Endocrine Cancer

The obesity epidemic in the United States may be slowing improvements in cancer mortality, according to a new analysis of over 50 million cancer and heart disease deaths.

“By integrating 20 years of cancer mortality data, we demonstrated that trends in obesity-associated cancer mortality showed signs of recent deceleration, consistent with recent findings for heart disease mortality,” Christy L. Avery, PhD, and associates wrote in JAMA Network Open.

Improvements in mortality related to heart disease slowed after 2011, a phenomenon that has been associated with rising obesity rates. The age-adjusted mortality rate (AAMR) declined at an average of 3.8 deaths per 100,000 persons from 1999 to 2011 but only 0.7 deaths per 100,000 from 2011 to 2018, based on data from the Centers for Disease Control and Prevention’s Wide-Ranging Online Data for Epidemiologic Research (WONDER).

To understand trends in cancer mortality and their possible connection with obesity, data for 1999-2018 from the WONDER database were divided into obesity-associated and non–obesity-associated categories and compared with heart disease mortality, they explained. The database included more than 50 million deaths that matched inclusion criteria.

The analysis showed there was difference between obesity-associated and non–obesity-associated cancers that was obscured when all cancer deaths were considered together. The average annual change in AAMR for obesity-associated cancers slowed from –1.19 deaths per 100,000 in 1999-2011 to –0.83 in 2011-2018, Dr. Avery and associates reported.

For non–obesity-associated cancers, the annual change in AAMR increased from –1.62 per 100,000 for 1999-2011 to –2.29 for 2011-2018, following the trend for all cancers: –1.48 per 100,000 during 1999-2011 and –1.77 in 2011-2018, they said.

“The largest mortality decreases were observed for melanoma of the skin and lung cancer, two cancers not associated with obesity. For obesity-associated cancers, stable or increasing mortality rates have been observed for liver and pancreatic cancer among both men and women as well as for uterine cancer among women,” the investigators wrote.

Demographically, however, the slowing improvement in mortality for obesity-associated cancers did not follow the trend for heart disease. The deceleration for cancer was more pronounced for women and for non-Hispanic Whites and not seen at all in non-Hispanic Asian/Pacific Islander individuals. “For heart disease, evidence of a deceleration was consistent across sex, race, and ethnicity,” they said.

There are “longstanding disparities in obesity” among various populations in the United States, and the recent trend of obesity occurring earlier in life may be having an effect. “Whether the findings of decelerating mortality rates potentially signal a changing profile of cancer and heart disease mortality as the consequences of the obesity epidemic are realized remains to be seen,” they concluded.

The investigators reported receiving grants from the National Institutes of Health during the conduct of the study, but no other disclosures were reported.

[email protected]

The obesity epidemic in the United States may be slowing improvements in cancer mortality, according to a new analysis of over 50 million cancer and heart disease deaths.

“By integrating 20 years of cancer mortality data, we demonstrated that trends in obesity-associated cancer mortality showed signs of recent deceleration, consistent with recent findings for heart disease mortality,” Christy L. Avery, PhD, and associates wrote in JAMA Network Open.

Improvements in mortality related to heart disease slowed after 2011, a phenomenon that has been associated with rising obesity rates. The age-adjusted mortality rate (AAMR) declined at an average of 3.8 deaths per 100,000 persons from 1999 to 2011 but only 0.7 deaths per 100,000 from 2011 to 2018, based on data from the Centers for Disease Control and Prevention’s Wide-Ranging Online Data for Epidemiologic Research (WONDER).

To understand trends in cancer mortality and their possible connection with obesity, data for 1999-2018 from the WONDER database were divided into obesity-associated and non–obesity-associated categories and compared with heart disease mortality, they explained. The database included more than 50 million deaths that matched inclusion criteria.

The analysis showed there was difference between obesity-associated and non–obesity-associated cancers that was obscured when all cancer deaths were considered together. The average annual change in AAMR for obesity-associated cancers slowed from –1.19 deaths per 100,000 in 1999-2011 to –0.83 in 2011-2018, Dr. Avery and associates reported.

For non–obesity-associated cancers, the annual change in AAMR increased from –1.62 per 100,000 for 1999-2011 to –2.29 for 2011-2018, following the trend for all cancers: –1.48 per 100,000 during 1999-2011 and –1.77 in 2011-2018, they said.

“The largest mortality decreases were observed for melanoma of the skin and lung cancer, two cancers not associated with obesity. For obesity-associated cancers, stable or increasing mortality rates have been observed for liver and pancreatic cancer among both men and women as well as for uterine cancer among women,” the investigators wrote.

Demographically, however, the slowing improvement in mortality for obesity-associated cancers did not follow the trend for heart disease. The deceleration for cancer was more pronounced for women and for non-Hispanic Whites and not seen at all in non-Hispanic Asian/Pacific Islander individuals. “For heart disease, evidence of a deceleration was consistent across sex, race, and ethnicity,” they said.

There are “longstanding disparities in obesity” among various populations in the United States, and the recent trend of obesity occurring earlier in life may be having an effect. “Whether the findings of decelerating mortality rates potentially signal a changing profile of cancer and heart disease mortality as the consequences of the obesity epidemic are realized remains to be seen,” they concluded.

The investigators reported receiving grants from the National Institutes of Health during the conduct of the study, but no other disclosures were reported.

[email protected]

The obesity epidemic in the United States may be slowing improvements in cancer mortality, according to a new analysis of over 50 million cancer and heart disease deaths.

“By integrating 20 years of cancer mortality data, we demonstrated that trends in obesity-associated cancer mortality showed signs of recent deceleration, consistent with recent findings for heart disease mortality,” Christy L. Avery, PhD, and associates wrote in JAMA Network Open.

Improvements in mortality related to heart disease slowed after 2011, a phenomenon that has been associated with rising obesity rates. The age-adjusted mortality rate (AAMR) declined at an average of 3.8 deaths per 100,000 persons from 1999 to 2011 but only 0.7 deaths per 100,000 from 2011 to 2018, based on data from the Centers for Disease Control and Prevention’s Wide-Ranging Online Data for Epidemiologic Research (WONDER).

To understand trends in cancer mortality and their possible connection with obesity, data for 1999-2018 from the WONDER database were divided into obesity-associated and non–obesity-associated categories and compared with heart disease mortality, they explained. The database included more than 50 million deaths that matched inclusion criteria.

The analysis showed there was difference between obesity-associated and non–obesity-associated cancers that was obscured when all cancer deaths were considered together. The average annual change in AAMR for obesity-associated cancers slowed from –1.19 deaths per 100,000 in 1999-2011 to –0.83 in 2011-2018, Dr. Avery and associates reported.

For non–obesity-associated cancers, the annual change in AAMR increased from –1.62 per 100,000 for 1999-2011 to –2.29 for 2011-2018, following the trend for all cancers: –1.48 per 100,000 during 1999-2011 and –1.77 in 2011-2018, they said.

“The largest mortality decreases were observed for melanoma of the skin and lung cancer, two cancers not associated with obesity. For obesity-associated cancers, stable or increasing mortality rates have been observed for liver and pancreatic cancer among both men and women as well as for uterine cancer among women,” the investigators wrote.

Demographically, however, the slowing improvement in mortality for obesity-associated cancers did not follow the trend for heart disease. The deceleration for cancer was more pronounced for women and for non-Hispanic Whites and not seen at all in non-Hispanic Asian/Pacific Islander individuals. “For heart disease, evidence of a deceleration was consistent across sex, race, and ethnicity,” they said.

There are “longstanding disparities in obesity” among various populations in the United States, and the recent trend of obesity occurring earlier in life may be having an effect. “Whether the findings of decelerating mortality rates potentially signal a changing profile of cancer and heart disease mortality as the consequences of the obesity epidemic are realized remains to be seen,” they concluded.

The investigators reported receiving grants from the National Institutes of Health during the conduct of the study, but no other disclosures were reported.

[email protected]

Hormonal therapies for the treatment of hormone-dependent breast and prostate cancer could raise the risk for myocardial infarction and stroke, and patients need to be closely monitored to allow early detection and treatment of cardiovascular disease (CVD), the American Heart Association says in a new scientific statement.
 

“The statement provides data on the risks of each type of hormonal therapy so clinicians can use it as a guide to help manage cardiovascular risks during cancer treatment,” Tochi Okwuosa, DO, chair of the writing group, said in a news release.

“A team-based approach to patient care that includes the oncology team, cardiologist, primary care clinician, dietitian, endocrinologist, and other health care professionals as appropriate is needed to work with each patient to manage and reduce the increased risk of heart disease and strokes associated with hormonal therapy in breast and prostate cancer treatment,” said Dr. Okwuosa, director of cardio-oncology services, Rush University Medical Center, Chicago.

The scientific statement was published online April 26 in Circulation: Genomic and Precision Medicine.

Hormone-dependent cancers, such as prostate and breast cancer, are the most common noncutaneous cancers in the United States and around the world. As hormonal therapies have markedly improved survival in these patients, CVD has emerged as a leading cause illness and death.

The increased CVD burden might be explained by the increasing average age of cancer survivors, leading to higher rates of age-related CV risk factors and coronary artery disease.

The writing group reviewed existing evidence from observational studies and randomized controlled trials on the cardiovascular impact of anticancer hormonal therapies.



Among the key findings:

• In patients with breast cancer,  has been shown to increase the risk for venous thromboembolic events, but to have somewhat protective to neutral effects on CVD risk burden and CVD events. Conversely, aromatase inhibitors have been shown to increase the risk for CVD risk factors and events, including MI and stroke.
• Androgen-deprivation therapy for prostate cancer appears to increase the risk for CV events, although gonadotrophin-releasing hormone (GnRH) antagonists are associated with a lower risk for CV events than are GnRH agonists. The oral antiandrogens appear to be associated with increased CVD risk as well, particularly when used for complete androgen blockade as combination GnRH/anti-androgen therapy.
• The duration of hormonal therapies has a significant impact on CVD risk; the longer patients receive hormonal therapy, the greater the risk. More research is needed to better define the risks associated with duration of treatment.
• The data are mixed on the impact of preexisting CV risk factors and CVD on CV events associated with hormonal therapy. Although the presence of baseline CV risk factors and CVD can increase CV events associated with aromatase inhibitors, it is not clear that tamoxifen does.
• Studies suggest that patients with prostate cancer and baseline CVD and CV risk factors have increased rates of CV events when treated with androgen-deprivation therapy.
• Although the prolonged use of some hormonal therapies worsens CV risk factors and , the effects of the duration of therapy on CV events are less clear.

The writing group noted that there are no definitive guidelines for the monitoring and management of hormonal therapy-related CVD risks.

The authors encourage clinicians to be alert for worsening CV problems in those with preexisting heart disease or risk factors, and to recognize that even patients without preexisting CV problems are at higher risk because of their exposure to hormonal therapies.

“For patients who have two or more cardiovascular risk factors, it is likely that referral to a cardiologist would be appropriate prior to beginning hormone treatment. For patients already receiving hormonal therapies, a discussion with the oncology team can help to determine if a cardiology referral is recommended,” Dr. Okwuosa said in the news release.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Cardio-Oncology Subcommittee of the Council on Clinical Cardiology and the Council on Genomic and Precision Medicine; the Council on Arteriosclerosis, Thrombosis, and Vascular Biology; and the Council on Cardiovascular Radiology and Intervention.

The research had no commercial funding. Dr. Okwuosa has disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Hormonal therapies for the treatment of hormone-dependent breast and prostate cancer could raise the risk for myocardial infarction and stroke, and patients need to be closely monitored to allow early detection and treatment of cardiovascular disease (CVD), the American Heart Association says in a new scientific statement.
 

“The statement provides data on the risks of each type of hormonal therapy so clinicians can use it as a guide to help manage cardiovascular risks during cancer treatment,” Tochi Okwuosa, DO, chair of the writing group, said in a news release.

“A team-based approach to patient care that includes the oncology team, cardiologist, primary care clinician, dietitian, endocrinologist, and other health care professionals as appropriate is needed to work with each patient to manage and reduce the increased risk of heart disease and strokes associated with hormonal therapy in breast and prostate cancer treatment,” said Dr. Okwuosa, director of cardio-oncology services, Rush University Medical Center, Chicago.

The scientific statement was published online April 26 in Circulation: Genomic and Precision Medicine.

Hormone-dependent cancers, such as prostate and breast cancer, are the most common noncutaneous cancers in the United States and around the world. As hormonal therapies have markedly improved survival in these patients, CVD has emerged as a leading cause illness and death.

The increased CVD burden might be explained by the increasing average age of cancer survivors, leading to higher rates of age-related CV risk factors and coronary artery disease.

The writing group reviewed existing evidence from observational studies and randomized controlled trials on the cardiovascular impact of anticancer hormonal therapies.



Among the key findings:

• In patients with breast cancer,  has been shown to increase the risk for venous thromboembolic events, but to have somewhat protective to neutral effects on CVD risk burden and CVD events. Conversely, aromatase inhibitors have been shown to increase the risk for CVD risk factors and events, including MI and stroke.
• Androgen-deprivation therapy for prostate cancer appears to increase the risk for CV events, although gonadotrophin-releasing hormone (GnRH) antagonists are associated with a lower risk for CV events than are GnRH agonists. The oral antiandrogens appear to be associated with increased CVD risk as well, particularly when used for complete androgen blockade as combination GnRH/anti-androgen therapy.
• The duration of hormonal therapies has a significant impact on CVD risk; the longer patients receive hormonal therapy, the greater the risk. More research is needed to better define the risks associated with duration of treatment.
• The data are mixed on the impact of preexisting CV risk factors and CVD on CV events associated with hormonal therapy. Although the presence of baseline CV risk factors and CVD can increase CV events associated with aromatase inhibitors, it is not clear that tamoxifen does.
• Studies suggest that patients with prostate cancer and baseline CVD and CV risk factors have increased rates of CV events when treated with androgen-deprivation therapy.
• Although the prolonged use of some hormonal therapies worsens CV risk factors and , the effects of the duration of therapy on CV events are less clear.

The writing group noted that there are no definitive guidelines for the monitoring and management of hormonal therapy-related CVD risks.

The authors encourage clinicians to be alert for worsening CV problems in those with preexisting heart disease or risk factors, and to recognize that even patients without preexisting CV problems are at higher risk because of their exposure to hormonal therapies.

“For patients who have two or more cardiovascular risk factors, it is likely that referral to a cardiologist would be appropriate prior to beginning hormone treatment. For patients already receiving hormonal therapies, a discussion with the oncology team can help to determine if a cardiology referral is recommended,” Dr. Okwuosa said in the news release.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Cardio-Oncology Subcommittee of the Council on Clinical Cardiology and the Council on Genomic and Precision Medicine; the Council on Arteriosclerosis, Thrombosis, and Vascular Biology; and the Council on Cardiovascular Radiology and Intervention.

The research had no commercial funding. Dr. Okwuosa has disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Hormonal therapies for the treatment of hormone-dependent breast and prostate cancer could raise the risk for myocardial infarction and stroke, and patients need to be closely monitored to allow early detection and treatment of cardiovascular disease (CVD), the American Heart Association says in a new scientific statement.
 

“The statement provides data on the risks of each type of hormonal therapy so clinicians can use it as a guide to help manage cardiovascular risks during cancer treatment,” Tochi Okwuosa, DO, chair of the writing group, said in a news release.

“A team-based approach to patient care that includes the oncology team, cardiologist, primary care clinician, dietitian, endocrinologist, and other health care professionals as appropriate is needed to work with each patient to manage and reduce the increased risk of heart disease and strokes associated with hormonal therapy in breast and prostate cancer treatment,” said Dr. Okwuosa, director of cardio-oncology services, Rush University Medical Center, Chicago.

The scientific statement was published online April 26 in Circulation: Genomic and Precision Medicine.

Hormone-dependent cancers, such as prostate and breast cancer, are the most common noncutaneous cancers in the United States and around the world. As hormonal therapies have markedly improved survival in these patients, CVD has emerged as a leading cause illness and death.

The increased CVD burden might be explained by the increasing average age of cancer survivors, leading to higher rates of age-related CV risk factors and coronary artery disease.

The writing group reviewed existing evidence from observational studies and randomized controlled trials on the cardiovascular impact of anticancer hormonal therapies.



Among the key findings:

• In patients with breast cancer,  has been shown to increase the risk for venous thromboembolic events, but to have somewhat protective to neutral effects on CVD risk burden and CVD events. Conversely, aromatase inhibitors have been shown to increase the risk for CVD risk factors and events, including MI and stroke.
• Androgen-deprivation therapy for prostate cancer appears to increase the risk for CV events, although gonadotrophin-releasing hormone (GnRH) antagonists are associated with a lower risk for CV events than are GnRH agonists. The oral antiandrogens appear to be associated with increased CVD risk as well, particularly when used for complete androgen blockade as combination GnRH/anti-androgen therapy.
• The duration of hormonal therapies has a significant impact on CVD risk; the longer patients receive hormonal therapy, the greater the risk. More research is needed to better define the risks associated with duration of treatment.
• The data are mixed on the impact of preexisting CV risk factors and CVD on CV events associated with hormonal therapy. Although the presence of baseline CV risk factors and CVD can increase CV events associated with aromatase inhibitors, it is not clear that tamoxifen does.
• Studies suggest that patients with prostate cancer and baseline CVD and CV risk factors have increased rates of CV events when treated with androgen-deprivation therapy.
• Although the prolonged use of some hormonal therapies worsens CV risk factors and , the effects of the duration of therapy on CV events are less clear.

The writing group noted that there are no definitive guidelines for the monitoring and management of hormonal therapy-related CVD risks.

The authors encourage clinicians to be alert for worsening CV problems in those with preexisting heart disease or risk factors, and to recognize that even patients without preexisting CV problems are at higher risk because of their exposure to hormonal therapies.

“For patients who have two or more cardiovascular risk factors, it is likely that referral to a cardiologist would be appropriate prior to beginning hormone treatment. For patients already receiving hormonal therapies, a discussion with the oncology team can help to determine if a cardiology referral is recommended,” Dr. Okwuosa said in the news release.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Cardio-Oncology Subcommittee of the Council on Clinical Cardiology and the Council on Genomic and Precision Medicine; the Council on Arteriosclerosis, Thrombosis, and Vascular Biology; and the Council on Cardiovascular Radiology and Intervention.

The research had no commercial funding. Dr. Okwuosa has disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

NEW ORLEANS – The 2015 American Thyroid Association risk stratification system for patients with differentiated thyroid cancer performed well in a real-world cohort with a high proportion of high-risk patients, according to a study presented at the annual meeting of the Endocrine Society.

“The 2015 ATA Risk Stratification System is an excellent predictor of both persisting disease and survival,” wrote Evert F.S. van Velsen, MD, and his colleagues at Erasmus Medical Center, Rotterdam, the Netherlands, in a poster accompanying the presentation.

Among a group of 236 patients with differentiated thyroid cancer (DTC), Dr. van Velsen and his coauthors looked at how the ATA high-risk criteria influenced patient response to therapy. By the end of the 14-year study period, initial gross extrathyroidal disease extension meant patients were much less likely to have an excellent response (odds ratio, 0.26; P less than .001), and much more likely to have persistent disease (OR, 2.57; P = .001).

Odds of having an excellent response were reduced by having high postoperative thyroglobulin levels (OR, 0.21; P less than .001), and persistent disease was more likely (OR, 2.39; P = .002).

Other high-risk criteria associated with significantly lower odds of excellent response included distant metastases (OR, 0.36), incomplete resection (OR, 0.51), and having follicular thyroid carcinoma (FTC) with extensive vascular invasion (OR, 0.27). All these risk factors also were associated with higher odds of persistent disease.

“Recurrence after no evidence of disease occurred in 14%” of the study population, said Dr. van Velsen and his coauthors, adding, “Clinicians should be aware of the relatively high recurrence risk, even after an excellent response to therapy.”

The study aimed to evaluate the 2015 ATA risk stratification system’s prognostic value in a population that included a relatively large proportion of high-risk DTC patients, to include many FTC patients. This work, they noted, augments previous assessments of the risk stratification system in lower-risk populations.

The authors noted that, in addition to predicting disease recurrence, the risk stratification system also worked as a predictor of disease-specific survival. Patients with structural incomplete response fared the worst, with a survival probability below 0.5 at 200 months on a Kaplan-Meier curve of disease-specific survival. Survival probability remained at 1.0 for patients with excellent response after first therapy and was intermediate for those with indeterminate response and biochemical incomplete response.

Overall mortality was higher in FTC patients. Over the study period, 31 of the 76 FTC patients (41%) died, compared with 39 of the PTC patients (24%; P = .010). In all, 28% of the FTC patients and 18% of the PTC patients died of thyroid cancer, but this difference didn’t reach statistical significance.

The retrospective study included adults with DTC meeting the 2015 ATA high-risk criteria who were diagnosed and/or treated at Erasmus Medical Center over a 13-year span ending in December 2015.

Overall, the investigators found 236 patients meeting inclusion criteria; 160 had papillary thyroid cancer (PTC), and the remaining 76 had FTC. The latter group were significantly older at baseline than PTC patients (64 versus 53 years), and were significantly less likely to undergo neck dissection (22% versus 55%).

In the full cohort, 96 patients (41%) had one high-risk factor, and an additional 74 (31%) had two risk factors. The remaining patients had three or more risk factors.

There was no between-group difference in the likelihood of receiving radioactive iodine treatment, but those with FTC had a lower cumulative radiation dose (195 versus 298 mCi; P less than .001).

More than half of patients (58%) had persistent disease after completing their first therapy. Of these, 51% had structural incomplete response and 7% had biochemical incomplete response. The response was indeterminate for about a quarter of the cohort, and the remaining 17% had an excellent initial response.

By the end of the study period, 55% of patients had persistent disease, and 51% had structural incomplete response (a more likely result for those with FTC than PTC). Just 4% had a biochemical incomplete response, and the response was indeterminate for 16%. Response was judged excellent for 29% of patients.

Dr. van Velsen and his coauthors reported that they had no relevant disclosures.

[email protected]

SOURCE: van Velsen EFS et al. ENDO 2019, Abstract MON-549.

NEW ORLEANS – The 2015 American Thyroid Association risk stratification system for patients with differentiated thyroid cancer performed well in a real-world cohort with a high proportion of high-risk patients, according to a study presented at the annual meeting of the Endocrine Society.

“The 2015 ATA Risk Stratification System is an excellent predictor of both persisting disease and survival,” wrote Evert F.S. van Velsen, MD, and his colleagues at Erasmus Medical Center, Rotterdam, the Netherlands, in a poster accompanying the presentation.

Among a group of 236 patients with differentiated thyroid cancer (DTC), Dr. van Velsen and his coauthors looked at how the ATA high-risk criteria influenced patient response to therapy. By the end of the 14-year study period, initial gross extrathyroidal disease extension meant patients were much less likely to have an excellent response (odds ratio, 0.26; P less than .001), and much more likely to have persistent disease (OR, 2.57; P = .001).

Odds of having an excellent response were reduced by having high postoperative thyroglobulin levels (OR, 0.21; P less than .001), and persistent disease was more likely (OR, 2.39; P = .002).

Other high-risk criteria associated with significantly lower odds of excellent response included distant metastases (OR, 0.36), incomplete resection (OR, 0.51), and having follicular thyroid carcinoma (FTC) with extensive vascular invasion (OR, 0.27). All these risk factors also were associated with higher odds of persistent disease.

“Recurrence after no evidence of disease occurred in 14%” of the study population, said Dr. van Velsen and his coauthors, adding, “Clinicians should be aware of the relatively high recurrence risk, even after an excellent response to therapy.”

The study aimed to evaluate the 2015 ATA risk stratification system’s prognostic value in a population that included a relatively large proportion of high-risk DTC patients, to include many FTC patients. This work, they noted, augments previous assessments of the risk stratification system in lower-risk populations.

The authors noted that, in addition to predicting disease recurrence, the risk stratification system also worked as a predictor of disease-specific survival. Patients with structural incomplete response fared the worst, with a survival probability below 0.5 at 200 months on a Kaplan-Meier curve of disease-specific survival. Survival probability remained at 1.0 for patients with excellent response after first therapy and was intermediate for those with indeterminate response and biochemical incomplete response.

Overall mortality was higher in FTC patients. Over the study period, 31 of the 76 FTC patients (41%) died, compared with 39 of the PTC patients (24%; P = .010). In all, 28% of the FTC patients and 18% of the PTC patients died of thyroid cancer, but this difference didn’t reach statistical significance.

The retrospective study included adults with DTC meeting the 2015 ATA high-risk criteria who were diagnosed and/or treated at Erasmus Medical Center over a 13-year span ending in December 2015.

Overall, the investigators found 236 patients meeting inclusion criteria; 160 had papillary thyroid cancer (PTC), and the remaining 76 had FTC. The latter group were significantly older at baseline than PTC patients (64 versus 53 years), and were significantly less likely to undergo neck dissection (22% versus 55%).

In the full cohort, 96 patients (41%) had one high-risk factor, and an additional 74 (31%) had two risk factors. The remaining patients had three or more risk factors.

There was no between-group difference in the likelihood of receiving radioactive iodine treatment, but those with FTC had a lower cumulative radiation dose (195 versus 298 mCi; P less than .001).

More than half of patients (58%) had persistent disease after completing their first therapy. Of these, 51% had structural incomplete response and 7% had biochemical incomplete response. The response was indeterminate for about a quarter of the cohort, and the remaining 17% had an excellent initial response.

By the end of the study period, 55% of patients had persistent disease, and 51% had structural incomplete response (a more likely result for those with FTC than PTC). Just 4% had a biochemical incomplete response, and the response was indeterminate for 16%. Response was judged excellent for 29% of patients.

Dr. van Velsen and his coauthors reported that they had no relevant disclosures.

[email protected]

SOURCE: van Velsen EFS et al. ENDO 2019, Abstract MON-549.

NEW ORLEANS – The 2015 American Thyroid Association risk stratification system for patients with differentiated thyroid cancer performed well in a real-world cohort with a high proportion of high-risk patients, according to a study presented at the annual meeting of the Endocrine Society.

“The 2015 ATA Risk Stratification System is an excellent predictor of both persisting disease and survival,” wrote Evert F.S. van Velsen, MD, and his colleagues at Erasmus Medical Center, Rotterdam, the Netherlands, in a poster accompanying the presentation.

Among a group of 236 patients with differentiated thyroid cancer (DTC), Dr. van Velsen and his coauthors looked at how the ATA high-risk criteria influenced patient response to therapy. By the end of the 14-year study period, initial gross extrathyroidal disease extension meant patients were much less likely to have an excellent response (odds ratio, 0.26; P less than .001), and much more likely to have persistent disease (OR, 2.57; P = .001).

Odds of having an excellent response were reduced by having high postoperative thyroglobulin levels (OR, 0.21; P less than .001), and persistent disease was more likely (OR, 2.39; P = .002).

Other high-risk criteria associated with significantly lower odds of excellent response included distant metastases (OR, 0.36), incomplete resection (OR, 0.51), and having follicular thyroid carcinoma (FTC) with extensive vascular invasion (OR, 0.27). All these risk factors also were associated with higher odds of persistent disease.

“Recurrence after no evidence of disease occurred in 14%” of the study population, said Dr. van Velsen and his coauthors, adding, “Clinicians should be aware of the relatively high recurrence risk, even after an excellent response to therapy.”

The study aimed to evaluate the 2015 ATA risk stratification system’s prognostic value in a population that included a relatively large proportion of high-risk DTC patients, to include many FTC patients. This work, they noted, augments previous assessments of the risk stratification system in lower-risk populations.

The authors noted that, in addition to predicting disease recurrence, the risk stratification system also worked as a predictor of disease-specific survival. Patients with structural incomplete response fared the worst, with a survival probability below 0.5 at 200 months on a Kaplan-Meier curve of disease-specific survival. Survival probability remained at 1.0 for patients with excellent response after first therapy and was intermediate for those with indeterminate response and biochemical incomplete response.

Overall mortality was higher in FTC patients. Over the study period, 31 of the 76 FTC patients (41%) died, compared with 39 of the PTC patients (24%; P = .010). In all, 28% of the FTC patients and 18% of the PTC patients died of thyroid cancer, but this difference didn’t reach statistical significance.

The retrospective study included adults with DTC meeting the 2015 ATA high-risk criteria who were diagnosed and/or treated at Erasmus Medical Center over a 13-year span ending in December 2015.

Overall, the investigators found 236 patients meeting inclusion criteria; 160 had papillary thyroid cancer (PTC), and the remaining 76 had FTC. The latter group were significantly older at baseline than PTC patients (64 versus 53 years), and were significantly less likely to undergo neck dissection (22% versus 55%).

In the full cohort, 96 patients (41%) had one high-risk factor, and an additional 74 (31%) had two risk factors. The remaining patients had three or more risk factors.

There was no between-group difference in the likelihood of receiving radioactive iodine treatment, but those with FTC had a lower cumulative radiation dose (195 versus 298 mCi; P less than .001).

More than half of patients (58%) had persistent disease after completing their first therapy. Of these, 51% had structural incomplete response and 7% had biochemical incomplete response. The response was indeterminate for about a quarter of the cohort, and the remaining 17% had an excellent initial response.

By the end of the study period, 55% of patients had persistent disease, and 51% had structural incomplete response (a more likely result for those with FTC than PTC). Just 4% had a biochemical incomplete response, and the response was indeterminate for 16%. Response was judged excellent for 29% of patients.

Dr. van Velsen and his coauthors reported that they had no relevant disclosures.

[email protected]

SOURCE: van Velsen EFS et al. ENDO 2019, Abstract MON-549.

A diagnosis of polycystic ovarian syndrome was associated with an increased risk of several cancers, based on an analysis of nearly 3.5 million women in a large Swedish database.

Women with PCOS had a sixfold increased risk of endometrial cancer, a tripling of endocrine gland cancers, and more than a doubling in the risk of ovarian and pancreatic cancers. Once women reached menopausal status, however, their cancer risk was comparable to that of women without a history of PCOS.

“Several carcinogenic processes are associated with PCOS, including dyslipidemia, hyperinsulinemia, and chronic inflammation,” wrote Weimin Ye, MD, PhD, of the Karolinska Institutet, Stockholm, and his colleagues. “Our study indicates that cancer may need to be added to the spectrum of long-term health consequences of PCOS and warrants increased surveillance among those patients.”

The research letter was published online in JAMA Oncology.

The team examined the relationship between PCOS and primary cancers in about 3.5 million women over a span of up to 24 years (1985-2009), although the mean follow-up time was not mentioned. To examine the potential impact of menopause, they conducted separate multivariate logistic regression analyses for those younger than 51 years, and those aged 51 years or older. The analyses controlled for use of some medications (metformin, oral contraceptives, and hormone therapy); as well as educational level (a proxy for socioeconomic status); smoking; parity (a proxy for fertility); parental cancers; and diabetes.

Overall, 14,764 women had been diagnosed with PCOS; they were a mean of 28 years at baseline and 182 developed a primary cancer 1 year or more after PCOS diagnosis.

These women had a 15% overall increased risk of cancer, compared with women without PCOS.

The risks for specific cancers also were increased, compared with women without PCOS, including endometrial (hazard ratio, 2.62), ovarian (HR, 2.16), endocrine (HR, 1.92), pancreatic (HR, 3.4), kidney (HR, 3.0), and skeletal and hematopoietic (HR, 1.69) cancers.

The risks were associated with younger age, however. In the group under age 51 years, the overall risk was 22% higher. The increased risk of specific cancers were endometrial (HR, 6.45), ovarian (HR, 2.55), pancreatic (HR, 6.68), kidney (HR, 4.57), and endocrine (not thyroid) gland (HR, 2.9) cancers.

The authors had no relevant financial disclosures.

[email protected]

SOURCE: Yin W et al. JAMA Oncol. 2018 Nov 29. doi:10.1001/jamaoncol.2018.5188.

A diagnosis of polycystic ovarian syndrome was associated with an increased risk of several cancers, based on an analysis of nearly 3.5 million women in a large Swedish database.

Women with PCOS had a sixfold increased risk of endometrial cancer, a tripling of endocrine gland cancers, and more than a doubling in the risk of ovarian and pancreatic cancers. Once women reached menopausal status, however, their cancer risk was comparable to that of women without a history of PCOS.

“Several carcinogenic processes are associated with PCOS, including dyslipidemia, hyperinsulinemia, and chronic inflammation,” wrote Weimin Ye, MD, PhD, of the Karolinska Institutet, Stockholm, and his colleagues. “Our study indicates that cancer may need to be added to the spectrum of long-term health consequences of PCOS and warrants increased surveillance among those patients.”

The research letter was published online in JAMA Oncology.

The team examined the relationship between PCOS and primary cancers in about 3.5 million women over a span of up to 24 years (1985-2009), although the mean follow-up time was not mentioned. To examine the potential impact of menopause, they conducted separate multivariate logistic regression analyses for those younger than 51 years, and those aged 51 years or older. The analyses controlled for use of some medications (metformin, oral contraceptives, and hormone therapy); as well as educational level (a proxy for socioeconomic status); smoking; parity (a proxy for fertility); parental cancers; and diabetes.

Overall, 14,764 women had been diagnosed with PCOS; they were a mean of 28 years at baseline and 182 developed a primary cancer 1 year or more after PCOS diagnosis.

These women had a 15% overall increased risk of cancer, compared with women without PCOS.

The risks for specific cancers also were increased, compared with women without PCOS, including endometrial (hazard ratio, 2.62), ovarian (HR, 2.16), endocrine (HR, 1.92), pancreatic (HR, 3.4), kidney (HR, 3.0), and skeletal and hematopoietic (HR, 1.69) cancers.

The risks were associated with younger age, however. In the group under age 51 years, the overall risk was 22% higher. The increased risk of specific cancers were endometrial (HR, 6.45), ovarian (HR, 2.55), pancreatic (HR, 6.68), kidney (HR, 4.57), and endocrine (not thyroid) gland (HR, 2.9) cancers.

The authors had no relevant financial disclosures.

[email protected]

SOURCE: Yin W et al. JAMA Oncol. 2018 Nov 29. doi:10.1001/jamaoncol.2018.5188.

A diagnosis of polycystic ovarian syndrome was associated with an increased risk of several cancers, based on an analysis of nearly 3.5 million women in a large Swedish database.

Women with PCOS had a sixfold increased risk of endometrial cancer, a tripling of endocrine gland cancers, and more than a doubling in the risk of ovarian and pancreatic cancers. Once women reached menopausal status, however, their cancer risk was comparable to that of women without a history of PCOS.

“Several carcinogenic processes are associated with PCOS, including dyslipidemia, hyperinsulinemia, and chronic inflammation,” wrote Weimin Ye, MD, PhD, of the Karolinska Institutet, Stockholm, and his colleagues. “Our study indicates that cancer may need to be added to the spectrum of long-term health consequences of PCOS and warrants increased surveillance among those patients.”

The research letter was published online in JAMA Oncology.

The team examined the relationship between PCOS and primary cancers in about 3.5 million women over a span of up to 24 years (1985-2009), although the mean follow-up time was not mentioned. To examine the potential impact of menopause, they conducted separate multivariate logistic regression analyses for those younger than 51 years, and those aged 51 years or older. The analyses controlled for use of some medications (metformin, oral contraceptives, and hormone therapy); as well as educational level (a proxy for socioeconomic status); smoking; parity (a proxy for fertility); parental cancers; and diabetes.

Overall, 14,764 women had been diagnosed with PCOS; they were a mean of 28 years at baseline and 182 developed a primary cancer 1 year or more after PCOS diagnosis.

These women had a 15% overall increased risk of cancer, compared with women without PCOS.

The risks for specific cancers also were increased, compared with women without PCOS, including endometrial (hazard ratio, 2.62), ovarian (HR, 2.16), endocrine (HR, 1.92), pancreatic (HR, 3.4), kidney (HR, 3.0), and skeletal and hematopoietic (HR, 1.69) cancers.

The risks were associated with younger age, however. In the group under age 51 years, the overall risk was 22% higher. The increased risk of specific cancers were endometrial (HR, 6.45), ovarian (HR, 2.55), pancreatic (HR, 6.68), kidney (HR, 4.57), and endocrine (not thyroid) gland (HR, 2.9) cancers.

The authors had no relevant financial disclosures.

[email protected]

SOURCE: Yin W et al. JAMA Oncol. 2018 Nov 29. doi:10.1001/jamaoncol.2018.5188.

Circulating tumor cells could be used to stratify patients with hormone receptor (HR)–positive, HER2-negative breast cancer for late recurrence risk, results of a secondary analysis of a randomized clinical trial suggest.

Risk of late clinical recurrence was about 13-fold higher among HR-positive patients with a positive circulating tumor cell (CTC) assay result, according to results of the study, published in JAMA Oncology.

“This prospectively conducted study offers a high level of evidence supporting the association between a positive CTC assay result and risk of clinical recurrence,” said Joseph A. Sparano, MD, of Albert Einstein College of Medicine, New York, and his coauthors.

The present study is the first to show that this CTC assay may play a role in determining late clinical recurrence after local and systemic adjuvant therapy, according to the investigators. The assay (CellSearch) is cleared by the Food and Drug Administration for enumeration of CTCs in patients with metastatic breast cancer.

The study is a secondary analysis of E5103, a phase 3 trial of adjuvant doxorubicin and cyclophosphamide followed by paclitaxel with bevacizumab in patients with HER2-negative stage II-III breast cancer. Investigators included a total of 547 patients who had no clinical evidence of recurrence between 4.5 and 7.5 years of registration in that trial.

Positive CTC assay results occurred in 26 of those patients (4.8%), they found.

At a median follow-up of 2.6 years, 24 patients had a clinical recurrence, including 23 HR-positive patients and just 1 HR-negative patient. Accordingly, the investigators focused most of their further analysis on the HR-positive subset.

A total of 7 of 23 patients with HR-positive disease (30.4%) had a positive CTC assay result.

A positive CTC result in HR-positive patients was associated with a 13.1-fold increased risk of recurrence, multivariate analysis showed.

Higher CTC burden appeared to be associated with a numerically higher recurrence risk in HR-positive patients, the investigators found. They saw recurrences in 16 of 335 patients with a CTC count of 0 cells per 7.5 mL blood (4.8%), compared with 2 of 12 patients with 1 cell per 7.5 mL blood (16.7%), and 5 of 6 patients with 2 or more cells per 7.5 mL (83.3%).

Taken together, these results provided proof of concept to support additional investigations of the CTC assay and other blood-based biomarker tests in the setting of late clinical recurrence in HR-positive patients, the researchers said.

They acknowledged several limitations of this study: It was small, it had relatively short follow-up, and it did not evaluate the CTC assay in the context of other assays.

“Notwithstanding proof of concept, further evaluation is required to confirm the clinical validity and determine the clinical utility of performing the CTC assay in this context,” Dr. Sparano and his coauthors wrote.

Late recurrences, or those that occur more than 5 years after diagnosis, account for about half of all recurrences among HR-positive receptive breast cancers, Dr. Sparano and his colleagues said.

The researchers had no conflicts of interest to report. The study was supported by grants from the National Cancer Institute, National Institutes of Health, Breast Cancer Research Foundation, and Susan G. Komen Foundation.

SOURCE: Sparano J et al. JAMA Oncol. 2018 Jul 26. doi: 10.1001/jamaoncol.2018.2574.

Circulating tumor cells could be used to stratify patients with hormone receptor (HR)–positive, HER2-negative breast cancer for late recurrence risk, results of a secondary analysis of a randomized clinical trial suggest.

Risk of late clinical recurrence was about 13-fold higher among HR-positive patients with a positive circulating tumor cell (CTC) assay result, according to results of the study, published in JAMA Oncology.

“This prospectively conducted study offers a high level of evidence supporting the association between a positive CTC assay result and risk of clinical recurrence,” said Joseph A. Sparano, MD, of Albert Einstein College of Medicine, New York, and his coauthors.

The present study is the first to show that this CTC assay may play a role in determining late clinical recurrence after local and systemic adjuvant therapy, according to the investigators. The assay (CellSearch) is cleared by the Food and Drug Administration for enumeration of CTCs in patients with metastatic breast cancer.

The study is a secondary analysis of E5103, a phase 3 trial of adjuvant doxorubicin and cyclophosphamide followed by paclitaxel with bevacizumab in patients with HER2-negative stage II-III breast cancer. Investigators included a total of 547 patients who had no clinical evidence of recurrence between 4.5 and 7.5 years of registration in that trial.

Positive CTC assay results occurred in 26 of those patients (4.8%), they found.

At a median follow-up of 2.6 years, 24 patients had a clinical recurrence, including 23 HR-positive patients and just 1 HR-negative patient. Accordingly, the investigators focused most of their further analysis on the HR-positive subset.

A total of 7 of 23 patients with HR-positive disease (30.4%) had a positive CTC assay result.

A positive CTC result in HR-positive patients was associated with a 13.1-fold increased risk of recurrence, multivariate analysis showed.

Higher CTC burden appeared to be associated with a numerically higher recurrence risk in HR-positive patients, the investigators found. They saw recurrences in 16 of 335 patients with a CTC count of 0 cells per 7.5 mL blood (4.8%), compared with 2 of 12 patients with 1 cell per 7.5 mL blood (16.7%), and 5 of 6 patients with 2 or more cells per 7.5 mL (83.3%).

Taken together, these results provided proof of concept to support additional investigations of the CTC assay and other blood-based biomarker tests in the setting of late clinical recurrence in HR-positive patients, the researchers said.

They acknowledged several limitations of this study: It was small, it had relatively short follow-up, and it did not evaluate the CTC assay in the context of other assays.

“Notwithstanding proof of concept, further evaluation is required to confirm the clinical validity and determine the clinical utility of performing the CTC assay in this context,” Dr. Sparano and his coauthors wrote.

Late recurrences, or those that occur more than 5 years after diagnosis, account for about half of all recurrences among HR-positive receptive breast cancers, Dr. Sparano and his colleagues said.

The researchers had no conflicts of interest to report. The study was supported by grants from the National Cancer Institute, National Institutes of Health, Breast Cancer Research Foundation, and Susan G. Komen Foundation.

SOURCE: Sparano J et al. JAMA Oncol. 2018 Jul 26. doi: 10.1001/jamaoncol.2018.2574.

Circulating tumor cells could be used to stratify patients with hormone receptor (HR)–positive, HER2-negative breast cancer for late recurrence risk, results of a secondary analysis of a randomized clinical trial suggest.

Risk of late clinical recurrence was about 13-fold higher among HR-positive patients with a positive circulating tumor cell (CTC) assay result, according to results of the study, published in JAMA Oncology.

“This prospectively conducted study offers a high level of evidence supporting the association between a positive CTC assay result and risk of clinical recurrence,” said Joseph A. Sparano, MD, of Albert Einstein College of Medicine, New York, and his coauthors.

The present study is the first to show that this CTC assay may play a role in determining late clinical recurrence after local and systemic adjuvant therapy, according to the investigators. The assay (CellSearch) is cleared by the Food and Drug Administration for enumeration of CTCs in patients with metastatic breast cancer.

The study is a secondary analysis of E5103, a phase 3 trial of adjuvant doxorubicin and cyclophosphamide followed by paclitaxel with bevacizumab in patients with HER2-negative stage II-III breast cancer. Investigators included a total of 547 patients who had no clinical evidence of recurrence between 4.5 and 7.5 years of registration in that trial.

Positive CTC assay results occurred in 26 of those patients (4.8%), they found.

At a median follow-up of 2.6 years, 24 patients had a clinical recurrence, including 23 HR-positive patients and just 1 HR-negative patient. Accordingly, the investigators focused most of their further analysis on the HR-positive subset.

A total of 7 of 23 patients with HR-positive disease (30.4%) had a positive CTC assay result.

A positive CTC result in HR-positive patients was associated with a 13.1-fold increased risk of recurrence, multivariate analysis showed.

Higher CTC burden appeared to be associated with a numerically higher recurrence risk in HR-positive patients, the investigators found. They saw recurrences in 16 of 335 patients with a CTC count of 0 cells per 7.5 mL blood (4.8%), compared with 2 of 12 patients with 1 cell per 7.5 mL blood (16.7%), and 5 of 6 patients with 2 or more cells per 7.5 mL (83.3%).

Taken together, these results provided proof of concept to support additional investigations of the CTC assay and other blood-based biomarker tests in the setting of late clinical recurrence in HR-positive patients, the researchers said.

They acknowledged several limitations of this study: It was small, it had relatively short follow-up, and it did not evaluate the CTC assay in the context of other assays.

“Notwithstanding proof of concept, further evaluation is required to confirm the clinical validity and determine the clinical utility of performing the CTC assay in this context,” Dr. Sparano and his coauthors wrote.

Late recurrences, or those that occur more than 5 years after diagnosis, account for about half of all recurrences among HR-positive receptive breast cancers, Dr. Sparano and his colleagues said.

The researchers had no conflicts of interest to report. The study was supported by grants from the National Cancer Institute, National Institutes of Health, Breast Cancer Research Foundation, and Susan G. Komen Foundation.

SOURCE: Sparano J et al. JAMA Oncol. 2018 Jul 26. doi: 10.1001/jamaoncol.2018.2574.

WASHINGTON – A majority of U.S. patients with presumed exocrine pancreatic insufficiency are likely going undiagnosed and untreated, and even those who get enzyme replacement therapy often receive too little, according to a recent analysis of insurance claims data from more than 48 million Americans.

Amid concerns that some people with nonspecific symptoms are overdiagnosed with exocrine pancreatic insufficiency (EPI) and hence getting unneeded treatment with pancreatic enzyme replacement therapy (PERT), it seems like substantial numbers of patients with legitimate pancreatic morbidity are often missed and are going untreated, Chris E. Forsmark, MD, said at the annual Digestive Disease Week^®. This includes patients with chronic pancreatitis, pancreatic cancer, and patients who underwent pancreatic resection surgery.

Mitchel L. Zoler/MDedge News

[email protected]

WASHINGTON – A majority of U.S. patients with presumed exocrine pancreatic insufficiency are likely going undiagnosed and untreated, and even those who get enzyme replacement therapy often receive too little, according to a recent analysis of insurance claims data from more than 48 million Americans.

Amid concerns that some people with nonspecific symptoms are overdiagnosed with exocrine pancreatic insufficiency (EPI) and hence getting unneeded treatment with pancreatic enzyme replacement therapy (PERT), it seems like substantial numbers of patients with legitimate pancreatic morbidity are often missed and are going untreated, Chris E. Forsmark, MD, said at the annual Digestive Disease Week^®. This includes patients with chronic pancreatitis, pancreatic cancer, and patients who underwent pancreatic resection surgery.

Mitchel L. Zoler/MDedge News

[email protected]

WASHINGTON – A majority of U.S. patients with presumed exocrine pancreatic insufficiency are likely going undiagnosed and untreated, and even those who get enzyme replacement therapy often receive too little, according to a recent analysis of insurance claims data from more than 48 million Americans.

Amid concerns that some people with nonspecific symptoms are overdiagnosed with exocrine pancreatic insufficiency (EPI) and hence getting unneeded treatment with pancreatic enzyme replacement therapy (PERT), it seems like substantial numbers of patients with legitimate pancreatic morbidity are often missed and are going untreated, Chris E. Forsmark, MD, said at the annual Digestive Disease Week^®. This includes patients with chronic pancreatitis, pancreatic cancer, and patients who underwent pancreatic resection surgery.

Mitchel L. Zoler/MDedge News

[email protected]

WASHINGTON – Patients with pancreatic cancer have a particular form of endocrine pancreatopathy distinct from that of type 2 diabetes mellitus (T2DM), with increased islet size but normal insulin to glucagon ratios and lower levels of islet amyloid.

“The endocrinopathies associated with type 2 diabetes mellitus and pancreatic cancer are distinct, the former represented by an increase in glucagon and the latter characterized by a reduction in islet size,” said Sajan Nagpal, MD, of the Mayo Clinic in Rochester, Minn., at Digestive Disease Week 2018^®. “These data lend insight to a unique pathophysiology of diabetes that results from pancreatic cancer.”

Prior to presenting his results, Dr. Nagpal pointed out an interesting relationship between pancreatic cancer and diabetes.

“Pancreatic cancer and diabetes have a very unique, two-way relationship. While long-standing diabetes [LSDM] increases the risk of developing pancreatic cancer by 1.5-2 times over a person’s lifetime, pancreatic cancer itself causes a paraneoplastic form of diabetes. A person with a new diagnosis of diabetes mellitus has a five to eight times increased risk of being diagnosed with pancreatic cancer as compared to the general population within 3 years.“

This form of diabetes is referred to as pancreatic cancer–induced new onset diabetes (PC-NOD).

Dr. Nagpal and his team conducted a study that included 46 patients: 16 patients with pancreatic cancer (5 with LSDM, 5 NOD, and 6 without diabetes mellitus), 15 patients with T2DM (9 LSDM, 6 NOD), and 15 controls matched for age and body mass index. NOD was defined as a diabetes mellitus diagnosis less than 3 years from the date of autopsy or pancreatic cancer diagnosis. All pancreatic specimens were resected from pancreatic cancer patients or obtained as autopsy specimens. Researchers performed islet morphometric studies utilizing immunofluorescence analysis with specific insulin and glucagon antibodies.

The results of the study showed that patients with pancreatic cancer had islet sizes that were about a third smaller than those in the patients with T2DM and the healthy controls (P = .005). This held true for both LSDM and NOD pancreatic cancer patients, compared with the T2DM and healthy control groups. Researchers also found that insulin to glucagon (I:G) ratios were preserved in pancreatic cancer patients, whereas they were lower in patients with T2DM because of a higher percentage of glucagon in the islets (P = .08). Additionally, islet amyloid was much higher in T2DM patients (66.7%) versus patients with diabetes associated with pancreatic cancer (55.6%) and healthy controls (13.3%; P = .01).

There were several limitations to this study, including the small number of patients in each group and how pancreatic islet characteristics can vary based on their location. Finally, ductal obstruction can cause changes to islet morphology.

Along with the pathological changes found by Dr. Nagpal and his research team, PC-NOD and T2DM also have unique clinical profiles. As patients with pancreatic cancer approach their diagnosis, they begin to lose weight. This begins about 1 year before the patient’s diagnosis of pancreatic cancer. Conversely, these patients have worsening fasting glucose levels despite the fact that they are losing weight. The paradoxical relationship between weight loss and hyperglycemia are what distinguishes PC-NOD from T2DM, according to Dr. Nagpal. In patients with PC-NOD, worsening hyperglycemia happens over a periods of months, compared with the gradual increase over the course of years seen in T2DM.

The differences between these diseases may be caused by differences in their pancreatopathy.

When discussing the pancreatopathy associated with T2DM, Dr. Nagpal pointed out that there is a decrease in the I:G ratio, compared with those seen in patients without diabetes. The prevailing theory is that this decrease in the I:G ratio is caused by beta-cell apoptosis and transdifferentiation to alpha-cells. T2DM patients also have increased amyloid deposits, the result of increased islet amyloid polypeptide.

”Pancreatic cancer provides subtle metabolic clues, such as worsening glucose tolerance and weight loss, that can serve as potential targets for its early detection.”

According to Dr. Nagpal, more research is needed on pathogenesis of PC-NOD. Identification of biomarkers for screening may be possible in patients with new onset diabetes.

Dr. Nagpal had no financial conflicts of interest to report.

[email protected]

SOURCE: Nagpal S et al. DDW 2018, Abstract 392.

WASHINGTON – Patients with pancreatic cancer have a particular form of endocrine pancreatopathy distinct from that of type 2 diabetes mellitus (T2DM), with increased islet size but normal insulin to glucagon ratios and lower levels of islet amyloid.

“The endocrinopathies associated with type 2 diabetes mellitus and pancreatic cancer are distinct, the former represented by an increase in glucagon and the latter characterized by a reduction in islet size,” said Sajan Nagpal, MD, of the Mayo Clinic in Rochester, Minn., at Digestive Disease Week 2018^®. “These data lend insight to a unique pathophysiology of diabetes that results from pancreatic cancer.”

Prior to presenting his results, Dr. Nagpal pointed out an interesting relationship between pancreatic cancer and diabetes.

“Pancreatic cancer and diabetes have a very unique, two-way relationship. While long-standing diabetes [LSDM] increases the risk of developing pancreatic cancer by 1.5-2 times over a person’s lifetime, pancreatic cancer itself causes a paraneoplastic form of diabetes. A person with a new diagnosis of diabetes mellitus has a five to eight times increased risk of being diagnosed with pancreatic cancer as compared to the general population within 3 years.“

This form of diabetes is referred to as pancreatic cancer–induced new onset diabetes (PC-NOD).

Dr. Nagpal and his team conducted a study that included 46 patients: 16 patients with pancreatic cancer (5 with LSDM, 5 NOD, and 6 without diabetes mellitus), 15 patients with T2DM (9 LSDM, 6 NOD), and 15 controls matched for age and body mass index. NOD was defined as a diabetes mellitus diagnosis less than 3 years from the date of autopsy or pancreatic cancer diagnosis. All pancreatic specimens were resected from pancreatic cancer patients or obtained as autopsy specimens. Researchers performed islet morphometric studies utilizing immunofluorescence analysis with specific insulin and glucagon antibodies.

The results of the study showed that patients with pancreatic cancer had islet sizes that were about a third smaller than those in the patients with T2DM and the healthy controls (P = .005). This held true for both LSDM and NOD pancreatic cancer patients, compared with the T2DM and healthy control groups. Researchers also found that insulin to glucagon (I:G) ratios were preserved in pancreatic cancer patients, whereas they were lower in patients with T2DM because of a higher percentage of glucagon in the islets (P = .08). Additionally, islet amyloid was much higher in T2DM patients (66.7%) versus patients with diabetes associated with pancreatic cancer (55.6%) and healthy controls (13.3%; P = .01).

There were several limitations to this study, including the small number of patients in each group and how pancreatic islet characteristics can vary based on their location. Finally, ductal obstruction can cause changes to islet morphology.

Along with the pathological changes found by Dr. Nagpal and his research team, PC-NOD and T2DM also have unique clinical profiles. As patients with pancreatic cancer approach their diagnosis, they begin to lose weight. This begins about 1 year before the patient’s diagnosis of pancreatic cancer. Conversely, these patients have worsening fasting glucose levels despite the fact that they are losing weight. The paradoxical relationship between weight loss and hyperglycemia are what distinguishes PC-NOD from T2DM, according to Dr. Nagpal. In patients with PC-NOD, worsening hyperglycemia happens over a periods of months, compared with the gradual increase over the course of years seen in T2DM.

The differences between these diseases may be caused by differences in their pancreatopathy.

When discussing the pancreatopathy associated with T2DM, Dr. Nagpal pointed out that there is a decrease in the I:G ratio, compared with those seen in patients without diabetes. The prevailing theory is that this decrease in the I:G ratio is caused by beta-cell apoptosis and transdifferentiation to alpha-cells. T2DM patients also have increased amyloid deposits, the result of increased islet amyloid polypeptide.

”Pancreatic cancer provides subtle metabolic clues, such as worsening glucose tolerance and weight loss, that can serve as potential targets for its early detection.”

According to Dr. Nagpal, more research is needed on pathogenesis of PC-NOD. Identification of biomarkers for screening may be possible in patients with new onset diabetes.

Dr. Nagpal had no financial conflicts of interest to report.

[email protected]

SOURCE: Nagpal S et al. DDW 2018, Abstract 392.

WASHINGTON – Patients with pancreatic cancer have a particular form of endocrine pancreatopathy distinct from that of type 2 diabetes mellitus (T2DM), with increased islet size but normal insulin to glucagon ratios and lower levels of islet amyloid.

“The endocrinopathies associated with type 2 diabetes mellitus and pancreatic cancer are distinct, the former represented by an increase in glucagon and the latter characterized by a reduction in islet size,” said Sajan Nagpal, MD, of the Mayo Clinic in Rochester, Minn., at Digestive Disease Week 2018^®. “These data lend insight to a unique pathophysiology of diabetes that results from pancreatic cancer.”

Prior to presenting his results, Dr. Nagpal pointed out an interesting relationship between pancreatic cancer and diabetes.

“Pancreatic cancer and diabetes have a very unique, two-way relationship. While long-standing diabetes [LSDM] increases the risk of developing pancreatic cancer by 1.5-2 times over a person’s lifetime, pancreatic cancer itself causes a paraneoplastic form of diabetes. A person with a new diagnosis of diabetes mellitus has a five to eight times increased risk of being diagnosed with pancreatic cancer as compared to the general population within 3 years.“

This form of diabetes is referred to as pancreatic cancer–induced new onset diabetes (PC-NOD).

Dr. Nagpal and his team conducted a study that included 46 patients: 16 patients with pancreatic cancer (5 with LSDM, 5 NOD, and 6 without diabetes mellitus), 15 patients with T2DM (9 LSDM, 6 NOD), and 15 controls matched for age and body mass index. NOD was defined as a diabetes mellitus diagnosis less than 3 years from the date of autopsy or pancreatic cancer diagnosis. All pancreatic specimens were resected from pancreatic cancer patients or obtained as autopsy specimens. Researchers performed islet morphometric studies utilizing immunofluorescence analysis with specific insulin and glucagon antibodies.

The results of the study showed that patients with pancreatic cancer had islet sizes that were about a third smaller than those in the patients with T2DM and the healthy controls (P = .005). This held true for both LSDM and NOD pancreatic cancer patients, compared with the T2DM and healthy control groups. Researchers also found that insulin to glucagon (I:G) ratios were preserved in pancreatic cancer patients, whereas they were lower in patients with T2DM because of a higher percentage of glucagon in the islets (P = .08). Additionally, islet amyloid was much higher in T2DM patients (66.7%) versus patients with diabetes associated with pancreatic cancer (55.6%) and healthy controls (13.3%; P = .01).

There were several limitations to this study, including the small number of patients in each group and how pancreatic islet characteristics can vary based on their location. Finally, ductal obstruction can cause changes to islet morphology.

Along with the pathological changes found by Dr. Nagpal and his research team, PC-NOD and T2DM also have unique clinical profiles. As patients with pancreatic cancer approach their diagnosis, they begin to lose weight. This begins about 1 year before the patient’s diagnosis of pancreatic cancer. Conversely, these patients have worsening fasting glucose levels despite the fact that they are losing weight. The paradoxical relationship between weight loss and hyperglycemia are what distinguishes PC-NOD from T2DM, according to Dr. Nagpal. In patients with PC-NOD, worsening hyperglycemia happens over a periods of months, compared with the gradual increase over the course of years seen in T2DM.

The differences between these diseases may be caused by differences in their pancreatopathy.

When discussing the pancreatopathy associated with T2DM, Dr. Nagpal pointed out that there is a decrease in the I:G ratio, compared with those seen in patients without diabetes. The prevailing theory is that this decrease in the I:G ratio is caused by beta-cell apoptosis and transdifferentiation to alpha-cells. T2DM patients also have increased amyloid deposits, the result of increased islet amyloid polypeptide.

”Pancreatic cancer provides subtle metabolic clues, such as worsening glucose tolerance and weight loss, that can serve as potential targets for its early detection.”

According to Dr. Nagpal, more research is needed on pathogenesis of PC-NOD. Identification of biomarkers for screening may be possible in patients with new onset diabetes.

Dr. Nagpal had no financial conflicts of interest to report.

[email protected]

SOURCE: Nagpal S et al. DDW 2018, Abstract 392.

CHICAGO – Cancer patients don’t necessarily have to come off immune checkpoint inhibitors if they develop diabetes, according to Priyanka Iyer, MD, an endocrinology fellow at MD Anderson Cancer Center, Houston.

“As long as we get glycemic control, they can continue,” she said at the annual meeting of the Endocrine Society.

Diabetes is a known side effect of immune checkpoint inhibitors (ICIs) but it’s rare, occurring in maybe 0.17% of patients, and its natural history and risk factors are unknown.

Median time to diabetes presentation after the start of ICI treatment was 12.3 weeks but ranged from 1 to 67.2 weeks. Half of the cases presented in diabetic ketoacidosis (DKA). Patients had upward trending hyperglycemia and most had diabetes symptoms for a while before diagnosis. They presented with a blood glucose above 250 mg/dL, and more than half above 500 mg/dL. Median hemoglobin A_1c at presentation was 8%, but ranged up to 12.5%.

Every patient required insulin, including the six that discontinued ICIs after developing diabetes. Diabetes resolved in just one patient at 10.2 months; she presented with DKA.

There were no obvious predisposing factors. None of the patients had histories of type 1 diabetes or other autoimmune disease. Five patients had well-controlled type 2 diabetes prior to ICI initiation; four had prediabetes. Some had family members with type 2 diabetes, but not type 1. Four had prior ICI exposure. Just three patients were on concomitant steroids.

A few patients also developed thyroid or pituitary dysfunction, which are more common side effects of ICIs.

The median age at diabetes presentation was 61 years and ranged from 32 to 82 years. The majority of patients were men, which reflects MD Anderson demographics, not a predisposing risk factor, Dr. Iyer said.

Melanoma was the most common cancer, followed by renal cell and prostate; patients had stage 2-4 disease. About half the subjects were on single agent anti-PD-1 treatment, about a third on anti-PD-1 combination treatment, and the rest on anti-PD-L1 combination therapy. C-peptide levels were below 0.9 ng/mL at diabetes diagnosis in most of the patients. Eleven of the 20 tested (55%) were positive for the pancreatic islet cell antibody GAD65.

The investigators had no disclosures. A funding source was not reported.

[email protected]

SOURCE: Iyer PC et al. Abstract OR05-5.

CHICAGO – Cancer patients don’t necessarily have to come off immune checkpoint inhibitors if they develop diabetes, according to Priyanka Iyer, MD, an endocrinology fellow at MD Anderson Cancer Center, Houston.

“As long as we get glycemic control, they can continue,” she said at the annual meeting of the Endocrine Society.

Diabetes is a known side effect of immune checkpoint inhibitors (ICIs) but it’s rare, occurring in maybe 0.17% of patients, and its natural history and risk factors are unknown.

Median time to diabetes presentation after the start of ICI treatment was 12.3 weeks but ranged from 1 to 67.2 weeks. Half of the cases presented in diabetic ketoacidosis (DKA). Patients had upward trending hyperglycemia and most had diabetes symptoms for a while before diagnosis. They presented with a blood glucose above 250 mg/dL, and more than half above 500 mg/dL. Median hemoglobin A_1c at presentation was 8%, but ranged up to 12.5%.

Every patient required insulin, including the six that discontinued ICIs after developing diabetes. Diabetes resolved in just one patient at 10.2 months; she presented with DKA.

There were no obvious predisposing factors. None of the patients had histories of type 1 diabetes or other autoimmune disease. Five patients had well-controlled type 2 diabetes prior to ICI initiation; four had prediabetes. Some had family members with type 2 diabetes, but not type 1. Four had prior ICI exposure. Just three patients were on concomitant steroids.

A few patients also developed thyroid or pituitary dysfunction, which are more common side effects of ICIs.

The median age at diabetes presentation was 61 years and ranged from 32 to 82 years. The majority of patients were men, which reflects MD Anderson demographics, not a predisposing risk factor, Dr. Iyer said.

Melanoma was the most common cancer, followed by renal cell and prostate; patients had stage 2-4 disease. About half the subjects were on single agent anti-PD-1 treatment, about a third on anti-PD-1 combination treatment, and the rest on anti-PD-L1 combination therapy. C-peptide levels were below 0.9 ng/mL at diabetes diagnosis in most of the patients. Eleven of the 20 tested (55%) were positive for the pancreatic islet cell antibody GAD65.

The investigators had no disclosures. A funding source was not reported.

[email protected]

SOURCE: Iyer PC et al. Abstract OR05-5.

CHICAGO – Cancer patients don’t necessarily have to come off immune checkpoint inhibitors if they develop diabetes, according to Priyanka Iyer, MD, an endocrinology fellow at MD Anderson Cancer Center, Houston.

“As long as we get glycemic control, they can continue,” she said at the annual meeting of the Endocrine Society.

Diabetes is a known side effect of immune checkpoint inhibitors (ICIs) but it’s rare, occurring in maybe 0.17% of patients, and its natural history and risk factors are unknown.

Median time to diabetes presentation after the start of ICI treatment was 12.3 weeks but ranged from 1 to 67.2 weeks. Half of the cases presented in diabetic ketoacidosis (DKA). Patients had upward trending hyperglycemia and most had diabetes symptoms for a while before diagnosis. They presented with a blood glucose above 250 mg/dL, and more than half above 500 mg/dL. Median hemoglobin A_1c at presentation was 8%, but ranged up to 12.5%.

Every patient required insulin, including the six that discontinued ICIs after developing diabetes. Diabetes resolved in just one patient at 10.2 months; she presented with DKA.

There were no obvious predisposing factors. None of the patients had histories of type 1 diabetes or other autoimmune disease. Five patients had well-controlled type 2 diabetes prior to ICI initiation; four had prediabetes. Some had family members with type 2 diabetes, but not type 1. Four had prior ICI exposure. Just three patients were on concomitant steroids.

A few patients also developed thyroid or pituitary dysfunction, which are more common side effects of ICIs.

The median age at diabetes presentation was 61 years and ranged from 32 to 82 years. The majority of patients were men, which reflects MD Anderson demographics, not a predisposing risk factor, Dr. Iyer said.

Melanoma was the most common cancer, followed by renal cell and prostate; patients had stage 2-4 disease. About half the subjects were on single agent anti-PD-1 treatment, about a third on anti-PD-1 combination treatment, and the rest on anti-PD-L1 combination therapy. C-peptide levels were below 0.9 ng/mL at diabetes diagnosis in most of the patients. Eleven of the 20 tested (55%) were positive for the pancreatic islet cell antibody GAD65.

The investigators had no disclosures. A funding source was not reported.

[email protected]

SOURCE: Iyer PC et al. Abstract OR05-5.

VICTORIA, B.C. – Several new and improved molecular classifiers show good performance for preoperatively assessing the nature of thyroid nodules, including histologic subsets that continue to pose diagnostic challenges, according to a trio of studies reported at the annual meeting of the American Thyroid Association.

ThyroSeq v3 classifier

In a prospective, blinded, multi-institutional study, investigators validated the ThyroSeq v3 genomic classifier, which uses next-generation sequencing to test for mutations, fusions, gene expression alterations, and copy number variations in 112 genes.

The validation cohort consisted of 234 patients from 10 centers who had thyroid nodules with Bethesda III to V cytology and known surgical outcome, with central pathology review, and successful molecular testing. In total, they had 257 fine needle aspiration samples.

Of the 247 samples from nodules having Bethesda III or IV cytology – those of greatest interest – 28% were cancer or noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP), reported senior author Yuri Nikiforov, MD, PhD, professor of pathology and director of the division of molecular & genomic pathology at the University of Pittsburgh Medical Center. “Both cancer and NIFTP are surgical diseases, so we felt they belong in one group,” he noted.

Afirma GSC with Hurthle classifiers

In a second study, investigators led by Quan-Yang Duh, MD, professor of surgery, division of general surgery, and chief, section of endocrine surgery, University of California, San Francisco, developed and validated a pair of classifiers to enhance performance of the Afirma platform among Hurthle cell specimens.

“The Hurthle cell lesions tend to give us trouble,” Dr. Duh said. On molecular analysis, those that are malignant seldom harbor mutations that would aid diagnosis, whereas those that are benign are usually classified as suspicious by the original Afirma Gene Expression Classifier (GEC).

“The specific group that is causing trouble are those that are Hurthle cell but not neoplasm, because they are the ones that give you the false positives,” Dr. Duh said. Therefore, it makes sense to stratify lesions on both of these factors, and then subject that specific subset to a more stringent threshold.

Afirma GSC with medullary thyroid cancer classifier

In a third study, investigators developed and validated a classifier for medullary thyroid cancer to be used with the Afirma GSC. They were led by Gregory Randolph, MD, professor of otolaryngology and the Claire and John Bertucci Endowed Chair in Thyroid Surgical Oncology at Harvard Medical School, and division chief of the general and thyroid/parathyroid endocrine surgical divisions at the Massachusetts Eye and Ear Infirmary, Boston.

Better preoperative identification of this cancer is key for several reasons, he maintained.

VICTORIA, B.C. – Several new and improved molecular classifiers show good performance for preoperatively assessing the nature of thyroid nodules, including histologic subsets that continue to pose diagnostic challenges, according to a trio of studies reported at the annual meeting of the American Thyroid Association.

ThyroSeq v3 classifier

In a prospective, blinded, multi-institutional study, investigators validated the ThyroSeq v3 genomic classifier, which uses next-generation sequencing to test for mutations, fusions, gene expression alterations, and copy number variations in 112 genes.

The validation cohort consisted of 234 patients from 10 centers who had thyroid nodules with Bethesda III to V cytology and known surgical outcome, with central pathology review, and successful molecular testing. In total, they had 257 fine needle aspiration samples.

Of the 247 samples from nodules having Bethesda III or IV cytology – those of greatest interest – 28% were cancer or noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP), reported senior author Yuri Nikiforov, MD, PhD, professor of pathology and director of the division of molecular & genomic pathology at the University of Pittsburgh Medical Center. “Both cancer and NIFTP are surgical diseases, so we felt they belong in one group,” he noted.

Afirma GSC with Hurthle classifiers

In a second study, investigators led by Quan-Yang Duh, MD, professor of surgery, division of general surgery, and chief, section of endocrine surgery, University of California, San Francisco, developed and validated a pair of classifiers to enhance performance of the Afirma platform among Hurthle cell specimens.

“The Hurthle cell lesions tend to give us trouble,” Dr. Duh said. On molecular analysis, those that are malignant seldom harbor mutations that would aid diagnosis, whereas those that are benign are usually classified as suspicious by the original Afirma Gene Expression Classifier (GEC).

“The specific group that is causing trouble are those that are Hurthle cell but not neoplasm, because they are the ones that give you the false positives,” Dr. Duh said. Therefore, it makes sense to stratify lesions on both of these factors, and then subject that specific subset to a more stringent threshold.

Afirma GSC with medullary thyroid cancer classifier

In a third study, investigators developed and validated a classifier for medullary thyroid cancer to be used with the Afirma GSC. They were led by Gregory Randolph, MD, professor of otolaryngology and the Claire and John Bertucci Endowed Chair in Thyroid Surgical Oncology at Harvard Medical School, and division chief of the general and thyroid/parathyroid endocrine surgical divisions at the Massachusetts Eye and Ear Infirmary, Boston.

Better preoperative identification of this cancer is key for several reasons, he maintained.

VICTORIA, B.C. – Several new and improved molecular classifiers show good performance for preoperatively assessing the nature of thyroid nodules, including histologic subsets that continue to pose diagnostic challenges, according to a trio of studies reported at the annual meeting of the American Thyroid Association.

ThyroSeq v3 classifier

In a prospective, blinded, multi-institutional study, investigators validated the ThyroSeq v3 genomic classifier, which uses next-generation sequencing to test for mutations, fusions, gene expression alterations, and copy number variations in 112 genes.

The validation cohort consisted of 234 patients from 10 centers who had thyroid nodules with Bethesda III to V cytology and known surgical outcome, with central pathology review, and successful molecular testing. In total, they had 257 fine needle aspiration samples.

Of the 247 samples from nodules having Bethesda III or IV cytology – those of greatest interest – 28% were cancer or noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP), reported senior author Yuri Nikiforov, MD, PhD, professor of pathology and director of the division of molecular & genomic pathology at the University of Pittsburgh Medical Center. “Both cancer and NIFTP are surgical diseases, so we felt they belong in one group,” he noted.

Afirma GSC with Hurthle classifiers

In a second study, investigators led by Quan-Yang Duh, MD, professor of surgery, division of general surgery, and chief, section of endocrine surgery, University of California, San Francisco, developed and validated a pair of classifiers to enhance performance of the Afirma platform among Hurthle cell specimens.

“The Hurthle cell lesions tend to give us trouble,” Dr. Duh said. On molecular analysis, those that are malignant seldom harbor mutations that would aid diagnosis, whereas those that are benign are usually classified as suspicious by the original Afirma Gene Expression Classifier (GEC).

“The specific group that is causing trouble are those that are Hurthle cell but not neoplasm, because they are the ones that give you the false positives,” Dr. Duh said. Therefore, it makes sense to stratify lesions on both of these factors, and then subject that specific subset to a more stringent threshold.

Afirma GSC with medullary thyroid cancer classifier

In a third study, investigators developed and validated a classifier for medullary thyroid cancer to be used with the Afirma GSC. They were led by Gregory Randolph, MD, professor of otolaryngology and the Claire and John Bertucci Endowed Chair in Thyroid Surgical Oncology at Harvard Medical School, and division chief of the general and thyroid/parathyroid endocrine surgical divisions at the Massachusetts Eye and Ear Infirmary, Boston.

Better preoperative identification of this cancer is key for several reasons, he maintained.

VICTORIA, B.C. – When it comes to the adverse effects of tyrosine kinase inhibitors (TKIs), hypothyroidism appears to have a bright side, according to a retrospective cohort study among patients with nonthyroid cancers.

While taking one of these targeted agents, roughly a quarter of patients became overtly hypothyroid, an adverse effect that appears to be due in part to immune destruction. Risk was higher for women and earlier in therapy.

Relative to counterparts who remained euthyroid, overtly hypothyroid patients were 44% less likely to die after other factors were taken into account.

Susan London, Frontline Medical News

VICTORIA, B.C. – When it comes to the adverse effects of tyrosine kinase inhibitors (TKIs), hypothyroidism appears to have a bright side, according to a retrospective cohort study among patients with nonthyroid cancers.

While taking one of these targeted agents, roughly a quarter of patients became overtly hypothyroid, an adverse effect that appears to be due in part to immune destruction. Risk was higher for women and earlier in therapy.

Relative to counterparts who remained euthyroid, overtly hypothyroid patients were 44% less likely to die after other factors were taken into account.

Susan London, Frontline Medical News

VICTORIA, B.C. – When it comes to the adverse effects of tyrosine kinase inhibitors (TKIs), hypothyroidism appears to have a bright side, according to a retrospective cohort study among patients with nonthyroid cancers.

While taking one of these targeted agents, roughly a quarter of patients became overtly hypothyroid, an adverse effect that appears to be due in part to immune destruction. Risk was higher for women and earlier in therapy.

Relative to counterparts who remained euthyroid, overtly hypothyroid patients were 44% less likely to die after other factors were taken into account.

Susan London, Frontline Medical News