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Early menopause linked with increased risk of heart problems
SEOUL, South Korea – Menopause before age 40 is associated with elevated risk of heart failure and atrial fibrillation, according to a study published in European Heart Journal, from the European Society of Cardiology (ESC). The study of more than 1.4 million women revealed that the younger the age at menopause, the higher the risk of heart failure and atrial fibrillation.
“Women with premature menopause should be aware that they may be more likely to develop heart failure or atrial fibrillation than their peers,” said study author Ga Eun Nam, MD, PhD, of Korea University College of Medicine, Seoul. “This may be good motivation to improve lifestyle habits known to be linked with heart disease, such as quitting smoking and exercising.”
Cardiovascular disease typically occurs up to 10 years later in women than men. Premenopausal women are thought to benefit from estrogen’s protective effect on the cardiovascular system. The cessation of menstruation and subsequent decline of estrogen levels may make women more vulnerable to cardiovascular disease.
A national population
Premature menopause affects 1% of women younger than 40 years, the ESC press release stated. Prior studies have found a link between premature (before age 40 years) and early (before age 45 years) menopause and cardiovascular disease overall, but the evidence for heart failure or atrial fibrillation alone is limited. This study examined the associations between premature menopause, age at menopause, and incident heart failure and atrial fibrillation. Data were obtained from the Korean National Health Insurance System (NHIS), which provides health screening at least every 2 years and includes 97% of the population.
The study included 1,401,175 postmenopausal women aged 30 years and older who completed the NHIS health checkup in 2009. Participants were monitored until the end of 2018 for new-onset heart failure and atrial fibrillation. Information was collected on demographics, health behaviors, and reproductive factors, including age at menopause and use of hormone replacement therapy (HRT). Age at menopause was split into four categories: younger than 40 years, 40-44 years, 45-49 years, and 50 years or older. Premature menopause was defined as having the final menstrual period before age 40 years.
Some 28,111 (2%) participants had a history of premature menopause. For these women, the average age at menopause was 36.7 years. The average age at study enrollment for women with and for those without a history of premature menopause was 60 and 61.5 years, respectively. During an average follow-up of 9.1 years, 42,699 (3.0%) developed heart failure, and 44,834 (3.2%) developed atrial fibrillation.
The researchers analyzed the association between history of premature menopause and incident heart failure and atrial fibrillation after adjusting for age, smoking, alcohol use, physical activity, income, body mass index, hypertension, type 2 diabetes, dyslipidemia, chronic kidney disease, coronary heart disease, HRT, and age at menarche. Women who experienced premature menopause had a 33% higher risk for heart failure and 9% higher risk for atrial fibrillation, compared with those who did not.
Reproductive history
The researchers then analyzed the associations between age at menopause and incidence of heart failure and atrial fibrillation after adjusting for the same factors as in the previous analyses. The risk for incident heart failure increased as the age at menopause decreased. Compared with women aged 50 years and older at menopause, those aged 45-49 years, 40-44 years, and younger than 40 years at menopause had 11%, 23%, and 39% greater risk for incident heart failure, respectively. Similarly, the risk for incident atrial fibrillation increased as the age at menopause decreased; the risk was 4%, 10%, and 11% higher for those aged 45-49 years, 40-44 years, and younger than 40 years at menopause, respectively, compared with women aged 50 years and older at menopause.
The authors said that several factors may explain the associations between menopausal age, heart failure, and atrial fibrillation, such as the drop in estrogen levels and changes in body fat distribution.
Dr. Nam concluded, “The misconception that heart disease primarily affects men has meant that sex-specific risk factors have been largely ignored. Evidence is growing that undergoing menopause before the age of 40 years may increase the likelihood of heart disease later in life. Our study indicates that reproductive history should be routinely considered in addition to traditional risk factors such as smoking when evaluating the future likelihood of heart failure and atrial fibrillation.”
A version of this article appeared on Medscape.com. This article was translated from the Medscape French edition.
SEOUL, South Korea – Menopause before age 40 is associated with elevated risk of heart failure and atrial fibrillation, according to a study published in European Heart Journal, from the European Society of Cardiology (ESC). The study of more than 1.4 million women revealed that the younger the age at menopause, the higher the risk of heart failure and atrial fibrillation.
“Women with premature menopause should be aware that they may be more likely to develop heart failure or atrial fibrillation than their peers,” said study author Ga Eun Nam, MD, PhD, of Korea University College of Medicine, Seoul. “This may be good motivation to improve lifestyle habits known to be linked with heart disease, such as quitting smoking and exercising.”
Cardiovascular disease typically occurs up to 10 years later in women than men. Premenopausal women are thought to benefit from estrogen’s protective effect on the cardiovascular system. The cessation of menstruation and subsequent decline of estrogen levels may make women more vulnerable to cardiovascular disease.
A national population
Premature menopause affects 1% of women younger than 40 years, the ESC press release stated. Prior studies have found a link between premature (before age 40 years) and early (before age 45 years) menopause and cardiovascular disease overall, but the evidence for heart failure or atrial fibrillation alone is limited. This study examined the associations between premature menopause, age at menopause, and incident heart failure and atrial fibrillation. Data were obtained from the Korean National Health Insurance System (NHIS), which provides health screening at least every 2 years and includes 97% of the population.
The study included 1,401,175 postmenopausal women aged 30 years and older who completed the NHIS health checkup in 2009. Participants were monitored until the end of 2018 for new-onset heart failure and atrial fibrillation. Information was collected on demographics, health behaviors, and reproductive factors, including age at menopause and use of hormone replacement therapy (HRT). Age at menopause was split into four categories: younger than 40 years, 40-44 years, 45-49 years, and 50 years or older. Premature menopause was defined as having the final menstrual period before age 40 years.
Some 28,111 (2%) participants had a history of premature menopause. For these women, the average age at menopause was 36.7 years. The average age at study enrollment for women with and for those without a history of premature menopause was 60 and 61.5 years, respectively. During an average follow-up of 9.1 years, 42,699 (3.0%) developed heart failure, and 44,834 (3.2%) developed atrial fibrillation.
The researchers analyzed the association between history of premature menopause and incident heart failure and atrial fibrillation after adjusting for age, smoking, alcohol use, physical activity, income, body mass index, hypertension, type 2 diabetes, dyslipidemia, chronic kidney disease, coronary heart disease, HRT, and age at menarche. Women who experienced premature menopause had a 33% higher risk for heart failure and 9% higher risk for atrial fibrillation, compared with those who did not.
Reproductive history
The researchers then analyzed the associations between age at menopause and incidence of heart failure and atrial fibrillation after adjusting for the same factors as in the previous analyses. The risk for incident heart failure increased as the age at menopause decreased. Compared with women aged 50 years and older at menopause, those aged 45-49 years, 40-44 years, and younger than 40 years at menopause had 11%, 23%, and 39% greater risk for incident heart failure, respectively. Similarly, the risk for incident atrial fibrillation increased as the age at menopause decreased; the risk was 4%, 10%, and 11% higher for those aged 45-49 years, 40-44 years, and younger than 40 years at menopause, respectively, compared with women aged 50 years and older at menopause.
The authors said that several factors may explain the associations between menopausal age, heart failure, and atrial fibrillation, such as the drop in estrogen levels and changes in body fat distribution.
Dr. Nam concluded, “The misconception that heart disease primarily affects men has meant that sex-specific risk factors have been largely ignored. Evidence is growing that undergoing menopause before the age of 40 years may increase the likelihood of heart disease later in life. Our study indicates that reproductive history should be routinely considered in addition to traditional risk factors such as smoking when evaluating the future likelihood of heart failure and atrial fibrillation.”
A version of this article appeared on Medscape.com. This article was translated from the Medscape French edition.
SEOUL, South Korea – Menopause before age 40 is associated with elevated risk of heart failure and atrial fibrillation, according to a study published in European Heart Journal, from the European Society of Cardiology (ESC). The study of more than 1.4 million women revealed that the younger the age at menopause, the higher the risk of heart failure and atrial fibrillation.
“Women with premature menopause should be aware that they may be more likely to develop heart failure or atrial fibrillation than their peers,” said study author Ga Eun Nam, MD, PhD, of Korea University College of Medicine, Seoul. “This may be good motivation to improve lifestyle habits known to be linked with heart disease, such as quitting smoking and exercising.”
Cardiovascular disease typically occurs up to 10 years later in women than men. Premenopausal women are thought to benefit from estrogen’s protective effect on the cardiovascular system. The cessation of menstruation and subsequent decline of estrogen levels may make women more vulnerable to cardiovascular disease.
A national population
Premature menopause affects 1% of women younger than 40 years, the ESC press release stated. Prior studies have found a link between premature (before age 40 years) and early (before age 45 years) menopause and cardiovascular disease overall, but the evidence for heart failure or atrial fibrillation alone is limited. This study examined the associations between premature menopause, age at menopause, and incident heart failure and atrial fibrillation. Data were obtained from the Korean National Health Insurance System (NHIS), which provides health screening at least every 2 years and includes 97% of the population.
The study included 1,401,175 postmenopausal women aged 30 years and older who completed the NHIS health checkup in 2009. Participants were monitored until the end of 2018 for new-onset heart failure and atrial fibrillation. Information was collected on demographics, health behaviors, and reproductive factors, including age at menopause and use of hormone replacement therapy (HRT). Age at menopause was split into four categories: younger than 40 years, 40-44 years, 45-49 years, and 50 years or older. Premature menopause was defined as having the final menstrual period before age 40 years.
Some 28,111 (2%) participants had a history of premature menopause. For these women, the average age at menopause was 36.7 years. The average age at study enrollment for women with and for those without a history of premature menopause was 60 and 61.5 years, respectively. During an average follow-up of 9.1 years, 42,699 (3.0%) developed heart failure, and 44,834 (3.2%) developed atrial fibrillation.
The researchers analyzed the association between history of premature menopause and incident heart failure and atrial fibrillation after adjusting for age, smoking, alcohol use, physical activity, income, body mass index, hypertension, type 2 diabetes, dyslipidemia, chronic kidney disease, coronary heart disease, HRT, and age at menarche. Women who experienced premature menopause had a 33% higher risk for heart failure and 9% higher risk for atrial fibrillation, compared with those who did not.
Reproductive history
The researchers then analyzed the associations between age at menopause and incidence of heart failure and atrial fibrillation after adjusting for the same factors as in the previous analyses. The risk for incident heart failure increased as the age at menopause decreased. Compared with women aged 50 years and older at menopause, those aged 45-49 years, 40-44 years, and younger than 40 years at menopause had 11%, 23%, and 39% greater risk for incident heart failure, respectively. Similarly, the risk for incident atrial fibrillation increased as the age at menopause decreased; the risk was 4%, 10%, and 11% higher for those aged 45-49 years, 40-44 years, and younger than 40 years at menopause, respectively, compared with women aged 50 years and older at menopause.
The authors said that several factors may explain the associations between menopausal age, heart failure, and atrial fibrillation, such as the drop in estrogen levels and changes in body fat distribution.
Dr. Nam concluded, “The misconception that heart disease primarily affects men has meant that sex-specific risk factors have been largely ignored. Evidence is growing that undergoing menopause before the age of 40 years may increase the likelihood of heart disease later in life. Our study indicates that reproductive history should be routinely considered in addition to traditional risk factors such as smoking when evaluating the future likelihood of heart failure and atrial fibrillation.”
A version of this article appeared on Medscape.com. This article was translated from the Medscape French edition.
Immune response may explain brain damage after COVID-19
It seems that the virus does not infect the brain directly. The scientists found evidence that antibodies – proteins produced by the immune system in response to viruses and other invaders – are involved in an attack on the cells lining the brain’s blood vessels, leading to inflammation and damage. The study was published in the journal Brain.
Brain tissue autopsy
“Patients often develop neurological complications with COVID-19, but the underlying pathophysiological process is not well understood,” Avindra Nath, MD, stated in a National Institutes of Health news release. Dr. Nath, who specializes in neuroimmunology, is the clinical director at the National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We had previously shown blood vessel damage and inflammation in patients’ brains at autopsy, but we didn’t understand the cause of the damage. I think in this paper we’ve gained important insight into the cascade of events.”
In this study, Dr. Nath and his team examined brain tissue from a subset of patients from their previous study. The nine individuals, ages 24-73 years, died shortly after contracting COVID-19. They were chosen because structural brain scans showed signs of blood vessel damage in the brain. The samples were compared with those from 10 controls. The team looked at neuroinflammation and immune responses using immunohistochemistry.
As in their earlier study, researchers found signs of leaky blood vessels based on the presence of blood proteins that normally do not cross the blood-brain barrier. This suggests that the tight junctions between the endothelial cells in the blood-brain barrier have been damaged.
Neurologic symptoms’ molecular basis
Dr. Nath and his colleagues discovered deposits of immune complexes on the surface of the cells. This finding is evidence that damage to endothelial cells was likely due to an immune response.
These observations suggest an antibody-mediated attack that activates endothelial cells. When endothelial cells are activated, they express proteins called adhesion molecules that cause platelets to stick together.
“Activation of the endothelial cells brings platelets that stick to the blood vessel walls, causing clots to form and leakage to occur. At the same time, the tight junctions between the endothelial cells get disrupted, causing them to leak,” Dr. Nath explained. “Once leakage occurs, immune cells such as macrophages may come to repair the damage, setting up inflammation. This, in turn, causes damage to neurons.”
Researchers found that in areas with damage to the endothelial cells, more than 300 genes showed decreased expression, whereas six genes were increased. These genes were associated with oxidative stress, DNA damage, and metabolic dysregulation. As the NIH news release notes, this may provide clues to the molecular basis of neurologic symptoms related to COVID-19 and offer potential therapeutic targets.
Together, these findings give insight into the immune response damaging the brain after COVID-19 infection. But it remains unclear what antigen the immune response is targeting, because the virus itself was not detected in the brain. It is possible that antibodies against the SARS-CoV-2 spike protein could bind to the angiotensin-converting enzyme 2 receptor used by the virus to enter cells. More research is needed to explore this hypothesis.
‘Brain fog’ explained?
The study may also have implications for understanding and treating long-term neurologic symptoms after COVID-19, which include headache, fatigue, loss of taste and smell, sleep problems, and “brain fog.” Had the patients in the study survived, the researchers believe they would likely have developed long COVID.
“It is quite possible that this same immune response persists in long COVID patients, resulting in neuronal injury,” said Dr. Nath. “There could be a small, indolent immune response that is continuing, which means that immune-modulating therapies might help these patients. So, these findings have very important therapeutic implications.”
The results suggest that treatments designed to prevent the development of the immune complexes observed in the study could be potential therapies for post-COVID neurologic symptoms.
This study was supported by the NINDS Division of Intramural Research (NS003130) and K23NS109284, the Roy J. Carver Foundation, and the Iowa Neuroscience Institute.
A version of this article first appeared on Medscape.com. This article was translated from Medscape French edition.
It seems that the virus does not infect the brain directly. The scientists found evidence that antibodies – proteins produced by the immune system in response to viruses and other invaders – are involved in an attack on the cells lining the brain’s blood vessels, leading to inflammation and damage. The study was published in the journal Brain.
Brain tissue autopsy
“Patients often develop neurological complications with COVID-19, but the underlying pathophysiological process is not well understood,” Avindra Nath, MD, stated in a National Institutes of Health news release. Dr. Nath, who specializes in neuroimmunology, is the clinical director at the National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We had previously shown blood vessel damage and inflammation in patients’ brains at autopsy, but we didn’t understand the cause of the damage. I think in this paper we’ve gained important insight into the cascade of events.”
In this study, Dr. Nath and his team examined brain tissue from a subset of patients from their previous study. The nine individuals, ages 24-73 years, died shortly after contracting COVID-19. They were chosen because structural brain scans showed signs of blood vessel damage in the brain. The samples were compared with those from 10 controls. The team looked at neuroinflammation and immune responses using immunohistochemistry.
As in their earlier study, researchers found signs of leaky blood vessels based on the presence of blood proteins that normally do not cross the blood-brain barrier. This suggests that the tight junctions between the endothelial cells in the blood-brain barrier have been damaged.
Neurologic symptoms’ molecular basis
Dr. Nath and his colleagues discovered deposits of immune complexes on the surface of the cells. This finding is evidence that damage to endothelial cells was likely due to an immune response.
These observations suggest an antibody-mediated attack that activates endothelial cells. When endothelial cells are activated, they express proteins called adhesion molecules that cause platelets to stick together.
“Activation of the endothelial cells brings platelets that stick to the blood vessel walls, causing clots to form and leakage to occur. At the same time, the tight junctions between the endothelial cells get disrupted, causing them to leak,” Dr. Nath explained. “Once leakage occurs, immune cells such as macrophages may come to repair the damage, setting up inflammation. This, in turn, causes damage to neurons.”
Researchers found that in areas with damage to the endothelial cells, more than 300 genes showed decreased expression, whereas six genes were increased. These genes were associated with oxidative stress, DNA damage, and metabolic dysregulation. As the NIH news release notes, this may provide clues to the molecular basis of neurologic symptoms related to COVID-19 and offer potential therapeutic targets.
Together, these findings give insight into the immune response damaging the brain after COVID-19 infection. But it remains unclear what antigen the immune response is targeting, because the virus itself was not detected in the brain. It is possible that antibodies against the SARS-CoV-2 spike protein could bind to the angiotensin-converting enzyme 2 receptor used by the virus to enter cells. More research is needed to explore this hypothesis.
‘Brain fog’ explained?
The study may also have implications for understanding and treating long-term neurologic symptoms after COVID-19, which include headache, fatigue, loss of taste and smell, sleep problems, and “brain fog.” Had the patients in the study survived, the researchers believe they would likely have developed long COVID.
“It is quite possible that this same immune response persists in long COVID patients, resulting in neuronal injury,” said Dr. Nath. “There could be a small, indolent immune response that is continuing, which means that immune-modulating therapies might help these patients. So, these findings have very important therapeutic implications.”
The results suggest that treatments designed to prevent the development of the immune complexes observed in the study could be potential therapies for post-COVID neurologic symptoms.
This study was supported by the NINDS Division of Intramural Research (NS003130) and K23NS109284, the Roy J. Carver Foundation, and the Iowa Neuroscience Institute.
A version of this article first appeared on Medscape.com. This article was translated from Medscape French edition.
It seems that the virus does not infect the brain directly. The scientists found evidence that antibodies – proteins produced by the immune system in response to viruses and other invaders – are involved in an attack on the cells lining the brain’s blood vessels, leading to inflammation and damage. The study was published in the journal Brain.
Brain tissue autopsy
“Patients often develop neurological complications with COVID-19, but the underlying pathophysiological process is not well understood,” Avindra Nath, MD, stated in a National Institutes of Health news release. Dr. Nath, who specializes in neuroimmunology, is the clinical director at the National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We had previously shown blood vessel damage and inflammation in patients’ brains at autopsy, but we didn’t understand the cause of the damage. I think in this paper we’ve gained important insight into the cascade of events.”
In this study, Dr. Nath and his team examined brain tissue from a subset of patients from their previous study. The nine individuals, ages 24-73 years, died shortly after contracting COVID-19. They were chosen because structural brain scans showed signs of blood vessel damage in the brain. The samples were compared with those from 10 controls. The team looked at neuroinflammation and immune responses using immunohistochemistry.
As in their earlier study, researchers found signs of leaky blood vessels based on the presence of blood proteins that normally do not cross the blood-brain barrier. This suggests that the tight junctions between the endothelial cells in the blood-brain barrier have been damaged.
Neurologic symptoms’ molecular basis
Dr. Nath and his colleagues discovered deposits of immune complexes on the surface of the cells. This finding is evidence that damage to endothelial cells was likely due to an immune response.
These observations suggest an antibody-mediated attack that activates endothelial cells. When endothelial cells are activated, they express proteins called adhesion molecules that cause platelets to stick together.
“Activation of the endothelial cells brings platelets that stick to the blood vessel walls, causing clots to form and leakage to occur. At the same time, the tight junctions between the endothelial cells get disrupted, causing them to leak,” Dr. Nath explained. “Once leakage occurs, immune cells such as macrophages may come to repair the damage, setting up inflammation. This, in turn, causes damage to neurons.”
Researchers found that in areas with damage to the endothelial cells, more than 300 genes showed decreased expression, whereas six genes were increased. These genes were associated with oxidative stress, DNA damage, and metabolic dysregulation. As the NIH news release notes, this may provide clues to the molecular basis of neurologic symptoms related to COVID-19 and offer potential therapeutic targets.
Together, these findings give insight into the immune response damaging the brain after COVID-19 infection. But it remains unclear what antigen the immune response is targeting, because the virus itself was not detected in the brain. It is possible that antibodies against the SARS-CoV-2 spike protein could bind to the angiotensin-converting enzyme 2 receptor used by the virus to enter cells. More research is needed to explore this hypothesis.
‘Brain fog’ explained?
The study may also have implications for understanding and treating long-term neurologic symptoms after COVID-19, which include headache, fatigue, loss of taste and smell, sleep problems, and “brain fog.” Had the patients in the study survived, the researchers believe they would likely have developed long COVID.
“It is quite possible that this same immune response persists in long COVID patients, resulting in neuronal injury,” said Dr. Nath. “There could be a small, indolent immune response that is continuing, which means that immune-modulating therapies might help these patients. So, these findings have very important therapeutic implications.”
The results suggest that treatments designed to prevent the development of the immune complexes observed in the study could be potential therapies for post-COVID neurologic symptoms.
This study was supported by the NINDS Division of Intramural Research (NS003130) and K23NS109284, the Roy J. Carver Foundation, and the Iowa Neuroscience Institute.
A version of this article first appeared on Medscape.com. This article was translated from Medscape French edition.
Cases of hepatitis of unknown origin in children raise alarm
After several cases of acute hepatitis of unknown origin in children in the United Kingdom were reported, further cases have now been reported in France (two cases), Denmark, Ireland, the Netherlands, and Spain. More than 80 cases have been reported overall, raising fears of an epidemic, according to a press release from the European Centre for Disease Prevention and Control (ECDC).
Furthermore, nine cases have allegedly been reported since last autumn in Alabama in the United States. These cases have mainly been in children aged 1-6 years.
Investigations are ongoing in all these countries, particularly as the “exact causes of these cases of acute hepatitis remain unknown.” Nevertheless, the team working on these cases in the United Kingdom believes that, based on clinical and epidemiologic data, the cause is probably infectious in origin.
Coordinated by the ECDC, European medical societies such as the European Association for the Study of the Liver and the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) are working together to promote information sharing, according to the European agency.
Potential infectious agent
For context, on April 5, the United Kingdom reported about 10 cases of acute hepatitis of unknown origin in children younger than 10 in Scotland with no underlying conditions. Seven days later, the UK reported that 61 additional cases were under investigation in England, Wales, and Northern Ireland, the majority of which were in children aged 2-5 years.
The cases in the United Kingdom presented with severe acute hepatitis, with increased liver enzyme levels (aspartate aminotransferase [AST] and alanine aminotransferase [ALT] levels above 500 IU/L), and most presented with jaundice. Some reported gastrointestinal symptoms such as abdominal pain, diarrhea, and vomiting in the previous weeks.
The majority had no fever.
Although no deaths had been reported at press time, some cases needed to be seen by a liver specialist in the hospital, and others had to undergo transplantation (six transplants in Europe and two in the United States).
Initial hypotheses have focused on a potential infectious agent or exposure to a toxin. No link to COVID-19 vaccination has been established.
Which type of hepatitis?
The ECDC reports that laboratory tests have ruled out the possibility of attributing the cases to type A, B, C, D, and E viral hepatitis. Of the 13 cases in Scotland, 3 tested positive for SARS-CoV-2, 5 were negative, and 2 had contracted COVID-19 over the course of the last 3 months.
One positive test for adenovirus was found in 5 of the 13 Scottish cases, out of the 11 that were tested. All the cases reported in the United States tested positive for an adenovirus, five of which were for adenovirus type 41, which is responsible for inflammation of the bowel. Investigations are ongoing to assess any possible involvement of this virus in other cases. It should be noted that adenoviruses can cause hepatitis in children, but generally only in those who are immunosuppressed.
The pandemic could be another possible explanation, Nancy Reau, MD, head of the hepatology department at Rush University, Chicago, told this news organization. “The possibility that these cases are linked to COVID still exists,” she said. Some cases in the United Kingdom tested positive for COVID-19; none of these children had received the COVID-19 vaccine.
“COVID has been regularly seen to raise liver markers. It has also been shown to affect organs other than the lungs,” she stated. “It could be the case that, as it evolves, this virus has the potential to cause hepatitis in children.”
A version of this article first appeared on Medscape.com.
After several cases of acute hepatitis of unknown origin in children in the United Kingdom were reported, further cases have now been reported in France (two cases), Denmark, Ireland, the Netherlands, and Spain. More than 80 cases have been reported overall, raising fears of an epidemic, according to a press release from the European Centre for Disease Prevention and Control (ECDC).
Furthermore, nine cases have allegedly been reported since last autumn in Alabama in the United States. These cases have mainly been in children aged 1-6 years.
Investigations are ongoing in all these countries, particularly as the “exact causes of these cases of acute hepatitis remain unknown.” Nevertheless, the team working on these cases in the United Kingdom believes that, based on clinical and epidemiologic data, the cause is probably infectious in origin.
Coordinated by the ECDC, European medical societies such as the European Association for the Study of the Liver and the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) are working together to promote information sharing, according to the European agency.
Potential infectious agent
For context, on April 5, the United Kingdom reported about 10 cases of acute hepatitis of unknown origin in children younger than 10 in Scotland with no underlying conditions. Seven days later, the UK reported that 61 additional cases were under investigation in England, Wales, and Northern Ireland, the majority of which were in children aged 2-5 years.
The cases in the United Kingdom presented with severe acute hepatitis, with increased liver enzyme levels (aspartate aminotransferase [AST] and alanine aminotransferase [ALT] levels above 500 IU/L), and most presented with jaundice. Some reported gastrointestinal symptoms such as abdominal pain, diarrhea, and vomiting in the previous weeks.
The majority had no fever.
Although no deaths had been reported at press time, some cases needed to be seen by a liver specialist in the hospital, and others had to undergo transplantation (six transplants in Europe and two in the United States).
Initial hypotheses have focused on a potential infectious agent or exposure to a toxin. No link to COVID-19 vaccination has been established.
Which type of hepatitis?
The ECDC reports that laboratory tests have ruled out the possibility of attributing the cases to type A, B, C, D, and E viral hepatitis. Of the 13 cases in Scotland, 3 tested positive for SARS-CoV-2, 5 were negative, and 2 had contracted COVID-19 over the course of the last 3 months.
One positive test for adenovirus was found in 5 of the 13 Scottish cases, out of the 11 that were tested. All the cases reported in the United States tested positive for an adenovirus, five of which were for adenovirus type 41, which is responsible for inflammation of the bowel. Investigations are ongoing to assess any possible involvement of this virus in other cases. It should be noted that adenoviruses can cause hepatitis in children, but generally only in those who are immunosuppressed.
The pandemic could be another possible explanation, Nancy Reau, MD, head of the hepatology department at Rush University, Chicago, told this news organization. “The possibility that these cases are linked to COVID still exists,” she said. Some cases in the United Kingdom tested positive for COVID-19; none of these children had received the COVID-19 vaccine.
“COVID has been regularly seen to raise liver markers. It has also been shown to affect organs other than the lungs,” she stated. “It could be the case that, as it evolves, this virus has the potential to cause hepatitis in children.”
A version of this article first appeared on Medscape.com.
After several cases of acute hepatitis of unknown origin in children in the United Kingdom were reported, further cases have now been reported in France (two cases), Denmark, Ireland, the Netherlands, and Spain. More than 80 cases have been reported overall, raising fears of an epidemic, according to a press release from the European Centre for Disease Prevention and Control (ECDC).
Furthermore, nine cases have allegedly been reported since last autumn in Alabama in the United States. These cases have mainly been in children aged 1-6 years.
Investigations are ongoing in all these countries, particularly as the “exact causes of these cases of acute hepatitis remain unknown.” Nevertheless, the team working on these cases in the United Kingdom believes that, based on clinical and epidemiologic data, the cause is probably infectious in origin.
Coordinated by the ECDC, European medical societies such as the European Association for the Study of the Liver and the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) are working together to promote information sharing, according to the European agency.
Potential infectious agent
For context, on April 5, the United Kingdom reported about 10 cases of acute hepatitis of unknown origin in children younger than 10 in Scotland with no underlying conditions. Seven days later, the UK reported that 61 additional cases were under investigation in England, Wales, and Northern Ireland, the majority of which were in children aged 2-5 years.
The cases in the United Kingdom presented with severe acute hepatitis, with increased liver enzyme levels (aspartate aminotransferase [AST] and alanine aminotransferase [ALT] levels above 500 IU/L), and most presented with jaundice. Some reported gastrointestinal symptoms such as abdominal pain, diarrhea, and vomiting in the previous weeks.
The majority had no fever.
Although no deaths had been reported at press time, some cases needed to be seen by a liver specialist in the hospital, and others had to undergo transplantation (six transplants in Europe and two in the United States).
Initial hypotheses have focused on a potential infectious agent or exposure to a toxin. No link to COVID-19 vaccination has been established.
Which type of hepatitis?
The ECDC reports that laboratory tests have ruled out the possibility of attributing the cases to type A, B, C, D, and E viral hepatitis. Of the 13 cases in Scotland, 3 tested positive for SARS-CoV-2, 5 were negative, and 2 had contracted COVID-19 over the course of the last 3 months.
One positive test for adenovirus was found in 5 of the 13 Scottish cases, out of the 11 that were tested. All the cases reported in the United States tested positive for an adenovirus, five of which were for adenovirus type 41, which is responsible for inflammation of the bowel. Investigations are ongoing to assess any possible involvement of this virus in other cases. It should be noted that adenoviruses can cause hepatitis in children, but generally only in those who are immunosuppressed.
The pandemic could be another possible explanation, Nancy Reau, MD, head of the hepatology department at Rush University, Chicago, told this news organization. “The possibility that these cases are linked to COVID still exists,” she said. Some cases in the United Kingdom tested positive for COVID-19; none of these children had received the COVID-19 vaccine.
“COVID has been regularly seen to raise liver markers. It has also been shown to affect organs other than the lungs,” she stated. “It could be the case that, as it evolves, this virus has the potential to cause hepatitis in children.”
A version of this article first appeared on Medscape.com.