California Gov. Gavin Newsom says the state government will manufacture its own low-cost insulin to make the drug more affordable for residents.

On July 7, he said he had just signed a state budget that includes $50 million for development of the insulin and another $50 million for a place to make it.

“Nothing, nothing epitomizes market failures more than the cost of insulin,” Gov. Newsom said in a video posted on the governor’s Twitter page. He noted that many Americans have out-of-pocket costs ranging from $300 to $500 per month for insulin, which is used to treat diabetes.

“In California, we know people should not go into debt to receive lifesaving medication,” he said.

Gov. Newsom said that when he first took office, he signed an executive order to launch California’s own prescription drug system and that the insulin initiative is the first step toward making that happen.

People who take insulin have long complained about its high price. A November 2021 report from The Lancet said 25% of the insulin patients in the United States struggle to pay for it.

The cost of insulin for patients with insurance ranges from $334 to $1,000 a month, ABC News said, citing the Kaiser Family Foundation.

Legislation in Congress would bring down the cost of insulin if passed, with one bill capping costs at $35 per month for patients with health insurance. But The Hill reported that some Republicans oppose the legislation because it would interfere with free markets and raise costs for drug companies.

The CDC says 37.3 million people in the United States – about 11.3% of the population – have diabetes, with 8.5 million of them undiagnosed.

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

California Gov. Gavin Newsom says the state government will manufacture its own low-cost insulin to make the drug more affordable for residents.

On July 7, he said he had just signed a state budget that includes $50 million for development of the insulin and another $50 million for a place to make it.

“Nothing, nothing epitomizes market failures more than the cost of insulin,” Gov. Newsom said in a video posted on the governor’s Twitter page. He noted that many Americans have out-of-pocket costs ranging from $300 to $500 per month for insulin, which is used to treat diabetes.

“In California, we know people should not go into debt to receive lifesaving medication,” he said.

Gov. Newsom said that when he first took office, he signed an executive order to launch California’s own prescription drug system and that the insulin initiative is the first step toward making that happen.

People who take insulin have long complained about its high price. A November 2021 report from The Lancet said 25% of the insulin patients in the United States struggle to pay for it.

The cost of insulin for patients with insurance ranges from $334 to $1,000 a month, ABC News said, citing the Kaiser Family Foundation.

Legislation in Congress would bring down the cost of insulin if passed, with one bill capping costs at $35 per month for patients with health insurance. But The Hill reported that some Republicans oppose the legislation because it would interfere with free markets and raise costs for drug companies.

The CDC says 37.3 million people in the United States – about 11.3% of the population – have diabetes, with 8.5 million of them undiagnosed.

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

California Gov. Gavin Newsom says the state government will manufacture its own low-cost insulin to make the drug more affordable for residents.

On July 7, he said he had just signed a state budget that includes $50 million for development of the insulin and another $50 million for a place to make it.

“Nothing, nothing epitomizes market failures more than the cost of insulin,” Gov. Newsom said in a video posted on the governor’s Twitter page. He noted that many Americans have out-of-pocket costs ranging from $300 to $500 per month for insulin, which is used to treat diabetes.

“In California, we know people should not go into debt to receive lifesaving medication,” he said.

Gov. Newsom said that when he first took office, he signed an executive order to launch California’s own prescription drug system and that the insulin initiative is the first step toward making that happen.

People who take insulin have long complained about its high price. A November 2021 report from The Lancet said 25% of the insulin patients in the United States struggle to pay for it.

The cost of insulin for patients with insurance ranges from $334 to $1,000 a month, ABC News said, citing the Kaiser Family Foundation.

Legislation in Congress would bring down the cost of insulin if passed, with one bill capping costs at $35 per month for patients with health insurance. But The Hill reported that some Republicans oppose the legislation because it would interfere with free markets and raise costs for drug companies.

The CDC says 37.3 million people in the United States – about 11.3% of the population – have diabetes, with 8.5 million of them undiagnosed.

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

Stephen Pribut, DPM, a sports medicine podiatrist based in Washington, has had many friends or family members ask him for medical advice. It’s a scenario every doctor will face at one point or another in their careers, and it’s never an easy one.

Dr. Pribut received a call from a friend about a sore shoulder from swimming, saying that his doctor had dismissed the potential for a rotator cuff injury. “Months later, images revealed it was a rotator cuff tear and he wanted my advice,” says Dr. Pribut.

Not being a shoulder specialist, Dr. Pribut limited his input. “I told him to consider a good physical therapist or a shoulder specialist and gave him some alternative strokes for swimming that hopefully wouldn’t aggravate the injury,” he explains.

But he admits some situations are challenging. “I had a relative asking about a third party with an ankle injury. I advised he hold off on using a balance board until things healed, and to make sure he went to see a specialist. Unfortunately, he went to his general practitioner who likely knows nothing about ankle anatomy,” says Dr. Pribut.

“I finally saw a photo, which revealed swelling higher up on the ankle and no evidence of a hematoma – much lower than we would see in an ankle ligament injury. I would like him to see a sports podiatrist or foot and ankle orthopedist, but now I have to stay calm when the advice isn’t followed,” he says.

Most doctors deal with the “curbside consult,” many times over, and most, according to a recent Medscape survey, will dole it out. When asked, “Do you give medical advice to your friends?” 96% of respondents answered yes.

Yazan Abou-Ismail, MD, assistant professor of medicine in the division of hematology at the University of Utah, Salt Lake City, has often faced questions from friends and family, particularly throughout the COVID-19 pandemic. “How you respond is something all physicians need to analyze carefully,” he says. “I get questions on a regular basis, but this greatly increased with COVID.”

“Sharing general information is okay, and it’s even a requirement that we educate on such topics,” says Dr. Abou-Ismail. “But if someone knows they have COVID, for instance, and wants advice on how to proceed, it’s important to send them to their primary care physician for an evaluation rather than give them instructions on care.”

Dr. Abou-Ismail says that most “curbside consulting” equates to lack of an ethical follow-up. “If you gave medical advice without having assessed them, you’re lacking the medical history, a physical exam, and you should not be giving advice,” he says. “This applies to follow-ups, too.”

Throughout the pandemic, Dr. Abou-Ismail’s requests for advice on COVID even extended to online inquiries, often from strangers. “This is not a place to do a formal assessment,” he reminds. “But there are certain types of advice you can offer appropriately.”

Dr. Abou-Ismail considers safe advice to be simple public health messages that stay far out of specifics. Things like “don’t smoke,” or “eat a healthy diet,” and “get enough sleep,” fall into this safety zone. Even, “What is XYZ disease?” or “How do COVID vaccines work?” are topics he says he answers comfortably.

“But telling someone you need a specific treatment for a condition is inappropriate,” he explains. “This is a general way of practicing medicine – your advice should never venture into the potential of doing harm.”

This approach is exactly in line with legal advice, according to Jeff Caesar Chukwuma, founder and senior partner at Chukwuma Law Group, Miami. “It doesn’t mean that doctors should never give medical advice to friends or family, but if they do, they should make sure to take several precautions to protect both themselves and their family and friends,” he says.

When the request for medical advice from an acquaintance migrates into areas in which a physician is not a specialist, sharing recommendations gets even trickier – and more ethically questionable.  

Says Mr. Chukwuma, “Doctors should avoid giving advice in areas outside their area of expertise to lower the possibility of providing erroneous or harmful information,” he says.

How to stay safe when asked for advice

The American Medical Association has weighed in on the topic. In the Code of Medical Ethics Opinion 1.2.1, the AMA states that, “Treating oneself or a member of one’s own family poses several challenges for physicians, including concerns about professional objectivity, patient autonomy, and informed consent.”

What about friends or acquaintances, however?

Even so, some respondents voiced their concerns with the scenario. Responses like, “Due to ethics, I would prefer they go and get first, second, and third opinions,” and “Usually the medical advice is very basic first aid (often mental health first aid), and if it’s anything remotely more complicated, I direct them to the appropriate provider.”

The AMA places advising friends in the same basket as advising and treating family members or oneself. In an article appearing in the AMA Journal of Ethics, Horacio Hojman, MD, of Tufts University School of Medicine, Boston, weighed in: “First and foremost, patients deserve objectivity from their doctors. When a physician is emotionally involved with a patient, that physician’s objectivity can be called into question.”

Why is medical advice so thorny when dealing with friends or relatives?

In some cases, a physician might not ask a friend relevant personal questions about his or her medical history, for instance. Or the friend might not want to share details with the doctor. In either case, the lack of information exchange can lead to improper advice.

The issue of giving medical advice to friends, family, and acquaintances can also wade into legal territory. “Personally or professionally, trust is the decisive factor that puts us at ease with the people we surround ourselves with,” says Mr. Chukwuma. “Nowhere is this truer than in medicine, where we approach doctors with some of the most sensitive matters in our lives and entrust our care to them, especially when the physician in question is a close friend or family member.”

Mr. Chukwuma points out that, while there are few strict legal prohibitions against doctors providing care or advice to family and friends, the AMA’s code of ethics states that such action should be reserved for rare situations, such as emergency settings or isolated settings where there is no other qualified physician available, or for minor, not long-term problems.

This was part of the equation for Dr. Pribut when helping his mother navigate her treatment for breast cancer. “With close relatives, offering advice and help can be very hard,” he says.

“This is to protect both patients and doctors,” says Mr. Chukwuma. “Although seeking advice from a family member or friend who is a doctor may be more convenient for a patient, they run the risk of receiving inadequate care by not going in for a formal medical visit complete with tests, medical examination, and follow-up care.”

Mr. Chukwuma offers guidance on how to share medical advice ethically and legally with family, friends, and acquaintances. “First, as much as possible, speak to general medical facts and knowledge rather than comment directly on the patient’s particular situation,” he says. “In the absence of thorough examination and tests, the doctor’s knowledge of a patient’s condition is limited, therefore, you should take care not to provide seemingly definitive answers on that patient’s unique condition in situations where they can’t rely on data to back up their advice and recommendations.”

The AMA’s Journal of Ethics article shares these tips for staying on the right side of the ethical line when dealing with friends and family members:

• Politely decline.
• Offer other forms of assistance – this might help a friend find the right qualified physician – as Dr. Pribut tends to do. Maybe help in navigating the sometimes-confusing health care system.
• Don’t hesitate in an emergency – the old “is there a doctor on board,” scenario on a plane when someone is in distress is a perfectly acceptable, and recommended, time to step in, even if it is a friend or family member.

Dr. Pribut, a long-time veteran of the tricky medical waters involving friends and family, has this to offer: “Be cautious and always stay in the realm of what you know,” he says. “Always encourage people to seek an opinion from a qualified doctor. Help them find a reputable doctor if that’s useful.”

Mr. Chukwuma adds also that doctors should stand firm when pushed by a friend or family member, especially when offering advice, even if it’s in the form of general education. “The doctor should make it clear to the family member or friend that their advice in no way takes the place of actual treatment or examination by a medical professional and that, if need be, the patient should seek formal medical help from another doctor, ideally one not related to or friends with the patient,” he says.

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

Stephen Pribut, DPM, a sports medicine podiatrist based in Washington, has had many friends or family members ask him for medical advice. It’s a scenario every doctor will face at one point or another in their careers, and it’s never an easy one.

Dr. Pribut received a call from a friend about a sore shoulder from swimming, saying that his doctor had dismissed the potential for a rotator cuff injury. “Months later, images revealed it was a rotator cuff tear and he wanted my advice,” says Dr. Pribut.

Not being a shoulder specialist, Dr. Pribut limited his input. “I told him to consider a good physical therapist or a shoulder specialist and gave him some alternative strokes for swimming that hopefully wouldn’t aggravate the injury,” he explains.

But he admits some situations are challenging. “I had a relative asking about a third party with an ankle injury. I advised he hold off on using a balance board until things healed, and to make sure he went to see a specialist. Unfortunately, he went to his general practitioner who likely knows nothing about ankle anatomy,” says Dr. Pribut.

“I finally saw a photo, which revealed swelling higher up on the ankle and no evidence of a hematoma – much lower than we would see in an ankle ligament injury. I would like him to see a sports podiatrist or foot and ankle orthopedist, but now I have to stay calm when the advice isn’t followed,” he says.

Most doctors deal with the “curbside consult,” many times over, and most, according to a recent Medscape survey, will dole it out. When asked, “Do you give medical advice to your friends?” 96% of respondents answered yes.

Yazan Abou-Ismail, MD, assistant professor of medicine in the division of hematology at the University of Utah, Salt Lake City, has often faced questions from friends and family, particularly throughout the COVID-19 pandemic. “How you respond is something all physicians need to analyze carefully,” he says. “I get questions on a regular basis, but this greatly increased with COVID.”

“Sharing general information is okay, and it’s even a requirement that we educate on such topics,” says Dr. Abou-Ismail. “But if someone knows they have COVID, for instance, and wants advice on how to proceed, it’s important to send them to their primary care physician for an evaluation rather than give them instructions on care.”

Dr. Abou-Ismail says that most “curbside consulting” equates to lack of an ethical follow-up. “If you gave medical advice without having assessed them, you’re lacking the medical history, a physical exam, and you should not be giving advice,” he says. “This applies to follow-ups, too.”

Throughout the pandemic, Dr. Abou-Ismail’s requests for advice on COVID even extended to online inquiries, often from strangers. “This is not a place to do a formal assessment,” he reminds. “But there are certain types of advice you can offer appropriately.”

Dr. Abou-Ismail considers safe advice to be simple public health messages that stay far out of specifics. Things like “don’t smoke,” or “eat a healthy diet,” and “get enough sleep,” fall into this safety zone. Even, “What is XYZ disease?” or “How do COVID vaccines work?” are topics he says he answers comfortably.

“But telling someone you need a specific treatment for a condition is inappropriate,” he explains. “This is a general way of practicing medicine – your advice should never venture into the potential of doing harm.”

This approach is exactly in line with legal advice, according to Jeff Caesar Chukwuma, founder and senior partner at Chukwuma Law Group, Miami. “It doesn’t mean that doctors should never give medical advice to friends or family, but if they do, they should make sure to take several precautions to protect both themselves and their family and friends,” he says.

When the request for medical advice from an acquaintance migrates into areas in which a physician is not a specialist, sharing recommendations gets even trickier – and more ethically questionable.  

Says Mr. Chukwuma, “Doctors should avoid giving advice in areas outside their area of expertise to lower the possibility of providing erroneous or harmful information,” he says.

How to stay safe when asked for advice

The American Medical Association has weighed in on the topic. In the Code of Medical Ethics Opinion 1.2.1, the AMA states that, “Treating oneself or a member of one’s own family poses several challenges for physicians, including concerns about professional objectivity, patient autonomy, and informed consent.”

What about friends or acquaintances, however?

Even so, some respondents voiced their concerns with the scenario. Responses like, “Due to ethics, I would prefer they go and get first, second, and third opinions,” and “Usually the medical advice is very basic first aid (often mental health first aid), and if it’s anything remotely more complicated, I direct them to the appropriate provider.”

The AMA places advising friends in the same basket as advising and treating family members or oneself. In an article appearing in the AMA Journal of Ethics, Horacio Hojman, MD, of Tufts University School of Medicine, Boston, weighed in: “First and foremost, patients deserve objectivity from their doctors. When a physician is emotionally involved with a patient, that physician’s objectivity can be called into question.”

Why is medical advice so thorny when dealing with friends or relatives?

In some cases, a physician might not ask a friend relevant personal questions about his or her medical history, for instance. Or the friend might not want to share details with the doctor. In either case, the lack of information exchange can lead to improper advice.

The issue of giving medical advice to friends, family, and acquaintances can also wade into legal territory. “Personally or professionally, trust is the decisive factor that puts us at ease with the people we surround ourselves with,” says Mr. Chukwuma. “Nowhere is this truer than in medicine, where we approach doctors with some of the most sensitive matters in our lives and entrust our care to them, especially when the physician in question is a close friend or family member.”

Mr. Chukwuma points out that, while there are few strict legal prohibitions against doctors providing care or advice to family and friends, the AMA’s code of ethics states that such action should be reserved for rare situations, such as emergency settings or isolated settings where there is no other qualified physician available, or for minor, not long-term problems.

This was part of the equation for Dr. Pribut when helping his mother navigate her treatment for breast cancer. “With close relatives, offering advice and help can be very hard,” he says.

“This is to protect both patients and doctors,” says Mr. Chukwuma. “Although seeking advice from a family member or friend who is a doctor may be more convenient for a patient, they run the risk of receiving inadequate care by not going in for a formal medical visit complete with tests, medical examination, and follow-up care.”

Mr. Chukwuma offers guidance on how to share medical advice ethically and legally with family, friends, and acquaintances. “First, as much as possible, speak to general medical facts and knowledge rather than comment directly on the patient’s particular situation,” he says. “In the absence of thorough examination and tests, the doctor’s knowledge of a patient’s condition is limited, therefore, you should take care not to provide seemingly definitive answers on that patient’s unique condition in situations where they can’t rely on data to back up their advice and recommendations.”

The AMA’s Journal of Ethics article shares these tips for staying on the right side of the ethical line when dealing with friends and family members:

• Politely decline.
• Offer other forms of assistance – this might help a friend find the right qualified physician – as Dr. Pribut tends to do. Maybe help in navigating the sometimes-confusing health care system.
• Don’t hesitate in an emergency – the old “is there a doctor on board,” scenario on a plane when someone is in distress is a perfectly acceptable, and recommended, time to step in, even if it is a friend or family member.

Dr. Pribut, a long-time veteran of the tricky medical waters involving friends and family, has this to offer: “Be cautious and always stay in the realm of what you know,” he says. “Always encourage people to seek an opinion from a qualified doctor. Help them find a reputable doctor if that’s useful.”

Mr. Chukwuma adds also that doctors should stand firm when pushed by a friend or family member, especially when offering advice, even if it’s in the form of general education. “The doctor should make it clear to the family member or friend that their advice in no way takes the place of actual treatment or examination by a medical professional and that, if need be, the patient should seek formal medical help from another doctor, ideally one not related to or friends with the patient,” he says.

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

Stephen Pribut, DPM, a sports medicine podiatrist based in Washington, has had many friends or family members ask him for medical advice. It’s a scenario every doctor will face at one point or another in their careers, and it’s never an easy one.

Dr. Pribut received a call from a friend about a sore shoulder from swimming, saying that his doctor had dismissed the potential for a rotator cuff injury. “Months later, images revealed it was a rotator cuff tear and he wanted my advice,” says Dr. Pribut.

Not being a shoulder specialist, Dr. Pribut limited his input. “I told him to consider a good physical therapist or a shoulder specialist and gave him some alternative strokes for swimming that hopefully wouldn’t aggravate the injury,” he explains.

But he admits some situations are challenging. “I had a relative asking about a third party with an ankle injury. I advised he hold off on using a balance board until things healed, and to make sure he went to see a specialist. Unfortunately, he went to his general practitioner who likely knows nothing about ankle anatomy,” says Dr. Pribut.

“I finally saw a photo, which revealed swelling higher up on the ankle and no evidence of a hematoma – much lower than we would see in an ankle ligament injury. I would like him to see a sports podiatrist or foot and ankle orthopedist, but now I have to stay calm when the advice isn’t followed,” he says.

Most doctors deal with the “curbside consult,” many times over, and most, according to a recent Medscape survey, will dole it out. When asked, “Do you give medical advice to your friends?” 96% of respondents answered yes.

Yazan Abou-Ismail, MD, assistant professor of medicine in the division of hematology at the University of Utah, Salt Lake City, has often faced questions from friends and family, particularly throughout the COVID-19 pandemic. “How you respond is something all physicians need to analyze carefully,” he says. “I get questions on a regular basis, but this greatly increased with COVID.”

“Sharing general information is okay, and it’s even a requirement that we educate on such topics,” says Dr. Abou-Ismail. “But if someone knows they have COVID, for instance, and wants advice on how to proceed, it’s important to send them to their primary care physician for an evaluation rather than give them instructions on care.”

Dr. Abou-Ismail says that most “curbside consulting” equates to lack of an ethical follow-up. “If you gave medical advice without having assessed them, you’re lacking the medical history, a physical exam, and you should not be giving advice,” he says. “This applies to follow-ups, too.”

Throughout the pandemic, Dr. Abou-Ismail’s requests for advice on COVID even extended to online inquiries, often from strangers. “This is not a place to do a formal assessment,” he reminds. “But there are certain types of advice you can offer appropriately.”

Dr. Abou-Ismail considers safe advice to be simple public health messages that stay far out of specifics. Things like “don’t smoke,” or “eat a healthy diet,” and “get enough sleep,” fall into this safety zone. Even, “What is XYZ disease?” or “How do COVID vaccines work?” are topics he says he answers comfortably.

“But telling someone you need a specific treatment for a condition is inappropriate,” he explains. “This is a general way of practicing medicine – your advice should never venture into the potential of doing harm.”

This approach is exactly in line with legal advice, according to Jeff Caesar Chukwuma, founder and senior partner at Chukwuma Law Group, Miami. “It doesn’t mean that doctors should never give medical advice to friends or family, but if they do, they should make sure to take several precautions to protect both themselves and their family and friends,” he says.

When the request for medical advice from an acquaintance migrates into areas in which a physician is not a specialist, sharing recommendations gets even trickier – and more ethically questionable.  

Says Mr. Chukwuma, “Doctors should avoid giving advice in areas outside their area of expertise to lower the possibility of providing erroneous or harmful information,” he says.

How to stay safe when asked for advice

The American Medical Association has weighed in on the topic. In the Code of Medical Ethics Opinion 1.2.1, the AMA states that, “Treating oneself or a member of one’s own family poses several challenges for physicians, including concerns about professional objectivity, patient autonomy, and informed consent.”

What about friends or acquaintances, however?

Even so, some respondents voiced their concerns with the scenario. Responses like, “Due to ethics, I would prefer they go and get first, second, and third opinions,” and “Usually the medical advice is very basic first aid (often mental health first aid), and if it’s anything remotely more complicated, I direct them to the appropriate provider.”

The AMA places advising friends in the same basket as advising and treating family members or oneself. In an article appearing in the AMA Journal of Ethics, Horacio Hojman, MD, of Tufts University School of Medicine, Boston, weighed in: “First and foremost, patients deserve objectivity from their doctors. When a physician is emotionally involved with a patient, that physician’s objectivity can be called into question.”

Why is medical advice so thorny when dealing with friends or relatives?

In some cases, a physician might not ask a friend relevant personal questions about his or her medical history, for instance. Or the friend might not want to share details with the doctor. In either case, the lack of information exchange can lead to improper advice.

The issue of giving medical advice to friends, family, and acquaintances can also wade into legal territory. “Personally or professionally, trust is the decisive factor that puts us at ease with the people we surround ourselves with,” says Mr. Chukwuma. “Nowhere is this truer than in medicine, where we approach doctors with some of the most sensitive matters in our lives and entrust our care to them, especially when the physician in question is a close friend or family member.”

Mr. Chukwuma points out that, while there are few strict legal prohibitions against doctors providing care or advice to family and friends, the AMA’s code of ethics states that such action should be reserved for rare situations, such as emergency settings or isolated settings where there is no other qualified physician available, or for minor, not long-term problems.

This was part of the equation for Dr. Pribut when helping his mother navigate her treatment for breast cancer. “With close relatives, offering advice and help can be very hard,” he says.

“This is to protect both patients and doctors,” says Mr. Chukwuma. “Although seeking advice from a family member or friend who is a doctor may be more convenient for a patient, they run the risk of receiving inadequate care by not going in for a formal medical visit complete with tests, medical examination, and follow-up care.”

Mr. Chukwuma offers guidance on how to share medical advice ethically and legally with family, friends, and acquaintances. “First, as much as possible, speak to general medical facts and knowledge rather than comment directly on the patient’s particular situation,” he says. “In the absence of thorough examination and tests, the doctor’s knowledge of a patient’s condition is limited, therefore, you should take care not to provide seemingly definitive answers on that patient’s unique condition in situations where they can’t rely on data to back up their advice and recommendations.”

The AMA’s Journal of Ethics article shares these tips for staying on the right side of the ethical line when dealing with friends and family members:

• Politely decline.
• Offer other forms of assistance – this might help a friend find the right qualified physician – as Dr. Pribut tends to do. Maybe help in navigating the sometimes-confusing health care system.
• Don’t hesitate in an emergency – the old “is there a doctor on board,” scenario on a plane when someone is in distress is a perfectly acceptable, and recommended, time to step in, even if it is a friend or family member.

Dr. Pribut, a long-time veteran of the tricky medical waters involving friends and family, has this to offer: “Be cautious and always stay in the realm of what you know,” he says. “Always encourage people to seek an opinion from a qualified doctor. Help them find a reputable doctor if that’s useful.”

Mr. Chukwuma adds also that doctors should stand firm when pushed by a friend or family member, especially when offering advice, even if it’s in the form of general education. “The doctor should make it clear to the family member or friend that their advice in no way takes the place of actual treatment or examination by a medical professional and that, if need be, the patient should seek formal medical help from another doctor, ideally one not related to or friends with the patient,” he says.

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

Medicare will cover the full cost of colonoscopy after a positive noninvasive fecal test beginning in 2023, largely in response to a year-long advocacy campaign.

The benefit expansion is a “huge win” for patients, according to the American Gastroenterological Association, because it represents the end of out-of-pocket costs for colorectal cancer (CRC) screening.

“The continuum is complete!” said John Inadomi, MD, AGAF, past president of the AGA and a champion of the initiative within the organization.

Colonoscopy after a positive fecal test was previously considered a diagnostic procedure and therefore not considered part of the screening process by the Affordable Care Act, allowing payers to charge patients. That is, until the AGA and partners, including the American Cancer Society Cancer Action Network and Fight Colorectal Cancer, pushed back. First, the organizations successfully campaigned to ensure that private payers would cover the follow-up procedure. Now, after multiple meetings with the United States Department of Health & Human Services and Centers for Medicare & Medicaid Services, their collaborative efforts will end screening costs for patients with Medicare, pending finalization of the rule this fall. If finalized, it will take effect Jan. 2, 2023.

The policy change will “directly advance health equity” the AGA said, particularly among “rural communities and communities of color,” which are disproportionally affected by CRC.

“Cost-sharing is a well-recognized barrier to screening and has resulted in disparities,” said David Lieberman, MD, AGAF, who met with the CMS multiple times on behalf of the AGA. “Patients can now engage in CRC screening programs and be confident that they will not face unexpected cost-sharing for colonoscopy after a positive noninvasive screening test.”

AGA president John Carethers, MD, AGAF, who also met with the CMS, noted that reducing barriers to CRC screening will ultimately reduce CRC mortality.

“This is a win for all patients and should elevate our nation’s screening rates while lowering the overall cancer burden, saving lives,” he said.

Dr. Inadomi, Dr. Carethers, and Dr. Lieberman serve on the scientific advisory board of Geneoscopy; Dr. Lieberman is also on the scientific advisory board for ColoWrap.

Medicare will cover the full cost of colonoscopy after a positive noninvasive fecal test beginning in 2023, largely in response to a year-long advocacy campaign.

The benefit expansion is a “huge win” for patients, according to the American Gastroenterological Association, because it represents the end of out-of-pocket costs for colorectal cancer (CRC) screening.

“The continuum is complete!” said John Inadomi, MD, AGAF, past president of the AGA and a champion of the initiative within the organization.

Colonoscopy after a positive fecal test was previously considered a diagnostic procedure and therefore not considered part of the screening process by the Affordable Care Act, allowing payers to charge patients. That is, until the AGA and partners, including the American Cancer Society Cancer Action Network and Fight Colorectal Cancer, pushed back. First, the organizations successfully campaigned to ensure that private payers would cover the follow-up procedure. Now, after multiple meetings with the United States Department of Health & Human Services and Centers for Medicare & Medicaid Services, their collaborative efforts will end screening costs for patients with Medicare, pending finalization of the rule this fall. If finalized, it will take effect Jan. 2, 2023.

The policy change will “directly advance health equity” the AGA said, particularly among “rural communities and communities of color,” which are disproportionally affected by CRC.

“Cost-sharing is a well-recognized barrier to screening and has resulted in disparities,” said David Lieberman, MD, AGAF, who met with the CMS multiple times on behalf of the AGA. “Patients can now engage in CRC screening programs and be confident that they will not face unexpected cost-sharing for colonoscopy after a positive noninvasive screening test.”

AGA president John Carethers, MD, AGAF, who also met with the CMS, noted that reducing barriers to CRC screening will ultimately reduce CRC mortality.

“This is a win for all patients and should elevate our nation’s screening rates while lowering the overall cancer burden, saving lives,” he said.

Dr. Inadomi, Dr. Carethers, and Dr. Lieberman serve on the scientific advisory board of Geneoscopy; Dr. Lieberman is also on the scientific advisory board for ColoWrap.

Medicare will cover the full cost of colonoscopy after a positive noninvasive fecal test beginning in 2023, largely in response to a year-long advocacy campaign.

The benefit expansion is a “huge win” for patients, according to the American Gastroenterological Association, because it represents the end of out-of-pocket costs for colorectal cancer (CRC) screening.

“The continuum is complete!” said John Inadomi, MD, AGAF, past president of the AGA and a champion of the initiative within the organization.

Colonoscopy after a positive fecal test was previously considered a diagnostic procedure and therefore not considered part of the screening process by the Affordable Care Act, allowing payers to charge patients. That is, until the AGA and partners, including the American Cancer Society Cancer Action Network and Fight Colorectal Cancer, pushed back. First, the organizations successfully campaigned to ensure that private payers would cover the follow-up procedure. Now, after multiple meetings with the United States Department of Health & Human Services and Centers for Medicare & Medicaid Services, their collaborative efforts will end screening costs for patients with Medicare, pending finalization of the rule this fall. If finalized, it will take effect Jan. 2, 2023.

The policy change will “directly advance health equity” the AGA said, particularly among “rural communities and communities of color,” which are disproportionally affected by CRC.

“Cost-sharing is a well-recognized barrier to screening and has resulted in disparities,” said David Lieberman, MD, AGAF, who met with the CMS multiple times on behalf of the AGA. “Patients can now engage in CRC screening programs and be confident that they will not face unexpected cost-sharing for colonoscopy after a positive noninvasive screening test.”

AGA president John Carethers, MD, AGAF, who also met with the CMS, noted that reducing barriers to CRC screening will ultimately reduce CRC mortality.

“This is a win for all patients and should elevate our nation’s screening rates while lowering the overall cancer burden, saving lives,” he said.

Dr. Inadomi, Dr. Carethers, and Dr. Lieberman serve on the scientific advisory board of Geneoscopy; Dr. Lieberman is also on the scientific advisory board for ColoWrap.

A new study among patients with inflammatory bowel disease (IBD) suggests that viral antigen persistence in the gut may contribute to post-acute COVID-19 syndrome.

Postacute COVID-19 syndrome is now understood to be a multiorgan condition with symptoms that may include fatigue, cognitive dysfunction, and pain. Poor baseline health and severe acute infection are risk factors for the condition, but nonhospitalized illness can also lead to persistent symptoms.

Researchers found that nearly two-thirds of IBD patients had persistence of the antigen in infected tissues up to 8 months after a mild (nonhospitalized) acute COVID-19 infection. The study is the first to tie gut antigen persistence to post-acute COVID symptoms, and the results imply that the antigen may lead to immune perturbation and ongoing symptoms.

The study was published online in Gastroenterology.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses the membrane-bound angiotensin-converting enzyme 2 to gain entry into cells, which is expressed in the brush border enterocytes, as well as elsewhere in the body.

Previous research using intestinal epithelial organoids confirmed that SARS-CoV-2 is capable of infecting the human epithelium and that the virus can be detected in anal swabs long after it is cleared from nasal passages.

One potential explanation is viral immune perturbation or inflammatory tissue injury. Supporting evidence includes neural accumulation of memory T cells in patients with neuropsychiatric symptoms such as malaise and depression, and similar changes are seen with age-related immune senescence and tissue injury. Hyperactivated B and T cells, as well as other innate immune cells, have also been linked to postacute COVID-19, as has heightened expression of proinflammatory cytokines.

To explore the potential role of persistent viral antigens, the researchers gathered biopsies during upper- and lower-gastrointestinal endoscopy in 46 patients with IBD whose prior COVID-19 infection (mean, 7.3 months previous) had been confirmed by polymerase chain reaction and who were seen at the IBD outpatient unit of the investigators’ institution. In all, 43.5% of patients were female, and the average age was 44.67 years. Overall, 67.4% had been diagnosed with Crohn’s disease, 28.3% with ulcerative colitis, and 4.3% had unclassified IBD; 23.9% had a history of exposure to anti–tumor necrosis factor therapy. Among patients in the study, 32 of the patients tested positive for mucosal SARS-CoV-2 RNA, and there was no association between the presence of viral RNA and IBD type.

The researchers found that 52%-70% of patients had antigen persistence in any gut segment, as measured by nucleocapsid immunofluorescence or expression of one of four viral transcripts. They detected persistence of the nucleocapsid in epithelial cells and CD8+ T cells. Viral antigens persisted in patients with and without exposure to immunosuppressive therapy, and there was no association with antigen persistence and severity of acute COVID-19 infection or the presence of inflammation at the time of the endoscopy.

The researchers believed that the persistent viral antigen reflects incomplete clearance from the original infection rather than a latent or persistent infection because they could not replicate the virus in biopsy samples. Most biopsies within a patient produced some, but not all, of the viral transcripts tested. The authors suggest that immunosuppressive therapy may lead to incomplete viral clearance. Some patients lacked humoral nucleocapsid IgG antibodies, especially among those with gut antigen persistence.

In fact, only patients with gut viral RNA persistence had symptoms of postacute COVID. “This observation strongly argues for a role of viral antigen persistence in postacute COVID-19 and it appears plausible that SARS-CoV-2 antigen persistence, possibly in infected tissues beyond the gut, could impact host immune responses underlying the postacute COVID-19 syndrome,” the researchers wrote.

There is precedent for such a phenomenon in influenza. Mouse models have shown that ineffective clearance can influence adaptive immune responses and memory T-cell formation in lymph nodes of the lung. Another report found that COVID-19 pneumonia survivors have persistent changes to pulmonary CD8+ T cells.

The study is limited by its small sample size and a lack of a replication cohort. The study was also conducted in IBD patients because the researchers believed they were at higher risk of COVID-19 infection, although the researchers note that viral antigen persistence has been observed 2 months after recovery from COVID-19 in patients without IBD or exposure to immunosuppressants.

The researchers call for studies in patients without IBD to determine whether viral antigen persistence is a key mechanism in postacute COVID-19.

The researchers have no relevant financial disclosures.

A new study among patients with inflammatory bowel disease (IBD) suggests that viral antigen persistence in the gut may contribute to post-acute COVID-19 syndrome.

Postacute COVID-19 syndrome is now understood to be a multiorgan condition with symptoms that may include fatigue, cognitive dysfunction, and pain. Poor baseline health and severe acute infection are risk factors for the condition, but nonhospitalized illness can also lead to persistent symptoms.

Researchers found that nearly two-thirds of IBD patients had persistence of the antigen in infected tissues up to 8 months after a mild (nonhospitalized) acute COVID-19 infection. The study is the first to tie gut antigen persistence to post-acute COVID symptoms, and the results imply that the antigen may lead to immune perturbation and ongoing symptoms.

The study was published online in Gastroenterology.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses the membrane-bound angiotensin-converting enzyme 2 to gain entry into cells, which is expressed in the brush border enterocytes, as well as elsewhere in the body.

Previous research using intestinal epithelial organoids confirmed that SARS-CoV-2 is capable of infecting the human epithelium and that the virus can be detected in anal swabs long after it is cleared from nasal passages.

One potential explanation is viral immune perturbation or inflammatory tissue injury. Supporting evidence includes neural accumulation of memory T cells in patients with neuropsychiatric symptoms such as malaise and depression, and similar changes are seen with age-related immune senescence and tissue injury. Hyperactivated B and T cells, as well as other innate immune cells, have also been linked to postacute COVID-19, as has heightened expression of proinflammatory cytokines.

To explore the potential role of persistent viral antigens, the researchers gathered biopsies during upper- and lower-gastrointestinal endoscopy in 46 patients with IBD whose prior COVID-19 infection (mean, 7.3 months previous) had been confirmed by polymerase chain reaction and who were seen at the IBD outpatient unit of the investigators’ institution. In all, 43.5% of patients were female, and the average age was 44.67 years. Overall, 67.4% had been diagnosed with Crohn’s disease, 28.3% with ulcerative colitis, and 4.3% had unclassified IBD; 23.9% had a history of exposure to anti–tumor necrosis factor therapy. Among patients in the study, 32 of the patients tested positive for mucosal SARS-CoV-2 RNA, and there was no association between the presence of viral RNA and IBD type.

The researchers found that 52%-70% of patients had antigen persistence in any gut segment, as measured by nucleocapsid immunofluorescence or expression of one of four viral transcripts. They detected persistence of the nucleocapsid in epithelial cells and CD8+ T cells. Viral antigens persisted in patients with and without exposure to immunosuppressive therapy, and there was no association with antigen persistence and severity of acute COVID-19 infection or the presence of inflammation at the time of the endoscopy.

The researchers believed that the persistent viral antigen reflects incomplete clearance from the original infection rather than a latent or persistent infection because they could not replicate the virus in biopsy samples. Most biopsies within a patient produced some, but not all, of the viral transcripts tested. The authors suggest that immunosuppressive therapy may lead to incomplete viral clearance. Some patients lacked humoral nucleocapsid IgG antibodies, especially among those with gut antigen persistence.

In fact, only patients with gut viral RNA persistence had symptoms of postacute COVID. “This observation strongly argues for a role of viral antigen persistence in postacute COVID-19 and it appears plausible that SARS-CoV-2 antigen persistence, possibly in infected tissues beyond the gut, could impact host immune responses underlying the postacute COVID-19 syndrome,” the researchers wrote.

There is precedent for such a phenomenon in influenza. Mouse models have shown that ineffective clearance can influence adaptive immune responses and memory T-cell formation in lymph nodes of the lung. Another report found that COVID-19 pneumonia survivors have persistent changes to pulmonary CD8+ T cells.

The study is limited by its small sample size and a lack of a replication cohort. The study was also conducted in IBD patients because the researchers believed they were at higher risk of COVID-19 infection, although the researchers note that viral antigen persistence has been observed 2 months after recovery from COVID-19 in patients without IBD or exposure to immunosuppressants.

The researchers call for studies in patients without IBD to determine whether viral antigen persistence is a key mechanism in postacute COVID-19.

The researchers have no relevant financial disclosures.

A new study among patients with inflammatory bowel disease (IBD) suggests that viral antigen persistence in the gut may contribute to post-acute COVID-19 syndrome.

Postacute COVID-19 syndrome is now understood to be a multiorgan condition with symptoms that may include fatigue, cognitive dysfunction, and pain. Poor baseline health and severe acute infection are risk factors for the condition, but nonhospitalized illness can also lead to persistent symptoms.

Researchers found that nearly two-thirds of IBD patients had persistence of the antigen in infected tissues up to 8 months after a mild (nonhospitalized) acute COVID-19 infection. The study is the first to tie gut antigen persistence to post-acute COVID symptoms, and the results imply that the antigen may lead to immune perturbation and ongoing symptoms.

The study was published online in Gastroenterology.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses the membrane-bound angiotensin-converting enzyme 2 to gain entry into cells, which is expressed in the brush border enterocytes, as well as elsewhere in the body.

Previous research using intestinal epithelial organoids confirmed that SARS-CoV-2 is capable of infecting the human epithelium and that the virus can be detected in anal swabs long after it is cleared from nasal passages.

One potential explanation is viral immune perturbation or inflammatory tissue injury. Supporting evidence includes neural accumulation of memory T cells in patients with neuropsychiatric symptoms such as malaise and depression, and similar changes are seen with age-related immune senescence and tissue injury. Hyperactivated B and T cells, as well as other innate immune cells, have also been linked to postacute COVID-19, as has heightened expression of proinflammatory cytokines.

To explore the potential role of persistent viral antigens, the researchers gathered biopsies during upper- and lower-gastrointestinal endoscopy in 46 patients with IBD whose prior COVID-19 infection (mean, 7.3 months previous) had been confirmed by polymerase chain reaction and who were seen at the IBD outpatient unit of the investigators’ institution. In all, 43.5% of patients were female, and the average age was 44.67 years. Overall, 67.4% had been diagnosed with Crohn’s disease, 28.3% with ulcerative colitis, and 4.3% had unclassified IBD; 23.9% had a history of exposure to anti–tumor necrosis factor therapy. Among patients in the study, 32 of the patients tested positive for mucosal SARS-CoV-2 RNA, and there was no association between the presence of viral RNA and IBD type.

The researchers found that 52%-70% of patients had antigen persistence in any gut segment, as measured by nucleocapsid immunofluorescence or expression of one of four viral transcripts. They detected persistence of the nucleocapsid in epithelial cells and CD8+ T cells. Viral antigens persisted in patients with and without exposure to immunosuppressive therapy, and there was no association with antigen persistence and severity of acute COVID-19 infection or the presence of inflammation at the time of the endoscopy.

The researchers believed that the persistent viral antigen reflects incomplete clearance from the original infection rather than a latent or persistent infection because they could not replicate the virus in biopsy samples. Most biopsies within a patient produced some, but not all, of the viral transcripts tested. The authors suggest that immunosuppressive therapy may lead to incomplete viral clearance. Some patients lacked humoral nucleocapsid IgG antibodies, especially among those with gut antigen persistence.

In fact, only patients with gut viral RNA persistence had symptoms of postacute COVID. “This observation strongly argues for a role of viral antigen persistence in postacute COVID-19 and it appears plausible that SARS-CoV-2 antigen persistence, possibly in infected tissues beyond the gut, could impact host immune responses underlying the postacute COVID-19 syndrome,” the researchers wrote.

There is precedent for such a phenomenon in influenza. Mouse models have shown that ineffective clearance can influence adaptive immune responses and memory T-cell formation in lymph nodes of the lung. Another report found that COVID-19 pneumonia survivors have persistent changes to pulmonary CD8+ T cells.

The study is limited by its small sample size and a lack of a replication cohort. The study was also conducted in IBD patients because the researchers believed they were at higher risk of COVID-19 infection, although the researchers note that viral antigen persistence has been observed 2 months after recovery from COVID-19 in patients without IBD or exposure to immunosuppressants.

The researchers call for studies in patients without IBD to determine whether viral antigen persistence is a key mechanism in postacute COVID-19.

The researchers have no relevant financial disclosures.

Cognitive impairment is a good predictor of physical disability progression in patients with multiple sclerosis (MS), new research suggests. In an analysis of more than 1,600 patients with secondary-progressive MS (SPMS), the likelihood of needing a wheelchair was almost doubled in those who had the worst scores on cognitive testing measures, compared with their counterparts who had the best scores.

“These findings should change our world view of MS,” study investigator Gavin Giovannoni, PhD, professor of neurology, Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, told attendees at the Congress of the European Academy of Neurology.

Expand data

Cognitive impairment occurs very early in the course of MS and is part of the disease, although to a greater or lesser degree depending on the patient, Dr. Giovannoni noted. Such impairment has a significant impact on quality of life for patients dealing with this disease, he added.

EXPAND was a phase 3 study of siponimod. Results showed the now-approved oral selective sphingosine 1–phosphate receptor modulator significantly reduced the risk for disability progression in patients with SPMS.

Using the EXPAND clinical trial database, the current researchers assessed 1,628 participants for an association between cognitive processing speed, as measured with the Symbol Digit Modality Test (SDMT), and physical disability progression, as measured with the Expanded Disability Status Scale (EDSS). A score of 7 or more on the EDSS indicates wheelchair dependence.

Dr. Giovannoni noted that cognitive processing speed is considered an indirect measure of thalamic network efficiency and functional brain reserve.

Investigators looked at both the core study, in which all patients continued on treatment or placebo for up to 37 months, and the core plus extension part, in which patients received treatment for up to 5 years.

They separated SDMT scores into quartiles: from worst (n = 435) to two intermediate quartiles (n = 808) to the best quartile (n = 385).
 

Wheelchair dependence

In addition, the researchers examined the predictive value by baseline SDMT, adjusting for treatment, age, gender, baseline EDSS score, baseline SCMT quartile, and treatment-by-baseline SCMT quartile interaction. On-study SDMT change (month 0-24) was also assessed after adjusting for treatment, age, gender, baseline EDS, baseline SCMT, and on-study change in SCMT quartile.

In the core study, those in the worst SDMT quartile at baseline were numerically more likely to reach deterioration to EDSS 7 or greater (wheelchair dependent), compared with patients in the best SDMT quartile (hazard ratio, 1.31; 95% confidence interval, .72-2.38; P = .371).

The short-term predictive value of baseline SDMT for reaching sustained EDSS of at least 7 was more obvious in the placebo arm than in the treatment arm.

Dr. Giovannoni said this is likely due to the treatment effect of siponimod preventing relatively more events in the worse quartile, and so reducing the risk for wheelchair dependency.

In the core plus extension part, there was an almost twofold increased risk for wheelchair dependence in the worse versus best SDMT groups (HR, 1.81; 95% CI, 1.17-2.78; P = .007).

Both baseline SDMT (HR, 1.81; P = .007) and on-study change in SDMT (HR, 1.73; P = .046) predicted wheelchair dependence in the long-term.
 

‘More important than a walking stick’

Measuring cognitive change over time “may be a more important predictor than a walking stick in terms of quality of life and outcomes, and it affects clinical decisionmaking,” said Dr. Giovannoni.

The findings are not novel, as post hoc analyses of other studies showed similar results. However, this new analysis adds more evidence to the importance of cognition in MS, Dr. Giovannoni noted.

“I have patients with EDSS of 0 or 1 who are profoundly disabled because of cognition. You shouldn’t just assume someone is not disabled because they don’t have physical disability,” he said.

However, Dr. Giovannoni noted that the study found an association and does not necessarily indicate a cause.
 

‘Valuable’ insights

Antonia Lefter, MD, of NeuroHope, Monza Oncologic Hospital, Bucharest, Romania, cochaired the session highlighting the research. Commenting on the study, she called this analysis from the “renowned” EXPAND study “valuable.”

In addition, it “underscores” the importance of assessing cognitive processing speed, as it may predict long-term disability progression in patients with SPMS, Dr. Lefter said.

The study was funded by Novartis Pharma AG, Basel, Switzerland. Dr. Giovannoni, a steering committee member of the EXPAND trial, reported receiving consulting fees from AbbVie, Actelion, Atara Bio, Biogen, Celgene, Sanofi-Genzyme, Genentech, GlaxoSmithKline, Merck-Serono, Novartis, Roche, and Reva. He has also received compensation for research from Biogen, Roche, Merck-Serono, Novartis, Sanofi-Genzyme, and Takeda. Dr. Lefter has reported no relevant financial relationships.

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

Cognitive impairment is a good predictor of physical disability progression in patients with multiple sclerosis (MS), new research suggests. In an analysis of more than 1,600 patients with secondary-progressive MS (SPMS), the likelihood of needing a wheelchair was almost doubled in those who had the worst scores on cognitive testing measures, compared with their counterparts who had the best scores.

“These findings should change our world view of MS,” study investigator Gavin Giovannoni, PhD, professor of neurology, Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, told attendees at the Congress of the European Academy of Neurology.

Expand data

Cognitive impairment occurs very early in the course of MS and is part of the disease, although to a greater or lesser degree depending on the patient, Dr. Giovannoni noted. Such impairment has a significant impact on quality of life for patients dealing with this disease, he added.

EXPAND was a phase 3 study of siponimod. Results showed the now-approved oral selective sphingosine 1–phosphate receptor modulator significantly reduced the risk for disability progression in patients with SPMS.

Using the EXPAND clinical trial database, the current researchers assessed 1,628 participants for an association between cognitive processing speed, as measured with the Symbol Digit Modality Test (SDMT), and physical disability progression, as measured with the Expanded Disability Status Scale (EDSS). A score of 7 or more on the EDSS indicates wheelchair dependence.

Dr. Giovannoni noted that cognitive processing speed is considered an indirect measure of thalamic network efficiency and functional brain reserve.

Investigators looked at both the core study, in which all patients continued on treatment or placebo for up to 37 months, and the core plus extension part, in which patients received treatment for up to 5 years.

They separated SDMT scores into quartiles: from worst (n = 435) to two intermediate quartiles (n = 808) to the best quartile (n = 385).
 

Wheelchair dependence

In addition, the researchers examined the predictive value by baseline SDMT, adjusting for treatment, age, gender, baseline EDSS score, baseline SCMT quartile, and treatment-by-baseline SCMT quartile interaction. On-study SDMT change (month 0-24) was also assessed after adjusting for treatment, age, gender, baseline EDS, baseline SCMT, and on-study change in SCMT quartile.

In the core study, those in the worst SDMT quartile at baseline were numerically more likely to reach deterioration to EDSS 7 or greater (wheelchair dependent), compared with patients in the best SDMT quartile (hazard ratio, 1.31; 95% confidence interval, .72-2.38; P = .371).

The short-term predictive value of baseline SDMT for reaching sustained EDSS of at least 7 was more obvious in the placebo arm than in the treatment arm.

Dr. Giovannoni said this is likely due to the treatment effect of siponimod preventing relatively more events in the worse quartile, and so reducing the risk for wheelchair dependency.

In the core plus extension part, there was an almost twofold increased risk for wheelchair dependence in the worse versus best SDMT groups (HR, 1.81; 95% CI, 1.17-2.78; P = .007).

Both baseline SDMT (HR, 1.81; P = .007) and on-study change in SDMT (HR, 1.73; P = .046) predicted wheelchair dependence in the long-term.
 

‘More important than a walking stick’

Measuring cognitive change over time “may be a more important predictor than a walking stick in terms of quality of life and outcomes, and it affects clinical decisionmaking,” said Dr. Giovannoni.

The findings are not novel, as post hoc analyses of other studies showed similar results. However, this new analysis adds more evidence to the importance of cognition in MS, Dr. Giovannoni noted.

“I have patients with EDSS of 0 or 1 who are profoundly disabled because of cognition. You shouldn’t just assume someone is not disabled because they don’t have physical disability,” he said.

However, Dr. Giovannoni noted that the study found an association and does not necessarily indicate a cause.
 

‘Valuable’ insights

Antonia Lefter, MD, of NeuroHope, Monza Oncologic Hospital, Bucharest, Romania, cochaired the session highlighting the research. Commenting on the study, she called this analysis from the “renowned” EXPAND study “valuable.”

In addition, it “underscores” the importance of assessing cognitive processing speed, as it may predict long-term disability progression in patients with SPMS, Dr. Lefter said.

The study was funded by Novartis Pharma AG, Basel, Switzerland. Dr. Giovannoni, a steering committee member of the EXPAND trial, reported receiving consulting fees from AbbVie, Actelion, Atara Bio, Biogen, Celgene, Sanofi-Genzyme, Genentech, GlaxoSmithKline, Merck-Serono, Novartis, Roche, and Reva. He has also received compensation for research from Biogen, Roche, Merck-Serono, Novartis, Sanofi-Genzyme, and Takeda. Dr. Lefter has reported no relevant financial relationships.

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

Cognitive impairment is a good predictor of physical disability progression in patients with multiple sclerosis (MS), new research suggests. In an analysis of more than 1,600 patients with secondary-progressive MS (SPMS), the likelihood of needing a wheelchair was almost doubled in those who had the worst scores on cognitive testing measures, compared with their counterparts who had the best scores.

“These findings should change our world view of MS,” study investigator Gavin Giovannoni, PhD, professor of neurology, Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, told attendees at the Congress of the European Academy of Neurology.

Expand data

Cognitive impairment occurs very early in the course of MS and is part of the disease, although to a greater or lesser degree depending on the patient, Dr. Giovannoni noted. Such impairment has a significant impact on quality of life for patients dealing with this disease, he added.

EXPAND was a phase 3 study of siponimod. Results showed the now-approved oral selective sphingosine 1–phosphate receptor modulator significantly reduced the risk for disability progression in patients with SPMS.

Using the EXPAND clinical trial database, the current researchers assessed 1,628 participants for an association between cognitive processing speed, as measured with the Symbol Digit Modality Test (SDMT), and physical disability progression, as measured with the Expanded Disability Status Scale (EDSS). A score of 7 or more on the EDSS indicates wheelchair dependence.

Dr. Giovannoni noted that cognitive processing speed is considered an indirect measure of thalamic network efficiency and functional brain reserve.

Investigators looked at both the core study, in which all patients continued on treatment or placebo for up to 37 months, and the core plus extension part, in which patients received treatment for up to 5 years.

They separated SDMT scores into quartiles: from worst (n = 435) to two intermediate quartiles (n = 808) to the best quartile (n = 385).
 

Wheelchair dependence

In addition, the researchers examined the predictive value by baseline SDMT, adjusting for treatment, age, gender, baseline EDSS score, baseline SCMT quartile, and treatment-by-baseline SCMT quartile interaction. On-study SDMT change (month 0-24) was also assessed after adjusting for treatment, age, gender, baseline EDS, baseline SCMT, and on-study change in SCMT quartile.

In the core study, those in the worst SDMT quartile at baseline were numerically more likely to reach deterioration to EDSS 7 or greater (wheelchair dependent), compared with patients in the best SDMT quartile (hazard ratio, 1.31; 95% confidence interval, .72-2.38; P = .371).

The short-term predictive value of baseline SDMT for reaching sustained EDSS of at least 7 was more obvious in the placebo arm than in the treatment arm.

Dr. Giovannoni said this is likely due to the treatment effect of siponimod preventing relatively more events in the worse quartile, and so reducing the risk for wheelchair dependency.

In the core plus extension part, there was an almost twofold increased risk for wheelchair dependence in the worse versus best SDMT groups (HR, 1.81; 95% CI, 1.17-2.78; P = .007).

Both baseline SDMT (HR, 1.81; P = .007) and on-study change in SDMT (HR, 1.73; P = .046) predicted wheelchair dependence in the long-term.
 

‘More important than a walking stick’

Measuring cognitive change over time “may be a more important predictor than a walking stick in terms of quality of life and outcomes, and it affects clinical decisionmaking,” said Dr. Giovannoni.

The findings are not novel, as post hoc analyses of other studies showed similar results. However, this new analysis adds more evidence to the importance of cognition in MS, Dr. Giovannoni noted.

“I have patients with EDSS of 0 or 1 who are profoundly disabled because of cognition. You shouldn’t just assume someone is not disabled because they don’t have physical disability,” he said.

However, Dr. Giovannoni noted that the study found an association and does not necessarily indicate a cause.
 

‘Valuable’ insights

Antonia Lefter, MD, of NeuroHope, Monza Oncologic Hospital, Bucharest, Romania, cochaired the session highlighting the research. Commenting on the study, she called this analysis from the “renowned” EXPAND study “valuable.”

In addition, it “underscores” the importance of assessing cognitive processing speed, as it may predict long-term disability progression in patients with SPMS, Dr. Lefter said.

The study was funded by Novartis Pharma AG, Basel, Switzerland. Dr. Giovannoni, a steering committee member of the EXPAND trial, reported receiving consulting fees from AbbVie, Actelion, Atara Bio, Biogen, Celgene, Sanofi-Genzyme, Genentech, GlaxoSmithKline, Merck-Serono, Novartis, Roche, and Reva. He has also received compensation for research from Biogen, Roche, Merck-Serono, Novartis, Sanofi-Genzyme, and Takeda. Dr. Lefter has reported no relevant financial relationships.

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

Chronic obstructive pulmonary disease (COPD) was among the significant predictors of hospital readmission in older adults with fractures, based on data from nearly 400 individuals.

Fractures in the elderly remain a major health concern, and readmissions are common; however, “The predictive factors for hospital readmission of elderly people with fractures are multifactorial and complex,” Lara Cristina da Cunha Guimarães, MSN, of State School of Public Health Candido Santiago, State Department of Health of Goiás (Brazil), and colleagues wrote.

Previous research suggests that readmissions risk may be greater in patients with preadmission conditions including pulmonary and cardiac disease, history of stroke and other neurological conditions, and other factors associated with aging in general, they said.

In a study published in the journal Injury , the researchers reviewed data from 376 adults aged 60 years and older in a trauma referral hospital in Brazil who had suffered fractures and were hospitalized between Sept. 1, 2016, and Feb. 28, 2017. The primary outcome was readmission up to one year after discharge from the initial hospitalization for fracture.

Approximately half of the patients experienced femur fractures (53.2%), and the most frequent cause was falling from standing height (72.9%). The overall incidence of readmission was 20.7%. A total of 30.5% of readmissions were related to the fracture, and surgical-site infections were the most common cause of fracture-related complications.

More than half (58.3%) of the readmissions were related to clinical complications.

In a multivariate analysis, several clinical factors not related to fractures were independently associated with readmission, including a previous diagnosis of COPD, age between 60 and 69 years, a fracture of the femur, and delirium at the time of the first hospitalization for fracture.

Pneumonia was the most frequent cause of clinical complications, reflecting data from other recent studies, the researchers noted. “Elderly people with COPD are more susceptible to infections, such as pneumonia, which was a cause of frequent readmissions in the population studied. The presence of COPD can contribute to imbalance in the pulmonary microbiome, mucus production and persistent inflammation of the airways, and structural damage, which increases exposure of the pulmonary mucosa to pathogens.” COPD also can be associated with cardiovascular, mental, and musculoskeletal diseases that can further complicate and delay recovery from fractures.

The study findings were limited by the potential for incomplete information in medical records. However, the results indicate a range of causes and conditions associated with hospital readmission after fractures in older adults, they said. Recognizing these factors can guide plans for transitions from hospital to home care to reduce complications and readmissions.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Chronic obstructive pulmonary disease (COPD) was among the significant predictors of hospital readmission in older adults with fractures, based on data from nearly 400 individuals.

Fractures in the elderly remain a major health concern, and readmissions are common; however, “The predictive factors for hospital readmission of elderly people with fractures are multifactorial and complex,” Lara Cristina da Cunha Guimarães, MSN, of State School of Public Health Candido Santiago, State Department of Health of Goiás (Brazil), and colleagues wrote.

Previous research suggests that readmissions risk may be greater in patients with preadmission conditions including pulmonary and cardiac disease, history of stroke and other neurological conditions, and other factors associated with aging in general, they said.

In a study published in the journal Injury , the researchers reviewed data from 376 adults aged 60 years and older in a trauma referral hospital in Brazil who had suffered fractures and were hospitalized between Sept. 1, 2016, and Feb. 28, 2017. The primary outcome was readmission up to one year after discharge from the initial hospitalization for fracture.

Approximately half of the patients experienced femur fractures (53.2%), and the most frequent cause was falling from standing height (72.9%). The overall incidence of readmission was 20.7%. A total of 30.5% of readmissions were related to the fracture, and surgical-site infections were the most common cause of fracture-related complications.

More than half (58.3%) of the readmissions were related to clinical complications.

In a multivariate analysis, several clinical factors not related to fractures were independently associated with readmission, including a previous diagnosis of COPD, age between 60 and 69 years, a fracture of the femur, and delirium at the time of the first hospitalization for fracture.

Pneumonia was the most frequent cause of clinical complications, reflecting data from other recent studies, the researchers noted. “Elderly people with COPD are more susceptible to infections, such as pneumonia, which was a cause of frequent readmissions in the population studied. The presence of COPD can contribute to imbalance in the pulmonary microbiome, mucus production and persistent inflammation of the airways, and structural damage, which increases exposure of the pulmonary mucosa to pathogens.” COPD also can be associated with cardiovascular, mental, and musculoskeletal diseases that can further complicate and delay recovery from fractures.

The study findings were limited by the potential for incomplete information in medical records. However, the results indicate a range of causes and conditions associated with hospital readmission after fractures in older adults, they said. Recognizing these factors can guide plans for transitions from hospital to home care to reduce complications and readmissions.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Chronic obstructive pulmonary disease (COPD) was among the significant predictors of hospital readmission in older adults with fractures, based on data from nearly 400 individuals.

Fractures in the elderly remain a major health concern, and readmissions are common; however, “The predictive factors for hospital readmission of elderly people with fractures are multifactorial and complex,” Lara Cristina da Cunha Guimarães, MSN, of State School of Public Health Candido Santiago, State Department of Health of Goiás (Brazil), and colleagues wrote.

Previous research suggests that readmissions risk may be greater in patients with preadmission conditions including pulmonary and cardiac disease, history of stroke and other neurological conditions, and other factors associated with aging in general, they said.

In a study published in the journal Injury , the researchers reviewed data from 376 adults aged 60 years and older in a trauma referral hospital in Brazil who had suffered fractures and were hospitalized between Sept. 1, 2016, and Feb. 28, 2017. The primary outcome was readmission up to one year after discharge from the initial hospitalization for fracture.

Approximately half of the patients experienced femur fractures (53.2%), and the most frequent cause was falling from standing height (72.9%). The overall incidence of readmission was 20.7%. A total of 30.5% of readmissions were related to the fracture, and surgical-site infections were the most common cause of fracture-related complications.

More than half (58.3%) of the readmissions were related to clinical complications.

In a multivariate analysis, several clinical factors not related to fractures were independently associated with readmission, including a previous diagnosis of COPD, age between 60 and 69 years, a fracture of the femur, and delirium at the time of the first hospitalization for fracture.

Pneumonia was the most frequent cause of clinical complications, reflecting data from other recent studies, the researchers noted. “Elderly people with COPD are more susceptible to infections, such as pneumonia, which was a cause of frequent readmissions in the population studied. The presence of COPD can contribute to imbalance in the pulmonary microbiome, mucus production and persistent inflammation of the airways, and structural damage, which increases exposure of the pulmonary mucosa to pathogens.” COPD also can be associated with cardiovascular, mental, and musculoskeletal diseases that can further complicate and delay recovery from fractures.

The study findings were limited by the potential for incomplete information in medical records. However, the results indicate a range of causes and conditions associated with hospital readmission after fractures in older adults, they said. Recognizing these factors can guide plans for transitions from hospital to home care to reduce complications and readmissions.

The study received no outside funding. The researchers had no financial conflicts to disclose.

Insulin injection therapy is one of the most widely used health care interventions to manage both type 1 and type 2 diabetes mellitus (T1DM/T2DM). Globally, more than 150 to 200 million people inject insulin into their upper posterior arms, buttocks, anterior and lateral thighs, or abdomen.^1,2 In an ideal world, every patient would be using the correct site and rotating their insulin injection sites in accordance with health care professional (HCP) recommendations—systematic injections in one general body location, at least 1 cm away from the previous injection.² Unfortunately, same-site insulin injection (repeatedly in the same region within 1 cm of previous injections) is a common mistake made by patients with DM—in one study, 63% of participants either did not rotate sites correctly or failed to do so at all.

Insulin-resistant cutaneous complications may occur as a result of same-site insulin injections. The most common is lipohypertrophy, reported in some studies in nearly 50% of patients with DM on insulin therapy.⁴ Other common cutaneous complications include lipoatrophy and amyloidosis. Injection-site acanthosis nigricans, although uncommon, has been reported in 18 cases in the literature.

Most articles suggest that same-site insulin injections decrease local insulin sensitivity and result in tissue hypertrophy because of the anabolic properties of insulin and increase in insulin binding to insulin-like growth factor-1 (IGF-1) receptor.^5-20 The hyperkeratotic growth and varying insulin absorption rates associated with these cutaneous complications increase chances of either hyper- or hypoglycemic episodes in patients.^10,11,13 It is the responsibility of the DM care professional to provide proper insulin-injection technique education and perform routine inspection of injection sites to reduce cutaneous complications of insulin therapy. The purpose of this article is to (1) describe a case of acanthosis nigricans resulting from insulin injection at the same site; (2) review case reports in the literature describing injection-site acanthosis nigricans resulting from same-site insulin injections; (3) describe localized cutaneous complications associated with the use of insulin; and (4) discuss clinical implications and lessons learned from the literature.

Case Presentation

A 75-year-old patient with an 8-year history of T2DM, as well as stable coronary artery disease, atrial fibrillation, hypertension, hyperlipidemia, chronic obstructive pulmonary disease, and stage 3 chronic kidney disease, presented with 2 discrete abdominal hyperpigmented plaques. At the time of the initial clinic visit, the patient was taking metformin 1000 mg twice daily and insulin glargine 40 units once daily. When insulin was initiated 7 years prior, the patient received neutral protamine Hagedorn (NPH) insulin for the first year and transitioned to insulin glargine. After 4 years of insulin therapy, insulin aspart was added and discontinued after 2 years. The patient’s hemoglobin A_1c (HbA_1c) was 6.8%, suggesting good glycemic control.

The patient reported 5 years of progressive, asymptomatic hyperpigmentation of the skin surrounding his insulin glargine injection sites and injecting in these same sites daily without rotation. He reported no additional skin changes or symptoms. He had noticed no skin changes while using NPH insulin during his first year of insulin therapy. On examination, the abdominal wall skin demonstrated 2 well-demarcated, nearly black, soft, velvety plaques, measuring 9 × 8 cm on the left side and 4 × 3.5 cm on the right, suggesting acanthosis nigricans (Figure 1A). The remainder of the skin examination, including the flexures, was normal. Of note, the patient received biweekly intramuscular testosterone injections in the gluteal region for secondary hypogonadism with no adverse dermatologic effects. A skin punch biopsy was performed and revealed epidermal papillomatosis and hyperkeratosis, confirming the clinical diagnosis of acanthosis nigricans (Figure 2).

After a review of insulin-injection technique at his clinic visit, the patient started rotating insulin injection sites over his entire abdomen, and the acanthosis nigricans partially improved. A few months later, the patient stopped rotating the insulin injection site, and the acanthosis nigricans worsened again. Because of worsening glycemic control, the patient was then started on insulin aspart. He did not develop any skin changes at the insulin aspart injection site, although he was not rotating its site of injection.

Subsequently, with reeducation and proper injection-site rotation, the patient had resolution of his acanthosis nigricans (Figure 1b).

Discussion

A review of the literature revealed 18 reported cases of acanthosis nigricans at sites of repeated insulin injection (Table).^5-20 Acanthosis nigricans at the site of insulin injection afflicts patients of any age, with cases observed in patients aged 14 to 75 years. Sixteen (84%) of 19 cases were male. Fourteen cases (73%) had T2DM; the rest of the patients had T1DM. The duration of insulin injection therapy prior to onset ranged from immediate to 13 years (median 4 years). Fourteen cases (73%) were reported on the abdomen; however, other sites, such as thighs and upper arm, also were reported. Lesions size varied from 12 to 360 cm². Two cases had associated amyloidosis. The average HbA_1c reported at presentation was 10%. Following insulin injection-site rotation, most of the cases reported improvement of both glycemic control and acanthosis nigricans appearance.

In the case described by Kudo and colleagues, a 59-year-old male patient with T2DM had been injecting insulin into the same spot on his abdomen for 10 years. He developed acanthosis nigricans and an amyloidoma so large and firm that it bent the needle when he injected insulin.¹¹

Most of the cases we found in the literature were after 2005 and associated with the use of human or analog insulin. These cases may be related to a bias, as cases may be easier to find in digital archives in the later years, when human or analog insulins have been in common use. Also noteworthy, in cases that reported dosage, most were not very high, and the highest daily dose was 240 IU/d. Ten reports of injection-site acanthosis nigricans were in dermatology journals; only 5 reports were in endocrinology journals and 3 in general medical journals, indicating possible less awareness of this phenomenon in other HCPs who care for patients with DM.

Complications of Same-Site Injections

Acanthosis nigricans. Commonly found in the armpits, neck folds, and groin, acanthosis nigricans is known as one of the calling cards for insulin resistance, obesity, and hyperinsulinemia.²¹ Acanthosis nigricans can be seen in people with or without DM and is not limited to those on insulin therapy. However, same-site insulin injections for 4 to 6 years also may result in injection-site acanthosis nigricans–like lesions because of factors such as insulin exposure at the local tissue level.¹⁶

Acanthosis nigricans development is characterized by hyperpigmented, hyperkeratotic, velvety, and sometimes verrucous plaques.⁶ Acanthosis nigricans surrounding repeated injection sites is hypothesized to develop as a result of localized hyperinsulinemia secondary to insulin resistance, which increases the stimulation of IGF, thereby causing epidermal hypertrophy.^5-20 If insulin injection therapy continues to be administered through the acanthosis nigricans lesion, it results in decreased insulin absorption, leading to poor glycemic control.¹³

Acanthosis nigricans associated with insulin injection is reversible. After rotation of injection sites, lesions either decrease in size or severity of appearance.^5-8,11 Also, by avoiding injection into the hyperkeratotic plaques and using normal subcutaneous tissue for injection, patients’ response to insulin improves, as measured by HbA_1c and by decreased daily insulin requirement.^{6-8,10,12,18-20}

Lipohypertrophy. This is characterized by an increase in localized adipose tissue and is the most common cutaneous complication of insulin therapy.² Lipohypertrophy presents as a firm, rubbery mass in the location of same-site insulin injections.²² Development of lipohypertrophy is suspected to be the result of either (1) anabolic effect of insulin on local adipocytes, promoting fat and protein synthesis; (2) an autoimmune response by immunoglobulin (Ig) G or IgE antibodies to insulin, immune response to insulin of different species, or to insulin injection techniques; or (3) repeated trauma to the injection site from repeated needle usage.^4,23

In a study assessing the prevalence of lipohypertrophy and its relation to insulin technique, 49.1% of participants with lipohypertrophy had glycemic variability compared with 6.5% of participants without lipohypertrophy.³ Johansson and colleagues described an impairment of insulin absorption in lipohypertrophic tissues, causing a 25% lower plasma insulin concentration compared with that of normal tissues.⁴ These findings suggest a significant effect of lipohypertrophy on insulin absorption—unnecessarily increasing insulin consumption and worsening glycemic control.

Primary prevention measures include injection site inspection and patient education about rotation and abstaining from needle reuse.²² If a patient already has signs of lipohypertrophy, data supports education and insulin injection technique practice as simple and effective means to reduce insulin action variability and increase glycemic control.²⁴

Lipoatrophy. Lipoatrophy is described as a local loss of subcutaneous adipose tissue often in the face, buttocks, legs and arm regions and can be rooted in genetic, immune, or drug-associated etiologies.²⁵ Insulin-induced lipoatrophy is suspected to be the result of tumor necrosis factor-α hyperproduction in reaction to insulin crystal presence at the injection site.^26,27 Overall, lipoatrophy development has decreased since the use of recombinant human insulin and analog insulin therapy.²⁸ The decrease is hypothesized to be due to increased subcutaneous tissue absorption rate of human insulin and its analog, decreasing overall adipocyte exposure to localized high insulin concentration.²⁷ Treatments for same-site insulin-derived lipoatrophy include changing injection sites and preparation of insulin.²⁶ When injection into the lipoatrophic site was avoided, glycemic control and lipoatrophy appearance improved.²⁶

Amyloidosis. Amyloidosis indicates the presence of an extracellular bundle of insoluble polymeric protein fibrils in tissues and organs.²⁹ Insulin-induced amyloidosis presents as a hard mass or ball near the injection site.²⁹ Insulin is one of many hormones that can form amyloid fibrils, and there have been several dozen cases reported of amyloid formation at the site of insulin injection.^29-31 Although insulin-derived amyloidosis is rare, it may be misdiagnosed as lipohypertrophy due to a lack of histopathologic testing or general awareness of the complication.²⁹

In a case series of 7 patients with amyloidosis, all patients had a mean HbA_1c of 9.3% (range, 8.5-10.2%) and averaged 1 IU/kg bodyweight before intervention.³⁰ After the discovery of the mass, participants were instructed to avoid injection into the amyloidoma, and average insulin requirements decreased to 0.48 IU/kg body weight (P = .40).³⁰ Patients with amyloidosis who rotated their injection sites experienced better glycemic control and decreased insulin requirements.³⁰

Pathophysiology of Localized Insulin Resistance

Insulin regulates glucose homeostasis in skeletal muscle and adipose tissue, increases hepatic and adipocyte lipid synthesis, and decreases adipocyte fatty acid release.³² Generalized insulin resistance occurs when target tissues have decreased glucose uptake in response to circulating insulin.³² Insulin resistance increases the amount of free insulin in surrounding tissues. At high concentrations, insulin fosters tissue growth by binding to IGF-1 receptors, stimulating hypertrophy and reproduction of keratinocytes and fibroblasts.³³ This pathophysiology helps explain the origin of localized acanthosis nigricans at same-site insulin injections.

Conclusions

Cutaneous complications are a local adverse effect of long-term failure to rotate insulin injection sites. Our case serves as a call to action for HCPs to improve education regarding insulin injection-site rotation, conduct routine injection-site inspection, and actively document cases as they occur to increase public awareness of these important complications.

If a patient with DM presents with unexplained poor glycemic control, consider questioning the patient about injection-site location and how often they are rotating the insulin injection site. Inspect the site for cutaneous complications. Of note, if a patient has a cutaneous complication due to insulin injection, adjust or decrease the insulin dosage when rotating sites to mitigate the risk of hypoglycemic episodes.

Improvement of glycemic control, cosmetic appearance of injection site, and insulin use all begin with skin inspection, injection technique education, and periodic review by a HCP.

Insulin injection therapy is one of the most widely used health care interventions to manage both type 1 and type 2 diabetes mellitus (T1DM/T2DM). Globally, more than 150 to 200 million people inject insulin into their upper posterior arms, buttocks, anterior and lateral thighs, or abdomen.^1,2 In an ideal world, every patient would be using the correct site and rotating their insulin injection sites in accordance with health care professional (HCP) recommendations—systematic injections in one general body location, at least 1 cm away from the previous injection.² Unfortunately, same-site insulin injection (repeatedly in the same region within 1 cm of previous injections) is a common mistake made by patients with DM—in one study, 63% of participants either did not rotate sites correctly or failed to do so at all.

Insulin-resistant cutaneous complications may occur as a result of same-site insulin injections. The most common is lipohypertrophy, reported in some studies in nearly 50% of patients with DM on insulin therapy.⁴ Other common cutaneous complications include lipoatrophy and amyloidosis. Injection-site acanthosis nigricans, although uncommon, has been reported in 18 cases in the literature.

Most articles suggest that same-site insulin injections decrease local insulin sensitivity and result in tissue hypertrophy because of the anabolic properties of insulin and increase in insulin binding to insulin-like growth factor-1 (IGF-1) receptor.^5-20 The hyperkeratotic growth and varying insulin absorption rates associated with these cutaneous complications increase chances of either hyper- or hypoglycemic episodes in patients.^10,11,13 It is the responsibility of the DM care professional to provide proper insulin-injection technique education and perform routine inspection of injection sites to reduce cutaneous complications of insulin therapy. The purpose of this article is to (1) describe a case of acanthosis nigricans resulting from insulin injection at the same site; (2) review case reports in the literature describing injection-site acanthosis nigricans resulting from same-site insulin injections; (3) describe localized cutaneous complications associated with the use of insulin; and (4) discuss clinical implications and lessons learned from the literature.

Case Presentation

A 75-year-old patient with an 8-year history of T2DM, as well as stable coronary artery disease, atrial fibrillation, hypertension, hyperlipidemia, chronic obstructive pulmonary disease, and stage 3 chronic kidney disease, presented with 2 discrete abdominal hyperpigmented plaques. At the time of the initial clinic visit, the patient was taking metformin 1000 mg twice daily and insulin glargine 40 units once daily. When insulin was initiated 7 years prior, the patient received neutral protamine Hagedorn (NPH) insulin for the first year and transitioned to insulin glargine. After 4 years of insulin therapy, insulin aspart was added and discontinued after 2 years. The patient’s hemoglobin A_1c (HbA_1c) was 6.8%, suggesting good glycemic control.

The patient reported 5 years of progressive, asymptomatic hyperpigmentation of the skin surrounding his insulin glargine injection sites and injecting in these same sites daily without rotation. He reported no additional skin changes or symptoms. He had noticed no skin changes while using NPH insulin during his first year of insulin therapy. On examination, the abdominal wall skin demonstrated 2 well-demarcated, nearly black, soft, velvety plaques, measuring 9 × 8 cm on the left side and 4 × 3.5 cm on the right, suggesting acanthosis nigricans (Figure 1A). The remainder of the skin examination, including the flexures, was normal. Of note, the patient received biweekly intramuscular testosterone injections in the gluteal region for secondary hypogonadism with no adverse dermatologic effects. A skin punch biopsy was performed and revealed epidermal papillomatosis and hyperkeratosis, confirming the clinical diagnosis of acanthosis nigricans (Figure 2).

After a review of insulin-injection technique at his clinic visit, the patient started rotating insulin injection sites over his entire abdomen, and the acanthosis nigricans partially improved. A few months later, the patient stopped rotating the insulin injection site, and the acanthosis nigricans worsened again. Because of worsening glycemic control, the patient was then started on insulin aspart. He did not develop any skin changes at the insulin aspart injection site, although he was not rotating its site of injection.

Subsequently, with reeducation and proper injection-site rotation, the patient had resolution of his acanthosis nigricans (Figure 1b).

Discussion

A review of the literature revealed 18 reported cases of acanthosis nigricans at sites of repeated insulin injection (Table).^5-20 Acanthosis nigricans at the site of insulin injection afflicts patients of any age, with cases observed in patients aged 14 to 75 years. Sixteen (84%) of 19 cases were male. Fourteen cases (73%) had T2DM; the rest of the patients had T1DM. The duration of insulin injection therapy prior to onset ranged from immediate to 13 years (median 4 years). Fourteen cases (73%) were reported on the abdomen; however, other sites, such as thighs and upper arm, also were reported. Lesions size varied from 12 to 360 cm². Two cases had associated amyloidosis. The average HbA_1c reported at presentation was 10%. Following insulin injection-site rotation, most of the cases reported improvement of both glycemic control and acanthosis nigricans appearance.

In the case described by Kudo and colleagues, a 59-year-old male patient with T2DM had been injecting insulin into the same spot on his abdomen for 10 years. He developed acanthosis nigricans and an amyloidoma so large and firm that it bent the needle when he injected insulin.¹¹

Most of the cases we found in the literature were after 2005 and associated with the use of human or analog insulin. These cases may be related to a bias, as cases may be easier to find in digital archives in the later years, when human or analog insulins have been in common use. Also noteworthy, in cases that reported dosage, most were not very high, and the highest daily dose was 240 IU/d. Ten reports of injection-site acanthosis nigricans were in dermatology journals; only 5 reports were in endocrinology journals and 3 in general medical journals, indicating possible less awareness of this phenomenon in other HCPs who care for patients with DM.

Complications of Same-Site Injections

Acanthosis nigricans. Commonly found in the armpits, neck folds, and groin, acanthosis nigricans is known as one of the calling cards for insulin resistance, obesity, and hyperinsulinemia.²¹ Acanthosis nigricans can be seen in people with or without DM and is not limited to those on insulin therapy. However, same-site insulin injections for 4 to 6 years also may result in injection-site acanthosis nigricans–like lesions because of factors such as insulin exposure at the local tissue level.¹⁶

Acanthosis nigricans development is characterized by hyperpigmented, hyperkeratotic, velvety, and sometimes verrucous plaques.⁶ Acanthosis nigricans surrounding repeated injection sites is hypothesized to develop as a result of localized hyperinsulinemia secondary to insulin resistance, which increases the stimulation of IGF, thereby causing epidermal hypertrophy.^5-20 If insulin injection therapy continues to be administered through the acanthosis nigricans lesion, it results in decreased insulin absorption, leading to poor glycemic control.¹³

Acanthosis nigricans associated with insulin injection is reversible. After rotation of injection sites, lesions either decrease in size or severity of appearance.^5-8,11 Also, by avoiding injection into the hyperkeratotic plaques and using normal subcutaneous tissue for injection, patients’ response to insulin improves, as measured by HbA_1c and by decreased daily insulin requirement.^{6-8,10,12,18-20}

Lipohypertrophy. This is characterized by an increase in localized adipose tissue and is the most common cutaneous complication of insulin therapy.² Lipohypertrophy presents as a firm, rubbery mass in the location of same-site insulin injections.²² Development of lipohypertrophy is suspected to be the result of either (1) anabolic effect of insulin on local adipocytes, promoting fat and protein synthesis; (2) an autoimmune response by immunoglobulin (Ig) G or IgE antibodies to insulin, immune response to insulin of different species, or to insulin injection techniques; or (3) repeated trauma to the injection site from repeated needle usage.^4,23

In a study assessing the prevalence of lipohypertrophy and its relation to insulin technique, 49.1% of participants with lipohypertrophy had glycemic variability compared with 6.5% of participants without lipohypertrophy.³ Johansson and colleagues described an impairment of insulin absorption in lipohypertrophic tissues, causing a 25% lower plasma insulin concentration compared with that of normal tissues.⁴ These findings suggest a significant effect of lipohypertrophy on insulin absorption—unnecessarily increasing insulin consumption and worsening glycemic control.

Primary prevention measures include injection site inspection and patient education about rotation and abstaining from needle reuse.²² If a patient already has signs of lipohypertrophy, data supports education and insulin injection technique practice as simple and effective means to reduce insulin action variability and increase glycemic control.²⁴

Lipoatrophy. Lipoatrophy is described as a local loss of subcutaneous adipose tissue often in the face, buttocks, legs and arm regions and can be rooted in genetic, immune, or drug-associated etiologies.²⁵ Insulin-induced lipoatrophy is suspected to be the result of tumor necrosis factor-α hyperproduction in reaction to insulin crystal presence at the injection site.^26,27 Overall, lipoatrophy development has decreased since the use of recombinant human insulin and analog insulin therapy.²⁸ The decrease is hypothesized to be due to increased subcutaneous tissue absorption rate of human insulin and its analog, decreasing overall adipocyte exposure to localized high insulin concentration.²⁷ Treatments for same-site insulin-derived lipoatrophy include changing injection sites and preparation of insulin.²⁶ When injection into the lipoatrophic site was avoided, glycemic control and lipoatrophy appearance improved.²⁶

Amyloidosis. Amyloidosis indicates the presence of an extracellular bundle of insoluble polymeric protein fibrils in tissues and organs.²⁹ Insulin-induced amyloidosis presents as a hard mass or ball near the injection site.²⁹ Insulin is one of many hormones that can form amyloid fibrils, and there have been several dozen cases reported of amyloid formation at the site of insulin injection.^29-31 Although insulin-derived amyloidosis is rare, it may be misdiagnosed as lipohypertrophy due to a lack of histopathologic testing or general awareness of the complication.²⁹

In a case series of 7 patients with amyloidosis, all patients had a mean HbA_1c of 9.3% (range, 8.5-10.2%) and averaged 1 IU/kg bodyweight before intervention.³⁰ After the discovery of the mass, participants were instructed to avoid injection into the amyloidoma, and average insulin requirements decreased to 0.48 IU/kg body weight (P = .40).³⁰ Patients with amyloidosis who rotated their injection sites experienced better glycemic control and decreased insulin requirements.³⁰

Pathophysiology of Localized Insulin Resistance

Insulin regulates glucose homeostasis in skeletal muscle and adipose tissue, increases hepatic and adipocyte lipid synthesis, and decreases adipocyte fatty acid release.³² Generalized insulin resistance occurs when target tissues have decreased glucose uptake in response to circulating insulin.³² Insulin resistance increases the amount of free insulin in surrounding tissues. At high concentrations, insulin fosters tissue growth by binding to IGF-1 receptors, stimulating hypertrophy and reproduction of keratinocytes and fibroblasts.³³ This pathophysiology helps explain the origin of localized acanthosis nigricans at same-site insulin injections.

Conclusions

Cutaneous complications are a local adverse effect of long-term failure to rotate insulin injection sites. Our case serves as a call to action for HCPs to improve education regarding insulin injection-site rotation, conduct routine injection-site inspection, and actively document cases as they occur to increase public awareness of these important complications.

If a patient with DM presents with unexplained poor glycemic control, consider questioning the patient about injection-site location and how often they are rotating the insulin injection site. Inspect the site for cutaneous complications. Of note, if a patient has a cutaneous complication due to insulin injection, adjust or decrease the insulin dosage when rotating sites to mitigate the risk of hypoglycemic episodes.

Improvement of glycemic control, cosmetic appearance of injection site, and insulin use all begin with skin inspection, injection technique education, and periodic review by a HCP.

Insulin injection therapy is one of the most widely used health care interventions to manage both type 1 and type 2 diabetes mellitus (T1DM/T2DM). Globally, more than 150 to 200 million people inject insulin into their upper posterior arms, buttocks, anterior and lateral thighs, or abdomen.^1,2 In an ideal world, every patient would be using the correct site and rotating their insulin injection sites in accordance with health care professional (HCP) recommendations—systematic injections in one general body location, at least 1 cm away from the previous injection.² Unfortunately, same-site insulin injection (repeatedly in the same region within 1 cm of previous injections) is a common mistake made by patients with DM—in one study, 63% of participants either did not rotate sites correctly or failed to do so at all.

Insulin-resistant cutaneous complications may occur as a result of same-site insulin injections. The most common is lipohypertrophy, reported in some studies in nearly 50% of patients with DM on insulin therapy.⁴ Other common cutaneous complications include lipoatrophy and amyloidosis. Injection-site acanthosis nigricans, although uncommon, has been reported in 18 cases in the literature.

Most articles suggest that same-site insulin injections decrease local insulin sensitivity and result in tissue hypertrophy because of the anabolic properties of insulin and increase in insulin binding to insulin-like growth factor-1 (IGF-1) receptor.^5-20 The hyperkeratotic growth and varying insulin absorption rates associated with these cutaneous complications increase chances of either hyper- or hypoglycemic episodes in patients.^10,11,13 It is the responsibility of the DM care professional to provide proper insulin-injection technique education and perform routine inspection of injection sites to reduce cutaneous complications of insulin therapy. The purpose of this article is to (1) describe a case of acanthosis nigricans resulting from insulin injection at the same site; (2) review case reports in the literature describing injection-site acanthosis nigricans resulting from same-site insulin injections; (3) describe localized cutaneous complications associated with the use of insulin; and (4) discuss clinical implications and lessons learned from the literature.

Case Presentation

A 75-year-old patient with an 8-year history of T2DM, as well as stable coronary artery disease, atrial fibrillation, hypertension, hyperlipidemia, chronic obstructive pulmonary disease, and stage 3 chronic kidney disease, presented with 2 discrete abdominal hyperpigmented plaques. At the time of the initial clinic visit, the patient was taking metformin 1000 mg twice daily and insulin glargine 40 units once daily. When insulin was initiated 7 years prior, the patient received neutral protamine Hagedorn (NPH) insulin for the first year and transitioned to insulin glargine. After 4 years of insulin therapy, insulin aspart was added and discontinued after 2 years. The patient’s hemoglobin A_1c (HbA_1c) was 6.8%, suggesting good glycemic control.

The patient reported 5 years of progressive, asymptomatic hyperpigmentation of the skin surrounding his insulin glargine injection sites and injecting in these same sites daily without rotation. He reported no additional skin changes or symptoms. He had noticed no skin changes while using NPH insulin during his first year of insulin therapy. On examination, the abdominal wall skin demonstrated 2 well-demarcated, nearly black, soft, velvety plaques, measuring 9 × 8 cm on the left side and 4 × 3.5 cm on the right, suggesting acanthosis nigricans (Figure 1A). The remainder of the skin examination, including the flexures, was normal. Of note, the patient received biweekly intramuscular testosterone injections in the gluteal region for secondary hypogonadism with no adverse dermatologic effects. A skin punch biopsy was performed and revealed epidermal papillomatosis and hyperkeratosis, confirming the clinical diagnosis of acanthosis nigricans (Figure 2).

After a review of insulin-injection technique at his clinic visit, the patient started rotating insulin injection sites over his entire abdomen, and the acanthosis nigricans partially improved. A few months later, the patient stopped rotating the insulin injection site, and the acanthosis nigricans worsened again. Because of worsening glycemic control, the patient was then started on insulin aspart. He did not develop any skin changes at the insulin aspart injection site, although he was not rotating its site of injection.

Subsequently, with reeducation and proper injection-site rotation, the patient had resolution of his acanthosis nigricans (Figure 1b).

Discussion

A review of the literature revealed 18 reported cases of acanthosis nigricans at sites of repeated insulin injection (Table).^5-20 Acanthosis nigricans at the site of insulin injection afflicts patients of any age, with cases observed in patients aged 14 to 75 years. Sixteen (84%) of 19 cases were male. Fourteen cases (73%) had T2DM; the rest of the patients had T1DM. The duration of insulin injection therapy prior to onset ranged from immediate to 13 years (median 4 years). Fourteen cases (73%) were reported on the abdomen; however, other sites, such as thighs and upper arm, also were reported. Lesions size varied from 12 to 360 cm². Two cases had associated amyloidosis. The average HbA_1c reported at presentation was 10%. Following insulin injection-site rotation, most of the cases reported improvement of both glycemic control and acanthosis nigricans appearance.

In the case described by Kudo and colleagues, a 59-year-old male patient with T2DM had been injecting insulin into the same spot on his abdomen for 10 years. He developed acanthosis nigricans and an amyloidoma so large and firm that it bent the needle when he injected insulin.¹¹

Most of the cases we found in the literature were after 2005 and associated with the use of human or analog insulin. These cases may be related to a bias, as cases may be easier to find in digital archives in the later years, when human or analog insulins have been in common use. Also noteworthy, in cases that reported dosage, most were not very high, and the highest daily dose was 240 IU/d. Ten reports of injection-site acanthosis nigricans were in dermatology journals; only 5 reports were in endocrinology journals and 3 in general medical journals, indicating possible less awareness of this phenomenon in other HCPs who care for patients with DM.

Complications of Same-Site Injections

Acanthosis nigricans. Commonly found in the armpits, neck folds, and groin, acanthosis nigricans is known as one of the calling cards for insulin resistance, obesity, and hyperinsulinemia.²¹ Acanthosis nigricans can be seen in people with or without DM and is not limited to those on insulin therapy. However, same-site insulin injections for 4 to 6 years also may result in injection-site acanthosis nigricans–like lesions because of factors such as insulin exposure at the local tissue level.¹⁶

Acanthosis nigricans development is characterized by hyperpigmented, hyperkeratotic, velvety, and sometimes verrucous plaques.⁶ Acanthosis nigricans surrounding repeated injection sites is hypothesized to develop as a result of localized hyperinsulinemia secondary to insulin resistance, which increases the stimulation of IGF, thereby causing epidermal hypertrophy.^5-20 If insulin injection therapy continues to be administered through the acanthosis nigricans lesion, it results in decreased insulin absorption, leading to poor glycemic control.¹³

Acanthosis nigricans associated with insulin injection is reversible. After rotation of injection sites, lesions either decrease in size or severity of appearance.^5-8,11 Also, by avoiding injection into the hyperkeratotic plaques and using normal subcutaneous tissue for injection, patients’ response to insulin improves, as measured by HbA_1c and by decreased daily insulin requirement.^{6-8,10,12,18-20}

Lipohypertrophy. This is characterized by an increase in localized adipose tissue and is the most common cutaneous complication of insulin therapy.² Lipohypertrophy presents as a firm, rubbery mass in the location of same-site insulin injections.²² Development of lipohypertrophy is suspected to be the result of either (1) anabolic effect of insulin on local adipocytes, promoting fat and protein synthesis; (2) an autoimmune response by immunoglobulin (Ig) G or IgE antibodies to insulin, immune response to insulin of different species, or to insulin injection techniques; or (3) repeated trauma to the injection site from repeated needle usage.^4,23

In a study assessing the prevalence of lipohypertrophy and its relation to insulin technique, 49.1% of participants with lipohypertrophy had glycemic variability compared with 6.5% of participants without lipohypertrophy.³ Johansson and colleagues described an impairment of insulin absorption in lipohypertrophic tissues, causing a 25% lower plasma insulin concentration compared with that of normal tissues.⁴ These findings suggest a significant effect of lipohypertrophy on insulin absorption—unnecessarily increasing insulin consumption and worsening glycemic control.

Primary prevention measures include injection site inspection and patient education about rotation and abstaining from needle reuse.²² If a patient already has signs of lipohypertrophy, data supports education and insulin injection technique practice as simple and effective means to reduce insulin action variability and increase glycemic control.²⁴

Lipoatrophy. Lipoatrophy is described as a local loss of subcutaneous adipose tissue often in the face, buttocks, legs and arm regions and can be rooted in genetic, immune, or drug-associated etiologies.²⁵ Insulin-induced lipoatrophy is suspected to be the result of tumor necrosis factor-α hyperproduction in reaction to insulin crystal presence at the injection site.^26,27 Overall, lipoatrophy development has decreased since the use of recombinant human insulin and analog insulin therapy.²⁸ The decrease is hypothesized to be due to increased subcutaneous tissue absorption rate of human insulin and its analog, decreasing overall adipocyte exposure to localized high insulin concentration.²⁷ Treatments for same-site insulin-derived lipoatrophy include changing injection sites and preparation of insulin.²⁶ When injection into the lipoatrophic site was avoided, glycemic control and lipoatrophy appearance improved.²⁶

Amyloidosis. Amyloidosis indicates the presence of an extracellular bundle of insoluble polymeric protein fibrils in tissues and organs.²⁹ Insulin-induced amyloidosis presents as a hard mass or ball near the injection site.²⁹ Insulin is one of many hormones that can form amyloid fibrils, and there have been several dozen cases reported of amyloid formation at the site of insulin injection.^29-31 Although insulin-derived amyloidosis is rare, it may be misdiagnosed as lipohypertrophy due to a lack of histopathologic testing or general awareness of the complication.²⁹

In a case series of 7 patients with amyloidosis, all patients had a mean HbA_1c of 9.3% (range, 8.5-10.2%) and averaged 1 IU/kg bodyweight before intervention.³⁰ After the discovery of the mass, participants were instructed to avoid injection into the amyloidoma, and average insulin requirements decreased to 0.48 IU/kg body weight (P = .40).³⁰ Patients with amyloidosis who rotated their injection sites experienced better glycemic control and decreased insulin requirements.³⁰

Pathophysiology of Localized Insulin Resistance

Insulin regulates glucose homeostasis in skeletal muscle and adipose tissue, increases hepatic and adipocyte lipid synthesis, and decreases adipocyte fatty acid release.³² Generalized insulin resistance occurs when target tissues have decreased glucose uptake in response to circulating insulin.³² Insulin resistance increases the amount of free insulin in surrounding tissues. At high concentrations, insulin fosters tissue growth by binding to IGF-1 receptors, stimulating hypertrophy and reproduction of keratinocytes and fibroblasts.³³ This pathophysiology helps explain the origin of localized acanthosis nigricans at same-site insulin injections.

Conclusions

Cutaneous complications are a local adverse effect of long-term failure to rotate insulin injection sites. Our case serves as a call to action for HCPs to improve education regarding insulin injection-site rotation, conduct routine injection-site inspection, and actively document cases as they occur to increase public awareness of these important complications.

If a patient with DM presents with unexplained poor glycemic control, consider questioning the patient about injection-site location and how often they are rotating the insulin injection site. Inspect the site for cutaneous complications. Of note, if a patient has a cutaneous complication due to insulin injection, adjust or decrease the insulin dosage when rotating sites to mitigate the risk of hypoglycemic episodes.

Improvement of glycemic control, cosmetic appearance of injection site, and insulin use all begin with skin inspection, injection technique education, and periodic review by a HCP.

Dupilumab Reduces Oral Corticosteroid Use in Patients With Corticosteroid-Dependent Severe Asthma. By Lawrence D. Sher, MD, et al.

Carriage and Transmission of Macrolide Resistance Genes in Patients With Chronic Respiratory Conditions and Their Close Contacts. By Yiming Wang, MSc, et al.

An Evaluation of Factors That Influence Referral to Pulmonary Rehabilitation Programs Among People With COPD. By Sarah Hug, BSc, et al.

Prevalence and Outcomes of Previously Healthy Adults Among Patients Hospitalized With Community-Onset Sepsis. By Mohammad Alrawashdeh, PhD, MSN, et al.

Screening Strategies for Pulmonary Hypertension in Patients With Interstitial Lung Disease: A Multidisciplinary Delphi Study. By Franck F. Rahaghi, MD, et al.

Race- and Ethnicity-Based Spirometry Reference Equations: Are They Accurate for Genetically Admixed Children? By Jonathan Witonsky, MD, et al.

No VTE Recurrence After 1-Year Follow Up of Hospitalized Patients With COVID-19 and a VTE Event: A Prospective Study. By Maxime Delrue, MD, PhD, et al.
 

Patient Perspectives on Longitudinal Adherence to Lung Cancer Screening. By Anna Holman, BS, et al.

Dupilumab Reduces Oral Corticosteroid Use in Patients With Corticosteroid-Dependent Severe Asthma. By Lawrence D. Sher, MD, et al.

Carriage and Transmission of Macrolide Resistance Genes in Patients With Chronic Respiratory Conditions and Their Close Contacts. By Yiming Wang, MSc, et al.

An Evaluation of Factors That Influence Referral to Pulmonary Rehabilitation Programs Among People With COPD. By Sarah Hug, BSc, et al.

Prevalence and Outcomes of Previously Healthy Adults Among Patients Hospitalized With Community-Onset Sepsis. By Mohammad Alrawashdeh, PhD, MSN, et al.

Screening Strategies for Pulmonary Hypertension in Patients With Interstitial Lung Disease: A Multidisciplinary Delphi Study. By Franck F. Rahaghi, MD, et al.

Race- and Ethnicity-Based Spirometry Reference Equations: Are They Accurate for Genetically Admixed Children? By Jonathan Witonsky, MD, et al.

No VTE Recurrence After 1-Year Follow Up of Hospitalized Patients With COVID-19 and a VTE Event: A Prospective Study. By Maxime Delrue, MD, PhD, et al.
 

Patient Perspectives on Longitudinal Adherence to Lung Cancer Screening. By Anna Holman, BS, et al.

Dupilumab Reduces Oral Corticosteroid Use in Patients With Corticosteroid-Dependent Severe Asthma. By Lawrence D. Sher, MD, et al.

Carriage and Transmission of Macrolide Resistance Genes in Patients With Chronic Respiratory Conditions and Their Close Contacts. By Yiming Wang, MSc, et al.

An Evaluation of Factors That Influence Referral to Pulmonary Rehabilitation Programs Among People With COPD. By Sarah Hug, BSc, et al.

Prevalence and Outcomes of Previously Healthy Adults Among Patients Hospitalized With Community-Onset Sepsis. By Mohammad Alrawashdeh, PhD, MSN, et al.

Screening Strategies for Pulmonary Hypertension in Patients With Interstitial Lung Disease: A Multidisciplinary Delphi Study. By Franck F. Rahaghi, MD, et al.

Race- and Ethnicity-Based Spirometry Reference Equations: Are They Accurate for Genetically Admixed Children? By Jonathan Witonsky, MD, et al.

No VTE Recurrence After 1-Year Follow Up of Hospitalized Patients With COVID-19 and a VTE Event: A Prospective Study. By Maxime Delrue, MD, PhD, et al.
 

Patient Perspectives on Longitudinal Adherence to Lung Cancer Screening. By Anna Holman, BS, et al.

After years of remote learning from behind computer screens, we’re kicking off the in-person CHEST 2022 meeting in Nashville, Tennessee, with a bang—or, more accurately, with a step kick, swivel, and stomp—at the Wildhorse Saloon.

The Wildhorse is famous for hosting daily line dancing lessons on the largest dance floor in the downtown area and for having a menu full of Nashville favorites, including Nashville hot chicken and a hearty selection of entrees (as well as a decadent bananas foster) with a “Jack Daniels” single barrel whiskey glaze.

The opening reception offers attendees the opportunity to relax and reconnect with their peers from across the fields of pulmonary, critical care, and sleep medicine before the jam-packed schedule of more than 300 educational sessions starts the following day.

But the fun doesn’t stop there. Attendees interested in exploring the city after hours have a host of options, from world-class music venues to iconic distilleries and restaurants. The Music City Center, where CHEST 2022 will be held, is located in the SoBro neighborhood of Nashville, not far from the Arts District, Downtown, and Music Row.

According to Nashville local and CHEST member Meredith Pugh, MD, MSCI, “it goes without saying that we have the best music scene in the country, but it’s a great place for outdoor activities and food.”

For those who don’t get their fill at the Wildhorse, Dr. Pugh recommends attendees check out the Assembly Food Hall (.3 miles from the convention center) to try the city’s famous Nashville Hot Chicken and a variety of other local options. And, don’t miss the many excellent options for BBQ. Fellow Nashville transplant and CHEST member Todd Rice, MD, FCCP, suggests Martin’s Bar-B-Que Joint and Jack’s Bar-B-Que—both within walking distance of the Music City Center—as well as other local options.

To learn more about everything Nashville has to offer, and get more recommendations from Drs. Rice and Pugh, check out the latest CHEST 2022 blog on chestnet.org

After years of remote learning from behind computer screens, we’re kicking off the in-person CHEST 2022 meeting in Nashville, Tennessee, with a bang—or, more accurately, with a step kick, swivel, and stomp—at the Wildhorse Saloon.

The Wildhorse is famous for hosting daily line dancing lessons on the largest dance floor in the downtown area and for having a menu full of Nashville favorites, including Nashville hot chicken and a hearty selection of entrees (as well as a decadent bananas foster) with a “Jack Daniels” single barrel whiskey glaze.

The opening reception offers attendees the opportunity to relax and reconnect with their peers from across the fields of pulmonary, critical care, and sleep medicine before the jam-packed schedule of more than 300 educational sessions starts the following day.

But the fun doesn’t stop there. Attendees interested in exploring the city after hours have a host of options, from world-class music venues to iconic distilleries and restaurants. The Music City Center, where CHEST 2022 will be held, is located in the SoBro neighborhood of Nashville, not far from the Arts District, Downtown, and Music Row.

According to Nashville local and CHEST member Meredith Pugh, MD, MSCI, “it goes without saying that we have the best music scene in the country, but it’s a great place for outdoor activities and food.”

For those who don’t get their fill at the Wildhorse, Dr. Pugh recommends attendees check out the Assembly Food Hall (.3 miles from the convention center) to try the city’s famous Nashville Hot Chicken and a variety of other local options. And, don’t miss the many excellent options for BBQ. Fellow Nashville transplant and CHEST member Todd Rice, MD, FCCP, suggests Martin’s Bar-B-Que Joint and Jack’s Bar-B-Que—both within walking distance of the Music City Center—as well as other local options.

To learn more about everything Nashville has to offer, and get more recommendations from Drs. Rice and Pugh, check out the latest CHEST 2022 blog on chestnet.org

After years of remote learning from behind computer screens, we’re kicking off the in-person CHEST 2022 meeting in Nashville, Tennessee, with a bang—or, more accurately, with a step kick, swivel, and stomp—at the Wildhorse Saloon.

The Wildhorse is famous for hosting daily line dancing lessons on the largest dance floor in the downtown area and for having a menu full of Nashville favorites, including Nashville hot chicken and a hearty selection of entrees (as well as a decadent bananas foster) with a “Jack Daniels” single barrel whiskey glaze.

The opening reception offers attendees the opportunity to relax and reconnect with their peers from across the fields of pulmonary, critical care, and sleep medicine before the jam-packed schedule of more than 300 educational sessions starts the following day.

But the fun doesn’t stop there. Attendees interested in exploring the city after hours have a host of options, from world-class music venues to iconic distilleries and restaurants. The Music City Center, where CHEST 2022 will be held, is located in the SoBro neighborhood of Nashville, not far from the Arts District, Downtown, and Music Row.

According to Nashville local and CHEST member Meredith Pugh, MD, MSCI, “it goes without saying that we have the best music scene in the country, but it’s a great place for outdoor activities and food.”

For those who don’t get their fill at the Wildhorse, Dr. Pugh recommends attendees check out the Assembly Food Hall (.3 miles from the convention center) to try the city’s famous Nashville Hot Chicken and a variety of other local options. And, don’t miss the many excellent options for BBQ. Fellow Nashville transplant and CHEST member Todd Rice, MD, FCCP, suggests Martin’s Bar-B-Que Joint and Jack’s Bar-B-Que—both within walking distance of the Music City Center—as well as other local options.

To learn more about everything Nashville has to offer, and get more recommendations from Drs. Rice and Pugh, check out the latest CHEST 2022 blog on chestnet.org