Hodgkin lymphoma (HL), originally named Hodgkin’s disease, is an uncommon monoclonal lymphoid tumor with high rates of recovery. Through multiple clinical and biological investigations, this disease has been classified into nodular lymphocyte-predominant Hodgkin lymphoma and classical Hodgkin lymphoma.
The clinical presentation and pathology of these two diseases are distinctly different. Almost all (95%) cases of Hodgkin lymphoma are attributed to classical Hodgkin lymphoma.
This disease is further divided into the following four subgroups:
Nodular Sclerosis Hodgkin lymphoma
Lymphocyte depleted Hodgkin lymphoma
Lymphocyte-rich Hodgkin lymphoma
Mixed Cellularity Hodgkin lymphoma
Hodgkin lymphomas have 4 distinct features which can be used to identify the disease:
Young adults are more prone to this disease
They often grow in cervical lymph nodes
Large mononuclear Hodgkin cells are scattered around with multinucleated cells in a mixture of non-neoplastic cells
T-lymphocytes are regularly found around neoplastic cells
4 out of 5 patients recover from Hodgkin Lymphoma, and it has a generally favorable prognosis for most patients.
Epidemiology
Hodgkin lymphoma is an uncommon malignancy in the United States, with an estimated incidence rate of 2.6 occurrences per 100,000 individuals. The disease accounts for 11% of all lymphomas diagnosed in the United States.
It has a bimodal distribution, with most affected patients being between the ages of 20 and 40, and another peak occurring between the ages of 55 and older. It is more prevalent in males than females, particularly in children, where 85 percent of occurrences occur in boys.
Hodgkin lymphoma with nodular sclerosis is more prevalent in young persons, whereas mixed cellularity Hodgkin lymphoma is more prevalent in older adults.
Given below is the incidence rates of all the subtypes of Classical Hodgkin lymphoma:
Nodular sclerosis classical HL (70%)
Mixed cellularity classical HL (25%)
Lymphocyte-rich classical HL (5%)
Lymphocyte-depleted classical HL (>1%)
Nodular lymphocyte-predominant Hodgkin lymphoma, accounts for around 5% of all Hodgkin lymphomas.
Anatomy
Pathophysiology
Unique neoplastic cells are present in both the classical and NLP-HL types of Hodgkin lymphoma. The Reed-Sternberg (RS) cell is a giant multinucleated neoplastic cell with two mirror-image nuclei inside a reactive cellular background.
For classical HL, the RS cell is pathognomonic. RS cells are produced from B cells with mutations in the IgH-variable region portion of the germinal center. Cytokines such as IL-5 and transforming growth factor-beta are secreted by the RS in order to recruit reactive cells. RS cells are often aneuploid, with no discernible cytogenetic abnormalities.
In the majority of isolated RS cells, conformational changes have been identified in the clonal lg gene. Immunohistochemistry stains for RS cells are positive for CD30, CD15, but typically negative for CD20 and CD45 that are positive only in neoplastic NLP-HL cells. In addition to CD15 and CD30, RS cells are usually positive for PAX5, CD25, HLA-DR, ICAM-1, Fascin, CD95 (apo-1/fas), TRAF1, CD40, and CD86. There are RS cell variants that include the Hodgkin cell, mummified cells, and lacunar cells. Hodgkin cells are mononuclear RS-cell variants.
Mummified cells show condensed cytoplasm and pyknotic reddish nuclei with smudgy chromatin. Lacunar cells have multilobulated nuclei, small nucleoli, and abundant, pale cytoplasm that often retracts during tissue fixation and sectioning, leaving the nucleus in what appears to be empty space (lacune-like space).
On the other hand, NLP-HL lacks the typical RS cells but has lymphocytic and histiocytic cells, which are characterized by larger cells with folded multilobulated nuclei (also known as “popcorn cells” or LP cells). The LP cells show a nucleus with multiple nucleoli that are basophilic and smaller than those seen in RS cells.
LP cells show clonally rearranged immunoglobulin genes that are only detected in isolated single LP cells. The LP cells are usually positive for C020, CD45, EMA, CD79a, CD75, BCL6, BOB.1, OCT2, and J chain.
Etiology
Hodgkin lymphoma’s exact cause is uncertain. However, Epstein-Barr virus (EBV) infection, autoimmune disorders, and immunosuppression all raise the chance of Hodgkin lymphoma. In Hodgkin lymphoma, there is additional evidence of a hereditary tendency. EBV was shown to be more prevalent in Hodgkin lymphoma subtypes with mixed cellularity and Hodgkin lymphomas which present lower levels of lymphocytes.
Immune deficiency has been considered as a probable cause of EBV-positive illness. No other virus has been identified as having a significant influence in the pathogenesis of Hodgkin lymphoma. Immunosuppression as a result of solid organ or hematopoietic cell transplantation, immunosuppressive medication therapy, or HIV infection all increase the chance of developing Hodgkin lymphoma.
HIV patients frequently present with an advanced stage of the infection, atypical lymph node locations, and a disappointing prognosis. Studies have discovered a tenfold increase in the risk of developing HL among same-sex siblings of Hodgkin lymphoma patients, implying that certain gene-environments are predisposed to developing Hodgkin lymphoma.
Genetics
Prognostic Factors
The prognoses of Hodgkin lymphoma cases are often decided based on 3 subgroups. The first stage, called the “Early-stage favorable”, in which the patient can be in the first or second stage of the disease without presenting any unfavorable risk factor.
The second sub-group also includes the first and second stage of Hodgkin lymphoma but with unfavorable risk factors. These include:
The present of 3 or more lymph nodes
A mass in the chest covering 1/3rd of the chest-width, or any lymph node that is larger than 10cm in length
Presence of disease affecting an organ outside the lymphatic system
Erythrocyte sedimentation rate above 50%
Symptoms such as fever, night sweats, or over 10% weight loss within 6 months
The last stage is the advanced stage, with the disease being in stage III or IV. The risk factors associated with this stage are:
Male Gender
Age 45<
Stage IV of the disease
Hemoglobin level: <10.5g/dL
Leukocytosis: condition in which the white blood count is over 15,000/mm³
Lymphocytopenia: condition in which the white blood cell count is 8% or more higher than the lymphocyte count, and/or the lymphocyte count is under 600/mm³
usual dose: 5.5-7.4 mg per m2 IV once every 7 days
Max: 18.5 mg per m2 once every seven days
The patient should not take a high dose if the white cell count reduces to 3000 cells per mm3
for days 1 and 15 of a 28-day cycle in combination with doxorubicin, vinblastine, and dacarbazine.
BEACOPP regimen: 0.25 to 0.5 units/kg IV on day 8 of a 28-day cycle in combination with procarbazine, etoposide, prednisone, and cyclophosphamide.
Stanford V regimen: 0.125 to 0.25 units/kg /dose in combination with mechlorethamine, vinblastine, doxorubicin, etoposide, and prednisone in weeks 2,4,6,8,10, and 12.
over 3 to 10 minutes once in 21 days.
Combination regimen: 25 mg/m^2 IV on days 1 and 15 every 28 days in combination with bleomycin, vinblastine, and dacarbazine for 2 to 4 cycles.
The drug is indicated for classical Hodgkin Lymphoma (cHL) or previously untreated cHL
First-line therapy for previously untreated Stage III cHL:
1.2 mg/kg intravenously every 2 weeks; do not exceed more than 120 mg/dose
Continue until 12 doses
cHL consolidation:
Indicated for cHL
Start the treatment within 4–6 weeks after auto-HSCT
1.8 mg/kg intravenously every 3 weeks; do not exceed 180 mg/dose
Continue until a maximum of 16 cycles, unacceptable toxicity, or disease progression
Relapsed cHL:
Indicated for cHL after failure
1.8 mg/kg intravenously every 3 weeks; do not exceed the dose of more than 180 mg/dose
Continue until disease progression or unacceptable toxicity
Systemic Anaplastic Large Cell Lymphoma:
Previously untreated-
ndicated for the treatment of sALCL that is previously untreated
1.8 mg/kg intravenously every 3 weeks for 6-8 doses; do not exceed the dose of more than 180 mg/dose
Relapsed sALCL
Indicated to treat (sALCL) after the failure of multiagent chemotherapy regimen
1.8 mg/kg intravenously every 3 weeks; do not exceed the dose of more than 180 mg/dose
ABVD (high-risk lymphoma) Children and adolescents :
0.25 - 0.5
unit/kg
Intravenous (IV)
on days 1 and 15 of a 28-day cycle for 2 to 6 cycles in combination with dacarbazine, vinblastine, and doxorubicin.
BEACOPP regimen: Children and adolescents
0.25 to 0.5 units/kg IV on day 7 of a 28-day cycle for 2 to 4 cycles in combination with procarbazine, etoposide, prednisone, and cyclophosphamide.
Stanford V regimen: Adolescents > 16 years
0.125 to 0.25 units/kg/dose IV in combination with mechlorethamine, vinblastine, doxorubicin, etoposide, and prednisone in weeks 2, 4, 6, 8, 10, and 12.
per day on day 1 of a 21-day cycle in combination with vincristine, prednisone, and cyclophosphamide.
25 mg/m^2 per day on days 1 and 2 of a 21-day cycle in combination with vincristine, prednisone, and cyclophosphamide.
For advanced-stage ABVD regimen: 25 mg/m^2 per day on days 0 and 14 of a 28-day cycle in combination with bleomycin, vinblastine, and dacarbazine.
Hodgkin lymphoma (HL), originally named Hodgkin’s disease, is an uncommon monoclonal lymphoid tumor with high rates of recovery. Through multiple clinical and biological investigations, this disease has been classified into nodular lymphocyte-predominant Hodgkin lymphoma and classical Hodgkin lymphoma.
The clinical presentation and pathology of these two diseases are distinctly different. Almost all (95%) cases of Hodgkin lymphoma are attributed to classical Hodgkin lymphoma.
This disease is further divided into the following four subgroups:
Nodular Sclerosis Hodgkin lymphoma
Lymphocyte depleted Hodgkin lymphoma
Lymphocyte-rich Hodgkin lymphoma
Mixed Cellularity Hodgkin lymphoma
Hodgkin lymphomas have 4 distinct features which can be used to identify the disease:
Young adults are more prone to this disease
They often grow in cervical lymph nodes
Large mononuclear Hodgkin cells are scattered around with multinucleated cells in a mixture of non-neoplastic cells
T-lymphocytes are regularly found around neoplastic cells
4 out of 5 patients recover from Hodgkin Lymphoma, and it has a generally favorable prognosis for most patients.
Hodgkin lymphoma is an uncommon malignancy in the United States, with an estimated incidence rate of 2.6 occurrences per 100,000 individuals. The disease accounts for 11% of all lymphomas diagnosed in the United States.
It has a bimodal distribution, with most affected patients being between the ages of 20 and 40, and another peak occurring between the ages of 55 and older. It is more prevalent in males than females, particularly in children, where 85 percent of occurrences occur in boys.
Hodgkin lymphoma with nodular sclerosis is more prevalent in young persons, whereas mixed cellularity Hodgkin lymphoma is more prevalent in older adults.
Given below is the incidence rates of all the subtypes of Classical Hodgkin lymphoma:
Nodular sclerosis classical HL (70%)
Mixed cellularity classical HL (25%)
Lymphocyte-rich classical HL (5%)
Lymphocyte-depleted classical HL (>1%)
Nodular lymphocyte-predominant Hodgkin lymphoma, accounts for around 5% of all Hodgkin lymphomas.
Unique neoplastic cells are present in both the classical and NLP-HL types of Hodgkin lymphoma. The Reed-Sternberg (RS) cell is a giant multinucleated neoplastic cell with two mirror-image nuclei inside a reactive cellular background.
For classical HL, the RS cell is pathognomonic. RS cells are produced from B cells with mutations in the IgH-variable region portion of the germinal center. Cytokines such as IL-5 and transforming growth factor-beta are secreted by the RS in order to recruit reactive cells. RS cells are often aneuploid, with no discernible cytogenetic abnormalities.
In the majority of isolated RS cells, conformational changes have been identified in the clonal lg gene. Immunohistochemistry stains for RS cells are positive for CD30, CD15, but typically negative for CD20 and CD45 that are positive only in neoplastic NLP-HL cells. In addition to CD15 and CD30, RS cells are usually positive for PAX5, CD25, HLA-DR, ICAM-1, Fascin, CD95 (apo-1/fas), TRAF1, CD40, and CD86. There are RS cell variants that include the Hodgkin cell, mummified cells, and lacunar cells. Hodgkin cells are mononuclear RS-cell variants.
Mummified cells show condensed cytoplasm and pyknotic reddish nuclei with smudgy chromatin. Lacunar cells have multilobulated nuclei, small nucleoli, and abundant, pale cytoplasm that often retracts during tissue fixation and sectioning, leaving the nucleus in what appears to be empty space (lacune-like space).
On the other hand, NLP-HL lacks the typical RS cells but has lymphocytic and histiocytic cells, which are characterized by larger cells with folded multilobulated nuclei (also known as “popcorn cells” or LP cells). The LP cells show a nucleus with multiple nucleoli that are basophilic and smaller than those seen in RS cells.
LP cells show clonally rearranged immunoglobulin genes that are only detected in isolated single LP cells. The LP cells are usually positive for C020, CD45, EMA, CD79a, CD75, BCL6, BOB.1, OCT2, and J chain.
Hodgkin lymphoma’s exact cause is uncertain. However, Epstein-Barr virus (EBV) infection, autoimmune disorders, and immunosuppression all raise the chance of Hodgkin lymphoma. In Hodgkin lymphoma, there is additional evidence of a hereditary tendency. EBV was shown to be more prevalent in Hodgkin lymphoma subtypes with mixed cellularity and Hodgkin lymphomas which present lower levels of lymphocytes.
Immune deficiency has been considered as a probable cause of EBV-positive illness. No other virus has been identified as having a significant influence in the pathogenesis of Hodgkin lymphoma. Immunosuppression as a result of solid organ or hematopoietic cell transplantation, immunosuppressive medication therapy, or HIV infection all increase the chance of developing Hodgkin lymphoma.
HIV patients frequently present with an advanced stage of the infection, atypical lymph node locations, and a disappointing prognosis. Studies have discovered a tenfold increase in the risk of developing HL among same-sex siblings of Hodgkin lymphoma patients, implying that certain gene-environments are predisposed to developing Hodgkin lymphoma.
The prognoses of Hodgkin lymphoma cases are often decided based on 3 subgroups. The first stage, called the “Early-stage favorable”, in which the patient can be in the first or second stage of the disease without presenting any unfavorable risk factor.
The second sub-group also includes the first and second stage of Hodgkin lymphoma but with unfavorable risk factors. These include:
The present of 3 or more lymph nodes
A mass in the chest covering 1/3rd of the chest-width, or any lymph node that is larger than 10cm in length
Presence of disease affecting an organ outside the lymphatic system
Erythrocyte sedimentation rate above 50%
Symptoms such as fever, night sweats, or over 10% weight loss within 6 months
The last stage is the advanced stage, with the disease being in stage III or IV. The risk factors associated with this stage are:
Male Gender
Age 45<
Stage IV of the disease
Hemoglobin level: <10.5g/dL
Leukocytosis: condition in which the white blood count is over 15,000/mm³
Lymphocytopenia: condition in which the white blood cell count is 8% or more higher than the lymphocyte count, and/or the lymphocyte count is under 600/mm³
usual dose: 5.5-7.4 mg per m2 IV once every 7 days
Max: 18.5 mg per m2 once every seven days
The patient should not take a high dose if the white cell count reduces to 3000 cells per mm3
for days 1 and 15 of a 28-day cycle in combination with doxorubicin, vinblastine, and dacarbazine.
BEACOPP regimen: 0.25 to 0.5 units/kg IV on day 8 of a 28-day cycle in combination with procarbazine, etoposide, prednisone, and cyclophosphamide.
Stanford V regimen: 0.125 to 0.25 units/kg /dose in combination with mechlorethamine, vinblastine, doxorubicin, etoposide, and prednisone in weeks 2,4,6,8,10, and 12.
over 3 to 10 minutes once in 21 days.
Combination regimen: 25 mg/m^2 IV on days 1 and 15 every 28 days in combination with bleomycin, vinblastine, and dacarbazine for 2 to 4 cycles.
The drug is indicated for classical Hodgkin Lymphoma (cHL) or previously untreated cHL
First-line therapy for previously untreated Stage III cHL:
1.2 mg/kg intravenously every 2 weeks; do not exceed more than 120 mg/dose
Continue until 12 doses
cHL consolidation:
Indicated for cHL
Start the treatment within 4–6 weeks after auto-HSCT
1.8 mg/kg intravenously every 3 weeks; do not exceed 180 mg/dose
Continue until a maximum of 16 cycles, unacceptable toxicity, or disease progression
Relapsed cHL:
Indicated for cHL after failure
1.8 mg/kg intravenously every 3 weeks; do not exceed the dose of more than 180 mg/dose
Continue until disease progression or unacceptable toxicity
Systemic Anaplastic Large Cell Lymphoma:
Previously untreated-
ndicated for the treatment of sALCL that is previously untreated
1.8 mg/kg intravenously every 3 weeks for 6-8 doses; do not exceed the dose of more than 180 mg/dose
Relapsed sALCL
Indicated to treat (sALCL) after the failure of multiagent chemotherapy regimen
1.8 mg/kg intravenously every 3 weeks; do not exceed the dose of more than 180 mg/dose
ABVD (high-risk lymphoma) Children and adolescents :
0.25 - 0.5
unit/kg
Intravenous (IV)
on days 1 and 15 of a 28-day cycle for 2 to 6 cycles in combination with dacarbazine, vinblastine, and doxorubicin.
BEACOPP regimen: Children and adolescents
0.25 to 0.5 units/kg IV on day 7 of a 28-day cycle for 2 to 4 cycles in combination with procarbazine, etoposide, prednisone, and cyclophosphamide.
Stanford V regimen: Adolescents > 16 years
0.125 to 0.25 units/kg/dose IV in combination with mechlorethamine, vinblastine, doxorubicin, etoposide, and prednisone in weeks 2, 4, 6, 8, 10, and 12.
per day on day 1 of a 21-day cycle in combination with vincristine, prednisone, and cyclophosphamide.
25 mg/m^2 per day on days 1 and 2 of a 21-day cycle in combination with vincristine, prednisone, and cyclophosphamide.
For advanced-stage ABVD regimen: 25 mg/m^2 per day on days 0 and 14 of a 28-day cycle in combination with bleomycin, vinblastine, and dacarbazine.
, repeat every 4 Weeks OR
375 mg/m² IV on Day 1; repeat every 15 Days
medtigo
Hodgkin lymphoma
Updated :
June 6, 2022
Hodgkin lymphoma (HL), originally named Hodgkin’s disease, is an uncommon monoclonal lymphoid tumor with high rates of recovery. Through multiple clinical and biological investigations, this disease has been classified into nodular lymphocyte-predominant Hodgkin lymphoma and classical Hodgkin lymphoma.
The clinical presentation and pathology of these two diseases are distinctly different. Almost all (95%) cases of Hodgkin lymphoma are attributed to classical Hodgkin lymphoma.
This disease is further divided into the following four subgroups:
Nodular Sclerosis Hodgkin lymphoma
Lymphocyte depleted Hodgkin lymphoma
Lymphocyte-rich Hodgkin lymphoma
Mixed Cellularity Hodgkin lymphoma
Hodgkin lymphomas have 4 distinct features which can be used to identify the disease:
Young adults are more prone to this disease
They often grow in cervical lymph nodes
Large mononuclear Hodgkin cells are scattered around with multinucleated cells in a mixture of non-neoplastic cells
T-lymphocytes are regularly found around neoplastic cells
4 out of 5 patients recover from Hodgkin Lymphoma, and it has a generally favorable prognosis for most patients.
Hodgkin lymphoma is an uncommon malignancy in the United States, with an estimated incidence rate of 2.6 occurrences per 100,000 individuals. The disease accounts for 11% of all lymphomas diagnosed in the United States.
It has a bimodal distribution, with most affected patients being between the ages of 20 and 40, and another peak occurring between the ages of 55 and older. It is more prevalent in males than females, particularly in children, where 85 percent of occurrences occur in boys.
Hodgkin lymphoma with nodular sclerosis is more prevalent in young persons, whereas mixed cellularity Hodgkin lymphoma is more prevalent in older adults.
Given below is the incidence rates of all the subtypes of Classical Hodgkin lymphoma:
Nodular sclerosis classical HL (70%)
Mixed cellularity classical HL (25%)
Lymphocyte-rich classical HL (5%)
Lymphocyte-depleted classical HL (>1%)
Nodular lymphocyte-predominant Hodgkin lymphoma, accounts for around 5% of all Hodgkin lymphomas.
Unique neoplastic cells are present in both the classical and NLP-HL types of Hodgkin lymphoma. The Reed-Sternberg (RS) cell is a giant multinucleated neoplastic cell with two mirror-image nuclei inside a reactive cellular background.
For classical HL, the RS cell is pathognomonic. RS cells are produced from B cells with mutations in the IgH-variable region portion of the germinal center. Cytokines such as IL-5 and transforming growth factor-beta are secreted by the RS in order to recruit reactive cells. RS cells are often aneuploid, with no discernible cytogenetic abnormalities.
In the majority of isolated RS cells, conformational changes have been identified in the clonal lg gene. Immunohistochemistry stains for RS cells are positive for CD30, CD15, but typically negative for CD20 and CD45 that are positive only in neoplastic NLP-HL cells. In addition to CD15 and CD30, RS cells are usually positive for PAX5, CD25, HLA-DR, ICAM-1, Fascin, CD95 (apo-1/fas), TRAF1, CD40, and CD86. There are RS cell variants that include the Hodgkin cell, mummified cells, and lacunar cells. Hodgkin cells are mononuclear RS-cell variants.
Mummified cells show condensed cytoplasm and pyknotic reddish nuclei with smudgy chromatin. Lacunar cells have multilobulated nuclei, small nucleoli, and abundant, pale cytoplasm that often retracts during tissue fixation and sectioning, leaving the nucleus in what appears to be empty space (lacune-like space).
On the other hand, NLP-HL lacks the typical RS cells but has lymphocytic and histiocytic cells, which are characterized by larger cells with folded multilobulated nuclei (also known as “popcorn cells” or LP cells). The LP cells show a nucleus with multiple nucleoli that are basophilic and smaller than those seen in RS cells.
LP cells show clonally rearranged immunoglobulin genes that are only detected in isolated single LP cells. The LP cells are usually positive for C020, CD45, EMA, CD79a, CD75, BCL6, BOB.1, OCT2, and J chain.
Hodgkin lymphoma’s exact cause is uncertain. However, Epstein-Barr virus (EBV) infection, autoimmune disorders, and immunosuppression all raise the chance of Hodgkin lymphoma. In Hodgkin lymphoma, there is additional evidence of a hereditary tendency. EBV was shown to be more prevalent in Hodgkin lymphoma subtypes with mixed cellularity and Hodgkin lymphomas which present lower levels of lymphocytes.
Immune deficiency has been considered as a probable cause of EBV-positive illness. No other virus has been identified as having a significant influence in the pathogenesis of Hodgkin lymphoma. Immunosuppression as a result of solid organ or hematopoietic cell transplantation, immunosuppressive medication therapy, or HIV infection all increase the chance of developing Hodgkin lymphoma.
HIV patients frequently present with an advanced stage of the infection, atypical lymph node locations, and a disappointing prognosis. Studies have discovered a tenfold increase in the risk of developing HL among same-sex siblings of Hodgkin lymphoma patients, implying that certain gene-environments are predisposed to developing Hodgkin lymphoma.
The prognoses of Hodgkin lymphoma cases are often decided based on 3 subgroups. The first stage, called the “Early-stage favorable”, in which the patient can be in the first or second stage of the disease without presenting any unfavorable risk factor.
The second sub-group also includes the first and second stage of Hodgkin lymphoma but with unfavorable risk factors. These include:
The present of 3 or more lymph nodes
A mass in the chest covering 1/3rd of the chest-width, or any lymph node that is larger than 10cm in length
Presence of disease affecting an organ outside the lymphatic system
Erythrocyte sedimentation rate above 50%
Symptoms such as fever, night sweats, or over 10% weight loss within 6 months
The last stage is the advanced stage, with the disease being in stage III or IV. The risk factors associated with this stage are:
Male Gender
Age 45<
Stage IV of the disease
Hemoglobin level: <10.5g/dL
Leukocytosis: condition in which the white blood count is over 15,000/mm³
Lymphocytopenia: condition in which the white blood cell count is 8% or more higher than the lymphocyte count, and/or the lymphocyte count is under 600/mm³
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