User login
Watch the inaugural Gastro Journal Club
We are delighted to introduce the Gastro Journal Club in which an author of a study published in Gastroenterology will present their paper followed by a Q&A. The inaugural Gastro Journal Club features Loren Laine, MD, professor of medicine (digestive diseases) at Yale University, New Haven, Conn., and was hosted by the McMaster University gastroenterology division. Dr. Laine presented his article “Vonoprazan Versus Lansoprazole for Healing and Maintenance of Healing of Erosive Esophagitis: A Randomized Trial,” published in the January 2023 issue of Gastroenterology.
If you are interested in participating, please contact [email protected].
Watch the inaugural Gastro Journal Club: https://rb.gy/j8mqm
We are delighted to introduce the Gastro Journal Club in which an author of a study published in Gastroenterology will present their paper followed by a Q&A. The inaugural Gastro Journal Club features Loren Laine, MD, professor of medicine (digestive diseases) at Yale University, New Haven, Conn., and was hosted by the McMaster University gastroenterology division. Dr. Laine presented his article “Vonoprazan Versus Lansoprazole for Healing and Maintenance of Healing of Erosive Esophagitis: A Randomized Trial,” published in the January 2023 issue of Gastroenterology.
If you are interested in participating, please contact [email protected].
Watch the inaugural Gastro Journal Club: https://rb.gy/j8mqm
We are delighted to introduce the Gastro Journal Club in which an author of a study published in Gastroenterology will present their paper followed by a Q&A. The inaugural Gastro Journal Club features Loren Laine, MD, professor of medicine (digestive diseases) at Yale University, New Haven, Conn., and was hosted by the McMaster University gastroenterology division. Dr. Laine presented his article “Vonoprazan Versus Lansoprazole for Healing and Maintenance of Healing of Erosive Esophagitis: A Randomized Trial,” published in the January 2023 issue of Gastroenterology.
If you are interested in participating, please contact [email protected].
Watch the inaugural Gastro Journal Club: https://rb.gy/j8mqm
Painful fingertip tumor in pregnancy
This friable vascular papule was most consistent with a lobular capillary hemangioma (LCH), also called a pyogenic granuloma. A shave biopsy was performed at the base of the tumor to confirm the diagnosis and rule out malignant pedunculated tumors, including nodular melanoma, angiosarcoma, and metastatic carcinoma.
LCHs are benign vascular growths that occur on the skin and mucosa, most often in children and young adults. Growth may occur rapidly over days to weeks and tumors may grow to several centimeters in size. Although LCHs are often painless, they do tend to bleed easily with minor trauma.
While the triggering mechanism is unknown, LCHs have been associated with infection, trauma, hormonal factors (especially in the second and third trimesters of pregnancy), and therapy with retinoids. About 5% of pregnancies are associated with the development of an LCH on the oral mucosa, usually in the second or third trimester.1
Treatment of LCHs is based on small case series and case reports. Individual tumors have a high likelihood of recurrence after a single treatment, so multiple visits for treatment are often recommended. Electrocautery is safe and effective with complete cure occurring after 2 sessions. Similarly, cryotherapy is safe and effective with excellent results after 3 treatment sessions. Cryotherapy may cause depigmentation in patients with darker skin types, so this should be discussed with patients with skin of color. Excision of small lesions is also safe and effective in a single session.2
This patient was treated with light electrodessication and curettage in 2 sessions with complete clearance.
Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.
1. Demir Y, Demir S, Aktepe F. Cutaneous lobular capillary hemangioma induced by pregnancy. J Cutan Pathol. 2004;31:77-80. doi: 10.1046/j.0303-6987.2004.0137.x
2. Lee J, Sinno H, Tahiri Y, et al. Treatment options for cutaneous pyogenic granulomas: a review. J Plast Reconstr Aesthet Surg. 2011;64:1216-1220. doi: 10.1016/j.bjps.2010.12.021
This friable vascular papule was most consistent with a lobular capillary hemangioma (LCH), also called a pyogenic granuloma. A shave biopsy was performed at the base of the tumor to confirm the diagnosis and rule out malignant pedunculated tumors, including nodular melanoma, angiosarcoma, and metastatic carcinoma.
LCHs are benign vascular growths that occur on the skin and mucosa, most often in children and young adults. Growth may occur rapidly over days to weeks and tumors may grow to several centimeters in size. Although LCHs are often painless, they do tend to bleed easily with minor trauma.
While the triggering mechanism is unknown, LCHs have been associated with infection, trauma, hormonal factors (especially in the second and third trimesters of pregnancy), and therapy with retinoids. About 5% of pregnancies are associated with the development of an LCH on the oral mucosa, usually in the second or third trimester.1
Treatment of LCHs is based on small case series and case reports. Individual tumors have a high likelihood of recurrence after a single treatment, so multiple visits for treatment are often recommended. Electrocautery is safe and effective with complete cure occurring after 2 sessions. Similarly, cryotherapy is safe and effective with excellent results after 3 treatment sessions. Cryotherapy may cause depigmentation in patients with darker skin types, so this should be discussed with patients with skin of color. Excision of small lesions is also safe and effective in a single session.2
This patient was treated with light electrodessication and curettage in 2 sessions with complete clearance.
Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.
This friable vascular papule was most consistent with a lobular capillary hemangioma (LCH), also called a pyogenic granuloma. A shave biopsy was performed at the base of the tumor to confirm the diagnosis and rule out malignant pedunculated tumors, including nodular melanoma, angiosarcoma, and metastatic carcinoma.
LCHs are benign vascular growths that occur on the skin and mucosa, most often in children and young adults. Growth may occur rapidly over days to weeks and tumors may grow to several centimeters in size. Although LCHs are often painless, they do tend to bleed easily with minor trauma.
While the triggering mechanism is unknown, LCHs have been associated with infection, trauma, hormonal factors (especially in the second and third trimesters of pregnancy), and therapy with retinoids. About 5% of pregnancies are associated with the development of an LCH on the oral mucosa, usually in the second or third trimester.1
Treatment of LCHs is based on small case series and case reports. Individual tumors have a high likelihood of recurrence after a single treatment, so multiple visits for treatment are often recommended. Electrocautery is safe and effective with complete cure occurring after 2 sessions. Similarly, cryotherapy is safe and effective with excellent results after 3 treatment sessions. Cryotherapy may cause depigmentation in patients with darker skin types, so this should be discussed with patients with skin of color. Excision of small lesions is also safe and effective in a single session.2
This patient was treated with light electrodessication and curettage in 2 sessions with complete clearance.
Photos and text for Photo Rounds Friday courtesy of Jonathan Karnes, MD (copyright retained). Dr. Karnes is the medical director of MDFMR Dermatology Services, Augusta, ME.
1. Demir Y, Demir S, Aktepe F. Cutaneous lobular capillary hemangioma induced by pregnancy. J Cutan Pathol. 2004;31:77-80. doi: 10.1046/j.0303-6987.2004.0137.x
2. Lee J, Sinno H, Tahiri Y, et al. Treatment options for cutaneous pyogenic granulomas: a review. J Plast Reconstr Aesthet Surg. 2011;64:1216-1220. doi: 10.1016/j.bjps.2010.12.021
1. Demir Y, Demir S, Aktepe F. Cutaneous lobular capillary hemangioma induced by pregnancy. J Cutan Pathol. 2004;31:77-80. doi: 10.1046/j.0303-6987.2004.0137.x
2. Lee J, Sinno H, Tahiri Y, et al. Treatment options for cutaneous pyogenic granulomas: a review. J Plast Reconstr Aesthet Surg. 2011;64:1216-1220. doi: 10.1016/j.bjps.2010.12.021
Minimally invasive surfactant shows some benefit in infants’ first 2 years
Results of the OPTIMIST follow-up study were published online in JAMA.
Researchers, led by Peter A. Dargaville, MD, department of paediatrics, Royal Hobart (Australia) Hospital, found that MIST, which involves administering surfactant via a thin catheter, compared with sham treatment, did not reduce the incidence of death or neurodevelopmental disability (NDD) by 2 years of age.
However, infants who received MIST had lower rates of poor respiratory outcomes during those first 2 years of life.
Study spanned 11 countries
The study was conducted in 33 tertiary neonatal intensive care units (NICUs) in 11 countries, including Australia, Canada, Israel, New Zealand, Qatar, Singapore, Slovenia, the Netherlands, Turkey, the United Kingdom, and the United States.
It included 486 infants 25-28 weeks old supported with CPAP; 453 had follow-up data available and data on the key secondary outcome were available for 434 infants.
The sham treatment consisted of only transient repositioning without airway instruments. Treating clinicians, outcome assessors, and parents were blinded to group status.
No significant difference in deaths, NDD
Death or NDD occurred in 36.3% of the patients in the MIST group and 36.1% in the control group (risk difference, 0%; 95% confidence interval, −7.6% to 7.7%; relative risk, 1.0; 95% confidence interval, 0.81-1.24).
Secondary respiratory outcomes were better in the MIST group:
- Hospitalization with respiratory illness occurred in 25.1% in the MIST group versus 38.2% in the control group (RR, 0.66; 95% CI, 0.54-0.81).
- Parent-reported wheezing or breathing difficulty occurred in 40.6% in the MIST group versus 53.6% in controls (RR, 0.76; 95% CI, 0.63-0.90).
- Asthma diagnosed by a physician was reported in 4.4% and 11.9% of MIST and control-group infants, respectively.
- Reported use of inhaled relievers (beta2 agonists) was 23.9% in the MIST group versus 38.7% in controls.
The previous study of early outcomes of deaths or bronchopulmonary dysplasia (BPD; chronic lung injury in preterm infants) was published by the same group of researchers in 2021.
Important benefit for respiratory health
Suhas G. Kallapur, MD, chief of the divisions of neonatology and developmental biology at University of California, Los Angeles, who was not part of either study, said: “This is one of the largest studies to date examining whether the MIST procedure for surfactant is beneficial in preterm babies born at 25-28 weeks’ gestation.”
Overall, when considering the 2021 and 2023 studies together, it appears that the MIST therapy has important benefits for respiratory health during a NICU stay and in early infancy, even though the primary outcome of death or NDD was not different between the treatment and control groups, Dr. Kallapur said.
“The slight (nonsignificant) increase in deaths in the MIST group was confined to the more immature babies – 25-26 weeks’ gestation at birth,” he pointed out. “In the bigger and more mature babies – 27-28 week gestation infants – the benefits of MIST therapy occurred without any increase in mortality, suggesting that this group of babies may be the group that stands to benefit most from this therapy.”
Dr. Kallapur said new data in the developmental origins of health and disease “now show that the trajectory of respiratory health in infancy is an important determinant of respiratory health into adulthood and older age.”
Therefore, the finding of benefit to respiratory health is particularly important, he said.
He noted that MIST or similar therapy is already in use in many NICUs throughout the world and that those already using it will likely feel vindicated by this study.
“Neonatologists who were on the sidelines will likely see these results – especially childhood respiratory outcomes – as a reason to initiate this procedure in all but the most immature preterm infants,” Dr. Kallapur says.
Dr. Dargaville reports personal fees from AbbVie and Chiesi Farmaceutici and provision of surfactant at reduced cost and support for conference travel from Chiesi Farmaceutici during the conduct of the study; in addition, Dr. Dargaville has been issued a patent for a catheter design. One coauthor reports grants from Chiesi Farmaceutici during the conduct of the study. Another coauthor reports serving as chief investigator for OPTI-SURF, an observational study on United Kingdom neonatal surfactant use in respiratory distress syndrome funded by Chiesi UK outside the submitted work. A third coauthor reports personal fees from Chiesi Farmaceutici outside the submitted work. This study was funded by grants from the Royal Hobart Hospital Research Foundation and the Australian National Health and Medical Research Council. Exogenous surfactant was provided at reduced cost by Chiesi Farmaceutici. Dr. Kallapur has no relevant financial relationships.
Results of the OPTIMIST follow-up study were published online in JAMA.
Researchers, led by Peter A. Dargaville, MD, department of paediatrics, Royal Hobart (Australia) Hospital, found that MIST, which involves administering surfactant via a thin catheter, compared with sham treatment, did not reduce the incidence of death or neurodevelopmental disability (NDD) by 2 years of age.
However, infants who received MIST had lower rates of poor respiratory outcomes during those first 2 years of life.
Study spanned 11 countries
The study was conducted in 33 tertiary neonatal intensive care units (NICUs) in 11 countries, including Australia, Canada, Israel, New Zealand, Qatar, Singapore, Slovenia, the Netherlands, Turkey, the United Kingdom, and the United States.
It included 486 infants 25-28 weeks old supported with CPAP; 453 had follow-up data available and data on the key secondary outcome were available for 434 infants.
The sham treatment consisted of only transient repositioning without airway instruments. Treating clinicians, outcome assessors, and parents were blinded to group status.
No significant difference in deaths, NDD
Death or NDD occurred in 36.3% of the patients in the MIST group and 36.1% in the control group (risk difference, 0%; 95% confidence interval, −7.6% to 7.7%; relative risk, 1.0; 95% confidence interval, 0.81-1.24).
Secondary respiratory outcomes were better in the MIST group:
- Hospitalization with respiratory illness occurred in 25.1% in the MIST group versus 38.2% in the control group (RR, 0.66; 95% CI, 0.54-0.81).
- Parent-reported wheezing or breathing difficulty occurred in 40.6% in the MIST group versus 53.6% in controls (RR, 0.76; 95% CI, 0.63-0.90).
- Asthma diagnosed by a physician was reported in 4.4% and 11.9% of MIST and control-group infants, respectively.
- Reported use of inhaled relievers (beta2 agonists) was 23.9% in the MIST group versus 38.7% in controls.
The previous study of early outcomes of deaths or bronchopulmonary dysplasia (BPD; chronic lung injury in preterm infants) was published by the same group of researchers in 2021.
Important benefit for respiratory health
Suhas G. Kallapur, MD, chief of the divisions of neonatology and developmental biology at University of California, Los Angeles, who was not part of either study, said: “This is one of the largest studies to date examining whether the MIST procedure for surfactant is beneficial in preterm babies born at 25-28 weeks’ gestation.”
Overall, when considering the 2021 and 2023 studies together, it appears that the MIST therapy has important benefits for respiratory health during a NICU stay and in early infancy, even though the primary outcome of death or NDD was not different between the treatment and control groups, Dr. Kallapur said.
“The slight (nonsignificant) increase in deaths in the MIST group was confined to the more immature babies – 25-26 weeks’ gestation at birth,” he pointed out. “In the bigger and more mature babies – 27-28 week gestation infants – the benefits of MIST therapy occurred without any increase in mortality, suggesting that this group of babies may be the group that stands to benefit most from this therapy.”
Dr. Kallapur said new data in the developmental origins of health and disease “now show that the trajectory of respiratory health in infancy is an important determinant of respiratory health into adulthood and older age.”
Therefore, the finding of benefit to respiratory health is particularly important, he said.
He noted that MIST or similar therapy is already in use in many NICUs throughout the world and that those already using it will likely feel vindicated by this study.
“Neonatologists who were on the sidelines will likely see these results – especially childhood respiratory outcomes – as a reason to initiate this procedure in all but the most immature preterm infants,” Dr. Kallapur says.
Dr. Dargaville reports personal fees from AbbVie and Chiesi Farmaceutici and provision of surfactant at reduced cost and support for conference travel from Chiesi Farmaceutici during the conduct of the study; in addition, Dr. Dargaville has been issued a patent for a catheter design. One coauthor reports grants from Chiesi Farmaceutici during the conduct of the study. Another coauthor reports serving as chief investigator for OPTI-SURF, an observational study on United Kingdom neonatal surfactant use in respiratory distress syndrome funded by Chiesi UK outside the submitted work. A third coauthor reports personal fees from Chiesi Farmaceutici outside the submitted work. This study was funded by grants from the Royal Hobart Hospital Research Foundation and the Australian National Health and Medical Research Council. Exogenous surfactant was provided at reduced cost by Chiesi Farmaceutici. Dr. Kallapur has no relevant financial relationships.
Results of the OPTIMIST follow-up study were published online in JAMA.
Researchers, led by Peter A. Dargaville, MD, department of paediatrics, Royal Hobart (Australia) Hospital, found that MIST, which involves administering surfactant via a thin catheter, compared with sham treatment, did not reduce the incidence of death or neurodevelopmental disability (NDD) by 2 years of age.
However, infants who received MIST had lower rates of poor respiratory outcomes during those first 2 years of life.
Study spanned 11 countries
The study was conducted in 33 tertiary neonatal intensive care units (NICUs) in 11 countries, including Australia, Canada, Israel, New Zealand, Qatar, Singapore, Slovenia, the Netherlands, Turkey, the United Kingdom, and the United States.
It included 486 infants 25-28 weeks old supported with CPAP; 453 had follow-up data available and data on the key secondary outcome were available for 434 infants.
The sham treatment consisted of only transient repositioning without airway instruments. Treating clinicians, outcome assessors, and parents were blinded to group status.
No significant difference in deaths, NDD
Death or NDD occurred in 36.3% of the patients in the MIST group and 36.1% in the control group (risk difference, 0%; 95% confidence interval, −7.6% to 7.7%; relative risk, 1.0; 95% confidence interval, 0.81-1.24).
Secondary respiratory outcomes were better in the MIST group:
- Hospitalization with respiratory illness occurred in 25.1% in the MIST group versus 38.2% in the control group (RR, 0.66; 95% CI, 0.54-0.81).
- Parent-reported wheezing or breathing difficulty occurred in 40.6% in the MIST group versus 53.6% in controls (RR, 0.76; 95% CI, 0.63-0.90).
- Asthma diagnosed by a physician was reported in 4.4% and 11.9% of MIST and control-group infants, respectively.
- Reported use of inhaled relievers (beta2 agonists) was 23.9% in the MIST group versus 38.7% in controls.
The previous study of early outcomes of deaths or bronchopulmonary dysplasia (BPD; chronic lung injury in preterm infants) was published by the same group of researchers in 2021.
Important benefit for respiratory health
Suhas G. Kallapur, MD, chief of the divisions of neonatology and developmental biology at University of California, Los Angeles, who was not part of either study, said: “This is one of the largest studies to date examining whether the MIST procedure for surfactant is beneficial in preterm babies born at 25-28 weeks’ gestation.”
Overall, when considering the 2021 and 2023 studies together, it appears that the MIST therapy has important benefits for respiratory health during a NICU stay and in early infancy, even though the primary outcome of death or NDD was not different between the treatment and control groups, Dr. Kallapur said.
“The slight (nonsignificant) increase in deaths in the MIST group was confined to the more immature babies – 25-26 weeks’ gestation at birth,” he pointed out. “In the bigger and more mature babies – 27-28 week gestation infants – the benefits of MIST therapy occurred without any increase in mortality, suggesting that this group of babies may be the group that stands to benefit most from this therapy.”
Dr. Kallapur said new data in the developmental origins of health and disease “now show that the trajectory of respiratory health in infancy is an important determinant of respiratory health into adulthood and older age.”
Therefore, the finding of benefit to respiratory health is particularly important, he said.
He noted that MIST or similar therapy is already in use in many NICUs throughout the world and that those already using it will likely feel vindicated by this study.
“Neonatologists who were on the sidelines will likely see these results – especially childhood respiratory outcomes – as a reason to initiate this procedure in all but the most immature preterm infants,” Dr. Kallapur says.
Dr. Dargaville reports personal fees from AbbVie and Chiesi Farmaceutici and provision of surfactant at reduced cost and support for conference travel from Chiesi Farmaceutici during the conduct of the study; in addition, Dr. Dargaville has been issued a patent for a catheter design. One coauthor reports grants from Chiesi Farmaceutici during the conduct of the study. Another coauthor reports serving as chief investigator for OPTI-SURF, an observational study on United Kingdom neonatal surfactant use in respiratory distress syndrome funded by Chiesi UK outside the submitted work. A third coauthor reports personal fees from Chiesi Farmaceutici outside the submitted work. This study was funded by grants from the Royal Hobart Hospital Research Foundation and the Australian National Health and Medical Research Council. Exogenous surfactant was provided at reduced cost by Chiesi Farmaceutici. Dr. Kallapur has no relevant financial relationships.
FROM JAMA
Fighting disparities in palliative and end-of-life care
Palliative care has been shown to improve quality of life, receipt of goal-concordant care, end-of-life decision-making, and improvement in pain and symptoms in individuals with serious illness. However, palliative and end-of-life care remain underutilized in racial and ethnic minorities.1 Health disparities such as access, quality of care, and health outcomes among minority groups exist in delivery and receipt of care within the health care system, and this includes the care of individuals with serious illness and at the end of life.1
Racial and ethnic minorities are less likely to receive goal-concordant care, participate in advance care planning, and have access to palliative care or hospice.2-4 They are more likely to die in a hospital, have inadequate pain and symptom management, and experience poor provider-patient communication.5-7 Other contributing factors include lack of knowledge of hospice and palliative care services, mistrust of the health care system, spiritual and religious beliefs, provider bias, and cultural beliefs.1
Despite these disparities, interventions have had limited success,8 and there are gaps in content, methods, and inclusion of racial and ethnic groups within palliative care research.7
Efforts to improve health equity for people with serious illness have been identified as an “urgent call to action.”1
A few recommended actionable items include delivering culturally competent care by ensuring availability of culturally and linguistically appropriate materials and information, education, and training for providers, and practicing cultural humility; contributing to workforce diversity by hiring and training diverse staff; and partnering with community organizations to build trust and to facilitate dissemination of culturally and linguistically appropriate information to providers in caring for their diverse patient populations.1,9
One of the first steps identified is to recognize that there is a problem and prioritize efforts to understand its “multifaceted nature.”10 This should occur on multiple levels including the individual (patient and caregiver), interpersonal (health care team), organization, and policy levels,10 and be done through clinical, research, and educational platforms.
At the interpersonal level, we as the health care team can start by reflecting, acknowledging biases, seeking educational and training opportunities on cross-cultural interactions, learning about cultural and spiritual beliefs, and developing skills in culturally and linguistically appropriate communication regarding goals of care and advance care planning.1,10
For those seeking resources, organizations such as the Center to Advance Palliative Care’s Project Equity and the American Academy of Hospice and Palliative Medicine have ongoing efforts to educate and train physicians and health care professionals to improve and understand health equity in palliative care by providing resource portals, toolkits, training, and general information.
It is imperative to move forward in actionable ways to address not only racial and ethnic disparities, but advance equity in serious illness care for health care organizations, providers, and policymakers.1
Dr. Kang is in the division of gerontology and geriatric medicine at the University of Washington, Seattle.
References
1. Barrett NJ et al. N C Med J. 2020;81:254-6.
2. Johnson KS et al. J Am Geriatr Soc. 2011;59:732-7.
3. Sharma RK et al. J Clin Oncol. 2015;33:3802-8.
4. Muni S et al. Chest. 2011;139:1025-33.
5. Anderson KO et al. J Pain. 2009;10:1187-204.
6. Mack JW et al. Arch Intern Med. 2010;170:1533-40.
7. Johnson KS. J Palliat Med. 2013;16(11):1329-34.
8. Brown CE et al. J Pain Symptom Manage. 2021;63(5):e465-e71.
9. Chambers B. Center for Advancing Palliative Care. July 9, 2020.
10. Koffman J et al. BMC Palliat Care. 2023;22(64):1-3.
Palliative care has been shown to improve quality of life, receipt of goal-concordant care, end-of-life decision-making, and improvement in pain and symptoms in individuals with serious illness. However, palliative and end-of-life care remain underutilized in racial and ethnic minorities.1 Health disparities such as access, quality of care, and health outcomes among minority groups exist in delivery and receipt of care within the health care system, and this includes the care of individuals with serious illness and at the end of life.1
Racial and ethnic minorities are less likely to receive goal-concordant care, participate in advance care planning, and have access to palliative care or hospice.2-4 They are more likely to die in a hospital, have inadequate pain and symptom management, and experience poor provider-patient communication.5-7 Other contributing factors include lack of knowledge of hospice and palliative care services, mistrust of the health care system, spiritual and religious beliefs, provider bias, and cultural beliefs.1
Despite these disparities, interventions have had limited success,8 and there are gaps in content, methods, and inclusion of racial and ethnic groups within palliative care research.7
Efforts to improve health equity for people with serious illness have been identified as an “urgent call to action.”1
A few recommended actionable items include delivering culturally competent care by ensuring availability of culturally and linguistically appropriate materials and information, education, and training for providers, and practicing cultural humility; contributing to workforce diversity by hiring and training diverse staff; and partnering with community organizations to build trust and to facilitate dissemination of culturally and linguistically appropriate information to providers in caring for their diverse patient populations.1,9
One of the first steps identified is to recognize that there is a problem and prioritize efforts to understand its “multifaceted nature.”10 This should occur on multiple levels including the individual (patient and caregiver), interpersonal (health care team), organization, and policy levels,10 and be done through clinical, research, and educational platforms.
At the interpersonal level, we as the health care team can start by reflecting, acknowledging biases, seeking educational and training opportunities on cross-cultural interactions, learning about cultural and spiritual beliefs, and developing skills in culturally and linguistically appropriate communication regarding goals of care and advance care planning.1,10
For those seeking resources, organizations such as the Center to Advance Palliative Care’s Project Equity and the American Academy of Hospice and Palliative Medicine have ongoing efforts to educate and train physicians and health care professionals to improve and understand health equity in palliative care by providing resource portals, toolkits, training, and general information.
It is imperative to move forward in actionable ways to address not only racial and ethnic disparities, but advance equity in serious illness care for health care organizations, providers, and policymakers.1
Dr. Kang is in the division of gerontology and geriatric medicine at the University of Washington, Seattle.
References
1. Barrett NJ et al. N C Med J. 2020;81:254-6.
2. Johnson KS et al. J Am Geriatr Soc. 2011;59:732-7.
3. Sharma RK et al. J Clin Oncol. 2015;33:3802-8.
4. Muni S et al. Chest. 2011;139:1025-33.
5. Anderson KO et al. J Pain. 2009;10:1187-204.
6. Mack JW et al. Arch Intern Med. 2010;170:1533-40.
7. Johnson KS. J Palliat Med. 2013;16(11):1329-34.
8. Brown CE et al. J Pain Symptom Manage. 2021;63(5):e465-e71.
9. Chambers B. Center for Advancing Palliative Care. July 9, 2020.
10. Koffman J et al. BMC Palliat Care. 2023;22(64):1-3.
Palliative care has been shown to improve quality of life, receipt of goal-concordant care, end-of-life decision-making, and improvement in pain and symptoms in individuals with serious illness. However, palliative and end-of-life care remain underutilized in racial and ethnic minorities.1 Health disparities such as access, quality of care, and health outcomes among minority groups exist in delivery and receipt of care within the health care system, and this includes the care of individuals with serious illness and at the end of life.1
Racial and ethnic minorities are less likely to receive goal-concordant care, participate in advance care planning, and have access to palliative care or hospice.2-4 They are more likely to die in a hospital, have inadequate pain and symptom management, and experience poor provider-patient communication.5-7 Other contributing factors include lack of knowledge of hospice and palliative care services, mistrust of the health care system, spiritual and religious beliefs, provider bias, and cultural beliefs.1
Despite these disparities, interventions have had limited success,8 and there are gaps in content, methods, and inclusion of racial and ethnic groups within palliative care research.7
Efforts to improve health equity for people with serious illness have been identified as an “urgent call to action.”1
A few recommended actionable items include delivering culturally competent care by ensuring availability of culturally and linguistically appropriate materials and information, education, and training for providers, and practicing cultural humility; contributing to workforce diversity by hiring and training diverse staff; and partnering with community organizations to build trust and to facilitate dissemination of culturally and linguistically appropriate information to providers in caring for their diverse patient populations.1,9
One of the first steps identified is to recognize that there is a problem and prioritize efforts to understand its “multifaceted nature.”10 This should occur on multiple levels including the individual (patient and caregiver), interpersonal (health care team), organization, and policy levels,10 and be done through clinical, research, and educational platforms.
At the interpersonal level, we as the health care team can start by reflecting, acknowledging biases, seeking educational and training opportunities on cross-cultural interactions, learning about cultural and spiritual beliefs, and developing skills in culturally and linguistically appropriate communication regarding goals of care and advance care planning.1,10
For those seeking resources, organizations such as the Center to Advance Palliative Care’s Project Equity and the American Academy of Hospice and Palliative Medicine have ongoing efforts to educate and train physicians and health care professionals to improve and understand health equity in palliative care by providing resource portals, toolkits, training, and general information.
It is imperative to move forward in actionable ways to address not only racial and ethnic disparities, but advance equity in serious illness care for health care organizations, providers, and policymakers.1
Dr. Kang is in the division of gerontology and geriatric medicine at the University of Washington, Seattle.
References
1. Barrett NJ et al. N C Med J. 2020;81:254-6.
2. Johnson KS et al. J Am Geriatr Soc. 2011;59:732-7.
3. Sharma RK et al. J Clin Oncol. 2015;33:3802-8.
4. Muni S et al. Chest. 2011;139:1025-33.
5. Anderson KO et al. J Pain. 2009;10:1187-204.
6. Mack JW et al. Arch Intern Med. 2010;170:1533-40.
7. Johnson KS. J Palliat Med. 2013;16(11):1329-34.
8. Brown CE et al. J Pain Symptom Manage. 2021;63(5):e465-e71.
9. Chambers B. Center for Advancing Palliative Care. July 9, 2020.
10. Koffman J et al. BMC Palliat Care. 2023;22(64):1-3.
Cold weather may challenge blood pressure control
A review of electronic health records of more than 60,000 U.S. adults being treated for hypertension found that on average, systolic BP rose by up to 1.7 mm Hg in the cold winter months, compared with the hot summer months.
On a population level, BP control rates decreased by up to 5% during the cold winter months, compared with control rates in the warm summer months.
“Some patients may benefit from increased pharmacological intervention to keep blood pressure controlled during the winter,” Robert Barrett, with the American Medical Association, Greenville, S.C., told this news organization.
“Individuals with hypertension or values near the range of hypertension may benefit from periodic blood pressure monitoring and improvements in physical activity and nutritional patterns during winter months to offset adverse effects from seasonal blood pressure changes,” Mr. Barrett added in a news release.
Mr. Barrett presented the study findings at the American Heart Association Hypertension Scientific Sessions 2023 in Boston.
Supportive data
Mr. Barrett explained that seasonal variation in BP has been previously documented, and as part of the evaluation for the AMA MAP Hypertension program, he and colleagues were interested in the effect of this variation on population control rates under standard metrics (visits with BP < 140/90 mm Hg).
They analyzed data from 60,676 men and women (mean age, 62 years) with hypertension from six health care organizations in the southeastern and midwestern United States that were participating in the quality improvement program.
During the roughly 5-year assessment period, none of the patients had changes in their antihypertensive medication, and all had at least one visit in each temperate season. The researchers estimated the seasonal effect on average systolic BP and BP control (defined as < 140/90 mm Hg).
Across a total of 453,787 visits, systolic BP during the winter averaged 0.47 mm Hg higher (95% confidence interval, 0.364-0.573) than the yearly average, with a significantly lower odds ratio for BP control (OR, 0.92; 95% CI, 0.91-0.94), the researchers report.
In contrast, average systolic BP was 0.92 mm Hg lower during the summer, with a higher likelihood of BP control (OR ,1.10; 95% CI, 1.07-1.12).
“Seasonal variation in blood pressure has a substantial effect on hypertension control, often defined as blood pressure < 140/90,” Barrett told this news organization.
“Patients with hypertension are less likely to have their blood pressure controlled during winter than summer months. If the blood pressure is very well controlled, for example to < 130/80, then seasonal variation will have little effect on control to < 140/90,” Mr. Barrett noted.
“However, if blood pressure is not well controlled, then patients near the 140/90 level could benefit from monitoring their blood pressure regularly, closer medical follow-up, and avoiding decreased physical activity and increased weight toward year end,” he added.
Wanpen Vongpatanasin, MD, clinical chair for the conference, said that it’s “well known that BP tends to lower during summer months and patients may be susceptible to dehydration and acute kidney injury when BP is too low, particularly when treated with certain medication such as diuretics.”
On the flip side, “cold weather predisposes to vasoconstriction as our blood vessel constrict to maintain core temperature and it could be challenging to manage BP. That’s why it is important for high BP patients to monitor home BP regularly,” said Dr. Vongpatanasin, professor of internal medicine and director of the hypertension section, cardiology division, UT Southwestern Medical Center, Dallas.
The study had no commercial funding. Mr. Barrett and Dr. Vongpatanasin have no relevant disclosures.
A version of this article first appeared on Medscape.com.
A review of electronic health records of more than 60,000 U.S. adults being treated for hypertension found that on average, systolic BP rose by up to 1.7 mm Hg in the cold winter months, compared with the hot summer months.
On a population level, BP control rates decreased by up to 5% during the cold winter months, compared with control rates in the warm summer months.
“Some patients may benefit from increased pharmacological intervention to keep blood pressure controlled during the winter,” Robert Barrett, with the American Medical Association, Greenville, S.C., told this news organization.
“Individuals with hypertension or values near the range of hypertension may benefit from periodic blood pressure monitoring and improvements in physical activity and nutritional patterns during winter months to offset adverse effects from seasonal blood pressure changes,” Mr. Barrett added in a news release.
Mr. Barrett presented the study findings at the American Heart Association Hypertension Scientific Sessions 2023 in Boston.
Supportive data
Mr. Barrett explained that seasonal variation in BP has been previously documented, and as part of the evaluation for the AMA MAP Hypertension program, he and colleagues were interested in the effect of this variation on population control rates under standard metrics (visits with BP < 140/90 mm Hg).
They analyzed data from 60,676 men and women (mean age, 62 years) with hypertension from six health care organizations in the southeastern and midwestern United States that were participating in the quality improvement program.
During the roughly 5-year assessment period, none of the patients had changes in their antihypertensive medication, and all had at least one visit in each temperate season. The researchers estimated the seasonal effect on average systolic BP and BP control (defined as < 140/90 mm Hg).
Across a total of 453,787 visits, systolic BP during the winter averaged 0.47 mm Hg higher (95% confidence interval, 0.364-0.573) than the yearly average, with a significantly lower odds ratio for BP control (OR, 0.92; 95% CI, 0.91-0.94), the researchers report.
In contrast, average systolic BP was 0.92 mm Hg lower during the summer, with a higher likelihood of BP control (OR ,1.10; 95% CI, 1.07-1.12).
“Seasonal variation in blood pressure has a substantial effect on hypertension control, often defined as blood pressure < 140/90,” Barrett told this news organization.
“Patients with hypertension are less likely to have their blood pressure controlled during winter than summer months. If the blood pressure is very well controlled, for example to < 130/80, then seasonal variation will have little effect on control to < 140/90,” Mr. Barrett noted.
“However, if blood pressure is not well controlled, then patients near the 140/90 level could benefit from monitoring their blood pressure regularly, closer medical follow-up, and avoiding decreased physical activity and increased weight toward year end,” he added.
Wanpen Vongpatanasin, MD, clinical chair for the conference, said that it’s “well known that BP tends to lower during summer months and patients may be susceptible to dehydration and acute kidney injury when BP is too low, particularly when treated with certain medication such as diuretics.”
On the flip side, “cold weather predisposes to vasoconstriction as our blood vessel constrict to maintain core temperature and it could be challenging to manage BP. That’s why it is important for high BP patients to monitor home BP regularly,” said Dr. Vongpatanasin, professor of internal medicine and director of the hypertension section, cardiology division, UT Southwestern Medical Center, Dallas.
The study had no commercial funding. Mr. Barrett and Dr. Vongpatanasin have no relevant disclosures.
A version of this article first appeared on Medscape.com.
A review of electronic health records of more than 60,000 U.S. adults being treated for hypertension found that on average, systolic BP rose by up to 1.7 mm Hg in the cold winter months, compared with the hot summer months.
On a population level, BP control rates decreased by up to 5% during the cold winter months, compared with control rates in the warm summer months.
“Some patients may benefit from increased pharmacological intervention to keep blood pressure controlled during the winter,” Robert Barrett, with the American Medical Association, Greenville, S.C., told this news organization.
“Individuals with hypertension or values near the range of hypertension may benefit from periodic blood pressure monitoring and improvements in physical activity and nutritional patterns during winter months to offset adverse effects from seasonal blood pressure changes,” Mr. Barrett added in a news release.
Mr. Barrett presented the study findings at the American Heart Association Hypertension Scientific Sessions 2023 in Boston.
Supportive data
Mr. Barrett explained that seasonal variation in BP has been previously documented, and as part of the evaluation for the AMA MAP Hypertension program, he and colleagues were interested in the effect of this variation on population control rates under standard metrics (visits with BP < 140/90 mm Hg).
They analyzed data from 60,676 men and women (mean age, 62 years) with hypertension from six health care organizations in the southeastern and midwestern United States that were participating in the quality improvement program.
During the roughly 5-year assessment period, none of the patients had changes in their antihypertensive medication, and all had at least one visit in each temperate season. The researchers estimated the seasonal effect on average systolic BP and BP control (defined as < 140/90 mm Hg).
Across a total of 453,787 visits, systolic BP during the winter averaged 0.47 mm Hg higher (95% confidence interval, 0.364-0.573) than the yearly average, with a significantly lower odds ratio for BP control (OR, 0.92; 95% CI, 0.91-0.94), the researchers report.
In contrast, average systolic BP was 0.92 mm Hg lower during the summer, with a higher likelihood of BP control (OR ,1.10; 95% CI, 1.07-1.12).
“Seasonal variation in blood pressure has a substantial effect on hypertension control, often defined as blood pressure < 140/90,” Barrett told this news organization.
“Patients with hypertension are less likely to have their blood pressure controlled during winter than summer months. If the blood pressure is very well controlled, for example to < 130/80, then seasonal variation will have little effect on control to < 140/90,” Mr. Barrett noted.
“However, if blood pressure is not well controlled, then patients near the 140/90 level could benefit from monitoring their blood pressure regularly, closer medical follow-up, and avoiding decreased physical activity and increased weight toward year end,” he added.
Wanpen Vongpatanasin, MD, clinical chair for the conference, said that it’s “well known that BP tends to lower during summer months and patients may be susceptible to dehydration and acute kidney injury when BP is too low, particularly when treated with certain medication such as diuretics.”
On the flip side, “cold weather predisposes to vasoconstriction as our blood vessel constrict to maintain core temperature and it could be challenging to manage BP. That’s why it is important for high BP patients to monitor home BP regularly,” said Dr. Vongpatanasin, professor of internal medicine and director of the hypertension section, cardiology division, UT Southwestern Medical Center, Dallas.
The study had no commercial funding. Mr. Barrett and Dr. Vongpatanasin have no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM HYPERTENSION 2023
Landmark obesity legislation reintroduced in Congress
(TROA) (H.R. 4818/S. 2407). This legislation is a vital first step in expanding access to obesity treatment as it would expand Medicare coverage to include screening and treatment of obesity by a diverse range of health care providers who provide obesity care. The bill also includes coverage of behavioral counseling, prescription drugs for long-term weight management, and other prevention and treatment options.
The passage of TROA could lead to improved obesity care options because many private insurance companies model their covered health benefits to reflect Medicare.
You can help lawmakers understand the urgent need for expanded access to affordable, effective obesity treatments and how greater access to these tools will equip you to better care for your patients.
Use the new obesity advocacy toolkit to find the tools and resources you need, including an email template, sample phone script, op-ed template, and more, to assist you in reaching out to your elected officials and urging them to support the passage of TROA.
(TROA) (H.R. 4818/S. 2407). This legislation is a vital first step in expanding access to obesity treatment as it would expand Medicare coverage to include screening and treatment of obesity by a diverse range of health care providers who provide obesity care. The bill also includes coverage of behavioral counseling, prescription drugs for long-term weight management, and other prevention and treatment options.
The passage of TROA could lead to improved obesity care options because many private insurance companies model their covered health benefits to reflect Medicare.
You can help lawmakers understand the urgent need for expanded access to affordable, effective obesity treatments and how greater access to these tools will equip you to better care for your patients.
Use the new obesity advocacy toolkit to find the tools and resources you need, including an email template, sample phone script, op-ed template, and more, to assist you in reaching out to your elected officials and urging them to support the passage of TROA.
(TROA) (H.R. 4818/S. 2407). This legislation is a vital first step in expanding access to obesity treatment as it would expand Medicare coverage to include screening and treatment of obesity by a diverse range of health care providers who provide obesity care. The bill also includes coverage of behavioral counseling, prescription drugs for long-term weight management, and other prevention and treatment options.
The passage of TROA could lead to improved obesity care options because many private insurance companies model their covered health benefits to reflect Medicare.
You can help lawmakers understand the urgent need for expanded access to affordable, effective obesity treatments and how greater access to these tools will equip you to better care for your patients.
Use the new obesity advocacy toolkit to find the tools and resources you need, including an email template, sample phone script, op-ed template, and more, to assist you in reaching out to your elected officials and urging them to support the passage of TROA.
FDA panel deems phenylephrine ineffective
The Nonprescription Drug Advisory Committee discussed the efficacy and pharmacokinetic data for phenylephrine. The committee’s next move is to determine if the drug’s status as Generally Recognized as Safe and Effective should be revoked. This would mean manufacturers would have to come up with new formulations, or products containing the drug would be removed from store shelves. NDAC did not disclose a timeline for assessing GRASE status.
The vote that formally declared phenylephrine ineffective was in line with a review of pharmacology and clinical data presented by the FDA on Sept. 11, which found that the oral bioavailability of the drug is less than 1%, compared with 38%, a number often cited in the literature and based on outdated technology.
A mechanism potentially responsible for inefficacy may be the half-life of phenylephrine.
“The half-life of the parent phenylephrine is much shorter than that of total phenylephrine, suggesting that the duration of action for active parent phenylephrine is far shorter than the monographed dosing interval of every 4 hours and is therefore open to question,” the review states.
The side effects of phenylephrine include headaches, insomnia, and nervousness. At higher doses, it can increase blood pressure.
The review also found that original studies used to support the efficacy of phenylephrine were inconclusive at best and contained potential methodological, statistical, and data integrity issues.
Pseudoephedrine is the only other nonprescription oral nasal decongestant on the retail market but is only available behind the counter due to its use as a potential narcotic.
Manufacturers have used phenylephrine instead of pseudoephedrine in many products due to this limitation.
Revoking the GRASE status of phenylephrine would leave patients without an over-the-counter option.
According to the FDA review, 242 million packages or bottles of phenylephrine products were sold in 2022, resulting in $1.76 billion in sales. A little over 50 million packages of pseudoephedrine were sold that same year, resulting in $542 million in sales.
“I think there’s a huge potential for consumer concern,” Diane B. Ginsburg, PhD, MS, RPh, the pharmacy practice division associate dean for Healthcare Partnerships at The University of Texas at Austin, said during the panel.
She said patients may be confused and concerned about the panel vote, especially those who feel they have benefitted from phenylephrine products. In the event of GRASE removal, she advised reassuring patients that phenylephrine is being pulled from shelves due to inefficacy rather than immediate health risks.
“The real positive here to me is the opportunity from an educational perspective to show consumers the fact that there are a lot more ways to treat” conditions that present with the symptom of congestion, such as rhinitis.
According to the FDA review, “most consumers may simply need instruction on the alternatives, including how to obtain ‘behind-the-counter’ pseudoephedrine or to use alternative treatments, including intranasal decongestants (including intranasal phenylephrine), intranasal steroids, intranasal antihistamines, or intranasal saline products.”
Despite these complications, “there are a number of potential benefits that would be derived by changing the GRASE status of oral phenylephrine.”
These include avoiding unnecessary costs of taking an ineffective drug, potential allergic reactions and side effects, and the risks of patients taking a higher dosage.
A version of this article appeared on Medscape.com.
The Nonprescription Drug Advisory Committee discussed the efficacy and pharmacokinetic data for phenylephrine. The committee’s next move is to determine if the drug’s status as Generally Recognized as Safe and Effective should be revoked. This would mean manufacturers would have to come up with new formulations, or products containing the drug would be removed from store shelves. NDAC did not disclose a timeline for assessing GRASE status.
The vote that formally declared phenylephrine ineffective was in line with a review of pharmacology and clinical data presented by the FDA on Sept. 11, which found that the oral bioavailability of the drug is less than 1%, compared with 38%, a number often cited in the literature and based on outdated technology.
A mechanism potentially responsible for inefficacy may be the half-life of phenylephrine.
“The half-life of the parent phenylephrine is much shorter than that of total phenylephrine, suggesting that the duration of action for active parent phenylephrine is far shorter than the monographed dosing interval of every 4 hours and is therefore open to question,” the review states.
The side effects of phenylephrine include headaches, insomnia, and nervousness. At higher doses, it can increase blood pressure.
The review also found that original studies used to support the efficacy of phenylephrine were inconclusive at best and contained potential methodological, statistical, and data integrity issues.
Pseudoephedrine is the only other nonprescription oral nasal decongestant on the retail market but is only available behind the counter due to its use as a potential narcotic.
Manufacturers have used phenylephrine instead of pseudoephedrine in many products due to this limitation.
Revoking the GRASE status of phenylephrine would leave patients without an over-the-counter option.
According to the FDA review, 242 million packages or bottles of phenylephrine products were sold in 2022, resulting in $1.76 billion in sales. A little over 50 million packages of pseudoephedrine were sold that same year, resulting in $542 million in sales.
“I think there’s a huge potential for consumer concern,” Diane B. Ginsburg, PhD, MS, RPh, the pharmacy practice division associate dean for Healthcare Partnerships at The University of Texas at Austin, said during the panel.
She said patients may be confused and concerned about the panel vote, especially those who feel they have benefitted from phenylephrine products. In the event of GRASE removal, she advised reassuring patients that phenylephrine is being pulled from shelves due to inefficacy rather than immediate health risks.
“The real positive here to me is the opportunity from an educational perspective to show consumers the fact that there are a lot more ways to treat” conditions that present with the symptom of congestion, such as rhinitis.
According to the FDA review, “most consumers may simply need instruction on the alternatives, including how to obtain ‘behind-the-counter’ pseudoephedrine or to use alternative treatments, including intranasal decongestants (including intranasal phenylephrine), intranasal steroids, intranasal antihistamines, or intranasal saline products.”
Despite these complications, “there are a number of potential benefits that would be derived by changing the GRASE status of oral phenylephrine.”
These include avoiding unnecessary costs of taking an ineffective drug, potential allergic reactions and side effects, and the risks of patients taking a higher dosage.
A version of this article appeared on Medscape.com.
The Nonprescription Drug Advisory Committee discussed the efficacy and pharmacokinetic data for phenylephrine. The committee’s next move is to determine if the drug’s status as Generally Recognized as Safe and Effective should be revoked. This would mean manufacturers would have to come up with new formulations, or products containing the drug would be removed from store shelves. NDAC did not disclose a timeline for assessing GRASE status.
The vote that formally declared phenylephrine ineffective was in line with a review of pharmacology and clinical data presented by the FDA on Sept. 11, which found that the oral bioavailability of the drug is less than 1%, compared with 38%, a number often cited in the literature and based on outdated technology.
A mechanism potentially responsible for inefficacy may be the half-life of phenylephrine.
“The half-life of the parent phenylephrine is much shorter than that of total phenylephrine, suggesting that the duration of action for active parent phenylephrine is far shorter than the monographed dosing interval of every 4 hours and is therefore open to question,” the review states.
The side effects of phenylephrine include headaches, insomnia, and nervousness. At higher doses, it can increase blood pressure.
The review also found that original studies used to support the efficacy of phenylephrine were inconclusive at best and contained potential methodological, statistical, and data integrity issues.
Pseudoephedrine is the only other nonprescription oral nasal decongestant on the retail market but is only available behind the counter due to its use as a potential narcotic.
Manufacturers have used phenylephrine instead of pseudoephedrine in many products due to this limitation.
Revoking the GRASE status of phenylephrine would leave patients without an over-the-counter option.
According to the FDA review, 242 million packages or bottles of phenylephrine products were sold in 2022, resulting in $1.76 billion in sales. A little over 50 million packages of pseudoephedrine were sold that same year, resulting in $542 million in sales.
“I think there’s a huge potential for consumer concern,” Diane B. Ginsburg, PhD, MS, RPh, the pharmacy practice division associate dean for Healthcare Partnerships at The University of Texas at Austin, said during the panel.
She said patients may be confused and concerned about the panel vote, especially those who feel they have benefitted from phenylephrine products. In the event of GRASE removal, she advised reassuring patients that phenylephrine is being pulled from shelves due to inefficacy rather than immediate health risks.
“The real positive here to me is the opportunity from an educational perspective to show consumers the fact that there are a lot more ways to treat” conditions that present with the symptom of congestion, such as rhinitis.
According to the FDA review, “most consumers may simply need instruction on the alternatives, including how to obtain ‘behind-the-counter’ pseudoephedrine or to use alternative treatments, including intranasal decongestants (including intranasal phenylephrine), intranasal steroids, intranasal antihistamines, or intranasal saline products.”
Despite these complications, “there are a number of potential benefits that would be derived by changing the GRASE status of oral phenylephrine.”
These include avoiding unnecessary costs of taking an ineffective drug, potential allergic reactions and side effects, and the risks of patients taking a higher dosage.
A version of this article appeared on Medscape.com.
Bad blood: Could brain bleeds be contagious?
This transcript has been edited for clarity.
How do you tell if a condition is caused by an infection?
It seems like an obvious question, right? In the post–van Leeuwenhoek era we can look at whatever part of the body is diseased under a microscope and see microbes – you know, the usual suspects.
Except when we can’t. And there are plenty of cases where we can’t: where the microbe is too small to be seen without more advanced imaging techniques, like with viruses; or when the pathogen is sparsely populated or hard to culture, like Mycobacterium.
Finding out that a condition is the result of an infection is not only an exercise for 19th century physicians. After all, it was 2008 when Barry Marshall and Robin Warren won their Nobel Prize for proving that stomach ulcers, long thought to be due to “stress,” were actually caused by a tiny microbe called Helicobacter pylori.
And this week, we are looking at a study which, once again, begins to suggest that a condition thought to be more or less random – cerebral amyloid angiopathy – may actually be the result of an infectious disease.
We’re talking about this paper, appearing in JAMA, which is just a great example of old-fashioned shoe-leather epidemiology. But let’s get up to speed on cerebral amyloid angiopathy (CAA) first.
CAA is characterized by the deposition of amyloid protein in the brain. While there are some genetic causes, they are quite rare, and most cases are thought to be idiopathic. Recent analyses suggest that somewhere between 5% and 7% of cognitively normal older adults have CAA, but the rate is much higher among those with intracerebral hemorrhage – brain bleeds. In fact, CAA is the second-most common cause of bleeding in the brain, second only to severe hypertension.
An article in Nature highlights cases that seemed to develop after the administration of cadaveric pituitary hormone.
Other studies have shown potential transmission via dura mater grafts and neurosurgical instruments. But despite those clues, no infectious organism has been identified. Some have suggested that the long latent period and difficulty of finding a responsible microbe points to a prion-like disease not yet known. But these studies are more or less case series. The new JAMA paper gives us, if not a smoking gun, a pretty decent set of fingerprints.
Here’s the idea: If CAA is caused by some infectious agent, it may be transmitted in the blood. We know that a decent percentage of people who have spontaneous brain bleeds have CAA. If those people donated blood in the past, maybe the people who received that blood would be at risk for brain bleeds too.
Of course, to really test that hypothesis, you’d need to know who every blood donor in a country was and every person who received that blood and all their subsequent diagnoses for basically their entire lives. No one has that kind of data, right?
Well, if you’ve been watching this space, you’ll know that a few countries do. Enter Sweden and Denmark, with their national electronic health record that captures all of this information, and much more, on every single person who lives or has lived in those countries since before 1970. Unbelievable.
So that’s exactly what the researchers, led by Jingchen Zhao at Karolinska (Sweden) University, did. They identified roughly 760,000 individuals in Sweden and 330,000 people in Denmark who had received a blood transfusion between 1970 and 2017.
Of course, most of those blood donors – 99% of them, actually – never went on to have any bleeding in the brain. It is a rare thing, fortunately.
But some of the donors did, on average within about 5 years of the time they donated blood. The researchers characterized each donor as either never having a brain bleed, having a single bleed, or having multiple bleeds. The latter is most strongly associated with CAA.
The big question: Would recipients who got blood from individuals who later on had brain bleeds, have brain bleeds themselves?
The answer is yes, though with an asterisk. You can see the results here. The risk of recipients having a brain bleed was lowest if the blood they received was from people who never had a brain bleed, higher if the individual had a single brain bleed, and highest if they got blood from a donor who would go on to have multiple brain bleeds.
All in all, individuals who received blood from someone who would later have multiple hemorrhages were three times more likely to themselves develop bleeds themselves. It’s fairly compelling evidence of a transmissible agent.
Of course, there are some potential confounders to consider here. Whose blood you get is not totally random. If, for example, people with type O blood are just more likely to have brain bleeds, then you could get results like this, as type O tends to donate to type O and both groups would have higher risk after donation. But the authors adjusted for blood type. They also adjusted for number of transfusions, calendar year, age, sex, and indication for transfusion.
Perhaps most compelling, and most clever, is that they used ischemic stroke as a negative control. Would people who received blood from someone who later had an ischemic stroke themselves be more likely to go on to have an ischemic stroke? No signal at all. It does not appear that there is a transmissible agent associated with ischemic stroke – only the brain bleeds.
I know what you’re thinking. What’s the agent? What’s the microbe, or virus, or prion, or toxin? The study gives us no insight there. These nationwide databases are awesome but they can only do so much. Because of the vagaries of medical coding and the difficulty of making the CAA diagnosis, the authors are using brain bleeds as a proxy here; we don’t even know for sure whether these were CAA-associated brain bleeds.
It’s also worth noting that there’s little we can do about this. None of the blood donors in this study had a brain bleed prior to donation; it’s not like we could screen people out of donating in the future. We have no test for whatever this agent is, if it even exists, nor do we have a potential treatment. Fortunately, whatever it is, it is extremely rare.
Still, this paper feels like a shot across the bow. At this point, the probability has shifted strongly away from CAA being a purely random disease and toward it being an infectious one. It may be time to round up some of the unusual suspects.
Dr. F. Perry Wilson is an associate professor of medicine and public health and director of Yale University’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
How do you tell if a condition is caused by an infection?
It seems like an obvious question, right? In the post–van Leeuwenhoek era we can look at whatever part of the body is diseased under a microscope and see microbes – you know, the usual suspects.
Except when we can’t. And there are plenty of cases where we can’t: where the microbe is too small to be seen without more advanced imaging techniques, like with viruses; or when the pathogen is sparsely populated or hard to culture, like Mycobacterium.
Finding out that a condition is the result of an infection is not only an exercise for 19th century physicians. After all, it was 2008 when Barry Marshall and Robin Warren won their Nobel Prize for proving that stomach ulcers, long thought to be due to “stress,” were actually caused by a tiny microbe called Helicobacter pylori.
And this week, we are looking at a study which, once again, begins to suggest that a condition thought to be more or less random – cerebral amyloid angiopathy – may actually be the result of an infectious disease.
We’re talking about this paper, appearing in JAMA, which is just a great example of old-fashioned shoe-leather epidemiology. But let’s get up to speed on cerebral amyloid angiopathy (CAA) first.
CAA is characterized by the deposition of amyloid protein in the brain. While there are some genetic causes, they are quite rare, and most cases are thought to be idiopathic. Recent analyses suggest that somewhere between 5% and 7% of cognitively normal older adults have CAA, but the rate is much higher among those with intracerebral hemorrhage – brain bleeds. In fact, CAA is the second-most common cause of bleeding in the brain, second only to severe hypertension.
An article in Nature highlights cases that seemed to develop after the administration of cadaveric pituitary hormone.
Other studies have shown potential transmission via dura mater grafts and neurosurgical instruments. But despite those clues, no infectious organism has been identified. Some have suggested that the long latent period and difficulty of finding a responsible microbe points to a prion-like disease not yet known. But these studies are more or less case series. The new JAMA paper gives us, if not a smoking gun, a pretty decent set of fingerprints.
Here’s the idea: If CAA is caused by some infectious agent, it may be transmitted in the blood. We know that a decent percentage of people who have spontaneous brain bleeds have CAA. If those people donated blood in the past, maybe the people who received that blood would be at risk for brain bleeds too.
Of course, to really test that hypothesis, you’d need to know who every blood donor in a country was and every person who received that blood and all their subsequent diagnoses for basically their entire lives. No one has that kind of data, right?
Well, if you’ve been watching this space, you’ll know that a few countries do. Enter Sweden and Denmark, with their national electronic health record that captures all of this information, and much more, on every single person who lives or has lived in those countries since before 1970. Unbelievable.
So that’s exactly what the researchers, led by Jingchen Zhao at Karolinska (Sweden) University, did. They identified roughly 760,000 individuals in Sweden and 330,000 people in Denmark who had received a blood transfusion between 1970 and 2017.
Of course, most of those blood donors – 99% of them, actually – never went on to have any bleeding in the brain. It is a rare thing, fortunately.
But some of the donors did, on average within about 5 years of the time they donated blood. The researchers characterized each donor as either never having a brain bleed, having a single bleed, or having multiple bleeds. The latter is most strongly associated with CAA.
The big question: Would recipients who got blood from individuals who later on had brain bleeds, have brain bleeds themselves?
The answer is yes, though with an asterisk. You can see the results here. The risk of recipients having a brain bleed was lowest if the blood they received was from people who never had a brain bleed, higher if the individual had a single brain bleed, and highest if they got blood from a donor who would go on to have multiple brain bleeds.
All in all, individuals who received blood from someone who would later have multiple hemorrhages were three times more likely to themselves develop bleeds themselves. It’s fairly compelling evidence of a transmissible agent.
Of course, there are some potential confounders to consider here. Whose blood you get is not totally random. If, for example, people with type O blood are just more likely to have brain bleeds, then you could get results like this, as type O tends to donate to type O and both groups would have higher risk after donation. But the authors adjusted for blood type. They also adjusted for number of transfusions, calendar year, age, sex, and indication for transfusion.
Perhaps most compelling, and most clever, is that they used ischemic stroke as a negative control. Would people who received blood from someone who later had an ischemic stroke themselves be more likely to go on to have an ischemic stroke? No signal at all. It does not appear that there is a transmissible agent associated with ischemic stroke – only the brain bleeds.
I know what you’re thinking. What’s the agent? What’s the microbe, or virus, or prion, or toxin? The study gives us no insight there. These nationwide databases are awesome but they can only do so much. Because of the vagaries of medical coding and the difficulty of making the CAA diagnosis, the authors are using brain bleeds as a proxy here; we don’t even know for sure whether these were CAA-associated brain bleeds.
It’s also worth noting that there’s little we can do about this. None of the blood donors in this study had a brain bleed prior to donation; it’s not like we could screen people out of donating in the future. We have no test for whatever this agent is, if it even exists, nor do we have a potential treatment. Fortunately, whatever it is, it is extremely rare.
Still, this paper feels like a shot across the bow. At this point, the probability has shifted strongly away from CAA being a purely random disease and toward it being an infectious one. It may be time to round up some of the unusual suspects.
Dr. F. Perry Wilson is an associate professor of medicine and public health and director of Yale University’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
How do you tell if a condition is caused by an infection?
It seems like an obvious question, right? In the post–van Leeuwenhoek era we can look at whatever part of the body is diseased under a microscope and see microbes – you know, the usual suspects.
Except when we can’t. And there are plenty of cases where we can’t: where the microbe is too small to be seen without more advanced imaging techniques, like with viruses; or when the pathogen is sparsely populated or hard to culture, like Mycobacterium.
Finding out that a condition is the result of an infection is not only an exercise for 19th century physicians. After all, it was 2008 when Barry Marshall and Robin Warren won their Nobel Prize for proving that stomach ulcers, long thought to be due to “stress,” were actually caused by a tiny microbe called Helicobacter pylori.
And this week, we are looking at a study which, once again, begins to suggest that a condition thought to be more or less random – cerebral amyloid angiopathy – may actually be the result of an infectious disease.
We’re talking about this paper, appearing in JAMA, which is just a great example of old-fashioned shoe-leather epidemiology. But let’s get up to speed on cerebral amyloid angiopathy (CAA) first.
CAA is characterized by the deposition of amyloid protein in the brain. While there are some genetic causes, they are quite rare, and most cases are thought to be idiopathic. Recent analyses suggest that somewhere between 5% and 7% of cognitively normal older adults have CAA, but the rate is much higher among those with intracerebral hemorrhage – brain bleeds. In fact, CAA is the second-most common cause of bleeding in the brain, second only to severe hypertension.
An article in Nature highlights cases that seemed to develop after the administration of cadaveric pituitary hormone.
Other studies have shown potential transmission via dura mater grafts and neurosurgical instruments. But despite those clues, no infectious organism has been identified. Some have suggested that the long latent period and difficulty of finding a responsible microbe points to a prion-like disease not yet known. But these studies are more or less case series. The new JAMA paper gives us, if not a smoking gun, a pretty decent set of fingerprints.
Here’s the idea: If CAA is caused by some infectious agent, it may be transmitted in the blood. We know that a decent percentage of people who have spontaneous brain bleeds have CAA. If those people donated blood in the past, maybe the people who received that blood would be at risk for brain bleeds too.
Of course, to really test that hypothesis, you’d need to know who every blood donor in a country was and every person who received that blood and all their subsequent diagnoses for basically their entire lives. No one has that kind of data, right?
Well, if you’ve been watching this space, you’ll know that a few countries do. Enter Sweden and Denmark, with their national electronic health record that captures all of this information, and much more, on every single person who lives or has lived in those countries since before 1970. Unbelievable.
So that’s exactly what the researchers, led by Jingchen Zhao at Karolinska (Sweden) University, did. They identified roughly 760,000 individuals in Sweden and 330,000 people in Denmark who had received a blood transfusion between 1970 and 2017.
Of course, most of those blood donors – 99% of them, actually – never went on to have any bleeding in the brain. It is a rare thing, fortunately.
But some of the donors did, on average within about 5 years of the time they donated blood. The researchers characterized each donor as either never having a brain bleed, having a single bleed, or having multiple bleeds. The latter is most strongly associated with CAA.
The big question: Would recipients who got blood from individuals who later on had brain bleeds, have brain bleeds themselves?
The answer is yes, though with an asterisk. You can see the results here. The risk of recipients having a brain bleed was lowest if the blood they received was from people who never had a brain bleed, higher if the individual had a single brain bleed, and highest if they got blood from a donor who would go on to have multiple brain bleeds.
All in all, individuals who received blood from someone who would later have multiple hemorrhages were three times more likely to themselves develop bleeds themselves. It’s fairly compelling evidence of a transmissible agent.
Of course, there are some potential confounders to consider here. Whose blood you get is not totally random. If, for example, people with type O blood are just more likely to have brain bleeds, then you could get results like this, as type O tends to donate to type O and both groups would have higher risk after donation. But the authors adjusted for blood type. They also adjusted for number of transfusions, calendar year, age, sex, and indication for transfusion.
Perhaps most compelling, and most clever, is that they used ischemic stroke as a negative control. Would people who received blood from someone who later had an ischemic stroke themselves be more likely to go on to have an ischemic stroke? No signal at all. It does not appear that there is a transmissible agent associated with ischemic stroke – only the brain bleeds.
I know what you’re thinking. What’s the agent? What’s the microbe, or virus, or prion, or toxin? The study gives us no insight there. These nationwide databases are awesome but they can only do so much. Because of the vagaries of medical coding and the difficulty of making the CAA diagnosis, the authors are using brain bleeds as a proxy here; we don’t even know for sure whether these were CAA-associated brain bleeds.
It’s also worth noting that there’s little we can do about this. None of the blood donors in this study had a brain bleed prior to donation; it’s not like we could screen people out of donating in the future. We have no test for whatever this agent is, if it even exists, nor do we have a potential treatment. Fortunately, whatever it is, it is extremely rare.
Still, this paper feels like a shot across the bow. At this point, the probability has shifted strongly away from CAA being a purely random disease and toward it being an infectious one. It may be time to round up some of the unusual suspects.
Dr. F. Perry Wilson is an associate professor of medicine and public health and director of Yale University’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
Stress, insomnia tied to increased AFib risk for older women
TOPLINE:
Eight psychosocial factors, grouped into two distinct clusters, are significantly associated with risk for atrial fibrillation in postmenopausal women, with insomnia and stressful life events (SLEs) being the most strongly associated with AFib, a large new study has found.
METHODOLOGY:
- In addition to traditional risk factors such as obesity, advanced age, ethnicity, smoking, alcohol, hypertension, diabetes, coronary artery disease, heart failure, and emotional and psychological distress may also affect AFib.
- The study included 83,736 postmenopausal women in the Women’s Health Initiative (mean age, 63.9 years; 88.1% White) who did not have AFib at baseline.
- From questionnaires, researchers collected information on psychosocial stressors and used hierarchical cluster analysis to identify patterns of psychosocial predictors.
- They separated these clusters into quartiles, identified associations between psychosocial exposure variables, and adjusted for traditional risk factors.
- Over an average follow-up of 10.5 years, 23,954 participants (28.6%) developed incident AFib.
TAKEAWAY:
- The analysis generated two clusters of distinct psychosocial variables that were significantly associated with AFib: the Stress Cluster, including SLEs, depressive symptoms, and insomnia; and the Strain Cluster, including three personality traits: optimism, cynical hostility, and emotional expressiveness; and two social measures: social support, and social strain.
- Those in the highest quartiles of both the Stress Cluster and the Strain Cluster had greater rates of AFib, compared with those in the lowest quartiles.
- In a final model, the association between SLEs (hazard ratio, 1.02; 95% confidence interval, 1.01-1.04) and insomnia (HR, 1.04; 95% CI, 1.03-1.06) were most strongly linked to increased incidence of AFib, and a sensitivity analysis using snoring as a surrogate marker for sleep apnea didn’t change this outcome, supporting the independent effect of insomnia on AFib.
- In subgroup analyses, the Stress Cluster had a stronger association with AFib incidence in younger (50-69 years) versus older women (70-79 years), and in non-Hispanic White and Asian women versus Hispanic and non-Hispanic Black women.
IN PRACTICE:
The results support the hypothesis that psychosocial predictors account for additional risk for AFib “above and beyond” traditional risk factors, the authors wrote. Identifying and addressing sex-specific, modifiable risk factors, including insomnia, “may help reduce the burden of AF[ib] in aging women.”
SOURCE:
The study was conducted by Susan X. Zhao, MD, division of cardiology, department of medicine, Santa Clara Valley Medical Center, San Jose, Calif., and colleagues. It was published online in the Journal of the American Heart Association.
LIMITATIONS:
The psychometric questionnaires were administered only at study entry, but psychosocial variables may change over time. Data on sleep apnea and other sleep disorders, which may confound the relationship between insomnia and AFib, were not available, and although the study included a sensitivity analysis controlling for snoring, this is an imperfect surrogate for sleep apnea. Generalizability to other demographic, racial, and ethnic groups is limited.
DISCLOSURES:
The Women’s Health Initiative program is funded by the National Heart, Lung, and Blood Institute; National Institutes of Health; and the Department of Health & Human Services. The authors have no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
Eight psychosocial factors, grouped into two distinct clusters, are significantly associated with risk for atrial fibrillation in postmenopausal women, with insomnia and stressful life events (SLEs) being the most strongly associated with AFib, a large new study has found.
METHODOLOGY:
- In addition to traditional risk factors such as obesity, advanced age, ethnicity, smoking, alcohol, hypertension, diabetes, coronary artery disease, heart failure, and emotional and psychological distress may also affect AFib.
- The study included 83,736 postmenopausal women in the Women’s Health Initiative (mean age, 63.9 years; 88.1% White) who did not have AFib at baseline.
- From questionnaires, researchers collected information on psychosocial stressors and used hierarchical cluster analysis to identify patterns of psychosocial predictors.
- They separated these clusters into quartiles, identified associations between psychosocial exposure variables, and adjusted for traditional risk factors.
- Over an average follow-up of 10.5 years, 23,954 participants (28.6%) developed incident AFib.
TAKEAWAY:
- The analysis generated two clusters of distinct psychosocial variables that were significantly associated with AFib: the Stress Cluster, including SLEs, depressive symptoms, and insomnia; and the Strain Cluster, including three personality traits: optimism, cynical hostility, and emotional expressiveness; and two social measures: social support, and social strain.
- Those in the highest quartiles of both the Stress Cluster and the Strain Cluster had greater rates of AFib, compared with those in the lowest quartiles.
- In a final model, the association between SLEs (hazard ratio, 1.02; 95% confidence interval, 1.01-1.04) and insomnia (HR, 1.04; 95% CI, 1.03-1.06) were most strongly linked to increased incidence of AFib, and a sensitivity analysis using snoring as a surrogate marker for sleep apnea didn’t change this outcome, supporting the independent effect of insomnia on AFib.
- In subgroup analyses, the Stress Cluster had a stronger association with AFib incidence in younger (50-69 years) versus older women (70-79 years), and in non-Hispanic White and Asian women versus Hispanic and non-Hispanic Black women.
IN PRACTICE:
The results support the hypothesis that psychosocial predictors account for additional risk for AFib “above and beyond” traditional risk factors, the authors wrote. Identifying and addressing sex-specific, modifiable risk factors, including insomnia, “may help reduce the burden of AF[ib] in aging women.”
SOURCE:
The study was conducted by Susan X. Zhao, MD, division of cardiology, department of medicine, Santa Clara Valley Medical Center, San Jose, Calif., and colleagues. It was published online in the Journal of the American Heart Association.
LIMITATIONS:
The psychometric questionnaires were administered only at study entry, but psychosocial variables may change over time. Data on sleep apnea and other sleep disorders, which may confound the relationship between insomnia and AFib, were not available, and although the study included a sensitivity analysis controlling for snoring, this is an imperfect surrogate for sleep apnea. Generalizability to other demographic, racial, and ethnic groups is limited.
DISCLOSURES:
The Women’s Health Initiative program is funded by the National Heart, Lung, and Blood Institute; National Institutes of Health; and the Department of Health & Human Services. The authors have no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
TOPLINE:
Eight psychosocial factors, grouped into two distinct clusters, are significantly associated with risk for atrial fibrillation in postmenopausal women, with insomnia and stressful life events (SLEs) being the most strongly associated with AFib, a large new study has found.
METHODOLOGY:
- In addition to traditional risk factors such as obesity, advanced age, ethnicity, smoking, alcohol, hypertension, diabetes, coronary artery disease, heart failure, and emotional and psychological distress may also affect AFib.
- The study included 83,736 postmenopausal women in the Women’s Health Initiative (mean age, 63.9 years; 88.1% White) who did not have AFib at baseline.
- From questionnaires, researchers collected information on psychosocial stressors and used hierarchical cluster analysis to identify patterns of psychosocial predictors.
- They separated these clusters into quartiles, identified associations between psychosocial exposure variables, and adjusted for traditional risk factors.
- Over an average follow-up of 10.5 years, 23,954 participants (28.6%) developed incident AFib.
TAKEAWAY:
- The analysis generated two clusters of distinct psychosocial variables that were significantly associated with AFib: the Stress Cluster, including SLEs, depressive symptoms, and insomnia; and the Strain Cluster, including three personality traits: optimism, cynical hostility, and emotional expressiveness; and two social measures: social support, and social strain.
- Those in the highest quartiles of both the Stress Cluster and the Strain Cluster had greater rates of AFib, compared with those in the lowest quartiles.
- In a final model, the association between SLEs (hazard ratio, 1.02; 95% confidence interval, 1.01-1.04) and insomnia (HR, 1.04; 95% CI, 1.03-1.06) were most strongly linked to increased incidence of AFib, and a sensitivity analysis using snoring as a surrogate marker for sleep apnea didn’t change this outcome, supporting the independent effect of insomnia on AFib.
- In subgroup analyses, the Stress Cluster had a stronger association with AFib incidence in younger (50-69 years) versus older women (70-79 years), and in non-Hispanic White and Asian women versus Hispanic and non-Hispanic Black women.
IN PRACTICE:
The results support the hypothesis that psychosocial predictors account for additional risk for AFib “above and beyond” traditional risk factors, the authors wrote. Identifying and addressing sex-specific, modifiable risk factors, including insomnia, “may help reduce the burden of AF[ib] in aging women.”
SOURCE:
The study was conducted by Susan X. Zhao, MD, division of cardiology, department of medicine, Santa Clara Valley Medical Center, San Jose, Calif., and colleagues. It was published online in the Journal of the American Heart Association.
LIMITATIONS:
The psychometric questionnaires were administered only at study entry, but psychosocial variables may change over time. Data on sleep apnea and other sleep disorders, which may confound the relationship between insomnia and AFib, were not available, and although the study included a sensitivity analysis controlling for snoring, this is an imperfect surrogate for sleep apnea. Generalizability to other demographic, racial, and ethnic groups is limited.
DISCLOSURES:
The Women’s Health Initiative program is funded by the National Heart, Lung, and Blood Institute; National Institutes of Health; and the Department of Health & Human Services. The authors have no relevant conflicts of interest.
A version of this article appeared on Medscape.com.
FROM JOURNAL OF THE AMERICAN HEART ASSOCIATION
Turmeric may be as effective as omeprazole for dyspepsia
TOPLINE:
METHODOLOGY:
- The researchers randomly assigned 206 patients to receive curcumin – the active ingredient in turmeric – alone; omeprazole alone; or curcumin plus omeprazole for 28 days. A total of 151 patients completed the study.
- Doses were two 250-mg curcumin pills four times daily, plus one placebo pill; one 20-mg omeprazole pill daily, plus two placebo pills four times daily; or two 250-mg curcumin pills four times daily, plus one 20-mg omeprazole pill once daily.
- Symptoms of functional dyspepsia were assessed on days 28 and 56 using the Severity of Dyspepsia Assessment (SODA) score.
TAKEAWAY:
- In the combined group, the curcumin-alone group, and the omeprazole-alone group, SODA scores for pain severity declined significantly by day 28 (–4.83, –5.46, and –6.22, respectively), as did scores for severity of other symptoms (–2.22, –2.32, and –2.31, respectively).
- Symptom improvements were even stronger by day 56 for pain (–7.19, –8.07, –8.85) and other symptoms (–4.09, –4.12, –3.71) in the same groups.
- Curcumin was safe and well tolerated, but satisfaction scores did not change significantly over time among those taking it, suggesting the possible need for improvement in its taste or smell.
- There was no synergistic effect between omeprazole and curcumin.
IN PRACTICE:
“The new findings from our study may justify considering curcumin in clinical practice. This multicenter, randomized, controlled trial provides highly reliable evidence for the treatment of functional dyspepsia,” the authors wrote.
SOURCE:
Pradermchai Kongkam, MD, of Chulalongkorn University, Bangkok, and Wichittra Khongkha of Chao Phraya Abhaibhubejhr Hospital, Prachin Buri, Thailand, are joint first authors. The study was published online in BMJ Evidence-Based Medicine.
LIMITATIONS:
A small number of participants in each group were lost to follow-up, and the follow-up period was short (less than 2 months) for all.
DISCLOSURES:
The study was funded by the Thai Traditional and Alternative Medicine Fund. The authors have disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- The researchers randomly assigned 206 patients to receive curcumin – the active ingredient in turmeric – alone; omeprazole alone; or curcumin plus omeprazole for 28 days. A total of 151 patients completed the study.
- Doses were two 250-mg curcumin pills four times daily, plus one placebo pill; one 20-mg omeprazole pill daily, plus two placebo pills four times daily; or two 250-mg curcumin pills four times daily, plus one 20-mg omeprazole pill once daily.
- Symptoms of functional dyspepsia were assessed on days 28 and 56 using the Severity of Dyspepsia Assessment (SODA) score.
TAKEAWAY:
- In the combined group, the curcumin-alone group, and the omeprazole-alone group, SODA scores for pain severity declined significantly by day 28 (–4.83, –5.46, and –6.22, respectively), as did scores for severity of other symptoms (–2.22, –2.32, and –2.31, respectively).
- Symptom improvements were even stronger by day 56 for pain (–7.19, –8.07, –8.85) and other symptoms (–4.09, –4.12, –3.71) in the same groups.
- Curcumin was safe and well tolerated, but satisfaction scores did not change significantly over time among those taking it, suggesting the possible need for improvement in its taste or smell.
- There was no synergistic effect between omeprazole and curcumin.
IN PRACTICE:
“The new findings from our study may justify considering curcumin in clinical practice. This multicenter, randomized, controlled trial provides highly reliable evidence for the treatment of functional dyspepsia,” the authors wrote.
SOURCE:
Pradermchai Kongkam, MD, of Chulalongkorn University, Bangkok, and Wichittra Khongkha of Chao Phraya Abhaibhubejhr Hospital, Prachin Buri, Thailand, are joint first authors. The study was published online in BMJ Evidence-Based Medicine.
LIMITATIONS:
A small number of participants in each group were lost to follow-up, and the follow-up period was short (less than 2 months) for all.
DISCLOSURES:
The study was funded by the Thai Traditional and Alternative Medicine Fund. The authors have disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- The researchers randomly assigned 206 patients to receive curcumin – the active ingredient in turmeric – alone; omeprazole alone; or curcumin plus omeprazole for 28 days. A total of 151 patients completed the study.
- Doses were two 250-mg curcumin pills four times daily, plus one placebo pill; one 20-mg omeprazole pill daily, plus two placebo pills four times daily; or two 250-mg curcumin pills four times daily, plus one 20-mg omeprazole pill once daily.
- Symptoms of functional dyspepsia were assessed on days 28 and 56 using the Severity of Dyspepsia Assessment (SODA) score.
TAKEAWAY:
- In the combined group, the curcumin-alone group, and the omeprazole-alone group, SODA scores for pain severity declined significantly by day 28 (–4.83, –5.46, and –6.22, respectively), as did scores for severity of other symptoms (–2.22, –2.32, and –2.31, respectively).
- Symptom improvements were even stronger by day 56 for pain (–7.19, –8.07, –8.85) and other symptoms (–4.09, –4.12, –3.71) in the same groups.
- Curcumin was safe and well tolerated, but satisfaction scores did not change significantly over time among those taking it, suggesting the possible need for improvement in its taste or smell.
- There was no synergistic effect between omeprazole and curcumin.
IN PRACTICE:
“The new findings from our study may justify considering curcumin in clinical practice. This multicenter, randomized, controlled trial provides highly reliable evidence for the treatment of functional dyspepsia,” the authors wrote.
SOURCE:
Pradermchai Kongkam, MD, of Chulalongkorn University, Bangkok, and Wichittra Khongkha of Chao Phraya Abhaibhubejhr Hospital, Prachin Buri, Thailand, are joint first authors. The study was published online in BMJ Evidence-Based Medicine.
LIMITATIONS:
A small number of participants in each group were lost to follow-up, and the follow-up period was short (less than 2 months) for all.
DISCLOSURES:
The study was funded by the Thai Traditional and Alternative Medicine Fund. The authors have disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
FROM BMJ EVIDENCE-BASED MEDICINE