Want to support free content?
Let us know who you are!
Why am I seeing this?
LearnOncology.ca is a free educational content provider. If you want to support our editors (powered by caffeine and no sleep), fill in the following info to let us know who is using the site. We use cookies to prevent this popup from coming up frequently. Continue using the site if you are happy with this.
The following module was designed following the objectives of the Oncology Goals and Objectives for Medical Students for lymphoma. Information on epidemiology, risk factors, screening, presentation, diagnosis, and treatment for non Hodgkin’s lymphoma is provided. By the end of this module, the following objectives should be addressed:
The lymphatic system consists of lymphoid organs and tissues. These include the spleen, thymus, tonsils, lymph nodes, bone marrow, and Peyer’s patches. Most of the lymphatic vessels empty into the thoracic duct, which itself empties into the venous system at the juncture of the left internal jugular vein and left subclavian vein. In contrast, lymph from the right arm, parts of the right thorax, and right side of the head and neck empty into the right lymphatic duct, which itself empties into the venous system at the juncture of the right internal jugular vein and right subclavian vein (1).
The lymphatic system is involved in two major processes: circulation and immune defense. Within the circulatory system, the lymphatic system provides a route through which fluid can travel between the interstitial spaces and blood. In particular, this is important for transfer of proteins between the interstitial space and blood. The lymphatic system is also important for absorption of nutrients, especially of fats (1).
The lymphatic system also plays an important role in immune defense. Lymphocytes are a major component of the lymphatic system, and are involved in both innate and acquired immunity. In addition, lymphoid tissue such as lymph nodes trap and remove foreign particles from the circulating lymph (1).
Lymphomas refer to a group of cancers that develop from cells in lymphoid organs / tissues. These cancers are heterogeneous in nature and can arise from various lymphocytes including B cells, T cells, and natural killer cells, or precursors of these cells. In addition, they can vary from indolent to aggressive. Classically, lymphoma is subdivided into Hodgkin's lymphoma and non Hodgkin's lymphoma (NHL). For purposes of this module, we will be discussing NHL (2).
NHL is a fairly common form of cancer. In Canada, the incidence is estimated at 5.0% of all cancers for males, and 4.1% for females. This makes it the 5th most common type of cancer in males, and the 6th in females (1). NHL is more common amongst older adults. The majority of those diagnosed are in the 65-75 age range, with a median age of diagnosis of 67 years (2). Geography and ethnicity also play a role in NHL. It is most common in Caucasians and Hispanics, and less common in Asian / Pacific Islanders and American Indian / Alaska Natives (2).
NHL is very common amongst those living with HIV. The RR has been reported as >100 when compared to the general population. Chronic antigenic stimulation and immune deficiency have been speculated as the cause for this association. Fortunately, the advent of highly active antiretroviral therapy (HAART) has reduced the risk considerably (1).
Those who undergo solid organ or allogeneic hematopoietic cell transplantation also have a markedly increased risk of developing NHL, with the RR approaching 100 (2). The mechanism for this is the long-term immunosuppressive therapy that these individuals are placed on to reduce the risk of organ rejection (3).
In addition to acquired immunodeficiency, there are a number of inherited immunodeficiency states that are associated with an increased incidence of lymphoma. These include Ataxia
Telangiectasia, Wiskott-Aldrich syndrome, and Klinefelter's syndrome among others (2).
Individuals with some autoimmune conditions have an increased risk of NHL. In particular, strong associations have been shown between systemic lupus erythematosus (RR: 7.4), rheumatoid arthritis (RR: 2.9), and Sjögren's syndrome (RR: 18.8). Other conditions with some association include celiac disease and psoriasis. It is currently unclear if it is related to the chronic inflammatory nature of the disease entities themselves or with the immunosuppressive agents used to treat these conditions (1).
The pathogenesis of many lymphomas are driven by viral and bacterial infections. Infection with Epstein-Barr virus (EBV) has been shown to increase the risk of Burkitt lymphoma. Interestingly, reactivation of EBV plays a role in the pathogenesis of a portion of the cases of NHL that are associated with HIV and immunosuppression following organ transplant (1).
Human herpes virus 8 (HHV-8) has been shown to be associated with an increased risk of primary effusion lymphoma, and human T-cell lymphotropic virus type 1 (HLTV-1) has been shown to be associated with increased risk of adult T-cell leukemia / lymphoma (4).
Heliobacter pylori (H.pylori) is a particular risk factor for mucosa associated lymphoid tissue (MALT) lymphoma, of which the proposed mechanism is through chronic inflammation (5). For those with gastric lymphoma there was an OR of 6.3 for having had a previous H.pylori infection (5). In addition, of 110 cases of gastric MALT lymphomas, H.pylori infection was found in 92% of them (6).
There is an array of genetic features that appear to predispose an individual to particular subtypes of NHL. Some of the implicated genes include the Th1/Th2 cytokine pathway genes encoding for: tissue necrosis factor (TNF) and interleukin-10 (IL-10), and cytokines involved in inflammatory responses and innate immune function (1,4). A more detailed discussion of particular genes and genetic conditions is available elsewhere (2).
There is a fairly exhaustive list of potential environmental exposures that lead to an increased risk of NHL. These include arsenic, pesticides, fungicides, organic solvents, hair dyes, lead, chloride, and asbestos. Additionally, agricultural work, welding, and the lumber industry have been linked to NHL. Finally, previous chemotherapy or radiation therapy has been associated with NHL, particularly as a late complication (1,2).
The presentation of NHL is inherently broad owing to the extensive anatomical range of the lymphatic system.
At the core of the presentation of NHL is the classic “painless, persistent, lymphadenopathy”, characterised as enlarged, generally more than 2 cm, painless lymph nodes that are firm/rubbery, mobile, and persistent. These enlarged lymph nodes themselves may cause local symptoms secondary to compression of surrounding structures such as blood vessels and nerves. This is estimated to constitute 66% of the NHL's initial presentation (1).
Within aggressive NHL subtypes, the acute or subacute development of a rapidly growing lymph node and constitutional symptoms may be the only symptoms. The most common example of this is Diffuse Large B Cell Lymphoma (2). Indolent NHL subtypes tend to have more slow growing lymph nodes that wax and wane in size; they less frequently have constitutional symptoms, and they may have organomegaly, namely splenomegaly and hepatomegaly. The most common example of this is Follicular Lymphoma (3). Symptoms associated with splenomegaly include left upper quadrant pain or discomfort and early satiety.
Primary “extranodal site” presentations of NHL also make up a significant portion, approximately 33%, of the initial presentation of NHL. Two major categories of extranodal site presentations include primary gastrointestinal lymphomas, and primary central nervous system lymphomas (1).
Primary gastrointestinal lymphomas may present with anorexia, nausea, vomiting, weight loss, and symptoms of gastrointestinal hemorrhage (i.e., hematemesis, melena, and persistent abdominal pain, particularly epigastric), visceral obstruction, and in some cases abdominal perforation (4). Primary central nervous system lymphomas present with headache, lethargy, and symptoms of neurological compromise including: focal neurological symptoms, paralysis, seizures, spinal cord compression, or meningitis (5).
Additionally, lymphoma can present as an anterior mediastinal mass, and thus should always be considered in the differential diagnosis. Classically, the differential for anterior mediastinal masses are made up of the 4 T’s (terrible lymphoma, thymic tumor, thyroid tumor, and teratoma) (6).
B Symptoms are defined as unexplained fevers >38.3°C, drenching night sweats, and unintentional weight loss. B symptoms are more commonly seen in aggressive subtypes of NHL, but may also be seen in indolent subtypes of NHL (7).
Paraneoplastic syndromes are very rare in NHL. For instance, there are case reports of Pareneoplastic myelopathy, autonomic ganglionopathy, and various forms of neuropathy.
The one exception appears to be dermato/poly-myositis which has been demonstrated to have an association with NHL (8).
Infiltration of the bone marrow by NHL can lead to anemia, thrombocytopenia, leukopenia, or pancytopenia. Deficiencies in these cell lines subsequently lead to specific patterns of symptoms. Anemia may present with fatigue, pallor, shortness or breath with exertion, and palpitations. Leukopenia may present with increased rate of infections or increased severity of infection. Thrombocytopenia may present with increased bruising, slower clotting, and petechiae (1).
Lymphadenopathy is defined as lymph nodes that are of abnormal size or consistency. It is typically a benign and self-limiting condition, but may require further workup (1).
The etiology of lymphadenopathy is varied. A proposed mnemonic is MIAMI, which stands for malignancy, infections, autoimmune disorders, miscellaneous, and iatrogenic (1). In primary care, viral or bacterial upper respiratory illnesses or nonspecific causes account for more than two-thirds of patients presenting with lymphadenopathy (2). Malignancy accounts for less than 1% (2).
It is important to assess for patient age, duration of lymphadenopathy, occupation, exposures, associated signs and symptoms, and location. Lymphadenopathy in children is typically benign or infectious. Likewise, lymphadenopathy lasting less than two weeks is generally not worrisome. Ask about past medical history, medications, family history, risk factors for NHL, vaccinations, occupation, travel, and any environmental, animal, or insect exposures. Assess for symptoms such as sore throat, malaise, arthralgies, rash, and constitutional symptoms. It is also important to elucidate if the lymphadenopathy is localized or generalized (1,2,3).
Assess the quality and size of the lymph nodes. In particular, pay attention to mobility, consistency, tenderness, and warmth. Features suggestive of benign lymph nodes include a size <1cm, soft rubbery texture, and mobility. Tender or painful nodes are largely non-specific. In contrast, features suggestive of metastatic disease are hard and irregular lymph nodes that are immobile and have a matted consistency. Lymph nodes that are hard and rubbery, mobile, and symmetric are suspicious for lymphoma. Malignant nodes are typically painless. (1,2,3).
The location of the lymph node may be of particular importance. Palpable axillary, inguinal, or submandibular lymph nodes can be found in healthy people (3). In contrast, abnormal locations for palpable lymph nodes are supraclavicular, popliteal, and iliac (1).
Finally, assess for any associated splenomegaly, hepatomegaly, rash, or arthritis and look for any associated ENT findings, such as changes in Waldeyer’s ring. This can help to point to a specific cause (2,3).
In general, if features of lymphadenopathy are suggestive of benign disease, reassurance can be provided. If findings are suggestive of infectious or autoimmune conditions, laboratory work-up should be pursued as necessary. Radiographic evaluation may be performed for cervical lymph nodes. Ultrasound is typically appropriate for initial evaluation of a suspicious node or nodes especially in young patients. CT may be appropriate in older patients or when there is suspicion of more widespread disease. A biopsy should be performed if the etiology is unknown. It should be arranged urgently if there are lymph node features suggestive of lymphoma or metastatic disease. Biopsy can be either a fine needle aspiration (FNA), core needle biopsy, or excisional biopsy, which is often strongly recommended if malignant disease is suspected (1). This excisional biopsy is recommended because FNA may not provide enough tissue to classify the disease.
There are no screening guidelines for NHL as of 2020.
In patients who present with clinical signs and symptoms suggestive of NHL, diagnostic evaluation should include a complete history and physical exam as discussed above, laboratory investigations, imaging studies, and excisional biopsy for pathology.
The general approach to laboratory evaluation of NHL includes (1):
A biopsy should be included in the workup of lymphadenopathy and is essential in the diagnosis of NHL. There are three potential options: fine-needle aspiration, core needle biopsy, and excisional biopsy. Generally, a fine needle aspiration is appropriate for suspected reactive lymph nodes or as an initial screening test. However, for definitive diagnosis, a full excisional biopsy should be performed, as this allows for evaluation of the cellular lymph node architecture. Therefore, in the setting of suspected lymphoma it is appropriate to go straight to excisional biopsy to allow for proper assessment. When biopsies are collected for evaluation of lymphoma, it is important to use the “Lymphoma Protocol”. This ensures that the samples are not sent in formalin which can compromise the diagnosis (2).
In addition to histological appearance, other tissue studies can be performed for further differentiation and profiling of lymphoma cells into specific subtypes of NHL. These include flow cytometry for immunophenotyping of lymphoid cells, and cytogenetic studies (3).
A bone marrow biopsy should also be considered for staging and prognosis in most cases of NHL, and a lumbar puncture should be performed in cases where there is high risk for CNS involvement (1,3).
Imaging is required for the staging of patients with NHL, and the optimal imaging modality is dependent on the suspected subtype of NHL. A CT neck, chest, abdomen and pelvis is a standard part of staging NHL, and this is often adequate for indolent NHL, though PET use may become standard for certain indolent lymphomas in the future. In aggressive NHL, however, FDG PET plays an important role in staging, assessment of treatment response, and directing therapy. The intensity of FDG avidity often correlates with histological aggressiveness. In addition, FDG-PET is also good at detecting extranodal NHL sites (1,3).
Non Hodgkin's lymphoma is classified following the 2016 WHO Classification of Lymphoid Malignancies (1). This divides NHL into two groups: those of B cell origin and those of T cell/natural killer (NK) cell origin. Within the B cell and T cell categories, two subdivisions are recognized: precursor neoplasms, which correspond to the earliest stages of differentiation, and more mature differentiated neoplasms. Within the B cell category, NHL can largely be characterized as either aggressive or indolent. Aggressive tumors require urgent treatment and are potentially curable. In contrast, indolent can generally be observed, but are largely incurable (2).
Burkitt lymphoma is derived from germinal center B cells. It is known for its highly aggressive nature, with a doubling time of <24 hours, presence of three distinct clinical forms, variable prevalence based on age, and association with EBV (2). The three clinical forms include the endemic, sporadic and immunodeficiency variants.
The endemic variant: found in Africa and New Guinea. It accounts for between 30-50% of pediatric cancer in these countries (3). It typically presents in the jaw / facial bones and spreads to primary and secondary sexual organs. It is EBV positive (2).
The sporadic variant: found in North America (NA) and Western Europe. It accounts for 30% of pediatric lymphoma, with a peak incidence age of 11, and less than 1% of adult lymphoma, with a median incidence age of 30 (4). It can present in the abdomen and spread to primary and secondary sexual organs as well as bone marrow and the CNS (2).
The immunodeficiency variant: which is typically seen in those with immunodeficiency, most commonly those who are HIV positive with a high CD4 count (5).
Among mature B cell lymphomas, DLBCL is the most common histologic subtype. It represents roughly one third of all cases. The median age of diagnosis is 64, and it is considered an aggressive subtype with patients often presenting with advanced stage disease. Many patients have constitutional symptoms at presentation and extra-nodal involvement is common in sites such as bone marrow, GI tract, liver, or skin (2).
MCL is an intermediate grade lymphoma, which accounts for about 6% of NHL. It is typically diagnosed around 63 years of age. Like indolent lymphomas it is generally not curable; however it requires more aggressive chemotherapy treatment in order to get an effective response (2). Two distinct types of MCL have been described. Classic MCL involves lymph nodes and extra nodal lymphatic sites. Leukemic MCL often spares lymph nodes and involves the peripheral blood, bone marrow, and spleen (6).
Among indolent NHL, MZL is the second most common type. It consists of 3 main subtypes.
Nodal MZL, which resembles follicular lymphoma and is treated similarly. Splenic MZL, which is most common in older Caucasian patients, presents with splenomegaly, lymphocytosis, and cytopenias; and is often associated with hepatitis C infection. The third subtype is MALT lymphoma, which is composed of extranodal tissue, most commonly the stomach, and is associated with chronic infections such as H.pylori and autoimmune conditions such as Sjogren's syndrome or Hashimoto's (2).
Follicular Lymphoma is the second most common form of NHL in NA and Europe, constituting 22% of NHL cases worldwide, and 30-35% in NA (2,7). It arises from germinal center B cells and is characterised by a pathognomonic follicular growth pattern. It classically presents initially as painless adenopathy in the cervical, axillary, inguinal, and/or femoral lymph node regions, with low rates of B symptoms, 20% (2,8). Because of its indolent nature, it is often diagnosed at an advanced stage, with 40% having splenic involvement, 50% having hepatic involvement, and 80% having involvement of the bone marrow (9).
SLL is considered to be the same disease as chronic lymphocytic leukemia (CLL) as they share the same genetic and molecular features. Notably, when the disease manifests in tissue or lymph nodes it is designated as SLL, while hematologic manifestations are classified as CLL (10).
It is possible for some subtypes of lymphoma to transform into other subtypes. For example, about 3% of follicular lymphomas are estimated to undergo histological transformation to DLBCL per year (2). Another example is Richter’s transformation, which describes when CLL converts to an aggressive lymphoma, typically DLBCL. When transformation of any kind is suspected the patient should be appropriately worked up (10).
ALCL is more common in pediatrics patients, where it accounts for about 10% of all pediatric lymphomas. It has several subtypes which have variable prognosis. Notably, there is a cutaneous variant, and a variant associated with breast implants. Typically, patients present with rapidly growing lymph nodes and constitutional symptoms (2).
AITL is the second most common T-cell lymphoma and accounts for roughly 20% of T-Cell lymphoma and 4% of all NHL. Patients may present with lymphadenopathy, hepatosplenomegaly, rash, arthritis, hemolytic anemia, and constitutional symptoms. The vast majority of patients will present with advanced stage disease, commonly with bone marrow involvement (2).
PTCL NOS is the most common type of T-Cell Lymphoma, and accounts for about 6% of all NHLs, and 15% of NHLs in adults. This category includes all entities not otherwise defined by the WHO classification. Patients generally present around 65 with advanced stage disease, which can include involvement of the bone marrow, liver, spleen, and skin. Constitutional symptoms are common, as is pruritus (2).
Otherwise known as cutaneous T-cell lymphoma, this is an indolent NHL with an age of onset around 55. It typically presents with eczematous or dermatitis skin lesions. The skin lesions are hard to diagnose early in the disease course as mycosis fungoides can mimic benign skin conditions. A high index of suspicion and careful observation and study over time may be necessitated. An aggressive form is known as Sezary syndrome and presents with generalized erythroderma and tumor cells in the blood (2).
The staging of NHL has been adapted over time. The previous iteration was the Ann arbor system. The current staging system is the “Lugano” Staging System, which is adapted from the Ann Arbor System. Although it is not part of the staging criteria for NHL the subscript “B” is useful clinically and added if B symptoms are present. The term “bulky” is generally added if the largest lymph node or involved mass is greater than 10cm (1).
Specific treatment of NHL lymphoma is complex. This treatment section will consist of a very high level overview of treatment options for NHL. Notably, each subtype of NHL has its own approach to treatment, and the treatment of lymphoma is also rapidly evolving. If you require a detailed overview of treatment regimens based on the subtype of NHL, there are other resources that provide excellent detail in this area.
We have chosen here to organize the treatment options into indolent vs aggressive forms of NHL. In general, indolent NHL are not curable, but can be observed and treated when symptomatic. However, there are some forms of limited stage indolent NHL that are curable. On the other hand, aggressive NHL is potentially curable but requires urgent treatment (1).
The treatment of NHL, like all malignancy, is dependent on patient, tumor, and treatment factors.
One particularly important discussion to have with patients being treated for NHL is fertility preservation via sperm or ovum banking. Recent advances have made infertility secondary to treatment less common, but nonetheless potential side effects should always be discussed with the patients.
Due to the slow growing nature of indolent NHL, observation MAY be appropriate, but there are specific scenarios it would not be the standard approach. If observation is chosen, patients are followed to check progression of the NHL. In the event that it progresses, or becomes symptomatic, treatment can be offered (2).
Radiation therapy is the standard treatment in limited stage indolent forms of NHL, and is especially effective for NHL with only one or a few lymph nodes affected. An example of a subtype of NHL that would be treated with RT alone when diagnosed in early stages is Follicular Lymphoma (3). Radiation therapy can result in cure in approximately 50% of cases.
Chemotherapy can be offered to patients with indolent NHL. Most commonly, a combination approach is elected, however single drugs may be given (2).
Single drug regimens include fludarabine, bendamustine, and chlorambucil. Common combination approaches used in the treatment of indolent NHL include CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone), CVP (cyclophosphamide, vincristine, and prednisone), or Bendamustine. For B-cell NHLs, chemotherapy is combined with the targeted therapy agent rituximab, which is a monoclonal antibody against CD20 which is found on B cells. These combinations are given the names: R-CHOP, R-CVP, and BR.
Immunotherapy consists of several different classes of drugs. These include monoclonal antibodies, cytokines, immune checkpoint inhibitors, immunomodulatory drugs, and chimeric antigen receptor T-cell therapy (CAR T cell therapy) (2).
There are currently over 10 different types of targeted immunotherapies that are used in the treatment of NHL. The specific targeted therapy used depends on the NHL subtype and patient responsiveness to other therapies. Targeted therapies can be used for some forms of limited stage indolent NHL. A common example is Rituximab, which is used in the treatment of B-cell lymphomas such as Follicular lymphoma (2,3). Rituximab has been considered a game changer in the treatment of many NHL as it has increased survival for many patients.
Chemotherapy tends to be the mainstay of treatment for both limited and advanced stage aggressive NHL. The commonly utilized chemotherapy regimens include: CHOP, R-CHOP, and Bendamustine / Rituximab also called BR. Other regimens such as dose-adjusted EPOCH-R can be used for high-risk or refractory or recurrent NHL. Radiation therapy is commonly given after chemotherapy to areas of residual disease or for palliation of symptoms due to lymph node masses or bone involvement (2).
Immunotherapy may be given as CNS prophylaxis, which functions to reduce / prevent the spread of NHL to the brain / spinal cord. Immunotherapy has been used to treat DLBCL which has been demonstrated to be refractory or is resistant to other forms of treatment. Specific examples for DLBCL are pembrolizumab, an immune checkpoint inhibitor, or CAR t cell therapy (2).
Targeted therapies such as monoclonal antibodies are also utilized to treat aggressive NHL. As previously mentioned, the specific targeted therapy agent is dependent on the NHL subtype and the patient responsiveness to other treatments. However, Rituximab remains the most common form of targeted immunotherapy, given to all patients with B cell NHL (2).
Radiation therapy may be given for localized NHL. However, in contrast to indolent NHL, it is not given alone if a curative approach is undertaken (unless the patient is not a chemoimmunotherapy candidate). Rather, radiotherapy is usually given adjuvantly after chemotherapy, such as in advanced stage DLBCL where it is used for residual PET positive disease (2).
Stem cell transplants can be used as part of the treatment for NHL. Some indications are as follows: the NHL has relapsed following treatment or the NHL is refractory to treatment. Generally, high dose chemotherapy, occasionally with total body radiation is used to kill both the healthy and cancerous cells in the bone marrow, and then healthy stem cells are given to replace the destroyed cells (2). Stem cell transplants can either be autologous (stem cells are harvested directly from the patient) or allogeneic (stem cells are harvested from a donor source). Donors for allogeneic stem cell transplants can be either siblings, a parent or child, or an unrelated donor, or from umbilical cord blood.
Some aggressive subtypes of NHL, such as Burkitt lymphoma or lymphoblastic lymphoma, are at high risk to spread into the CNS. For these forms of NHL, CNS prophylaxis is standard. Other subtypes, such as DLBCL, may have a particularly high risk of CNS recurrence that merits CNS prophylaxis in certain cases. CNS prophylaxis can include intrathecal methotrexate, high-dose systemic methotrexate, or intrathecal chemotherapy (2,3).
While there is not a prognostic index that includes all forms of indolent NHL, a predictive model has been developed for follicular lymphoma. It is known as the Follicular Lymphoma International Prognostic Index (FLIPI). The FLIPI model is based on several risk factors including age, LDH, hemoglobin, stage, and number of nodal areas. Notably, the treatment received did not include rituximab as the model was created prior to its availability (1).
The International Prognostic Index (IPI) for NHL was created to give a prognostic score for aggressive NHL (2). It should be noted that while this index provides a prognostic estimate, a more accurate prognosis is highly dependent on the histopathology of the NHL. In addition, the original IPI did not include rituximab in the study, and rituximab has since become a commonly used treatment modality. A modified IPI has been created which looks at the new advent of R-CHOP regimens for DLBCL (3). The models are based on several risk factors including age, tumor stage, performance status, number of extranodal sites, and LDH (2,3).
Specific follow up depends on the histological subtype and the clinical setting. A general summary has been provided below which provides a high level approach contrasting aggressive versus indolent NHL follow up. However, it is prudent to find the unique follow up schedule for your patient’s histological subtype.
In addition, patients treated for NHL can be young, so it is appropriate to consider late effects of therapy in your follow up. For example, think about endocrinopathies, infertility, and secondary cancers, and refer to specialists as indicated.
For aggressive lymphomas such as DLBCL or Burkitt lymphoma, the likelihood of relapses decreases with time. As such, the follow up schedule tends to taper off. These visits should include a history, physical exam, CBC, metabolic panel, and LDH. Currently, surveillance with imaging such as PET is not generally not recommended (1). However, this should be guided by the patient’s symptoms as there may be some benefit in certain circumstances.
For indolent lymphomas such as follicular lymphoma or mantle cell lymphoma the likelihood of recurrence remains the same or increases with time. Therefore, an appropriate follow up regimen consists of visits every 3-6 months indefinitely. These visits should include a history, physical exam, CBC, metabolic panel, and LDH. The role of surveillance imaging is uncertain (1).
Use your mouse to click through the slides and answer each question in the text box provided.
Note: This case can be completed on an iPad. To do this download the (free) Articulate Mobile Player for the iPad by clicking here.
