California’s highest court has revived a high-profile lawsuit that could have a major impact on whether insurers can punish physicians who refer patients to out-of-network providers.

The case, which has bounced around courts in the Golden State since 2012, pits the nearly 50,000-member California Medical Association (CMA) against Aetna, one of the nation’s largest health insurers. The physician group alleges that Aetna illegally retaliated against physicians who sent patients to certain out-of-network clinics.

Out-of-network providers and clinics were involved in just 4.7% of professional medical claims in 2020, according to a federal report released July 6, 2023. Such claims are more likely than others to be denied, and they result in unexpected medical bills, which have led to the passage of state and federal laws that target “surprise billing.”

In a July 17 ruling, the California Supreme Court unanimously resurrected the CMA v. Aetna case after a judge and a state appeals court killed it on the grounds that the CMA - which is affiliated with the American Medical Association (AMA) - had no standing to sue Aetna. The high state court declared that the CMA could sue on its own behalf, but the justices noted that their ruling says nothing about the merits of the case.

The ruling appears to mean that CMA’s lawsuit will head back to Superior Court in Los Angeles County. The outcome of the case won’t have a direct national effect, since the case is in state court, not federal court. However, state rulings can influence the thinking of judges elsewhere.

The case, filed in 2012, alleges that Aetna harmed patient care by harassing and sacking contract physicians who referred patients to out-of-network ambulatory surgery centers.

According to the new ruling, Aetna responded by saying that “its policy, rather than interfering in medical judgments, was designed simply to encourage participating physicians, consistent with their judgment, to use in-network care providers, such as ambulatory surgery centers, and was adopted in part in response to physicians referring patients to facilities in which they had financial interests.”

In a 2012 letter to CMA, as reported by the Los Angeles Times, an Aetna attorney went further and claimed that “physicians and their business partners secure outsized and improper windfalls at the expense of Aetna’s plan members and employer plan sponsors.”

The CMA received support for its lawsuit via friend-of-the-court legal briefs from the California attorney general, city attorneys for several major California cities, the AMA, several major labor unions, the AIDS Healthcare Foundation, and the advocacy organization Consumer Watchdog. The U.S. Chamber of Commerce, the California Association of Health Plans, and the Association of California Life and Health Insurance Companies filed briefs supporting Aetna.

Aetna, now part of CVS Health, declined to comment about the new ruling.

The CMA released a statement from its president, internist/hospitalist Donaldo M. Hernandez, MD: “The practice of threatening physicians who refer patients to out-of-network providers is unlawful, and we are pleased that the court agrees that CMA has the right to challenge these practices in court.”

In an interview, research professor emeritus Jack Hoadley, PhD, of the Health Policy Institute at Georgetown University’s McCourt School of Public Policy, noted that many health plans don’t cover out-of-network care. Those that do – including PPOs and hybrid plans – often require that patients pay a larger share of the total cost or pay a separate or higher deductible, he said.

So why would an insurer punish doctors who refer patients to health care providers who are outside the insurer’s approved network? In some cases, patients may blame insurers when they’re forced to pay higher rates for out-of-network care, Dr. Hoadley said. Insurers may also be miffed when physicians send patients out of network, he said, because insurers contract with physicians to send a certain number of patients within the insurer’s network.

The federal No Surprises Act, passed by Congress in 2020, hasn’t decreased tension between providers and insurers over out-of-network fees, Dr. Hoadley said. As the effects of the law are hammered out in court, he said, there’s still an adversarial relationship.

In California, the out-of-network landscape changed 3 years before the No Surprises Act. In 2017, the state passed its own no-surprise-billing law, which “protects consumers from surprise medical bills when they get non-emergency services, go to an in-network health facility and receive care from an out-of-network provider without their consent.” In these cases, the law says patients need to pay only in accordance with in-network cost sharing.

In 2019, a USC-Brookings Schaeffer Initiative for Health Policy report found signs that out-of-network care was fading in California other than in the emergency setting, possibly as a result of the law.

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

California’s highest court has revived a high-profile lawsuit that could have a major impact on whether insurers can punish physicians who refer patients to out-of-network providers.

The case, which has bounced around courts in the Golden State since 2012, pits the nearly 50,000-member California Medical Association (CMA) against Aetna, one of the nation’s largest health insurers. The physician group alleges that Aetna illegally retaliated against physicians who sent patients to certain out-of-network clinics.

Out-of-network providers and clinics were involved in just 4.7% of professional medical claims in 2020, according to a federal report released July 6, 2023. Such claims are more likely than others to be denied, and they result in unexpected medical bills, which have led to the passage of state and federal laws that target “surprise billing.”

In a July 17 ruling, the California Supreme Court unanimously resurrected the CMA v. Aetna case after a judge and a state appeals court killed it on the grounds that the CMA - which is affiliated with the American Medical Association (AMA) - had no standing to sue Aetna. The high state court declared that the CMA could sue on its own behalf, but the justices noted that their ruling says nothing about the merits of the case.

The ruling appears to mean that CMA’s lawsuit will head back to Superior Court in Los Angeles County. The outcome of the case won’t have a direct national effect, since the case is in state court, not federal court. However, state rulings can influence the thinking of judges elsewhere.

The case, filed in 2012, alleges that Aetna harmed patient care by harassing and sacking contract physicians who referred patients to out-of-network ambulatory surgery centers.

According to the new ruling, Aetna responded by saying that “its policy, rather than interfering in medical judgments, was designed simply to encourage participating physicians, consistent with their judgment, to use in-network care providers, such as ambulatory surgery centers, and was adopted in part in response to physicians referring patients to facilities in which they had financial interests.”

In a 2012 letter to CMA, as reported by the Los Angeles Times, an Aetna attorney went further and claimed that “physicians and their business partners secure outsized and improper windfalls at the expense of Aetna’s plan members and employer plan sponsors.”

The CMA received support for its lawsuit via friend-of-the-court legal briefs from the California attorney general, city attorneys for several major California cities, the AMA, several major labor unions, the AIDS Healthcare Foundation, and the advocacy organization Consumer Watchdog. The U.S. Chamber of Commerce, the California Association of Health Plans, and the Association of California Life and Health Insurance Companies filed briefs supporting Aetna.

Aetna, now part of CVS Health, declined to comment about the new ruling.

The CMA released a statement from its president, internist/hospitalist Donaldo M. Hernandez, MD: “The practice of threatening physicians who refer patients to out-of-network providers is unlawful, and we are pleased that the court agrees that CMA has the right to challenge these practices in court.”

In an interview, research professor emeritus Jack Hoadley, PhD, of the Health Policy Institute at Georgetown University’s McCourt School of Public Policy, noted that many health plans don’t cover out-of-network care. Those that do – including PPOs and hybrid plans – often require that patients pay a larger share of the total cost or pay a separate or higher deductible, he said.

So why would an insurer punish doctors who refer patients to health care providers who are outside the insurer’s approved network? In some cases, patients may blame insurers when they’re forced to pay higher rates for out-of-network care, Dr. Hoadley said. Insurers may also be miffed when physicians send patients out of network, he said, because insurers contract with physicians to send a certain number of patients within the insurer’s network.

The federal No Surprises Act, passed by Congress in 2020, hasn’t decreased tension between providers and insurers over out-of-network fees, Dr. Hoadley said. As the effects of the law are hammered out in court, he said, there’s still an adversarial relationship.

In California, the out-of-network landscape changed 3 years before the No Surprises Act. In 2017, the state passed its own no-surprise-billing law, which “protects consumers from surprise medical bills when they get non-emergency services, go to an in-network health facility and receive care from an out-of-network provider without their consent.” In these cases, the law says patients need to pay only in accordance with in-network cost sharing.

In 2019, a USC-Brookings Schaeffer Initiative for Health Policy report found signs that out-of-network care was fading in California other than in the emergency setting, possibly as a result of the law.

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

California’s highest court has revived a high-profile lawsuit that could have a major impact on whether insurers can punish physicians who refer patients to out-of-network providers.

The case, which has bounced around courts in the Golden State since 2012, pits the nearly 50,000-member California Medical Association (CMA) against Aetna, one of the nation’s largest health insurers. The physician group alleges that Aetna illegally retaliated against physicians who sent patients to certain out-of-network clinics.

Out-of-network providers and clinics were involved in just 4.7% of professional medical claims in 2020, according to a federal report released July 6, 2023. Such claims are more likely than others to be denied, and they result in unexpected medical bills, which have led to the passage of state and federal laws that target “surprise billing.”

In a July 17 ruling, the California Supreme Court unanimously resurrected the CMA v. Aetna case after a judge and a state appeals court killed it on the grounds that the CMA - which is affiliated with the American Medical Association (AMA) - had no standing to sue Aetna. The high state court declared that the CMA could sue on its own behalf, but the justices noted that their ruling says nothing about the merits of the case.

The ruling appears to mean that CMA’s lawsuit will head back to Superior Court in Los Angeles County. The outcome of the case won’t have a direct national effect, since the case is in state court, not federal court. However, state rulings can influence the thinking of judges elsewhere.

The case, filed in 2012, alleges that Aetna harmed patient care by harassing and sacking contract physicians who referred patients to out-of-network ambulatory surgery centers.

According to the new ruling, Aetna responded by saying that “its policy, rather than interfering in medical judgments, was designed simply to encourage participating physicians, consistent with their judgment, to use in-network care providers, such as ambulatory surgery centers, and was adopted in part in response to physicians referring patients to facilities in which they had financial interests.”

In a 2012 letter to CMA, as reported by the Los Angeles Times, an Aetna attorney went further and claimed that “physicians and their business partners secure outsized and improper windfalls at the expense of Aetna’s plan members and employer plan sponsors.”

The CMA received support for its lawsuit via friend-of-the-court legal briefs from the California attorney general, city attorneys for several major California cities, the AMA, several major labor unions, the AIDS Healthcare Foundation, and the advocacy organization Consumer Watchdog. The U.S. Chamber of Commerce, the California Association of Health Plans, and the Association of California Life and Health Insurance Companies filed briefs supporting Aetna.

Aetna, now part of CVS Health, declined to comment about the new ruling.

The CMA released a statement from its president, internist/hospitalist Donaldo M. Hernandez, MD: “The practice of threatening physicians who refer patients to out-of-network providers is unlawful, and we are pleased that the court agrees that CMA has the right to challenge these practices in court.”

In an interview, research professor emeritus Jack Hoadley, PhD, of the Health Policy Institute at Georgetown University’s McCourt School of Public Policy, noted that many health plans don’t cover out-of-network care. Those that do – including PPOs and hybrid plans – often require that patients pay a larger share of the total cost or pay a separate or higher deductible, he said.

So why would an insurer punish doctors who refer patients to health care providers who are outside the insurer’s approved network? In some cases, patients may blame insurers when they’re forced to pay higher rates for out-of-network care, Dr. Hoadley said. Insurers may also be miffed when physicians send patients out of network, he said, because insurers contract with physicians to send a certain number of patients within the insurer’s network.

The federal No Surprises Act, passed by Congress in 2020, hasn’t decreased tension between providers and insurers over out-of-network fees, Dr. Hoadley said. As the effects of the law are hammered out in court, he said, there’s still an adversarial relationship.

In California, the out-of-network landscape changed 3 years before the No Surprises Act. In 2017, the state passed its own no-surprise-billing law, which “protects consumers from surprise medical bills when they get non-emergency services, go to an in-network health facility and receive care from an out-of-network provider without their consent.” In these cases, the law says patients need to pay only in accordance with in-network cost sharing.

In 2019, a USC-Brookings Schaeffer Initiative for Health Policy report found signs that out-of-network care was fading in California other than in the emergency setting, possibly as a result of the law.

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

Social isolation in older individuals has been linked to reduced brain volume in regions associated with memory, a new study shows.

Further, the association between social isolation and reduced brain volume appears to be at least partly mediated by depressive symptoms.

“We believe that efforts should be made to reduce social isolation among the elderly as much as possible,” investigator Toshiharu Ninomiya, MD, PhD, professor of epidemiology and public health at Kyushu University in Fukuoka, Japan, said in an interview.

The study was published online in Neurology.
 

A dementia prevention strategy

Dr. Ninomiya noted there have been several studies suggesting that social interaction is beneficial in preventing cognitive decline and the onset of dementia.

In addition, recent epidemiological studies have shown social isolation is associated with a risk for cognitive decline and dementia.

Although the investigators note that very little is known about the link between the two, some studies have shown that social isolation is linked with depressive symptoms in older adults, and late-life depression has been associated with brain atrophy.

To explore the potential link between social isolation and brain atrophy, as well as the role of depression as a potential mediator, the investigators studied nearly 9,000 citizens aged 65 and older as part of the Japan Prospective Studies Collaboration for Aging and Dementia (JPSC-AD), an ongoing, community-based nationwide cohort study of dementia in Japan.

Participants were recruited from eight research sites across Japan, and each had a baseline MRI scan between 2016 and 2018. The investigators excluded those with a dementia diagnosis at baseline. Self-reported frequency of social contact was categorized as every day, several times a week, several times a month, or seldom.

Participants also answered questions about medical history and treatment, antihypertensive or antidiabetic medications, exercise, current alcohol intake, and smoking habits. Depressive symptoms were assessed with the Geriatric Depression Scale. Of the participants, 57% were women, and the mean age was 73 years.
 

Lower brain volume

Total brain volume was lower in those with the lowest frequency of social contact vs. those with the highest frequency (67.3% vs. 67.8%). Less social contact was also linked to smaller temporal lobe, occipital lobe, cingulum, hippocampus, and amygdala volumes.

White matter lesion volume increased with fewer social interactions, from 0.26% in the most social group to 0.30% in the least.

Cognitive function was higher in participants who had daily social contact, compared with those who had the least contact (28 vs. 27 on the Mini-Mental State Examination; P < .001). Scores between 25 and 30 are considered normal.

Depressive symptoms were lower in the daily contact group, compared with the seldom-contact group (P < .001).

The team also found that lower frequency of social contact was significantly associated with the smaller superior, middle, or inferior temporal gyrus; and a smaller fusiform gyrus, transverse temporal gyrus, temporal pole, and entorhinal cortex, among other subregions.

Mediation analyses indicated that depressive symptoms accounted for only 15%-29% of the associations of lower frequency of social contact with each regional volume.
 

Worse physical health

The results also showed that socially isolated participants were more likely to have diabetes, to have hypertension, to smoke, and to be physically inactive.

“Cardiovascular risk factors have been reported to cause endothelial dysfunction in the brain, which could in turn lead to problems in maintaining microcirculation and blood-brain barrier function,” the investigators write.

Some epidemiological studies have associated cardiovascular risk factors with brain atrophy, they noted, which could have been one of the underlying mechanisms.

Another possibility is that reduced cognitive stimulation due to social isolation may cause brain atrophy, they add.

“Ultimately,” Dr. Ninomiya said, “the detailed mechanism of the relationship between social isolation and brain volume is not yet clear.”

He also said more research is needed to know whether the findings would apply to people in other countries.

In an accompanying editorial, Alexa Walter, PhD, and Danielle Sandsmark, MD, PhD, from the University of Pennsylvania, Philadelphia, note that  isolation has been associated with many adverse health outcomes, including increased risk of heart disease, stroke, and premature death.

“Given these findings, future work considering social health factors in the context of neurological disease is an important area of research to consider. Additionally, leveraging other existing longitudinal studies could provide us with an opportunity to better understand these relationships within populations and inform public policy to address these issues,” Dr. Walter and Dr. Sandsmark write.

The study was funded by the Japan Agency for Medical Research and Development and Suntory Holdings Limited. Dr. Ninomiya reports receiving grants from Suntory Holdings Limited.

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

Social isolation in older individuals has been linked to reduced brain volume in regions associated with memory, a new study shows.

Further, the association between social isolation and reduced brain volume appears to be at least partly mediated by depressive symptoms.

“We believe that efforts should be made to reduce social isolation among the elderly as much as possible,” investigator Toshiharu Ninomiya, MD, PhD, professor of epidemiology and public health at Kyushu University in Fukuoka, Japan, said in an interview.

The study was published online in Neurology.
 

A dementia prevention strategy

Dr. Ninomiya noted there have been several studies suggesting that social interaction is beneficial in preventing cognitive decline and the onset of dementia.

In addition, recent epidemiological studies have shown social isolation is associated with a risk for cognitive decline and dementia.

Although the investigators note that very little is known about the link between the two, some studies have shown that social isolation is linked with depressive symptoms in older adults, and late-life depression has been associated with brain atrophy.

To explore the potential link between social isolation and brain atrophy, as well as the role of depression as a potential mediator, the investigators studied nearly 9,000 citizens aged 65 and older as part of the Japan Prospective Studies Collaboration for Aging and Dementia (JPSC-AD), an ongoing, community-based nationwide cohort study of dementia in Japan.

Participants were recruited from eight research sites across Japan, and each had a baseline MRI scan between 2016 and 2018. The investigators excluded those with a dementia diagnosis at baseline. Self-reported frequency of social contact was categorized as every day, several times a week, several times a month, or seldom.

Participants also answered questions about medical history and treatment, antihypertensive or antidiabetic medications, exercise, current alcohol intake, and smoking habits. Depressive symptoms were assessed with the Geriatric Depression Scale. Of the participants, 57% were women, and the mean age was 73 years.
 

Lower brain volume

Total brain volume was lower in those with the lowest frequency of social contact vs. those with the highest frequency (67.3% vs. 67.8%). Less social contact was also linked to smaller temporal lobe, occipital lobe, cingulum, hippocampus, and amygdala volumes.

White matter lesion volume increased with fewer social interactions, from 0.26% in the most social group to 0.30% in the least.

Cognitive function was higher in participants who had daily social contact, compared with those who had the least contact (28 vs. 27 on the Mini-Mental State Examination; P < .001). Scores between 25 and 30 are considered normal.

Depressive symptoms were lower in the daily contact group, compared with the seldom-contact group (P < .001).

The team also found that lower frequency of social contact was significantly associated with the smaller superior, middle, or inferior temporal gyrus; and a smaller fusiform gyrus, transverse temporal gyrus, temporal pole, and entorhinal cortex, among other subregions.

Mediation analyses indicated that depressive symptoms accounted for only 15%-29% of the associations of lower frequency of social contact with each regional volume.
 

Worse physical health

The results also showed that socially isolated participants were more likely to have diabetes, to have hypertension, to smoke, and to be physically inactive.

“Cardiovascular risk factors have been reported to cause endothelial dysfunction in the brain, which could in turn lead to problems in maintaining microcirculation and blood-brain barrier function,” the investigators write.

Some epidemiological studies have associated cardiovascular risk factors with brain atrophy, they noted, which could have been one of the underlying mechanisms.

Another possibility is that reduced cognitive stimulation due to social isolation may cause brain atrophy, they add.

“Ultimately,” Dr. Ninomiya said, “the detailed mechanism of the relationship between social isolation and brain volume is not yet clear.”

He also said more research is needed to know whether the findings would apply to people in other countries.

In an accompanying editorial, Alexa Walter, PhD, and Danielle Sandsmark, MD, PhD, from the University of Pennsylvania, Philadelphia, note that  isolation has been associated with many adverse health outcomes, including increased risk of heart disease, stroke, and premature death.

“Given these findings, future work considering social health factors in the context of neurological disease is an important area of research to consider. Additionally, leveraging other existing longitudinal studies could provide us with an opportunity to better understand these relationships within populations and inform public policy to address these issues,” Dr. Walter and Dr. Sandsmark write.

The study was funded by the Japan Agency for Medical Research and Development and Suntory Holdings Limited. Dr. Ninomiya reports receiving grants from Suntory Holdings Limited.

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

Social isolation in older individuals has been linked to reduced brain volume in regions associated with memory, a new study shows.

Further, the association between social isolation and reduced brain volume appears to be at least partly mediated by depressive symptoms.

“We believe that efforts should be made to reduce social isolation among the elderly as much as possible,” investigator Toshiharu Ninomiya, MD, PhD, professor of epidemiology and public health at Kyushu University in Fukuoka, Japan, said in an interview.

The study was published online in Neurology.
 

A dementia prevention strategy

Dr. Ninomiya noted there have been several studies suggesting that social interaction is beneficial in preventing cognitive decline and the onset of dementia.

In addition, recent epidemiological studies have shown social isolation is associated with a risk for cognitive decline and dementia.

Although the investigators note that very little is known about the link between the two, some studies have shown that social isolation is linked with depressive symptoms in older adults, and late-life depression has been associated with brain atrophy.

To explore the potential link between social isolation and brain atrophy, as well as the role of depression as a potential mediator, the investigators studied nearly 9,000 citizens aged 65 and older as part of the Japan Prospective Studies Collaboration for Aging and Dementia (JPSC-AD), an ongoing, community-based nationwide cohort study of dementia in Japan.

Participants were recruited from eight research sites across Japan, and each had a baseline MRI scan between 2016 and 2018. The investigators excluded those with a dementia diagnosis at baseline. Self-reported frequency of social contact was categorized as every day, several times a week, several times a month, or seldom.

Participants also answered questions about medical history and treatment, antihypertensive or antidiabetic medications, exercise, current alcohol intake, and smoking habits. Depressive symptoms were assessed with the Geriatric Depression Scale. Of the participants, 57% were women, and the mean age was 73 years.
 

Lower brain volume

Total brain volume was lower in those with the lowest frequency of social contact vs. those with the highest frequency (67.3% vs. 67.8%). Less social contact was also linked to smaller temporal lobe, occipital lobe, cingulum, hippocampus, and amygdala volumes.

White matter lesion volume increased with fewer social interactions, from 0.26% in the most social group to 0.30% in the least.

Cognitive function was higher in participants who had daily social contact, compared with those who had the least contact (28 vs. 27 on the Mini-Mental State Examination; P < .001). Scores between 25 and 30 are considered normal.

Depressive symptoms were lower in the daily contact group, compared with the seldom-contact group (P < .001).

The team also found that lower frequency of social contact was significantly associated with the smaller superior, middle, or inferior temporal gyrus; and a smaller fusiform gyrus, transverse temporal gyrus, temporal pole, and entorhinal cortex, among other subregions.

Mediation analyses indicated that depressive symptoms accounted for only 15%-29% of the associations of lower frequency of social contact with each regional volume.
 

Worse physical health

The results also showed that socially isolated participants were more likely to have diabetes, to have hypertension, to smoke, and to be physically inactive.

“Cardiovascular risk factors have been reported to cause endothelial dysfunction in the brain, which could in turn lead to problems in maintaining microcirculation and blood-brain barrier function,” the investigators write.

Some epidemiological studies have associated cardiovascular risk factors with brain atrophy, they noted, which could have been one of the underlying mechanisms.

Another possibility is that reduced cognitive stimulation due to social isolation may cause brain atrophy, they add.

“Ultimately,” Dr. Ninomiya said, “the detailed mechanism of the relationship between social isolation and brain volume is not yet clear.”

He also said more research is needed to know whether the findings would apply to people in other countries.

In an accompanying editorial, Alexa Walter, PhD, and Danielle Sandsmark, MD, PhD, from the University of Pennsylvania, Philadelphia, note that  isolation has been associated with many adverse health outcomes, including increased risk of heart disease, stroke, and premature death.

“Given these findings, future work considering social health factors in the context of neurological disease is an important area of research to consider. Additionally, leveraging other existing longitudinal studies could provide us with an opportunity to better understand these relationships within populations and inform public policy to address these issues,” Dr. Walter and Dr. Sandsmark write.

The study was funded by the Japan Agency for Medical Research and Development and Suntory Holdings Limited. Dr. Ninomiya reports receiving grants from Suntory Holdings Limited.

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

Stiff arteries may cause, rather than be a consequence of, metabolic syndrome, results of a longitudinal birth cohort study show.

New research published in the American Journal of Physiology found that arterial stiffness occurred before the presence of metabolic syndrome. A progressive rise in stiffness was associated with a cumulative increase in risk for the condition among the 3,862 people studied over a 7-year period starting in late adolescence. 

Results revealed a notable sex difference: Arterial stiffness increased the risk for metabolic syndrome by 9% for males but only by 1% for females. Males were also five times more likely than females to have metabolic syndrome.

“It seems metabolic syndrome has a new risk factor we haven’t thought about,” said author Andrew O. Agbaje, MD, clinical epidemiologist and researcher, University of Eastern Finland, Kuopio.

Arterial stiffness previously was associated with metabolic syndrome in numerous studies. But the new work is the first to find evidence for causality, Dr. Agbaje said in an interview.

“Interventions have focused on addressing the components of metabolic syndrome such as obesity, dyslipidemia, hyperglycemia, and hypertension,” Dr. Agbaje said. “But arterial stiffness may independently cause metabolic syndrome in 1 out of 10 male teens. I encourage clinicians to think about its role in preventing and managing metabolic syndrome, not just as a consequence but as a cause.”

The results have important implications for physicians, according to Sissi Cossio, MD, pediatric endocrinologist, Pediatrix Medical Group, Fort Lauderdale, Fla.

“The fact that arterial stiffness progression preceded metabolic syndrome is important because it could be used as an earlier detection marker of disease,” Dr. Cossio said.

To conduct the study, Dr. Agbaje and his research team used data collected by the Avon Longitudinal Study of Parents and Children at the University of Bristol in England. Arterial stiffness was measured using carotid-femoral pulse wave velocity, the speed of blood flow from the upper to the lower aorta. They assessed for metabolic syndrome by the presence of three or more risk factors, including high cholesterol, high triglycerides, and high trunk fat mass.

Participants were studied starting in gestation in the early 1990s, and were measured for arterial stiffness and metabolic syndrome starting at age 17 through age 24.

The overall risk for metabolic syndrome doubled within the 7-year study period of follow-up between 2009 and 2017, indicating that early intervention during adolescence is essential. 

Dr. Agbaje recommended that physicians start treating arterial stiffness and other markers of metabolic syndrome as early as possible, noting that, “potentially irreversible cardiovascular health damage might occur after age 17.” 

Arterial stiffness can be negated through physical activity and dietary changes that lower inflammation. Physicians should refer at-risk teens to a preventative clinic where they can be monitored and receive repeated measurements of arterial stiffness, lipid levels, blood pressure, glucose levels, and obesity every 3 months, Dr. Agbaje said.

“The health progress made after a year would be an indicator for physicians whether a more aggressive therapeutic approach is needed since it takes about 7 years for the risk of metabolic syndrome attributed to arterial stiffness to worsen remarkably in the young population,” he said.

Dr. Agbaje pointed to a few potential pathways through which arterial stiffness might create a disease cascade. Stiffer arteries disrupt blood flow to the liver and pancreas, which could adversely affect their functioning, he said. Damage to these organs may increase insulin and LDL cholesterol blood levels, increasing the risk for metabolic syndrome.

Arterial stiffness also can lead to higher blood pressure and insulin resistance, potentially inducing musculogenesis and vasculogenesis. The resulting excessive muscle mass may also increase the risk for the condition, he said.

Dr. Cossio acknowledged that treatments for metabolic syndrome become less effective with age, but emphasized that reversal is possible in adults with lifestyle changes and medications.

“Early detection will give patients the best chance at reversing the disease, and [primary care physicians] are a key factor in this process,” she said.

Dr. Cossio said that at-risk teens should receive treatment in a weight loss or endocrinology clinic. Treatment may include behavioral, surgical, and pharmacotherapeutic interventions.

“Teens with signs of insulin resistance and impaired fasting glucose, acanthosis, or prediabetes, should start metformin as the first line of therapy,” Dr. Cossio said. 

For weight management, she recommends antiobesity medications such as liraglutide, semaglutide, and the combination of phentermine/topiramate in children aged 12 years or older. In teenagers 16 years or older, phentermine alone is another option.

The research group that conducted the study reported received funding from the Jenny and Antti Wihuri Foundation, the North Savo Regional Fund and Central Finnish Cultural Foundation, the Aarne Koskelo Foundation, the Foundation for Pediatric Research, and the Finnish Foundation for Cardiovascular Research, among others. The authors declared no conflicts of interest, financial or otherwise.
 

A version of this article appeared on Medscape.com.

Stiff arteries may cause, rather than be a consequence of, metabolic syndrome, results of a longitudinal birth cohort study show.

New research published in the American Journal of Physiology found that arterial stiffness occurred before the presence of metabolic syndrome. A progressive rise in stiffness was associated with a cumulative increase in risk for the condition among the 3,862 people studied over a 7-year period starting in late adolescence. 

Results revealed a notable sex difference: Arterial stiffness increased the risk for metabolic syndrome by 9% for males but only by 1% for females. Males were also five times more likely than females to have metabolic syndrome.

“It seems metabolic syndrome has a new risk factor we haven’t thought about,” said author Andrew O. Agbaje, MD, clinical epidemiologist and researcher, University of Eastern Finland, Kuopio.

Arterial stiffness previously was associated with metabolic syndrome in numerous studies. But the new work is the first to find evidence for causality, Dr. Agbaje said in an interview.

“Interventions have focused on addressing the components of metabolic syndrome such as obesity, dyslipidemia, hyperglycemia, and hypertension,” Dr. Agbaje said. “But arterial stiffness may independently cause metabolic syndrome in 1 out of 10 male teens. I encourage clinicians to think about its role in preventing and managing metabolic syndrome, not just as a consequence but as a cause.”

The results have important implications for physicians, according to Sissi Cossio, MD, pediatric endocrinologist, Pediatrix Medical Group, Fort Lauderdale, Fla.

“The fact that arterial stiffness progression preceded metabolic syndrome is important because it could be used as an earlier detection marker of disease,” Dr. Cossio said.

To conduct the study, Dr. Agbaje and his research team used data collected by the Avon Longitudinal Study of Parents and Children at the University of Bristol in England. Arterial stiffness was measured using carotid-femoral pulse wave velocity, the speed of blood flow from the upper to the lower aorta. They assessed for metabolic syndrome by the presence of three or more risk factors, including high cholesterol, high triglycerides, and high trunk fat mass.

Participants were studied starting in gestation in the early 1990s, and were measured for arterial stiffness and metabolic syndrome starting at age 17 through age 24.

The overall risk for metabolic syndrome doubled within the 7-year study period of follow-up between 2009 and 2017, indicating that early intervention during adolescence is essential. 

Dr. Agbaje recommended that physicians start treating arterial stiffness and other markers of metabolic syndrome as early as possible, noting that, “potentially irreversible cardiovascular health damage might occur after age 17.” 

Arterial stiffness can be negated through physical activity and dietary changes that lower inflammation. Physicians should refer at-risk teens to a preventative clinic where they can be monitored and receive repeated measurements of arterial stiffness, lipid levels, blood pressure, glucose levels, and obesity every 3 months, Dr. Agbaje said.

“The health progress made after a year would be an indicator for physicians whether a more aggressive therapeutic approach is needed since it takes about 7 years for the risk of metabolic syndrome attributed to arterial stiffness to worsen remarkably in the young population,” he said.

Dr. Agbaje pointed to a few potential pathways through which arterial stiffness might create a disease cascade. Stiffer arteries disrupt blood flow to the liver and pancreas, which could adversely affect their functioning, he said. Damage to these organs may increase insulin and LDL cholesterol blood levels, increasing the risk for metabolic syndrome.

Arterial stiffness also can lead to higher blood pressure and insulin resistance, potentially inducing musculogenesis and vasculogenesis. The resulting excessive muscle mass may also increase the risk for the condition, he said.

Dr. Cossio acknowledged that treatments for metabolic syndrome become less effective with age, but emphasized that reversal is possible in adults with lifestyle changes and medications.

“Early detection will give patients the best chance at reversing the disease, and [primary care physicians] are a key factor in this process,” she said.

Dr. Cossio said that at-risk teens should receive treatment in a weight loss or endocrinology clinic. Treatment may include behavioral, surgical, and pharmacotherapeutic interventions.

“Teens with signs of insulin resistance and impaired fasting glucose, acanthosis, or prediabetes, should start metformin as the first line of therapy,” Dr. Cossio said. 

For weight management, she recommends antiobesity medications such as liraglutide, semaglutide, and the combination of phentermine/topiramate in children aged 12 years or older. In teenagers 16 years or older, phentermine alone is another option.

The research group that conducted the study reported received funding from the Jenny and Antti Wihuri Foundation, the North Savo Regional Fund and Central Finnish Cultural Foundation, the Aarne Koskelo Foundation, the Foundation for Pediatric Research, and the Finnish Foundation for Cardiovascular Research, among others. The authors declared no conflicts of interest, financial or otherwise.
 

A version of this article appeared on Medscape.com.

Stiff arteries may cause, rather than be a consequence of, metabolic syndrome, results of a longitudinal birth cohort study show.

New research published in the American Journal of Physiology found that arterial stiffness occurred before the presence of metabolic syndrome. A progressive rise in stiffness was associated with a cumulative increase in risk for the condition among the 3,862 people studied over a 7-year period starting in late adolescence. 

Results revealed a notable sex difference: Arterial stiffness increased the risk for metabolic syndrome by 9% for males but only by 1% for females. Males were also five times more likely than females to have metabolic syndrome.

“It seems metabolic syndrome has a new risk factor we haven’t thought about,” said author Andrew O. Agbaje, MD, clinical epidemiologist and researcher, University of Eastern Finland, Kuopio.

Arterial stiffness previously was associated with metabolic syndrome in numerous studies. But the new work is the first to find evidence for causality, Dr. Agbaje said in an interview.

“Interventions have focused on addressing the components of metabolic syndrome such as obesity, dyslipidemia, hyperglycemia, and hypertension,” Dr. Agbaje said. “But arterial stiffness may independently cause metabolic syndrome in 1 out of 10 male teens. I encourage clinicians to think about its role in preventing and managing metabolic syndrome, not just as a consequence but as a cause.”

The results have important implications for physicians, according to Sissi Cossio, MD, pediatric endocrinologist, Pediatrix Medical Group, Fort Lauderdale, Fla.

“The fact that arterial stiffness progression preceded metabolic syndrome is important because it could be used as an earlier detection marker of disease,” Dr. Cossio said.

To conduct the study, Dr. Agbaje and his research team used data collected by the Avon Longitudinal Study of Parents and Children at the University of Bristol in England. Arterial stiffness was measured using carotid-femoral pulse wave velocity, the speed of blood flow from the upper to the lower aorta. They assessed for metabolic syndrome by the presence of three or more risk factors, including high cholesterol, high triglycerides, and high trunk fat mass.

Participants were studied starting in gestation in the early 1990s, and were measured for arterial stiffness and metabolic syndrome starting at age 17 through age 24.

The overall risk for metabolic syndrome doubled within the 7-year study period of follow-up between 2009 and 2017, indicating that early intervention during adolescence is essential. 

Dr. Agbaje recommended that physicians start treating arterial stiffness and other markers of metabolic syndrome as early as possible, noting that, “potentially irreversible cardiovascular health damage might occur after age 17.” 

Arterial stiffness can be negated through physical activity and dietary changes that lower inflammation. Physicians should refer at-risk teens to a preventative clinic where they can be monitored and receive repeated measurements of arterial stiffness, lipid levels, blood pressure, glucose levels, and obesity every 3 months, Dr. Agbaje said.

“The health progress made after a year would be an indicator for physicians whether a more aggressive therapeutic approach is needed since it takes about 7 years for the risk of metabolic syndrome attributed to arterial stiffness to worsen remarkably in the young population,” he said.

Dr. Agbaje pointed to a few potential pathways through which arterial stiffness might create a disease cascade. Stiffer arteries disrupt blood flow to the liver and pancreas, which could adversely affect their functioning, he said. Damage to these organs may increase insulin and LDL cholesterol blood levels, increasing the risk for metabolic syndrome.

Arterial stiffness also can lead to higher blood pressure and insulin resistance, potentially inducing musculogenesis and vasculogenesis. The resulting excessive muscle mass may also increase the risk for the condition, he said.

Dr. Cossio acknowledged that treatments for metabolic syndrome become less effective with age, but emphasized that reversal is possible in adults with lifestyle changes and medications.

“Early detection will give patients the best chance at reversing the disease, and [primary care physicians] are a key factor in this process,” she said.

Dr. Cossio said that at-risk teens should receive treatment in a weight loss or endocrinology clinic. Treatment may include behavioral, surgical, and pharmacotherapeutic interventions.

“Teens with signs of insulin resistance and impaired fasting glucose, acanthosis, or prediabetes, should start metformin as the first line of therapy,” Dr. Cossio said. 

For weight management, she recommends antiobesity medications such as liraglutide, semaglutide, and the combination of phentermine/topiramate in children aged 12 years or older. In teenagers 16 years or older, phentermine alone is another option.

The research group that conducted the study reported received funding from the Jenny and Antti Wihuri Foundation, the North Savo Regional Fund and Central Finnish Cultural Foundation, the Aarne Koskelo Foundation, the Foundation for Pediatric Research, and the Finnish Foundation for Cardiovascular Research, among others. The authors declared no conflicts of interest, financial or otherwise.
 

A version of this article appeared on Medscape.com.

Abbott is recalling the Amplatzer steerable delivery sheath, used to deliver the Amplatzer Amulet left atrial appendage occluder during cardiac catheterization, because of an increased risk of air embolism, the Food and Drug Administration has announced.

Air embolism can lead to injuries such as acute reduction in blood flow to the heart (indicated by ST elevation), tachycardia, bradycardia, hypotension, and oxygen desaturation, as well as stroke and death, the FDA said in a recall notice.

Because of the potential for serious injury or death, the agency has identified this as a class I recall, the most serious type.

To date, Abbott has reported 26 incidents, 16 injuries, and no deaths related to this issue.

According to the recall notice, the overall reported incidence rate of observed or potential cases of air embolism during procedures in which the product was used is 0.77%.

The recall includes 672 devices (model: ASDS-14F-075) that were distributed from Oct. 4, 2022, to Feb. 22, 2023.

Abbott sent a medical device recall notice to customers in June asking them to return any remaining unused Amplatzer steerable delivery sheaths to Abbott and to complete an enclosed acknowledgment form.

The company advises use of the fixed curve TorqVue 45° x 45° delivery system for future Amplatzer Amulet left atrial appendage occluder implants.

Customers with questions about this recall should contact their local Abbott representative or Abbott support at 1-800-544-1664 (option 2).

A version of this article appeared on Medscape.com.

Abbott is recalling the Amplatzer steerable delivery sheath, used to deliver the Amplatzer Amulet left atrial appendage occluder during cardiac catheterization, because of an increased risk of air embolism, the Food and Drug Administration has announced.

Air embolism can lead to injuries such as acute reduction in blood flow to the heart (indicated by ST elevation), tachycardia, bradycardia, hypotension, and oxygen desaturation, as well as stroke and death, the FDA said in a recall notice.

Because of the potential for serious injury or death, the agency has identified this as a class I recall, the most serious type.

To date, Abbott has reported 26 incidents, 16 injuries, and no deaths related to this issue.

According to the recall notice, the overall reported incidence rate of observed or potential cases of air embolism during procedures in which the product was used is 0.77%.

The recall includes 672 devices (model: ASDS-14F-075) that were distributed from Oct. 4, 2022, to Feb. 22, 2023.

Abbott sent a medical device recall notice to customers in June asking them to return any remaining unused Amplatzer steerable delivery sheaths to Abbott and to complete an enclosed acknowledgment form.

The company advises use of the fixed curve TorqVue 45° x 45° delivery system for future Amplatzer Amulet left atrial appendage occluder implants.

Customers with questions about this recall should contact their local Abbott representative or Abbott support at 1-800-544-1664 (option 2).

A version of this article appeared on Medscape.com.

Abbott is recalling the Amplatzer steerable delivery sheath, used to deliver the Amplatzer Amulet left atrial appendage occluder during cardiac catheterization, because of an increased risk of air embolism, the Food and Drug Administration has announced.

Air embolism can lead to injuries such as acute reduction in blood flow to the heart (indicated by ST elevation), tachycardia, bradycardia, hypotension, and oxygen desaturation, as well as stroke and death, the FDA said in a recall notice.

Because of the potential for serious injury or death, the agency has identified this as a class I recall, the most serious type.

To date, Abbott has reported 26 incidents, 16 injuries, and no deaths related to this issue.

According to the recall notice, the overall reported incidence rate of observed or potential cases of air embolism during procedures in which the product was used is 0.77%.

The recall includes 672 devices (model: ASDS-14F-075) that were distributed from Oct. 4, 2022, to Feb. 22, 2023.

Abbott sent a medical device recall notice to customers in June asking them to return any remaining unused Amplatzer steerable delivery sheaths to Abbott and to complete an enclosed acknowledgment form.

The company advises use of the fixed curve TorqVue 45° x 45° delivery system for future Amplatzer Amulet left atrial appendage occluder implants.

Customers with questions about this recall should contact their local Abbott representative or Abbott support at 1-800-544-1664 (option 2).

A version of this article appeared on Medscape.com.

TOPLINE

The use of magnetic resonance–guided daily adaptive stereotactic body radiotherapy for patients with prostate cancer reduces the risk of acute urinary side effects of grade 2 or higher by 44% and the risk of acute bowel side effects of grade 2 or higher by 60%, compared with standard CT-guided SBRT (CT‐SBRT).

METHODOLOGY

• With the use of magnetic resonance–guided daily adaptive SBRT, clinicians can customize radiation dosing to accommodate changes in prostate anatomy during treatment, which may also make SBRT safer and less toxic for patients.
• To determine whether this approach does reduce patient side effects, investigators ran a meta-analysis that included 29 studies with 2547 patients comparing the incidence of short-term, physician-assessed bowel and genitourinary side effects between the MRI-guided approach and standard CT-SBRT.
• The investigators reported no statistically significant differences in age, prescribed radiation doses, planning target volumes, or International Prostatism Symptom Scores between the two groups; the use of rectal spacers and the number of patients who received pelvic lymph node radiation were low in both.
• The average window for collecting acute toxicity data was 70 days in the MRI-guided investigations and 94 days in CT-SBRT investigations.

TAKEAWAY

• The pooled estimate for acute grade 2 or higher genitourinary toxicity was 16% with MRI-guided SBRT versus 28% with CT-SBRT (odds ratio, 0.56; P = .04).
• The pooled estimate for grade 2 or higher gastrointestinal toxicity was 4% with the MRI approach versus 9% with CT-SBRT (OR, 0.40; P = .04).
• There were no differences in grade 3 or higher events, which were rare, between the groups.
• There was also no difference in toxicity among CT‐SBRT studies that used fiducial markers and those that did not.

IN PRACTICE

“These findings suggest that the technical advantages in precision of radiotherapy delivery afforded by [MRI-guided] SBRT translate to measurable clinical benefit,” the authors concluded. Potential reasons for the reduced risk of acute toxicity with the MRI-guided approach include “daily online adaptive planning, MRI‐based contouring that results in smaller treatment volumes, and MRI tracking, all of which may facilitate the precision and accuracy of treatment delivery.”

SOURCE

The study was led by Jonathan Leeman, MD, of the Dana-Farber Cancer Institute, Boston, and was published July 24 in Cancer.

LIMITATIONS

• The analysis did not account for differences in dosimetry, radiation planning, and toxicity management and assessment between the studies.
• Late toxicity and cancer control rates were not tracked and may have differed between the two approaches.

DISCLOSURES

• No external funding was reported.
• The investigators reported grants and consulting, personal, and other payments from Novartis, AstraZeneca, Janssen, and other companies.

A version of this article appeared on Medscape.com.

TOPLINE

The use of magnetic resonance–guided daily adaptive stereotactic body radiotherapy for patients with prostate cancer reduces the risk of acute urinary side effects of grade 2 or higher by 44% and the risk of acute bowel side effects of grade 2 or higher by 60%, compared with standard CT-guided SBRT (CT‐SBRT).

METHODOLOGY

• With the use of magnetic resonance–guided daily adaptive SBRT, clinicians can customize radiation dosing to accommodate changes in prostate anatomy during treatment, which may also make SBRT safer and less toxic for patients.
• To determine whether this approach does reduce patient side effects, investigators ran a meta-analysis that included 29 studies with 2547 patients comparing the incidence of short-term, physician-assessed bowel and genitourinary side effects between the MRI-guided approach and standard CT-SBRT.
• The investigators reported no statistically significant differences in age, prescribed radiation doses, planning target volumes, or International Prostatism Symptom Scores between the two groups; the use of rectal spacers and the number of patients who received pelvic lymph node radiation were low in both.
• The average window for collecting acute toxicity data was 70 days in the MRI-guided investigations and 94 days in CT-SBRT investigations.

TAKEAWAY

• The pooled estimate for acute grade 2 or higher genitourinary toxicity was 16% with MRI-guided SBRT versus 28% with CT-SBRT (odds ratio, 0.56; P = .04).
• The pooled estimate for grade 2 or higher gastrointestinal toxicity was 4% with the MRI approach versus 9% with CT-SBRT (OR, 0.40; P = .04).
• There were no differences in grade 3 or higher events, which were rare, between the groups.
• There was also no difference in toxicity among CT‐SBRT studies that used fiducial markers and those that did not.

IN PRACTICE

“These findings suggest that the technical advantages in precision of radiotherapy delivery afforded by [MRI-guided] SBRT translate to measurable clinical benefit,” the authors concluded. Potential reasons for the reduced risk of acute toxicity with the MRI-guided approach include “daily online adaptive planning, MRI‐based contouring that results in smaller treatment volumes, and MRI tracking, all of which may facilitate the precision and accuracy of treatment delivery.”

SOURCE

The study was led by Jonathan Leeman, MD, of the Dana-Farber Cancer Institute, Boston, and was published July 24 in Cancer.

LIMITATIONS

• The analysis did not account for differences in dosimetry, radiation planning, and toxicity management and assessment between the studies.
• Late toxicity and cancer control rates were not tracked and may have differed between the two approaches.

DISCLOSURES

• No external funding was reported.
• The investigators reported grants and consulting, personal, and other payments from Novartis, AstraZeneca, Janssen, and other companies.

A version of this article appeared on Medscape.com.

TOPLINE

The use of magnetic resonance–guided daily adaptive stereotactic body radiotherapy for patients with prostate cancer reduces the risk of acute urinary side effects of grade 2 or higher by 44% and the risk of acute bowel side effects of grade 2 or higher by 60%, compared with standard CT-guided SBRT (CT‐SBRT).

METHODOLOGY

• With the use of magnetic resonance–guided daily adaptive SBRT, clinicians can customize radiation dosing to accommodate changes in prostate anatomy during treatment, which may also make SBRT safer and less toxic for patients.
• To determine whether this approach does reduce patient side effects, investigators ran a meta-analysis that included 29 studies with 2547 patients comparing the incidence of short-term, physician-assessed bowel and genitourinary side effects between the MRI-guided approach and standard CT-SBRT.
• The investigators reported no statistically significant differences in age, prescribed radiation doses, planning target volumes, or International Prostatism Symptom Scores between the two groups; the use of rectal spacers and the number of patients who received pelvic lymph node radiation were low in both.
• The average window for collecting acute toxicity data was 70 days in the MRI-guided investigations and 94 days in CT-SBRT investigations.

TAKEAWAY

• The pooled estimate for acute grade 2 or higher genitourinary toxicity was 16% with MRI-guided SBRT versus 28% with CT-SBRT (odds ratio, 0.56; P = .04).
• The pooled estimate for grade 2 or higher gastrointestinal toxicity was 4% with the MRI approach versus 9% with CT-SBRT (OR, 0.40; P = .04).
• There were no differences in grade 3 or higher events, which were rare, between the groups.
• There was also no difference in toxicity among CT‐SBRT studies that used fiducial markers and those that did not.

IN PRACTICE

“These findings suggest that the technical advantages in precision of radiotherapy delivery afforded by [MRI-guided] SBRT translate to measurable clinical benefit,” the authors concluded. Potential reasons for the reduced risk of acute toxicity with the MRI-guided approach include “daily online adaptive planning, MRI‐based contouring that results in smaller treatment volumes, and MRI tracking, all of which may facilitate the precision and accuracy of treatment delivery.”

SOURCE

The study was led by Jonathan Leeman, MD, of the Dana-Farber Cancer Institute, Boston, and was published July 24 in Cancer.

LIMITATIONS

• The analysis did not account for differences in dosimetry, radiation planning, and toxicity management and assessment between the studies.
• Late toxicity and cancer control rates were not tracked and may have differed between the two approaches.

DISCLOSURES

• No external funding was reported.
• The investigators reported grants and consulting, personal, and other payments from Novartis, AstraZeneca, Janssen, and other companies.

A version of this article appeared on Medscape.com.

Family members with pulmonary fibrosis showed correlations for predicted forced vital capacity trajectories and computed tomography patterns, based on data from 101 individuals in 45 families.

Patients with familial pulmonary fibrosis (FPF), defined as fibrotic interstitial lung disease among two or more first-degree or second-degree relatives, have worse survival than that of patients with sporadic pulmonary fibrosis, wrote Tinne Goos, MD, of KU Leuven, Belgium, and colleagues. Diagnosis of FPF diagnosis is mainly based on family history, and data on intrafamilial correlations are lacking, they said.

In a study published in the journal Chest, the researchers identified FPF patients treated at a single center. The study population included 101 patients from 45 families; most of these (34) were siblings. Overall, 61.4% of the participants were men, 69.3% were ever-smokers, and 84.2% had idiopathic pulmonary fibrosis.

The analysis included data on computed tomography (CT) scanning and predicted forced vital capacity (FVC%), as well as age at diagnosis, treatment type, gender, smoking history, and date of diagnosis.

Overall, FVC%predicted was significantly correlated within families, with a correlation of 0.75. The annual change in FVC was –158.2 mL, and the annual change in FVC%predicted was –6.3%.

Sixty-five patients received antifibrotic treatment, and 18 received immunosuppressive treatment. Immunosuppressive treatment remained significantly correlated among families in a multivariate analysis, with a correlation of 0.77.

“Age at diagnosis correlated within a generation, while patients from a second generation were diagnosed younger,” the researchers noted. The current study findings and results from other studies suggest a genetic basis for FPF age of onset, and determining an age range for screening unaffected relatives based on the age at diagnosis of affected relatives might be useful, they said.

In addition, 42.2% of families showed concordance of CT scan patterns. Typical usual interstitial pneumonia (UIP) appeared in 35 patients, atypical UIP in 36 patients, UIP with emphysema in 9 patients, and findings incompatible with UIP in 21 patients.

The study findings were limited by several factors including the retrospective design and use of data from a single center, as well as by the changes in clinical practice guidelines between 2004 and 2019, with increases in genetic testing, the researchers noted.

However, the current study is the first known to report on FVC evolution within families in FPF, they said. Future studies of both intra- and interfamilial correlation and variability are needed to identify the genetic and environmental factors that may affect disease manifestation and progression, they concluded.

The study was supported by Research Foundation-Flanders. Dr. Goos had no financial conflicts to disclose.

Family members with pulmonary fibrosis showed correlations for predicted forced vital capacity trajectories and computed tomography patterns, based on data from 101 individuals in 45 families.

Patients with familial pulmonary fibrosis (FPF), defined as fibrotic interstitial lung disease among two or more first-degree or second-degree relatives, have worse survival than that of patients with sporadic pulmonary fibrosis, wrote Tinne Goos, MD, of KU Leuven, Belgium, and colleagues. Diagnosis of FPF diagnosis is mainly based on family history, and data on intrafamilial correlations are lacking, they said.

In a study published in the journal Chest, the researchers identified FPF patients treated at a single center. The study population included 101 patients from 45 families; most of these (34) were siblings. Overall, 61.4% of the participants were men, 69.3% were ever-smokers, and 84.2% had idiopathic pulmonary fibrosis.

The analysis included data on computed tomography (CT) scanning and predicted forced vital capacity (FVC%), as well as age at diagnosis, treatment type, gender, smoking history, and date of diagnosis.

Overall, FVC%predicted was significantly correlated within families, with a correlation of 0.75. The annual change in FVC was –158.2 mL, and the annual change in FVC%predicted was –6.3%.

Sixty-five patients received antifibrotic treatment, and 18 received immunosuppressive treatment. Immunosuppressive treatment remained significantly correlated among families in a multivariate analysis, with a correlation of 0.77.

“Age at diagnosis correlated within a generation, while patients from a second generation were diagnosed younger,” the researchers noted. The current study findings and results from other studies suggest a genetic basis for FPF age of onset, and determining an age range for screening unaffected relatives based on the age at diagnosis of affected relatives might be useful, they said.

In addition, 42.2% of families showed concordance of CT scan patterns. Typical usual interstitial pneumonia (UIP) appeared in 35 patients, atypical UIP in 36 patients, UIP with emphysema in 9 patients, and findings incompatible with UIP in 21 patients.

The study findings were limited by several factors including the retrospective design and use of data from a single center, as well as by the changes in clinical practice guidelines between 2004 and 2019, with increases in genetic testing, the researchers noted.

However, the current study is the first known to report on FVC evolution within families in FPF, they said. Future studies of both intra- and interfamilial correlation and variability are needed to identify the genetic and environmental factors that may affect disease manifestation and progression, they concluded.

The study was supported by Research Foundation-Flanders. Dr. Goos had no financial conflicts to disclose.

Family members with pulmonary fibrosis showed correlations for predicted forced vital capacity trajectories and computed tomography patterns, based on data from 101 individuals in 45 families.

Patients with familial pulmonary fibrosis (FPF), defined as fibrotic interstitial lung disease among two or more first-degree or second-degree relatives, have worse survival than that of patients with sporadic pulmonary fibrosis, wrote Tinne Goos, MD, of KU Leuven, Belgium, and colleagues. Diagnosis of FPF diagnosis is mainly based on family history, and data on intrafamilial correlations are lacking, they said.

In a study published in the journal Chest, the researchers identified FPF patients treated at a single center. The study population included 101 patients from 45 families; most of these (34) were siblings. Overall, 61.4% of the participants were men, 69.3% were ever-smokers, and 84.2% had idiopathic pulmonary fibrosis.

The analysis included data on computed tomography (CT) scanning and predicted forced vital capacity (FVC%), as well as age at diagnosis, treatment type, gender, smoking history, and date of diagnosis.

Overall, FVC%predicted was significantly correlated within families, with a correlation of 0.75. The annual change in FVC was –158.2 mL, and the annual change in FVC%predicted was –6.3%.

Sixty-five patients received antifibrotic treatment, and 18 received immunosuppressive treatment. Immunosuppressive treatment remained significantly correlated among families in a multivariate analysis, with a correlation of 0.77.

“Age at diagnosis correlated within a generation, while patients from a second generation were diagnosed younger,” the researchers noted. The current study findings and results from other studies suggest a genetic basis for FPF age of onset, and determining an age range for screening unaffected relatives based on the age at diagnosis of affected relatives might be useful, they said.

In addition, 42.2% of families showed concordance of CT scan patterns. Typical usual interstitial pneumonia (UIP) appeared in 35 patients, atypical UIP in 36 patients, UIP with emphysema in 9 patients, and findings incompatible with UIP in 21 patients.

The study findings were limited by several factors including the retrospective design and use of data from a single center, as well as by the changes in clinical practice guidelines between 2004 and 2019, with increases in genetic testing, the researchers noted.

However, the current study is the first known to report on FVC evolution within families in FPF, they said. Future studies of both intra- and interfamilial correlation and variability are needed to identify the genetic and environmental factors that may affect disease manifestation and progression, they concluded.

The study was supported by Research Foundation-Flanders. Dr. Goos had no financial conflicts to disclose.

The Diagnosis: Scrotal Calcinosis

Scrotal calcinosis is a rare benign disease that results from the deposition of calcium, magnesium, phosphate, and carbonate within the dermis and subcutaneous layer of the skin in the absence of underlying systemic disease or serum calcium and phosphorus abnormalities.^1,2 Lesions usually are asymptomatic but can be mildly painful or pruritic. They usually present in childhood or early adulthood as yellow-white firm nodules ranging in size from a few millimeters to a few centimeters that increase in size and number over time. Additionally, lesions can ulcerate and discharge a chalklike exudative material. Although benign in nature, the quality-of-life impact in patients with this condition can be substantial, specifically regarding cosmesis, which may cause patients to feel embarrassed and even avoid sexual activity. This condition rarely has been associated with infection.¹

Our patient elected to undergo surgical excision under local anesthesia, and the lesions were sent for histopathologic examination. His postoperative course was unremarkable, and he was pleased with the cosmetic result of the surgery (Figure 1). Histopathology revealed calcified deposits that appeared as intradermal basophilic nodules lacking an epithelial lining (Figure 2), consistent with the diagnosis of scrotal calcinosis.² No recurrence of the lesions was documented over the course of 18 months.

The pathogenesis of this condition is not clear. Most research supports scrotal calcinosis resulting from dystrophic calcification of epidermal inclusion cysts.³ There have been cases of scrotal calcinosis coinciding with epidermal inclusion cysts of the scrotum in varying stages of inflammation (some intact and some ruptured).² Some research also suggests dystrophic calcification of eccrine epithelial cysts and degenerated dartos muscle as the origin of scrotal calcinosis.³

The differential diagnosis for this case included calcified steatocystoma multiplex, eruptive xanthomas, nodular scabies, and epidermal inclusion cysts. Steatocystoma multiplex can be inherited in an autosomal-dominant fashion or can develop sporadically with mutations in the KRT17 gene.⁴ It is characterized by multiple sebum-filled, cystic lesions of the pilosebaceous unit that may become calcified. Calcified lesions appear as yellow, firm, irregularly shaped papules or nodules ranging from a few millimeters to centimeters in size. Cysts can develop anywhere on the body with a predilection for the chest, upper extremities, axillae, trunk, groin, and scrotum.⁴ Histologically, our patient’s lesions were not associated with the pilosebaceous unit. Additionally, our patient denied a family history of similar skin lesions, which made calcified steatocystoma multiplex an unlikely diagnosis.

Eruptive xanthomas result from localized deposition of lipids within the dermis, typically in the setting of dyslipidemia or poorly controlled diabetes mellitus. They commonly appear on the extremities or buttocks as pruritic crops of yellow-red papules or nodules that are a few millimeters in size. Although our patient has a history of hyperlipidemia, his lesions differed substantially from eruptive xanthomas in clinical presentation.

Nodular scabies is a manifestation of classic scabies that presents with intensely pruritic erythematous papules and nodules that are a few millimeters in size and commonly occur on the axillae, groin, and genitalia. Our patient’s skin lesions were not pruritic and differed in appearance from nodular scabies.

Although research indicates scrotal calcinosis may result from dystrophic calcification of epidermal inclusion cysts,² the latter present as dome-shaped, flesh-colored nodules with central pores representing the opening of hair follicles. Our patient lacked characteristic findings of epidermal inclusion cysts on histology.

The preferred treatment for scrotal calcinosis is surgical excision, which improves the aesthetic appearance, relieves itch, and removes ulcerative lesions.⁵ Additionally, surgical excision provides histological diagnostic confirmation. Recurrence with incomplete excision is possible; therefore, all lesions should be completely excised to reduce the risk for recurrence.³

The Diagnosis: Scrotal Calcinosis

Scrotal calcinosis is a rare benign disease that results from the deposition of calcium, magnesium, phosphate, and carbonate within the dermis and subcutaneous layer of the skin in the absence of underlying systemic disease or serum calcium and phosphorus abnormalities.^1,2 Lesions usually are asymptomatic but can be mildly painful or pruritic. They usually present in childhood or early adulthood as yellow-white firm nodules ranging in size from a few millimeters to a few centimeters that increase in size and number over time. Additionally, lesions can ulcerate and discharge a chalklike exudative material. Although benign in nature, the quality-of-life impact in patients with this condition can be substantial, specifically regarding cosmesis, which may cause patients to feel embarrassed and even avoid sexual activity. This condition rarely has been associated with infection.¹

Our patient elected to undergo surgical excision under local anesthesia, and the lesions were sent for histopathologic examination. His postoperative course was unremarkable, and he was pleased with the cosmetic result of the surgery (Figure 1). Histopathology revealed calcified deposits that appeared as intradermal basophilic nodules lacking an epithelial lining (Figure 2), consistent with the diagnosis of scrotal calcinosis.² No recurrence of the lesions was documented over the course of 18 months.

The pathogenesis of this condition is not clear. Most research supports scrotal calcinosis resulting from dystrophic calcification of epidermal inclusion cysts.³ There have been cases of scrotal calcinosis coinciding with epidermal inclusion cysts of the scrotum in varying stages of inflammation (some intact and some ruptured).² Some research also suggests dystrophic calcification of eccrine epithelial cysts and degenerated dartos muscle as the origin of scrotal calcinosis.³

The differential diagnosis for this case included calcified steatocystoma multiplex, eruptive xanthomas, nodular scabies, and epidermal inclusion cysts. Steatocystoma multiplex can be inherited in an autosomal-dominant fashion or can develop sporadically with mutations in the KRT17 gene.⁴ It is characterized by multiple sebum-filled, cystic lesions of the pilosebaceous unit that may become calcified. Calcified lesions appear as yellow, firm, irregularly shaped papules or nodules ranging from a few millimeters to centimeters in size. Cysts can develop anywhere on the body with a predilection for the chest, upper extremities, axillae, trunk, groin, and scrotum.⁴ Histologically, our patient’s lesions were not associated with the pilosebaceous unit. Additionally, our patient denied a family history of similar skin lesions, which made calcified steatocystoma multiplex an unlikely diagnosis.

Eruptive xanthomas result from localized deposition of lipids within the dermis, typically in the setting of dyslipidemia or poorly controlled diabetes mellitus. They commonly appear on the extremities or buttocks as pruritic crops of yellow-red papules or nodules that are a few millimeters in size. Although our patient has a history of hyperlipidemia, his lesions differed substantially from eruptive xanthomas in clinical presentation.

Nodular scabies is a manifestation of classic scabies that presents with intensely pruritic erythematous papules and nodules that are a few millimeters in size and commonly occur on the axillae, groin, and genitalia. Our patient’s skin lesions were not pruritic and differed in appearance from nodular scabies.

Although research indicates scrotal calcinosis may result from dystrophic calcification of epidermal inclusion cysts,² the latter present as dome-shaped, flesh-colored nodules with central pores representing the opening of hair follicles. Our patient lacked characteristic findings of epidermal inclusion cysts on histology.

The preferred treatment for scrotal calcinosis is surgical excision, which improves the aesthetic appearance, relieves itch, and removes ulcerative lesions.⁵ Additionally, surgical excision provides histological diagnostic confirmation. Recurrence with incomplete excision is possible; therefore, all lesions should be completely excised to reduce the risk for recurrence.³

The Diagnosis: Scrotal Calcinosis

Scrotal calcinosis is a rare benign disease that results from the deposition of calcium, magnesium, phosphate, and carbonate within the dermis and subcutaneous layer of the skin in the absence of underlying systemic disease or serum calcium and phosphorus abnormalities.^1,2 Lesions usually are asymptomatic but can be mildly painful or pruritic. They usually present in childhood or early adulthood as yellow-white firm nodules ranging in size from a few millimeters to a few centimeters that increase in size and number over time. Additionally, lesions can ulcerate and discharge a chalklike exudative material. Although benign in nature, the quality-of-life impact in patients with this condition can be substantial, specifically regarding cosmesis, which may cause patients to feel embarrassed and even avoid sexual activity. This condition rarely has been associated with infection.¹

Our patient elected to undergo surgical excision under local anesthesia, and the lesions were sent for histopathologic examination. His postoperative course was unremarkable, and he was pleased with the cosmetic result of the surgery (Figure 1). Histopathology revealed calcified deposits that appeared as intradermal basophilic nodules lacking an epithelial lining (Figure 2), consistent with the diagnosis of scrotal calcinosis.² No recurrence of the lesions was documented over the course of 18 months.

The pathogenesis of this condition is not clear. Most research supports scrotal calcinosis resulting from dystrophic calcification of epidermal inclusion cysts.³ There have been cases of scrotal calcinosis coinciding with epidermal inclusion cysts of the scrotum in varying stages of inflammation (some intact and some ruptured).² Some research also suggests dystrophic calcification of eccrine epithelial cysts and degenerated dartos muscle as the origin of scrotal calcinosis.³

The differential diagnosis for this case included calcified steatocystoma multiplex, eruptive xanthomas, nodular scabies, and epidermal inclusion cysts. Steatocystoma multiplex can be inherited in an autosomal-dominant fashion or can develop sporadically with mutations in the KRT17 gene.⁴ It is characterized by multiple sebum-filled, cystic lesions of the pilosebaceous unit that may become calcified. Calcified lesions appear as yellow, firm, irregularly shaped papules or nodules ranging from a few millimeters to centimeters in size. Cysts can develop anywhere on the body with a predilection for the chest, upper extremities, axillae, trunk, groin, and scrotum.⁴ Histologically, our patient’s lesions were not associated with the pilosebaceous unit. Additionally, our patient denied a family history of similar skin lesions, which made calcified steatocystoma multiplex an unlikely diagnosis.

Eruptive xanthomas result from localized deposition of lipids within the dermis, typically in the setting of dyslipidemia or poorly controlled diabetes mellitus. They commonly appear on the extremities or buttocks as pruritic crops of yellow-red papules or nodules that are a few millimeters in size. Although our patient has a history of hyperlipidemia, his lesions differed substantially from eruptive xanthomas in clinical presentation.

Nodular scabies is a manifestation of classic scabies that presents with intensely pruritic erythematous papules and nodules that are a few millimeters in size and commonly occur on the axillae, groin, and genitalia. Our patient’s skin lesions were not pruritic and differed in appearance from nodular scabies.

Although research indicates scrotal calcinosis may result from dystrophic calcification of epidermal inclusion cysts,² the latter present as dome-shaped, flesh-colored nodules with central pores representing the opening of hair follicles. Our patient lacked characteristic findings of epidermal inclusion cysts on histology.

The preferred treatment for scrotal calcinosis is surgical excision, which improves the aesthetic appearance, relieves itch, and removes ulcerative lesions.⁵ Additionally, surgical excision provides histological diagnostic confirmation. Recurrence with incomplete excision is possible; therefore, all lesions should be completely excised to reduce the risk for recurrence.³

With the Food and Drug Administration’s full stamp of approval in hand, Leqembi (lecanemab) is poised to catapult us into a new era of treatment for Alzheimer’s disease. And now that the donanemab trial data are out, there’s another antiamyloid drug waiting in the wings.

To finally have true disease-modifying therapies for Alzheimer’s disease is a massive step forward for a field that’s been plagued with disappointment. But these drugs come with serious concerns and unknowns. They will require complex decision-making, putting doctors, patients, and their families in a medical quandary.

Striking the right balance between cautious optimism and realistic expectations will be a formidable challenge.
 

Managing patient and family expectations

These drugs are no magic bullet. They slow down the dementia’s progression, buying patients more time (on the order of months) before they begin to experience significant worsening. We’ll need a lot more information from research and clinical experience before we can understand how meaningful that treatment effect is. Right now, it is unclear whether eligible patients and their families will even perceive tangible differences.

In the CLARITY-AD trial, participants on lecanemab experienced a 27% slowing in the rate of cognitive decline over 18 months. Donanemab was shown to slow decline in memory and cognition by about 35% over the same time frame in the TRAILBLAZER-ALZ 2 trial. That translates to more time for patients and their families to enjoy independence, maintain normal life, and stave off the most distressing parts of the disease.

But what happens after 18 months of treatment – will the treatment effect magnify or dissipate? How much time are we really buying in the long run? Counseling patients and their families is made all the more difficult when the answers to important questions like these remain to be seen.
 

Only a sliver of Alzheimer’s patients are current candidates

The fact is that most patients living with Alzheimer’s disease will not qualify for treatment with these drugs. Lecanemab is approved for people with early-stage disease, meaning their dementia is mild or they have mild cognitive impairment, which is a precursor to full-blown Alzheimer’s disease. Of the 6 million people in the United States living with Alzheimer’s, about 1.5 million are estimated to fall into that category. We can expect to see a similar qualifier for donanemab if it receives FDA approval, especially because that trial suggested a more pronounced treatment effect for patients in the earliest stages of the disease.

Even if a patient hits the sweet spot where they have just enough cognitive impairment, but not too much, they aren’t technically therapeutic candidates until prerequisite testing confirms amyloid protein accumulation in the brain via PET scan or cerebrospinal fluid analysis.

Even then, the FDA’s boxed warning for lecanemab recommends that patients undergo genetic testing for the apo E4 mutation to identify those at a particularly high risk for severe adverse effects including brain bleeding and swelling. This recommendation is not unreasonable considering that 15% of the Alzheimer’s population has two copies of the apo E4 mutation and fall into that high-risk group.
 

Significant risks

Antiamyloid drugs are well-known to cause serious side effects. In the lecanemab trial, 13% of participants receiving Leqembi experienced brain swelling (vs. 2% of participants receiving placebo) and 17% of participants had brain bleeding (vs. 9% of participants on placebo). In the donanemab trial, brain bleeding occurred in 31.4% of participants on the drug (vs. 13.6% on placebo) and swelling occurred in 24% (vs. 2.1% receiving placebo). Thankfully, in both trials, most of these adverse events did not produce significant symptoms, but in rare cases these events caused severe or catastrophic neurologic injury, including death.

How can we best guide patients and their families to weigh the uncertain benefits against potentially serious risks? We can start by considering the patient characteristics most likely to portend increased risk for serious side effects: apo E4 mutations, blood thinner use, and the presence of microhemorrhages on brain imaging. But after that, we’re left with a lot of uncertainty in terms of which patients are most likely to see meaningful clinical improvements from the drug and unknown factors that may increase the risks of treatment.
 

A costly therapy

Medicare plans to cover 80% of lecanemab’s steep cost of $26,500 per year. Still, that will leave many patients with a hefty copay, potentially over $6,000 per year. But that only scratches the surface. Consider the frequent medical visits, repeated brain scans, laboratory tests, and infusion center appointments. It’s been estimated that all-in, the treatment will actually cost about $90,000 per year.

Yes, Medicare will reimburse a large portion of that cost, but it adds up to an estimated $2 billion per year for about 85,000 patients. This will probably spur increases to Medicare premiums, among other economic consequences for the health care system.

We’ll probably have to wait for an FDA approval decision before we know where donanemab will be priced.
 

Logistical challenges could be a rate-limiting step

Ask anyone who’s tried to see a neurologist recently, and they’ll tell you that the wait for a new patient appointment is months long. The shortage of neurologists in the United States is already a crisis, and there are even fewer cognitive neurologists. How long will patients be forced to wait for their diagnosis?

Many geriatricians will get comfortable prescribing these drugs, but will our already overburdened primary care providers have the bandwidth to do the same? It’s a tall order.

A new world of Alzheimer’s treatments also means that the infrastructure of our health care systems will need to be ramped up. Lecanemab infusions are administered every 2 weeks and donanemab every 4 weeks. Infusion centers will need to accommodate a lot more patients. And those patients will need frequent brain scans, so neuroimaging centers will need to increase their capacity to perform many more brain MRI and PET scans.
 

Antiamyloid drugs: An exciting first step

The bottom line is that these drugs aren’t the Alzheimer’s holy grail: An accessible treatment that could stop the disease in its tracks or reverse cognitive impairment. They are, however, a very promising breakthrough.

Yes, there are a ton of kinks to work out here, but this is an exciting start. Alzheimer’s research is entering a renaissance era that will hopefully bring more groundbreaking developments. Better biomarkers to facilitate faster, easier diagnosis. More drugs that go beyond amyloid proteins for their therapeutic targets. Treatments for later-stage disease. Drugs that prevent dementia altogether.

Ultimately, these new antiamyloid beta drugs are an exciting indication that we will eventually have a toolkit of Alzheimer’s drugs to choose from. For now, we’ve taken a solid step forward and there is ample reason to be hopeful for the future.

Dr. Croll is assistant professor of neurology at Temple University, Philadelphia. She reported no relevant conflicts of interest.

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

With the Food and Drug Administration’s full stamp of approval in hand, Leqembi (lecanemab) is poised to catapult us into a new era of treatment for Alzheimer’s disease. And now that the donanemab trial data are out, there’s another antiamyloid drug waiting in the wings.

To finally have true disease-modifying therapies for Alzheimer’s disease is a massive step forward for a field that’s been plagued with disappointment. But these drugs come with serious concerns and unknowns. They will require complex decision-making, putting doctors, patients, and their families in a medical quandary.

Striking the right balance between cautious optimism and realistic expectations will be a formidable challenge.
 

Managing patient and family expectations

These drugs are no magic bullet. They slow down the dementia’s progression, buying patients more time (on the order of months) before they begin to experience significant worsening. We’ll need a lot more information from research and clinical experience before we can understand how meaningful that treatment effect is. Right now, it is unclear whether eligible patients and their families will even perceive tangible differences.

In the CLARITY-AD trial, participants on lecanemab experienced a 27% slowing in the rate of cognitive decline over 18 months. Donanemab was shown to slow decline in memory and cognition by about 35% over the same time frame in the TRAILBLAZER-ALZ 2 trial. That translates to more time for patients and their families to enjoy independence, maintain normal life, and stave off the most distressing parts of the disease.

But what happens after 18 months of treatment – will the treatment effect magnify or dissipate? How much time are we really buying in the long run? Counseling patients and their families is made all the more difficult when the answers to important questions like these remain to be seen.
 

Only a sliver of Alzheimer’s patients are current candidates

The fact is that most patients living with Alzheimer’s disease will not qualify for treatment with these drugs. Lecanemab is approved for people with early-stage disease, meaning their dementia is mild or they have mild cognitive impairment, which is a precursor to full-blown Alzheimer’s disease. Of the 6 million people in the United States living with Alzheimer’s, about 1.5 million are estimated to fall into that category. We can expect to see a similar qualifier for donanemab if it receives FDA approval, especially because that trial suggested a more pronounced treatment effect for patients in the earliest stages of the disease.

Even if a patient hits the sweet spot where they have just enough cognitive impairment, but not too much, they aren’t technically therapeutic candidates until prerequisite testing confirms amyloid protein accumulation in the brain via PET scan or cerebrospinal fluid analysis.

Even then, the FDA’s boxed warning for lecanemab recommends that patients undergo genetic testing for the apo E4 mutation to identify those at a particularly high risk for severe adverse effects including brain bleeding and swelling. This recommendation is not unreasonable considering that 15% of the Alzheimer’s population has two copies of the apo E4 mutation and fall into that high-risk group.
 

Significant risks

Antiamyloid drugs are well-known to cause serious side effects. In the lecanemab trial, 13% of participants receiving Leqembi experienced brain swelling (vs. 2% of participants receiving placebo) and 17% of participants had brain bleeding (vs. 9% of participants on placebo). In the donanemab trial, brain bleeding occurred in 31.4% of participants on the drug (vs. 13.6% on placebo) and swelling occurred in 24% (vs. 2.1% receiving placebo). Thankfully, in both trials, most of these adverse events did not produce significant symptoms, but in rare cases these events caused severe or catastrophic neurologic injury, including death.

How can we best guide patients and their families to weigh the uncertain benefits against potentially serious risks? We can start by considering the patient characteristics most likely to portend increased risk for serious side effects: apo E4 mutations, blood thinner use, and the presence of microhemorrhages on brain imaging. But after that, we’re left with a lot of uncertainty in terms of which patients are most likely to see meaningful clinical improvements from the drug and unknown factors that may increase the risks of treatment.
 

A costly therapy

Medicare plans to cover 80% of lecanemab’s steep cost of $26,500 per year. Still, that will leave many patients with a hefty copay, potentially over $6,000 per year. But that only scratches the surface. Consider the frequent medical visits, repeated brain scans, laboratory tests, and infusion center appointments. It’s been estimated that all-in, the treatment will actually cost about $90,000 per year.

Yes, Medicare will reimburse a large portion of that cost, but it adds up to an estimated $2 billion per year for about 85,000 patients. This will probably spur increases to Medicare premiums, among other economic consequences for the health care system.

We’ll probably have to wait for an FDA approval decision before we know where donanemab will be priced.
 

Logistical challenges could be a rate-limiting step

Ask anyone who’s tried to see a neurologist recently, and they’ll tell you that the wait for a new patient appointment is months long. The shortage of neurologists in the United States is already a crisis, and there are even fewer cognitive neurologists. How long will patients be forced to wait for their diagnosis?

Many geriatricians will get comfortable prescribing these drugs, but will our already overburdened primary care providers have the bandwidth to do the same? It’s a tall order.

A new world of Alzheimer’s treatments also means that the infrastructure of our health care systems will need to be ramped up. Lecanemab infusions are administered every 2 weeks and donanemab every 4 weeks. Infusion centers will need to accommodate a lot more patients. And those patients will need frequent brain scans, so neuroimaging centers will need to increase their capacity to perform many more brain MRI and PET scans.
 

Antiamyloid drugs: An exciting first step

The bottom line is that these drugs aren’t the Alzheimer’s holy grail: An accessible treatment that could stop the disease in its tracks or reverse cognitive impairment. They are, however, a very promising breakthrough.

Yes, there are a ton of kinks to work out here, but this is an exciting start. Alzheimer’s research is entering a renaissance era that will hopefully bring more groundbreaking developments. Better biomarkers to facilitate faster, easier diagnosis. More drugs that go beyond amyloid proteins for their therapeutic targets. Treatments for later-stage disease. Drugs that prevent dementia altogether.

Ultimately, these new antiamyloid beta drugs are an exciting indication that we will eventually have a toolkit of Alzheimer’s drugs to choose from. For now, we’ve taken a solid step forward and there is ample reason to be hopeful for the future.

Dr. Croll is assistant professor of neurology at Temple University, Philadelphia. She reported no relevant conflicts of interest.

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

With the Food and Drug Administration’s full stamp of approval in hand, Leqembi (lecanemab) is poised to catapult us into a new era of treatment for Alzheimer’s disease. And now that the donanemab trial data are out, there’s another antiamyloid drug waiting in the wings.

To finally have true disease-modifying therapies for Alzheimer’s disease is a massive step forward for a field that’s been plagued with disappointment. But these drugs come with serious concerns and unknowns. They will require complex decision-making, putting doctors, patients, and their families in a medical quandary.

Striking the right balance between cautious optimism and realistic expectations will be a formidable challenge.
 

Managing patient and family expectations

These drugs are no magic bullet. They slow down the dementia’s progression, buying patients more time (on the order of months) before they begin to experience significant worsening. We’ll need a lot more information from research and clinical experience before we can understand how meaningful that treatment effect is. Right now, it is unclear whether eligible patients and their families will even perceive tangible differences.

In the CLARITY-AD trial, participants on lecanemab experienced a 27% slowing in the rate of cognitive decline over 18 months. Donanemab was shown to slow decline in memory and cognition by about 35% over the same time frame in the TRAILBLAZER-ALZ 2 trial. That translates to more time for patients and their families to enjoy independence, maintain normal life, and stave off the most distressing parts of the disease.

But what happens after 18 months of treatment – will the treatment effect magnify or dissipate? How much time are we really buying in the long run? Counseling patients and their families is made all the more difficult when the answers to important questions like these remain to be seen.
 

Only a sliver of Alzheimer’s patients are current candidates

The fact is that most patients living with Alzheimer’s disease will not qualify for treatment with these drugs. Lecanemab is approved for people with early-stage disease, meaning their dementia is mild or they have mild cognitive impairment, which is a precursor to full-blown Alzheimer’s disease. Of the 6 million people in the United States living with Alzheimer’s, about 1.5 million are estimated to fall into that category. We can expect to see a similar qualifier for donanemab if it receives FDA approval, especially because that trial suggested a more pronounced treatment effect for patients in the earliest stages of the disease.

Even if a patient hits the sweet spot where they have just enough cognitive impairment, but not too much, they aren’t technically therapeutic candidates until prerequisite testing confirms amyloid protein accumulation in the brain via PET scan or cerebrospinal fluid analysis.

Even then, the FDA’s boxed warning for lecanemab recommends that patients undergo genetic testing for the apo E4 mutation to identify those at a particularly high risk for severe adverse effects including brain bleeding and swelling. This recommendation is not unreasonable considering that 15% of the Alzheimer’s population has two copies of the apo E4 mutation and fall into that high-risk group.
 

Significant risks

Antiamyloid drugs are well-known to cause serious side effects. In the lecanemab trial, 13% of participants receiving Leqembi experienced brain swelling (vs. 2% of participants receiving placebo) and 17% of participants had brain bleeding (vs. 9% of participants on placebo). In the donanemab trial, brain bleeding occurred in 31.4% of participants on the drug (vs. 13.6% on placebo) and swelling occurred in 24% (vs. 2.1% receiving placebo). Thankfully, in both trials, most of these adverse events did not produce significant symptoms, but in rare cases these events caused severe or catastrophic neurologic injury, including death.

How can we best guide patients and their families to weigh the uncertain benefits against potentially serious risks? We can start by considering the patient characteristics most likely to portend increased risk for serious side effects: apo E4 mutations, blood thinner use, and the presence of microhemorrhages on brain imaging. But after that, we’re left with a lot of uncertainty in terms of which patients are most likely to see meaningful clinical improvements from the drug and unknown factors that may increase the risks of treatment.
 

A costly therapy

Medicare plans to cover 80% of lecanemab’s steep cost of $26,500 per year. Still, that will leave many patients with a hefty copay, potentially over $6,000 per year. But that only scratches the surface. Consider the frequent medical visits, repeated brain scans, laboratory tests, and infusion center appointments. It’s been estimated that all-in, the treatment will actually cost about $90,000 per year.

Yes, Medicare will reimburse a large portion of that cost, but it adds up to an estimated $2 billion per year for about 85,000 patients. This will probably spur increases to Medicare premiums, among other economic consequences for the health care system.

We’ll probably have to wait for an FDA approval decision before we know where donanemab will be priced.
 

Logistical challenges could be a rate-limiting step

Ask anyone who’s tried to see a neurologist recently, and they’ll tell you that the wait for a new patient appointment is months long. The shortage of neurologists in the United States is already a crisis, and there are even fewer cognitive neurologists. How long will patients be forced to wait for their diagnosis?

Many geriatricians will get comfortable prescribing these drugs, but will our already overburdened primary care providers have the bandwidth to do the same? It’s a tall order.

A new world of Alzheimer’s treatments also means that the infrastructure of our health care systems will need to be ramped up. Lecanemab infusions are administered every 2 weeks and donanemab every 4 weeks. Infusion centers will need to accommodate a lot more patients. And those patients will need frequent brain scans, so neuroimaging centers will need to increase their capacity to perform many more brain MRI and PET scans.
 

Antiamyloid drugs: An exciting first step

The bottom line is that these drugs aren’t the Alzheimer’s holy grail: An accessible treatment that could stop the disease in its tracks or reverse cognitive impairment. They are, however, a very promising breakthrough.

Yes, there are a ton of kinks to work out here, but this is an exciting start. Alzheimer’s research is entering a renaissance era that will hopefully bring more groundbreaking developments. Better biomarkers to facilitate faster, easier diagnosis. More drugs that go beyond amyloid proteins for their therapeutic targets. Treatments for later-stage disease. Drugs that prevent dementia altogether.

Ultimately, these new antiamyloid beta drugs are an exciting indication that we will eventually have a toolkit of Alzheimer’s drugs to choose from. For now, we’ve taken a solid step forward and there is ample reason to be hopeful for the future.

Dr. Croll is assistant professor of neurology at Temple University, Philadelphia. She reported no relevant conflicts of interest.

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

To the Editor:

Methemoglobinemia (MetHb) is a condition caused by elevated levels of methemoglobin in the blood, which leads to an overall reduced ability of red blood cells to release oxygen to tissues, causing tissue hypoxia. Methemoglobinemia may be congenital or acquired. Various antibiotics and local anesthetics have been reported to induce acquired MetHb.¹ We describe an adult who presented with MetHb resulting from excessive topical application of local anesthetics for painful scrotal ulcers.

A 54-year-old man presented with multiple scrotal and penile shaft ulcers of a few weeks’ duration with no systemic concerns. His medical history included chronic hepatitis C virus (HCV) and lumbar disc disease. Physical examination revealed multiple erosions and ulcers on an erythematous base involving the scrotal skin and distal penile shaft (Figure). Histopathology revealed acute leukocytoclastic vasculitis, and a laboratory workup was positive for mixed cryoglobulinemia that was thought to be HCV related. The patient was started on a systemic corticosteroid treatment in addition to sofosbuvir-velpatasvir for the treatment of HCV-related mixed cryoglobulinemic vasculitis. Concomitantly, the patient self-treated for pain with a local anesthetic cream containing lidocaine 2.5% and prilocaine 2.5%, applying it excessively every few hours daily for 2 weeks. He also intermittently used occlusive dressings.

After 2 weeks of application, the patient developed lightheadedness and shortness of breath. He returned and was admitted for further evaluation. He had dyspnea and tachypnea of 22 breaths per minute. He also had mild tachycardia (109 beats per minute). He did not have a fever, and his blood pressure was normal. The oxygen saturation measured in ambient room air by pulse oximetry was 82%. A neurologic examination was normal except for mild drowsiness. The lungs were clear, and heart sounds were normal. A 12-lead electrocardiogram also was normal. A complete blood cell count showed severe macrocytic anemia with a hemoglobin level of 7 g/dL, which was a severe decline from the patient’s baseline level of 14 g/dL (reference range, 13–17 g/dL). A MetHb blood level of 11% was reported on co-oximetry. An arterial blood gas analysis revealed a pH of 7.46; partial pressure of carbon dioxide of 41 mm Hg; and partial pressure of oxygen of 63 mm Hg. The haptoglobin level was low at 2.6 mg/dL (reference range, 30–200 mg/dL). An absolute reticulocyte count was markedly elevated at 0.4×10⁶/mL (reference range, 0.03–0.08×10⁶/mL), lactate dehydrogenase was elevated at 430 U/L (reference range, 125–220 U/L), and indirect billirubin was high at 0.9 mg/dL (reference range, 0–0.5 mg/dL), consistent with hemolytic anemia. Electrolyte serum levels and renal function tests were within reference range. A diagnosis of MetHb induced by the lidocaine-prilocaine cream was rendered, and intravenous methylene blue 72 mg (1 mg/kg) was administered over 10 minutes. Within the next 60 minutes, the patient’s drowsiness and arterial desaturation resolved. A subsequent MetHb measurement taken several hours later was reduced to 4%. The patient remained asymptomatic and was eventually discharged.

Methemoglobinemia is an altered state of hemoglobin where the ferrous (Fe2⁺) ions of heme are oxidized to the ferric (Fe3⁺) state. These ferric ions are unable to bind oxygen, resulting in impaired oxygen delivery to tissues.¹ Local anesthetics, which are strong oxidizers, have been reported to induce MetHb.² In our patient, the extensive use of lidocaine 2.5%–prilocaine 2.5% cream resulted in severe life-threatening MetHb. The oxidizing properties of local anesthetics can be attributed to their chemical structure. Benzocaine is metabolized to potent oxidizers such as aniline, phenylhydroxylamine, and nitrobenzene.³ Prilocaine and another potent oxidizer, ortho-toluidine, which is a metabolite of prilocaine, can oxidize the iron in hemoglobin from ferrous (Fe2⁺) to ferric (Fe3⁺), leading to MetHb.^2,3

Cases of anesthetic-induced MetHb primarily are associated with overuse of the product by applying it to large surface areas or using it for prolonged periods of time. In one case report, the occlusive dressing of the lidocaine-prilocaine cream applied to skin of the legs that was already abraded by laser epilation therapy resulted in MetHb.⁴ In our patient, applying the topical anesthetic to the eroded high-absorptive mucosal surface of the scrotal skin and the use of occlusive dressings increased the risk for toxicity. Absorption from scrotal skin is 40-times higher than the forearm.⁵ The face, axillae, and scalp also exhibit increased absorption compared to the forearm—10-, 4-, and 3-times higher, respectively.

In recent years, the use of topical anesthetics has greatly expanded due to the popularity of aesthetic and cosmetic procedures. These procedures often are performed in an outpatient setting.⁶ Dermatologists should be well aware of MetHb as a serious adverse effect and guide patients accordingly, as patients do not tend to consider a local anesthetic to be a drug. Drug interactions also may affect free lidocaine concentrations by liver cytochrome P450 metabolism; although this was not the case with our patient, special attention should be given to potential interactions that may exacerbate this serious adverse effect. Consideration should be given to patients applying the anesthetic to areas with high absorption capacity.

To the Editor:

Methemoglobinemia (MetHb) is a condition caused by elevated levels of methemoglobin in the blood, which leads to an overall reduced ability of red blood cells to release oxygen to tissues, causing tissue hypoxia. Methemoglobinemia may be congenital or acquired. Various antibiotics and local anesthetics have been reported to induce acquired MetHb.¹ We describe an adult who presented with MetHb resulting from excessive topical application of local anesthetics for painful scrotal ulcers.

A 54-year-old man presented with multiple scrotal and penile shaft ulcers of a few weeks’ duration with no systemic concerns. His medical history included chronic hepatitis C virus (HCV) and lumbar disc disease. Physical examination revealed multiple erosions and ulcers on an erythematous base involving the scrotal skin and distal penile shaft (Figure). Histopathology revealed acute leukocytoclastic vasculitis, and a laboratory workup was positive for mixed cryoglobulinemia that was thought to be HCV related. The patient was started on a systemic corticosteroid treatment in addition to sofosbuvir-velpatasvir for the treatment of HCV-related mixed cryoglobulinemic vasculitis. Concomitantly, the patient self-treated for pain with a local anesthetic cream containing lidocaine 2.5% and prilocaine 2.5%, applying it excessively every few hours daily for 2 weeks. He also intermittently used occlusive dressings.

After 2 weeks of application, the patient developed lightheadedness and shortness of breath. He returned and was admitted for further evaluation. He had dyspnea and tachypnea of 22 breaths per minute. He also had mild tachycardia (109 beats per minute). He did not have a fever, and his blood pressure was normal. The oxygen saturation measured in ambient room air by pulse oximetry was 82%. A neurologic examination was normal except for mild drowsiness. The lungs were clear, and heart sounds were normal. A 12-lead electrocardiogram also was normal. A complete blood cell count showed severe macrocytic anemia with a hemoglobin level of 7 g/dL, which was a severe decline from the patient’s baseline level of 14 g/dL (reference range, 13–17 g/dL). A MetHb blood level of 11% was reported on co-oximetry. An arterial blood gas analysis revealed a pH of 7.46; partial pressure of carbon dioxide of 41 mm Hg; and partial pressure of oxygen of 63 mm Hg. The haptoglobin level was low at 2.6 mg/dL (reference range, 30–200 mg/dL). An absolute reticulocyte count was markedly elevated at 0.4×10⁶/mL (reference range, 0.03–0.08×10⁶/mL), lactate dehydrogenase was elevated at 430 U/L (reference range, 125–220 U/L), and indirect billirubin was high at 0.9 mg/dL (reference range, 0–0.5 mg/dL), consistent with hemolytic anemia. Electrolyte serum levels and renal function tests were within reference range. A diagnosis of MetHb induced by the lidocaine-prilocaine cream was rendered, and intravenous methylene blue 72 mg (1 mg/kg) was administered over 10 minutes. Within the next 60 minutes, the patient’s drowsiness and arterial desaturation resolved. A subsequent MetHb measurement taken several hours later was reduced to 4%. The patient remained asymptomatic and was eventually discharged.

Methemoglobinemia is an altered state of hemoglobin where the ferrous (Fe2⁺) ions of heme are oxidized to the ferric (Fe3⁺) state. These ferric ions are unable to bind oxygen, resulting in impaired oxygen delivery to tissues.¹ Local anesthetics, which are strong oxidizers, have been reported to induce MetHb.² In our patient, the extensive use of lidocaine 2.5%–prilocaine 2.5% cream resulted in severe life-threatening MetHb. The oxidizing properties of local anesthetics can be attributed to their chemical structure. Benzocaine is metabolized to potent oxidizers such as aniline, phenylhydroxylamine, and nitrobenzene.³ Prilocaine and another potent oxidizer, ortho-toluidine, which is a metabolite of prilocaine, can oxidize the iron in hemoglobin from ferrous (Fe2⁺) to ferric (Fe3⁺), leading to MetHb.^2,3

Cases of anesthetic-induced MetHb primarily are associated with overuse of the product by applying it to large surface areas or using it for prolonged periods of time. In one case report, the occlusive dressing of the lidocaine-prilocaine cream applied to skin of the legs that was already abraded by laser epilation therapy resulted in MetHb.⁴ In our patient, applying the topical anesthetic to the eroded high-absorptive mucosal surface of the scrotal skin and the use of occlusive dressings increased the risk for toxicity. Absorption from scrotal skin is 40-times higher than the forearm.⁵ The face, axillae, and scalp also exhibit increased absorption compared to the forearm—10-, 4-, and 3-times higher, respectively.

In recent years, the use of topical anesthetics has greatly expanded due to the popularity of aesthetic and cosmetic procedures. These procedures often are performed in an outpatient setting.⁶ Dermatologists should be well aware of MetHb as a serious adverse effect and guide patients accordingly, as patients do not tend to consider a local anesthetic to be a drug. Drug interactions also may affect free lidocaine concentrations by liver cytochrome P450 metabolism; although this was not the case with our patient, special attention should be given to potential interactions that may exacerbate this serious adverse effect. Consideration should be given to patients applying the anesthetic to areas with high absorption capacity.

To the Editor:

Methemoglobinemia (MetHb) is a condition caused by elevated levels of methemoglobin in the blood, which leads to an overall reduced ability of red blood cells to release oxygen to tissues, causing tissue hypoxia. Methemoglobinemia may be congenital or acquired. Various antibiotics and local anesthetics have been reported to induce acquired MetHb.¹ We describe an adult who presented with MetHb resulting from excessive topical application of local anesthetics for painful scrotal ulcers.

A 54-year-old man presented with multiple scrotal and penile shaft ulcers of a few weeks’ duration with no systemic concerns. His medical history included chronic hepatitis C virus (HCV) and lumbar disc disease. Physical examination revealed multiple erosions and ulcers on an erythematous base involving the scrotal skin and distal penile shaft (Figure). Histopathology revealed acute leukocytoclastic vasculitis, and a laboratory workup was positive for mixed cryoglobulinemia that was thought to be HCV related. The patient was started on a systemic corticosteroid treatment in addition to sofosbuvir-velpatasvir for the treatment of HCV-related mixed cryoglobulinemic vasculitis. Concomitantly, the patient self-treated for pain with a local anesthetic cream containing lidocaine 2.5% and prilocaine 2.5%, applying it excessively every few hours daily for 2 weeks. He also intermittently used occlusive dressings.

After 2 weeks of application, the patient developed lightheadedness and shortness of breath. He returned and was admitted for further evaluation. He had dyspnea and tachypnea of 22 breaths per minute. He also had mild tachycardia (109 beats per minute). He did not have a fever, and his blood pressure was normal. The oxygen saturation measured in ambient room air by pulse oximetry was 82%. A neurologic examination was normal except for mild drowsiness. The lungs were clear, and heart sounds were normal. A 12-lead electrocardiogram also was normal. A complete blood cell count showed severe macrocytic anemia with a hemoglobin level of 7 g/dL, which was a severe decline from the patient’s baseline level of 14 g/dL (reference range, 13–17 g/dL). A MetHb blood level of 11% was reported on co-oximetry. An arterial blood gas analysis revealed a pH of 7.46; partial pressure of carbon dioxide of 41 mm Hg; and partial pressure of oxygen of 63 mm Hg. The haptoglobin level was low at 2.6 mg/dL (reference range, 30–200 mg/dL). An absolute reticulocyte count was markedly elevated at 0.4×10⁶/mL (reference range, 0.03–0.08×10⁶/mL), lactate dehydrogenase was elevated at 430 U/L (reference range, 125–220 U/L), and indirect billirubin was high at 0.9 mg/dL (reference range, 0–0.5 mg/dL), consistent with hemolytic anemia. Electrolyte serum levels and renal function tests were within reference range. A diagnosis of MetHb induced by the lidocaine-prilocaine cream was rendered, and intravenous methylene blue 72 mg (1 mg/kg) was administered over 10 minutes. Within the next 60 minutes, the patient’s drowsiness and arterial desaturation resolved. A subsequent MetHb measurement taken several hours later was reduced to 4%. The patient remained asymptomatic and was eventually discharged.

Methemoglobinemia is an altered state of hemoglobin where the ferrous (Fe2⁺) ions of heme are oxidized to the ferric (Fe3⁺) state. These ferric ions are unable to bind oxygen, resulting in impaired oxygen delivery to tissues.¹ Local anesthetics, which are strong oxidizers, have been reported to induce MetHb.² In our patient, the extensive use of lidocaine 2.5%–prilocaine 2.5% cream resulted in severe life-threatening MetHb. The oxidizing properties of local anesthetics can be attributed to their chemical structure. Benzocaine is metabolized to potent oxidizers such as aniline, phenylhydroxylamine, and nitrobenzene.³ Prilocaine and another potent oxidizer, ortho-toluidine, which is a metabolite of prilocaine, can oxidize the iron in hemoglobin from ferrous (Fe2⁺) to ferric (Fe3⁺), leading to MetHb.^2,3

Cases of anesthetic-induced MetHb primarily are associated with overuse of the product by applying it to large surface areas or using it for prolonged periods of time. In one case report, the occlusive dressing of the lidocaine-prilocaine cream applied to skin of the legs that was already abraded by laser epilation therapy resulted in MetHb.⁴ In our patient, applying the topical anesthetic to the eroded high-absorptive mucosal surface of the scrotal skin and the use of occlusive dressings increased the risk for toxicity. Absorption from scrotal skin is 40-times higher than the forearm.⁵ The face, axillae, and scalp also exhibit increased absorption compared to the forearm—10-, 4-, and 3-times higher, respectively.

In recent years, the use of topical anesthetics has greatly expanded due to the popularity of aesthetic and cosmetic procedures. These procedures often are performed in an outpatient setting.⁶ Dermatologists should be well aware of MetHb as a serious adverse effect and guide patients accordingly, as patients do not tend to consider a local anesthetic to be a drug. Drug interactions also may affect free lidocaine concentrations by liver cytochrome P450 metabolism; although this was not the case with our patient, special attention should be given to potential interactions that may exacerbate this serious adverse effect. Consideration should be given to patients applying the anesthetic to areas with high absorption capacity.

This transcript has been edited for clarity.

If a picture is worth a thousand words, then a CT scan of the chest might as well be Atlas Shrugged. When you think of the sheer information content in one of those scans, it becomes immediately clear that our usual method of CT scan interpretation must be leaving a lot on the table. After all, we can go through all that information and come out with simply “normal” and call it a day.
 

Of course, radiologists can glean a lot from a CT scan, but they are trained to look for abnormalities. They can find pneumonia, emboli, fractures, and pneumothoraces, but the presence or absence of life-threatening abnormalities is still just a fraction of the data contained within a CT scan.

Pulling out more data from those images – data that may not indicate disease per se, but nevertheless tell us something important about patients and their risks – might just fall to those entities that are primed to take a bunch of data and interpret it in new ways: artificial intelligence (AI).

I’m thinking about AI and CT scans this week thanks to this study, appearing in the journal Radiology, from Kaiwen Xu and colleagues at Vanderbilt.

In a previous study, the team had developed an AI algorithm to take chest CT images and convert that data into information about body composition: skeletal muscle mass, fat mass, muscle lipid content – that sort of thing.

courtesy HHS Author Manuscripts

courtesy GitHub

courtesy Radiology

courtesy Radiology

courtesy Radiology

courtesy Radiology

courtesy Dr. F. Perry Wilson

F. Perry Wilson, MD, MSCE, is associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no conflicts of interest.

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

This transcript has been edited for clarity.

If a picture is worth a thousand words, then a CT scan of the chest might as well be Atlas Shrugged. When you think of the sheer information content in one of those scans, it becomes immediately clear that our usual method of CT scan interpretation must be leaving a lot on the table. After all, we can go through all that information and come out with simply “normal” and call it a day.
 

Of course, radiologists can glean a lot from a CT scan, but they are trained to look for abnormalities. They can find pneumonia, emboli, fractures, and pneumothoraces, but the presence or absence of life-threatening abnormalities is still just a fraction of the data contained within a CT scan.

Pulling out more data from those images – data that may not indicate disease per se, but nevertheless tell us something important about patients and their risks – might just fall to those entities that are primed to take a bunch of data and interpret it in new ways: artificial intelligence (AI).

I’m thinking about AI and CT scans this week thanks to this study, appearing in the journal Radiology, from Kaiwen Xu and colleagues at Vanderbilt.

In a previous study, the team had developed an AI algorithm to take chest CT images and convert that data into information about body composition: skeletal muscle mass, fat mass, muscle lipid content – that sort of thing.

courtesy HHS Author Manuscripts

courtesy GitHub

courtesy Radiology

courtesy Radiology

courtesy Radiology

courtesy Radiology

courtesy Dr. F. Perry Wilson

F. Perry Wilson, MD, MSCE, is associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no conflicts of interest.

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

This transcript has been edited for clarity.

If a picture is worth a thousand words, then a CT scan of the chest might as well be Atlas Shrugged. When you think of the sheer information content in one of those scans, it becomes immediately clear that our usual method of CT scan interpretation must be leaving a lot on the table. After all, we can go through all that information and come out with simply “normal” and call it a day.
 

Of course, radiologists can glean a lot from a CT scan, but they are trained to look for abnormalities. They can find pneumonia, emboli, fractures, and pneumothoraces, but the presence or absence of life-threatening abnormalities is still just a fraction of the data contained within a CT scan.

Pulling out more data from those images – data that may not indicate disease per se, but nevertheless tell us something important about patients and their risks – might just fall to those entities that are primed to take a bunch of data and interpret it in new ways: artificial intelligence (AI).

I’m thinking about AI and CT scans this week thanks to this study, appearing in the journal Radiology, from Kaiwen Xu and colleagues at Vanderbilt.

In a previous study, the team had developed an AI algorithm to take chest CT images and convert that data into information about body composition: skeletal muscle mass, fat mass, muscle lipid content – that sort of thing.

courtesy HHS Author Manuscripts

courtesy GitHub

courtesy Radiology

courtesy Radiology

courtesy Radiology

courtesy Radiology

courtesy Dr. F. Perry Wilson

F. Perry Wilson, MD, MSCE, is associate professor of medicine and public health and director of Yale’s Clinical and Translational Research Accelerator in New Haven, Conn. He reported no conflicts of interest.

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