TOPLINE:

Atopic dermatitis (AD) in early childhood is associated with an increased risk for inflammatory bowel disease (IBD) later in life, but atopic manifestations are generally not associated with IBD.

METHODOLOGY:

• Studies examining the link between atopy and IBD have yielded inconsistent results. Many of these studies included adults, introducing recall bias, or relied on physician diagnoses that might have overlooked mild cases.
• Researchers analyzed prospectively collected data on 83,311 children from two cohort studies, ABIS (1997-1999) and MoBa (1999-2008), who were followed up from birth until 2021 or a diagnosis of IBD.
• Information on parents was collected prospectively via questionnaires on any atopy their children might have developed by the age of 3 years. Atopy included conditions such as AD, asthma, food allergy, or allergic rhinitis.

TAKEAWAY:

• A total of 301 participants were diagnosed with IBD over 1,174,756 person-years of follow-up. By the age of 3 years, 31,671 children (38%) were reported to have any atopic manifestation.
• Children with AD at the age of 3 years demonstrated a significantly higher risk for IBD (pooled adjusted hazard ratio [aHR], 1.46), Crohn’s disease (pooled aHR, 1.53), and ulcerative colitis (pooled aHR, 1.78).
• Any atopic manifestation by the age of 3 years was not associated with a subsequent risk for IBD, Crohn’s disease, or ulcerative colitis, nor were analyses focused on early-life food-related allergy, asthma, and allergic rhinitis.

IN PRACTICE:

According to the authors, these findings suggested potential shared underlying causes between AD and IBD, which could help identify individuals at risk, and “a deeper understanding could significantly benefit the development of novel treatment approaches capable of effectively addressing both conditions, consequently enhancing patient outcomes.”

SOURCE:

This study, led by Tereza Lerchova, MD, PhD, Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, was published online in The Journal of Pediatrics.

LIMITATIONS:

The findings of this study were mostly related to childhood-onset IBD instead of IBD in adult life. Lower participation in the MoBa study could limit generalizability to a broader population. In addition, there might have been lower participation from families without atopic manifestations.

DISCLOSURES:

The study was funded by the Swedish Society for Medical Research, Swedish Research Council, and ALF and supported by grants from the Swedish Child Diabetes Foundation, Swedish Council for Working Life and Social Research, Swedish Research Council, Medical Research Council of Southeast Sweden, JDRF Wallenberg Foundation, Linkoping University, and Joanna Cocozza Foundation. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Atopic dermatitis (AD) in early childhood is associated with an increased risk for inflammatory bowel disease (IBD) later in life, but atopic manifestations are generally not associated with IBD.

METHODOLOGY:

• Studies examining the link between atopy and IBD have yielded inconsistent results. Many of these studies included adults, introducing recall bias, or relied on physician diagnoses that might have overlooked mild cases.
• Researchers analyzed prospectively collected data on 83,311 children from two cohort studies, ABIS (1997-1999) and MoBa (1999-2008), who were followed up from birth until 2021 or a diagnosis of IBD.
• Information on parents was collected prospectively via questionnaires on any atopy their children might have developed by the age of 3 years. Atopy included conditions such as AD, asthma, food allergy, or allergic rhinitis.

TAKEAWAY:

• A total of 301 participants were diagnosed with IBD over 1,174,756 person-years of follow-up. By the age of 3 years, 31,671 children (38%) were reported to have any atopic manifestation.
• Children with AD at the age of 3 years demonstrated a significantly higher risk for IBD (pooled adjusted hazard ratio [aHR], 1.46), Crohn’s disease (pooled aHR, 1.53), and ulcerative colitis (pooled aHR, 1.78).
• Any atopic manifestation by the age of 3 years was not associated with a subsequent risk for IBD, Crohn’s disease, or ulcerative colitis, nor were analyses focused on early-life food-related allergy, asthma, and allergic rhinitis.

IN PRACTICE:

According to the authors, these findings suggested potential shared underlying causes between AD and IBD, which could help identify individuals at risk, and “a deeper understanding could significantly benefit the development of novel treatment approaches capable of effectively addressing both conditions, consequently enhancing patient outcomes.”

SOURCE:

This study, led by Tereza Lerchova, MD, PhD, Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, was published online in The Journal of Pediatrics.

LIMITATIONS:

The findings of this study were mostly related to childhood-onset IBD instead of IBD in adult life. Lower participation in the MoBa study could limit generalizability to a broader population. In addition, there might have been lower participation from families without atopic manifestations.

DISCLOSURES:

The study was funded by the Swedish Society for Medical Research, Swedish Research Council, and ALF and supported by grants from the Swedish Child Diabetes Foundation, Swedish Council for Working Life and Social Research, Swedish Research Council, Medical Research Council of Southeast Sweden, JDRF Wallenberg Foundation, Linkoping University, and Joanna Cocozza Foundation. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

Atopic dermatitis (AD) in early childhood is associated with an increased risk for inflammatory bowel disease (IBD) later in life, but atopic manifestations are generally not associated with IBD.

METHODOLOGY:

• Studies examining the link between atopy and IBD have yielded inconsistent results. Many of these studies included adults, introducing recall bias, or relied on physician diagnoses that might have overlooked mild cases.
• Researchers analyzed prospectively collected data on 83,311 children from two cohort studies, ABIS (1997-1999) and MoBa (1999-2008), who were followed up from birth until 2021 or a diagnosis of IBD.
• Information on parents was collected prospectively via questionnaires on any atopy their children might have developed by the age of 3 years. Atopy included conditions such as AD, asthma, food allergy, or allergic rhinitis.

TAKEAWAY:

• A total of 301 participants were diagnosed with IBD over 1,174,756 person-years of follow-up. By the age of 3 years, 31,671 children (38%) were reported to have any atopic manifestation.
• Children with AD at the age of 3 years demonstrated a significantly higher risk for IBD (pooled adjusted hazard ratio [aHR], 1.46), Crohn’s disease (pooled aHR, 1.53), and ulcerative colitis (pooled aHR, 1.78).
• Any atopic manifestation by the age of 3 years was not associated with a subsequent risk for IBD, Crohn’s disease, or ulcerative colitis, nor were analyses focused on early-life food-related allergy, asthma, and allergic rhinitis.

IN PRACTICE:

According to the authors, these findings suggested potential shared underlying causes between AD and IBD, which could help identify individuals at risk, and “a deeper understanding could significantly benefit the development of novel treatment approaches capable of effectively addressing both conditions, consequently enhancing patient outcomes.”

SOURCE:

This study, led by Tereza Lerchova, MD, PhD, Department of Pediatrics, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden, was published online in The Journal of Pediatrics.

LIMITATIONS:

The findings of this study were mostly related to childhood-onset IBD instead of IBD in adult life. Lower participation in the MoBa study could limit generalizability to a broader population. In addition, there might have been lower participation from families without atopic manifestations.

DISCLOSURES:

The study was funded by the Swedish Society for Medical Research, Swedish Research Council, and ALF and supported by grants from the Swedish Child Diabetes Foundation, Swedish Council for Working Life and Social Research, Swedish Research Council, Medical Research Council of Southeast Sweden, JDRF Wallenberg Foundation, Linkoping University, and Joanna Cocozza Foundation. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

The acronym AIDS is redundant, loaded with stigma, and potentially harmful, according to a group of specialists who suggest replacing the term with “advanced HIV.”

The acronym AIDS has “outlived its usefulness and we should transition toward a more descriptive language that aligns with contemporary challenges in HIV,” reports Isaac Núñez, MD, from the Department of Medical Education, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán in Mexico City, Mexico, and colleagues.

People generally associate the acronym AIDS with patients who have no available treatment options and a short life expectancy, said Dr. Núñez. That mischaracterization may affect treatment decisions by patients and clinicians and could result in exaggerated infection-control measures.

Using the HIV/AIDS combination erroneously implies equivalence and can mislead the public and clinicians, which the authors explained in their Viewpoint article published in The Lancet HIV.
 

Original Reason for the Term

AIDS, which stands for acquired immunodeficiency syndrome, was coined in 1982 by the US Centers for Disease Control and Prevention (CDC) to name a disease with an unknown cause that affected people with weakened cell-mediated immunity.

“When HIV was found to be the cause of the disease (labeled HIV in 1986), the term AIDS, strictly speaking, became unnecessary,” Dr. Núñez said.

AIDS was originally intended as a case definition for surveillance purposes, and treatment decisions were based on whether patients met the case definition for AIDS, he pointed out.

“The fact that some people still do so in this day and age shows that this is not only unhelpful, but misleading and even harmful,” he noted. Without the label AIDS, clinicians can focus on whether and for how long people have been on treatment, whether they recently switched treatment, and other factors that will help determine appropriate care.
 

Some Organizations Removed AIDS From Their Names

Some organizations have already removed AIDS from their names. For example, the International AIDS Society–USA, which issues guidelines on antiretroviral treatment, changed its name to the International Antiviral Society–USA. 

In 2017, the name of AIDS.gov was changed to HIV.gov. In its explanation, the group wrote, “Today, people with HIV who are diagnosed early, linked to care, start antiretroviral therapy, and take it as prescribed can achieve life-long viral suppression that prevents HIV infection from progressing to AIDS.”

A different view on the term AIDS comes from Greg Millett, MPH, vice president at the Foundation for AIDS Research (amfAR) and the director of amfAR’s Public Policy Office. 

Although he believes that AIDS is an anachronistic term, as a researcher for more than 30 years in the field; a policy director in Washington; a scientist; and a person living with HIV, “it feels like a distinction without a difference. At least from where I sit, there are far more pressing issues that we’re facing as an HIV community,” Millett shared. 

For instance, “we’re seeing that global, as well as domestic, HIV funding is in, by far, the most precarious position that I’ve ever seen in the field. Calling it AIDS or HIV makes no difference in trying to alleviate that jeopardy,” he said.

Millett also said that the stigma and persecution and, in some cases, criminalization of people living with HIV or AIDS is pervasive and won’t go away with a name change, which is a point the authors also acknowledged.

“We need to focus on the social determinants of health,” he said. “That is the thing that is going to move the needle among people living with HIV, not nomenclature.”

Millett likens the argument to the one between Black and African American. “As a Black American, I remember fierce debates in the early ‘90s over whether we should be called African Americans or Blacks. Some argued that African American carried greater dignity and would help with self-esteem and address inequities by emphasizing that we are American. Many others said that it doesn’t make a difference.”

“It is clear that being called African American has not fixed intractable issues like poverty, structural racism, or inequities in incarceration,” he pointed out.
 

End the Epidemic, Not the Name 

The authors misinterpret the impact of the term on stigma, said James W. Curran, MD, MPH, dean emeritus of the Rollins School of Public Health and professor of epidemiology and global health at Emory University, both in Atlanta, Georgia. The term AIDS “is more likely attributed to the fatal nature of the infection itself,” without treatment, he explained, and the mode of transmission, exacerbated by homophobia.

“The term has been in widespread use for 40 years and recognized worldwide,” Dr. Curran, who led the nation’s efforts in the battle against HIV and AIDS at the CDC for 15 years before joining Emory as dean, said.

He also worries about the continued trajectory of lives lost: “Over 35 million people worldwide have perished from HIV/AIDS, including over 500,000 per year now.”

Meanwhile, “global programs such as PEPFAR [the US President’s Emergency Plan for AIDS Relief] are under fire and threatened by Congress as no longer necessary. Removing AIDS from the terminology may add to confusion,” making people think “that the epidemic is over,” he said.

Although the authors argue that keeping the term may cause harm, eliminating it might worsen a different kind of harm. “There is a risk that abolishing the term will further de-emphasize the importance of the problem, with no significant impact on stigma,” Dr. Curran added.

A version of this article appeared on Medscape.com.

The acronym AIDS is redundant, loaded with stigma, and potentially harmful, according to a group of specialists who suggest replacing the term with “advanced HIV.”

The acronym AIDS has “outlived its usefulness and we should transition toward a more descriptive language that aligns with contemporary challenges in HIV,” reports Isaac Núñez, MD, from the Department of Medical Education, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán in Mexico City, Mexico, and colleagues.

People generally associate the acronym AIDS with patients who have no available treatment options and a short life expectancy, said Dr. Núñez. That mischaracterization may affect treatment decisions by patients and clinicians and could result in exaggerated infection-control measures.

Using the HIV/AIDS combination erroneously implies equivalence and can mislead the public and clinicians, which the authors explained in their Viewpoint article published in The Lancet HIV.
 

Original Reason for the Term

AIDS, which stands for acquired immunodeficiency syndrome, was coined in 1982 by the US Centers for Disease Control and Prevention (CDC) to name a disease with an unknown cause that affected people with weakened cell-mediated immunity.

“When HIV was found to be the cause of the disease (labeled HIV in 1986), the term AIDS, strictly speaking, became unnecessary,” Dr. Núñez said.

AIDS was originally intended as a case definition for surveillance purposes, and treatment decisions were based on whether patients met the case definition for AIDS, he pointed out.

“The fact that some people still do so in this day and age shows that this is not only unhelpful, but misleading and even harmful,” he noted. Without the label AIDS, clinicians can focus on whether and for how long people have been on treatment, whether they recently switched treatment, and other factors that will help determine appropriate care.
 

Some Organizations Removed AIDS From Their Names

Some organizations have already removed AIDS from their names. For example, the International AIDS Society–USA, which issues guidelines on antiretroviral treatment, changed its name to the International Antiviral Society–USA. 

In 2017, the name of AIDS.gov was changed to HIV.gov. In its explanation, the group wrote, “Today, people with HIV who are diagnosed early, linked to care, start antiretroviral therapy, and take it as prescribed can achieve life-long viral suppression that prevents HIV infection from progressing to AIDS.”

A different view on the term AIDS comes from Greg Millett, MPH, vice president at the Foundation for AIDS Research (amfAR) and the director of amfAR’s Public Policy Office. 

Although he believes that AIDS is an anachronistic term, as a researcher for more than 30 years in the field; a policy director in Washington; a scientist; and a person living with HIV, “it feels like a distinction without a difference. At least from where I sit, there are far more pressing issues that we’re facing as an HIV community,” Millett shared. 

For instance, “we’re seeing that global, as well as domestic, HIV funding is in, by far, the most precarious position that I’ve ever seen in the field. Calling it AIDS or HIV makes no difference in trying to alleviate that jeopardy,” he said.

Millett also said that the stigma and persecution and, in some cases, criminalization of people living with HIV or AIDS is pervasive and won’t go away with a name change, which is a point the authors also acknowledged.

“We need to focus on the social determinants of health,” he said. “That is the thing that is going to move the needle among people living with HIV, not nomenclature.”

Millett likens the argument to the one between Black and African American. “As a Black American, I remember fierce debates in the early ‘90s over whether we should be called African Americans or Blacks. Some argued that African American carried greater dignity and would help with self-esteem and address inequities by emphasizing that we are American. Many others said that it doesn’t make a difference.”

“It is clear that being called African American has not fixed intractable issues like poverty, structural racism, or inequities in incarceration,” he pointed out.
 

End the Epidemic, Not the Name 

The authors misinterpret the impact of the term on stigma, said James W. Curran, MD, MPH, dean emeritus of the Rollins School of Public Health and professor of epidemiology and global health at Emory University, both in Atlanta, Georgia. The term AIDS “is more likely attributed to the fatal nature of the infection itself,” without treatment, he explained, and the mode of transmission, exacerbated by homophobia.

“The term has been in widespread use for 40 years and recognized worldwide,” Dr. Curran, who led the nation’s efforts in the battle against HIV and AIDS at the CDC for 15 years before joining Emory as dean, said.

He also worries about the continued trajectory of lives lost: “Over 35 million people worldwide have perished from HIV/AIDS, including over 500,000 per year now.”

Meanwhile, “global programs such as PEPFAR [the US President’s Emergency Plan for AIDS Relief] are under fire and threatened by Congress as no longer necessary. Removing AIDS from the terminology may add to confusion,” making people think “that the epidemic is over,” he said.

Although the authors argue that keeping the term may cause harm, eliminating it might worsen a different kind of harm. “There is a risk that abolishing the term will further de-emphasize the importance of the problem, with no significant impact on stigma,” Dr. Curran added.

A version of this article appeared on Medscape.com.

The acronym AIDS is redundant, loaded with stigma, and potentially harmful, according to a group of specialists who suggest replacing the term with “advanced HIV.”

The acronym AIDS has “outlived its usefulness and we should transition toward a more descriptive language that aligns with contemporary challenges in HIV,” reports Isaac Núñez, MD, from the Department of Medical Education, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán in Mexico City, Mexico, and colleagues.

People generally associate the acronym AIDS with patients who have no available treatment options and a short life expectancy, said Dr. Núñez. That mischaracterization may affect treatment decisions by patients and clinicians and could result in exaggerated infection-control measures.

Using the HIV/AIDS combination erroneously implies equivalence and can mislead the public and clinicians, which the authors explained in their Viewpoint article published in The Lancet HIV.
 

Original Reason for the Term

AIDS, which stands for acquired immunodeficiency syndrome, was coined in 1982 by the US Centers for Disease Control and Prevention (CDC) to name a disease with an unknown cause that affected people with weakened cell-mediated immunity.

“When HIV was found to be the cause of the disease (labeled HIV in 1986), the term AIDS, strictly speaking, became unnecessary,” Dr. Núñez said.

AIDS was originally intended as a case definition for surveillance purposes, and treatment decisions were based on whether patients met the case definition for AIDS, he pointed out.

“The fact that some people still do so in this day and age shows that this is not only unhelpful, but misleading and even harmful,” he noted. Without the label AIDS, clinicians can focus on whether and for how long people have been on treatment, whether they recently switched treatment, and other factors that will help determine appropriate care.
 

Some Organizations Removed AIDS From Their Names

Some organizations have already removed AIDS from their names. For example, the International AIDS Society–USA, which issues guidelines on antiretroviral treatment, changed its name to the International Antiviral Society–USA. 

In 2017, the name of AIDS.gov was changed to HIV.gov. In its explanation, the group wrote, “Today, people with HIV who are diagnosed early, linked to care, start antiretroviral therapy, and take it as prescribed can achieve life-long viral suppression that prevents HIV infection from progressing to AIDS.”

A different view on the term AIDS comes from Greg Millett, MPH, vice president at the Foundation for AIDS Research (amfAR) and the director of amfAR’s Public Policy Office. 

Although he believes that AIDS is an anachronistic term, as a researcher for more than 30 years in the field; a policy director in Washington; a scientist; and a person living with HIV, “it feels like a distinction without a difference. At least from where I sit, there are far more pressing issues that we’re facing as an HIV community,” Millett shared. 

For instance, “we’re seeing that global, as well as domestic, HIV funding is in, by far, the most precarious position that I’ve ever seen in the field. Calling it AIDS or HIV makes no difference in trying to alleviate that jeopardy,” he said.

Millett also said that the stigma and persecution and, in some cases, criminalization of people living with HIV or AIDS is pervasive and won’t go away with a name change, which is a point the authors also acknowledged.

“We need to focus on the social determinants of health,” he said. “That is the thing that is going to move the needle among people living with HIV, not nomenclature.”

Millett likens the argument to the one between Black and African American. “As a Black American, I remember fierce debates in the early ‘90s over whether we should be called African Americans or Blacks. Some argued that African American carried greater dignity and would help with self-esteem and address inequities by emphasizing that we are American. Many others said that it doesn’t make a difference.”

“It is clear that being called African American has not fixed intractable issues like poverty, structural racism, or inequities in incarceration,” he pointed out.
 

End the Epidemic, Not the Name 

The authors misinterpret the impact of the term on stigma, said James W. Curran, MD, MPH, dean emeritus of the Rollins School of Public Health and professor of epidemiology and global health at Emory University, both in Atlanta, Georgia. The term AIDS “is more likely attributed to the fatal nature of the infection itself,” without treatment, he explained, and the mode of transmission, exacerbated by homophobia.

“The term has been in widespread use for 40 years and recognized worldwide,” Dr. Curran, who led the nation’s efforts in the battle against HIV and AIDS at the CDC for 15 years before joining Emory as dean, said.

He also worries about the continued trajectory of lives lost: “Over 35 million people worldwide have perished from HIV/AIDS, including over 500,000 per year now.”

Meanwhile, “global programs such as PEPFAR [the US President’s Emergency Plan for AIDS Relief] are under fire and threatened by Congress as no longer necessary. Removing AIDS from the terminology may add to confusion,” making people think “that the epidemic is over,” he said.

Although the authors argue that keeping the term may cause harm, eliminating it might worsen a different kind of harm. “There is a risk that abolishing the term will further de-emphasize the importance of the problem, with no significant impact on stigma,” Dr. Curran added.

A version of this article appeared on Medscape.com.

A new American Gastroenterological Association (AGA) clinical practice update shines a light on cannabinoid hyperemesis syndrome (CHS).

CHS, which is triggered by chronic cannabis usage and manifests with GI and autonomic symptoms, is on the rise in the United States, yet underdiagnosis remains a challenge and clinical data are scarce, reported lead update panelist Alberto Rubio Tapia, MD, of Cleveland Clinic, Cleveland, Ohio, and colleagues.

Courtesy Cleveland Clinic

“Although cannabis use has been reported for many decades, some of its unique adverse effects of nausea, vomiting, and abdominal pain, termed CHS, were noted relatively recently,” the panelists wrote in Gastroenterology. “The objective of this article was to help practitioners define the appropriate approach to the diagnosis and management of CHS.”

According to the update, the typical CHS patient is male with a years-long history of daily or near-daily cannabis use. Paradoxically, while cannabis use drives this condition, some patients with CHS report that cannabis use relieves their symptoms.The update describes CHS as a subtype of cyclical vomiting syndrome (CVS), and offers diagnostic criteria for CHS, reproduced below verbatim:

• Clinical features: stereotypical episodic vomiting resembling CVS in terms of onset, with frequency 3 or more times annually;
• Cannabis use patterns: duration of cannabis use more than 1 year before symptom onset; frequency more than 4 times per week, on average;
• Cannabis cessation: resolution of symptoms after a period of abstinence from cannabis use for at least 6 months, or at least equal to the total duration of 3 typical vomiting cycles in that patient.

As CHS is a subtype of CVS, the update also provides an outline and management guide for this broader condition, which is characterized by four phases: inter-episodic, prodromal, emetic, and recovery.

During the inter-episodic phase, patients will have minimal or no symptoms, although almost one third will describe dyspepsia or nausea. Prophylactic medications in this period include tricyclics, mitochondrial supplements like CoQ10 and vitamin B12, NK1 antagonists, and anticonvulsants.

The prodromal phase is characterized by abdominal pain and nausea with a duration of 30-90 minutes. During this time patients may have autonomic symptoms like sweating and feeling hot or cold. Psychological symptoms may include feelings of panic and being “out of control.” Abortive medications are appropriate during this period, according to the update, like triptans and antiemetics.

Next comes the emetic phase, in which patients exhibit “relentless vomiting,” retching, abdominal pain, neurological symptoms and extreme thirst. Because an empty stomach may provide relief, inducing emesis may be considered, along with rest in a quiet dark room and supportive care.

Finally, the vomiting subsides during the recovery phase, when it is possible to restart oral intake and resume normal activities.

While this framework may be useful when managing patients with CHS, intervention should be centered around cannabis cessation, according to the update.

“For long-term management, counseling to achieve marijuana cessation and tricyclic antidepressants, such as amitriptyline, are the mainstay of therapy,” Dr. Rubio Tapia and colleagues wrote.

Advising patients to stop cannabis “cold turkey” is not recommended, they added, as this may bring on withdrawal symptoms, and it tends to be ineffective in this population, which has a high recidivism rate.

“Co-management with a psychologist or psychiatrist may be helpful for patients who have a lack of response to standard therapies or extensive psychiatric comorbidity,” the panelists wrote. “Anxiety and depression are very common associated conditions.”

Dr. Rubio Tapia and colleagues concluded with a call for more research.

“Further understanding of CHS pathophysiology and evidence-based therapies are urgently needed,” they wrote.

This update was commissioned and approved by the AGA. The update panelists disclosed relationships with Evoke Pharma, RedHill Biopharma, Takeda, and others.

A new American Gastroenterological Association (AGA) clinical practice update shines a light on cannabinoid hyperemesis syndrome (CHS).

CHS, which is triggered by chronic cannabis usage and manifests with GI and autonomic symptoms, is on the rise in the United States, yet underdiagnosis remains a challenge and clinical data are scarce, reported lead update panelist Alberto Rubio Tapia, MD, of Cleveland Clinic, Cleveland, Ohio, and colleagues.

Courtesy Cleveland Clinic

“Although cannabis use has been reported for many decades, some of its unique adverse effects of nausea, vomiting, and abdominal pain, termed CHS, were noted relatively recently,” the panelists wrote in Gastroenterology. “The objective of this article was to help practitioners define the appropriate approach to the diagnosis and management of CHS.”

According to the update, the typical CHS patient is male with a years-long history of daily or near-daily cannabis use. Paradoxically, while cannabis use drives this condition, some patients with CHS report that cannabis use relieves their symptoms.The update describes CHS as a subtype of cyclical vomiting syndrome (CVS), and offers diagnostic criteria for CHS, reproduced below verbatim:

• Clinical features: stereotypical episodic vomiting resembling CVS in terms of onset, with frequency 3 or more times annually;
• Cannabis use patterns: duration of cannabis use more than 1 year before symptom onset; frequency more than 4 times per week, on average;
• Cannabis cessation: resolution of symptoms after a period of abstinence from cannabis use for at least 6 months, or at least equal to the total duration of 3 typical vomiting cycles in that patient.

As CHS is a subtype of CVS, the update also provides an outline and management guide for this broader condition, which is characterized by four phases: inter-episodic, prodromal, emetic, and recovery.

During the inter-episodic phase, patients will have minimal or no symptoms, although almost one third will describe dyspepsia or nausea. Prophylactic medications in this period include tricyclics, mitochondrial supplements like CoQ10 and vitamin B12, NK1 antagonists, and anticonvulsants.

The prodromal phase is characterized by abdominal pain and nausea with a duration of 30-90 minutes. During this time patients may have autonomic symptoms like sweating and feeling hot or cold. Psychological symptoms may include feelings of panic and being “out of control.” Abortive medications are appropriate during this period, according to the update, like triptans and antiemetics.

Next comes the emetic phase, in which patients exhibit “relentless vomiting,” retching, abdominal pain, neurological symptoms and extreme thirst. Because an empty stomach may provide relief, inducing emesis may be considered, along with rest in a quiet dark room and supportive care.

Finally, the vomiting subsides during the recovery phase, when it is possible to restart oral intake and resume normal activities.

While this framework may be useful when managing patients with CHS, intervention should be centered around cannabis cessation, according to the update.

“For long-term management, counseling to achieve marijuana cessation and tricyclic antidepressants, such as amitriptyline, are the mainstay of therapy,” Dr. Rubio Tapia and colleagues wrote.

Advising patients to stop cannabis “cold turkey” is not recommended, they added, as this may bring on withdrawal symptoms, and it tends to be ineffective in this population, which has a high recidivism rate.

“Co-management with a psychologist or psychiatrist may be helpful for patients who have a lack of response to standard therapies or extensive psychiatric comorbidity,” the panelists wrote. “Anxiety and depression are very common associated conditions.”

Dr. Rubio Tapia and colleagues concluded with a call for more research.

“Further understanding of CHS pathophysiology and evidence-based therapies are urgently needed,” they wrote.

This update was commissioned and approved by the AGA. The update panelists disclosed relationships with Evoke Pharma, RedHill Biopharma, Takeda, and others.

A new American Gastroenterological Association (AGA) clinical practice update shines a light on cannabinoid hyperemesis syndrome (CHS).

CHS, which is triggered by chronic cannabis usage and manifests with GI and autonomic symptoms, is on the rise in the United States, yet underdiagnosis remains a challenge and clinical data are scarce, reported lead update panelist Alberto Rubio Tapia, MD, of Cleveland Clinic, Cleveland, Ohio, and colleagues.

Courtesy Cleveland Clinic

“Although cannabis use has been reported for many decades, some of its unique adverse effects of nausea, vomiting, and abdominal pain, termed CHS, were noted relatively recently,” the panelists wrote in Gastroenterology. “The objective of this article was to help practitioners define the appropriate approach to the diagnosis and management of CHS.”

According to the update, the typical CHS patient is male with a years-long history of daily or near-daily cannabis use. Paradoxically, while cannabis use drives this condition, some patients with CHS report that cannabis use relieves their symptoms.The update describes CHS as a subtype of cyclical vomiting syndrome (CVS), and offers diagnostic criteria for CHS, reproduced below verbatim:

• Clinical features: stereotypical episodic vomiting resembling CVS in terms of onset, with frequency 3 or more times annually;
• Cannabis use patterns: duration of cannabis use more than 1 year before symptom onset; frequency more than 4 times per week, on average;
• Cannabis cessation: resolution of symptoms after a period of abstinence from cannabis use for at least 6 months, or at least equal to the total duration of 3 typical vomiting cycles in that patient.

As CHS is a subtype of CVS, the update also provides an outline and management guide for this broader condition, which is characterized by four phases: inter-episodic, prodromal, emetic, and recovery.

During the inter-episodic phase, patients will have minimal or no symptoms, although almost one third will describe dyspepsia or nausea. Prophylactic medications in this period include tricyclics, mitochondrial supplements like CoQ10 and vitamin B12, NK1 antagonists, and anticonvulsants.

The prodromal phase is characterized by abdominal pain and nausea with a duration of 30-90 minutes. During this time patients may have autonomic symptoms like sweating and feeling hot or cold. Psychological symptoms may include feelings of panic and being “out of control.” Abortive medications are appropriate during this period, according to the update, like triptans and antiemetics.

Next comes the emetic phase, in which patients exhibit “relentless vomiting,” retching, abdominal pain, neurological symptoms and extreme thirst. Because an empty stomach may provide relief, inducing emesis may be considered, along with rest in a quiet dark room and supportive care.

Finally, the vomiting subsides during the recovery phase, when it is possible to restart oral intake and resume normal activities.

While this framework may be useful when managing patients with CHS, intervention should be centered around cannabis cessation, according to the update.

“For long-term management, counseling to achieve marijuana cessation and tricyclic antidepressants, such as amitriptyline, are the mainstay of therapy,” Dr. Rubio Tapia and colleagues wrote.

Advising patients to stop cannabis “cold turkey” is not recommended, they added, as this may bring on withdrawal symptoms, and it tends to be ineffective in this population, which has a high recidivism rate.

“Co-management with a psychologist or psychiatrist may be helpful for patients who have a lack of response to standard therapies or extensive psychiatric comorbidity,” the panelists wrote. “Anxiety and depression are very common associated conditions.”

Dr. Rubio Tapia and colleagues concluded with a call for more research.

“Further understanding of CHS pathophysiology and evidence-based therapies are urgently needed,” they wrote.

This update was commissioned and approved by the AGA. The update panelists disclosed relationships with Evoke Pharma, RedHill Biopharma, Takeda, and others.

Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL)–targeting therapies still hold promise for treating cholangiocarcinoma (CCA) despite disappointing results in previous preclinical research, primarily due to the adaptive resistance and unexpected immune modulation, according to investigators.

Those prior studies evaluated a combination of immunotherapy and TRAIL agonism, but selective TRAIL antagonism shows greater potential via dual ligand/receptor (TRAIL/TRAIL-R) targeting to block immunosuppression, reported lead author Emilien J. Loeuillard, PhD, of Mayo Clinic, Rochester, Minnesota, and colleagues.

Courtesy Dr. Emilien J. Loeuillard

“The TRAIL/TRAIL-R system has garnered considerable interest in cancer biology, especially as a potential anticancer therapy,” the investigators wrote in Cellular and Molecular Gastroenterology and Hepatology. “However, TRAIL-R agonists have had very limited anticancer activity in human beings, challenging this concept of TRAIL as an anticancer agent.”

This may be because they were working in the wrong direction, Dr. Loeuillard and colleagues suggested, citing recent work linking TRAIL with tumor proliferation and invasion, possibly via modification of the tumor immune microenvironment.

Exact mechanisms of modification, however, remain unclear. While TRAIL has been associated with tumor-promoting effects like induction of a promyeloid secretome in adenocarcinoma, it has also been linked with anticancer effects like activation of natural killer cells and cytotoxic T lymphocytes.

“Thus, the potency and hierarchy of TRAIL anticancer vs procancer processes in cancer biology has yet to be defined,” the investigators wrote.

While TRAIL ligation of cognate receptors has been previously investigated and shown to trigger proapoptotic signaling pathways, noncanonical TRAIL-mediated signaling remains largely unexplored, particularly in CCA.

The present study evaluated TRAIL biology in CCA using immunocompetent mouse models.

These experiments showed that noncanonical TRAIL signaling immunosuppresses the tumor microenvironment by increasing quantity and activity of myeloid-derived suppressor cells (MDSCs). Blocking noncanonical TRAIL signaling by selective deletion of TRAIL-R in immune cells had significantly reduced tumor volumes alongside fewer MDSCs, driven by FLICE inhibitory protein (cFLIP)-dependent nuclear factor kappa-B activation (NF-kappa-B) in MDSCs, which has antiapoptotic activity. While MDSCs present one possible target in this chain of immunosuppression, “therapeutic strategies for targeting MDSCs are limited,” the investigators wrote, noting that available myeloid modulators have fallen short in clinical trials.

Instead, cFLIP may be a convincing option, they suggested, as targeting cFLIP can sensitize cancer cells to proapoptotic TRAIL signaling. What’s more, cFLIP appears to protect MDSCs from TRAIL-mediated apoptosis, so taking out this barrier could render MDSCs susceptible to therapy.

“Our studies suggest that switching prosurvival/proliferation TRAIL signaling to canonical proapoptotic TRAIL signaling will promote MDSC apoptosis, which in turn has therapeutic implications for CCA suppression,” the investigators wrote.

Hope therefore remains for targeting TRAIL in patients with CCA, but with selective antagonism instead of agonism, as previously attempted.

“In summary, our findings support the role of selective therapeutic targeting of TRAIL-positive cancer cells in an effort to block TRAIL/TRAIL-R–mediated tumor immunosuppression,” Dr. Loeuillard and colleagues concluded.

This study was funded by the Cholangiocarcinoma Foundation and the Mayo Clinic Eagles 5th District Cancer Telethon Funds for Research Fellowship Program, the CTSA/National Center for Advancing Translational Science, the National Institutes of Health/National Cancer Institute, and others. The investigators disclosed no conflicts of interest.

Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL)–targeting therapies still hold promise for treating cholangiocarcinoma (CCA) despite disappointing results in previous preclinical research, primarily due to the adaptive resistance and unexpected immune modulation, according to investigators.

Those prior studies evaluated a combination of immunotherapy and TRAIL agonism, but selective TRAIL antagonism shows greater potential via dual ligand/receptor (TRAIL/TRAIL-R) targeting to block immunosuppression, reported lead author Emilien J. Loeuillard, PhD, of Mayo Clinic, Rochester, Minnesota, and colleagues.

Courtesy Dr. Emilien J. Loeuillard

“The TRAIL/TRAIL-R system has garnered considerable interest in cancer biology, especially as a potential anticancer therapy,” the investigators wrote in Cellular and Molecular Gastroenterology and Hepatology. “However, TRAIL-R agonists have had very limited anticancer activity in human beings, challenging this concept of TRAIL as an anticancer agent.”

This may be because they were working in the wrong direction, Dr. Loeuillard and colleagues suggested, citing recent work linking TRAIL with tumor proliferation and invasion, possibly via modification of the tumor immune microenvironment.

Exact mechanisms of modification, however, remain unclear. While TRAIL has been associated with tumor-promoting effects like induction of a promyeloid secretome in adenocarcinoma, it has also been linked with anticancer effects like activation of natural killer cells and cytotoxic T lymphocytes.

“Thus, the potency and hierarchy of TRAIL anticancer vs procancer processes in cancer biology has yet to be defined,” the investigators wrote.

While TRAIL ligation of cognate receptors has been previously investigated and shown to trigger proapoptotic signaling pathways, noncanonical TRAIL-mediated signaling remains largely unexplored, particularly in CCA.

The present study evaluated TRAIL biology in CCA using immunocompetent mouse models.

These experiments showed that noncanonical TRAIL signaling immunosuppresses the tumor microenvironment by increasing quantity and activity of myeloid-derived suppressor cells (MDSCs). Blocking noncanonical TRAIL signaling by selective deletion of TRAIL-R in immune cells had significantly reduced tumor volumes alongside fewer MDSCs, driven by FLICE inhibitory protein (cFLIP)-dependent nuclear factor kappa-B activation (NF-kappa-B) in MDSCs, which has antiapoptotic activity. While MDSCs present one possible target in this chain of immunosuppression, “therapeutic strategies for targeting MDSCs are limited,” the investigators wrote, noting that available myeloid modulators have fallen short in clinical trials.

Instead, cFLIP may be a convincing option, they suggested, as targeting cFLIP can sensitize cancer cells to proapoptotic TRAIL signaling. What’s more, cFLIP appears to protect MDSCs from TRAIL-mediated apoptosis, so taking out this barrier could render MDSCs susceptible to therapy.

“Our studies suggest that switching prosurvival/proliferation TRAIL signaling to canonical proapoptotic TRAIL signaling will promote MDSC apoptosis, which in turn has therapeutic implications for CCA suppression,” the investigators wrote.

Hope therefore remains for targeting TRAIL in patients with CCA, but with selective antagonism instead of agonism, as previously attempted.

“In summary, our findings support the role of selective therapeutic targeting of TRAIL-positive cancer cells in an effort to block TRAIL/TRAIL-R–mediated tumor immunosuppression,” Dr. Loeuillard and colleagues concluded.

This study was funded by the Cholangiocarcinoma Foundation and the Mayo Clinic Eagles 5th District Cancer Telethon Funds for Research Fellowship Program, the CTSA/National Center for Advancing Translational Science, the National Institutes of Health/National Cancer Institute, and others. The investigators disclosed no conflicts of interest.

Tumor necrosis factor–related apoptosis-inducing ligand (TRAIL)–targeting therapies still hold promise for treating cholangiocarcinoma (CCA) despite disappointing results in previous preclinical research, primarily due to the adaptive resistance and unexpected immune modulation, according to investigators.

Those prior studies evaluated a combination of immunotherapy and TRAIL agonism, but selective TRAIL antagonism shows greater potential via dual ligand/receptor (TRAIL/TRAIL-R) targeting to block immunosuppression, reported lead author Emilien J. Loeuillard, PhD, of Mayo Clinic, Rochester, Minnesota, and colleagues.

Courtesy Dr. Emilien J. Loeuillard

“The TRAIL/TRAIL-R system has garnered considerable interest in cancer biology, especially as a potential anticancer therapy,” the investigators wrote in Cellular and Molecular Gastroenterology and Hepatology. “However, TRAIL-R agonists have had very limited anticancer activity in human beings, challenging this concept of TRAIL as an anticancer agent.”

This may be because they were working in the wrong direction, Dr. Loeuillard and colleagues suggested, citing recent work linking TRAIL with tumor proliferation and invasion, possibly via modification of the tumor immune microenvironment.

Exact mechanisms of modification, however, remain unclear. While TRAIL has been associated with tumor-promoting effects like induction of a promyeloid secretome in adenocarcinoma, it has also been linked with anticancer effects like activation of natural killer cells and cytotoxic T lymphocytes.

“Thus, the potency and hierarchy of TRAIL anticancer vs procancer processes in cancer biology has yet to be defined,” the investigators wrote.

While TRAIL ligation of cognate receptors has been previously investigated and shown to trigger proapoptotic signaling pathways, noncanonical TRAIL-mediated signaling remains largely unexplored, particularly in CCA.

The present study evaluated TRAIL biology in CCA using immunocompetent mouse models.

These experiments showed that noncanonical TRAIL signaling immunosuppresses the tumor microenvironment by increasing quantity and activity of myeloid-derived suppressor cells (MDSCs). Blocking noncanonical TRAIL signaling by selective deletion of TRAIL-R in immune cells had significantly reduced tumor volumes alongside fewer MDSCs, driven by FLICE inhibitory protein (cFLIP)-dependent nuclear factor kappa-B activation (NF-kappa-B) in MDSCs, which has antiapoptotic activity. While MDSCs present one possible target in this chain of immunosuppression, “therapeutic strategies for targeting MDSCs are limited,” the investigators wrote, noting that available myeloid modulators have fallen short in clinical trials.

Instead, cFLIP may be a convincing option, they suggested, as targeting cFLIP can sensitize cancer cells to proapoptotic TRAIL signaling. What’s more, cFLIP appears to protect MDSCs from TRAIL-mediated apoptosis, so taking out this barrier could render MDSCs susceptible to therapy.

“Our studies suggest that switching prosurvival/proliferation TRAIL signaling to canonical proapoptotic TRAIL signaling will promote MDSC apoptosis, which in turn has therapeutic implications for CCA suppression,” the investigators wrote.

Hope therefore remains for targeting TRAIL in patients with CCA, but with selective antagonism instead of agonism, as previously attempted.

“In summary, our findings support the role of selective therapeutic targeting of TRAIL-positive cancer cells in an effort to block TRAIL/TRAIL-R–mediated tumor immunosuppression,” Dr. Loeuillard and colleagues concluded.

This study was funded by the Cholangiocarcinoma Foundation and the Mayo Clinic Eagles 5th District Cancer Telethon Funds for Research Fellowship Program, the CTSA/National Center for Advancing Translational Science, the National Institutes of Health/National Cancer Institute, and others. The investigators disclosed no conflicts of interest.

Histologic inflammation in women with inflammatory bowel disease (IBD) may lead to reduced fertility, according to a Swedish nationwide cohort study.

Reduced fertility was linked with histologic inflammation even in the absence of clinical disease activity, highlighting the importance of achieving deep remission in women planning pregnancy, reported lead author Karl Mårild, MD, PhD, of Sahlgrenska Academy, Gothenburg, Sweden, and colleagues.

“Reduced female fertility (ie, number of live births) is believed to be primarily confined to women with clinically active IBD, especially in Crohn’s disease (CD), where symptoms may inhibit sexual activity, and inflammation may affect the fallopian tubes and ovaries,” the investigators wrote in Gastroenterology. “Despite the increasing appreciation of histologic activity in IBD, its association with female fertility has not been clarified, including whether histologic activity in the absence of clinical disease activity impairs fertility.”

Courtesy University of Gothenburg

Dr. Mårild and colleagues aimed to address this knowledge gap by analyzing fertility rates and histologic inflammation or IBD activity in two cohorts of women with IBD aged 15-44 years. The first group included approximately 21,000 women with and without histologic inflammation from 1990 to 2016. The second group included approximately 25,000 women with or without IBD clinical activity from 2006 to 2020. In each group, the relationship between fertility and IBD was compared with fertility in matched general population comparator individuals.

This approach showed that clinical IBD activity was associated with an adjusted fertility rate ratio (aFRR) of 0.76 (95% CI, 0.72-0.79), which equates to one fewer child per six women with 10 years of clinical activity. Impacts on fertility were similar for UC (aFRR, 0.75) and CD (aFRR, 0.76).

“Fertility rates were notably reduced during periods of clinical IBD activity and, contrary to a generally accepted belief, equally reduced in clinically active UC and CD,” the investigators wrote. “Besides inflammation, clinically active IBD may reduce fertility through psychological mechanisms (eg, depression), dyspareunia (especially in perianal CD), bowel pain, urgency, and other symptoms that hinder sexual activity.”

Compared with histologic remission, histologic inflammation was also associated with reduced fertility (aFRR, 0.90). This means that in periods of histologic inflammation, 6.35 live births occurred per 100 person-years of follow-up, compared with 7.09 lives births for periods of histologic remission. This amounts to one fewer child per 14 women with 10 years of histologic inflammation.

Finally, the study revealed that, in women with clinically quiescent IBD, those with histologic inflammation had significantly reduced fertility, compared with those in histologic remission (aFRR, 0.85). This association persisted after controlling for contraceptive use.

“Even if histologic inflammation was associated with an overall modest fertility reduction … its impact on the individual might be substantial, with potential ramifications beyond reproductive health, given that reduced female fertility is linked to poor quality of life and mental health,” Dr. Mårild and colleagues wrote. “At a societal level, involuntary childlessness causes high and increasing costs, highlighting the need to focus on preventable causes of reduced fertility.”

The investigators suggested that inflammation may be driving infertility by reducing ovulation and fertilization, or by reducing endometrial receptivity, which increases risk of pregnancy loss.

“This is the first study, to our knowledge, to show reduced fertility during histologic inflammation in IBD compared to histologic remission,” the investigators wrote. “Our findings suggest that achieving histologic remission may improve the fertility of women with IBD, even in the absence of clinically defined disease activity.”

The investigators disclosed relationships with AbbVie, Pfizer, Janssen, and others.

Histologic inflammation in women with inflammatory bowel disease (IBD) may lead to reduced fertility, according to a Swedish nationwide cohort study.

Reduced fertility was linked with histologic inflammation even in the absence of clinical disease activity, highlighting the importance of achieving deep remission in women planning pregnancy, reported lead author Karl Mårild, MD, PhD, of Sahlgrenska Academy, Gothenburg, Sweden, and colleagues.

“Reduced female fertility (ie, number of live births) is believed to be primarily confined to women with clinically active IBD, especially in Crohn’s disease (CD), where symptoms may inhibit sexual activity, and inflammation may affect the fallopian tubes and ovaries,” the investigators wrote in Gastroenterology. “Despite the increasing appreciation of histologic activity in IBD, its association with female fertility has not been clarified, including whether histologic activity in the absence of clinical disease activity impairs fertility.”

Courtesy University of Gothenburg

Dr. Mårild and colleagues aimed to address this knowledge gap by analyzing fertility rates and histologic inflammation or IBD activity in two cohorts of women with IBD aged 15-44 years. The first group included approximately 21,000 women with and without histologic inflammation from 1990 to 2016. The second group included approximately 25,000 women with or without IBD clinical activity from 2006 to 2020. In each group, the relationship between fertility and IBD was compared with fertility in matched general population comparator individuals.

This approach showed that clinical IBD activity was associated with an adjusted fertility rate ratio (aFRR) of 0.76 (95% CI, 0.72-0.79), which equates to one fewer child per six women with 10 years of clinical activity. Impacts on fertility were similar for UC (aFRR, 0.75) and CD (aFRR, 0.76).

“Fertility rates were notably reduced during periods of clinical IBD activity and, contrary to a generally accepted belief, equally reduced in clinically active UC and CD,” the investigators wrote. “Besides inflammation, clinically active IBD may reduce fertility through psychological mechanisms (eg, depression), dyspareunia (especially in perianal CD), bowel pain, urgency, and other symptoms that hinder sexual activity.”

Compared with histologic remission, histologic inflammation was also associated with reduced fertility (aFRR, 0.90). This means that in periods of histologic inflammation, 6.35 live births occurred per 100 person-years of follow-up, compared with 7.09 lives births for periods of histologic remission. This amounts to one fewer child per 14 women with 10 years of histologic inflammation.

Finally, the study revealed that, in women with clinically quiescent IBD, those with histologic inflammation had significantly reduced fertility, compared with those in histologic remission (aFRR, 0.85). This association persisted after controlling for contraceptive use.

“Even if histologic inflammation was associated with an overall modest fertility reduction … its impact on the individual might be substantial, with potential ramifications beyond reproductive health, given that reduced female fertility is linked to poor quality of life and mental health,” Dr. Mårild and colleagues wrote. “At a societal level, involuntary childlessness causes high and increasing costs, highlighting the need to focus on preventable causes of reduced fertility.”

The investigators suggested that inflammation may be driving infertility by reducing ovulation and fertilization, or by reducing endometrial receptivity, which increases risk of pregnancy loss.

“This is the first study, to our knowledge, to show reduced fertility during histologic inflammation in IBD compared to histologic remission,” the investigators wrote. “Our findings suggest that achieving histologic remission may improve the fertility of women with IBD, even in the absence of clinically defined disease activity.”

The investigators disclosed relationships with AbbVie, Pfizer, Janssen, and others.

Histologic inflammation in women with inflammatory bowel disease (IBD) may lead to reduced fertility, according to a Swedish nationwide cohort study.

Reduced fertility was linked with histologic inflammation even in the absence of clinical disease activity, highlighting the importance of achieving deep remission in women planning pregnancy, reported lead author Karl Mårild, MD, PhD, of Sahlgrenska Academy, Gothenburg, Sweden, and colleagues.

“Reduced female fertility (ie, number of live births) is believed to be primarily confined to women with clinically active IBD, especially in Crohn’s disease (CD), where symptoms may inhibit sexual activity, and inflammation may affect the fallopian tubes and ovaries,” the investigators wrote in Gastroenterology. “Despite the increasing appreciation of histologic activity in IBD, its association with female fertility has not been clarified, including whether histologic activity in the absence of clinical disease activity impairs fertility.”

Courtesy University of Gothenburg

Dr. Mårild and colleagues aimed to address this knowledge gap by analyzing fertility rates and histologic inflammation or IBD activity in two cohorts of women with IBD aged 15-44 years. The first group included approximately 21,000 women with and without histologic inflammation from 1990 to 2016. The second group included approximately 25,000 women with or without IBD clinical activity from 2006 to 2020. In each group, the relationship between fertility and IBD was compared with fertility in matched general population comparator individuals.

This approach showed that clinical IBD activity was associated with an adjusted fertility rate ratio (aFRR) of 0.76 (95% CI, 0.72-0.79), which equates to one fewer child per six women with 10 years of clinical activity. Impacts on fertility were similar for UC (aFRR, 0.75) and CD (aFRR, 0.76).

“Fertility rates were notably reduced during periods of clinical IBD activity and, contrary to a generally accepted belief, equally reduced in clinically active UC and CD,” the investigators wrote. “Besides inflammation, clinically active IBD may reduce fertility through psychological mechanisms (eg, depression), dyspareunia (especially in perianal CD), bowel pain, urgency, and other symptoms that hinder sexual activity.”

Compared with histologic remission, histologic inflammation was also associated with reduced fertility (aFRR, 0.90). This means that in periods of histologic inflammation, 6.35 live births occurred per 100 person-years of follow-up, compared with 7.09 lives births for periods of histologic remission. This amounts to one fewer child per 14 women with 10 years of histologic inflammation.

Finally, the study revealed that, in women with clinically quiescent IBD, those with histologic inflammation had significantly reduced fertility, compared with those in histologic remission (aFRR, 0.85). This association persisted after controlling for contraceptive use.

“Even if histologic inflammation was associated with an overall modest fertility reduction … its impact on the individual might be substantial, with potential ramifications beyond reproductive health, given that reduced female fertility is linked to poor quality of life and mental health,” Dr. Mårild and colleagues wrote. “At a societal level, involuntary childlessness causes high and increasing costs, highlighting the need to focus on preventable causes of reduced fertility.”

The investigators suggested that inflammation may be driving infertility by reducing ovulation and fertilization, or by reducing endometrial receptivity, which increases risk of pregnancy loss.

“This is the first study, to our knowledge, to show reduced fertility during histologic inflammation in IBD compared to histologic remission,” the investigators wrote. “Our findings suggest that achieving histologic remission may improve the fertility of women with IBD, even in the absence of clinically defined disease activity.”

The investigators disclosed relationships with AbbVie, Pfizer, Janssen, and others.

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The AGA Research Foundation, the charitable arm of the American Gastroenterological Association (AGA), plays an important role in medical research by providing grants to young scientists at a critical time in their career. The AGA Research Foundation’s mission is to raise funds to support young researchers in gastroenterology and hepatology.

The research program of the AGA has had an important impact on digestive disease research for the last 30 years. Ninety percent of investigators who received an AGA Research Scholar Award over the past 10 years have stayed in gastroenterology and hepatology research.

AGA grants have led to discoveries, including new approaches to down-regulate intestinal inflammation, a test for genetic predisposition to colon cancer, and autoimmune liver disease treatments. The importance of these awards is evidenced by the fact that virtually every major advance leading to the understanding, prevention, treatment, and cure of digestive diseases has been made in the research laboratory of a talented young investigator.

At a time when funds from the National Institutes of Health and other traditional sources of support are in decline, the AGA Research Foundation is committed and ready to support young investigators and fund discoveries that will continue to improve GI practice and better patient care.

The AGA Research Foundation provides a key source of funding at a critical juncture in a young researcher’s career. By joining AGA members and donors in donating to the AGA Research Foundation, you will ensure that researchers have opportunities to continue their life-saving work.

The AGA Research Foundation, the charitable arm of the American Gastroenterological Association (AGA), plays an important role in medical research by providing grants to young scientists at a critical time in their career. The AGA Research Foundation’s mission is to raise funds to support young researchers in gastroenterology and hepatology.

The research program of the AGA has had an important impact on digestive disease research for the last 30 years. Ninety percent of investigators who received an AGA Research Scholar Award over the past 10 years have stayed in gastroenterology and hepatology research.

AGA grants have led to discoveries, including new approaches to down-regulate intestinal inflammation, a test for genetic predisposition to colon cancer, and autoimmune liver disease treatments. The importance of these awards is evidenced by the fact that virtually every major advance leading to the understanding, prevention, treatment, and cure of digestive diseases has been made in the research laboratory of a talented young investigator.

At a time when funds from the National Institutes of Health and other traditional sources of support are in decline, the AGA Research Foundation is committed and ready to support young investigators and fund discoveries that will continue to improve GI practice and better patient care.

The AGA Research Foundation provides a key source of funding at a critical juncture in a young researcher’s career. By joining AGA members and donors in donating to the AGA Research Foundation, you will ensure that researchers have opportunities to continue their life-saving work.

The AGA Research Foundation, the charitable arm of the American Gastroenterological Association (AGA), plays an important role in medical research by providing grants to young scientists at a critical time in their career. The AGA Research Foundation’s mission is to raise funds to support young researchers in gastroenterology and hepatology.

The research program of the AGA has had an important impact on digestive disease research for the last 30 years. Ninety percent of investigators who received an AGA Research Scholar Award over the past 10 years have stayed in gastroenterology and hepatology research.

AGA grants have led to discoveries, including new approaches to down-regulate intestinal inflammation, a test for genetic predisposition to colon cancer, and autoimmune liver disease treatments. The importance of these awards is evidenced by the fact that virtually every major advance leading to the understanding, prevention, treatment, and cure of digestive diseases has been made in the research laboratory of a talented young investigator.

At a time when funds from the National Institutes of Health and other traditional sources of support are in decline, the AGA Research Foundation is committed and ready to support young investigators and fund discoveries that will continue to improve GI practice and better patient care.

The AGA Research Foundation provides a key source of funding at a critical juncture in a young researcher’s career. By joining AGA members and donors in donating to the AGA Research Foundation, you will ensure that researchers have opportunities to continue their life-saving work.

We are looking forward to seeing you in our hometown for Digestive Disease Week® (DDW) 2024!

As you plan your schedule, here’s a listing of AGA’s free networking events. For more details and featured programming, visit www.gastro.org/DDW.

American Gastroenterological Association

Meetups at AGA Central (L Street Bridge)

Network with like-minded attendees, build your #AGAGastroSquad and enjoy refreshments at our meetups.

Saturday, May 18

• 3 p.m.: Advocacy champions meetup – A “thank you” for everyone who supported our grassroots advocacy efforts this year!

Sunday, May 19

• 11 a.m.: NPPA meetup
• 1 p.m.: Dietitian meetup
• 3 p.m.: IBD meetup – Happy World IBD Day!

Monday, May 20

• 11 a.m.: Trainee meetup – Mingle with AGA journal editors!
• 1 p.m.: Psychologists meetup
• 3 p.m.: Clinician meetup

Tuesday, May 21

• 11 a.m.: Innovator meetup

RSVP and add to your calendar: www.signupgenius.com/go/10C0E4EA4AE2DA2F5C43-48529281-agacentral#/

Additional events for trainees

We have more opportunities for you to network at DDW! The following events all take place on Sunday, May 19.

• 10 a.m.: Live recording: Small Talk, Big Topics – Mingle with fellow trainees and early career GIs during a live recording of AGA’s podcast. Our hosts will interview fellowship program director Dr. Janice Jou.

[Location: AGA Central (L Street Bridge)]

• 1 p.m.: Meet-the-Experts: AGA Leadership – Held in the DDW Trainee and Early Career Lounge, these sessions are an opportunity for early career attendees to get tips from those further along in their career.

[Location: DDW Trainee and Early Career Lounge]

• 2 p.m.: AGA/DHPA Networking Hour – Join us for an hour of guided networking and 4-way Jeopardy!

[Location: DDW Trainee and Early Career Lounge]

We are looking forward to seeing you in our hometown for Digestive Disease Week® (DDW) 2024!

As you plan your schedule, here’s a listing of AGA’s free networking events. For more details and featured programming, visit www.gastro.org/DDW.

American Gastroenterological Association

Meetups at AGA Central (L Street Bridge)

Network with like-minded attendees, build your #AGAGastroSquad and enjoy refreshments at our meetups.

Saturday, May 18

• 3 p.m.: Advocacy champions meetup – A “thank you” for everyone who supported our grassroots advocacy efforts this year!

Sunday, May 19

• 11 a.m.: NPPA meetup
• 1 p.m.: Dietitian meetup
• 3 p.m.: IBD meetup – Happy World IBD Day!

Monday, May 20

• 11 a.m.: Trainee meetup – Mingle with AGA journal editors!
• 1 p.m.: Psychologists meetup
• 3 p.m.: Clinician meetup

Tuesday, May 21

• 11 a.m.: Innovator meetup

RSVP and add to your calendar: www.signupgenius.com/go/10C0E4EA4AE2DA2F5C43-48529281-agacentral#/

Additional events for trainees

We have more opportunities for you to network at DDW! The following events all take place on Sunday, May 19.

• 10 a.m.: Live recording: Small Talk, Big Topics – Mingle with fellow trainees and early career GIs during a live recording of AGA’s podcast. Our hosts will interview fellowship program director Dr. Janice Jou.

[Location: AGA Central (L Street Bridge)]

• 1 p.m.: Meet-the-Experts: AGA Leadership – Held in the DDW Trainee and Early Career Lounge, these sessions are an opportunity for early career attendees to get tips from those further along in their career.

[Location: DDW Trainee and Early Career Lounge]

• 2 p.m.: AGA/DHPA Networking Hour – Join us for an hour of guided networking and 4-way Jeopardy!

[Location: DDW Trainee and Early Career Lounge]

We are looking forward to seeing you in our hometown for Digestive Disease Week® (DDW) 2024!

As you plan your schedule, here’s a listing of AGA’s free networking events. For more details and featured programming, visit www.gastro.org/DDW.

American Gastroenterological Association

Meetups at AGA Central (L Street Bridge)

Network with like-minded attendees, build your #AGAGastroSquad and enjoy refreshments at our meetups.

Saturday, May 18

• 3 p.m.: Advocacy champions meetup – A “thank you” for everyone who supported our grassroots advocacy efforts this year!

Sunday, May 19

• 11 a.m.: NPPA meetup
• 1 p.m.: Dietitian meetup
• 3 p.m.: IBD meetup – Happy World IBD Day!

Monday, May 20

• 11 a.m.: Trainee meetup – Mingle with AGA journal editors!
• 1 p.m.: Psychologists meetup
• 3 p.m.: Clinician meetup

Tuesday, May 21

• 11 a.m.: Innovator meetup

RSVP and add to your calendar: www.signupgenius.com/go/10C0E4EA4AE2DA2F5C43-48529281-agacentral#/

Additional events for trainees

We have more opportunities for you to network at DDW! The following events all take place on Sunday, May 19.

• 10 a.m.: Live recording: Small Talk, Big Topics – Mingle with fellow trainees and early career GIs during a live recording of AGA’s podcast. Our hosts will interview fellowship program director Dr. Janice Jou.

[Location: AGA Central (L Street Bridge)]

• 1 p.m.: Meet-the-Experts: AGA Leadership – Held in the DDW Trainee and Early Career Lounge, these sessions are an opportunity for early career attendees to get tips from those further along in their career.

[Location: DDW Trainee and Early Career Lounge]

• 2 p.m.: AGA/DHPA Networking Hour – Join us for an hour of guided networking and 4-way Jeopardy!

[Location: DDW Trainee and Early Career Lounge]

Rep. Yadira Caraveo, MD (D-CO), recently introduced the Colorectal Cancer Early Detection Act along with Reps. Donald Payne Jr. (D-NJ), Haley Stevens (D-MI), and Terri Sewell (D-AL).

The Colorectal Cancer Early Detection Act would award grants to states to promote colorectal cancer prevention and early detection efforts to individuals under age 45.

• Screen increased risk and high-risk individuals under age 45 for colorectal cancer.
• Provide appropriate referrals for medical treatment.
• Develop and carry out a public education and awareness campaign for the detection and control of CRC.
• Improve the education and training of health providers in detecting and controlling CRC.
• Establish mechanisms through which states can monitor the quality of CRC screening procedures.
• Develop strategies to assess family history and genetic predispositions to CRC.
• Design patient and clinician decision support tools for CRC.
• Conduct surveillance to determine other risk factors for CRC in this population.

“Colorectal cancer is the second-leading cause of cancer death in the US and is increasing at an alarming rate in younger people. AGA celebrates Rep. Caraveo’s work to address this trend through education and awareness” said Barbara Jung, MD, AGA President.

We look forward to working with our congressional champions to increase screening rates and reverse the trend of early onset colorectal cancer!

Rep. Yadira Caraveo, MD (D-CO), recently introduced the Colorectal Cancer Early Detection Act along with Reps. Donald Payne Jr. (D-NJ), Haley Stevens (D-MI), and Terri Sewell (D-AL).

The Colorectal Cancer Early Detection Act would award grants to states to promote colorectal cancer prevention and early detection efforts to individuals under age 45.

• Screen increased risk and high-risk individuals under age 45 for colorectal cancer.
• Provide appropriate referrals for medical treatment.
• Develop and carry out a public education and awareness campaign for the detection and control of CRC.
• Improve the education and training of health providers in detecting and controlling CRC.
• Establish mechanisms through which states can monitor the quality of CRC screening procedures.
• Develop strategies to assess family history and genetic predispositions to CRC.
• Design patient and clinician decision support tools for CRC.
• Conduct surveillance to determine other risk factors for CRC in this population.

“Colorectal cancer is the second-leading cause of cancer death in the US and is increasing at an alarming rate in younger people. AGA celebrates Rep. Caraveo’s work to address this trend through education and awareness” said Barbara Jung, MD, AGA President.

We look forward to working with our congressional champions to increase screening rates and reverse the trend of early onset colorectal cancer!

Rep. Yadira Caraveo, MD (D-CO), recently introduced the Colorectal Cancer Early Detection Act along with Reps. Donald Payne Jr. (D-NJ), Haley Stevens (D-MI), and Terri Sewell (D-AL).

The Colorectal Cancer Early Detection Act would award grants to states to promote colorectal cancer prevention and early detection efforts to individuals under age 45.

• Screen increased risk and high-risk individuals under age 45 for colorectal cancer.
• Provide appropriate referrals for medical treatment.
• Develop and carry out a public education and awareness campaign for the detection and control of CRC.
• Improve the education and training of health providers in detecting and controlling CRC.
• Establish mechanisms through which states can monitor the quality of CRC screening procedures.
• Develop strategies to assess family history and genetic predispositions to CRC.
• Design patient and clinician decision support tools for CRC.
• Conduct surveillance to determine other risk factors for CRC in this population.

“Colorectal cancer is the second-leading cause of cancer death in the US and is increasing at an alarming rate in younger people. AGA celebrates Rep. Caraveo’s work to address this trend through education and awareness” said Barbara Jung, MD, AGA President.

We look forward to working with our congressional champions to increase screening rates and reverse the trend of early onset colorectal cancer!

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