𝔖 Scriptorium
✩   LIBER   ✩

📁

Hodgkin Lymphoma. A Comprehensive Overview

✍ Scribed by Andreas Engert, Anas Younes (eds.)


Publisher
Springer
Year
2020
Tongue
English
Leaves
496
Edition
3
Category
Library

⬇  Acquire This Volume

No coin nor oath required. For personal study only.

✩ Table of Contents


Preface
Contents
Part I: Epidemiology and Pathogenesis
1: Epidemiology of Hodgkin Lymphoma
1.1 Introduction
1.2 Definition and Histological Classification (WHO)
1.3 Hodgkin Lymphoma Occurrence
1.3.1 Overall Incidence
1.3.2 Age-Specific Incidence Patterns Vary Geographically
1.3.2.1 Historical Patterns
1.3.2.2 Modern Age-Specific Incidence Patterns
1.3.2.3 Age-Specific Incidence Patterns for Hodgkin Lymphoma Subtypes
1.3.3 Incidence Trends
1.3.4 Classifications for Epidemiological Studies: Multi-disease Models
1.3.5 Classifications by Age at Diagnosis, Histology and Tumour Epstein-Barr Virus Status
1.3.6 Overlap Between Epidemiological Classifications of Hodgkin Lymphoma
1.4 Familial Accumulation of Hodgkin Lymphoma: Genetic Predisposition
1.4.1 Genetic Studies: Genome-Wide Association Studies
1.4.1.1 Hodgkin Lymphoma Subtype-Specific Associations in Genetic Analyses
1.5 Risk Factors
1.5.1 Prevailing Hypotheses in Hodgkin Lymphoma Epidemiology
1.5.1.1 Childhood Socio- Economic Environment
1.5.2 Anthropometry
1.5.3 Medical History
1.5.3.1 Infections
Epstein-Barr Virus Infection: Infectious Mononucleosis
Epstein-Barr Virus Infection: Serological Evidence
Epstein-Barr Virus Infection: Variation in Tumour Prevalence
A Four-Disease Model for Hodgkin Lymphoma
Other Childhood Infections
1.5.3.2 Primary and Secondary Immune Deficiencies
1.5.3.3 Autoimmune and Allergic Disorders
Autoimmune and Allergic/Atopic Diseases
1.5.3.4 Medications
1.5.4 Environmental Exposures
1.5.4.1 Ultraviolet Light
1.5.4.2 Tobacco
1.5.4.3 Alcohol
1.6 Conclusion
References
2: The Role of Viruses in the Genesis of Hodgkin Lymphoma
2.1 Introduction
2.2 Hodgkin Lymphoma and Epstein-Barr Virus
2.2.1 Epstein-Barr Virus and the Pathogenesis of Hodgkin Lymphoma
2.2.2 Risk Factors for Epstein-Barr Virus-Associated Hodgkin Lymphoma
2.2.3 Epstein-Barr Virus and Hodgkin Lymphoma: A Causative Association?
2.2.4 Epstein-Barr Virus and the Clinicopathological Features of Hodgkin Lymphoma
2.3 Epstein-Barr Virus-Negative Hodgkin Lymphoma Cases
2.3.1 Hodgkin Lymphoma and Herpesviruses Other Than Epstein-Barr Virus
2.3.2 Polyomaviruses and Hodgkin Lymphoma
2.3.3 Measles Virus and Hodgkin Lymphoma
2.3.4 The Virome, Anelloviruses, and Hodgkin Lymphoma
2.4 Conclusions
References
3: Pathology and Molecular Pathology of Hodgkin Lymphoma
3.1 Subclassification and Pathology
3.1.1 Nodular Lymphocyte-Predominant Hodgkin Lymphoma
3.1.2 Classical Hodgkin Lymphoma: The HRS Cells
3.1.2.1 Nodular Sclerosis Classical Hodgkin Lymphoma
3.1.2.2 Mixed Cellularity Classical Hodgkin Lymphoma
3.1.2.3 Lymphocyte-Depleted Classical Hodgkin Lymphoma
3.1.2.4 Lymphocyte-Rich Classical Hodgkin Lymphoma
3.2 Differential Diagnosis
3.3 Histogenesis of HRS and LP Cells
3.3.1 Cellular Origin of HRS and LP Cells
3.3.2 Relationship of Hodgkin Cells and Reed-Sternberg Cells and Putative HRS Cell Precursors
3.4 Genetic Lesions
3.5 Deregulated Transcription Factor Networks and Signaling Pathways
3.5.1 The Lost B Cell Phenotype
3.5.2 Constitutive Activation of Multiple Signaling Pathways
3.6 Anti-apoptotic Mechanisms
References
4: Microenvironment, Cross-Talk, and Immune Escape Mechanisms
4.1 Microenvironment
4.1.1 Hodgkin Lymphoma Subtypes
4.1.2 Epstein-Barr Virus
4.1.3 Human Immunodeficiency Virus
4.1.4 T Cell Subsets in cHL
4.1.5 T Cell Subsets in NLPHL
4.1.6 Fibrosis and Sclerosis
4.1.7 Eosinophils, Plasma Cells, Mast Cells, and B Cells
4.2 Cross-Talk between HRS Cells and Microenvironment (Fig. 4.4)
4.2.1 Factors Supporting Tumor Growth
4.2.2 Shaping the Environment
4.3 Immune Escape Mechanisms (Fig. 4.4)
4.3.1 Antigen Presentation
4.3.2 HLA Class I Expression
4.3.3 HLA Class II Expression
4.3.4 Immune Checkpoints
4.3.5 Immunosuppression
4.4 Prognostic Impact of the Microenvironment
4.5 Conclusion
References
5: What Have We Learnt from Genomics and Transcriptomics in Classic Hodgkin Lymphoma
5.1 Introduction
5.2 Genomics of Hodgkin and Reed-Sternberg Cells
5.2.1 Cytokine Signaling
5.2.2 NF-ÎșB Signaling
5.2.3 PI3K/AKT/mTOR Signaling
5.2.4 Immune Escape
5.3 The Transcriptome of HRS Cells
5.4 Microenvironment Profiling
5.5 Biomarker-Driven Prognostication and Risk Stratification in cHL
5.6 Conclusions and Future Perspective
References
Part II: Diagnosis and First-Line Treatment
6: Clinical Evaluation
6.1 Presenting Manifestations
6.2 Physical Findings and Laboratory Abnormalities
6.3 Pathologic Diagnosis: The Biopsy
6.4 Staging Systems for Hodgkin Lymphoma
6.5 Imaging Evaluation of the Extent of Disease
6.6 Clinical Evaluation During Therapy
6.7 Definition of the Response to Treatment
6.8 Complete Remission
6.9 Follow-Up Management
6.10 Conclusion
References
7: Functional Imaging in Hodgkin Lymphoma
7.1 Introduction
7.2 History of Imaging in Hodgkin Lymphoma
7.3 Background of PET and the FDG Tracer
7.3.1 Basic Principles of PET
7.3.2 The FDG Tracer
7.4 PET in Clinical Management of Hodgkin Lymphoma
7.4.1 Staging
7.4.2 Early Assessment of Chemosensitivity
7.4.3 Final Response Assessment
7.4.4 Interpretation Criteria
7.4.4.1 Interim PET Scan
7.4.4.2 End-of-Treatment PET Scan
7.4.5 Treatment Response Assessment to Immune Checkpoint Inhibitors
7.4.6 PET in Radiotherapy Planning
7.4.7 PET for Response Prediction During Salvage Treatment
7.4.8 PET for Follow-Up of HL Patients in Complete Remission
7.5 PET Response-Adapted Therapy
7.5.1 Early-Stage HL
7.5.2 Advanced-Stage HL
7.5.3 Post-chemotherapy PET/CT-Driven Consolidation Radiotherapy
7.5.4 PET/CT-Adapted Therapy in Relapsed HL
7.6 Toward Revised Criteria for PET Scan Interpretation
7.6.1 Qualitative vs. Semiquantitative Assessment
7.6.1.1 From Anatomical to Functional Imaging
7.6.1.2 Toward New Criteria for Response Assessment of New Drugs
7.6.1.3 Biomarker Integration in Response Criteria
7.6.2 Interim PET
7.6.3 End-of-Treatment PET
7.7 FDG-PET/MRI
7.8 Future Perspectives
7.8.1 Other Tracers
7.8.2 Quantitative Methods for PET Reading (SUV, MTV, TLG)
7.8.2.1 Semiquantitative Assessment
7.8.2.2 Metabolic Tumor Volume
7.9 General Recommendations for the Use of PET in HL
References
8: Prognostic Factors
8.1 Historical Perspective
8.2 Prognostic Factors
8.2.1 Definition and Use
8.2.2 Types of Prognostic Factors
8.2.3 Different End Points
8.2.4 Types and Analyses of Prognostic Studies
8.2.5 Predictive Factors
8.3 Prognostic Factors across Stages
8.4 Early-Stage Hodgkin Lymphoma
8.5 Advanced-Stage Hodgkin Lymphoma
8.5.1 Pretreatment Prognostic Factors in Advanced-Stage Hodgkin Lymphoma
8.5.2 Interim PET as Prognostic Factor in Advanced-Stage Hodgkin Lymphoma
8.5.3 Prognostic Indices in Advanced-Stage Hodgkin Lymphoma
8.6 Prognostic Factors in Relapsed or Refractory Hodgkin Lymphoma
8.6.1 Patients Treated for r/r HL with Conventional Treatment
8.6.2 Treatment with High-Dose Chemotherapy and Autologous Stem Cell Transplantation
8.6.3 Patients’ Prognostic Indices or Scores in r/r HL Treated with Novel Agents
8.6.4 Prognostic Factors for Treatment with Novel Agents in r/r HL
8.7 Conclusion and Future Aspects
References
9: Principles of Radiation Therapy for Hodgkin Lymphoma
9.1 Principles of Radiation Therapy of Hodgkin Lymphoma
9.2 The Evolution of Radiotherapy for HL
9.3 Indications for Radiation Therapy in HL
9.3.1 Lymphocyte-Predominant HL
9.3.2 Classic Hodgkin: Stage I–II
9.3.3 Stage III–IV HL
9.3.4 RT in Salvage Programs for Refractory and Relapsed HL
9.4 Radiation Fields and Volumes: Principles and Design
9.4.1 Extended-Field Radiation Therapy
9.4.2 Involved-Field Radiation Therapy
9.4.3 Involved-Site Radiation Therapy (ISRT): The New Standard Volume for HL
9.4.3.1 ISRT When RT Is the Primary Treatment
9.4.3.2 ISRT When RT Is Part of Combined-Modality Treatment
9.4.4 Involved-Node Radiation Therapy (INRT): A Special Case of ISRT
9.4.5 Volume Definitions for Planning ISRT and INRT
9.4.5.1 Volume of Interest Acquisition
9.4.5.2 Determination of Gross Tumor Volume (GTV)
Pre-chemotherapy (or Presurgery) GTV
No Chemotherapy or Post-chemotherapy GTV
9.4.5.3 Determination of Clinical Target Volume (CTV)
9.4.5.4 Determination of Internal Target Volume (ITV)
9.4.5.5 Determination of Planning Target Volume (PTV)
9.4.6 Determination of Organs at Risk (OAR)
9.4.6.1 Lung
9.4.6.2 Heart
9.4.6.3 Thyroid
9.4.6.4 Second Cancers
9.4.7 Consolidation Volume Radiation Therapy (CVRT)
9.5 Dose Considerations and Recommendations
9.5.1 The Significance of Reducing the Radiation Dose
9.5.2 Dose Recommendations
9.6 New Aspects of Radiation Volume Definition and Treatment Delivery
9.6.1 New Technologies
9.6.2 Deep Inspiration Breath Hold
9.7 Proton Therapy
9.8 Common Side Effects and Supportive Care During Radiation Therapy
9.8.1 Common Acute Side Effects
9.8.2 Uncommon Early Side Effects
9.8.3 Supportive Care During Treatment
9.8.4 Follow-Up After Treatment
References
10: Principles of Chemotherapy in Hodgkin Lymphoma
10.1 Historical Introduction
10.2 Chemotherapy Applied to Advanced-Stage Hodgkin Lymphoma: Theories and Practice
10.2.1 Classes of Active Classical Agents in HL (Table 10.1)
10.2.2 Polychemotherapy: Models and Comparative Clinical Studies (Tables 10.2 and 10.3)
10.2.2.1 MOPP and Derivatives
10.2.2.2 ABVD and Derivatives
10.2.2.3 The Dose/Response Relationship: Norton and Simon Model
Dose/Response Relationships and Treatment Tolerance: An Individual Characteristic?
10.2.2.4 Sustained/Weekly Regimens
10.2.2.5 Escalated-Dose Regimens
10.2.2.6 High-Dose Treatment and Autologous Stem Cell Transplantation as Part of Initial Therapy
10.2.2.7 Risk-Adapted Regimens Based on PET
10.2.2.8 Incorporation of Antibody-Drug Conjugate in Primary Treatment of Advanced-Stage cHL
10.3 Chemotherapy Treatment for Recurrent and Refractory Hodgkin Lymphoma
10.3.1 New Systemic Treatments
10.4 Conclusions
References
11: Treatment of Early Favorable Hodgkin Lymphoma
11.1 Introduction
11.2 Defining Favorable Early-Stage Disease
11.2.1 Staging
11.2.2 Prognostic Factors
11.3 Radiotherapy Alone
11.4 Late Treatment Effects and Mortality
11.5 Combined Modality Treatment
11.5.1 Radiotherapy Alone Versus CMT
11.5.2 Optimal Number of Cycles of Chemotherapy
11.5.3 Optimal Chemotherapy Combination
11.5.4 Optimal Radiation Dose
11.5.5 Optimal Radiation Field Size
11.6 Chemotherapy Alone
11.7 Treatment Adaptation Based on PET Scan Response
11.8 Recommendations and Future Directions
References
12: Treatment of Early Unfavorable Hodgkin Lymphoma
12.1 Prognostic Factors
12.1.1 Definition
12.1.2 New Prognostic Factors
12.2 Long-Term Side Effects
12.3 Non-PET-Adapted Treatment Strategies
12.3.1 Fields and Dose of Radiotherapy
12.3.2 Chemotherapy
12.3.3 Chemotherapy Alone
12.4 PET-Adapted Treatment Strategies
12.4.1 Interim PET
12.4.2 Clinical Trials
12.4.2.1 Rapid Study
12.4.2.2 H10 Study
12.4.2.3 Other Studies
12.4.2.4 Management of iPET-Positive Patients
12.5 ESMO and NCCN Recommendations
12.6 New Drugs
12.6.1 Brentuximab Vedotin
12.6.2 Checkpoint Inhibitors
12.7 Conclusions and Future Strategies
References
13: Treatment of Advanced-Stage Hodgkin Lymphoma
13.1 Introduction and Early History of Combination Chemotherapy
13.2 Fourth-Generation Regimens
13.2.1 Hybrid and Alternating Regimens
13.2.2 BEACOPP Escalated
13.3 ABVD or BEACOPP Escalated as Standard First-Line Treatment?
13.4 Outcome Prediction
13.4.1 The International Prognostic Score
13.4.2 Positron Emission Tomography
13.5 Response-Adapted Therapy
13.5.1 De-escalation of Therapy in Early Responders
13.5.2 Escalation of Therapy in Early Nonresponders
13.6 Introduction of Brentuximab Vedotin into First-Line Treatment
13.7 Introducing Programmed-Death-1 Inhibitors into First-Line Treatment
13.8 The Role of Radiotherapy
13.9 Summary
References
14: Optimizing Decision Making in Hodgkin Lymphoma
14.1 Treatment Choices and Individualized Care
14.2 Treatment-Related Late Effects and Associated Human Cost
14.3 Risk, Impact, and Variability of Treatment-Related Late Effects
14.4 Paucity of Harmonized Data to Guide Providers and Patients Towards Individualized Treatment Choices
14.5 Disease Classification and Prognostication
14.6 Simulation Modeling
14.6.1 Low-Dose CT Scan for Lung Cancer
14.6.2 Diffuse Large B-Cell Lymphoma (DLBCL)
14.7 Decision Models in Hodgkin Lymphoma (HL)
14.8 Conclusion
References
Part III: Special Clinical Situations
15: Pediatric Hodgkin Lymphoma
15.1 Introduction
15.1.1 Comparison of Pediatric/Adolescent Vs. Adult HL
15.1.2 Classical Pediatric Hodgkin Lymphoma (PHL)
15.1.2.1 Overall Strategies
15.1.2.2 Low-Risk (Early Favorable) Disease
15.1.2.3 Intermediate- and High-Risk (Advanced, Unfavorable) Disease
15.1.2.4 Future Considerations in Classical Pediatric and Adolescent HL
15.1.3 Nodular Lymphocyte-Predominant HL (NLPHL)
15.1.4 Recurrence, Relapse, and Salvage in PHL
15.1.4.1 Introduction
15.1.4.2 Standard-Dose Salvage Chemotherapy Regimens
15.1.4.3 Prognostic Factors at Relapse in Pediatric HL: Standard-Dose Chemoradiotherapy Vs. High-Dose Chemotherapy/Stem Cell Transplantation
15.1.4.4 Role of Radiotherapy in Relapsed Hodgkin Lymphoma
15.1.4.5 High-Dose Chemotherapy and Autologous Stem Cell Transplant
15.1.4.6 High-Dose Chemotherapy and Allogeneic Stem Cell Transplantation
15.1.4.7 Brentuximab Vedotin and Checkpoint Inhibitors
15.1.5 Late Effects
15.1.5.1 Cardiac Toxicities
15.1.5.2 Pulmonary Toxicities
15.1.5.3 Thyroid Toxicities
15.1.5.4 Secondary Malignancies
15.1.6 Summary/Future Directions
References
16: The Management of Older Patients with Hodgkin Lymphoma
16.1 Introduction
16.2 Epidemiology
16.3 Pathology
16.4 Clinical Presentation
16.5 Age Issues Affecting Treatment and Outcome
16.5.1 Comorbidity
16.5.2 Therapy-Associated Toxicity
16.6 Therapy
16.6.1 Early Stages
16.6.2 Advanced Stages
16.6.2.1 Earlier Data
16.6.2.2 Contemporary Data
16.6.3 Relapsed Patients
16.7 Conclusions and Perspectives
References
17: Nodular Lymphocyte-Predominant Hodgkin Lymphoma
17.1 Introduction
17.2 Pathology of NLPHL
17.3 Differential Diagnosis
17.4 Transformation to NHL
17.5 Clinical Characteristics
17.6 Treatment of Early Favorable NLPHL
17.7 Treatment of Early Unfavorable and Advanced NLPHL
17.8 Treatment of Relapsed NLPHL
17.9 Risk Factors
17.10 Summary and Conclusions
References
18: The Management of Hodgkin Lymphoma During Pregnancy
18.1 Introduction
18.2 Diagnostic Approach to HL during Pregnancy
18.3 Outcomes of Mother and Child in HL Coincident with Pregnancy
18.4 Treatment of Hodgkin Lymphoma during Pregnancy
18.4.1 General Therapeutic Principles
18.4.2 Early-Stage HL during Pregnancy
18.4.3 Use of Chemotherapy for Symptomatic or Advanced-Stage HL in Pregnant Patients
18.5 Fetal Outcomes
18.6 Planning the Delivery and Managing the Postpartum Period in Patients with HL
18.7 Relapsed HL and Concomitant Pregnancy
18.8 Conclusions
References
19: The Management of HIV-Hodgkin Lymphoma
19.1 Introduction
19.2 Epidemiology
19.2.1 CD4 T-Cell Counts and Risk of HIV-HL
19.3 Pathology
19.4 Clinical Presentation and Prognostic Factors
19.4.1 Prognostic Factors
19.5 Management
19.5.1 Primary Chemotherapy
19.5.1.1 Stage-Adapted Approach
19.5.1.2 PET-Adapted Approach
19.5.1.3 Brentuximab Vedotin with Chemotherapy
19.5.1.4 Combination Antiretroviral Therapy (cART)
19.5.2 Relapsed and Resistant Disease
19.5.2.1 Brentuximab Vedotin
19.5.2.2 Checkpoint Inhibitors
References
Part IV: Relapsed and Refractory Disease
20: Relapsed and Refractory Hodgkin Lymphoma
20.1 Introduction
20.2 Prognostic Factors in Relapsed and Refractory Hodgkin Lymphoma
20.3 Salvage Therapy
20.4 Pre-ASCT FDG-PET
20.5 Salvage Radiotherapy
20.6 HDCT Regimens
20.7 Tandem HDCT/ASCT
20.8 Posttransplant Therapy
20.9 Allogeneic Transplantation after Reduced Conditioning in Hodgkin Lymphoma
References
21: Allogeneic Transplantation for Relapsed Hodgkin Lymphoma
21.1 Introduction
21.2 Myeloablative Allogeneic Stem Cell Transplantation in Hodgkin Lymphoma: A Historical Perspective
21.3 Reduced-Intensity Regimens
21.4 Prognostic Factors of Long-Term Outcome for Allogeneic SCT
21.5 Evidence for Graft Versus Hodgkin Lymphoma
21.6 Role of Allogeneic SCT in Autograft Failures
21.7 Moving Allogeneic Stem Cell Transplantation to Earlier Stages of the Disease
21.8 Role of Allogeneic SCT in the Pediatric Population
21.9 Alternative Donor Transplants
21.10 Role of Allogeneic Stem Cell Transplantation in the Era of New Drugs
References
22: Targeting CD30 in Patients with Hodgkin Lymphoma
22.1 Introduction
22.2 Structure and Function of CD30
22.3 Therapeutic Targeting of CD30
22.4 Monoclonal Antibodies
22.5 Bispecific Monoclonal Antibodies
22.6 Radiolabeled Antibodies
22.7 Chimeric Antigen Receptor (CAR) T-Cell Therapy
22.8 Antibody-Drug Conjugates
22.8.1 Single-Agent Experience with Brentuximab Vedotin
22.9 Safety and Tolerability of Brentuximab Vedotin
22.9.1 Brentuximab Vedotin in Frontline Setting for HL
22.9.1.1 Early-Stage Disease
22.9.1.2 Advanced-Stage Disease
22.9.1.3 Elderly Patients
22.9.2 Brentuximab Vedotin Pre-ASCT
22.9.3 Brentuximab Vedotin Maintenance Post Autologous Stem Cell Transplant
22.9.4 Brentuximab Vedotin-Based Combinations in Posttransplant Settings
22.10 Conclusions
References
23: Hodgkin Lymphoma and PD-1 Blockade
23.1 Introduction
23.2 Early Clinical Trials
23.3 Measuring Response to PD-1 Blockade: Pseudoprogression and Treatment Beyond Progression
23.4 Minimal Residual Disease in cHL
23.5 Mechanisms of Response and Resistance
23.6 PD-1 Blockade-Based Combination Treatments and Use in Earlier Lines of Therapy
23.6.1 Frontline Therapy
23.6.2 First Relapse: Salvage Therapy
23.6.3 Maintenance Following ASCT
23.6.4 Combination Approaches in Multiply Relapsed/Refractory Patients
23.6.5 Impact of PD-1 Blockade on Subsequent Therapies
23.7 PD-1 Blockade and Allogeneic Stem Cell Transplantation
23.8 Conclusion
References
24: Other New Agents for Hodgkin Lymphoma
24.1 PI3K/Akt/mTOR Pathway
24.2 HDAC Inhibitors
24.3 Lenalidomide
24.4 Emerging Therapies
24.5 Conclusion
References
Part V: Survivorship
25: Quality of Life in Hodgkin Lymphoma
25.1 Quality of Life in Hodgkin Lymphoma
25.2 Health-Related Quality-of-Life Assessment
25.2.1 HRQoL Instruments
25.2.2 HRQoL in Special Patient Groups
25.3 HRQoL in Clinical Trials for Hodgkin Lymphoma
25.3.1 Lessons from Retrospective and Cross-Sectional Studies
25.3.2 Results from Prospective Trials
25.4 Conclusions
References
26: Second Malignancy Risk After Treatment of Hodgkin Lymphoma
26.1 Introduction
26.2 Methods of Assessing Second Cancer Risk
26.3 Magnitude of the Risk Increase of Second Malignancy, Temporal Patterns, and Age Effects
26.4 Contributors to Second Cancer Risk
26.4.1 Radiation Therapy
26.4.2 Chemotherapy
26.4.3 Genetic Factors
26.5 Risk of Selected Second Malignancies
26.5.1 Risk Factors for Leukemia
26.5.2 Risk Factors of Non-Hodgkin Lymphoma (NHL)
26.5.3 Risk Factors for Breast Cancer
26.5.4 Risk Factors for Lung Cancer
26.6 Clinical Implications
References
27: Cardiovascular and Pulmonary Late Effects
27.1 Cardiovascular Toxicity
27.1.1 Chemotherapy-Associated Cardiotoxicity
27.1.1.1 General Aspects of Chemotherapy-Associated Cardiotoxicity
27.1.1.2 Prevention of Chemotherapy-Associated Cardiotoxicity
27.1.1.3 Surveillance for and Management of Chemotherapy-Associated Cardiotoxicity
27.1.2 Radiation-Associated Cardiotoxicity
27.1.2.1 General Aspects of Radiation-Associated Cardiotoxicity
27.1.2.2 Dose-Response Relationships for Radiation-Associated Cardiotoxicity
27.1.2.3 Other Risk Factors for Radiation-Associated Cardiotoxicity
27.1.2.4 Imaging of and Screening for Radiation-Associated Cardiotoxicity
27.1.2.5 Prevention and Management of Radiation-Associated Cardiotoxicity
27.1.3 Radiation-Associated Cerebrovascular Toxicity
27.1.3.1 Radiation-Associated Stroke and Transient Ischemic Attack
27.1.3.2 Prevention and Screening for Radiation Damage to Carotid Arteries
27.1.3.3 Management of Radiation-Associated Carotid Artery Damage
27.1.4 Radiation-Associated Damage to Other Major Arteries
27.2 Late Pulmonary Toxicity
27.2.1 Chemotherapy-Associated Pulmonary Toxicity
27.2.1.1 General Aspects of Chemotherapy-Associated Pulmonary Toxicity
27.2.1.2 Bleomycin
27.2.1.3 Other Agents Leading to Pulmonary Toxicity
27.2.1.4 Prevention of Chemotherapy-Associated Pulmonary Toxicity
27.2.1.5 Management of Chemotherapy-Associated Pulmonary Toxicity
27.2.2 Radiation-Associated Pulmonary Toxicity
27.2.2.1 General Aspects of Radiation-Associated Pulmonary Toxicity
27.2.2.2 Prevention of Radiation-Associated Pulmonary Toxicity
27.2.2.3 Management of Radiation-Associated Pulmonary Toxicity
27.2.2.4 Combined Toxicity
27.3 Conclusion
References
28: Gonadal Dysfunction and Fertility Preservation in Hodgkin Lymphoma Patients
28.1 Introduction
28.2 Gonadal Dysfunction in Men
28.2.1 Male Reproductive Physiology
28.2.2 Hodgkin Lymphoma and Male Gonadal Dysfunction
28.2.3 Treatment-Related Gonadal Dysfunction
28.2.4 Predictive Factors for Gonadal Dysfunction and Damage
28.2.5 Hormonal Analyses to Assess Testicular Function After Therapy
28.2.6 Endocrine Hypogonadism After Chemotherapy in Men
28.2.7 Fertility Preservation in Men: Preventative Pretreatment Strategies and Management After Chemotherapy
28.3 Gonadal Dysfunction in Women
28.3.1 Female Reproductive Physiology
28.3.2 Treatment-Related Infertility
28.3.3 Posttreatment Assessment of Ovarian Reserve with Anti-MĂŒllerian Hormone Levels
28.3.3.1 Reduced Ovarian Reserve Prior to Therapy
28.3.3.2 Hypogonadism in Women
28.3.4 Radiation Therapy
28.3.5 Preventative Treatment Strategies in Women
28.3.6 Pharmacological Prevention of Gonadal Damage
28.3.6.1 GnRH Agonists (GnRHa) During Chemotherapy
28.3.7 Cryopreservation of Oocytes/Ovarian Tissue
28.3.7.1 Ovarian Stimulation and Cryopreservation of Fertilized and Unfertilized Oocytes
28.3.7.2 Cryopreservation of Ovarian Tissue
Combination of Different Fertility-Preserving Techniques
28.3.8 Transposition of the Ovaries
28.3.9 Premature Menopause
28.3.10 Fertility and Late Effects in HL Survivors
28.4 Conclusions
References
29: Cancer-Related Fatigue in Hodgkin Lymphoma
29.1 Introduction
29.2 Assessment of CRF
29.3 Prevalence of CRF and Time of Occurrence
29.4 The Longitudinal Course of CRF
29.5 The Impact of Treatment Intensity on Long-Term CRF
29.6 Predictors of Long-Term CRF
29.7 Impact of Persistent CRF on Treatment Outcome and Social Reintegration
29.8 Management of CRF
29.9 Summary and Conclusion
References


📜 SIMILAR VOLUMES


Hodgkin Lymphoma: A Comprehensive Overvi
✍ Andreas Engert, Anas Younes (eds.) 📂 Library 📅 2015 🏛 Springer International Publishing 🌐 English

<p>This book examines in detail the current treatment options for first-line, relapsed, and refractory Hodgkin lymphoma and the management appropriate in special clinical circumstances, including in the elderly, pregnant women, and those with lymphocyte-predominant disease. Careful attention is devo

Hodgkin Lymphoma: A Comprehensive Update
✍ Sally L. Glaser, Ellen T. Chang, Christina A. Clarke, Theresa H. Keegan (auth.), 📂 Library 📅 2011 🏛 Springer Berlin Heidelberg 🌐 English

This book provides a well-illustrated, comprehensive, and up-to-date account of Hodgkin lymphoma. Epidemiology, pathogenesis, and the role of the microenvironment are examined in detail. The initial clinical evaluation and use of staging systems are fully discussed, and prognostic factors are carefu

Hodgkin Lymphoma
✍ Richard T. Hoppe, Peter M. Mauch, James O. Armitage, Volker Diehl, Lawrence M. W 📂 Library 📅 2007 🏛 Lippincott Williams & Wilkins 🌐 English

The definitive text on Hodgkin lymphoma is now in its thoroughly revised, updated Second Edition. More than 100 recognized authorities from all parts of the world provide comprehensive, current information on every aspect of Hodgkin lymphoma, including etiology, epidemiology, biology, pathology, eva