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Interventional Chest/Diagnostic Procedures: Evolving approaches to manage central airway obstruction

Central airway obstruction (CAO) is a major cause of morbidity and mortality in patients with malignant and nonmalignant pulmonary disorders (Ernst et al. Am J Respir Crit Care Med. 2004;169:1278). It is associated with postobstructive pneumonia, respiratory compromise, and even respiratory failure. It often precludes the patients with malignancy from getting definitive treatment, such as surgical resection or chemotherapy. Therapeutic bronchoscopy using a rigid bronchoscope plays a central role in managing these patients.

Different modalities used during therapeutic bronchoscopy include debridement, airway dilation, and different heat therapies, such as laser, electrocautery, and argon plasma coagulation (Bolliger et al. Eur Respir J. 2006;27:1258). Airway stents are often placed to achieve durable airway patency. Endobronchial therapies with delayed effect include brachytherapy, photodynamic therapy, and cryotherapy (Vergnon et al. Eur Respir J. 2006;28:200). There is improvement in symptom control, quality of life, and spirometry with successful bronchoscopic intervention (Mahmood et al. Respiration. 2015;89:404). Patients with respiratory failure secondary to CAO can be weaned from mechanical ventilation (Murgu et al. Respiration. 2012;84:55).

It is often difficult to predict which patients will have a successful bronchoscopic intervention. Endobronchial disease and stent placement have been associated with successful outcome (Ost et al. Chest. 2015;147:1282). Patients with unsuccessful bronchoscopic intervention often have a poor prognosis, despite concurrent chemotherapy and radiation (Mahmood et al. Respiration. 2015;89:404).

As more fellowship programs are offering training in rigid bronchoscopy, there is a need to standardize the training and use validated tools to assess competency. RIGID-TASC (Rigid bronchoscopy Tool for Assessment of Skills and Competence) is one such tool, which can be utilized for this purpose to provide objective feedback to the trainee (Mahmood et al. Ann Am Thor Soc. 2016. doi: 10.1513/ Epub ahead of print).

 

Dr. Kamran Mahmood

Kamran Mahmood, MD, MPH, FCCP

Steering Committee Member

Pediatric Chest Medicine: CHEST Foundation campaign to fight difficult-to-control asthma

The CHEST Foundation and the Asthma and Allergy Network have joined forces to combat difficult-to-control asthma with the campaign “Asthma: Take Action. Take Control.” Affecting approximately 235 million people worldwide, asthma morbidity continues to have a significant impact on quality of life for both children and adults with asthma. In the United States alone, it accounts for health-care costs of approximately 60 billion dollars.

The campaign educates patients, caregivers, families, and health-care providers about current treatment options for asthma, highlights the importance of specialist referrals, and encourages patients to participate with their health-care provider to achieve asthma control. Because asthma may fall into this difficult-to-control category for many reasons, including poor adherence, unresponsiveness to conventional therapies, failure to recognize and manage triggers, and co-morbidities, this campaign developed materials to improve health literacy so that patients can take an active and informed role in asthma self-management. Written in an easy to understand format and language, the “Take Control” campaign highlights four key steps:

• Tell your doctor when it’s hard to breathe.

• Ask your doctor for an asthma action plan.

• Practice your asthma action plan.

• Know that asthma shouldn’t hold you back.

Newly developed materials include tips and resources for children and adults to learn about asthma and raise awareness about difficult-to-control asthma. These materials can be found at asthma.chestnet.org.

 

Dr. Mary Cataletto

Mary Cataletto MD, FCCP

Steering Committee Member

Pulmonary Physiology, Function, and Rehabilitation: Current clinical usefulness of the PETCO2 during exercise testing

Dynamic measurement of the PETCO2 in cardiopulmonary exercise testing may demonstrate unique changes throughout exercise in specific diseases and is often underutilized during interpretation. Though it can be affected by hyperventilation and the VD/VT relationship, normally it rises from rest to lactate threshold (LT), then declines from peak exercise through recovery (Ramos RP, et al. Pulm Med. 2013;2013:359021. doi: 10.1155/2013/359021.) In severe pulmonary hypertension and shunts, the reverse occurs, declining in early exercise and then rising during recovery (Sun XG, et al. Circulation. 2002;105[1]:54). Blunting or reversal of this exercise decline in PETCO2 has been correlated with clinical improvement in therapeutic trials (Oudiz RJ, et al. Eur J Heart Fail. 2007;9[9]:917). Studies in severe CHF have correlated prognosis with lower values at rest and greater decline from rest to peak exercise, the latter being affected by adequacy of effort and assessed by RQ. They, however, do not take into account the normal rise and fall before and after LT (Arena R, et al. Am Heart J. 2008;156[5]:982) (Hoshimoto-Iwamoto M, et al. J Physiol Sci. 2009;59[1]:49). In pulmonary hypertension, as the disease progresses, the unique reversal of the normal slopes of the PETCO2 that occurs, negative in early exercise and positive during recovery in association with an excessive alveolar ventilator response, needs further clinical investigation and correlation (Yasunobu Y, et al. Chest. 2005;127[5]:1637). The dynamic changes that occur in the PETCO2 throughout exercise may be an additional tool to use in selective conditions to more accurately assess prognosis and monitor response to therapy.

 

 

 

Dr. Said Chaaban

Said Chaaban, MD; and Zachary Morris, MD, FCCP

Steering Committee Members

Pulmonary Vascular Disease: Estrogen in PAH: Is it good or bad?

The role of sex hormones in the development and perpetuation of pulmonary arterial hypertension (PAH) continues to be an open field of active research. Epidemiology reveals that PAH is more prevalent in women in both idiopathic and heritable cases.1 On the other hand, data demonstrate that prognosis of PAH in men is worse than in women and, in animal research, estrogens provide a protective effect. This constitutes the “estrogen paradox.” Estrogen plays a protective role in the vasculature, modulating proliferative and vasoactive signaling by direct and receptor-mediated mechanisms.2,3 In animal models of PAH, estrogen increases nitric oxide and prostacyclin production and decreases endothelin-1, resulting in beneficial vascular effects.4 However, the Women’s Health Initiative revealed that hormone replacement therapy increases the risk for adverse cardiovascular events.5 In familial PAH, estrogen is a potent mitogen of pulmonary vascular smooth muscle cells.6 A recently published study, first in humans, by Ventetuolo et al.7 showed higher levels of estrogen (E2) and lower level of dehydroepiandrosterone-sulfate (DHEAS) in men with PAH, compared with normal men without cardiovascular disease (MESA study), supporting the role of the estrogen pathway in the development of PAH. Experimental data implicate estrogens as promoters of vascular proliferation and cell damage but also as inhibitors of pulmonary vasoreactivity. In vitro, estrogen is mitogenic and promotes proliferation of pulmonary vascular smooth muscle cells.6 Despite advances, the role of sex and estrogen in PAH is not fully understood. More preclinical and clinical data are necessary to establish a potential role for estrogen-based therapies in this disease.

 

Dr. Hector Cajigas

Sandeep Sahay, MD; and Hector R Cajigas, MD

Steering Committee Members

References

1. Frost AE, et al. Chest. 2011;139:128.

2. Brouchet L, et al. Circulation. 2001;103:423.

3. Pendaries C, et al. Proc Natl Acad Sci USA. 2002;99:2205.

4. Lahm T, et al. Shock. 2008;30:660.

5. Manson JE, et al. N Engl J Med. 2003;349:523.

6. Farhat MY, et al. Br J Pharmacol. 1992;107:679.

7. Ventetuolo CE, et al. Am J Respir Crit Care Med. 2016;193:1168.

Thoracic Oncology: The “new” lung cancer staging system

Definition of lung cancer stage is an essential part of defining prognosis, developing treatment plans, and conducting and reporting on clinical research studies. The stage classification system is determined by the American Joint Committee on Cancer (AJCC) and Union for International Cancer Control (UICC). The 7th edition of the lung cancer staging system, published in 2009, was a landmark effort based on a large multicenter international database created by the Staging and Prognostic Factors (SPFC) of the International Association for the Study of Lung Cancer (IASLC) and backed by careful validation and statistical analysis.

The IASLC Lung Cancer Staging Committee has been working on the 8th edition of the TNM classification for lung cancer. The database used for analysis consists of 94,708 patients diagnosed between 1999 and 2010, and included cases from 35 sources and 16 countries. Multiple analyses were performed to assess the ability of T, N, and M descriptors to predict prognosis and to identify new cutpoints for inclusion in the eight edition.1-3 The proposed changes include new cutpoints for the T component based on 1-cm increments, new categories for the N component, a new M category to specifically identify patients with oligometastatic disease, and multiple updates to the overall TNM stage groupings.4 In addition, the proposal includes recommendations for coding T stage for subsolid nodules and assessment of tumor size in part-solid nodules.5 These proposed changes will be submitted to the UICC and AJCC for inclusion in the eighth edition and will be enacted in January 2017.

 

Dr. Anil Vachani

Anil Vachani, MD, FCCP

NetWork Vice-Chair

References

1. Rami-Porta R, et al. J Thorac Oncol. 2015;10:990.

2. Eberhardt WEE, et al. J Thorac Oncol. 2015;10:1515.

3. Asamura H, et al. J Thorac Oncol. 2015;10:1675.

4. Goldstraw P, et al. J Thorac Oncol. 2016;11:39.

5. Travis WD, et al. J Thorac Oncol. 2016;11:1204.

Publications
Sections

Interventional Chest/Diagnostic Procedures: Evolving approaches to manage central airway obstruction

Central airway obstruction (CAO) is a major cause of morbidity and mortality in patients with malignant and nonmalignant pulmonary disorders (Ernst et al. Am J Respir Crit Care Med. 2004;169:1278). It is associated with postobstructive pneumonia, respiratory compromise, and even respiratory failure. It often precludes the patients with malignancy from getting definitive treatment, such as surgical resection or chemotherapy. Therapeutic bronchoscopy using a rigid bronchoscope plays a central role in managing these patients.

Different modalities used during therapeutic bronchoscopy include debridement, airway dilation, and different heat therapies, such as laser, electrocautery, and argon plasma coagulation (Bolliger et al. Eur Respir J. 2006;27:1258). Airway stents are often placed to achieve durable airway patency. Endobronchial therapies with delayed effect include brachytherapy, photodynamic therapy, and cryotherapy (Vergnon et al. Eur Respir J. 2006;28:200). There is improvement in symptom control, quality of life, and spirometry with successful bronchoscopic intervention (Mahmood et al. Respiration. 2015;89:404). Patients with respiratory failure secondary to CAO can be weaned from mechanical ventilation (Murgu et al. Respiration. 2012;84:55).

It is often difficult to predict which patients will have a successful bronchoscopic intervention. Endobronchial disease and stent placement have been associated with successful outcome (Ost et al. Chest. 2015;147:1282). Patients with unsuccessful bronchoscopic intervention often have a poor prognosis, despite concurrent chemotherapy and radiation (Mahmood et al. Respiration. 2015;89:404).

As more fellowship programs are offering training in rigid bronchoscopy, there is a need to standardize the training and use validated tools to assess competency. RIGID-TASC (Rigid bronchoscopy Tool for Assessment of Skills and Competence) is one such tool, which can be utilized for this purpose to provide objective feedback to the trainee (Mahmood et al. Ann Am Thor Soc. 2016. doi: 10.1513/ Epub ahead of print).

 

Dr. Kamran Mahmood

Kamran Mahmood, MD, MPH, FCCP

Steering Committee Member

Pediatric Chest Medicine: CHEST Foundation campaign to fight difficult-to-control asthma

The CHEST Foundation and the Asthma and Allergy Network have joined forces to combat difficult-to-control asthma with the campaign “Asthma: Take Action. Take Control.” Affecting approximately 235 million people worldwide, asthma morbidity continues to have a significant impact on quality of life for both children and adults with asthma. In the United States alone, it accounts for health-care costs of approximately 60 billion dollars.

The campaign educates patients, caregivers, families, and health-care providers about current treatment options for asthma, highlights the importance of specialist referrals, and encourages patients to participate with their health-care provider to achieve asthma control. Because asthma may fall into this difficult-to-control category for many reasons, including poor adherence, unresponsiveness to conventional therapies, failure to recognize and manage triggers, and co-morbidities, this campaign developed materials to improve health literacy so that patients can take an active and informed role in asthma self-management. Written in an easy to understand format and language, the “Take Control” campaign highlights four key steps:

• Tell your doctor when it’s hard to breathe.

• Ask your doctor for an asthma action plan.

• Practice your asthma action plan.

• Know that asthma shouldn’t hold you back.

Newly developed materials include tips and resources for children and adults to learn about asthma and raise awareness about difficult-to-control asthma. These materials can be found at asthma.chestnet.org.

 

Dr. Mary Cataletto

Mary Cataletto MD, FCCP

Steering Committee Member

Pulmonary Physiology, Function, and Rehabilitation: Current clinical usefulness of the PETCO2 during exercise testing

Dynamic measurement of the PETCO2 in cardiopulmonary exercise testing may demonstrate unique changes throughout exercise in specific diseases and is often underutilized during interpretation. Though it can be affected by hyperventilation and the VD/VT relationship, normally it rises from rest to lactate threshold (LT), then declines from peak exercise through recovery (Ramos RP, et al. Pulm Med. 2013;2013:359021. doi: 10.1155/2013/359021.) In severe pulmonary hypertension and shunts, the reverse occurs, declining in early exercise and then rising during recovery (Sun XG, et al. Circulation. 2002;105[1]:54). Blunting or reversal of this exercise decline in PETCO2 has been correlated with clinical improvement in therapeutic trials (Oudiz RJ, et al. Eur J Heart Fail. 2007;9[9]:917). Studies in severe CHF have correlated prognosis with lower values at rest and greater decline from rest to peak exercise, the latter being affected by adequacy of effort and assessed by RQ. They, however, do not take into account the normal rise and fall before and after LT (Arena R, et al. Am Heart J. 2008;156[5]:982) (Hoshimoto-Iwamoto M, et al. J Physiol Sci. 2009;59[1]:49). In pulmonary hypertension, as the disease progresses, the unique reversal of the normal slopes of the PETCO2 that occurs, negative in early exercise and positive during recovery in association with an excessive alveolar ventilator response, needs further clinical investigation and correlation (Yasunobu Y, et al. Chest. 2005;127[5]:1637). The dynamic changes that occur in the PETCO2 throughout exercise may be an additional tool to use in selective conditions to more accurately assess prognosis and monitor response to therapy.

 

 

 

Dr. Said Chaaban

Said Chaaban, MD; and Zachary Morris, MD, FCCP

Steering Committee Members

Pulmonary Vascular Disease: Estrogen in PAH: Is it good or bad?

The role of sex hormones in the development and perpetuation of pulmonary arterial hypertension (PAH) continues to be an open field of active research. Epidemiology reveals that PAH is more prevalent in women in both idiopathic and heritable cases.1 On the other hand, data demonstrate that prognosis of PAH in men is worse than in women and, in animal research, estrogens provide a protective effect. This constitutes the “estrogen paradox.” Estrogen plays a protective role in the vasculature, modulating proliferative and vasoactive signaling by direct and receptor-mediated mechanisms.2,3 In animal models of PAH, estrogen increases nitric oxide and prostacyclin production and decreases endothelin-1, resulting in beneficial vascular effects.4 However, the Women’s Health Initiative revealed that hormone replacement therapy increases the risk for adverse cardiovascular events.5 In familial PAH, estrogen is a potent mitogen of pulmonary vascular smooth muscle cells.6 A recently published study, first in humans, by Ventetuolo et al.7 showed higher levels of estrogen (E2) and lower level of dehydroepiandrosterone-sulfate (DHEAS) in men with PAH, compared with normal men without cardiovascular disease (MESA study), supporting the role of the estrogen pathway in the development of PAH. Experimental data implicate estrogens as promoters of vascular proliferation and cell damage but also as inhibitors of pulmonary vasoreactivity. In vitro, estrogen is mitogenic and promotes proliferation of pulmonary vascular smooth muscle cells.6 Despite advances, the role of sex and estrogen in PAH is not fully understood. More preclinical and clinical data are necessary to establish a potential role for estrogen-based therapies in this disease.

 

Dr. Hector Cajigas

Sandeep Sahay, MD; and Hector R Cajigas, MD

Steering Committee Members

References

1. Frost AE, et al. Chest. 2011;139:128.

2. Brouchet L, et al. Circulation. 2001;103:423.

3. Pendaries C, et al. Proc Natl Acad Sci USA. 2002;99:2205.

4. Lahm T, et al. Shock. 2008;30:660.

5. Manson JE, et al. N Engl J Med. 2003;349:523.

6. Farhat MY, et al. Br J Pharmacol. 1992;107:679.

7. Ventetuolo CE, et al. Am J Respir Crit Care Med. 2016;193:1168.

Thoracic Oncology: The “new” lung cancer staging system

Definition of lung cancer stage is an essential part of defining prognosis, developing treatment plans, and conducting and reporting on clinical research studies. The stage classification system is determined by the American Joint Committee on Cancer (AJCC) and Union for International Cancer Control (UICC). The 7th edition of the lung cancer staging system, published in 2009, was a landmark effort based on a large multicenter international database created by the Staging and Prognostic Factors (SPFC) of the International Association for the Study of Lung Cancer (IASLC) and backed by careful validation and statistical analysis.

The IASLC Lung Cancer Staging Committee has been working on the 8th edition of the TNM classification for lung cancer. The database used for analysis consists of 94,708 patients diagnosed between 1999 and 2010, and included cases from 35 sources and 16 countries. Multiple analyses were performed to assess the ability of T, N, and M descriptors to predict prognosis and to identify new cutpoints for inclusion in the eight edition.1-3 The proposed changes include new cutpoints for the T component based on 1-cm increments, new categories for the N component, a new M category to specifically identify patients with oligometastatic disease, and multiple updates to the overall TNM stage groupings.4 In addition, the proposal includes recommendations for coding T stage for subsolid nodules and assessment of tumor size in part-solid nodules.5 These proposed changes will be submitted to the UICC and AJCC for inclusion in the eighth edition and will be enacted in January 2017.

 

Dr. Anil Vachani

Anil Vachani, MD, FCCP

NetWork Vice-Chair

References

1. Rami-Porta R, et al. J Thorac Oncol. 2015;10:990.

2. Eberhardt WEE, et al. J Thorac Oncol. 2015;10:1515.

3. Asamura H, et al. J Thorac Oncol. 2015;10:1675.

4. Goldstraw P, et al. J Thorac Oncol. 2016;11:39.

5. Travis WD, et al. J Thorac Oncol. 2016;11:1204.

Interventional Chest/Diagnostic Procedures: Evolving approaches to manage central airway obstruction

Central airway obstruction (CAO) is a major cause of morbidity and mortality in patients with malignant and nonmalignant pulmonary disorders (Ernst et al. Am J Respir Crit Care Med. 2004;169:1278). It is associated with postobstructive pneumonia, respiratory compromise, and even respiratory failure. It often precludes the patients with malignancy from getting definitive treatment, such as surgical resection or chemotherapy. Therapeutic bronchoscopy using a rigid bronchoscope plays a central role in managing these patients.

Different modalities used during therapeutic bronchoscopy include debridement, airway dilation, and different heat therapies, such as laser, electrocautery, and argon plasma coagulation (Bolliger et al. Eur Respir J. 2006;27:1258). Airway stents are often placed to achieve durable airway patency. Endobronchial therapies with delayed effect include brachytherapy, photodynamic therapy, and cryotherapy (Vergnon et al. Eur Respir J. 2006;28:200). There is improvement in symptom control, quality of life, and spirometry with successful bronchoscopic intervention (Mahmood et al. Respiration. 2015;89:404). Patients with respiratory failure secondary to CAO can be weaned from mechanical ventilation (Murgu et al. Respiration. 2012;84:55).

It is often difficult to predict which patients will have a successful bronchoscopic intervention. Endobronchial disease and stent placement have been associated with successful outcome (Ost et al. Chest. 2015;147:1282). Patients with unsuccessful bronchoscopic intervention often have a poor prognosis, despite concurrent chemotherapy and radiation (Mahmood et al. Respiration. 2015;89:404).

As more fellowship programs are offering training in rigid bronchoscopy, there is a need to standardize the training and use validated tools to assess competency. RIGID-TASC (Rigid bronchoscopy Tool for Assessment of Skills and Competence) is one such tool, which can be utilized for this purpose to provide objective feedback to the trainee (Mahmood et al. Ann Am Thor Soc. 2016. doi: 10.1513/ Epub ahead of print).

 

Dr. Kamran Mahmood

Kamran Mahmood, MD, MPH, FCCP

Steering Committee Member

Pediatric Chest Medicine: CHEST Foundation campaign to fight difficult-to-control asthma

The CHEST Foundation and the Asthma and Allergy Network have joined forces to combat difficult-to-control asthma with the campaign “Asthma: Take Action. Take Control.” Affecting approximately 235 million people worldwide, asthma morbidity continues to have a significant impact on quality of life for both children and adults with asthma. In the United States alone, it accounts for health-care costs of approximately 60 billion dollars.

The campaign educates patients, caregivers, families, and health-care providers about current treatment options for asthma, highlights the importance of specialist referrals, and encourages patients to participate with their health-care provider to achieve asthma control. Because asthma may fall into this difficult-to-control category for many reasons, including poor adherence, unresponsiveness to conventional therapies, failure to recognize and manage triggers, and co-morbidities, this campaign developed materials to improve health literacy so that patients can take an active and informed role in asthma self-management. Written in an easy to understand format and language, the “Take Control” campaign highlights four key steps:

• Tell your doctor when it’s hard to breathe.

• Ask your doctor for an asthma action plan.

• Practice your asthma action plan.

• Know that asthma shouldn’t hold you back.

Newly developed materials include tips and resources for children and adults to learn about asthma and raise awareness about difficult-to-control asthma. These materials can be found at asthma.chestnet.org.

 

Dr. Mary Cataletto

Mary Cataletto MD, FCCP

Steering Committee Member

Pulmonary Physiology, Function, and Rehabilitation: Current clinical usefulness of the PETCO2 during exercise testing

Dynamic measurement of the PETCO2 in cardiopulmonary exercise testing may demonstrate unique changes throughout exercise in specific diseases and is often underutilized during interpretation. Though it can be affected by hyperventilation and the VD/VT relationship, normally it rises from rest to lactate threshold (LT), then declines from peak exercise through recovery (Ramos RP, et al. Pulm Med. 2013;2013:359021. doi: 10.1155/2013/359021.) In severe pulmonary hypertension and shunts, the reverse occurs, declining in early exercise and then rising during recovery (Sun XG, et al. Circulation. 2002;105[1]:54). Blunting or reversal of this exercise decline in PETCO2 has been correlated with clinical improvement in therapeutic trials (Oudiz RJ, et al. Eur J Heart Fail. 2007;9[9]:917). Studies in severe CHF have correlated prognosis with lower values at rest and greater decline from rest to peak exercise, the latter being affected by adequacy of effort and assessed by RQ. They, however, do not take into account the normal rise and fall before and after LT (Arena R, et al. Am Heart J. 2008;156[5]:982) (Hoshimoto-Iwamoto M, et al. J Physiol Sci. 2009;59[1]:49). In pulmonary hypertension, as the disease progresses, the unique reversal of the normal slopes of the PETCO2 that occurs, negative in early exercise and positive during recovery in association with an excessive alveolar ventilator response, needs further clinical investigation and correlation (Yasunobu Y, et al. Chest. 2005;127[5]:1637). The dynamic changes that occur in the PETCO2 throughout exercise may be an additional tool to use in selective conditions to more accurately assess prognosis and monitor response to therapy.

 

 

 

Dr. Said Chaaban

Said Chaaban, MD; and Zachary Morris, MD, FCCP

Steering Committee Members

Pulmonary Vascular Disease: Estrogen in PAH: Is it good or bad?

The role of sex hormones in the development and perpetuation of pulmonary arterial hypertension (PAH) continues to be an open field of active research. Epidemiology reveals that PAH is more prevalent in women in both idiopathic and heritable cases.1 On the other hand, data demonstrate that prognosis of PAH in men is worse than in women and, in animal research, estrogens provide a protective effect. This constitutes the “estrogen paradox.” Estrogen plays a protective role in the vasculature, modulating proliferative and vasoactive signaling by direct and receptor-mediated mechanisms.2,3 In animal models of PAH, estrogen increases nitric oxide and prostacyclin production and decreases endothelin-1, resulting in beneficial vascular effects.4 However, the Women’s Health Initiative revealed that hormone replacement therapy increases the risk for adverse cardiovascular events.5 In familial PAH, estrogen is a potent mitogen of pulmonary vascular smooth muscle cells.6 A recently published study, first in humans, by Ventetuolo et al.7 showed higher levels of estrogen (E2) and lower level of dehydroepiandrosterone-sulfate (DHEAS) in men with PAH, compared with normal men without cardiovascular disease (MESA study), supporting the role of the estrogen pathway in the development of PAH. Experimental data implicate estrogens as promoters of vascular proliferation and cell damage but also as inhibitors of pulmonary vasoreactivity. In vitro, estrogen is mitogenic and promotes proliferation of pulmonary vascular smooth muscle cells.6 Despite advances, the role of sex and estrogen in PAH is not fully understood. More preclinical and clinical data are necessary to establish a potential role for estrogen-based therapies in this disease.

 

Dr. Hector Cajigas

Sandeep Sahay, MD; and Hector R Cajigas, MD

Steering Committee Members

References

1. Frost AE, et al. Chest. 2011;139:128.

2. Brouchet L, et al. Circulation. 2001;103:423.

3. Pendaries C, et al. Proc Natl Acad Sci USA. 2002;99:2205.

4. Lahm T, et al. Shock. 2008;30:660.

5. Manson JE, et al. N Engl J Med. 2003;349:523.

6. Farhat MY, et al. Br J Pharmacol. 1992;107:679.

7. Ventetuolo CE, et al. Am J Respir Crit Care Med. 2016;193:1168.

Thoracic Oncology: The “new” lung cancer staging system

Definition of lung cancer stage is an essential part of defining prognosis, developing treatment plans, and conducting and reporting on clinical research studies. The stage classification system is determined by the American Joint Committee on Cancer (AJCC) and Union for International Cancer Control (UICC). The 7th edition of the lung cancer staging system, published in 2009, was a landmark effort based on a large multicenter international database created by the Staging and Prognostic Factors (SPFC) of the International Association for the Study of Lung Cancer (IASLC) and backed by careful validation and statistical analysis.

The IASLC Lung Cancer Staging Committee has been working on the 8th edition of the TNM classification for lung cancer. The database used for analysis consists of 94,708 patients diagnosed between 1999 and 2010, and included cases from 35 sources and 16 countries. Multiple analyses were performed to assess the ability of T, N, and M descriptors to predict prognosis and to identify new cutpoints for inclusion in the eight edition.1-3 The proposed changes include new cutpoints for the T component based on 1-cm increments, new categories for the N component, a new M category to specifically identify patients with oligometastatic disease, and multiple updates to the overall TNM stage groupings.4 In addition, the proposal includes recommendations for coding T stage for subsolid nodules and assessment of tumor size in part-solid nodules.5 These proposed changes will be submitted to the UICC and AJCC for inclusion in the eighth edition and will be enacted in January 2017.

 

Dr. Anil Vachani

Anil Vachani, MD, FCCP

NetWork Vice-Chair

References

1. Rami-Porta R, et al. J Thorac Oncol. 2015;10:990.

2. Eberhardt WEE, et al. J Thorac Oncol. 2015;10:1515.

3. Asamura H, et al. J Thorac Oncol. 2015;10:1675.

4. Goldstraw P, et al. J Thorac Oncol. 2016;11:39.

5. Travis WD, et al. J Thorac Oncol. 2016;11:1204.

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