Non-Hodgkin lymphoma

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

Non-Hodgkin lymphomas (NHLs), are diverse group of blood cancers that include any kind of lymphoma except Hodgkin’s lymphomas. Lymphomas are types of cancer derived from lymphocytes, a type of white blood cell. Non-Hodgkin lymphoma may be classified into subtypes according to updated WHO classification and rate of growth. There are no established causes for non-Hodgkin lymphoma. Non-Hodgkin lymphoma must be differentiated from Hodgkin’s disease, viral infections, metastatic carcinoma, and autoimmune diseases. In 2015, the incidence of non-Hodgkin lymphoma was estimated to be 24 cases per 100,000 individuals in the United States. In the United States, the age-adjusted prevalence of non-Hodgkin lymphoma is 131.1 per 100,000 individuals in 2011. The known risk factors in the development of non-Hodgkin lymphoma are weakened immune system, autoimmune disorders, certain infections and previous cancer treatment. Other possible risk factors include positive family history of non-Hodgkin lymphoma, exposure to pesticides, exposure to trichloroethylene, diet, obesity, hair dyes, and occupational exposures. Common complications of non-Hodgkin lymphoma include autoimmune hemolytic anemia and infection. The indolent non-Hodgkin lymphoma types are associated with a relatively good prognosis. According to the Ann Arbor staging system, there are four stages of non-Hodgkin lymphoma based on the number of nodes and extra nodal involvement. The most common symptom of non-Hodgkin lymphoma is painless swelling of the lymph nodes in the neck, underarm (axilla), or groin. Other symptoms of non-Hodgkin lymphoma may include fever, weight loss, poor appetite, night sweats, constant fatigue, itchy skin, reddened patches on the skin, cough, shortness of breath, abdominal pain or swelling, constipation, nausea, vomiting, headache, concentration problems, personality changes, and seizures. Common physical examination findings of non-Hodgkin lymphoma include fever, pruritus, petechiae, chest tenderness, abdominal tenderness, hepatomegaly, splenomegaly, peripheral lymphadenopathy, seizures, and central lymphadenopathy. Laboratory tests for non-Hodgkin lymphoma include complete blood count (CBC), blood chemistry studies, HIV blood test, and hepatitis B blood test. On chest x ray, non-Hodgkin lymphoma is characterized by nodules and pleural effusion. CT and MRI scan may be helpful in the diagnosis of non-Hodgkin lymphoma. On ultrasound, non-Hodgkin lymphoma is characterized by hepatomegaly and splenomegaly. Lymph node or extra nodal tissue biopsy is diagnostic of non-Hodgkin lymphoma. PET and bone scan may be helpful in the diagnosis of non-Hodgkin lymphoma. Other diagnostic studies for the diagnosis of non-Hodgkin lymphoma include bone marrow aspiration, bone marrow biopsy, and lumbar puncture. The predominant therapy for non-Hodgkin lymphoma is chemotherapy. Adjunctive radiation, immunotherapy, and stem cell transplantation may be required. Surgical intervention is not recommended for the management of non-Hodgkin lymphoma.

Non-Hodgkin lymphoma may be classified into subtypes according to updated WHO classification and rate of growth.

There are no established causes for non-Hodgkin lymphoma.

Non-Hodgkin lymphoma must be differentiated from Hodgkin’s disease, viral infections, metastatic carcinoma, and autoimmune diseases.

In 2015, the incidence of non-Hodgkin lymphoma was estimated to be 24 cases per 100,000 individuals in the United States. In the United States, the age-adjusted prevalence of non-Hodgkin lymphoma is 131.1 per 100,000 individuals in 2011.

The known risk factors in the development of non-Hodgkin lymphoma are weakened immune system, autoimmune disorders, certain infections and previous cancer treatment. Other possible risk factors include positive family history of non-Hodgkin lymphoma, exposure to pesticides, exposure to trichloroethylene, diet, obesity, hair dyes, and occupational exposures.

Common complications of non-Hodgkin lymphoma include autoimmune hemolytic anemia and infection. The indolent non-Hodgkin lymphoma types are associated with a relatively good prognosis.

According to the Ann Arbor staging system, there are four stages of non-Hodgkin lymphoma based on the number of nodes and extra nodal involvement.

The most common symptom of non-Hodgkin lymphoma is painless swelling of the lymph nodes in the neck, underarm (axilla), or groin. Other symptoms of non-Hodgkin lymphoma may include fever, weight loss, poor appetite, night sweats, constant fatigue, itchy skin, reddened patches on the skin, cough, shortness of breath, abdominal pain or swelling, constipation, nausea, vomiting, headache, concentration problems, personality changes, and seizures.

Common physical examination findings of non-Hodgkin lymphoma include fever, pruritus, petechiae, chest tenderness, abdominal tenderness, hepatomegaly, splenomegaly, peripheral lymphadenopathy, seizures, and central lymphadenopathy.

Laboratory tests for non-Hodgkin lymphoma include complete blood count (CBC), blood chemistry studies, HIV blood test, and hepatitis B blood test.

On chest x ray, non-Hodgkin lymphoma is characterized by nodules and pleural effusion.

Chest, abdomen, and pelvis CT scan may be helpful in the diagnosis of non-Hodgkin lymphoma.

MRI may be helpful in the diagnosis of non-Hodgkin lymphoma.

On ultrasound, non-Hodgkin lymphoma is characterized by hepatomegaly and splenomegaly.

Lymph node or extra nodal tissue biopsy is diagnostic of non-Hodgkin lymphoma.

PET and bone scan may be helpful in the diagnosis of non-Hodgkin lymphoma.

Other diagnostic studies for the diagnosis of non-Hodgkin lymphoma include bone marrow aspiration, bone marrow biopsy, and lumbar puncture.

The predominant therapy for non-Hodgkin lymphoma is chemotherapy. Adjunctive radiation, immunotherapy, and stem cell transplantation may be required.

Surgical intervention is not recommended for the management of non-Hodgkin lymphoma.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

In 1864 and 1865, Virchow and Cohnheim independently described non-Hodgkin lymphoma and called it lymphosarcoma and psedoleukemia respectively. In 1997, FDA approved rituximab, to treat patients with B-cell non-Hodgkin lymphoma that did not responds to other treatments Since then, tremendous efforts of many scientists have been continuing to provide more precise and comprehensive with pathology, staging, and treatment of Hodgkin’s lymphoma.

• In 1864, Virchow, a German physician, described lymph node enlargement not related to leukemia as lymphosarcoma (a subdivision of aleukimic type of leukemias).
• In 1865, Cohnheim, a German-Jewish physician, used the term pseudolukemia to describe all common lymphadenopathy and splenomegaly.
• In 1871, Bilroth, a Prussian-born Austrian surgeon, was the first to described a case of non-Hodgkin lymphoma, and coined the term malignant lymphoma.^[1]
• In 1958, Denis Parsons Burkitt, an Irish surgeon, first discovered Burkitt’s lymphoma while working in Africa.^[2]
• In 1925, follicular lymphoma was described by Brill and Symmers, independently.^[3]
• In 1956, Henry Rappaport and his colleagues proposed the Rappaport classification, based on cellular morphology. This became the first widely accepted classification of non-Hodgkin lymphomas.
• In 1966, Armed Forces Institute of Pathology (AFIP) modified the the Rappaport classification in the “Tumors of the Hematopoietic System”.^[4]
• In 1982, National Cancer Institute introduced the working formulation, an amalgamation translating all previous classifications, which defined three grades of non-Hodgkin lymphoma.^[5]
• In 1992, Banks first coined the term mantle cell lymphoma (MCL).^[6]
• In 1994, the Revised European-American Classification of Lymphoid Neoplasms (REAL) classified non-Hodgkin’s lymphoma, based on immunologic, genetic and clinical characteristics of the disorders in addition to histopathologic characteristics of the tumor cells.^[7]
• Since 2008 the World Health Organisation (WHO) has been starting a project with committees of international hematopathologists and oncologists, who have developed lists and definitions of disease entities to ensure that the classification will be helpful to clinicians. They proposed their first approach in 2008 and after that, the relevant Clinical Advisory Committee (CAC) updates its latest revision every few years.^[8][9]
• The latest revision of classification of neoplastic diseases of the haematopoietic and lymphoid tissues by World Health Organisation (WHO) was done in 2016.^[10]

• In 1997, FDA approved rituximab, to treat patients with B-cell non-Hodgkin lymphoma that did not responds to other treatments.^[11]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

Non-Hodgkin lymphoma may be classified into subtypes according to updated WHO classification and rate of growth.

• Non-Hodgkin lymphoma may be classified according to updated WHO classification into 2 groups:^[1][2]

• B-cell neoplasms
• T-cell and putative NK-cell neoplasms

• Non-Hodgkin lymphoma may be classified based on rate of growth into 2 groups:^[3]

• Low-grade or Indolent lymphoma
• High-grade or Aggressive lymphoma

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

Non Hodgkin’s Lymphoma (NHL) represents a heterogeneous group of diseases with varied clinical presentation and histological appearance.It arises from cell of the lymphoid system, tumors are mainly derived from B lymphocytes, but are also from T lymphocytes, or natural killer cells. Lymphomas rise from different stages of B and T cell differentiation. Aberrations in the tightly controlled steps of B cell development can lead to oncogenesis. These aberrations are mainly seen in form of chromosomal translocation. About 85% of NHL’s are of B-cell origin and only 15% are derived from T/NK cells. Two specific lymphomas, follicular lymphoma and diffuse large B cell lymphoma, account for about 65% of all non-Hodgkin lymphomas.

• Lymphomas can arise from different stages of B cell development:
• B cell development starts in the primary lymphoid tissue, the bone marrow and subsequent maturation takes place in secondary lymphoid tissue (spleen and lymph nodes).
• At the germinal centers of secondary lymphoid tissue B cells encounter antigens via T cells and then undergo affinity maturation to produce immunoglobulins of high affinity.
• It supports rapid B-cell proliferation for immunoglobulin affinity maturation and production of antibody diversity through two processes know as somatic hypermutation (SHM) and immunoglobulin class switching.
• Both of these processes require rapid cell turnover and multiple double stranded DNA breaks, which is error-prone.
• Somatically acquired genetic alterations ( mainly translocations) of these processes is probably the underlying cause of lymphomagenesis.

• The major subtypes of non-hodgkin lymphoma (NHL) include the following:
  • Mature B-cell neoplasms:
    • Diffuse large B cell lymphoma
    • Follicular lymphoma
    • Burkitt lymphoma
    • Mantle cell lymphoma
    • Hairy cell leukemia
    • Extranodal marginal zone lymphoma
    • Splenic marginal zone lymphoma
    • Plasma cell myeloma
  • Mature T and NK neoplasms:
    • Adult T-cell lymphoma
    • Mycosis fungoides
    • Sezary syndrome
    • Peripheral T cell lymphoma

• About 85% of NHLs are of B-cell origin and only 15% are derived from T/NK cells.^[1]
• The small remainder stems from macrophages.
• These tumors are characterized by the level of differentiation, the size of the cell of origin, the origin cell’s rate of proliferation, and the histological pattern of growth.
• Lymphomas of small lymphocytes generally have a more indolent course than those of large lymphocytes, which may have intermediate-grade or high-grade aggressiveness.
• Two specific lymphomas, follicular lymphoma and diffuse large B cell lymphoma, account for about 65% of all non-Hodgkin lymphomas.
• The gene-expression profiles of almost all non-Hodgkin lymphomas are a reflection of the equivalent healthy cell of origin from which the lymphoma is derived.^[1]
• Follicular lymphoma most commonly results from the t(14;18)(q32;q21) translocation; this translocation places BCL2 (which encodes B-cell CLL/lymphoma 2) under control of the IGH enhancer element, leading to constitutive BCL2 expression.^[2]
• BCL-2 is an anti-apoptotic protein, and the t(14;18)(q32;q21) translocation results in markedly elevated expression of BCL-2, which blocks the healthy germinal center default program of apoptotic cell death and represents a defining pathogenic feature of follicular lymphoma.^[2][3]
• Similarly, mantle cell lymphoma is characterised by the t(11;14)(q13;q32) translocation, which leads to the deregulated expression of cyclin D1.^[4]
• Moreover, burkitt lymphoma overexpresses MYC as a result of the t(8;14)(q24;q32) translocation or variants.
• Recurrent translocations are less common in peripheral T-cell lymphomas than in other types of lymphoma, and examples include the characteristic t(2;5) (p23;q35) translocation seen in anaplastic lymphoma kinase (ALK)-positive anaplastic T-cell lymphoma and the t(5;9)(q33;q22) translocation associated with follicular T-cell lymphoma.^[5]
• Recurrent translocations including t(6;7) (p25;q32) and recurrent gene fusions involving the tumour-suppressor gene TP63 are characteristic of ALK-negative anaplastic T-cell lymphoma.^[5][6]
  

The development of non-Hodgkin lymphoma is the result of multiple genetic mutations such as:^[7][8]

• Mutations of the B-cell receptor genes and NFKB pathway.
• RNA splicing mutations in the small lymphocytic lymphoma.
• Genetic mutations in histone formation:^[9]
  • MLL2
  • MEF2B
  • EZH2
  • CREBBP
  • EP300
  • MLL2
  • KMT2D
• Mutations in CDKN2A alters cell cycle control and affects JAK–STAT signalling.
• Upregulation of key signalling pathways such as CD79B, MYD88, CARD11.
• Block to terminal differentiation such as BCL6 translocations and loss of PRDM1.

• Several conditions are associated with non-Hodgkin’s lymphoma depending on the type. However, Epstein Barr virus, human immunodeficiency virus, and hepatitis C infection are commonly present.

• For information on gross pathology findings of Follicular lymphoma, click here.
• For information on gross pathology findings of Mantle cell lymphoma, click here.
• For information on gross pathology findings of Hairy cell leukemia, click here.
• For information on gross pathology findings of Splenic marginal zone lymphoma, click here.
• For information on gross pathology findings of Mycosis fungoides, click here.
• For information on gross pathology findings of Peripheral T cell lymphoma, click here.

• For information on microscopic pathology findings of Follicular lymphoma, click here.
• For information on microscopic pathology findings of Mantle cell lymphoma, click here.
• For information on microscopic pathology findings of Hairy cell leukemia, click here.
• For information on microscopic pathology findings of Splenic marginal zone lymphoma, click here.
• For information on microscopic pathology findings of Mycosis fungoides, click here.
• For information on microscopic pathology findings of Peripheral T cell lymphoma, click here.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

Non Hodgkin lymphoma may arise due to genetic causes, immunodeficiency state, infection, environmental factor, and chronic inflammation.

• There are no life-threatening causes of non Hodgkin lymphoma (NHL), however complications resulting from untreated non Hodgkin lymphoma is common.

Common causes of non Hodgkin lymphoma may include:

• Chromosomal translocation
• Infections
• Environmental factor
• Immunodeficiency state
• Chronic inflammation

• Chromosomal translocations play a vital role in the pathogenesis of many lymphomas.^[1]
• The t(14;18)(q32;q21) translocation is the most common chromosomal abnormality associated with Non Hodgkin Lymphoma.
• It occurs in 85% of follicular lymphomas and 28% of higher-grade Non Hodgkin Lymphoma.^[2]
• This results in the juxtaposition of the bcl -2 apoptotic inhibitor oncogene at chromosome band 18q21 to the heavy chain region of the immunoglobulin (Ig) locus within chromosome band 14q32..
• The t(11;14)(q13;q32) translocation has association with mantle cell lymphoma.^[3]
• It causes overexpression of bcl -1 (cyclin D1/PRAD 1), a cell-cycle regulator on chromosome band 11q13.^[4]
• The 8q24 translocations causes c-myc dysregulation.^[5][6]
• It is frequently seen in high-grade small noncleaved lymphomas such as Burkitt lymphoma, including the one associated with HIV infection.
• The t(2;5)(p23;q35) translocation occurs between the nucleophosmin (NPM) gene and the anaplastic lymphoma kinase (ALK1) gene.^[4][7]
• This results in the expression of a fusion protein found in a majority of anaplastic large cell lymphomas.
• Two chromosomal translocations, t(11;18)(q21;q21) and t(1;14)(p22;132), are associated with mucosa-associated lymphoid tissue (MALT) lymphomas.
• The more common type such as t[11;18][q21;q21] translocates the apoptosis inhibitor AP12 gene with the MALT1 gene; resulting in the expression of an aberrant fusion protein.
• The other translocation, t(1;14)(p22;132), involves the translocation of the bcl -10 gene to the immunoglobulin gene enhancer region.

• Some viruses are involved in the pathogenesis of Non Hodgkin Lymphoma because of their ability to induce chronic antigenic stimulation and cytokine dysregulation resulting in uncontrolled B- or T-cell stimulation, proliferation, and lymphomagenesis.
• Epstein-Barr virus (EBV) is a DNA virus that is associated with Burkitt lymphoma, lymphomas in immunocompromised patients; and sinonasal lymphoma.
• Human T-cell leukemia virus type 1 (HTLV-1) causes a latent infection due to reverse transcription ability in activated T-helper cells.
• It is endemic in certain areas of Japan and the Caribbean islands, and approximately 5% of carriers develop adult T-cell leukemia or lymphoma.
• Hepatitis C virus (HCV) is associated with the development of clonal B-cell expansions, lymphoplasmacytic lymphoma; and Waldenström macroglobulinemia especially in the setting of essential mixed cryoglobulinemia.
• Kaposi sarcoma–associated herpesvirus (KSHV) is associated with body cavity lymphomas in patients with immunocompromised state and in patients with multicentric Castleman disease.
• Helicobacter pylori infection is associated with the development of gastrointestinal lymphomassuch as gastric mucosa-associated lymphoid tissue (MALT) lymphomas.

Environmental factors associated with Non Hodgkin Lymphoma include:^[8][9]

• Pesticides
• Herbicides
• Solvents
• Organic chemicals
• Wood preservatives
• Dusts
• Hair dye
• Chemotherapy
• Radiation exposure
• Smoking

Immunodeficiency states associated with Non Hodgkin Lymphoma include:^[2]

• Congenital immunodeficiency states
  • Severe combined immunodeficiency disease (SCID)
  • Wiskott-Aldrich syndrome
• Acquired immunodeficiency states
  • AIDS
• Induced immunodeficiency states
  • Immunosuppression

Autoimmune disorders associated with Non Hodgkin Lymphoma include:^[10][11]

• Sjögren syndrome
• Hashimoto thyroiditis
• Celiac disease

List the causes of the disease in alphabetical order:

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[5]

Non-Hodgkin lymphoma must be differentiated from Hodgkin’s disease, viral infections, metastatic carcinoma, and autoimmune diseases.

Non-Hodgkin lymphoma must be differentiated from common disorders with localized or generalized lymphadenopathy such as:

• Neoplasm

• Hodgkin’s disease
• Chronic lymphocytic leukemia
• Small cell carcinoma of the lung
• Melanoma
• Lymphomatoid granulomatosis
• Angioimmunoblastic lymphadenopathy
• Giant lymph node hyperplasia (Castleman disease)

• Infections

• Syphilis
• Brucellosis
• Infectious mononucleosis
• CMV
• HIV
• Cat scratch disease
• Tuberculosis
• Toxoplasmosis

• Autoimmune diseases

• Systemic lupus erythematosus
• Sjögren’s syndrome
• Sarcoidosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

In 2015, the incidence of non-Hodgkin lymphoma was estimated to be 24 cases per 100,000 individuals in the United States. In the United States, the age-adjusted prevalence of non-Hodgkin lymphoma is 131.1 per 100,000 individuals in 2011.

• Non-Hodgkin lymphoma (NHL) is the most common hematologic malignancy in the world.^[1]
• NHL ranks as the 7th most common cancer among males and the 6th most common cancer among females.^[1]

• The incidence/prevalence of non Hodgkin lymphoma is approximately 13.2 per 100,000 individuals worldwide.^[1][2]

• Non Hodgkin lymphoma is the 6th most common cause of cancer related death in the world.^[1]

• Patients of all age groups may develop non Hodgkin lymphoma.^[3]
• B and T cell lymphoblastic lymphoma/leukemia occurs most frequently in children and adults greater than 65 years of age.
• Burkitt’s Lymphoma affects individuals between 20–64 years of age.
• Primary mediastinal large B-cell lymphoma has a median age of 35.

• Non Hodgkin lymphoma usually affects individuals of the Caucasian race.^[4]
• In the US, the relative risk (RR) of HIV-associated NHL in African-American is half that of Caucasians (RR 22.3, 95% CI, 17.1–29 vs. RR 46.2, 95% CI, 38.8–55) mainly due to ethnic variations in immune system regulatory genes.^[5]

• Men are more commonly affected by non Hodgkin lymphoma than women. The Male to female ratio is approximately 1.5:1 to 3:1.^[6][7][8]

• The majority of non Hodgkin lymphoma cases are reported in North America, Africa and East Asia.^[9]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

The known risk factors in the development of non-Hodgkin lymphoma are weakened immune system, autoimmune disorders, certain infections, and previous cancer treatment. Other possible risk factors include positive family history of non-Hodgkin lymphoma, exposure to pesticides, exposure to trichloroethylene, diet, obesity, hair dyes, and occupational exposures.

The known risk factors in the development of non-Hodgkin lymphoma are:^{[1][2][3][4][5][6]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

According to the the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for Non-Hodgkin lymphoma.

According to the the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for Non-Hodgkin lymphoma.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Preeti Singh, M.B.B.S.[2]

Common complications of non-Hodgkin lymphoma include lymphadenopathy, disseminated intravascular coagulation, superior vena cava (SVC) syndrome, autoimmune hemolytic anemia and infection. The indolent non-Hodgkin lymphoma types are associated with a relatively good prognosis. The 5-year relative survival rate of patients with NHL is 71.4%.

Common complications of non-Hodgkin lymphoma include:^[1]

• Lymphadenopathy especially cervical lymphadenopathy
• Cytopenias such as neutropenia, anemia and thrombocytopenia secondary to bone marrow infiltration
• Autoimmune hemolytic anemia
• Bleeding secondary to thrombocytopenia
• Disseminated intravascular coagulation (DIC)
• Infection secondary to neutropenia
• Cardiac problems secondary to large pericardial effusion
• Cardiac arrhythmias secondary to cardiac metastases
• Respiratory problems secondary to pleural effusion
• Superior vena cava (SVC) syndrome secondary to a large mediastinal tumor
• Spinal cord compression secondary to vertebral metastases
• Neurologic problems secondary to primary CNS lymphoma or lymphomatous meningitis
• Gastrointestinal obstruction, perforation, and bleeding in a patient with MALT lymphoma
• Pain secondary to tumor invasion
• Lymphocytosis in leukemic phase of disease

• The 5-year relative survival rate of patients with NHL is 71.4%.^[2]
• The survival rate has steadily improved over the last 2 decades, thanks to improvements in medical and nursing care, the advent of novel therapeutic strategies (ie, monoclonal antibodies), validation of biomarkers of response, and the implementation of tailored treatment.
• The prognosis for patients with NHL depends on the following factors:^[2]
  • Tumor histology
  • Tumor stage
  • Patient age
  • Tumor bulk
  • Performance status
  • Serum lactate dehydrogenase (LDH) level
  • Beta2-microglobulin level

• The International Prognostic Index (IPI), which was originally designed as a prognostic factor model for aggressive non Hodgkin lymphoma (NHL) appears to be useful for predicting the outcome of patients with low-grade lymphoma and mantle cell lymphoma.^[2][3]
• This index is used to identify patients at high risk of relapse, based on specific sites of involvement, including bone marrow, CNS, liver, testis, lung, and spleen.
• Clinical features included in the IPI that are independently predictive of survival include the following:
  • Age – Younger than 60 years versus older than 60 years
  • LDH level – Within the reference range versus elevated
  • Performance status – Eastern Cooperative Oncology Group ( ECOG) grade 0-1 versus 2-4
  • Ann Arbor stage – Stage I-II versus III-IV
  • Number of extranodal sites – Zero to 1 versus more than 1
• With this model, relapse-free and overall survival rates at 5 years are as follows:
  • 0-1 risk factors – 75%
  • 2-3 risk factors – 50%
  • 4-5 risk factors – 25%

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Study of choice Biopsy is the gold standard test for the diagnosis of non-Hodgkin’s lymphoma

A biopsy is needed to make a diagnosis. A surgeon removes a sample of tissue, which a pathologist can examine under a microscope to check for cancer cells. A biopsy for non-Hodgkin’s lymphoma is usually taken from lymph nodes that are enlarged, but other tissues may be sampled as well. Biopsies in internal lymph nodes can also taken as needle biopsies under the guidance of CT scans. Rarely, an operation called a laparotomy may be performed. During this operation, a surgeon cuts into the abdomen and removes samples of tissue to be checked under a microscope.

The doctor may also order tests that produce pictures of the inside of the body. These may include:

• X-rays: Pictures of areas inside the body created by high-energy radiation.
• CT scan (computed tomography scan, also known as a “CAT scan”): A series of detailed pictures of areas inside the body. The pictures are created by a computer linked to an x-ray machine.
• PET scan (positron emission tomography scan): This is an imaging test that detects uptake of a radioactive tracer by the tumor. More often, the PET scan can be combined with the CT scan.
• MRI (magnetic resonance imaging): Detailed pictures of areas inside the body produced with a powerful magnet linked to a computer.

• Lymphangiogram: Pictures of the lymphatic system taken with x-rays after a special dye is injected to outline the lymph nodes and vessels. This test is not used as often because of the adoption of CT scan and the PET scan technologies.
• Gallium scan: Gallium is a rare metal that behaves in the body in a fashion similar to iron, so that it concentrates in areas of inflammation or rapid cell-division, and hence is useful for imaging the entire lymphatic system for staging of lymphoma once the presence of the disease has been confirmed. PET scans have supplanted gallium scans for evaluation and follow up of NHL.

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