Rheumatology News

The death of a patient comes with many challenges for physicians, including a range of emotional and professional issues. Beyond those concerns, some physicians and their practices must also consider how to collect on any outstanding bill that might go unpaid after a patient’s death.

“When a patient passes away, obviously there is, unfortunately, a lot of paperwork and stress for families, and it’s a very difficult situation,” says Shikha Jain, MD, an oncologist and associate professor of medicine at the University of Illinois at Chicago. “Talking about finances in that moment can be difficult and uncomfortable, and one thing I’d recommend is that the physicians themselves not get involved.”

Instead, Dr. Jain said, someone in the billing department in the practice or the hospital should take a lead on dealing with any outstanding debts.

“That doctor-patient relationship is a very precious relationship, so you don’t want to mix that financial aspect of providing care with the doctor-patient relationship,” Dr. Jain said. “That’s one thing that’s really important.”

The best approach in such situations is for practices to have a standing policy in place that dictates how to handle bills once a patient has died.

In most cases, the executor of the patient’s will must inform all creditors, including doctors, that the decedent has died, but sometimes there’s a delay.
 

Hoping the doctor’s office writes it off

“Even though the person in charge of the estate is supposed to contact the doctor’s office and let them know when a patient has passed, that doesn’t always happen,” says Hope Wen, head of billing at practice management platform Soundry Health. “It can be very challenging to track down that information, and sometimes they’re just crossing their fingers hoping that the doctor’s office will just write off the balance, which they often do.”

Some offices use a service that compares accounts receivable lists to Social Security death files and state records to identify deaths more quickly. Some physicians might also use a debt collection agency or an attorney who has experience collecting decedent debts and dealing with executors and probate courts.

Once the practice becomes aware that a patient has died, it can no longer send communications to the name and address on file, although it can continue to go through the billing process with the insurer for any bills incurred up to the date of the death.

At that point, the estate becomes responsible for the debt, and all communication must go to the executor of the estate (in some states, this might be called a personal representative). The office can reach out to any contacts on file to see if they are able to identify the executor.

“You want to do that in a compassionate way,” says Jack Brown III, JD, MBA, president of Gulf Coast Collection Bureau. “You’ll tell them you’re sorry for their loss, but you’re wondering who is responsible for the estate. Once you’ve identified that person and gotten their letter of administration from the probate court or a power of attorney, then you can speak with that person as if they were the patient.”

The names of executors are also public record and are available through the probate court (sometimes called the surrogate court) in the county where the decedent lived.

“Even if there’s no will or no executive named, the court will appoint an administrator for the estate, which is usually a family member,” said Robert Bernstein, an estate lawyer in Parsippany, N.J. “Their information will be on file in the court.”
 

Insurance coverage

Typically, insurance will pay for treatment (after deductibles and copays) up until the date of the patient’s death. But, of course, it can take months for some insurance companies to make their final payments, allowing physicians to know exactly how much they’re owed by that estate. In such cases, it’s important for physicians to know the rules in the decedent’s state for how long they have to file a claim.

Most states require that claims occur within 6-9 months of the person’s death. However, in some states, claimants can continue to file for much longer if the estate has not yet paid out all of its assets.

“Sometimes there is real estate to sell or a business to wind down, and it can take years for the estate to distribute all of the assets,” Mr. Bernstein says. “If it’s a year later and they still haven’t distributed the assets, the physician can still file the claim and should be paid.”

In some cases, especially if the decedent received compassionate, quality care, their family will want to make good on any outstanding debts to the health care providers who took care of their loved ones in their final days. In other cases, especially when a family member has had a long illness, their assets have been depleted over time or were transferred to other family members so that there is little left in the estate itself when the patient dies.

Regardless of other circumstances, the estate alone is responsible for such payments, and family members, including spouses and children, typically have no liability. (Though rarely enforced, some states do have filial responsibility laws that could hold children responsible for their parents’ debts, including unpaid medical bills. In addition, states with community property laws might require a surviving spouse to cover their partner’s debt, even after death.)

The probate process varies from state to state, but in general, the probate system and the executor will gather all existing assets and then notify all creditors about how to submit a claim. Typically, the claim will need to include information about how much is owed and documentation, such as bills and an explanation of benefits to back up the claim. It should be borne in mind that even those who’ve passed away have privacy protections under the Health Insurance Portability and Accountability Act, so practices must be careful as to how much information they’re sharing through their claim.

Once the estate has received all the claims, the executor will follow a priority of claims, starting with secured creditors. Typically, medical bills, especially those incurred in the last 90 days of the decedent’s life, have priority in the probate process, Mr. Brown says.
 

How to minimize losses

In that case, the practice would write off the unpaid debt as a business loss. If there are not enough assets in the estate to pay all claims, the executor will follow a state schedule that apportions those assets that are available.

There are some steps that practices can take to protect themselves from incurring such losses. For example, before beginning treatment, practices might consider asking patients to name a guarantor, who will essentially promise to cover any outstanding debts that the patient incurs.

To be binding, the office will need a signature from both the patient and the guarantor. Some offices may also keep a patient credit card number on file with written authorization that they can use to pay bills that are past due, although this payment method would no longer be valid after a patient dies.

While it’s important for all physicians to document and verify the financial information for their patients, oncologists often must consider an additional layer of fiduciary responsibility when it comes to their patients. Ms. Wen suggests that oncology offices check in with insurance companies to determine whether a patient has exhausted their benefits.

“That can happen with cancer patients, depending on how long they’ve been receiving treatment and what type of treatment they’ve been getting,” she said. “Some of the clinical trials, insurance will pay for them, but they’re really expensive and can get toward that max. So knowing where they are with their insurance coverage is big.”

When time is of the essence, some patients will choose to go forward with a treatment before receiving insurance approval. In those cases, the office must have an additional conversation in which the costs of the treatment are discussed. The office should obtain written confirmation of who will pay if the insurer does not, Ms. Wen said. While it’s the patient’s responsibility to keep track of their insurance benefits, oncology practices and hospitals must also exercise due diligence in monitoring the benefits that are available.

“That’s part of their contract with insurance companies if they’re in network, helping patients understand their benefits,” Ms. Wen saids.

It’s also important for practices to keep clear, consistent records to make it easier to identify outstanding bills and the correct contact information for them. If bills had gone unpaid prior to a patient’s death and the office started legal action and received a judgment, that claim would typically go ahead of other creditors’ claims.

Dr. Jain says that some practices might also consider keeping a financial adviser or social worker on staff who can assist patients and their families with understanding their out-of-pocket costs for treatment.

“Financial toxicity in oncology and medical care is a very real problem,” she says. “At the beginning of the relationship, I recommend that my patients get set up with a financial specialist that can help them navigate that aspect, not only when a patient passes away but during the process of receiving treatment, so they’re not shocked by the bills.”

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

The death of a patient comes with many challenges for physicians, including a range of emotional and professional issues. Beyond those concerns, some physicians and their practices must also consider how to collect on any outstanding bill that might go unpaid after a patient’s death.

“When a patient passes away, obviously there is, unfortunately, a lot of paperwork and stress for families, and it’s a very difficult situation,” says Shikha Jain, MD, an oncologist and associate professor of medicine at the University of Illinois at Chicago. “Talking about finances in that moment can be difficult and uncomfortable, and one thing I’d recommend is that the physicians themselves not get involved.”

Instead, Dr. Jain said, someone in the billing department in the practice or the hospital should take a lead on dealing with any outstanding debts.

“That doctor-patient relationship is a very precious relationship, so you don’t want to mix that financial aspect of providing care with the doctor-patient relationship,” Dr. Jain said. “That’s one thing that’s really important.”

The best approach in such situations is for practices to have a standing policy in place that dictates how to handle bills once a patient has died.

In most cases, the executor of the patient’s will must inform all creditors, including doctors, that the decedent has died, but sometimes there’s a delay.
 

Hoping the doctor’s office writes it off

“Even though the person in charge of the estate is supposed to contact the doctor’s office and let them know when a patient has passed, that doesn’t always happen,” says Hope Wen, head of billing at practice management platform Soundry Health. “It can be very challenging to track down that information, and sometimes they’re just crossing their fingers hoping that the doctor’s office will just write off the balance, which they often do.”

Some offices use a service that compares accounts receivable lists to Social Security death files and state records to identify deaths more quickly. Some physicians might also use a debt collection agency or an attorney who has experience collecting decedent debts and dealing with executors and probate courts.

Once the practice becomes aware that a patient has died, it can no longer send communications to the name and address on file, although it can continue to go through the billing process with the insurer for any bills incurred up to the date of the death.

At that point, the estate becomes responsible for the debt, and all communication must go to the executor of the estate (in some states, this might be called a personal representative). The office can reach out to any contacts on file to see if they are able to identify the executor.

“You want to do that in a compassionate way,” says Jack Brown III, JD, MBA, president of Gulf Coast Collection Bureau. “You’ll tell them you’re sorry for their loss, but you’re wondering who is responsible for the estate. Once you’ve identified that person and gotten their letter of administration from the probate court or a power of attorney, then you can speak with that person as if they were the patient.”

The names of executors are also public record and are available through the probate court (sometimes called the surrogate court) in the county where the decedent lived.

“Even if there’s no will or no executive named, the court will appoint an administrator for the estate, which is usually a family member,” said Robert Bernstein, an estate lawyer in Parsippany, N.J. “Their information will be on file in the court.”
 

Insurance coverage

Typically, insurance will pay for treatment (after deductibles and copays) up until the date of the patient’s death. But, of course, it can take months for some insurance companies to make their final payments, allowing physicians to know exactly how much they’re owed by that estate. In such cases, it’s important for physicians to know the rules in the decedent’s state for how long they have to file a claim.

Most states require that claims occur within 6-9 months of the person’s death. However, in some states, claimants can continue to file for much longer if the estate has not yet paid out all of its assets.

“Sometimes there is real estate to sell or a business to wind down, and it can take years for the estate to distribute all of the assets,” Mr. Bernstein says. “If it’s a year later and they still haven’t distributed the assets, the physician can still file the claim and should be paid.”

In some cases, especially if the decedent received compassionate, quality care, their family will want to make good on any outstanding debts to the health care providers who took care of their loved ones in their final days. In other cases, especially when a family member has had a long illness, their assets have been depleted over time or were transferred to other family members so that there is little left in the estate itself when the patient dies.

Regardless of other circumstances, the estate alone is responsible for such payments, and family members, including spouses and children, typically have no liability. (Though rarely enforced, some states do have filial responsibility laws that could hold children responsible for their parents’ debts, including unpaid medical bills. In addition, states with community property laws might require a surviving spouse to cover their partner’s debt, even after death.)

The probate process varies from state to state, but in general, the probate system and the executor will gather all existing assets and then notify all creditors about how to submit a claim. Typically, the claim will need to include information about how much is owed and documentation, such as bills and an explanation of benefits to back up the claim. It should be borne in mind that even those who’ve passed away have privacy protections under the Health Insurance Portability and Accountability Act, so practices must be careful as to how much information they’re sharing through their claim.

Once the estate has received all the claims, the executor will follow a priority of claims, starting with secured creditors. Typically, medical bills, especially those incurred in the last 90 days of the decedent’s life, have priority in the probate process, Mr. Brown says.
 

How to minimize losses

In that case, the practice would write off the unpaid debt as a business loss. If there are not enough assets in the estate to pay all claims, the executor will follow a state schedule that apportions those assets that are available.

There are some steps that practices can take to protect themselves from incurring such losses. For example, before beginning treatment, practices might consider asking patients to name a guarantor, who will essentially promise to cover any outstanding debts that the patient incurs.

To be binding, the office will need a signature from both the patient and the guarantor. Some offices may also keep a patient credit card number on file with written authorization that they can use to pay bills that are past due, although this payment method would no longer be valid after a patient dies.

While it’s important for all physicians to document and verify the financial information for their patients, oncologists often must consider an additional layer of fiduciary responsibility when it comes to their patients. Ms. Wen suggests that oncology offices check in with insurance companies to determine whether a patient has exhausted their benefits.

“That can happen with cancer patients, depending on how long they’ve been receiving treatment and what type of treatment they’ve been getting,” she said. “Some of the clinical trials, insurance will pay for them, but they’re really expensive and can get toward that max. So knowing where they are with their insurance coverage is big.”

When time is of the essence, some patients will choose to go forward with a treatment before receiving insurance approval. In those cases, the office must have an additional conversation in which the costs of the treatment are discussed. The office should obtain written confirmation of who will pay if the insurer does not, Ms. Wen said. While it’s the patient’s responsibility to keep track of their insurance benefits, oncology practices and hospitals must also exercise due diligence in monitoring the benefits that are available.

“That’s part of their contract with insurance companies if they’re in network, helping patients understand their benefits,” Ms. Wen saids.

It’s also important for practices to keep clear, consistent records to make it easier to identify outstanding bills and the correct contact information for them. If bills had gone unpaid prior to a patient’s death and the office started legal action and received a judgment, that claim would typically go ahead of other creditors’ claims.

Dr. Jain says that some practices might also consider keeping a financial adviser or social worker on staff who can assist patients and their families with understanding their out-of-pocket costs for treatment.

“Financial toxicity in oncology and medical care is a very real problem,” she says. “At the beginning of the relationship, I recommend that my patients get set up with a financial specialist that can help them navigate that aspect, not only when a patient passes away but during the process of receiving treatment, so they’re not shocked by the bills.”

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

The death of a patient comes with many challenges for physicians, including a range of emotional and professional issues. Beyond those concerns, some physicians and their practices must also consider how to collect on any outstanding bill that might go unpaid after a patient’s death.

“When a patient passes away, obviously there is, unfortunately, a lot of paperwork and stress for families, and it’s a very difficult situation,” says Shikha Jain, MD, an oncologist and associate professor of medicine at the University of Illinois at Chicago. “Talking about finances in that moment can be difficult and uncomfortable, and one thing I’d recommend is that the physicians themselves not get involved.”

Instead, Dr. Jain said, someone in the billing department in the practice or the hospital should take a lead on dealing with any outstanding debts.

“That doctor-patient relationship is a very precious relationship, so you don’t want to mix that financial aspect of providing care with the doctor-patient relationship,” Dr. Jain said. “That’s one thing that’s really important.”

The best approach in such situations is for practices to have a standing policy in place that dictates how to handle bills once a patient has died.

In most cases, the executor of the patient’s will must inform all creditors, including doctors, that the decedent has died, but sometimes there’s a delay.
 

Hoping the doctor’s office writes it off

“Even though the person in charge of the estate is supposed to contact the doctor’s office and let them know when a patient has passed, that doesn’t always happen,” says Hope Wen, head of billing at practice management platform Soundry Health. “It can be very challenging to track down that information, and sometimes they’re just crossing their fingers hoping that the doctor’s office will just write off the balance, which they often do.”

Some offices use a service that compares accounts receivable lists to Social Security death files and state records to identify deaths more quickly. Some physicians might also use a debt collection agency or an attorney who has experience collecting decedent debts and dealing with executors and probate courts.

Once the practice becomes aware that a patient has died, it can no longer send communications to the name and address on file, although it can continue to go through the billing process with the insurer for any bills incurred up to the date of the death.

At that point, the estate becomes responsible for the debt, and all communication must go to the executor of the estate (in some states, this might be called a personal representative). The office can reach out to any contacts on file to see if they are able to identify the executor.

“You want to do that in a compassionate way,” says Jack Brown III, JD, MBA, president of Gulf Coast Collection Bureau. “You’ll tell them you’re sorry for their loss, but you’re wondering who is responsible for the estate. Once you’ve identified that person and gotten their letter of administration from the probate court or a power of attorney, then you can speak with that person as if they were the patient.”

The names of executors are also public record and are available through the probate court (sometimes called the surrogate court) in the county where the decedent lived.

“Even if there’s no will or no executive named, the court will appoint an administrator for the estate, which is usually a family member,” said Robert Bernstein, an estate lawyer in Parsippany, N.J. “Their information will be on file in the court.”
 

Insurance coverage

Typically, insurance will pay for treatment (after deductibles and copays) up until the date of the patient’s death. But, of course, it can take months for some insurance companies to make their final payments, allowing physicians to know exactly how much they’re owed by that estate. In such cases, it’s important for physicians to know the rules in the decedent’s state for how long they have to file a claim.

Most states require that claims occur within 6-9 months of the person’s death. However, in some states, claimants can continue to file for much longer if the estate has not yet paid out all of its assets.

“Sometimes there is real estate to sell or a business to wind down, and it can take years for the estate to distribute all of the assets,” Mr. Bernstein says. “If it’s a year later and they still haven’t distributed the assets, the physician can still file the claim and should be paid.”

In some cases, especially if the decedent received compassionate, quality care, their family will want to make good on any outstanding debts to the health care providers who took care of their loved ones in their final days. In other cases, especially when a family member has had a long illness, their assets have been depleted over time or were transferred to other family members so that there is little left in the estate itself when the patient dies.

Regardless of other circumstances, the estate alone is responsible for such payments, and family members, including spouses and children, typically have no liability. (Though rarely enforced, some states do have filial responsibility laws that could hold children responsible for their parents’ debts, including unpaid medical bills. In addition, states with community property laws might require a surviving spouse to cover their partner’s debt, even after death.)

The probate process varies from state to state, but in general, the probate system and the executor will gather all existing assets and then notify all creditors about how to submit a claim. Typically, the claim will need to include information about how much is owed and documentation, such as bills and an explanation of benefits to back up the claim. It should be borne in mind that even those who’ve passed away have privacy protections under the Health Insurance Portability and Accountability Act, so practices must be careful as to how much information they’re sharing through their claim.

Once the estate has received all the claims, the executor will follow a priority of claims, starting with secured creditors. Typically, medical bills, especially those incurred in the last 90 days of the decedent’s life, have priority in the probate process, Mr. Brown says.
 

How to minimize losses

In that case, the practice would write off the unpaid debt as a business loss. If there are not enough assets in the estate to pay all claims, the executor will follow a state schedule that apportions those assets that are available.

There are some steps that practices can take to protect themselves from incurring such losses. For example, before beginning treatment, practices might consider asking patients to name a guarantor, who will essentially promise to cover any outstanding debts that the patient incurs.

To be binding, the office will need a signature from both the patient and the guarantor. Some offices may also keep a patient credit card number on file with written authorization that they can use to pay bills that are past due, although this payment method would no longer be valid after a patient dies.

While it’s important for all physicians to document and verify the financial information for their patients, oncologists often must consider an additional layer of fiduciary responsibility when it comes to their patients. Ms. Wen suggests that oncology offices check in with insurance companies to determine whether a patient has exhausted their benefits.

“That can happen with cancer patients, depending on how long they’ve been receiving treatment and what type of treatment they’ve been getting,” she said. “Some of the clinical trials, insurance will pay for them, but they’re really expensive and can get toward that max. So knowing where they are with their insurance coverage is big.”

When time is of the essence, some patients will choose to go forward with a treatment before receiving insurance approval. In those cases, the office must have an additional conversation in which the costs of the treatment are discussed. The office should obtain written confirmation of who will pay if the insurer does not, Ms. Wen said. While it’s the patient’s responsibility to keep track of their insurance benefits, oncology practices and hospitals must also exercise due diligence in monitoring the benefits that are available.

“That’s part of their contract with insurance companies if they’re in network, helping patients understand their benefits,” Ms. Wen saids.

It’s also important for practices to keep clear, consistent records to make it easier to identify outstanding bills and the correct contact information for them. If bills had gone unpaid prior to a patient’s death and the office started legal action and received a judgment, that claim would typically go ahead of other creditors’ claims.

Dr. Jain says that some practices might also consider keeping a financial adviser or social worker on staff who can assist patients and their families with understanding their out-of-pocket costs for treatment.

“Financial toxicity in oncology and medical care is a very real problem,” she says. “At the beginning of the relationship, I recommend that my patients get set up with a financial specialist that can help them navigate that aspect, not only when a patient passes away but during the process of receiving treatment, so they’re not shocked by the bills.”

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

People with long COVID have specific biomarkers in their blood, according to results of a study published in Nature. 

The findings may be a step toward creating blood tests to positively identify people with long COVID so specialized treatments can be employed, researchers said.

 “This is a decisive step forward in the development of valid and reliable blood testing protocols for long COVID,” said David Putrino, PhD., lead author and professor of rehabilitation and human performance and director of the Abilities Research Center at Icahn Mount Sinai Health System, New York.

Researchers from the Icahn School of Medicine at Mount Sinai and Yale School of Medicine looked at blood samples from about 270 people between January 2021 and June 2022. The people had never been infected with COVID, had fully recovered from an infection, or still showed symptoms at least four months after infection.

Using machine learning, the research teams were able to differentiate between people with and without long COVID with 96% accuracy based on distinctive features in the blood samples, according to a news release from Mount Sinai.

People with long COVID had abnormal T-cell activity and low levels of the hormone cortisol. Cortisol helps people feel alert and awake, which would explain why people with long COVID often report fatigue, NBC News said in a report on the study.

“It was one of the findings that most definitively separated the folks with long Covid from the people without long Covid,” Dr. Putrino told NBC News.

The study also found that long COVID appears to reactivate latent viruses including Epstein-Barr and mononucleosis, the study said.

The blood tests could allow doctors to come up with specialized treatments in people who report a wide variety of long COVID symptoms, Dr. Putrino said. 

“There is no ‘silver bullet’ for treating long COVID, because it is an illness that infiltrates complex systems such as the immune and hormonal regulation,” he said.

The Centers for Disease Control and Prevention says about one in five Americans who had COVID still have long COVID. Symptoms include fatigue, brain fog, dizziness, digestive problems, and loss of smell and taste.

A version of this article appeared on WebMD.com.

People with long COVID have specific biomarkers in their blood, according to results of a study published in Nature. 

The findings may be a step toward creating blood tests to positively identify people with long COVID so specialized treatments can be employed, researchers said.

 “This is a decisive step forward in the development of valid and reliable blood testing protocols for long COVID,” said David Putrino, PhD., lead author and professor of rehabilitation and human performance and director of the Abilities Research Center at Icahn Mount Sinai Health System, New York.

Researchers from the Icahn School of Medicine at Mount Sinai and Yale School of Medicine looked at blood samples from about 270 people between January 2021 and June 2022. The people had never been infected with COVID, had fully recovered from an infection, or still showed symptoms at least four months after infection.

Using machine learning, the research teams were able to differentiate between people with and without long COVID with 96% accuracy based on distinctive features in the blood samples, according to a news release from Mount Sinai.

People with long COVID had abnormal T-cell activity and low levels of the hormone cortisol. Cortisol helps people feel alert and awake, which would explain why people with long COVID often report fatigue, NBC News said in a report on the study.

“It was one of the findings that most definitively separated the folks with long Covid from the people without long Covid,” Dr. Putrino told NBC News.

The study also found that long COVID appears to reactivate latent viruses including Epstein-Barr and mononucleosis, the study said.

The blood tests could allow doctors to come up with specialized treatments in people who report a wide variety of long COVID symptoms, Dr. Putrino said. 

“There is no ‘silver bullet’ for treating long COVID, because it is an illness that infiltrates complex systems such as the immune and hormonal regulation,” he said.

The Centers for Disease Control and Prevention says about one in five Americans who had COVID still have long COVID. Symptoms include fatigue, brain fog, dizziness, digestive problems, and loss of smell and taste.

A version of this article appeared on WebMD.com.

People with long COVID have specific biomarkers in their blood, according to results of a study published in Nature. 

The findings may be a step toward creating blood tests to positively identify people with long COVID so specialized treatments can be employed, researchers said.

 “This is a decisive step forward in the development of valid and reliable blood testing protocols for long COVID,” said David Putrino, PhD., lead author and professor of rehabilitation and human performance and director of the Abilities Research Center at Icahn Mount Sinai Health System, New York.

Researchers from the Icahn School of Medicine at Mount Sinai and Yale School of Medicine looked at blood samples from about 270 people between January 2021 and June 2022. The people had never been infected with COVID, had fully recovered from an infection, or still showed symptoms at least four months after infection.

Using machine learning, the research teams were able to differentiate between people with and without long COVID with 96% accuracy based on distinctive features in the blood samples, according to a news release from Mount Sinai.

People with long COVID had abnormal T-cell activity and low levels of the hormone cortisol. Cortisol helps people feel alert and awake, which would explain why people with long COVID often report fatigue, NBC News said in a report on the study.

“It was one of the findings that most definitively separated the folks with long Covid from the people without long Covid,” Dr. Putrino told NBC News.

The study also found that long COVID appears to reactivate latent viruses including Epstein-Barr and mononucleosis, the study said.

The blood tests could allow doctors to come up with specialized treatments in people who report a wide variety of long COVID symptoms, Dr. Putrino said. 

“There is no ‘silver bullet’ for treating long COVID, because it is an illness that infiltrates complex systems such as the immune and hormonal regulation,” he said.

The Centers for Disease Control and Prevention says about one in five Americans who had COVID still have long COVID. Symptoms include fatigue, brain fog, dizziness, digestive problems, and loss of smell and taste.

A version of this article appeared on WebMD.com.

Vitamin D deficiency appears to render people more vulnerable to canagliflozin’s adverse effects on bone health, whereas vitamin D3 supplementation appears protective of individuals with vitamin D deficiency.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are beneficial for treating type 2 diabetes and reducing cardiovascular and kidney disease risk. However, some, but not all, trial data have linked the SLGT2 inhibitor canagliflozin to increased fracture risk. That particular agent has been reported to accelerate loss of bone mineral density, which could contribute to fracture risk. Other drugs in the class have also been implicated in worsening markers of bone health.

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

Vitamin D deficiency appears to render people more vulnerable to canagliflozin’s adverse effects on bone health, whereas vitamin D3 supplementation appears protective of individuals with vitamin D deficiency.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are beneficial for treating type 2 diabetes and reducing cardiovascular and kidney disease risk. However, some, but not all, trial data have linked the SLGT2 inhibitor canagliflozin to increased fracture risk. That particular agent has been reported to accelerate loss of bone mineral density, which could contribute to fracture risk. Other drugs in the class have also been implicated in worsening markers of bone health.

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

Vitamin D deficiency appears to render people more vulnerable to canagliflozin’s adverse effects on bone health, whereas vitamin D3 supplementation appears protective of individuals with vitamin D deficiency.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are beneficial for treating type 2 diabetes and reducing cardiovascular and kidney disease risk. However, some, but not all, trial data have linked the SLGT2 inhibitor canagliflozin to increased fracture risk. That particular agent has been reported to accelerate loss of bone mineral density, which could contribute to fracture risk. Other drugs in the class have also been implicated in worsening markers of bone health.

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

LEIPZIG, GERMANY – With age comes illness: Cancer, cardiovascular and neurodegenerative diseases, increased infections, and autoimmune diseases such as rheumatism become more common. This is because the immune system also ages. In the case of autoimmune diseases, this aging happens particularly quickly.

“There is this phenomenon of premature aging of the immune system,” said Cornelia Weyand, PhD, director of Stanford (Calif.) University’s Center for Translational Medicine at the German Rheumatology Congress 2023. In healthy people, the immune system begins to age at age 20. From that point on, the thymus gland, which reaches peak function at 14-15 years old, plays an increasingly minor role. “At age 50 years, the aging process of the immune system gains momentum.”

“What’s good about this is that the T and B cells age together, but all a little differently, each system by itself,” said Thomas Dörner, MD, PhD, head of consultation hours for clinical hemostaseology at the Charité University Hospitals in Berlin.

While the reduced formation of naive T cells can be attributed to the regression of the thymus gland, the naive B cells are a consequence of age-related, fatty bone marrow degeneration. The influence of adipocyte-derived tumor necrosis factor (TNF)–alpha also causes the bone marrow to develop B cells more and more weakly and slowly. “Through this [process], the preimmune range of B-cells decreases and becomes less healthy than in a young person.”
 

‘Inflamm-aging’

“In the periphery, we have identified a process we call “inflamm-aging,” where the cytokines interferon-gamma, interleukin (IL)–10, and IL-17 play a predominant role. This also alters the primary and secondary immune response,” said Dr. Dörner. Here, decreasing stimulation via the B-cell receptor by aging T-lymphocytes makes a difference.

As we age, the immune system restructures itself completely. “Protective immunity regresses and the inferior immunity emerges,” explained Dr. Weyand. Wounds heal more poorly, the protective action against infections and above all malignancies, as well as the immune response to vaccinations, decreases.

The increased occurrence of neurodegenerative, cardiovascular, and autoimmune diseases is not because of a loss of function, but rather to newly gained, undesired functions. These are associated with inflammatory changes. Hence, the term inflamm-aging.

With the B cells, functional germinal centers in the lymphoid organs and protective antibodies become rarer, and age-associated B cells accumulate. As Dr. Dörner emphasized, these cells are not under the command of the B-cell receptor and are independent of the cytokine BAFF (B-cell activating factor). Instead, they react to signals that are sent from the toll-like receptors 7 and 9.

This potentially also explains the increased development of autoantibodies in older people and the association of viral and autoimmune diseases. This means that age-associated B cells develop more frequently, such as with rheumatoid arthritis, scleroderma, and systemic lupus erythematosus. “There are good data that show that they are triggered by infections and that they are specialized to form autoantibodies,” Dr. Weyand said about the age-associated B cells.
 

‘Bad old T cells’

Under the influence of genetic stop-and-go signals, the composition of the T-cell population also changes over the course of our lives. It becomes less diverse. T-helper cells become less common, and as a result, terminally differentiated effector memory T cells become more common. According to Dr. Weyand, herein lies the problem. “These cells are not just lazy, old cells that sit around. Unfortunately, they are also malicious. What we see in both the T- and B-cell systems is that they become increasingly innate with age,” he said. “They are not quite so precise or good.”

In turn, myeloid cells are less active in old age because of phagocytosis and antigen presentation, and they get more mutations. They are released more often from the bone marrow, produce more cytokines, and essentially contribute to inflamm-aging.
 

Power sources fail

In her cellular and microbiological investigations, Dr. Weyand has devoted a lot of time to studying why T cells age prematurely in patients with RA. The key was in the cellular microbiology. “We learned how the T-cell aging process translates into metabolic reprogramming of the T cells – how a good, strong, and protective T cell transforms into a disease-inducing T cell.”

At the center of premature T-cell aging in RA are disrupted mitochondrial function and insufficient communication of the mitochondria with the lysosomes and the endoplasmic reticulum.

T cells of RA patients (RA T cells) contain less MRE11A, compared with those in healthy people. This is a nuclease that allows the repair of breaks in DNA. If MRE11A is inhibited, then senescent T cells accumulate and form proinflammatory cytokines such as IL-B, IL-6, and TNF. “This is the trio that we rheumatologists are always concerned with.”

Since mitochondrial DNA repair is essential for maintaining mitochondrial fitness, the cellular power sources in patients with RA cannot provide as much energy in the form of adenosine triphosphate as in healthy people. Metabolically, they are not so fit, Dr. Weyand said.
 

Inflammatory cell death

In fact, all metabolic pathways in the T cells are reduced. The bioenergetic failure has consequences. “Unfortunately, as the mitochondrion ages, its DNA leaks into the cytosol,” explained Dr. Weyand. “Cells do not like this.” This is because DNA activates inflammasomes in the cytosol via caspase-1. This process results in a highly inflammatory cell death: pyroptosis. Subsequently, there is no trace of the cells in the tissue. “RA patients’ synovial tissue is a graveyard of dying T cells.”

In the lysosomes, the cells’ “intestine,” problems arise because patients with RA can no longer activate the adenosine monophosphate–activated protein kinase enzyme. It does not receive the lipid tail it needs to take its position as energy sensor on the lysosomal membrane. As a result, its antagonist, mTOR – both usually keep each other in check – gains the upper hand. According to Dr. Weyand, “mTOR has a party.” It activates and stresses the cells.

Additional changes affect the endoplasmic reticulum (ER). “This is where all of your proteins are synthesized and packaged to migrate from within to outside the cell, or to the cell membrane.” Compared with healthy T cells, RA T cells have around 50% more ER. “The less that mitochondria work, the larger the ER. It gets really fat.”

Mitochondria communicate with the ER via aspartate, oxaloacetate, and malate. In so doing, they control their size. RA T cells appear to be aspartate deficient. In animal models, amino acids had an anti-inflammatory effect.

When sequencing the mRNA bound to the ER, Dr. Weyand and her colleagues encountered the building blocks for TNF. “There is more than three times as much mRNA as TNF. It transforms these T cells into TNF superproducers,” said the rheumatologist. “No wonder this kind of cell is proinflammatory – it forms precisely that cytokine on which you focus every day.”

This article was translated from Medscape’s German edition. A version of this article first appeared on Medscape.com.

LEIPZIG, GERMANY – With age comes illness: Cancer, cardiovascular and neurodegenerative diseases, increased infections, and autoimmune diseases such as rheumatism become more common. This is because the immune system also ages. In the case of autoimmune diseases, this aging happens particularly quickly.

“There is this phenomenon of premature aging of the immune system,” said Cornelia Weyand, PhD, director of Stanford (Calif.) University’s Center for Translational Medicine at the German Rheumatology Congress 2023. In healthy people, the immune system begins to age at age 20. From that point on, the thymus gland, which reaches peak function at 14-15 years old, plays an increasingly minor role. “At age 50 years, the aging process of the immune system gains momentum.”

“What’s good about this is that the T and B cells age together, but all a little differently, each system by itself,” said Thomas Dörner, MD, PhD, head of consultation hours for clinical hemostaseology at the Charité University Hospitals in Berlin.

While the reduced formation of naive T cells can be attributed to the regression of the thymus gland, the naive B cells are a consequence of age-related, fatty bone marrow degeneration. The influence of adipocyte-derived tumor necrosis factor (TNF)–alpha also causes the bone marrow to develop B cells more and more weakly and slowly. “Through this [process], the preimmune range of B-cells decreases and becomes less healthy than in a young person.”
 

‘Inflamm-aging’

“In the periphery, we have identified a process we call “inflamm-aging,” where the cytokines interferon-gamma, interleukin (IL)–10, and IL-17 play a predominant role. This also alters the primary and secondary immune response,” said Dr. Dörner. Here, decreasing stimulation via the B-cell receptor by aging T-lymphocytes makes a difference.

As we age, the immune system restructures itself completely. “Protective immunity regresses and the inferior immunity emerges,” explained Dr. Weyand. Wounds heal more poorly, the protective action against infections and above all malignancies, as well as the immune response to vaccinations, decreases.

The increased occurrence of neurodegenerative, cardiovascular, and autoimmune diseases is not because of a loss of function, but rather to newly gained, undesired functions. These are associated with inflammatory changes. Hence, the term inflamm-aging.

With the B cells, functional germinal centers in the lymphoid organs and protective antibodies become rarer, and age-associated B cells accumulate. As Dr. Dörner emphasized, these cells are not under the command of the B-cell receptor and are independent of the cytokine BAFF (B-cell activating factor). Instead, they react to signals that are sent from the toll-like receptors 7 and 9.

This potentially also explains the increased development of autoantibodies in older people and the association of viral and autoimmune diseases. This means that age-associated B cells develop more frequently, such as with rheumatoid arthritis, scleroderma, and systemic lupus erythematosus. “There are good data that show that they are triggered by infections and that they are specialized to form autoantibodies,” Dr. Weyand said about the age-associated B cells.
 

‘Bad old T cells’

Under the influence of genetic stop-and-go signals, the composition of the T-cell population also changes over the course of our lives. It becomes less diverse. T-helper cells become less common, and as a result, terminally differentiated effector memory T cells become more common. According to Dr. Weyand, herein lies the problem. “These cells are not just lazy, old cells that sit around. Unfortunately, they are also malicious. What we see in both the T- and B-cell systems is that they become increasingly innate with age,” he said. “They are not quite so precise or good.”

In turn, myeloid cells are less active in old age because of phagocytosis and antigen presentation, and they get more mutations. They are released more often from the bone marrow, produce more cytokines, and essentially contribute to inflamm-aging.
 

Power sources fail

In her cellular and microbiological investigations, Dr. Weyand has devoted a lot of time to studying why T cells age prematurely in patients with RA. The key was in the cellular microbiology. “We learned how the T-cell aging process translates into metabolic reprogramming of the T cells – how a good, strong, and protective T cell transforms into a disease-inducing T cell.”

At the center of premature T-cell aging in RA are disrupted mitochondrial function and insufficient communication of the mitochondria with the lysosomes and the endoplasmic reticulum.

T cells of RA patients (RA T cells) contain less MRE11A, compared with those in healthy people. This is a nuclease that allows the repair of breaks in DNA. If MRE11A is inhibited, then senescent T cells accumulate and form proinflammatory cytokines such as IL-B, IL-6, and TNF. “This is the trio that we rheumatologists are always concerned with.”

Since mitochondrial DNA repair is essential for maintaining mitochondrial fitness, the cellular power sources in patients with RA cannot provide as much energy in the form of adenosine triphosphate as in healthy people. Metabolically, they are not so fit, Dr. Weyand said.
 

Inflammatory cell death

In fact, all metabolic pathways in the T cells are reduced. The bioenergetic failure has consequences. “Unfortunately, as the mitochondrion ages, its DNA leaks into the cytosol,” explained Dr. Weyand. “Cells do not like this.” This is because DNA activates inflammasomes in the cytosol via caspase-1. This process results in a highly inflammatory cell death: pyroptosis. Subsequently, there is no trace of the cells in the tissue. “RA patients’ synovial tissue is a graveyard of dying T cells.”

In the lysosomes, the cells’ “intestine,” problems arise because patients with RA can no longer activate the adenosine monophosphate–activated protein kinase enzyme. It does not receive the lipid tail it needs to take its position as energy sensor on the lysosomal membrane. As a result, its antagonist, mTOR – both usually keep each other in check – gains the upper hand. According to Dr. Weyand, “mTOR has a party.” It activates and stresses the cells.

Additional changes affect the endoplasmic reticulum (ER). “This is where all of your proteins are synthesized and packaged to migrate from within to outside the cell, or to the cell membrane.” Compared with healthy T cells, RA T cells have around 50% more ER. “The less that mitochondria work, the larger the ER. It gets really fat.”

Mitochondria communicate with the ER via aspartate, oxaloacetate, and malate. In so doing, they control their size. RA T cells appear to be aspartate deficient. In animal models, amino acids had an anti-inflammatory effect.

When sequencing the mRNA bound to the ER, Dr. Weyand and her colleagues encountered the building blocks for TNF. “There is more than three times as much mRNA as TNF. It transforms these T cells into TNF superproducers,” said the rheumatologist. “No wonder this kind of cell is proinflammatory – it forms precisely that cytokine on which you focus every day.”

This article was translated from Medscape’s German edition. A version of this article first appeared on Medscape.com.

LEIPZIG, GERMANY – With age comes illness: Cancer, cardiovascular and neurodegenerative diseases, increased infections, and autoimmune diseases such as rheumatism become more common. This is because the immune system also ages. In the case of autoimmune diseases, this aging happens particularly quickly.

“There is this phenomenon of premature aging of the immune system,” said Cornelia Weyand, PhD, director of Stanford (Calif.) University’s Center for Translational Medicine at the German Rheumatology Congress 2023. In healthy people, the immune system begins to age at age 20. From that point on, the thymus gland, which reaches peak function at 14-15 years old, plays an increasingly minor role. “At age 50 years, the aging process of the immune system gains momentum.”

“What’s good about this is that the T and B cells age together, but all a little differently, each system by itself,” said Thomas Dörner, MD, PhD, head of consultation hours for clinical hemostaseology at the Charité University Hospitals in Berlin.

While the reduced formation of naive T cells can be attributed to the regression of the thymus gland, the naive B cells are a consequence of age-related, fatty bone marrow degeneration. The influence of adipocyte-derived tumor necrosis factor (TNF)–alpha also causes the bone marrow to develop B cells more and more weakly and slowly. “Through this [process], the preimmune range of B-cells decreases and becomes less healthy than in a young person.”
 

‘Inflamm-aging’

“In the periphery, we have identified a process we call “inflamm-aging,” where the cytokines interferon-gamma, interleukin (IL)–10, and IL-17 play a predominant role. This also alters the primary and secondary immune response,” said Dr. Dörner. Here, decreasing stimulation via the B-cell receptor by aging T-lymphocytes makes a difference.

As we age, the immune system restructures itself completely. “Protective immunity regresses and the inferior immunity emerges,” explained Dr. Weyand. Wounds heal more poorly, the protective action against infections and above all malignancies, as well as the immune response to vaccinations, decreases.

The increased occurrence of neurodegenerative, cardiovascular, and autoimmune diseases is not because of a loss of function, but rather to newly gained, undesired functions. These are associated with inflammatory changes. Hence, the term inflamm-aging.

With the B cells, functional germinal centers in the lymphoid organs and protective antibodies become rarer, and age-associated B cells accumulate. As Dr. Dörner emphasized, these cells are not under the command of the B-cell receptor and are independent of the cytokine BAFF (B-cell activating factor). Instead, they react to signals that are sent from the toll-like receptors 7 and 9.

This potentially also explains the increased development of autoantibodies in older people and the association of viral and autoimmune diseases. This means that age-associated B cells develop more frequently, such as with rheumatoid arthritis, scleroderma, and systemic lupus erythematosus. “There are good data that show that they are triggered by infections and that they are specialized to form autoantibodies,” Dr. Weyand said about the age-associated B cells.
 

‘Bad old T cells’

Under the influence of genetic stop-and-go signals, the composition of the T-cell population also changes over the course of our lives. It becomes less diverse. T-helper cells become less common, and as a result, terminally differentiated effector memory T cells become more common. According to Dr. Weyand, herein lies the problem. “These cells are not just lazy, old cells that sit around. Unfortunately, they are also malicious. What we see in both the T- and B-cell systems is that they become increasingly innate with age,” he said. “They are not quite so precise or good.”

In turn, myeloid cells are less active in old age because of phagocytosis and antigen presentation, and they get more mutations. They are released more often from the bone marrow, produce more cytokines, and essentially contribute to inflamm-aging.
 

Power sources fail

In her cellular and microbiological investigations, Dr. Weyand has devoted a lot of time to studying why T cells age prematurely in patients with RA. The key was in the cellular microbiology. “We learned how the T-cell aging process translates into metabolic reprogramming of the T cells – how a good, strong, and protective T cell transforms into a disease-inducing T cell.”

At the center of premature T-cell aging in RA are disrupted mitochondrial function and insufficient communication of the mitochondria with the lysosomes and the endoplasmic reticulum.

T cells of RA patients (RA T cells) contain less MRE11A, compared with those in healthy people. This is a nuclease that allows the repair of breaks in DNA. If MRE11A is inhibited, then senescent T cells accumulate and form proinflammatory cytokines such as IL-B, IL-6, and TNF. “This is the trio that we rheumatologists are always concerned with.”

Since mitochondrial DNA repair is essential for maintaining mitochondrial fitness, the cellular power sources in patients with RA cannot provide as much energy in the form of adenosine triphosphate as in healthy people. Metabolically, they are not so fit, Dr. Weyand said.
 

Inflammatory cell death

In fact, all metabolic pathways in the T cells are reduced. The bioenergetic failure has consequences. “Unfortunately, as the mitochondrion ages, its DNA leaks into the cytosol,” explained Dr. Weyand. “Cells do not like this.” This is because DNA activates inflammasomes in the cytosol via caspase-1. This process results in a highly inflammatory cell death: pyroptosis. Subsequently, there is no trace of the cells in the tissue. “RA patients’ synovial tissue is a graveyard of dying T cells.”

In the lysosomes, the cells’ “intestine,” problems arise because patients with RA can no longer activate the adenosine monophosphate–activated protein kinase enzyme. It does not receive the lipid tail it needs to take its position as energy sensor on the lysosomal membrane. As a result, its antagonist, mTOR – both usually keep each other in check – gains the upper hand. According to Dr. Weyand, “mTOR has a party.” It activates and stresses the cells.

Additional changes affect the endoplasmic reticulum (ER). “This is where all of your proteins are synthesized and packaged to migrate from within to outside the cell, or to the cell membrane.” Compared with healthy T cells, RA T cells have around 50% more ER. “The less that mitochondria work, the larger the ER. It gets really fat.”

Mitochondria communicate with the ER via aspartate, oxaloacetate, and malate. In so doing, they control their size. RA T cells appear to be aspartate deficient. In animal models, amino acids had an anti-inflammatory effect.

When sequencing the mRNA bound to the ER, Dr. Weyand and her colleagues encountered the building blocks for TNF. “There is more than three times as much mRNA as TNF. It transforms these T cells into TNF superproducers,” said the rheumatologist. “No wonder this kind of cell is proinflammatory – it forms precisely that cytokine on which you focus every day.”

This article was translated from Medscape’s German edition. A version of this article first appeared on Medscape.com.

TOPLINE:

Blood samples from healthy adults show an inhibition of neutrophil extracellular trap formation (NET) after 1 week of daily ginger supplements.

METHODOLOGY:

• Researchers recruited nine healthy adults aged 18-38 years to receive a 100-mg oral ginger supplement daily for 7 consecutive days.
• Blood samples were collected at baseline and on days 7 and 14, with isolation of neutrophils, peripheral blood mononuclear cells, and plasma.
• The researchers measured NET formation (NETosis) as a way to show the effect of ginger on inflammation.

TAKEAWAY:

• Measures of neutrophil cyclic AMP (cAMP) were significantly higher after 7 days of ginger supplements, compared with baseline levels, although these levels returned to near baseline by 1 week after discontinuing ginger consumption.
• Oral ginger supplements reduced neutrophil phosphodiesterase (PDE) activity by 40% from baseline, similar to results seen with synthetic PDE4 inhibitors.
• The results build on previous studies showing inhibition of neutrophil hyperactivity in mice with antiphospholipid syndrome and lupus after injection with a purified ginger preparation.
• Researchers replicated the results showing effects of oral ginger on neutrophils in eight additional healthy adults who also showed reduced NETosis and increased cAMP after 1 week of ginger supplements.

IN PRACTICE:

The results show biologic support for the potential of ginger to affect neutrophil function in humans; therefore, “ginger may have a real ability to complement treatment programs that are already underway,” said corresponding author Jason Knight, MD, of the University of Michigan, Ann Arbor, in a press release.

SOURCE:

First author Ramadan A. Ali, MD, of the University of Michigan, Ann Arbor, and colleagues reported their study in JCI Insight.

LIMITATIONS:

More research is needed in humans with inflammatory and autoimmune diseases to confirm the findings and explore ginger as an adjuvant therapeutic intervention.

DISCLOSURES:

The study received no outside funding. The researchers report no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

Blood samples from healthy adults show an inhibition of neutrophil extracellular trap formation (NET) after 1 week of daily ginger supplements.

METHODOLOGY:

• Researchers recruited nine healthy adults aged 18-38 years to receive a 100-mg oral ginger supplement daily for 7 consecutive days.
• Blood samples were collected at baseline and on days 7 and 14, with isolation of neutrophils, peripheral blood mononuclear cells, and plasma.
• The researchers measured NET formation (NETosis) as a way to show the effect of ginger on inflammation.

TAKEAWAY:

• Measures of neutrophil cyclic AMP (cAMP) were significantly higher after 7 days of ginger supplements, compared with baseline levels, although these levels returned to near baseline by 1 week after discontinuing ginger consumption.
• Oral ginger supplements reduced neutrophil phosphodiesterase (PDE) activity by 40% from baseline, similar to results seen with synthetic PDE4 inhibitors.
• The results build on previous studies showing inhibition of neutrophil hyperactivity in mice with antiphospholipid syndrome and lupus after injection with a purified ginger preparation.
• Researchers replicated the results showing effects of oral ginger on neutrophils in eight additional healthy adults who also showed reduced NETosis and increased cAMP after 1 week of ginger supplements.

IN PRACTICE:

The results show biologic support for the potential of ginger to affect neutrophil function in humans; therefore, “ginger may have a real ability to complement treatment programs that are already underway,” said corresponding author Jason Knight, MD, of the University of Michigan, Ann Arbor, in a press release.

SOURCE:

First author Ramadan A. Ali, MD, of the University of Michigan, Ann Arbor, and colleagues reported their study in JCI Insight.

LIMITATIONS:

More research is needed in humans with inflammatory and autoimmune diseases to confirm the findings and explore ginger as an adjuvant therapeutic intervention.

DISCLOSURES:

The study received no outside funding. The researchers report no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

Blood samples from healthy adults show an inhibition of neutrophil extracellular trap formation (NET) after 1 week of daily ginger supplements.

METHODOLOGY:

• Researchers recruited nine healthy adults aged 18-38 years to receive a 100-mg oral ginger supplement daily for 7 consecutive days.
• Blood samples were collected at baseline and on days 7 and 14, with isolation of neutrophils, peripheral blood mononuclear cells, and plasma.
• The researchers measured NET formation (NETosis) as a way to show the effect of ginger on inflammation.

TAKEAWAY:

• Measures of neutrophil cyclic AMP (cAMP) were significantly higher after 7 days of ginger supplements, compared with baseline levels, although these levels returned to near baseline by 1 week after discontinuing ginger consumption.
• Oral ginger supplements reduced neutrophil phosphodiesterase (PDE) activity by 40% from baseline, similar to results seen with synthetic PDE4 inhibitors.
• The results build on previous studies showing inhibition of neutrophil hyperactivity in mice with antiphospholipid syndrome and lupus after injection with a purified ginger preparation.
• Researchers replicated the results showing effects of oral ginger on neutrophils in eight additional healthy adults who also showed reduced NETosis and increased cAMP after 1 week of ginger supplements.

IN PRACTICE:

The results show biologic support for the potential of ginger to affect neutrophil function in humans; therefore, “ginger may have a real ability to complement treatment programs that are already underway,” said corresponding author Jason Knight, MD, of the University of Michigan, Ann Arbor, in a press release.

SOURCE:

First author Ramadan A. Ali, MD, of the University of Michigan, Ann Arbor, and colleagues reported their study in JCI Insight.

LIMITATIONS:

More research is needed in humans with inflammatory and autoimmune diseases to confirm the findings and explore ginger as an adjuvant therapeutic intervention.

DISCLOSURES:

The study received no outside funding. The researchers report no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

Drug use disorder increased the likelihood of in-hospital mortality more than 10-fold in patients with ankylosing spondylitis (AS), compared with patients who did not die while hospitalized.

METHODOLOGY:

• Researchers reviewed data from 2,125 adults with AS who were hospitalized between 2015 and 2017, using the Cerner Health Facts Database.
• The final analysis included 41 patients with AS who died while hospitalized and 260 random control patients with AS who did not die.
• The mean age of the deceased patients with AS was 70 years, 85% were male, and 81% were White; 71% had hypertension, 32% had kidney disease, and 22% had congestive heart failure.

TAKEAWAY:

• Among the patients with AS, cardiovascular disease was the most frequent cause of death, followed by infection, respiratory failure, and fracture/trauma in 15, 14, 8, and 7 patients, respectively. (Some patients had more than one cause of death recorded in the discharge summary.)
• The most common cardiac causes of death were myocardial infarction and cardiac arrest, while the top causes of acute respiratory failure were pneumonia and pulmonary embolism.
• Drug abuse, including opioid dependence, was significantly associated with death among hospitalized patients with AS (adjusted odds ratio, 10.9; P = .001).
• Heart failure and kidney disease were the comorbidities most strongly associated with mortality; the odds of death in the presence of heart failure rose 2.76-fold, and it increased 2.46-fold in the presence of kidney disease.

IN PRACTICE:

Underlying comorbidities, especially cardiac and renal, are associated with mortality in AS, and patients should be screened early on for these comorbidities to help reduce the odds of death.

SOURCE:

First author Mohamad Bittar, MD, of the University of Tennessee Health Science Center, Memphis, and colleagues reported their findings in Clinical Rheumatology).

LIMITATIONS:

The study lacked AS-specific data such as disease activity scores, which were not in the database. Also missing were variables linked to disease activity and mortality, including smoking, BMI levels, and C-reactive protein levels.

DISCLOSURES:

The study received no outside funding. Several coauthors disclosed financial relationships with UCB, Amgen, Pfizer, AbbVie, Novartis, and Eli Lilly.

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

TOPLINE:

Drug use disorder increased the likelihood of in-hospital mortality more than 10-fold in patients with ankylosing spondylitis (AS), compared with patients who did not die while hospitalized.

METHODOLOGY:

• Researchers reviewed data from 2,125 adults with AS who were hospitalized between 2015 and 2017, using the Cerner Health Facts Database.
• The final analysis included 41 patients with AS who died while hospitalized and 260 random control patients with AS who did not die.
• The mean age of the deceased patients with AS was 70 years, 85% were male, and 81% were White; 71% had hypertension, 32% had kidney disease, and 22% had congestive heart failure.

TAKEAWAY:

• Among the patients with AS, cardiovascular disease was the most frequent cause of death, followed by infection, respiratory failure, and fracture/trauma in 15, 14, 8, and 7 patients, respectively. (Some patients had more than one cause of death recorded in the discharge summary.)
• The most common cardiac causes of death were myocardial infarction and cardiac arrest, while the top causes of acute respiratory failure were pneumonia and pulmonary embolism.
• Drug abuse, including opioid dependence, was significantly associated with death among hospitalized patients with AS (adjusted odds ratio, 10.9; P = .001).
• Heart failure and kidney disease were the comorbidities most strongly associated with mortality; the odds of death in the presence of heart failure rose 2.76-fold, and it increased 2.46-fold in the presence of kidney disease.

IN PRACTICE:

Underlying comorbidities, especially cardiac and renal, are associated with mortality in AS, and patients should be screened early on for these comorbidities to help reduce the odds of death.

SOURCE:

First author Mohamad Bittar, MD, of the University of Tennessee Health Science Center, Memphis, and colleagues reported their findings in Clinical Rheumatology).

LIMITATIONS:

The study lacked AS-specific data such as disease activity scores, which were not in the database. Also missing were variables linked to disease activity and mortality, including smoking, BMI levels, and C-reactive protein levels.

DISCLOSURES:

The study received no outside funding. Several coauthors disclosed financial relationships with UCB, Amgen, Pfizer, AbbVie, Novartis, and Eli Lilly.

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

TOPLINE:

Drug use disorder increased the likelihood of in-hospital mortality more than 10-fold in patients with ankylosing spondylitis (AS), compared with patients who did not die while hospitalized.

METHODOLOGY:

• Researchers reviewed data from 2,125 adults with AS who were hospitalized between 2015 and 2017, using the Cerner Health Facts Database.
• The final analysis included 41 patients with AS who died while hospitalized and 260 random control patients with AS who did not die.
• The mean age of the deceased patients with AS was 70 years, 85% were male, and 81% were White; 71% had hypertension, 32% had kidney disease, and 22% had congestive heart failure.

TAKEAWAY:

• Among the patients with AS, cardiovascular disease was the most frequent cause of death, followed by infection, respiratory failure, and fracture/trauma in 15, 14, 8, and 7 patients, respectively. (Some patients had more than one cause of death recorded in the discharge summary.)
• The most common cardiac causes of death were myocardial infarction and cardiac arrest, while the top causes of acute respiratory failure were pneumonia and pulmonary embolism.
• Drug abuse, including opioid dependence, was significantly associated with death among hospitalized patients with AS (adjusted odds ratio, 10.9; P = .001).
• Heart failure and kidney disease were the comorbidities most strongly associated with mortality; the odds of death in the presence of heart failure rose 2.76-fold, and it increased 2.46-fold in the presence of kidney disease.

IN PRACTICE:

Underlying comorbidities, especially cardiac and renal, are associated with mortality in AS, and patients should be screened early on for these comorbidities to help reduce the odds of death.

SOURCE:

First author Mohamad Bittar, MD, of the University of Tennessee Health Science Center, Memphis, and colleagues reported their findings in Clinical Rheumatology).

LIMITATIONS:

The study lacked AS-specific data such as disease activity scores, which were not in the database. Also missing were variables linked to disease activity and mortality, including smoking, BMI levels, and C-reactive protein levels.

DISCLOSURES:

The study received no outside funding. Several coauthors disclosed financial relationships with UCB, Amgen, Pfizer, AbbVie, Novartis, and Eli Lilly.

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

MILAN – Numerous unresolved questions surround progressive pulmonary fibrosis (PPF) treatment, according to Elisabeth Bendstrup, MD, PhD, a researcher and clinical professor in the department of clinical medicine – department of respiratory diseases and allergy, Aarhus (Denmark) University, Denmark. These questions regard the optimal timing for treatment initiation, the role of available medications, either as monotherapy or in combination, and nonpharmacologic support options.

What’s in the toolbox?

Pulmonologists who manage PPF have a range of treatment options at their disposal. This includes careful patient observation, with treatment initiation based on clinical necessity. The therapeutic arsenal comprises immunomodulatory treatments, antifibrotic agents, palliative and supportive care, and, for a minority of patients, lung transplantation.

“Once a patient is diagnosed with PPF, it is important to remember that the diagnostic criteria from the guidelines are not exactly the same of those accepted for the reimbursement of antifibrotic treatments in different countries,” Dr. Bendstrup said, suggesting that nonclinical considerations could also potentially influence the treatment choice. She spoke at the annual congress of the European Respiratory Society.

Michael Kreuter, MD, director of the Lung Center at the University Hospital in Mainz, Germany, provided insight into the introduction of antifibrotic drugs for the treatment of PPF. Drawing from nearly a decade ago when the first antifibrotic medication was approved for idiopathic pulmonary fibrosis (IPF), Dr. Kreuter noted its effectiveness in slowing disease progression, although it does not reverse it. Subsequently, the discovery that non-IPF diseases, such as rheumatoid arthritis, exhibited IPF-like behavior led to the exploration of the use of the same drugs for similar conditions, even if not IPF.

“That’s how antifibrotic treatments came into place. Now we have more trials and data to be discussed in the future,” Dr. Kreuter added. He highlighted that antifibrotic drugs are effective for several diseases. Most of those diseases are treated with different anti-inflammatory drugs, which makes it difficult to decide when to start antifibrotic therapy and how to eventually combine it with different pharmacologic approaches.
 

A pivotal starting point

One of the primary challenges faced by pulmonologists in the management of PPF is determining the appropriate timing for initiating treatment, a question only partially addressed by existing guidelines. Dr. Bendstrup advocated for a comprehensive baseline evaluation. Factors to be considered include symptom burden, the severity of lung decline, radiologic characteristics, signs of alveolar inflammation, progression risk factors, quality of life, patient preferences, and medical history. “All these should be best discussed in a multidisciplinary team, including pulmonologists, nurses, experts in palliative care, occupational physicians, and more,” she said.

Current guidelines recommend nintedanib for PPF treatment for patients who have failed standard management for fibrotic interstitial lung disease (ILD) other than IPF. However, the definition of “standard management” remains a topic of debate, and it is acknowledged that evidence-based guidance for a standard of care varies among patients. Dr. Bendstrup pointed out the limited guidance clinicians receive from these guidelines. “As clinicians, we are not left with very much help from here.”
 

Choosing the right approach

Dr. Bendstrup delved into the factors influencing the choice between antifibrotic and anti-inflammatory therapies. This decision hinges on whether the patient presents with a predominantly inflammatory or a fibrotic progressive phenotype. Certain clinical characteristics contribute to the decision. Factors such as younger age, female gender, and the presence of connective tissue disease lean toward an inflammatory phenotype. Radiologic patterns, such as organized pneumonia, hypersensitivity pneumonia, or usual interstitial pneumonia–like patterns also provide valuable clues. Additionally, genetics plays a role, with shorter telomeres indicating a more fibrotic phenotype and an increased risk of immunomodulatory treatment side effects in non-IPF ILDs.

Bendstrup referred to a recent position paper on treatment recommendations and many other studies that support the use of different treatments for patients with PPF. The authors highlighted limited evidence for immunomodulation in fibrotic ILD, though such treatment is generally used except for ILD associated with systemic sclerosis. Moreover, the guidelines conditionally recommend nintedanib and call for further research on pirfenidone in PPF.

“We need intelligent, well-designed trials looking at subgroups of patients at higher risk, maybe based on molecular identification. We also need to have good biomarkers to better classify our patients based on disease behavior and treatment response. There’s a lot of discussion of biomarkers for progression, much less – if any – on biomarkers for the response to treatment. And we need them as well,” Dr. Bendstrup said in an interview.
 

The role of supportive care

Effective PPF treatment extends beyond pharmacologic interventions. It encompasses symptom management, patient education on vaccination and smoking cessation, and fostering social support networks. Psychological support, supplemental oxygen therapy, and pulmonary rehabilitation are integral components of care.

Elisabeth Robertson, a PPF patient representative from the United Kingdom, emphasized the importance of palliative care, not just in end-of-life scenarios but throughout the patient’s journey. Palliative care encompasses symptom alleviation, enabling patients to stay at home when possible, addressing mental health, and preparing for the end of life. Such holistic care can significantly enhance the patient’s quality of life.

The cochair of the session, Marlies S. Wijsenbeek, MD, PhD, pulmonary physician and head of the ILD Centre at the Erasmus University Medical Centre, Rotterdam, the Netherlands, underscored that palliative care begins at diagnosis and involves managing symptom burdens. “Supportive care also includes nurses, as they are precious for the patients while answering their questions and can help save time for the doctors,” she said in an interview.

In the discussion on treatment decisions, experts agreed on the pivotal role of patients in decision-making. However, Dr. Kreuter highlighted two critical factors that influence successful patient-doctor interactions: the cultural backgrounds of patients and their relatives, and the attitudes of health care providers.

Dr. Bendstrup has received honoraria or consultation fees from Boehringer Ingelheim, Roche, Astra Zeneca, Chiesi, and Daiichi Sankyo. Ms. Robertson disclosed no relevant financial relationships.

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

MILAN – Numerous unresolved questions surround progressive pulmonary fibrosis (PPF) treatment, according to Elisabeth Bendstrup, MD, PhD, a researcher and clinical professor in the department of clinical medicine – department of respiratory diseases and allergy, Aarhus (Denmark) University, Denmark. These questions regard the optimal timing for treatment initiation, the role of available medications, either as monotherapy or in combination, and nonpharmacologic support options.

What’s in the toolbox?

Pulmonologists who manage PPF have a range of treatment options at their disposal. This includes careful patient observation, with treatment initiation based on clinical necessity. The therapeutic arsenal comprises immunomodulatory treatments, antifibrotic agents, palliative and supportive care, and, for a minority of patients, lung transplantation.

“Once a patient is diagnosed with PPF, it is important to remember that the diagnostic criteria from the guidelines are not exactly the same of those accepted for the reimbursement of antifibrotic treatments in different countries,” Dr. Bendstrup said, suggesting that nonclinical considerations could also potentially influence the treatment choice. She spoke at the annual congress of the European Respiratory Society.

Michael Kreuter, MD, director of the Lung Center at the University Hospital in Mainz, Germany, provided insight into the introduction of antifibrotic drugs for the treatment of PPF. Drawing from nearly a decade ago when the first antifibrotic medication was approved for idiopathic pulmonary fibrosis (IPF), Dr. Kreuter noted its effectiveness in slowing disease progression, although it does not reverse it. Subsequently, the discovery that non-IPF diseases, such as rheumatoid arthritis, exhibited IPF-like behavior led to the exploration of the use of the same drugs for similar conditions, even if not IPF.

“That’s how antifibrotic treatments came into place. Now we have more trials and data to be discussed in the future,” Dr. Kreuter added. He highlighted that antifibrotic drugs are effective for several diseases. Most of those diseases are treated with different anti-inflammatory drugs, which makes it difficult to decide when to start antifibrotic therapy and how to eventually combine it with different pharmacologic approaches.
 

A pivotal starting point

One of the primary challenges faced by pulmonologists in the management of PPF is determining the appropriate timing for initiating treatment, a question only partially addressed by existing guidelines. Dr. Bendstrup advocated for a comprehensive baseline evaluation. Factors to be considered include symptom burden, the severity of lung decline, radiologic characteristics, signs of alveolar inflammation, progression risk factors, quality of life, patient preferences, and medical history. “All these should be best discussed in a multidisciplinary team, including pulmonologists, nurses, experts in palliative care, occupational physicians, and more,” she said.

Current guidelines recommend nintedanib for PPF treatment for patients who have failed standard management for fibrotic interstitial lung disease (ILD) other than IPF. However, the definition of “standard management” remains a topic of debate, and it is acknowledged that evidence-based guidance for a standard of care varies among patients. Dr. Bendstrup pointed out the limited guidance clinicians receive from these guidelines. “As clinicians, we are not left with very much help from here.”
 

Choosing the right approach

Dr. Bendstrup delved into the factors influencing the choice between antifibrotic and anti-inflammatory therapies. This decision hinges on whether the patient presents with a predominantly inflammatory or a fibrotic progressive phenotype. Certain clinical characteristics contribute to the decision. Factors such as younger age, female gender, and the presence of connective tissue disease lean toward an inflammatory phenotype. Radiologic patterns, such as organized pneumonia, hypersensitivity pneumonia, or usual interstitial pneumonia–like patterns also provide valuable clues. Additionally, genetics plays a role, with shorter telomeres indicating a more fibrotic phenotype and an increased risk of immunomodulatory treatment side effects in non-IPF ILDs.

Bendstrup referred to a recent position paper on treatment recommendations and many other studies that support the use of different treatments for patients with PPF. The authors highlighted limited evidence for immunomodulation in fibrotic ILD, though such treatment is generally used except for ILD associated with systemic sclerosis. Moreover, the guidelines conditionally recommend nintedanib and call for further research on pirfenidone in PPF.

“We need intelligent, well-designed trials looking at subgroups of patients at higher risk, maybe based on molecular identification. We also need to have good biomarkers to better classify our patients based on disease behavior and treatment response. There’s a lot of discussion of biomarkers for progression, much less – if any – on biomarkers for the response to treatment. And we need them as well,” Dr. Bendstrup said in an interview.
 

The role of supportive care

Effective PPF treatment extends beyond pharmacologic interventions. It encompasses symptom management, patient education on vaccination and smoking cessation, and fostering social support networks. Psychological support, supplemental oxygen therapy, and pulmonary rehabilitation are integral components of care.

Elisabeth Robertson, a PPF patient representative from the United Kingdom, emphasized the importance of palliative care, not just in end-of-life scenarios but throughout the patient’s journey. Palliative care encompasses symptom alleviation, enabling patients to stay at home when possible, addressing mental health, and preparing for the end of life. Such holistic care can significantly enhance the patient’s quality of life.

The cochair of the session, Marlies S. Wijsenbeek, MD, PhD, pulmonary physician and head of the ILD Centre at the Erasmus University Medical Centre, Rotterdam, the Netherlands, underscored that palliative care begins at diagnosis and involves managing symptom burdens. “Supportive care also includes nurses, as they are precious for the patients while answering their questions and can help save time for the doctors,” she said in an interview.

In the discussion on treatment decisions, experts agreed on the pivotal role of patients in decision-making. However, Dr. Kreuter highlighted two critical factors that influence successful patient-doctor interactions: the cultural backgrounds of patients and their relatives, and the attitudes of health care providers.

Dr. Bendstrup has received honoraria or consultation fees from Boehringer Ingelheim, Roche, Astra Zeneca, Chiesi, and Daiichi Sankyo. Ms. Robertson disclosed no relevant financial relationships.

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

MILAN – Numerous unresolved questions surround progressive pulmonary fibrosis (PPF) treatment, according to Elisabeth Bendstrup, MD, PhD, a researcher and clinical professor in the department of clinical medicine – department of respiratory diseases and allergy, Aarhus (Denmark) University, Denmark. These questions regard the optimal timing for treatment initiation, the role of available medications, either as monotherapy or in combination, and nonpharmacologic support options.

What’s in the toolbox?

Pulmonologists who manage PPF have a range of treatment options at their disposal. This includes careful patient observation, with treatment initiation based on clinical necessity. The therapeutic arsenal comprises immunomodulatory treatments, antifibrotic agents, palliative and supportive care, and, for a minority of patients, lung transplantation.

“Once a patient is diagnosed with PPF, it is important to remember that the diagnostic criteria from the guidelines are not exactly the same of those accepted for the reimbursement of antifibrotic treatments in different countries,” Dr. Bendstrup said, suggesting that nonclinical considerations could also potentially influence the treatment choice. She spoke at the annual congress of the European Respiratory Society.

Michael Kreuter, MD, director of the Lung Center at the University Hospital in Mainz, Germany, provided insight into the introduction of antifibrotic drugs for the treatment of PPF. Drawing from nearly a decade ago when the first antifibrotic medication was approved for idiopathic pulmonary fibrosis (IPF), Dr. Kreuter noted its effectiveness in slowing disease progression, although it does not reverse it. Subsequently, the discovery that non-IPF diseases, such as rheumatoid arthritis, exhibited IPF-like behavior led to the exploration of the use of the same drugs for similar conditions, even if not IPF.

“That’s how antifibrotic treatments came into place. Now we have more trials and data to be discussed in the future,” Dr. Kreuter added. He highlighted that antifibrotic drugs are effective for several diseases. Most of those diseases are treated with different anti-inflammatory drugs, which makes it difficult to decide when to start antifibrotic therapy and how to eventually combine it with different pharmacologic approaches.
 

A pivotal starting point

One of the primary challenges faced by pulmonologists in the management of PPF is determining the appropriate timing for initiating treatment, a question only partially addressed by existing guidelines. Dr. Bendstrup advocated for a comprehensive baseline evaluation. Factors to be considered include symptom burden, the severity of lung decline, radiologic characteristics, signs of alveolar inflammation, progression risk factors, quality of life, patient preferences, and medical history. “All these should be best discussed in a multidisciplinary team, including pulmonologists, nurses, experts in palliative care, occupational physicians, and more,” she said.

Current guidelines recommend nintedanib for PPF treatment for patients who have failed standard management for fibrotic interstitial lung disease (ILD) other than IPF. However, the definition of “standard management” remains a topic of debate, and it is acknowledged that evidence-based guidance for a standard of care varies among patients. Dr. Bendstrup pointed out the limited guidance clinicians receive from these guidelines. “As clinicians, we are not left with very much help from here.”
 

Choosing the right approach

Dr. Bendstrup delved into the factors influencing the choice between antifibrotic and anti-inflammatory therapies. This decision hinges on whether the patient presents with a predominantly inflammatory or a fibrotic progressive phenotype. Certain clinical characteristics contribute to the decision. Factors such as younger age, female gender, and the presence of connective tissue disease lean toward an inflammatory phenotype. Radiologic patterns, such as organized pneumonia, hypersensitivity pneumonia, or usual interstitial pneumonia–like patterns also provide valuable clues. Additionally, genetics plays a role, with shorter telomeres indicating a more fibrotic phenotype and an increased risk of immunomodulatory treatment side effects in non-IPF ILDs.

Bendstrup referred to a recent position paper on treatment recommendations and many other studies that support the use of different treatments for patients with PPF. The authors highlighted limited evidence for immunomodulation in fibrotic ILD, though such treatment is generally used except for ILD associated with systemic sclerosis. Moreover, the guidelines conditionally recommend nintedanib and call for further research on pirfenidone in PPF.

“We need intelligent, well-designed trials looking at subgroups of patients at higher risk, maybe based on molecular identification. We also need to have good biomarkers to better classify our patients based on disease behavior and treatment response. There’s a lot of discussion of biomarkers for progression, much less – if any – on biomarkers for the response to treatment. And we need them as well,” Dr. Bendstrup said in an interview.
 

The role of supportive care

Effective PPF treatment extends beyond pharmacologic interventions. It encompasses symptom management, patient education on vaccination and smoking cessation, and fostering social support networks. Psychological support, supplemental oxygen therapy, and pulmonary rehabilitation are integral components of care.

Elisabeth Robertson, a PPF patient representative from the United Kingdom, emphasized the importance of palliative care, not just in end-of-life scenarios but throughout the patient’s journey. Palliative care encompasses symptom alleviation, enabling patients to stay at home when possible, addressing mental health, and preparing for the end of life. Such holistic care can significantly enhance the patient’s quality of life.

The cochair of the session, Marlies S. Wijsenbeek, MD, PhD, pulmonary physician and head of the ILD Centre at the Erasmus University Medical Centre, Rotterdam, the Netherlands, underscored that palliative care begins at diagnosis and involves managing symptom burdens. “Supportive care also includes nurses, as they are precious for the patients while answering their questions and can help save time for the doctors,” she said in an interview.

In the discussion on treatment decisions, experts agreed on the pivotal role of patients in decision-making. However, Dr. Kreuter highlighted two critical factors that influence successful patient-doctor interactions: the cultural backgrounds of patients and their relatives, and the attitudes of health care providers.

Dr. Bendstrup has received honoraria or consultation fees from Boehringer Ingelheim, Roche, Astra Zeneca, Chiesi, and Daiichi Sankyo. Ms. Robertson disclosed no relevant financial relationships.

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

TOPLINE:

In a large cross-sectional study, nearly one-third of patients with severe psoriasis met criteria for coronary microvascular dysfunction (CMD).

METHODOLOGY:

• Prior studies with small sample sizes have shown that CMD predicts poor cardiovascular outcomes in patients with severe psoriasis.
• In a prospective multicenter study, researchers enrolled 448 patients with moderate to severe psoriasis with no documented clinical cardiovascular disease who underwent transthoracic Doppler echocardiography to evaluate coronary microcirculation.
• The outcome variable of interest was CMD, defined as a coronary flow rate of 2.5 mL or less.
• The researchers used multivariable linear regression to model the associations of the characteristics of patients with psoriasis with CMD.

TAKEAWAY:

• Of the 448 patients, 141 (31.5%) showed CMD.
• Multivariable regression revealed four variables independently associated with CMD: higher Psoriasis Area Severity Index (PASI) score (per unit, odds ratio, 1.058; P < .001), duration of psoriasis (per year; OR, 1.046; P < .001), the presence of psoriatic arthritis (OR, 1.938; P = .015), and hypertension (OR, 2.169; P = .010).
• An increase of 1 point in the PASI score and 1 year of psoriasis duration were associated with a 5.8% and a 4.6% increased risk for CMD, respectively.

IN PRACTICE:

“We should diagnose and actively search for microvascular dysfunction in patients with psoriasis, as this population is at particularly high risk,” the researchers wrote.

SOURCE:

Stefano Piaserico, MD, PhD, of the University of Padova (Italy), led the research. The study was published in the Journal of Investigative Dermatology.

LIMITATIONS:

A small proportion of patients in the study were being treated for psoriasis, and other tools for assessing CMD were not used, such as PET-CT and cardiovascular MRI.

DISCLOSURES:

The authors reported having no relevant financial disclosures.

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

TOPLINE:

In a large cross-sectional study, nearly one-third of patients with severe psoriasis met criteria for coronary microvascular dysfunction (CMD).

METHODOLOGY:

• Prior studies with small sample sizes have shown that CMD predicts poor cardiovascular outcomes in patients with severe psoriasis.
• In a prospective multicenter study, researchers enrolled 448 patients with moderate to severe psoriasis with no documented clinical cardiovascular disease who underwent transthoracic Doppler echocardiography to evaluate coronary microcirculation.
• The outcome variable of interest was CMD, defined as a coronary flow rate of 2.5 mL or less.
• The researchers used multivariable linear regression to model the associations of the characteristics of patients with psoriasis with CMD.

TAKEAWAY:

• Of the 448 patients, 141 (31.5%) showed CMD.
• Multivariable regression revealed four variables independently associated with CMD: higher Psoriasis Area Severity Index (PASI) score (per unit, odds ratio, 1.058; P < .001), duration of psoriasis (per year; OR, 1.046; P < .001), the presence of psoriatic arthritis (OR, 1.938; P = .015), and hypertension (OR, 2.169; P = .010).
• An increase of 1 point in the PASI score and 1 year of psoriasis duration were associated with a 5.8% and a 4.6% increased risk for CMD, respectively.

IN PRACTICE:

“We should diagnose and actively search for microvascular dysfunction in patients with psoriasis, as this population is at particularly high risk,” the researchers wrote.

SOURCE:

Stefano Piaserico, MD, PhD, of the University of Padova (Italy), led the research. The study was published in the Journal of Investigative Dermatology.

LIMITATIONS:

A small proportion of patients in the study were being treated for psoriasis, and other tools for assessing CMD were not used, such as PET-CT and cardiovascular MRI.

DISCLOSURES:

The authors reported having no relevant financial disclosures.

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

TOPLINE:

In a large cross-sectional study, nearly one-third of patients with severe psoriasis met criteria for coronary microvascular dysfunction (CMD).

METHODOLOGY:

• Prior studies with small sample sizes have shown that CMD predicts poor cardiovascular outcomes in patients with severe psoriasis.
• In a prospective multicenter study, researchers enrolled 448 patients with moderate to severe psoriasis with no documented clinical cardiovascular disease who underwent transthoracic Doppler echocardiography to evaluate coronary microcirculation.
• The outcome variable of interest was CMD, defined as a coronary flow rate of 2.5 mL or less.
• The researchers used multivariable linear regression to model the associations of the characteristics of patients with psoriasis with CMD.

TAKEAWAY:

• Of the 448 patients, 141 (31.5%) showed CMD.
• Multivariable regression revealed four variables independently associated with CMD: higher Psoriasis Area Severity Index (PASI) score (per unit, odds ratio, 1.058; P < .001), duration of psoriasis (per year; OR, 1.046; P < .001), the presence of psoriatic arthritis (OR, 1.938; P = .015), and hypertension (OR, 2.169; P = .010).
• An increase of 1 point in the PASI score and 1 year of psoriasis duration were associated with a 5.8% and a 4.6% increased risk for CMD, respectively.

IN PRACTICE:

“We should diagnose and actively search for microvascular dysfunction in patients with psoriasis, as this population is at particularly high risk,” the researchers wrote.

SOURCE:

Stefano Piaserico, MD, PhD, of the University of Padova (Italy), led the research. The study was published in the Journal of Investigative Dermatology.

LIMITATIONS:

A small proportion of patients in the study were being treated for psoriasis, and other tools for assessing CMD were not used, such as PET-CT and cardiovascular MRI.

DISCLOSURES:

The authors reported having no relevant financial disclosures.

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

Editor’s note: As of this writing, the following proposed health insurance policy from Blue Cross and Blue Shield of North Carolina is still active. The Coalition of State Rheumatology Organizations and other rheumatology advocacy groups are in ongoing discussions with the health insurer and hope to have major changes to this policy implemented.

While AI has been in our world for years, it is expanding by the minute, perhaps by the nanosecond, within the health care sector. The $6.7 billion dollar health care AI market in 2020 is expected to climb to more than $120 billion by 2028. There are many questions regarding the application of AI in our world. Is it a mere instructional algorithm that computes things in a much faster way, or does it create a new story based on the information it has access to? Does it engender excitement or fear ... or both? Remember HAL? As we have seen throughout history with new inventions and technologies, there are risks and rewards. Even the best can have harmful unintended consequences. AI is no different, particularly when it comes to health care. In this case, AI can get a bad name if it is utilized along with biased data input and bad policy.

Shared savings

Here is where “shared savings” comes into play. A shared savings program starts with a baseline cost analysis of a particular care plan and then tracks costs (performance) going forward after certain changes to the original care plan are instituted. If savings are accrued when compared with baseline spending, those savings are shared with the providers of the care. Depending on how the shared savings program is implemented, the optics can be very bad if it appears as though physicians are being paid to reduce care.

‘The volunteer opportunity’

Recently, Blue Cross and Blue Shield of North Carolina, in partnership with Outcomes Matter Innovations, a data analysis company that uses AI/machine-learning technology, offered rheumatologists a new voluntary shared savings, value-based care (VBC) “opportunity.” Rheumatologists would be able to “utilize a web-based machine-learning technology platform that suggests evidence-based care pathways” in the treatment of rheumatoid arthritis and psoriatic arthritis (PsA). The VBC/shared savings model uses the AI platform to propose two different pathways. One model would delay the start of biologics or Janus kinase inhibitors (JAKi), and the second model would taper and/or stop biologics or JAKi altogether.

Delaying the start of biologics/JAKi would be achieved through “methotrexate optimization” and/or the use of triple therapy with methotrexate, sulfasalazine, and hydroxychloroquine. The other model would recommend tapering biologic/JAKi dosing in patients in remission or low disease activity and might even suggest a “medication holiday.”

The intention of this 3-year VBC/shared savings program is to reduce costs and create savings by reducing the use of biologics or JAKi. A tangential question might be, “Reduce costs and create savings for whom?” Apparently, the patients will not reap any of the cost savings, as this is proposed to be a shared savings program with the savings going to the physicians and the insurance company. Perhaps the idea is that patients will benefit by reducing unneeded expensive medications.
 

How will it work?

A cost baseline will be established on biologic and JAKi use prior to the start of the program. Once started, there will be a calculation of savings based on biologic/JAKi use going forward. It was stated that physicians would receive 22% of the total costs saved. In one flyer, it was estimated that, with methotrexate optimization, rheumatologists could be paid an average of $1,527 a month per patient per month of delay before starting a biologic or JAKi.

The American College of Rheumatology has guidelines for the treatment of RA and PsA, and while optimizing methotrexate and triple therapy is mentioned, tapering or stopping treatment with biologics or JAKi is not. Additionally, after lack of response at 3 months, the standard of care is to change to a more effective treatment, which for most patients is a biologic disease-modifying antirheumatic drug (DMARD). It could be construed that rheumatologists are being monetarily incentivized to reduce the use of expensive medications through ways that are not included in ACR guidelines and are not standard of care.

What if after the medication holiday the patient cannot recapture control of their disease? Is there a liability concern? Remember, there is no institutional review board or informed patient consent for this VBC data gathering model.

How will a patient feel knowing that their physician was paid to withhold care, or even worse, if a patient is not told of this and then finds out later? Not only are the optics for this suboptimal (at best), where does the liability fall if the patient does not do well and it comes out that their rheumatologist was paid to reduce the care, particularly in a way that is not supported in the guideline. Clearly, this appears to be a clinical study without an institutional review board and without patient consent.

There are also the data that are collected from this voluntary “opportunity.” A valid question would be, “What kind of data will this produce if rheumatologists are paid to delay, reduce, or stop the use of biologics/JAKi?” Is it possible that physicians may subconsciously delay putting patients on a biologic and taper more rapidly because of the reimbursement? This could lead to faulty, biased, AI-generated data that erroneously show this type of care is working. It would not be unheard of to wonder whether this once-voluntary opportunity might evolve into mandatory policy because now, they have “data to prove it.” … only this time there is no shared savings.
 

Low disease activity results in long-term savings

This is not meant to be an indictment of AI in health care, value-based care, or shared savings programs. In reality, AI had very little to do with how poorly this program was presented. Hopefully, it will bring about further discussions on how to achieve savings without sacrificing care. In fact, optimal care in RA and PsA is probably one of the best ways to save money in the long run. Nowhere in this program is there any mention of the high cost associated with uncontrolled disease activity in patients with RA or PsA. The downstream costs can be enormous when long- and short-term sequelae are taken into consideration: joint replacements, cardiovascular disease, certain kinds of malignancies, and all the side effects of increased steroid usage are just a few of the consequences we see with uncontrolled disease activity. It is only recently that we have been able to achieve low disease activity and remission in our patients. The rush to get patients off these medications is not the answer to achieving long-term savings. In addition to the very bad optics of paying rheumatologists to delay, taper, or stop using expensive mediations in their patients, the ultimate data achieved will be biased, and the only real winner will be the health insurance company.

Again, AI machine-learning and shared saving programs are not the guilty parties here. In fact, AI may be helpful in coming up with solutions to long-term health care costs, whether in the realm of economics or scientific research. CSRO and our state member organizations continue to educate the health insurance company on the significant drawbacks to this “volunteer opportunity.” Let’s hope a more reasonable program is put forward with AI-generated data that can be trusted. Hopefully not with a platform named “HAL,” for those of you old enough to remember “2001: A Space Odyssey.”

Dr. Feldman is a rheumatologist in private practice with The Rheumatology Group in New Orleans. She is the CSRO’s vice president of advocacy and government affairs and its immediate past president, as well as past chair of the Alliance for Safe Biologic Medicines and a past member of the American College of Rheumatology insurance subcommittee. You can reach her at [email protected].

Editor’s note: As of this writing, the following proposed health insurance policy from Blue Cross and Blue Shield of North Carolina is still active. The Coalition of State Rheumatology Organizations and other rheumatology advocacy groups are in ongoing discussions with the health insurer and hope to have major changes to this policy implemented.

While AI has been in our world for years, it is expanding by the minute, perhaps by the nanosecond, within the health care sector. The $6.7 billion dollar health care AI market in 2020 is expected to climb to more than $120 billion by 2028. There are many questions regarding the application of AI in our world. Is it a mere instructional algorithm that computes things in a much faster way, or does it create a new story based on the information it has access to? Does it engender excitement or fear ... or both? Remember HAL? As we have seen throughout history with new inventions and technologies, there are risks and rewards. Even the best can have harmful unintended consequences. AI is no different, particularly when it comes to health care. In this case, AI can get a bad name if it is utilized along with biased data input and bad policy.

Shared savings

Here is where “shared savings” comes into play. A shared savings program starts with a baseline cost analysis of a particular care plan and then tracks costs (performance) going forward after certain changes to the original care plan are instituted. If savings are accrued when compared with baseline spending, those savings are shared with the providers of the care. Depending on how the shared savings program is implemented, the optics can be very bad if it appears as though physicians are being paid to reduce care.

‘The volunteer opportunity’

Recently, Blue Cross and Blue Shield of North Carolina, in partnership with Outcomes Matter Innovations, a data analysis company that uses AI/machine-learning technology, offered rheumatologists a new voluntary shared savings, value-based care (VBC) “opportunity.” Rheumatologists would be able to “utilize a web-based machine-learning technology platform that suggests evidence-based care pathways” in the treatment of rheumatoid arthritis and psoriatic arthritis (PsA). The VBC/shared savings model uses the AI platform to propose two different pathways. One model would delay the start of biologics or Janus kinase inhibitors (JAKi), and the second model would taper and/or stop biologics or JAKi altogether.

Delaying the start of biologics/JAKi would be achieved through “methotrexate optimization” and/or the use of triple therapy with methotrexate, sulfasalazine, and hydroxychloroquine. The other model would recommend tapering biologic/JAKi dosing in patients in remission or low disease activity and might even suggest a “medication holiday.”

The intention of this 3-year VBC/shared savings program is to reduce costs and create savings by reducing the use of biologics or JAKi. A tangential question might be, “Reduce costs and create savings for whom?” Apparently, the patients will not reap any of the cost savings, as this is proposed to be a shared savings program with the savings going to the physicians and the insurance company. Perhaps the idea is that patients will benefit by reducing unneeded expensive medications.
 

How will it work?

A cost baseline will be established on biologic and JAKi use prior to the start of the program. Once started, there will be a calculation of savings based on biologic/JAKi use going forward. It was stated that physicians would receive 22% of the total costs saved. In one flyer, it was estimated that, with methotrexate optimization, rheumatologists could be paid an average of $1,527 a month per patient per month of delay before starting a biologic or JAKi.

The American College of Rheumatology has guidelines for the treatment of RA and PsA, and while optimizing methotrexate and triple therapy is mentioned, tapering or stopping treatment with biologics or JAKi is not. Additionally, after lack of response at 3 months, the standard of care is to change to a more effective treatment, which for most patients is a biologic disease-modifying antirheumatic drug (DMARD). It could be construed that rheumatologists are being monetarily incentivized to reduce the use of expensive medications through ways that are not included in ACR guidelines and are not standard of care.

What if after the medication holiday the patient cannot recapture control of their disease? Is there a liability concern? Remember, there is no institutional review board or informed patient consent for this VBC data gathering model.

How will a patient feel knowing that their physician was paid to withhold care, or even worse, if a patient is not told of this and then finds out later? Not only are the optics for this suboptimal (at best), where does the liability fall if the patient does not do well and it comes out that their rheumatologist was paid to reduce the care, particularly in a way that is not supported in the guideline. Clearly, this appears to be a clinical study without an institutional review board and without patient consent.

There are also the data that are collected from this voluntary “opportunity.” A valid question would be, “What kind of data will this produce if rheumatologists are paid to delay, reduce, or stop the use of biologics/JAKi?” Is it possible that physicians may subconsciously delay putting patients on a biologic and taper more rapidly because of the reimbursement? This could lead to faulty, biased, AI-generated data that erroneously show this type of care is working. It would not be unheard of to wonder whether this once-voluntary opportunity might evolve into mandatory policy because now, they have “data to prove it.” … only this time there is no shared savings.
 

Low disease activity results in long-term savings

This is not meant to be an indictment of AI in health care, value-based care, or shared savings programs. In reality, AI had very little to do with how poorly this program was presented. Hopefully, it will bring about further discussions on how to achieve savings without sacrificing care. In fact, optimal care in RA and PsA is probably one of the best ways to save money in the long run. Nowhere in this program is there any mention of the high cost associated with uncontrolled disease activity in patients with RA or PsA. The downstream costs can be enormous when long- and short-term sequelae are taken into consideration: joint replacements, cardiovascular disease, certain kinds of malignancies, and all the side effects of increased steroid usage are just a few of the consequences we see with uncontrolled disease activity. It is only recently that we have been able to achieve low disease activity and remission in our patients. The rush to get patients off these medications is not the answer to achieving long-term savings. In addition to the very bad optics of paying rheumatologists to delay, taper, or stop using expensive mediations in their patients, the ultimate data achieved will be biased, and the only real winner will be the health insurance company.

Again, AI machine-learning and shared saving programs are not the guilty parties here. In fact, AI may be helpful in coming up with solutions to long-term health care costs, whether in the realm of economics or scientific research. CSRO and our state member organizations continue to educate the health insurance company on the significant drawbacks to this “volunteer opportunity.” Let’s hope a more reasonable program is put forward with AI-generated data that can be trusted. Hopefully not with a platform named “HAL,” for those of you old enough to remember “2001: A Space Odyssey.”

Dr. Feldman is a rheumatologist in private practice with The Rheumatology Group in New Orleans. She is the CSRO’s vice president of advocacy and government affairs and its immediate past president, as well as past chair of the Alliance for Safe Biologic Medicines and a past member of the American College of Rheumatology insurance subcommittee. You can reach her at [email protected].

Editor’s note: As of this writing, the following proposed health insurance policy from Blue Cross and Blue Shield of North Carolina is still active. The Coalition of State Rheumatology Organizations and other rheumatology advocacy groups are in ongoing discussions with the health insurer and hope to have major changes to this policy implemented.

While AI has been in our world for years, it is expanding by the minute, perhaps by the nanosecond, within the health care sector. The $6.7 billion dollar health care AI market in 2020 is expected to climb to more than $120 billion by 2028. There are many questions regarding the application of AI in our world. Is it a mere instructional algorithm that computes things in a much faster way, or does it create a new story based on the information it has access to? Does it engender excitement or fear ... or both? Remember HAL? As we have seen throughout history with new inventions and technologies, there are risks and rewards. Even the best can have harmful unintended consequences. AI is no different, particularly when it comes to health care. In this case, AI can get a bad name if it is utilized along with biased data input and bad policy.

Shared savings

Here is where “shared savings” comes into play. A shared savings program starts with a baseline cost analysis of a particular care plan and then tracks costs (performance) going forward after certain changes to the original care plan are instituted. If savings are accrued when compared with baseline spending, those savings are shared with the providers of the care. Depending on how the shared savings program is implemented, the optics can be very bad if it appears as though physicians are being paid to reduce care.

‘The volunteer opportunity’

Recently, Blue Cross and Blue Shield of North Carolina, in partnership with Outcomes Matter Innovations, a data analysis company that uses AI/machine-learning technology, offered rheumatologists a new voluntary shared savings, value-based care (VBC) “opportunity.” Rheumatologists would be able to “utilize a web-based machine-learning technology platform that suggests evidence-based care pathways” in the treatment of rheumatoid arthritis and psoriatic arthritis (PsA). The VBC/shared savings model uses the AI platform to propose two different pathways. One model would delay the start of biologics or Janus kinase inhibitors (JAKi), and the second model would taper and/or stop biologics or JAKi altogether.

Delaying the start of biologics/JAKi would be achieved through “methotrexate optimization” and/or the use of triple therapy with methotrexate, sulfasalazine, and hydroxychloroquine. The other model would recommend tapering biologic/JAKi dosing in patients in remission or low disease activity and might even suggest a “medication holiday.”

The intention of this 3-year VBC/shared savings program is to reduce costs and create savings by reducing the use of biologics or JAKi. A tangential question might be, “Reduce costs and create savings for whom?” Apparently, the patients will not reap any of the cost savings, as this is proposed to be a shared savings program with the savings going to the physicians and the insurance company. Perhaps the idea is that patients will benefit by reducing unneeded expensive medications.
 

How will it work?

A cost baseline will be established on biologic and JAKi use prior to the start of the program. Once started, there will be a calculation of savings based on biologic/JAKi use going forward. It was stated that physicians would receive 22% of the total costs saved. In one flyer, it was estimated that, with methotrexate optimization, rheumatologists could be paid an average of $1,527 a month per patient per month of delay before starting a biologic or JAKi.

The American College of Rheumatology has guidelines for the treatment of RA and PsA, and while optimizing methotrexate and triple therapy is mentioned, tapering or stopping treatment with biologics or JAKi is not. Additionally, after lack of response at 3 months, the standard of care is to change to a more effective treatment, which for most patients is a biologic disease-modifying antirheumatic drug (DMARD). It could be construed that rheumatologists are being monetarily incentivized to reduce the use of expensive medications through ways that are not included in ACR guidelines and are not standard of care.

What if after the medication holiday the patient cannot recapture control of their disease? Is there a liability concern? Remember, there is no institutional review board or informed patient consent for this VBC data gathering model.

How will a patient feel knowing that their physician was paid to withhold care, or even worse, if a patient is not told of this and then finds out later? Not only are the optics for this suboptimal (at best), where does the liability fall if the patient does not do well and it comes out that their rheumatologist was paid to reduce the care, particularly in a way that is not supported in the guideline. Clearly, this appears to be a clinical study without an institutional review board and without patient consent.

There are also the data that are collected from this voluntary “opportunity.” A valid question would be, “What kind of data will this produce if rheumatologists are paid to delay, reduce, or stop the use of biologics/JAKi?” Is it possible that physicians may subconsciously delay putting patients on a biologic and taper more rapidly because of the reimbursement? This could lead to faulty, biased, AI-generated data that erroneously show this type of care is working. It would not be unheard of to wonder whether this once-voluntary opportunity might evolve into mandatory policy because now, they have “data to prove it.” … only this time there is no shared savings.
 

Low disease activity results in long-term savings

This is not meant to be an indictment of AI in health care, value-based care, or shared savings programs. In reality, AI had very little to do with how poorly this program was presented. Hopefully, it will bring about further discussions on how to achieve savings without sacrificing care. In fact, optimal care in RA and PsA is probably one of the best ways to save money in the long run. Nowhere in this program is there any mention of the high cost associated with uncontrolled disease activity in patients with RA or PsA. The downstream costs can be enormous when long- and short-term sequelae are taken into consideration: joint replacements, cardiovascular disease, certain kinds of malignancies, and all the side effects of increased steroid usage are just a few of the consequences we see with uncontrolled disease activity. It is only recently that we have been able to achieve low disease activity and remission in our patients. The rush to get patients off these medications is not the answer to achieving long-term savings. In addition to the very bad optics of paying rheumatologists to delay, taper, or stop using expensive mediations in their patients, the ultimate data achieved will be biased, and the only real winner will be the health insurance company.

Again, AI machine-learning and shared saving programs are not the guilty parties here. In fact, AI may be helpful in coming up with solutions to long-term health care costs, whether in the realm of economics or scientific research. CSRO and our state member organizations continue to educate the health insurance company on the significant drawbacks to this “volunteer opportunity.” Let’s hope a more reasonable program is put forward with AI-generated data that can be trusted. Hopefully not with a platform named “HAL,” for those of you old enough to remember “2001: A Space Odyssey.”

Dr. Feldman is a rheumatologist in private practice with The Rheumatology Group in New Orleans. She is the CSRO’s vice president of advocacy and government affairs and its immediate past president, as well as past chair of the Alliance for Safe Biologic Medicines and a past member of the American College of Rheumatology insurance subcommittee. You can reach her at [email protected].

This transcript has been edited for clarity.

Let’s assume, for the sake of argument, that I am a healthy 43-year old man. Nevertheless, I am interested in getting my vitamin D level checked. My primary care doc says it’s unnecessary, but that doesn’t matter because a variety of direct-to-consumer testing companies will do it without a doctor’s prescription – for a fee of course.

Is that okay? Should I be able to get the test?

What if instead of my vitamin D level, I want to test my testosterone level, or my PSA, or my cadmium level, or my Lyme disease antibodies, or even have a full-body MRI scan? All of these tests are available from a variety of direct-to-consumer testing companies. If I am willing to pay, should I be able to get those too?

These questions are becoming more and more common, because the direct-to-consumer testing market is exploding.

We’re talking about direct-to-consumer testing, thanks to this paper: Policies of US Companies Offering Direct-to-Consumer Laboratory Tests, appearing in JAMA Internal Medicine, which characterizes the testing practices of direct-to-consumer testing companies.

But before we get to the study, a word on this market. Direct-to-consumer lab testing is projected to be a $2 billion industry by 2025, and lab testing megacorporations Quest Diagnostics and Labcorp are both jumping headlong into this space.

Why is this happening? A couple of reasons, I think. First, the increasing cost of health care has led payers to place significant restrictions on what tests can be ordered and under what circumstances. Physicians are all too familiar with the “prior authorization” system that seeks to limit even the tests we think would benefit our patients.

Frustrated with such a system, it’s no wonder that patients are increasingly deciding to go it on their own. Sure, insurance won’t cover these tests, but the prices are transparent and competition actually keeps them somewhat reasonable. So, is this a win-win? Shouldn’t we allow people to get the tests they want, at least if they are willing to pay for it?

Of course, it’s not quite that simple. If the tests are normal, or negative, then sure – no harm, no foul. But when they are positive, everything changes. What happens when the PSA test I got myself via a direct-to-consumer testing company comes back elevated? Well, at that point, I am right back into the traditional mode of medicine – seeing my doctor, probably getting repeat testing, biopsies, etc., – and some payer will be on the hook for that, which is to say that all of us will be on the hook for that.

One other reason direct-to-consumer testing is getting more popular is a more difficult-to-characterize phenomenon which I might call postpandemic individualism. I’ve seen this across several domains, but I think in some ways the pandemic led people to focus more attention on themselves, perhaps because we were so isolated from each other. Optimizing health through data – whether using a fitness tracking watch, meticulously counting macronutrient intake, or ordering your own lab tests – may be a form of exerting control over a universe that feels increasingly chaotic. But what do I know? I’m not a psychologist.

The study characterizes a total of 21 direct-to-consumer testing companies. They offer a variety of services, as you can see here, with the majority in the endocrine space: thyroid, diabetes, men’s and women’s health. A smattering of companies offer more esoteric testing, such as heavy metals and Lyme disease.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

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

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

This transcript has been edited for clarity.

Let’s assume, for the sake of argument, that I am a healthy 43-year old man. Nevertheless, I am interested in getting my vitamin D level checked. My primary care doc says it’s unnecessary, but that doesn’t matter because a variety of direct-to-consumer testing companies will do it without a doctor’s prescription – for a fee of course.

Is that okay? Should I be able to get the test?

What if instead of my vitamin D level, I want to test my testosterone level, or my PSA, or my cadmium level, or my Lyme disease antibodies, or even have a full-body MRI scan? All of these tests are available from a variety of direct-to-consumer testing companies. If I am willing to pay, should I be able to get those too?

These questions are becoming more and more common, because the direct-to-consumer testing market is exploding.

We’re talking about direct-to-consumer testing, thanks to this paper: Policies of US Companies Offering Direct-to-Consumer Laboratory Tests, appearing in JAMA Internal Medicine, which characterizes the testing practices of direct-to-consumer testing companies.

But before we get to the study, a word on this market. Direct-to-consumer lab testing is projected to be a $2 billion industry by 2025, and lab testing megacorporations Quest Diagnostics and Labcorp are both jumping headlong into this space.

Why is this happening? A couple of reasons, I think. First, the increasing cost of health care has led payers to place significant restrictions on what tests can be ordered and under what circumstances. Physicians are all too familiar with the “prior authorization” system that seeks to limit even the tests we think would benefit our patients.

Frustrated with such a system, it’s no wonder that patients are increasingly deciding to go it on their own. Sure, insurance won’t cover these tests, but the prices are transparent and competition actually keeps them somewhat reasonable. So, is this a win-win? Shouldn’t we allow people to get the tests they want, at least if they are willing to pay for it?

Of course, it’s not quite that simple. If the tests are normal, or negative, then sure – no harm, no foul. But when they are positive, everything changes. What happens when the PSA test I got myself via a direct-to-consumer testing company comes back elevated? Well, at that point, I am right back into the traditional mode of medicine – seeing my doctor, probably getting repeat testing, biopsies, etc., – and some payer will be on the hook for that, which is to say that all of us will be on the hook for that.

One other reason direct-to-consumer testing is getting more popular is a more difficult-to-characterize phenomenon which I might call postpandemic individualism. I’ve seen this across several domains, but I think in some ways the pandemic led people to focus more attention on themselves, perhaps because we were so isolated from each other. Optimizing health through data – whether using a fitness tracking watch, meticulously counting macronutrient intake, or ordering your own lab tests – may be a form of exerting control over a universe that feels increasingly chaotic. But what do I know? I’m not a psychologist.

The study characterizes a total of 21 direct-to-consumer testing companies. They offer a variety of services, as you can see here, with the majority in the endocrine space: thyroid, diabetes, men’s and women’s health. A smattering of companies offer more esoteric testing, such as heavy metals and Lyme disease.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

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

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

This transcript has been edited for clarity.

Let’s assume, for the sake of argument, that I am a healthy 43-year old man. Nevertheless, I am interested in getting my vitamin D level checked. My primary care doc says it’s unnecessary, but that doesn’t matter because a variety of direct-to-consumer testing companies will do it without a doctor’s prescription – for a fee of course.

Is that okay? Should I be able to get the test?

What if instead of my vitamin D level, I want to test my testosterone level, or my PSA, or my cadmium level, or my Lyme disease antibodies, or even have a full-body MRI scan? All of these tests are available from a variety of direct-to-consumer testing companies. If I am willing to pay, should I be able to get those too?

These questions are becoming more and more common, because the direct-to-consumer testing market is exploding.

We’re talking about direct-to-consumer testing, thanks to this paper: Policies of US Companies Offering Direct-to-Consumer Laboratory Tests, appearing in JAMA Internal Medicine, which characterizes the testing practices of direct-to-consumer testing companies.

But before we get to the study, a word on this market. Direct-to-consumer lab testing is projected to be a $2 billion industry by 2025, and lab testing megacorporations Quest Diagnostics and Labcorp are both jumping headlong into this space.

Why is this happening? A couple of reasons, I think. First, the increasing cost of health care has led payers to place significant restrictions on what tests can be ordered and under what circumstances. Physicians are all too familiar with the “prior authorization” system that seeks to limit even the tests we think would benefit our patients.

Frustrated with such a system, it’s no wonder that patients are increasingly deciding to go it on their own. Sure, insurance won’t cover these tests, but the prices are transparent and competition actually keeps them somewhat reasonable. So, is this a win-win? Shouldn’t we allow people to get the tests they want, at least if they are willing to pay for it?

Of course, it’s not quite that simple. If the tests are normal, or negative, then sure – no harm, no foul. But when they are positive, everything changes. What happens when the PSA test I got myself via a direct-to-consumer testing company comes back elevated? Well, at that point, I am right back into the traditional mode of medicine – seeing my doctor, probably getting repeat testing, biopsies, etc., – and some payer will be on the hook for that, which is to say that all of us will be on the hook for that.

One other reason direct-to-consumer testing is getting more popular is a more difficult-to-characterize phenomenon which I might call postpandemic individualism. I’ve seen this across several domains, but I think in some ways the pandemic led people to focus more attention on themselves, perhaps because we were so isolated from each other. Optimizing health through data – whether using a fitness tracking watch, meticulously counting macronutrient intake, or ordering your own lab tests – may be a form of exerting control over a universe that feels increasingly chaotic. But what do I know? I’m not a psychologist.

The study characterizes a total of 21 direct-to-consumer testing companies. They offer a variety of services, as you can see here, with the majority in the endocrine space: thyroid, diabetes, men’s and women’s health. A smattering of companies offer more esoteric testing, such as heavy metals and Lyme disease.

Dr. F. Perry Wilson

Dr. F. Perry Wilson

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

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