis
• Most common type diagnosed
• About 70%
• Lacunar cells seen
• CD15, 30 positive
• EBV negative
• Only subtype without a male predominance
• Seen in younger patients with stage I-II disease.
• Differential diagnosis: Large cell Non Hodgkin lymphoma, carcinoma,
germ cell tumour and thymoma.

2. Mixed Cellularity
• Constitutes about 20%
• More than 50% present as stage III or IV disease
• Biphasic incidence, peaking in young adults and again in adults
older than 55
• CD15, 30, EBV positive
• Presents in advanced stages
• Tendency to involve spleen, bone marrow.
• Differential diagnosis: Some cases of MCHL display an interfollicular
growth pattern. Such cases may be difficult to distinguish from peripheral
T-cell lymphomas. Lennert’s lymphoma (diffuse mixed T-cell ML with
excessive histiocytes). Diffuse follicular lymphoma.

3. Lymphocyte Depleted
• Constitutes <5%
• Worst prognosis of all subtypes
• Older males, rare in children
• Present as febrile illness with
pancytopenia, hepatomegaly, and no
peripheral lymphadenopathy
• Advanced stage, Stage IV
• The biologic hallmark of LDHL is a
collapse of cell-mediated immunity,
HIV infection
• RS cells CD15+, CD30+; most EBV+
• Differential Diagnosis: Large cell Non-
Hodgkin’s lymphoma. Nodular
sclerosis HL

4. Lymphocyte-Rich
• RS cells CD15+, CD30+; 40% EBV+
• Uncommon
• M > F
• Tends to be seen in older adults
• This is an uncommon form of classical HL
• Reactive lymphocytes make up the vast majority of the cellular infiltrate.
In most cases, involved lymph nodes are diffusely effaced, but vague
nodularity due to the presence of residual B-cell follicles is sometimes
seen.
• Differential Diagnosis: This entity is distinguished from the lymphocyte
predominance type by the presence of frequent mononuclear variants and
diagnostic Reed-Sternberg cells with a “classical” immunophenotypic
profile.
• Very good to excellent prognosis.

Spread
• Generally a well behaved spread of disease through contiguous LN groups,
(especially NS and LP); <5% show non-contiguous spread
• May have direct extension into perinodal tissue.
• 85% of Stage I/II disease are above diaphragm.
• Spleen: if >400g, almost always positive.
• Liver: if positive, spleen and retroperitoneal LN’s are also positive.

PROGNOSIS
• Clinical stage
• Extranodal involvement bad (especially if distant rather than by direct
spread)
• Degree of splenic involvement: ≥5 nodules poor prognosis
• Age: >50 yrs unfavorable
• Sex and race: Black males worse than white females
• Microscopic type: LP and NS best, MC intermediate, LD worst (less
important with current treatment protocols)
• Laboratory findings: decreased hematocrit, elevated LDH, raised ESR,
elevated serum levels of CD30, soluble CD25 have negative prognosis.
• CD15- lack of expression is a negative prognostic factor.

Chemotherapy
Regimen Medication Regimen Medication
1. ABVD
(US)
•ADRIAMYCIN
•BLEOMYCIN
•VINBLASTINE
•DACARBAZINE
2. STANFORD V
(NEW)
•ADRIAMYCIN
•BLEOMYCIN
•VINBLASTINE
•VINCRISTINE
•PREDNISONE
•MECHLORETHAMINE
ETOPOSIDE
3. MOPP •Mechlorethamine
• Vincristine
•Procarbazine
• Prednisone
4. BEACOPP
(EUROPE)
•BLEOMYCIN
•ETOPOSIDE
•ADRIAMYCIN
•CYCLOPHOSPHAMIDE
•ONCOVIN
•PROCARBAZINE
•PREDNISONE

Radiotherapy
• Radiation therapy is the most effective single thrapeutic agent for treating
Hodgkin lymphoma.
• The main objective of radiation in Hodgkin lymphoma is to treat involved
and contiguous field.
• Radiotherapy can be given by
1. 2D planning
2. 3D planning
3. IFRT
• Involved field radiotherapy is the most commonly used technique at
present. It targets a smaller area rather than a classical extended field.

Complications
• Autologous bone marrow transplantation can cure half of patients who fail
effective chemotherapy regimens.
• Because of the very high cure rate in patients with Hodgkin's disease,
long-term complications have become a major focus for clinical research.
The most serious late side effects include secondary malignancies, cardiac
injury, infertility and Lhermitte's syndrome.

NHL – Lymphadenopathy

Non-Hodgkin’s lymphomas-definition
and epidemiology
1. Definition: malignant disease of the lymphoid
system, highly heterogeneous, both histologically
and clinically.
2. Epidemiology:
- annual incidence: 5-10 new cases per 100 000 persons,
- age distribution: middle-age patients and the elderly,
- males are affected more often than females (1.5:1.0).

Non-Hodgkin’s lymphomas-Clinical features
1. Constitutional symptoms (fever, night sweats, weight
loss)
2. Lymphadenopathy
(cervical, supraclavicular, axillary, inguinal, mediastinal,
retroperitoneal, mesenteric, pelvic).
3. Mediastinal adenopathy (T cell lymphoma)
4. Extralymphatic involvement (gastrointestinal, testicular
masses, solitary bone lesions, CNS).
5. Unexplained anemia and thrombocytopenia ( bone
marrow infiltration).

Histologic classification of non-Hodgkin’s
lymphomas - Working Formulation (WF)
1. Low grade
2. Intermediate grade
3. High grade

Treatment results of aggressive advanced
non-Hodgkin’s lymphomas using different
chemotherapy programs
1. First-generation: CHOP
- CR: 50-55%. Long-term survival: 35-50 %.
2. Second-generation: mBACOD, ProMACO-MOPP
- CR: 70-80%. Long-term survival: 50-60%.
3. Third-generation: MACOP-B
- CR: 84%. Long-term survival: 75%
- CR: 52-57%. Long-term survival: 47-56%

Treatment results of aggressive non-Hodgkin’s
lymphomas according to the risk group
Risk group No of risk CR 5-year
survival
__________________factors ________%______________%______
Low 0,1 87 73
Low intermediate 2 67 50
High intermediate 3 55 43
High 4,5 44 26

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Cervical lymph adenopathy

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Cervical lymph adenopathy