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Will this trial help solve chronic back pain?
Chronic pain, and back pain in particular, is among the most frequent concerns for patients in the primary care setting. Roughly 8% of adults in the United States say they suffer from chronic low back pain, and many of them say the pain is significant enough to impair their ability to move, work, and otherwise enjoy life. All this, despite decades of research and countless millions in funding to find the optimal approach to treating chronic pain.
As the United States crawls out of the opioid epidemic, a group of pain specialists is hoping to identify effective, personalized approaches to managing back pain. Daniel Clauw, MD, professor of anesthesiology, internal medicine, and psychiatry at the University of Michigan, Ann Arbor, is helping lead the BEST trial. With projected enrollment of nearly 800 patients, BEST will be the largest federally funded clinical trial of interventions to treat chronic low back pain.
In an interview, The interview has been edited for length and clarity.
What are your thoughts on the current state of primary care physicians’ understanding and management of pain?
Primary care physicians need a lot of help in demystifying the diagnosis and treatment of any kind of pain, but back pain is a really good place to start. When it comes to back pain, most primary care physicians are not any more knowledgeable than a layperson.
What has the opioid debacle-cum-tragedy taught you about pain management, particular as regards people with chronic pain?
I don’t feel opioids should ever be used to treat chronic low back pain. The few long-term studies that have been performed using opioids for longer than 3 months suggest that they often make pain worse rather than just failing to make pain better – and we know they are associated with a significantly increased all-cause mortality with increased deaths from myocardial infarction, accidents, and suicides, in addition to overdose.
Given how many patients experience back pain, how did we come to the point at which primary care physicians are so ill equipped?
We’ve had terrible pain curricula in medical schools. To give you an example: I’m one of the leading pain experts in the world and I’m not allowed to teach our medical students their pain curriculum. The students learn about neurophysiology and the anatomy of the nerves, not what’s relevant in pain.
This is notorious in medical school: Curricula are almost impossible to modify and change. So it starts with poor training in medical school. And then, regardless of what education they do or don’t get in medical school, a lot of their education about pain management is through our residencies – mainly in inpatient settings, where you’re really seeing the management of acute pain and not the management of chronic pain.
People get more accustomed to managing acute pain, where opioids are a reasonable option. It’s just that when you start managing subacute or chronic pain, opioids don’t work as well.
The other big problem is that historically, most people trained in medicine think that if you have pain in your elbow, there’s got to be something wrong in your elbow. This third mechanism of pain, central sensitization – or nociplastic pain – the kind of pain that we see in fibromyalgia, headache, and low back pain, where the pain is coming from the brain – that’s confusing to people. People can have pain without any damage or inflammation to that region of the body.
Physicians are trained that if there’s pain, there’s something wrong and we have to do surgery or there’s been some trauma. Most chronic pain is none of that. There’s a big disconnect between how people are trained, and then when they go out and are seeing a tremendous number of people with chronic pain.
What are the different types of pain, and how should they inform clinicians’ understanding about what approaches might work for managing their patients in pain?
The way the central nervous system responds to pain is analogous to the loudness of an electric guitar. You can make an electric guitar louder either by strumming the strings harder or by turning up the amplifier. For many people with fibromyalgia, low back pain, and endometriosis, for example, the problem is really more that the amplifier is turned up too high rather than its being that the guitar is strummed too strongly. That kind of pain where the pain is not due to anatomic damage or inflammation is particularly flummoxing for providers.
Can you explain the design of the new study?
It’s a 13-site study looking at four treatments: enhanced self-care, cognitive-behavioral therapy, physical therapy, and duloxetine. It’s a big precision medicine trial, trying to take everything we’ve learned and putting it all into one big study.
We’re using a SMART design, which randomizes people to two of those treatments, unless they are very much improved from the first treatment. To be eligible for the trial, you have to be able to be randomized to three of the four treatments, and people can’t choose which of the four they get.
We give them one of those treatments for 12 weeks, and at the end of 12 weeks we make the call – “Did you respond or not respond?” – and then we go back to the phenotypic data we collected at the beginning of that trial and say, “What information at baseline that we collected predicts that someone is going to respond better to duloxetine or worse to duloxetine?” And then we create the phenotype that responds best to each of those four treatments.
None of our treatments works so well that someone doesn’t end up getting randomized to a second treatment. About 85% of people so far need a second treatment because they still have enough pain that they want more relief. But the nice thing about that is we’ve already done all the functional brain imaging and all these really expensive and time-consuming things.
We’re hoping to have around 700-800 people total in this trial, which means that around 170 people will get randomized to each of the four initial treatments. No one’s ever done a study that has functional brain imaging and all these other things in it with more than 80 or 100 people. The scale of this is totally unprecedented.
Given that the individual therapies don’t appear to be all that successful on their own, what is your goal?
The primary aim is to match the phenotypic characteristics of a patient with chronic low back pain with treatment response to each of these four treatments. So at the end, we can give clinicians information on which of the patients is going to respond to physical therapy, for instance.
Right now, about one out of three people respond to most treatments for pain. We think by doing a trial like this, we can take treatments that work in one out of three people and make them work in one out of two or two out of three people just by using them in the right people.
How do you differentiate between these types of pain in your study?
We phenotype people by asking them a number of questions. We also do brain imaging, look at their back with MRI, test biomechanics, and then give them four different treatments that we know work in groups of people with low back pain.
We think one of the first parts of the phenotype is, do they have pain just in their back? Or do they have pain in their back plus a lot of other body regions? Because the more body regions that people have pain in, the more likely it is that this is an amplifier problem rather than a guitar problem.
Treatments like physical therapy, surgery, and injections are going to work better for people in whom the pain is a guitar problem rather than an amplifier problem. And drugs like duloxetine, which works in the brain, and cognitive-behavioral therapy are going to work a lot better in the people with pain in multiple sites besides the back.
To pick up on your metaphor, do any symptoms help clinicians differentiate between the guitar and the amplifier?
Sleep problems, fatigue, memory problems, and mood problems are common in patients with chronic pain and are more common with amplifier pain. Because again, those are all central nervous system problems. And so we see that the people that have anxiety, depression, and a lot of distress are more likely to have this kind of pain.
Does medical imaging help?
There’s a terrible relationship between what you see on an MRI of the back and whether someone has pain or how severe the pain is going to be. There’s always going to be individuals that have a lot of anatomic damage who don’t have any pain because they happen to be on the other end of the continuum from fibromyalgia; they’re actually pain-insensitive people.
What are your thoughts about ketamine as a possible treatment for chronic pain?
I have a mentee who’s doing a ketamine trial. We’re doing psilocybin trials in patients with fibromyalgia. Ketamine is such a dirty drug; it has so many different mechanisms of action. It does have some psychedelic effects, but it also is an NMDA blocker. It really has so many different effects.
I think it’s being thrown around like water in settings where we don’t yet know it to be efficacious. Even the data in treatment-refractory depression are pretty weak, but we’re so desperate to do something for those patients. If you’re trying to harness the psychedelic properties of ketamine, I think there’s other psychedelics that are a lot more interesting, which is why we’re using psilocybin for a subset of patients. Most of us in the pain field think that the psychedelics will work best for the people with chronic pain who have a lot of comorbid psychiatric illness, especially the ones with a lot of trauma. These drugs will allow us therapeutically to get at a lot of these patients with the side-by-side psychotherapy that’s being done as people are getting care in the medicalized setting.
Dr. Clauw reported conflicts of interest with Pfizer, Tonix, Theravance, Zynerba, Samumed, Aptinyx, Daiichi Sankyo, Intec, Regeneron, Teva, Lundbeck, Virios, and Cerephex.
A version of this article first appeared on Medscape.com.
Chronic pain, and back pain in particular, is among the most frequent concerns for patients in the primary care setting. Roughly 8% of adults in the United States say they suffer from chronic low back pain, and many of them say the pain is significant enough to impair their ability to move, work, and otherwise enjoy life. All this, despite decades of research and countless millions in funding to find the optimal approach to treating chronic pain.
As the United States crawls out of the opioid epidemic, a group of pain specialists is hoping to identify effective, personalized approaches to managing back pain. Daniel Clauw, MD, professor of anesthesiology, internal medicine, and psychiatry at the University of Michigan, Ann Arbor, is helping lead the BEST trial. With projected enrollment of nearly 800 patients, BEST will be the largest federally funded clinical trial of interventions to treat chronic low back pain.
In an interview, The interview has been edited for length and clarity.
What are your thoughts on the current state of primary care physicians’ understanding and management of pain?
Primary care physicians need a lot of help in demystifying the diagnosis and treatment of any kind of pain, but back pain is a really good place to start. When it comes to back pain, most primary care physicians are not any more knowledgeable than a layperson.
What has the opioid debacle-cum-tragedy taught you about pain management, particular as regards people with chronic pain?
I don’t feel opioids should ever be used to treat chronic low back pain. The few long-term studies that have been performed using opioids for longer than 3 months suggest that they often make pain worse rather than just failing to make pain better – and we know they are associated with a significantly increased all-cause mortality with increased deaths from myocardial infarction, accidents, and suicides, in addition to overdose.
Given how many patients experience back pain, how did we come to the point at which primary care physicians are so ill equipped?
We’ve had terrible pain curricula in medical schools. To give you an example: I’m one of the leading pain experts in the world and I’m not allowed to teach our medical students their pain curriculum. The students learn about neurophysiology and the anatomy of the nerves, not what’s relevant in pain.
This is notorious in medical school: Curricula are almost impossible to modify and change. So it starts with poor training in medical school. And then, regardless of what education they do or don’t get in medical school, a lot of their education about pain management is through our residencies – mainly in inpatient settings, where you’re really seeing the management of acute pain and not the management of chronic pain.
People get more accustomed to managing acute pain, where opioids are a reasonable option. It’s just that when you start managing subacute or chronic pain, opioids don’t work as well.
The other big problem is that historically, most people trained in medicine think that if you have pain in your elbow, there’s got to be something wrong in your elbow. This third mechanism of pain, central sensitization – or nociplastic pain – the kind of pain that we see in fibromyalgia, headache, and low back pain, where the pain is coming from the brain – that’s confusing to people. People can have pain without any damage or inflammation to that region of the body.
Physicians are trained that if there’s pain, there’s something wrong and we have to do surgery or there’s been some trauma. Most chronic pain is none of that. There’s a big disconnect between how people are trained, and then when they go out and are seeing a tremendous number of people with chronic pain.
What are the different types of pain, and how should they inform clinicians’ understanding about what approaches might work for managing their patients in pain?
The way the central nervous system responds to pain is analogous to the loudness of an electric guitar. You can make an electric guitar louder either by strumming the strings harder or by turning up the amplifier. For many people with fibromyalgia, low back pain, and endometriosis, for example, the problem is really more that the amplifier is turned up too high rather than its being that the guitar is strummed too strongly. That kind of pain where the pain is not due to anatomic damage or inflammation is particularly flummoxing for providers.
Can you explain the design of the new study?
It’s a 13-site study looking at four treatments: enhanced self-care, cognitive-behavioral therapy, physical therapy, and duloxetine. It’s a big precision medicine trial, trying to take everything we’ve learned and putting it all into one big study.
We’re using a SMART design, which randomizes people to two of those treatments, unless they are very much improved from the first treatment. To be eligible for the trial, you have to be able to be randomized to three of the four treatments, and people can’t choose which of the four they get.
We give them one of those treatments for 12 weeks, and at the end of 12 weeks we make the call – “Did you respond or not respond?” – and then we go back to the phenotypic data we collected at the beginning of that trial and say, “What information at baseline that we collected predicts that someone is going to respond better to duloxetine or worse to duloxetine?” And then we create the phenotype that responds best to each of those four treatments.
None of our treatments works so well that someone doesn’t end up getting randomized to a second treatment. About 85% of people so far need a second treatment because they still have enough pain that they want more relief. But the nice thing about that is we’ve already done all the functional brain imaging and all these really expensive and time-consuming things.
We’re hoping to have around 700-800 people total in this trial, which means that around 170 people will get randomized to each of the four initial treatments. No one’s ever done a study that has functional brain imaging and all these other things in it with more than 80 or 100 people. The scale of this is totally unprecedented.
Given that the individual therapies don’t appear to be all that successful on their own, what is your goal?
The primary aim is to match the phenotypic characteristics of a patient with chronic low back pain with treatment response to each of these four treatments. So at the end, we can give clinicians information on which of the patients is going to respond to physical therapy, for instance.
Right now, about one out of three people respond to most treatments for pain. We think by doing a trial like this, we can take treatments that work in one out of three people and make them work in one out of two or two out of three people just by using them in the right people.
How do you differentiate between these types of pain in your study?
We phenotype people by asking them a number of questions. We also do brain imaging, look at their back with MRI, test biomechanics, and then give them four different treatments that we know work in groups of people with low back pain.
We think one of the first parts of the phenotype is, do they have pain just in their back? Or do they have pain in their back plus a lot of other body regions? Because the more body regions that people have pain in, the more likely it is that this is an amplifier problem rather than a guitar problem.
Treatments like physical therapy, surgery, and injections are going to work better for people in whom the pain is a guitar problem rather than an amplifier problem. And drugs like duloxetine, which works in the brain, and cognitive-behavioral therapy are going to work a lot better in the people with pain in multiple sites besides the back.
To pick up on your metaphor, do any symptoms help clinicians differentiate between the guitar and the amplifier?
Sleep problems, fatigue, memory problems, and mood problems are common in patients with chronic pain and are more common with amplifier pain. Because again, those are all central nervous system problems. And so we see that the people that have anxiety, depression, and a lot of distress are more likely to have this kind of pain.
Does medical imaging help?
There’s a terrible relationship between what you see on an MRI of the back and whether someone has pain or how severe the pain is going to be. There’s always going to be individuals that have a lot of anatomic damage who don’t have any pain because they happen to be on the other end of the continuum from fibromyalgia; they’re actually pain-insensitive people.
What are your thoughts about ketamine as a possible treatment for chronic pain?
I have a mentee who’s doing a ketamine trial. We’re doing psilocybin trials in patients with fibromyalgia. Ketamine is such a dirty drug; it has so many different mechanisms of action. It does have some psychedelic effects, but it also is an NMDA blocker. It really has so many different effects.
I think it’s being thrown around like water in settings where we don’t yet know it to be efficacious. Even the data in treatment-refractory depression are pretty weak, but we’re so desperate to do something for those patients. If you’re trying to harness the psychedelic properties of ketamine, I think there’s other psychedelics that are a lot more interesting, which is why we’re using psilocybin for a subset of patients. Most of us in the pain field think that the psychedelics will work best for the people with chronic pain who have a lot of comorbid psychiatric illness, especially the ones with a lot of trauma. These drugs will allow us therapeutically to get at a lot of these patients with the side-by-side psychotherapy that’s being done as people are getting care in the medicalized setting.
Dr. Clauw reported conflicts of interest with Pfizer, Tonix, Theravance, Zynerba, Samumed, Aptinyx, Daiichi Sankyo, Intec, Regeneron, Teva, Lundbeck, Virios, and Cerephex.
A version of this article first appeared on Medscape.com.
Chronic pain, and back pain in particular, is among the most frequent concerns for patients in the primary care setting. Roughly 8% of adults in the United States say they suffer from chronic low back pain, and many of them say the pain is significant enough to impair their ability to move, work, and otherwise enjoy life. All this, despite decades of research and countless millions in funding to find the optimal approach to treating chronic pain.
As the United States crawls out of the opioid epidemic, a group of pain specialists is hoping to identify effective, personalized approaches to managing back pain. Daniel Clauw, MD, professor of anesthesiology, internal medicine, and psychiatry at the University of Michigan, Ann Arbor, is helping lead the BEST trial. With projected enrollment of nearly 800 patients, BEST will be the largest federally funded clinical trial of interventions to treat chronic low back pain.
In an interview, The interview has been edited for length and clarity.
What are your thoughts on the current state of primary care physicians’ understanding and management of pain?
Primary care physicians need a lot of help in demystifying the diagnosis and treatment of any kind of pain, but back pain is a really good place to start. When it comes to back pain, most primary care physicians are not any more knowledgeable than a layperson.
What has the opioid debacle-cum-tragedy taught you about pain management, particular as regards people with chronic pain?
I don’t feel opioids should ever be used to treat chronic low back pain. The few long-term studies that have been performed using opioids for longer than 3 months suggest that they often make pain worse rather than just failing to make pain better – and we know they are associated with a significantly increased all-cause mortality with increased deaths from myocardial infarction, accidents, and suicides, in addition to overdose.
Given how many patients experience back pain, how did we come to the point at which primary care physicians are so ill equipped?
We’ve had terrible pain curricula in medical schools. To give you an example: I’m one of the leading pain experts in the world and I’m not allowed to teach our medical students their pain curriculum. The students learn about neurophysiology and the anatomy of the nerves, not what’s relevant in pain.
This is notorious in medical school: Curricula are almost impossible to modify and change. So it starts with poor training in medical school. And then, regardless of what education they do or don’t get in medical school, a lot of their education about pain management is through our residencies – mainly in inpatient settings, where you’re really seeing the management of acute pain and not the management of chronic pain.
People get more accustomed to managing acute pain, where opioids are a reasonable option. It’s just that when you start managing subacute or chronic pain, opioids don’t work as well.
The other big problem is that historically, most people trained in medicine think that if you have pain in your elbow, there’s got to be something wrong in your elbow. This third mechanism of pain, central sensitization – or nociplastic pain – the kind of pain that we see in fibromyalgia, headache, and low back pain, where the pain is coming from the brain – that’s confusing to people. People can have pain without any damage or inflammation to that region of the body.
Physicians are trained that if there’s pain, there’s something wrong and we have to do surgery or there’s been some trauma. Most chronic pain is none of that. There’s a big disconnect between how people are trained, and then when they go out and are seeing a tremendous number of people with chronic pain.
What are the different types of pain, and how should they inform clinicians’ understanding about what approaches might work for managing their patients in pain?
The way the central nervous system responds to pain is analogous to the loudness of an electric guitar. You can make an electric guitar louder either by strumming the strings harder or by turning up the amplifier. For many people with fibromyalgia, low back pain, and endometriosis, for example, the problem is really more that the amplifier is turned up too high rather than its being that the guitar is strummed too strongly. That kind of pain where the pain is not due to anatomic damage or inflammation is particularly flummoxing for providers.
Can you explain the design of the new study?
It’s a 13-site study looking at four treatments: enhanced self-care, cognitive-behavioral therapy, physical therapy, and duloxetine. It’s a big precision medicine trial, trying to take everything we’ve learned and putting it all into one big study.
We’re using a SMART design, which randomizes people to two of those treatments, unless they are very much improved from the first treatment. To be eligible for the trial, you have to be able to be randomized to three of the four treatments, and people can’t choose which of the four they get.
We give them one of those treatments for 12 weeks, and at the end of 12 weeks we make the call – “Did you respond or not respond?” – and then we go back to the phenotypic data we collected at the beginning of that trial and say, “What information at baseline that we collected predicts that someone is going to respond better to duloxetine or worse to duloxetine?” And then we create the phenotype that responds best to each of those four treatments.
None of our treatments works so well that someone doesn’t end up getting randomized to a second treatment. About 85% of people so far need a second treatment because they still have enough pain that they want more relief. But the nice thing about that is we’ve already done all the functional brain imaging and all these really expensive and time-consuming things.
We’re hoping to have around 700-800 people total in this trial, which means that around 170 people will get randomized to each of the four initial treatments. No one’s ever done a study that has functional brain imaging and all these other things in it with more than 80 or 100 people. The scale of this is totally unprecedented.
Given that the individual therapies don’t appear to be all that successful on their own, what is your goal?
The primary aim is to match the phenotypic characteristics of a patient with chronic low back pain with treatment response to each of these four treatments. So at the end, we can give clinicians information on which of the patients is going to respond to physical therapy, for instance.
Right now, about one out of three people respond to most treatments for pain. We think by doing a trial like this, we can take treatments that work in one out of three people and make them work in one out of two or two out of three people just by using them in the right people.
How do you differentiate between these types of pain in your study?
We phenotype people by asking them a number of questions. We also do brain imaging, look at their back with MRI, test biomechanics, and then give them four different treatments that we know work in groups of people with low back pain.
We think one of the first parts of the phenotype is, do they have pain just in their back? Or do they have pain in their back plus a lot of other body regions? Because the more body regions that people have pain in, the more likely it is that this is an amplifier problem rather than a guitar problem.
Treatments like physical therapy, surgery, and injections are going to work better for people in whom the pain is a guitar problem rather than an amplifier problem. And drugs like duloxetine, which works in the brain, and cognitive-behavioral therapy are going to work a lot better in the people with pain in multiple sites besides the back.
To pick up on your metaphor, do any symptoms help clinicians differentiate between the guitar and the amplifier?
Sleep problems, fatigue, memory problems, and mood problems are common in patients with chronic pain and are more common with amplifier pain. Because again, those are all central nervous system problems. And so we see that the people that have anxiety, depression, and a lot of distress are more likely to have this kind of pain.
Does medical imaging help?
There’s a terrible relationship between what you see on an MRI of the back and whether someone has pain or how severe the pain is going to be. There’s always going to be individuals that have a lot of anatomic damage who don’t have any pain because they happen to be on the other end of the continuum from fibromyalgia; they’re actually pain-insensitive people.
What are your thoughts about ketamine as a possible treatment for chronic pain?
I have a mentee who’s doing a ketamine trial. We’re doing psilocybin trials in patients with fibromyalgia. Ketamine is such a dirty drug; it has so many different mechanisms of action. It does have some psychedelic effects, but it also is an NMDA blocker. It really has so many different effects.
I think it’s being thrown around like water in settings where we don’t yet know it to be efficacious. Even the data in treatment-refractory depression are pretty weak, but we’re so desperate to do something for those patients. If you’re trying to harness the psychedelic properties of ketamine, I think there’s other psychedelics that are a lot more interesting, which is why we’re using psilocybin for a subset of patients. Most of us in the pain field think that the psychedelics will work best for the people with chronic pain who have a lot of comorbid psychiatric illness, especially the ones with a lot of trauma. These drugs will allow us therapeutically to get at a lot of these patients with the side-by-side psychotherapy that’s being done as people are getting care in the medicalized setting.
Dr. Clauw reported conflicts of interest with Pfizer, Tonix, Theravance, Zynerba, Samumed, Aptinyx, Daiichi Sankyo, Intec, Regeneron, Teva, Lundbeck, Virios, and Cerephex.
A version of this article first appeared on Medscape.com.
Why doctors should take end-of-life decisions back from insurers, says physician
Sadly, the medical business has descended to this: Some insurers are combing health records to find and target customers with a 50% chance of dying in the next 18 months. Those companies then work to persuade customers to switch into palliative and hospice care.
And more of this automated end-of-life medicine appears to be on the way.
What’s gained is cost savings. What’s lost is empathy and humanity.
Doctor colleagues have warned for decades about the rise of the bean-counters in medicine. Yes, health care is a business, but it should be a higher calling, too. We serve, we heal, we protect, and we comfort.
There are times, however, when the people who try to squeeze the most money out of medicine try to gain too much influence over the people who actually engage in medicine. I think the rise of phone bank boiler rooms, built on business incentives to move patients into cheaper hospice care, should be a bridge too far for our profession.
End-of-life care is one of the most sensitive and emotionally rewarding things a doctor can do. Hospice can be an excellent choice for fully informed patients and families, but we should not be turning over these decisions to artificial intelligence, spreadsheets, and crunchers of big data.
At the same time, we should realize that the end-of-life phone banks have not evolved from nowhere. The reality is that dying is expensive. The last year of life accounts for 13%-25% of all spending on Medicare, according to numerous studies. That’s more than $200 billion a year for just one part of one federal health care program. Much of that money goes to hospitals, where end-of-life patients amass average charges of $6,000 per day.
All this spending runs counter to the wishes of most Americans. According to a Kaiser Family Foundation poll, 9 out of 10 adults say they don’t want their families to be burdened financially by their end-of-life medical care. Given the choice, 7 out of 10 Americans say they want to die at home; fewer than 1 in 10 say they want to die in a hospital.
And far more people (71%) think it’s more important to die without pain or stress than to extend life as long as possible (19%).
It’s crucial for us to get this right. Within 11 years, the U.S. Census projects that seniors will outnumber kids for the first time in history: We’ll have 77 million people age 65 or older and 76.5 million age 18 or under. And many of those seniors have medical and functional conditions that signal they are nearing end of life.
As chief medical officer of a complete senior health company, and as a physician with more than 3 decades of personal experience in geriatrics, I know we can improve the final chapter of life for our older adults and our taxpayers. If medical professionals don’t do a better job with patients at the end of life, then key decisions increasingly will be driven by the money-centered phone banks.
The single biggest improvement is having a frank and direct talk with senior patients about end-of-life wishes. Remarkably, only 1 in 10 Americans say they’ve ever had an end-of-life conversation with their doctor or health care provider – no heartfelt talk about what quality of life looks like under different treatment options. Only half ever discussed the topic with a spouse or loved one.
As a result, the default end-of-life care regimen for many is to extend life at any cost, even though most Americans tell pollsters they don’t truly want that. Doctors must focus on thorough informed consent with patients before major medical crises hurt patient cognition.
Another key is for specialists and general care doctors to do a better job consulting with each other. Two of every 3 seniors have several chronic conditions, or multimorbidities; that status worsens to include 8 of every 10 seniors after age 80. That means seniors often have multiple doctors who work in their own silos and fail to communicate the competing risks and benefits of diagnostic and treatment options. The result is fragmented plans that are difficult to follow and often as likely to harm complex patients as help them.
We all know that 90-year-old people shouldn’t be on 15 drugs, and yet too many are. Big Pharma has made it easy for doctors to add new medications, but I don’t think there’s even a class in medical school to teach clinicians how to trim the medicine list. When a drug is causing side effects, the sad reality is that most doctors add another medication to treat the side effect, as opposed to removing the offending agent. We need to end this practice known as drug cascading.
Doctors need training on how to unwind prescriptions. For example, too many seniors are being prescribed atypical antipsychotics off label for dementia. Overtreatment of geriatric diabetes and hypertension causes weakness and falls. Overprescribing antibiotics for frail patients whose bladders are colonized with bacteria too often leads to colitis. We need to question why our seniors are on so many drugs.
Doctors, patients, and families should be discussing quality of life as much as quantity of life.
I’ve spent my career taking care of older people. It’s rare for me to get a phone call saying an older person died and nobody expected it. We all know that we will die, but we spend so little time talking about it and preparing for it. A great disservice will be done to patients, doctors, and the medical profession if we let the phone banks take over.
Dr. Schneeman is a geriatrician and chief medical officer for Lifespark, a senior health company based in Minneapolis.
A version of this article appeared on Medscape.com.
Sadly, the medical business has descended to this: Some insurers are combing health records to find and target customers with a 50% chance of dying in the next 18 months. Those companies then work to persuade customers to switch into palliative and hospice care.
And more of this automated end-of-life medicine appears to be on the way.
What’s gained is cost savings. What’s lost is empathy and humanity.
Doctor colleagues have warned for decades about the rise of the bean-counters in medicine. Yes, health care is a business, but it should be a higher calling, too. We serve, we heal, we protect, and we comfort.
There are times, however, when the people who try to squeeze the most money out of medicine try to gain too much influence over the people who actually engage in medicine. I think the rise of phone bank boiler rooms, built on business incentives to move patients into cheaper hospice care, should be a bridge too far for our profession.
End-of-life care is one of the most sensitive and emotionally rewarding things a doctor can do. Hospice can be an excellent choice for fully informed patients and families, but we should not be turning over these decisions to artificial intelligence, spreadsheets, and crunchers of big data.
At the same time, we should realize that the end-of-life phone banks have not evolved from nowhere. The reality is that dying is expensive. The last year of life accounts for 13%-25% of all spending on Medicare, according to numerous studies. That’s more than $200 billion a year for just one part of one federal health care program. Much of that money goes to hospitals, where end-of-life patients amass average charges of $6,000 per day.
All this spending runs counter to the wishes of most Americans. According to a Kaiser Family Foundation poll, 9 out of 10 adults say they don’t want their families to be burdened financially by their end-of-life medical care. Given the choice, 7 out of 10 Americans say they want to die at home; fewer than 1 in 10 say they want to die in a hospital.
And far more people (71%) think it’s more important to die without pain or stress than to extend life as long as possible (19%).
It’s crucial for us to get this right. Within 11 years, the U.S. Census projects that seniors will outnumber kids for the first time in history: We’ll have 77 million people age 65 or older and 76.5 million age 18 or under. And many of those seniors have medical and functional conditions that signal they are nearing end of life.
As chief medical officer of a complete senior health company, and as a physician with more than 3 decades of personal experience in geriatrics, I know we can improve the final chapter of life for our older adults and our taxpayers. If medical professionals don’t do a better job with patients at the end of life, then key decisions increasingly will be driven by the money-centered phone banks.
The single biggest improvement is having a frank and direct talk with senior patients about end-of-life wishes. Remarkably, only 1 in 10 Americans say they’ve ever had an end-of-life conversation with their doctor or health care provider – no heartfelt talk about what quality of life looks like under different treatment options. Only half ever discussed the topic with a spouse or loved one.
As a result, the default end-of-life care regimen for many is to extend life at any cost, even though most Americans tell pollsters they don’t truly want that. Doctors must focus on thorough informed consent with patients before major medical crises hurt patient cognition.
Another key is for specialists and general care doctors to do a better job consulting with each other. Two of every 3 seniors have several chronic conditions, or multimorbidities; that status worsens to include 8 of every 10 seniors after age 80. That means seniors often have multiple doctors who work in their own silos and fail to communicate the competing risks and benefits of diagnostic and treatment options. The result is fragmented plans that are difficult to follow and often as likely to harm complex patients as help them.
We all know that 90-year-old people shouldn’t be on 15 drugs, and yet too many are. Big Pharma has made it easy for doctors to add new medications, but I don’t think there’s even a class in medical school to teach clinicians how to trim the medicine list. When a drug is causing side effects, the sad reality is that most doctors add another medication to treat the side effect, as opposed to removing the offending agent. We need to end this practice known as drug cascading.
Doctors need training on how to unwind prescriptions. For example, too many seniors are being prescribed atypical antipsychotics off label for dementia. Overtreatment of geriatric diabetes and hypertension causes weakness and falls. Overprescribing antibiotics for frail patients whose bladders are colonized with bacteria too often leads to colitis. We need to question why our seniors are on so many drugs.
Doctors, patients, and families should be discussing quality of life as much as quantity of life.
I’ve spent my career taking care of older people. It’s rare for me to get a phone call saying an older person died and nobody expected it. We all know that we will die, but we spend so little time talking about it and preparing for it. A great disservice will be done to patients, doctors, and the medical profession if we let the phone banks take over.
Dr. Schneeman is a geriatrician and chief medical officer for Lifespark, a senior health company based in Minneapolis.
A version of this article appeared on Medscape.com.
Sadly, the medical business has descended to this: Some insurers are combing health records to find and target customers with a 50% chance of dying in the next 18 months. Those companies then work to persuade customers to switch into palliative and hospice care.
And more of this automated end-of-life medicine appears to be on the way.
What’s gained is cost savings. What’s lost is empathy and humanity.
Doctor colleagues have warned for decades about the rise of the bean-counters in medicine. Yes, health care is a business, but it should be a higher calling, too. We serve, we heal, we protect, and we comfort.
There are times, however, when the people who try to squeeze the most money out of medicine try to gain too much influence over the people who actually engage in medicine. I think the rise of phone bank boiler rooms, built on business incentives to move patients into cheaper hospice care, should be a bridge too far for our profession.
End-of-life care is one of the most sensitive and emotionally rewarding things a doctor can do. Hospice can be an excellent choice for fully informed patients and families, but we should not be turning over these decisions to artificial intelligence, spreadsheets, and crunchers of big data.
At the same time, we should realize that the end-of-life phone banks have not evolved from nowhere. The reality is that dying is expensive. The last year of life accounts for 13%-25% of all spending on Medicare, according to numerous studies. That’s more than $200 billion a year for just one part of one federal health care program. Much of that money goes to hospitals, where end-of-life patients amass average charges of $6,000 per day.
All this spending runs counter to the wishes of most Americans. According to a Kaiser Family Foundation poll, 9 out of 10 adults say they don’t want their families to be burdened financially by their end-of-life medical care. Given the choice, 7 out of 10 Americans say they want to die at home; fewer than 1 in 10 say they want to die in a hospital.
And far more people (71%) think it’s more important to die without pain or stress than to extend life as long as possible (19%).
It’s crucial for us to get this right. Within 11 years, the U.S. Census projects that seniors will outnumber kids for the first time in history: We’ll have 77 million people age 65 or older and 76.5 million age 18 or under. And many of those seniors have medical and functional conditions that signal they are nearing end of life.
As chief medical officer of a complete senior health company, and as a physician with more than 3 decades of personal experience in geriatrics, I know we can improve the final chapter of life for our older adults and our taxpayers. If medical professionals don’t do a better job with patients at the end of life, then key decisions increasingly will be driven by the money-centered phone banks.
The single biggest improvement is having a frank and direct talk with senior patients about end-of-life wishes. Remarkably, only 1 in 10 Americans say they’ve ever had an end-of-life conversation with their doctor or health care provider – no heartfelt talk about what quality of life looks like under different treatment options. Only half ever discussed the topic with a spouse or loved one.
As a result, the default end-of-life care regimen for many is to extend life at any cost, even though most Americans tell pollsters they don’t truly want that. Doctors must focus on thorough informed consent with patients before major medical crises hurt patient cognition.
Another key is for specialists and general care doctors to do a better job consulting with each other. Two of every 3 seniors have several chronic conditions, or multimorbidities; that status worsens to include 8 of every 10 seniors after age 80. That means seniors often have multiple doctors who work in their own silos and fail to communicate the competing risks and benefits of diagnostic and treatment options. The result is fragmented plans that are difficult to follow and often as likely to harm complex patients as help them.
We all know that 90-year-old people shouldn’t be on 15 drugs, and yet too many are. Big Pharma has made it easy for doctors to add new medications, but I don’t think there’s even a class in medical school to teach clinicians how to trim the medicine list. When a drug is causing side effects, the sad reality is that most doctors add another medication to treat the side effect, as opposed to removing the offending agent. We need to end this practice known as drug cascading.
Doctors need training on how to unwind prescriptions. For example, too many seniors are being prescribed atypical antipsychotics off label for dementia. Overtreatment of geriatric diabetes and hypertension causes weakness and falls. Overprescribing antibiotics for frail patients whose bladders are colonized with bacteria too often leads to colitis. We need to question why our seniors are on so many drugs.
Doctors, patients, and families should be discussing quality of life as much as quantity of life.
I’ve spent my career taking care of older people. It’s rare for me to get a phone call saying an older person died and nobody expected it. We all know that we will die, but we spend so little time talking about it and preparing for it. A great disservice will be done to patients, doctors, and the medical profession if we let the phone banks take over.
Dr. Schneeman is a geriatrician and chief medical officer for Lifespark, a senior health company based in Minneapolis.
A version of this article appeared on Medscape.com.
Who owns your genes?
Who owns your genes? The assumption of any sane person would be that he or she owns his or her own genes. I mean, how dumb a question is that?
Yet, in 2007, Dov Michaeli, MD, PhD, described how an American company had claimed ownership of genetic materials and believed that it had the right to commercialize those naturally occurring bits of DNA. Myriad Genetics began by patenting mutations of BRCA. Dr. Michaeli issued a call for action to support early efforts to pass legislation to restore and preserve individual ownership of one’s own genes. This is a historically important quick read/watch/listen. Give it a click.
In related legislation, the Genetic Information Nondiscrimination Act (GINA), originally introduced by New York Rep. Louise Slaughter in 1995, was ultimately spearheaded by California Rep. Xavier Becerra (now Secretary of Health & Human Services) to passage by the House of Representatives on April 25, 2007, by a vote of 420-9-3. Led by Sen. Edward Kennedy of Massachusetts, it was passed by the Senate on April 24, 2008, by a vote of 95-0. President George W. Bush signed the bill into law on May 21, 2008.
GINA is a landmark piece of legislation that protects Americans. It prohibits employers and health insurers from discriminating against people on the basis of their genetic information, and it also prohibits the use of genetic information in life insurance and long-term care insurance.
Its impact has been immense. GINA has been indispensable in promoting progress in the field of human genetics. By safeguarding individuals against discrimination based on genetic information, it has encouraged broader participation in research, built public trust, and stimulated advancements in genetic testing and personalized medicine. GINA’s impact extends beyond borders and has influenced much of the rest of the world.
As important as GINA was to the field, more was needed. National legislation to protect ownership of genetic materials has, despite many attempts, still not become law in the United States. However, in our system of divided government and balance of power, we also have independent courts.
June 13, 2023, was the 10th anniversary of another landmark event. The legal case is that of the Association for Molecular Pathology v. Myriad Genetics, a Salt Lake City–based biotech company that held patents on isolated DNA sequences associated with breast and ovarian cancer. The AMP, joined by several other organizations and researchers, challenged Myriad’s gene patents, arguing that human genes are naturally occurring and, therefore, should not be subject to patenting. In a unanimous decision, the Supreme Court held that naturally occurring DNA segments are products of nature and therefore are not eligible for patent protection.
This was a pivotal decision in the field of human genetics and had a broad impact on genetic research. The decision clarified that naturally occurring DNA sequences cannot be patented, which means that researchers are free to use these sequences in their research without fear of patent infringement. This has led to a vast increase in the amount of genetic research being conducted, and it has also led to the development of new genetic tests and treatments.
The numbers of genetic research papers published in scientific journals and of genetic tests available to consumers have increased significantly, while the cost of genetic testing has decreased significantly. The AMP v. Myriad decision is likely to continue to have an impact for many years to come.
Thank you, common sense, activist American molecular pathologists, Congress, the President, and the Supreme Court for siding with the people.Dr. Lundbert is editor in chief of Cancer Commons. He has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Who owns your genes? The assumption of any sane person would be that he or she owns his or her own genes. I mean, how dumb a question is that?
Yet, in 2007, Dov Michaeli, MD, PhD, described how an American company had claimed ownership of genetic materials and believed that it had the right to commercialize those naturally occurring bits of DNA. Myriad Genetics began by patenting mutations of BRCA. Dr. Michaeli issued a call for action to support early efforts to pass legislation to restore and preserve individual ownership of one’s own genes. This is a historically important quick read/watch/listen. Give it a click.
In related legislation, the Genetic Information Nondiscrimination Act (GINA), originally introduced by New York Rep. Louise Slaughter in 1995, was ultimately spearheaded by California Rep. Xavier Becerra (now Secretary of Health & Human Services) to passage by the House of Representatives on April 25, 2007, by a vote of 420-9-3. Led by Sen. Edward Kennedy of Massachusetts, it was passed by the Senate on April 24, 2008, by a vote of 95-0. President George W. Bush signed the bill into law on May 21, 2008.
GINA is a landmark piece of legislation that protects Americans. It prohibits employers and health insurers from discriminating against people on the basis of their genetic information, and it also prohibits the use of genetic information in life insurance and long-term care insurance.
Its impact has been immense. GINA has been indispensable in promoting progress in the field of human genetics. By safeguarding individuals against discrimination based on genetic information, it has encouraged broader participation in research, built public trust, and stimulated advancements in genetic testing and personalized medicine. GINA’s impact extends beyond borders and has influenced much of the rest of the world.
As important as GINA was to the field, more was needed. National legislation to protect ownership of genetic materials has, despite many attempts, still not become law in the United States. However, in our system of divided government and balance of power, we also have independent courts.
June 13, 2023, was the 10th anniversary of another landmark event. The legal case is that of the Association for Molecular Pathology v. Myriad Genetics, a Salt Lake City–based biotech company that held patents on isolated DNA sequences associated with breast and ovarian cancer. The AMP, joined by several other organizations and researchers, challenged Myriad’s gene patents, arguing that human genes are naturally occurring and, therefore, should not be subject to patenting. In a unanimous decision, the Supreme Court held that naturally occurring DNA segments are products of nature and therefore are not eligible for patent protection.
This was a pivotal decision in the field of human genetics and had a broad impact on genetic research. The decision clarified that naturally occurring DNA sequences cannot be patented, which means that researchers are free to use these sequences in their research without fear of patent infringement. This has led to a vast increase in the amount of genetic research being conducted, and it has also led to the development of new genetic tests and treatments.
The numbers of genetic research papers published in scientific journals and of genetic tests available to consumers have increased significantly, while the cost of genetic testing has decreased significantly. The AMP v. Myriad decision is likely to continue to have an impact for many years to come.
Thank you, common sense, activist American molecular pathologists, Congress, the President, and the Supreme Court for siding with the people.Dr. Lundbert is editor in chief of Cancer Commons. He has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Who owns your genes? The assumption of any sane person would be that he or she owns his or her own genes. I mean, how dumb a question is that?
Yet, in 2007, Dov Michaeli, MD, PhD, described how an American company had claimed ownership of genetic materials and believed that it had the right to commercialize those naturally occurring bits of DNA. Myriad Genetics began by patenting mutations of BRCA. Dr. Michaeli issued a call for action to support early efforts to pass legislation to restore and preserve individual ownership of one’s own genes. This is a historically important quick read/watch/listen. Give it a click.
In related legislation, the Genetic Information Nondiscrimination Act (GINA), originally introduced by New York Rep. Louise Slaughter in 1995, was ultimately spearheaded by California Rep. Xavier Becerra (now Secretary of Health & Human Services) to passage by the House of Representatives on April 25, 2007, by a vote of 420-9-3. Led by Sen. Edward Kennedy of Massachusetts, it was passed by the Senate on April 24, 2008, by a vote of 95-0. President George W. Bush signed the bill into law on May 21, 2008.
GINA is a landmark piece of legislation that protects Americans. It prohibits employers and health insurers from discriminating against people on the basis of their genetic information, and it also prohibits the use of genetic information in life insurance and long-term care insurance.
Its impact has been immense. GINA has been indispensable in promoting progress in the field of human genetics. By safeguarding individuals against discrimination based on genetic information, it has encouraged broader participation in research, built public trust, and stimulated advancements in genetic testing and personalized medicine. GINA’s impact extends beyond borders and has influenced much of the rest of the world.
As important as GINA was to the field, more was needed. National legislation to protect ownership of genetic materials has, despite many attempts, still not become law in the United States. However, in our system of divided government and balance of power, we also have independent courts.
June 13, 2023, was the 10th anniversary of another landmark event. The legal case is that of the Association for Molecular Pathology v. Myriad Genetics, a Salt Lake City–based biotech company that held patents on isolated DNA sequences associated with breast and ovarian cancer. The AMP, joined by several other organizations and researchers, challenged Myriad’s gene patents, arguing that human genes are naturally occurring and, therefore, should not be subject to patenting. In a unanimous decision, the Supreme Court held that naturally occurring DNA segments are products of nature and therefore are not eligible for patent protection.
This was a pivotal decision in the field of human genetics and had a broad impact on genetic research. The decision clarified that naturally occurring DNA sequences cannot be patented, which means that researchers are free to use these sequences in their research without fear of patent infringement. This has led to a vast increase in the amount of genetic research being conducted, and it has also led to the development of new genetic tests and treatments.
The numbers of genetic research papers published in scientific journals and of genetic tests available to consumers have increased significantly, while the cost of genetic testing has decreased significantly. The AMP v. Myriad decision is likely to continue to have an impact for many years to come.
Thank you, common sense, activist American molecular pathologists, Congress, the President, and the Supreme Court for siding with the people.Dr. Lundbert is editor in chief of Cancer Commons. He has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Ten tips for boosting patient communication
This transcript has been edited for clarity.
Here are 10 ways to improve health communication with patients.
No. 1: Be an active listener
The first tip is to be an active listener and help guide the history-taking process by asking for clarification when needed.
Quickly figure out the patient’s chief complaint. Which symptom is the most severe?
Ask them for symptom-modifying factors, such as onset, duration, frequency, and a pain description. Is the abdominal pain sharp or crampy, dull and achy, or pressure-like? What makes the symptoms better or worse?
As many of us were taught in medical school, 80% of the diagnosis is in a patient’s history and description.
No. 2: Ask questions that resonate with patients
What can we do to help elicit an accurate history from the patient when they’re not providing the needed information or being helpful enough?
The easiest way is to ask your patient in a completely different way but one that resonates with them. For instance, ask how the abdominal pain is affecting their quality of life. That will help focus the history taking and encourage the patient to share details.
Does the pain keep them awake at night? Are they able to eat a normal-sized meal? Or are they forced to eat tiny snacks? Is the pain interfering with work or school?
By providing a framework, the patient will be more passionate about sharing the details of their history.
No. 3: Help patients organize their story
Sometimes, patients provide details in a nonchronological order, jumping all over the place.
A super helpful technique is to explain to the patient that you have a story to write for your computer note, and for them to think back to when they first started noticing their abdominal pain or rectal bleeding symptoms. When were the most-severe episodes? How frequent are the episodes? What’s the volume of their rectal bleeding?
If the patient realizes that you’re trying to write a story synopsis, they will provide information in a much more organized way.
No. 4: Determine patient’s language preference
Quickly determine the patient’s language preference. We want patients to feel extremely comfortable.
Whenever possible, use a certified interpreter. Language phone lines, in-person interpreters, and video conferencing are widely available today. It’s worth investing in this technology so that we can provide the best possible care to immigrants and refugees.
Conversely, avoid using family members as interpreters because they may not be adequately trained in medical vocabulary.
No. 5: Use simple language
When providing explanations, use simple language that your patient can understand and identify with.
For example, use analogies like “the heart is a pump” or the diverticula are thin areas of the colon that can bleed if the blood vessel is too close to the surface.
No. 6: Determine level of medical literacy
Determine your patient’s level of medical literacy. Some of our patients did not graduate from high school. Some patients can’t read very well. Therefore, your discharge instructions and handouts should sometimes be written on a third-grade level.
If patients can’t read, write medication instructions with symbols. Draw a sun for medications that are supposed to be taken in the morning and draw a moon if a medication is supposed to be taken at night.
Always very carefully review the instructions with the patient.
No. 7: Check in with the patient
During the visit, frequently check in with the patient to make sure that they understand what you’re asking or what you’re trying to explain to them.
No. 8: Include family member as patient advocate
If the patient is accompanied by a family member, help them serve in the important role as a patient advocate.
If the family member wants to take notes, encourage them because that provides an awesome value.
Sometimes patients can forget clinic and hospital medical conversations, and that family member might be the key to improving your patient’s health.
No. 9: Follow-up with the patient
If your clinic has the capability, follow up with a patient the next day to make sure that they understood everything.
Check to make sure the patient was able to pick up all of the medications that you prescribed.
Check that laboratory tests are arranged or completed.
Check that important procedures, such as esophagogastroduodenoscopy and colonoscopy, and imaging, such as ultrasounds and CTs, are scheduled.
No. 10: Identify barriers to care
Have fun talking with a patient. Find out what they do for a living. Build a rapport. Listen to their stressors in life.
Try to identify any barriers to care or external stressors, like taking care of a sick parent, which might interfere with their scheduling an important diagnostic colonoscopy for rectal bleeding.
Good luck incorporating these communication strategies into your clinic and hospital work. Together, we can help improve the delivery of health care.
Dr. Levy is a gastroenterologist at the University of Chicago. In 2017, Dr. Levy, a previous Fulbright Fellow in France, also started a gastroenterology clinic for refugees resettling in Chicago. His clinical projects focus on the development of colorectal cancer screening campaigns. Dr. Levy, who recently gave a TEDx Talk about building health education campaigns using music and concerts, organizes Tune It Up: A Concert To Raise Colorectal Cancer Awareness with the American College of Gastroenterology (ACG). He frequently publishes on a variety of gastroenterology topics and serves on ACG’s Public Relations Committee and FDA-Related Matters Committee. He has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Here are 10 ways to improve health communication with patients.
No. 1: Be an active listener
The first tip is to be an active listener and help guide the history-taking process by asking for clarification when needed.
Quickly figure out the patient’s chief complaint. Which symptom is the most severe?
Ask them for symptom-modifying factors, such as onset, duration, frequency, and a pain description. Is the abdominal pain sharp or crampy, dull and achy, or pressure-like? What makes the symptoms better or worse?
As many of us were taught in medical school, 80% of the diagnosis is in a patient’s history and description.
No. 2: Ask questions that resonate with patients
What can we do to help elicit an accurate history from the patient when they’re not providing the needed information or being helpful enough?
The easiest way is to ask your patient in a completely different way but one that resonates with them. For instance, ask how the abdominal pain is affecting their quality of life. That will help focus the history taking and encourage the patient to share details.
Does the pain keep them awake at night? Are they able to eat a normal-sized meal? Or are they forced to eat tiny snacks? Is the pain interfering with work or school?
By providing a framework, the patient will be more passionate about sharing the details of their history.
No. 3: Help patients organize their story
Sometimes, patients provide details in a nonchronological order, jumping all over the place.
A super helpful technique is to explain to the patient that you have a story to write for your computer note, and for them to think back to when they first started noticing their abdominal pain or rectal bleeding symptoms. When were the most-severe episodes? How frequent are the episodes? What’s the volume of their rectal bleeding?
If the patient realizes that you’re trying to write a story synopsis, they will provide information in a much more organized way.
No. 4: Determine patient’s language preference
Quickly determine the patient’s language preference. We want patients to feel extremely comfortable.
Whenever possible, use a certified interpreter. Language phone lines, in-person interpreters, and video conferencing are widely available today. It’s worth investing in this technology so that we can provide the best possible care to immigrants and refugees.
Conversely, avoid using family members as interpreters because they may not be adequately trained in medical vocabulary.
No. 5: Use simple language
When providing explanations, use simple language that your patient can understand and identify with.
For example, use analogies like “the heart is a pump” or the diverticula are thin areas of the colon that can bleed if the blood vessel is too close to the surface.
No. 6: Determine level of medical literacy
Determine your patient’s level of medical literacy. Some of our patients did not graduate from high school. Some patients can’t read very well. Therefore, your discharge instructions and handouts should sometimes be written on a third-grade level.
If patients can’t read, write medication instructions with symbols. Draw a sun for medications that are supposed to be taken in the morning and draw a moon if a medication is supposed to be taken at night.
Always very carefully review the instructions with the patient.
No. 7: Check in with the patient
During the visit, frequently check in with the patient to make sure that they understand what you’re asking or what you’re trying to explain to them.
No. 8: Include family member as patient advocate
If the patient is accompanied by a family member, help them serve in the important role as a patient advocate.
If the family member wants to take notes, encourage them because that provides an awesome value.
Sometimes patients can forget clinic and hospital medical conversations, and that family member might be the key to improving your patient’s health.
No. 9: Follow-up with the patient
If your clinic has the capability, follow up with a patient the next day to make sure that they understood everything.
Check to make sure the patient was able to pick up all of the medications that you prescribed.
Check that laboratory tests are arranged or completed.
Check that important procedures, such as esophagogastroduodenoscopy and colonoscopy, and imaging, such as ultrasounds and CTs, are scheduled.
No. 10: Identify barriers to care
Have fun talking with a patient. Find out what they do for a living. Build a rapport. Listen to their stressors in life.
Try to identify any barriers to care or external stressors, like taking care of a sick parent, which might interfere with their scheduling an important diagnostic colonoscopy for rectal bleeding.
Good luck incorporating these communication strategies into your clinic and hospital work. Together, we can help improve the delivery of health care.
Dr. Levy is a gastroenterologist at the University of Chicago. In 2017, Dr. Levy, a previous Fulbright Fellow in France, also started a gastroenterology clinic for refugees resettling in Chicago. His clinical projects focus on the development of colorectal cancer screening campaigns. Dr. Levy, who recently gave a TEDx Talk about building health education campaigns using music and concerts, organizes Tune It Up: A Concert To Raise Colorectal Cancer Awareness with the American College of Gastroenterology (ACG). He frequently publishes on a variety of gastroenterology topics and serves on ACG’s Public Relations Committee and FDA-Related Matters Committee. He has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Here are 10 ways to improve health communication with patients.
No. 1: Be an active listener
The first tip is to be an active listener and help guide the history-taking process by asking for clarification when needed.
Quickly figure out the patient’s chief complaint. Which symptom is the most severe?
Ask them for symptom-modifying factors, such as onset, duration, frequency, and a pain description. Is the abdominal pain sharp or crampy, dull and achy, or pressure-like? What makes the symptoms better or worse?
As many of us were taught in medical school, 80% of the diagnosis is in a patient’s history and description.
No. 2: Ask questions that resonate with patients
What can we do to help elicit an accurate history from the patient when they’re not providing the needed information or being helpful enough?
The easiest way is to ask your patient in a completely different way but one that resonates with them. For instance, ask how the abdominal pain is affecting their quality of life. That will help focus the history taking and encourage the patient to share details.
Does the pain keep them awake at night? Are they able to eat a normal-sized meal? Or are they forced to eat tiny snacks? Is the pain interfering with work or school?
By providing a framework, the patient will be more passionate about sharing the details of their history.
No. 3: Help patients organize their story
Sometimes, patients provide details in a nonchronological order, jumping all over the place.
A super helpful technique is to explain to the patient that you have a story to write for your computer note, and for them to think back to when they first started noticing their abdominal pain or rectal bleeding symptoms. When were the most-severe episodes? How frequent are the episodes? What’s the volume of their rectal bleeding?
If the patient realizes that you’re trying to write a story synopsis, they will provide information in a much more organized way.
No. 4: Determine patient’s language preference
Quickly determine the patient’s language preference. We want patients to feel extremely comfortable.
Whenever possible, use a certified interpreter. Language phone lines, in-person interpreters, and video conferencing are widely available today. It’s worth investing in this technology so that we can provide the best possible care to immigrants and refugees.
Conversely, avoid using family members as interpreters because they may not be adequately trained in medical vocabulary.
No. 5: Use simple language
When providing explanations, use simple language that your patient can understand and identify with.
For example, use analogies like “the heart is a pump” or the diverticula are thin areas of the colon that can bleed if the blood vessel is too close to the surface.
No. 6: Determine level of medical literacy
Determine your patient’s level of medical literacy. Some of our patients did not graduate from high school. Some patients can’t read very well. Therefore, your discharge instructions and handouts should sometimes be written on a third-grade level.
If patients can’t read, write medication instructions with symbols. Draw a sun for medications that are supposed to be taken in the morning and draw a moon if a medication is supposed to be taken at night.
Always very carefully review the instructions with the patient.
No. 7: Check in with the patient
During the visit, frequently check in with the patient to make sure that they understand what you’re asking or what you’re trying to explain to them.
No. 8: Include family member as patient advocate
If the patient is accompanied by a family member, help them serve in the important role as a patient advocate.
If the family member wants to take notes, encourage them because that provides an awesome value.
Sometimes patients can forget clinic and hospital medical conversations, and that family member might be the key to improving your patient’s health.
No. 9: Follow-up with the patient
If your clinic has the capability, follow up with a patient the next day to make sure that they understood everything.
Check to make sure the patient was able to pick up all of the medications that you prescribed.
Check that laboratory tests are arranged or completed.
Check that important procedures, such as esophagogastroduodenoscopy and colonoscopy, and imaging, such as ultrasounds and CTs, are scheduled.
No. 10: Identify barriers to care
Have fun talking with a patient. Find out what they do for a living. Build a rapport. Listen to their stressors in life.
Try to identify any barriers to care or external stressors, like taking care of a sick parent, which might interfere with their scheduling an important diagnostic colonoscopy for rectal bleeding.
Good luck incorporating these communication strategies into your clinic and hospital work. Together, we can help improve the delivery of health care.
Dr. Levy is a gastroenterologist at the University of Chicago. In 2017, Dr. Levy, a previous Fulbright Fellow in France, also started a gastroenterology clinic for refugees resettling in Chicago. His clinical projects focus on the development of colorectal cancer screening campaigns. Dr. Levy, who recently gave a TEDx Talk about building health education campaigns using music and concerts, organizes Tune It Up: A Concert To Raise Colorectal Cancer Awareness with the American College of Gastroenterology (ACG). He frequently publishes on a variety of gastroenterology topics and serves on ACG’s Public Relations Committee and FDA-Related Matters Committee. He has disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The unique approach involved in age-specific concerns surrounding young patients with breast cancer
This transcript has been edited for clarity.
Dr. Partridge:
Olivia, let’s get started. What kinds of things do we need to think about when we’re seeing a young patient in clinic, beyond the usual things we think about for patients with breast cancer?
Dr. Pagani: The idea of selecting age as a determinant of care of young women is because they have specific issues, which are different from older, premenopausal patients but also older patients in general. We need to take care of many things, which can go from their job, family, fertility, and all these things are specific to these women and can impact their treatment, survivorship issues, side effects, and long-term problems. It’s a different world, compared with other patients with breast cancer.
Dr. Partridge: One of the areas that you and I have been very deep in the weeds in is the fertility issues. That’s obviously one of the things that’s pretty age-specific. There are some new data around that that we’re excited about. What do we think about when we think about trying to have a pregnancy or not after a breast cancer diagnosis?
Dr. Pagani: Yeah. I think it’s great times for that because we succeeded in building up a very important trial, which broke a taboo that was there for many, many decades: You had breast cancer so forget your pregnancy desire.
Despite many retrospective data from many groups that suggested pregnancy after breast cancer was not detrimental, there were so many obstacles for these women to address their pregnancy desire. I think we succeeded in explaining and showing in a quite solid way that if you desire a baby after breast cancer, you can try to have him or her.
Dr. Partridge: This was called the POSITIVE trial, with early findings published in the New England Journal of Medicine this past year, which was very exciting. Let’s dig a little deeper into that. Is this relevant for all patients with breast cancer or select patients with breast cancer who want to get pregnant?
Dr. Pagani: The accrual of the trial was open to all patients with stage I-III disease, but the majority of the patients were low risk, which means that the majority were node negative with small tumors. I think, so far, we can say that in low-risk women, pregnancy after breast cancer can be discussed and planned.
Summarizing, I think the evidence is for low-risk patients with early breast cancer. A minority had huge tumors or node-positive disease.
Dr. Partridge: It’s nice to be able to have these data to say a temporary interruption of endocrine therapy – not coming off forever, getting back on – was not associated with any worsening in terms of their breast cancer events in the future, which is great news for the women who are diagnosed when they’re trying to get pregnant and build their families or not having completed their families. It’s been fantastic.
What about for our patients with advanced disease who come in, and we’re treating them more to try and manage the cancer and improve their survival and quality of life, but cure may not be the goal. How do we manage the fertility issues for them?
Dr. Pagani: This is, I think, still an open issue despite overall survival for many women with advanced disease, especially HER2 positive or endocrine responsive; it is improving and it’s getting better and better. There are few women with oligometastatic disease that can be cured.
We are not yet there. At the Advanced Breast Cancer conference, we started to open the door to say that fertility should be discussed with patients with advanced breast cancer as well. We cannot recommend to patients with advanced breast cancer to pursue a pregnancy.
We have no data. For sure, this needs to be taken into account and discussed openly with all the patients who desire to discuss this.
Dr. Partridge: Yes. To help people to either grieve their losses or find alternative ways to build their family, I think, is something that we focus on.
How to optimize the plan of care for young patients
Dr. Partridge: Shifting gears into the psychosocial, we know that our young women of all stages have a harder time adjusting to a breast cancer diagnosis for good reason. It’s not normative at all to be dealing with a lot of the slings and arrows that our young women deal with at the age that they do. How do you manage that in your clinic, Olivia?
Dr. Pagani: Well, I think it’s always tough. One of the problems, which is also true for early breast cancer in general, which I think is common to you as well, is that in our society many women get breast cancer before even having thought of their family planning. That’s many of them in our reality.
In other countries, maybe they have already two to three children. In our countries, they are aged 30-35 years with no children, no stable relationship, and then are faced with all these things, and their pregnancy desire can be blown up because they understand there is no time, especially if they are metastatic. This can be devastating.
We are not very good at that yet. I think we need to develop better tools, better competence, and knowledge to support them to this extent as well.
Dr. Partridge: I know that whether people want kids or not, the diagnosis of breast cancer has financial toxicity and the inconvenience of going through this kind of experience while managing a busy life. Many of our patients, especially our young patients, are trying to develop their careers, to graduate from schools, and to grow a nest egg. They’re not retired yet, on average.
I agree that we have a large amount of work to do. The one thing I try and do is always bring in our social workers and our psychosocial supportive care providers for our young patients; not that I don’t bring them in for everybody that needs them, but our young patients on average seem to need them a little bit more just because it can be just so hard on them from a psychosocial and emotional standpoint, don’t you think?
Dr. Pagani: Yes, I think so. Do you have any specific program going on at Harvard?
Dr. Partridge: We do. We’ve built a program for young women that focuses on their unique and specific needs that capitalizes on groups that are already there. We have a social work department. We just have smoothed the pathway, and we send our young people in there more quickly and have some dedicated support groups and one-to-one interventions where patients can guide other young patients. We’ve built out the supportive care for these young patients and programming.
The other big area we’ve developed that’s not unique to young age but certainly enhanced in our young patients is genetics. We have a big genetic component at our cancer center. The young patients, more so than any other group, need to have the genetic counseling and the genetic testing not only to know about future risks and about their families but also to inform their treatment decisions these days. Do you want to comment on that?
Dr. Pagani: Yes, of course. Genetic counseling, especially for the most common BRCA1 and BRCA2, can change their local treatment (e.g., bilateral mastectomy instead of conservative surgery) but they have also to take care of their ovaries. They need to think of prophylactic oophorectomy, which makes fertility and pregnancy even more complicated. For them, it’s much more complex to address everything.
I think it’s really very complex, and I think we need a better understanding of all the nuances. Sometimes, we really do not consider, as you mentioned, that not every woman desires to have a baby.
The occurrence of breast cancer can wake up a desire that was not conscious but becomes conscious because you feel that you will not be able to do that. With the social support, the psychological support, and support groups – we have a very strong breast cancer support group for younger women — they could face these things. The young women support group was supportive of the POSITIVE trial: they helped to develop and financed a video, which was very helpful to promote POSITIVE.
I think that having a relationship or a network between patients, health professionals, social workers, and psychologists can help everyone, including those who want to become mothers, those who cannot, and those who do not want to.
Dr. Partridge: I think that’s great, Olivia. I think you rounded it out by just shining a light on these issues for our young patients and elevating it to being okay to talk about these issues. I think historically, it’s been: “You’ve got breast cancer, forget about this. We just need to get you to a better survival.”
We’re increasingly recognizing for patients of all ages, but particularly our young patients, that just surviving through breast cancer or cancer in general is not enough. We need to help people live the best and fullest life possible in their survivorship.
Education and communication: Key aspects moving forward
Dr. Pagani: I think another issue we need really to improve is health professional competence and knowledge. After you presented the POSITIVE trial in San Antonio, I had many calls with patients. They told me, “Well, I had this information, but my gynecologist, my oncologist, or my general practitioner still discouraged me.” This is a great barrier.
I think we need to do more to teach the health professionals. Otherwise, what we do is never enough because it will be blocked. They are scared and they do not want to go against their doctors. I think this is a very big conflict.
Dr. Partridge: That’s a really important point, and I appreciate you bringing it up. We as clinicians and educators who are building the research base need to really get it out there.
Dr. Pagani is a professor at the University of Geneva. Dr. Partridge is professor of medicine at Harvard Medical School and vice chair of clinical oncology at Dana-Farber Cancer Institute, both in Boston. Dr. Pagani reported conflicts of interest with PRIME, Roche, Eli Lilly, Novartis, Takeda, Pfizer, and Debiopharm. Dr. Partridge reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Dr. Partridge:
Olivia, let’s get started. What kinds of things do we need to think about when we’re seeing a young patient in clinic, beyond the usual things we think about for patients with breast cancer?
Dr. Pagani: The idea of selecting age as a determinant of care of young women is because they have specific issues, which are different from older, premenopausal patients but also older patients in general. We need to take care of many things, which can go from their job, family, fertility, and all these things are specific to these women and can impact their treatment, survivorship issues, side effects, and long-term problems. It’s a different world, compared with other patients with breast cancer.
Dr. Partridge: One of the areas that you and I have been very deep in the weeds in is the fertility issues. That’s obviously one of the things that’s pretty age-specific. There are some new data around that that we’re excited about. What do we think about when we think about trying to have a pregnancy or not after a breast cancer diagnosis?
Dr. Pagani: Yeah. I think it’s great times for that because we succeeded in building up a very important trial, which broke a taboo that was there for many, many decades: You had breast cancer so forget your pregnancy desire.
Despite many retrospective data from many groups that suggested pregnancy after breast cancer was not detrimental, there were so many obstacles for these women to address their pregnancy desire. I think we succeeded in explaining and showing in a quite solid way that if you desire a baby after breast cancer, you can try to have him or her.
Dr. Partridge: This was called the POSITIVE trial, with early findings published in the New England Journal of Medicine this past year, which was very exciting. Let’s dig a little deeper into that. Is this relevant for all patients with breast cancer or select patients with breast cancer who want to get pregnant?
Dr. Pagani: The accrual of the trial was open to all patients with stage I-III disease, but the majority of the patients were low risk, which means that the majority were node negative with small tumors. I think, so far, we can say that in low-risk women, pregnancy after breast cancer can be discussed and planned.
Summarizing, I think the evidence is for low-risk patients with early breast cancer. A minority had huge tumors or node-positive disease.
Dr. Partridge: It’s nice to be able to have these data to say a temporary interruption of endocrine therapy – not coming off forever, getting back on – was not associated with any worsening in terms of their breast cancer events in the future, which is great news for the women who are diagnosed when they’re trying to get pregnant and build their families or not having completed their families. It’s been fantastic.
What about for our patients with advanced disease who come in, and we’re treating them more to try and manage the cancer and improve their survival and quality of life, but cure may not be the goal. How do we manage the fertility issues for them?
Dr. Pagani: This is, I think, still an open issue despite overall survival for many women with advanced disease, especially HER2 positive or endocrine responsive; it is improving and it’s getting better and better. There are few women with oligometastatic disease that can be cured.
We are not yet there. At the Advanced Breast Cancer conference, we started to open the door to say that fertility should be discussed with patients with advanced breast cancer as well. We cannot recommend to patients with advanced breast cancer to pursue a pregnancy.
We have no data. For sure, this needs to be taken into account and discussed openly with all the patients who desire to discuss this.
Dr. Partridge: Yes. To help people to either grieve their losses or find alternative ways to build their family, I think, is something that we focus on.
How to optimize the plan of care for young patients
Dr. Partridge: Shifting gears into the psychosocial, we know that our young women of all stages have a harder time adjusting to a breast cancer diagnosis for good reason. It’s not normative at all to be dealing with a lot of the slings and arrows that our young women deal with at the age that they do. How do you manage that in your clinic, Olivia?
Dr. Pagani: Well, I think it’s always tough. One of the problems, which is also true for early breast cancer in general, which I think is common to you as well, is that in our society many women get breast cancer before even having thought of their family planning. That’s many of them in our reality.
In other countries, maybe they have already two to three children. In our countries, they are aged 30-35 years with no children, no stable relationship, and then are faced with all these things, and their pregnancy desire can be blown up because they understand there is no time, especially if they are metastatic. This can be devastating.
We are not very good at that yet. I think we need to develop better tools, better competence, and knowledge to support them to this extent as well.
Dr. Partridge: I know that whether people want kids or not, the diagnosis of breast cancer has financial toxicity and the inconvenience of going through this kind of experience while managing a busy life. Many of our patients, especially our young patients, are trying to develop their careers, to graduate from schools, and to grow a nest egg. They’re not retired yet, on average.
I agree that we have a large amount of work to do. The one thing I try and do is always bring in our social workers and our psychosocial supportive care providers for our young patients; not that I don’t bring them in for everybody that needs them, but our young patients on average seem to need them a little bit more just because it can be just so hard on them from a psychosocial and emotional standpoint, don’t you think?
Dr. Pagani: Yes, I think so. Do you have any specific program going on at Harvard?
Dr. Partridge: We do. We’ve built a program for young women that focuses on their unique and specific needs that capitalizes on groups that are already there. We have a social work department. We just have smoothed the pathway, and we send our young people in there more quickly and have some dedicated support groups and one-to-one interventions where patients can guide other young patients. We’ve built out the supportive care for these young patients and programming.
The other big area we’ve developed that’s not unique to young age but certainly enhanced in our young patients is genetics. We have a big genetic component at our cancer center. The young patients, more so than any other group, need to have the genetic counseling and the genetic testing not only to know about future risks and about their families but also to inform their treatment decisions these days. Do you want to comment on that?
Dr. Pagani: Yes, of course. Genetic counseling, especially for the most common BRCA1 and BRCA2, can change their local treatment (e.g., bilateral mastectomy instead of conservative surgery) but they have also to take care of their ovaries. They need to think of prophylactic oophorectomy, which makes fertility and pregnancy even more complicated. For them, it’s much more complex to address everything.
I think it’s really very complex, and I think we need a better understanding of all the nuances. Sometimes, we really do not consider, as you mentioned, that not every woman desires to have a baby.
The occurrence of breast cancer can wake up a desire that was not conscious but becomes conscious because you feel that you will not be able to do that. With the social support, the psychological support, and support groups – we have a very strong breast cancer support group for younger women — they could face these things. The young women support group was supportive of the POSITIVE trial: they helped to develop and financed a video, which was very helpful to promote POSITIVE.
I think that having a relationship or a network between patients, health professionals, social workers, and psychologists can help everyone, including those who want to become mothers, those who cannot, and those who do not want to.
Dr. Partridge: I think that’s great, Olivia. I think you rounded it out by just shining a light on these issues for our young patients and elevating it to being okay to talk about these issues. I think historically, it’s been: “You’ve got breast cancer, forget about this. We just need to get you to a better survival.”
We’re increasingly recognizing for patients of all ages, but particularly our young patients, that just surviving through breast cancer or cancer in general is not enough. We need to help people live the best and fullest life possible in their survivorship.
Education and communication: Key aspects moving forward
Dr. Pagani: I think another issue we need really to improve is health professional competence and knowledge. After you presented the POSITIVE trial in San Antonio, I had many calls with patients. They told me, “Well, I had this information, but my gynecologist, my oncologist, or my general practitioner still discouraged me.” This is a great barrier.
I think we need to do more to teach the health professionals. Otherwise, what we do is never enough because it will be blocked. They are scared and they do not want to go against their doctors. I think this is a very big conflict.
Dr. Partridge: That’s a really important point, and I appreciate you bringing it up. We as clinicians and educators who are building the research base need to really get it out there.
Dr. Pagani is a professor at the University of Geneva. Dr. Partridge is professor of medicine at Harvard Medical School and vice chair of clinical oncology at Dana-Farber Cancer Institute, both in Boston. Dr. Pagani reported conflicts of interest with PRIME, Roche, Eli Lilly, Novartis, Takeda, Pfizer, and Debiopharm. Dr. Partridge reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Dr. Partridge:
Olivia, let’s get started. What kinds of things do we need to think about when we’re seeing a young patient in clinic, beyond the usual things we think about for patients with breast cancer?
Dr. Pagani: The idea of selecting age as a determinant of care of young women is because they have specific issues, which are different from older, premenopausal patients but also older patients in general. We need to take care of many things, which can go from their job, family, fertility, and all these things are specific to these women and can impact their treatment, survivorship issues, side effects, and long-term problems. It’s a different world, compared with other patients with breast cancer.
Dr. Partridge: One of the areas that you and I have been very deep in the weeds in is the fertility issues. That’s obviously one of the things that’s pretty age-specific. There are some new data around that that we’re excited about. What do we think about when we think about trying to have a pregnancy or not after a breast cancer diagnosis?
Dr. Pagani: Yeah. I think it’s great times for that because we succeeded in building up a very important trial, which broke a taboo that was there for many, many decades: You had breast cancer so forget your pregnancy desire.
Despite many retrospective data from many groups that suggested pregnancy after breast cancer was not detrimental, there were so many obstacles for these women to address their pregnancy desire. I think we succeeded in explaining and showing in a quite solid way that if you desire a baby after breast cancer, you can try to have him or her.
Dr. Partridge: This was called the POSITIVE trial, with early findings published in the New England Journal of Medicine this past year, which was very exciting. Let’s dig a little deeper into that. Is this relevant for all patients with breast cancer or select patients with breast cancer who want to get pregnant?
Dr. Pagani: The accrual of the trial was open to all patients with stage I-III disease, but the majority of the patients were low risk, which means that the majority were node negative with small tumors. I think, so far, we can say that in low-risk women, pregnancy after breast cancer can be discussed and planned.
Summarizing, I think the evidence is for low-risk patients with early breast cancer. A minority had huge tumors or node-positive disease.
Dr. Partridge: It’s nice to be able to have these data to say a temporary interruption of endocrine therapy – not coming off forever, getting back on – was not associated with any worsening in terms of their breast cancer events in the future, which is great news for the women who are diagnosed when they’re trying to get pregnant and build their families or not having completed their families. It’s been fantastic.
What about for our patients with advanced disease who come in, and we’re treating them more to try and manage the cancer and improve their survival and quality of life, but cure may not be the goal. How do we manage the fertility issues for them?
Dr. Pagani: This is, I think, still an open issue despite overall survival for many women with advanced disease, especially HER2 positive or endocrine responsive; it is improving and it’s getting better and better. There are few women with oligometastatic disease that can be cured.
We are not yet there. At the Advanced Breast Cancer conference, we started to open the door to say that fertility should be discussed with patients with advanced breast cancer as well. We cannot recommend to patients with advanced breast cancer to pursue a pregnancy.
We have no data. For sure, this needs to be taken into account and discussed openly with all the patients who desire to discuss this.
Dr. Partridge: Yes. To help people to either grieve their losses or find alternative ways to build their family, I think, is something that we focus on.
How to optimize the plan of care for young patients
Dr. Partridge: Shifting gears into the psychosocial, we know that our young women of all stages have a harder time adjusting to a breast cancer diagnosis for good reason. It’s not normative at all to be dealing with a lot of the slings and arrows that our young women deal with at the age that they do. How do you manage that in your clinic, Olivia?
Dr. Pagani: Well, I think it’s always tough. One of the problems, which is also true for early breast cancer in general, which I think is common to you as well, is that in our society many women get breast cancer before even having thought of their family planning. That’s many of them in our reality.
In other countries, maybe they have already two to three children. In our countries, they are aged 30-35 years with no children, no stable relationship, and then are faced with all these things, and their pregnancy desire can be blown up because they understand there is no time, especially if they are metastatic. This can be devastating.
We are not very good at that yet. I think we need to develop better tools, better competence, and knowledge to support them to this extent as well.
Dr. Partridge: I know that whether people want kids or not, the diagnosis of breast cancer has financial toxicity and the inconvenience of going through this kind of experience while managing a busy life. Many of our patients, especially our young patients, are trying to develop their careers, to graduate from schools, and to grow a nest egg. They’re not retired yet, on average.
I agree that we have a large amount of work to do. The one thing I try and do is always bring in our social workers and our psychosocial supportive care providers for our young patients; not that I don’t bring them in for everybody that needs them, but our young patients on average seem to need them a little bit more just because it can be just so hard on them from a psychosocial and emotional standpoint, don’t you think?
Dr. Pagani: Yes, I think so. Do you have any specific program going on at Harvard?
Dr. Partridge: We do. We’ve built a program for young women that focuses on their unique and specific needs that capitalizes on groups that are already there. We have a social work department. We just have smoothed the pathway, and we send our young people in there more quickly and have some dedicated support groups and one-to-one interventions where patients can guide other young patients. We’ve built out the supportive care for these young patients and programming.
The other big area we’ve developed that’s not unique to young age but certainly enhanced in our young patients is genetics. We have a big genetic component at our cancer center. The young patients, more so than any other group, need to have the genetic counseling and the genetic testing not only to know about future risks and about their families but also to inform their treatment decisions these days. Do you want to comment on that?
Dr. Pagani: Yes, of course. Genetic counseling, especially for the most common BRCA1 and BRCA2, can change their local treatment (e.g., bilateral mastectomy instead of conservative surgery) but they have also to take care of their ovaries. They need to think of prophylactic oophorectomy, which makes fertility and pregnancy even more complicated. For them, it’s much more complex to address everything.
I think it’s really very complex, and I think we need a better understanding of all the nuances. Sometimes, we really do not consider, as you mentioned, that not every woman desires to have a baby.
The occurrence of breast cancer can wake up a desire that was not conscious but becomes conscious because you feel that you will not be able to do that. With the social support, the psychological support, and support groups – we have a very strong breast cancer support group for younger women — they could face these things. The young women support group was supportive of the POSITIVE trial: they helped to develop and financed a video, which was very helpful to promote POSITIVE.
I think that having a relationship or a network between patients, health professionals, social workers, and psychologists can help everyone, including those who want to become mothers, those who cannot, and those who do not want to.
Dr. Partridge: I think that’s great, Olivia. I think you rounded it out by just shining a light on these issues for our young patients and elevating it to being okay to talk about these issues. I think historically, it’s been: “You’ve got breast cancer, forget about this. We just need to get you to a better survival.”
We’re increasingly recognizing for patients of all ages, but particularly our young patients, that just surviving through breast cancer or cancer in general is not enough. We need to help people live the best and fullest life possible in their survivorship.
Education and communication: Key aspects moving forward
Dr. Pagani: I think another issue we need really to improve is health professional competence and knowledge. After you presented the POSITIVE trial in San Antonio, I had many calls with patients. They told me, “Well, I had this information, but my gynecologist, my oncologist, or my general practitioner still discouraged me.” This is a great barrier.
I think we need to do more to teach the health professionals. Otherwise, what we do is never enough because it will be blocked. They are scared and they do not want to go against their doctors. I think this is a very big conflict.
Dr. Partridge: That’s a really important point, and I appreciate you bringing it up. We as clinicians and educators who are building the research base need to really get it out there.
Dr. Pagani is a professor at the University of Geneva. Dr. Partridge is professor of medicine at Harvard Medical School and vice chair of clinical oncology at Dana-Farber Cancer Institute, both in Boston. Dr. Pagani reported conflicts of interest with PRIME, Roche, Eli Lilly, Novartis, Takeda, Pfizer, and Debiopharm. Dr. Partridge reported no conflicts of interest.
A version of this article first appeared on Medscape.com.
Weekend Botox training: Shortcut to cash or risky business?
This transcript has been edited for clarity.
Dr. Patel: A friend recently joked with me and said, “I wish you were a dermatologist so you could hook me up with Botox and fillers.” Well, little does this friend know that I could be a certified cosmetic injector just after a weekend course. Botox parties, here I come?
I can’t blame any health care professional for having a side hustle. People are burned out, want to supplement their income, or scale back clinical hours. According to one Medscape survey, almost 40% of physicians do have some form of a side hustle, whether it is consulting, speaking engagements, being an expert witness, or moonlighting. I know plenty of doctors and nurses who have taken on Botox injecting as a way to make some extra cash.
Now, going back to me and smoothing out wrinkles. I’m a pediatric hospitalist. I’ve never injected an aesthetic product in anyone’s face. When it comes to sharp objects and faces, I’ve sewn lacerations and drained abscesses. In my world, when we talk about botulinum toxin, we’re usually talking about botulism or the therapeutic treatment of migraines and muscle spasms – pathology.
The National Laser Institute has a 2-day Botox and dermal filler training. “Our 2-day Botox and filler course will also teach you how to build a practice and capitalize on the enormous Botox and dermal filler market that exists in the United States.” That’s a lot to cover in 2 days. They even have lunch breaks.
Just from a quick search, I even found an online video course for $1,500. For an additional fee, you can have a live, hands-on component. There are so many trainings out there, including one that’s only 8 hours long, offered by Empire Medical. I also went and spoke with an employee at Empire Medical who told me that because I’m an MD, if I do the course, I can use my certificate and go directly to a manufacturer, buy Botox, and start injecting right away.
Now, is this training actually sufficient for me to go and get good results while minimizing adverse effects like brow ptosis, dry eyes, and asymmetry? I have no idea. According to a review from the Journal of Cosmetic Dermatology, it’s crucial to understand anatomic landmarks, muscle function, baseline asymmetry, potential migration of the toxin, and site-specific precautions.
Okay, that sounds really intimidating, but people still do it. I saw a Business Insider article about a hospitalist who took a 2-day Botox course and then, to her credit, she trained under supervision for an additional 6 months. She then started hosting Botox parties and each time was making $3,500 to upwards of $20,000.
Let’s do some quick mental math. If I were to go online and buy Botox for $3-$6 a unit and then charge patients $15 a unit, and then I consider that in areas like the forehead or in between the eyes – I read that could take 25-50 units – and I repeat this for multiple patients, I can make a few thousand dollars. Well, I may have to adjust my prices according to the market, obviously, because I did see some Groupons advertising $10 per unit.
Who can get in on some Botox cosmetic cash action? Well, physicians can right away. For other health care professionals, it depends on the state. For example, in California, dentists cannot get Botox solely for cosmetic purposes, whereas in Arizona, they can. Generally speaking, NPs and PAs require some type of physician oversight or supervision, but again, it depends on the state.
Oh, and fun fact: Connecticut outright banned Botox parties and said that Botox must be performed “in a medical spa or licensed health care facility and by a Connecticut-licensed health care provider within his or her scope of practice.”
It definitely worries me that someone could go online or go overseas, buy Botox, claim to be a health care professional, and literally commit fraud. I found stories out there such as a couple in San Jose who are giving out Botox from their home without a license. They got arrested. Also, a woman in Alabama who lied about being a licensed dermatologist and did the same, or another woman in Los Angeles who got arrested after selling counterfeit Botox to undercover law enforcement. Surely, there are plenty more cases out there like this.
I asked Dr. Jacqueline Watchmaker, a board-certified dermatologist at U.S. Dermatology Partners in Arizona who has an expertise in cosmetic procedures, what she thought about the booming med spa industry and what, if any, regulatory changes she wanted to see.
Jacqueline Watchmaker, MD: I do think the fact that people can just go to a 1- or 2-day injection course and inject filler and Botox is concerning. I think the lack of regulation surrounding this topic is also very concerning.
There’s so much that goes into being a skilled injector. It’s an intricate knowledge of facial anatomy, which takes weeks, if not months, to really master. There’s actually injection technique, which can be very complex depending on the part of the face that you’re injecting. Even more important, it’s how to prevent complications, but also how to deal with complications if they do occur. There’s no way that these weekend injection courses are able to cover those topics in a thorough and satisfactory manner.
I see complications from med spas all the time, and I think it’s people going to injectors who are not skilled. They don’t know their anatomy, they don’t know the appropriate filler to use, and then heaven forbid there is a complication, they don’t know how to manage the complication – and then those patients get sent to me.
I think patients sometimes forget that these cosmetic procedures are true medical procedures. You need sterile technique. Again, you need to know the anatomy. It can look easy on social media, but there’s a large amount of thought behind it. I think there needs to be more regulation around this topic.
Dr. Patel: In one study, out of 400 people who received a cosmetic procedure, 50 reported an adverse event, such as discoloration or burns, and these adverse events were more likely to occur if a nonphysician was doing the procedure. Granted, this was a small study. You can’t make a generalization out of it, but this does add to the argument that there needs to be more regulation and oversight.
Let’s be real. The cosmetic injection side hustle is alive and well, but I’m good. I’m not going there. Maybe there should be some more quality control. At Botox parties, do people even ask if their injectors are certified or where they bought their vials?
You might be thinking that this isn’t a big deal because it’s just Botox. Let me ask you all a question: If you or your family member were going to go get Botox or another cosmetic injection, would it still not be a big deal?
Dr. Patel is a pediatric hospitalist, television producer, media contributor, and digital health enthusiast. He splits his time between New York City and San Francisco, as he is on faculty at Columbia University/Morgan Stanley Children’s Hospital and UCSF Benioff Children’s Hospital. He reported conflicts of interest with Medumo.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Dr. Patel: A friend recently joked with me and said, “I wish you were a dermatologist so you could hook me up with Botox and fillers.” Well, little does this friend know that I could be a certified cosmetic injector just after a weekend course. Botox parties, here I come?
I can’t blame any health care professional for having a side hustle. People are burned out, want to supplement their income, or scale back clinical hours. According to one Medscape survey, almost 40% of physicians do have some form of a side hustle, whether it is consulting, speaking engagements, being an expert witness, or moonlighting. I know plenty of doctors and nurses who have taken on Botox injecting as a way to make some extra cash.
Now, going back to me and smoothing out wrinkles. I’m a pediatric hospitalist. I’ve never injected an aesthetic product in anyone’s face. When it comes to sharp objects and faces, I’ve sewn lacerations and drained abscesses. In my world, when we talk about botulinum toxin, we’re usually talking about botulism or the therapeutic treatment of migraines and muscle spasms – pathology.
The National Laser Institute has a 2-day Botox and dermal filler training. “Our 2-day Botox and filler course will also teach you how to build a practice and capitalize on the enormous Botox and dermal filler market that exists in the United States.” That’s a lot to cover in 2 days. They even have lunch breaks.
Just from a quick search, I even found an online video course for $1,500. For an additional fee, you can have a live, hands-on component. There are so many trainings out there, including one that’s only 8 hours long, offered by Empire Medical. I also went and spoke with an employee at Empire Medical who told me that because I’m an MD, if I do the course, I can use my certificate and go directly to a manufacturer, buy Botox, and start injecting right away.
Now, is this training actually sufficient for me to go and get good results while minimizing adverse effects like brow ptosis, dry eyes, and asymmetry? I have no idea. According to a review from the Journal of Cosmetic Dermatology, it’s crucial to understand anatomic landmarks, muscle function, baseline asymmetry, potential migration of the toxin, and site-specific precautions.
Okay, that sounds really intimidating, but people still do it. I saw a Business Insider article about a hospitalist who took a 2-day Botox course and then, to her credit, she trained under supervision for an additional 6 months. She then started hosting Botox parties and each time was making $3,500 to upwards of $20,000.
Let’s do some quick mental math. If I were to go online and buy Botox for $3-$6 a unit and then charge patients $15 a unit, and then I consider that in areas like the forehead or in between the eyes – I read that could take 25-50 units – and I repeat this for multiple patients, I can make a few thousand dollars. Well, I may have to adjust my prices according to the market, obviously, because I did see some Groupons advertising $10 per unit.
Who can get in on some Botox cosmetic cash action? Well, physicians can right away. For other health care professionals, it depends on the state. For example, in California, dentists cannot get Botox solely for cosmetic purposes, whereas in Arizona, they can. Generally speaking, NPs and PAs require some type of physician oversight or supervision, but again, it depends on the state.
Oh, and fun fact: Connecticut outright banned Botox parties and said that Botox must be performed “in a medical spa or licensed health care facility and by a Connecticut-licensed health care provider within his or her scope of practice.”
It definitely worries me that someone could go online or go overseas, buy Botox, claim to be a health care professional, and literally commit fraud. I found stories out there such as a couple in San Jose who are giving out Botox from their home without a license. They got arrested. Also, a woman in Alabama who lied about being a licensed dermatologist and did the same, or another woman in Los Angeles who got arrested after selling counterfeit Botox to undercover law enforcement. Surely, there are plenty more cases out there like this.
I asked Dr. Jacqueline Watchmaker, a board-certified dermatologist at U.S. Dermatology Partners in Arizona who has an expertise in cosmetic procedures, what she thought about the booming med spa industry and what, if any, regulatory changes she wanted to see.
Jacqueline Watchmaker, MD: I do think the fact that people can just go to a 1- or 2-day injection course and inject filler and Botox is concerning. I think the lack of regulation surrounding this topic is also very concerning.
There’s so much that goes into being a skilled injector. It’s an intricate knowledge of facial anatomy, which takes weeks, if not months, to really master. There’s actually injection technique, which can be very complex depending on the part of the face that you’re injecting. Even more important, it’s how to prevent complications, but also how to deal with complications if they do occur. There’s no way that these weekend injection courses are able to cover those topics in a thorough and satisfactory manner.
I see complications from med spas all the time, and I think it’s people going to injectors who are not skilled. They don’t know their anatomy, they don’t know the appropriate filler to use, and then heaven forbid there is a complication, they don’t know how to manage the complication – and then those patients get sent to me.
I think patients sometimes forget that these cosmetic procedures are true medical procedures. You need sterile technique. Again, you need to know the anatomy. It can look easy on social media, but there’s a large amount of thought behind it. I think there needs to be more regulation around this topic.
Dr. Patel: In one study, out of 400 people who received a cosmetic procedure, 50 reported an adverse event, such as discoloration or burns, and these adverse events were more likely to occur if a nonphysician was doing the procedure. Granted, this was a small study. You can’t make a generalization out of it, but this does add to the argument that there needs to be more regulation and oversight.
Let’s be real. The cosmetic injection side hustle is alive and well, but I’m good. I’m not going there. Maybe there should be some more quality control. At Botox parties, do people even ask if their injectors are certified or where they bought their vials?
You might be thinking that this isn’t a big deal because it’s just Botox. Let me ask you all a question: If you or your family member were going to go get Botox or another cosmetic injection, would it still not be a big deal?
Dr. Patel is a pediatric hospitalist, television producer, media contributor, and digital health enthusiast. He splits his time between New York City and San Francisco, as he is on faculty at Columbia University/Morgan Stanley Children’s Hospital and UCSF Benioff Children’s Hospital. He reported conflicts of interest with Medumo.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Dr. Patel: A friend recently joked with me and said, “I wish you were a dermatologist so you could hook me up with Botox and fillers.” Well, little does this friend know that I could be a certified cosmetic injector just after a weekend course. Botox parties, here I come?
I can’t blame any health care professional for having a side hustle. People are burned out, want to supplement their income, or scale back clinical hours. According to one Medscape survey, almost 40% of physicians do have some form of a side hustle, whether it is consulting, speaking engagements, being an expert witness, or moonlighting. I know plenty of doctors and nurses who have taken on Botox injecting as a way to make some extra cash.
Now, going back to me and smoothing out wrinkles. I’m a pediatric hospitalist. I’ve never injected an aesthetic product in anyone’s face. When it comes to sharp objects and faces, I’ve sewn lacerations and drained abscesses. In my world, when we talk about botulinum toxin, we’re usually talking about botulism or the therapeutic treatment of migraines and muscle spasms – pathology.
The National Laser Institute has a 2-day Botox and dermal filler training. “Our 2-day Botox and filler course will also teach you how to build a practice and capitalize on the enormous Botox and dermal filler market that exists in the United States.” That’s a lot to cover in 2 days. They even have lunch breaks.
Just from a quick search, I even found an online video course for $1,500. For an additional fee, you can have a live, hands-on component. There are so many trainings out there, including one that’s only 8 hours long, offered by Empire Medical. I also went and spoke with an employee at Empire Medical who told me that because I’m an MD, if I do the course, I can use my certificate and go directly to a manufacturer, buy Botox, and start injecting right away.
Now, is this training actually sufficient for me to go and get good results while minimizing adverse effects like brow ptosis, dry eyes, and asymmetry? I have no idea. According to a review from the Journal of Cosmetic Dermatology, it’s crucial to understand anatomic landmarks, muscle function, baseline asymmetry, potential migration of the toxin, and site-specific precautions.
Okay, that sounds really intimidating, but people still do it. I saw a Business Insider article about a hospitalist who took a 2-day Botox course and then, to her credit, she trained under supervision for an additional 6 months. She then started hosting Botox parties and each time was making $3,500 to upwards of $20,000.
Let’s do some quick mental math. If I were to go online and buy Botox for $3-$6 a unit and then charge patients $15 a unit, and then I consider that in areas like the forehead or in between the eyes – I read that could take 25-50 units – and I repeat this for multiple patients, I can make a few thousand dollars. Well, I may have to adjust my prices according to the market, obviously, because I did see some Groupons advertising $10 per unit.
Who can get in on some Botox cosmetic cash action? Well, physicians can right away. For other health care professionals, it depends on the state. For example, in California, dentists cannot get Botox solely for cosmetic purposes, whereas in Arizona, they can. Generally speaking, NPs and PAs require some type of physician oversight or supervision, but again, it depends on the state.
Oh, and fun fact: Connecticut outright banned Botox parties and said that Botox must be performed “in a medical spa or licensed health care facility and by a Connecticut-licensed health care provider within his or her scope of practice.”
It definitely worries me that someone could go online or go overseas, buy Botox, claim to be a health care professional, and literally commit fraud. I found stories out there such as a couple in San Jose who are giving out Botox from their home without a license. They got arrested. Also, a woman in Alabama who lied about being a licensed dermatologist and did the same, or another woman in Los Angeles who got arrested after selling counterfeit Botox to undercover law enforcement. Surely, there are plenty more cases out there like this.
I asked Dr. Jacqueline Watchmaker, a board-certified dermatologist at U.S. Dermatology Partners in Arizona who has an expertise in cosmetic procedures, what she thought about the booming med spa industry and what, if any, regulatory changes she wanted to see.
Jacqueline Watchmaker, MD: I do think the fact that people can just go to a 1- or 2-day injection course and inject filler and Botox is concerning. I think the lack of regulation surrounding this topic is also very concerning.
There’s so much that goes into being a skilled injector. It’s an intricate knowledge of facial anatomy, which takes weeks, if not months, to really master. There’s actually injection technique, which can be very complex depending on the part of the face that you’re injecting. Even more important, it’s how to prevent complications, but also how to deal with complications if they do occur. There’s no way that these weekend injection courses are able to cover those topics in a thorough and satisfactory manner.
I see complications from med spas all the time, and I think it’s people going to injectors who are not skilled. They don’t know their anatomy, they don’t know the appropriate filler to use, and then heaven forbid there is a complication, they don’t know how to manage the complication – and then those patients get sent to me.
I think patients sometimes forget that these cosmetic procedures are true medical procedures. You need sterile technique. Again, you need to know the anatomy. It can look easy on social media, but there’s a large amount of thought behind it. I think there needs to be more regulation around this topic.
Dr. Patel: In one study, out of 400 people who received a cosmetic procedure, 50 reported an adverse event, such as discoloration or burns, and these adverse events were more likely to occur if a nonphysician was doing the procedure. Granted, this was a small study. You can’t make a generalization out of it, but this does add to the argument that there needs to be more regulation and oversight.
Let’s be real. The cosmetic injection side hustle is alive and well, but I’m good. I’m not going there. Maybe there should be some more quality control. At Botox parties, do people even ask if their injectors are certified or where they bought their vials?
You might be thinking that this isn’t a big deal because it’s just Botox. Let me ask you all a question: If you or your family member were going to go get Botox or another cosmetic injection, would it still not be a big deal?
Dr. Patel is a pediatric hospitalist, television producer, media contributor, and digital health enthusiast. He splits his time between New York City and San Francisco, as he is on faculty at Columbia University/Morgan Stanley Children’s Hospital and UCSF Benioff Children’s Hospital. He reported conflicts of interest with Medumo.
A version of this article first appeared on Medscape.com.
The four questions you should ask about sexual health
This transcript has been edited for clarity.
When I went to med school, we were taught to take a sexual history. Do you smoke? Do you drink? Do you do drugs? Do you have sex? Men, women, or both? And that was it. We’re telling patients that sex is a vice, something that is dangerous and that you should feel bad about. But sex is how we’re all here and how we even continue as a species. We must get comfortable as doctors talking to our patients about sexual medicine.
What if we move away from sex being in the vice category – the part of the social history that’s the bad stuff you shouldn’t be doing? Maybe we should bring it into the review of systems.
As a very basic first step, I like to ask patients four things. As a sexual medicine doctor, I deal with these four things: libido, arousal, orgasm, and pain.
Why are these important? These are the things our patients really care about; 2.3 of every 1,000 people got divorced in 2021.
Libido. Women who have distressing low sexual desire have sex on average two and a half times per month. We call this mercy sex or duty sex. I don’t know what the half time per month looks like, but people genuinely care about desire and their doctors don’t really know that.
We have a biopsychosocial toolbox to help our patients. Let me give you an example: Antidepressants can have sexual side effects. Could there be medications in our toolbox that can help our patients? Of course there can, and there are. What about education or talk therapy? We should be asking our patients what they care about and why they care about it so we can help them achieve their quality-of-life goals.
Arousal. What about arousal? Did you know that erections are a marker of cardiovascular disease in men? We know this to be true for men, and I’m certain the research would be no different for women. We know that there are many biological causes for decrease in arousal, including sleep apnea, diabetes, hypertension, and smoking. I can convince a lot of men to quit smoking because I tell them it’s bad for their penis. We have to understand what our patients care about and then advise them on why we think we can help improve these issues.
Orgasm. How about orgasm? Have you ever been asked whether you can orgasm? Have you ever been asked whether you have questions about orgasm? About 15%-20% of women report having an orgasm disorder, and we rarely talk about this in an exam room. I’ve certainly never been asked, and everybody knows what I do for a living. Not to mention all the men that I and my colleagues see who have really distressing premature ejaculation or delayed orgasm. This is pathophysiology at its finest and most complex. It is so interesting, and we have so much to learn and understand about orgasm in general.
Pain. Finally, ask about pain. It seems obvious that we should be asking our patients about their pain, which includes pelvic pain, but oftentimes we avoid talking about private parts. Pain affects not just our patients, but also their partners and their families, when our patients can’t sit without discomfort, if they can’t go and perform the daily activities that bring them joy and belonging. We have to really work with our toolbox in a biopsychosocial manner to help our patients. I often use the incredible rehabilitation specialists called pelvic floor physical therapists.
Remember, we’re talking about libido, arousal, orgasm, and pain. Sex is important to us as a species. It’s important to our patients. Ask nonjudgmental and open-ended questions. You actually may be the only doctor to ever do so.
Dr. Rubin is an assistant clinical professor, department of urology, Georgetown University, Washington. She reported conflicts of interest with Sprout, Maternal Medical, Absorption Pharmaceuticals, GSK, and Endo.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
When I went to med school, we were taught to take a sexual history. Do you smoke? Do you drink? Do you do drugs? Do you have sex? Men, women, or both? And that was it. We’re telling patients that sex is a vice, something that is dangerous and that you should feel bad about. But sex is how we’re all here and how we even continue as a species. We must get comfortable as doctors talking to our patients about sexual medicine.
What if we move away from sex being in the vice category – the part of the social history that’s the bad stuff you shouldn’t be doing? Maybe we should bring it into the review of systems.
As a very basic first step, I like to ask patients four things. As a sexual medicine doctor, I deal with these four things: libido, arousal, orgasm, and pain.
Why are these important? These are the things our patients really care about; 2.3 of every 1,000 people got divorced in 2021.
Libido. Women who have distressing low sexual desire have sex on average two and a half times per month. We call this mercy sex or duty sex. I don’t know what the half time per month looks like, but people genuinely care about desire and their doctors don’t really know that.
We have a biopsychosocial toolbox to help our patients. Let me give you an example: Antidepressants can have sexual side effects. Could there be medications in our toolbox that can help our patients? Of course there can, and there are. What about education or talk therapy? We should be asking our patients what they care about and why they care about it so we can help them achieve their quality-of-life goals.
Arousal. What about arousal? Did you know that erections are a marker of cardiovascular disease in men? We know this to be true for men, and I’m certain the research would be no different for women. We know that there are many biological causes for decrease in arousal, including sleep apnea, diabetes, hypertension, and smoking. I can convince a lot of men to quit smoking because I tell them it’s bad for their penis. We have to understand what our patients care about and then advise them on why we think we can help improve these issues.
Orgasm. How about orgasm? Have you ever been asked whether you can orgasm? Have you ever been asked whether you have questions about orgasm? About 15%-20% of women report having an orgasm disorder, and we rarely talk about this in an exam room. I’ve certainly never been asked, and everybody knows what I do for a living. Not to mention all the men that I and my colleagues see who have really distressing premature ejaculation or delayed orgasm. This is pathophysiology at its finest and most complex. It is so interesting, and we have so much to learn and understand about orgasm in general.
Pain. Finally, ask about pain. It seems obvious that we should be asking our patients about their pain, which includes pelvic pain, but oftentimes we avoid talking about private parts. Pain affects not just our patients, but also their partners and their families, when our patients can’t sit without discomfort, if they can’t go and perform the daily activities that bring them joy and belonging. We have to really work with our toolbox in a biopsychosocial manner to help our patients. I often use the incredible rehabilitation specialists called pelvic floor physical therapists.
Remember, we’re talking about libido, arousal, orgasm, and pain. Sex is important to us as a species. It’s important to our patients. Ask nonjudgmental and open-ended questions. You actually may be the only doctor to ever do so.
Dr. Rubin is an assistant clinical professor, department of urology, Georgetown University, Washington. She reported conflicts of interest with Sprout, Maternal Medical, Absorption Pharmaceuticals, GSK, and Endo.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
When I went to med school, we were taught to take a sexual history. Do you smoke? Do you drink? Do you do drugs? Do you have sex? Men, women, or both? And that was it. We’re telling patients that sex is a vice, something that is dangerous and that you should feel bad about. But sex is how we’re all here and how we even continue as a species. We must get comfortable as doctors talking to our patients about sexual medicine.
What if we move away from sex being in the vice category – the part of the social history that’s the bad stuff you shouldn’t be doing? Maybe we should bring it into the review of systems.
As a very basic first step, I like to ask patients four things. As a sexual medicine doctor, I deal with these four things: libido, arousal, orgasm, and pain.
Why are these important? These are the things our patients really care about; 2.3 of every 1,000 people got divorced in 2021.
Libido. Women who have distressing low sexual desire have sex on average two and a half times per month. We call this mercy sex or duty sex. I don’t know what the half time per month looks like, but people genuinely care about desire and their doctors don’t really know that.
We have a biopsychosocial toolbox to help our patients. Let me give you an example: Antidepressants can have sexual side effects. Could there be medications in our toolbox that can help our patients? Of course there can, and there are. What about education or talk therapy? We should be asking our patients what they care about and why they care about it so we can help them achieve their quality-of-life goals.
Arousal. What about arousal? Did you know that erections are a marker of cardiovascular disease in men? We know this to be true for men, and I’m certain the research would be no different for women. We know that there are many biological causes for decrease in arousal, including sleep apnea, diabetes, hypertension, and smoking. I can convince a lot of men to quit smoking because I tell them it’s bad for their penis. We have to understand what our patients care about and then advise them on why we think we can help improve these issues.
Orgasm. How about orgasm? Have you ever been asked whether you can orgasm? Have you ever been asked whether you have questions about orgasm? About 15%-20% of women report having an orgasm disorder, and we rarely talk about this in an exam room. I’ve certainly never been asked, and everybody knows what I do for a living. Not to mention all the men that I and my colleagues see who have really distressing premature ejaculation or delayed orgasm. This is pathophysiology at its finest and most complex. It is so interesting, and we have so much to learn and understand about orgasm in general.
Pain. Finally, ask about pain. It seems obvious that we should be asking our patients about their pain, which includes pelvic pain, but oftentimes we avoid talking about private parts. Pain affects not just our patients, but also their partners and their families, when our patients can’t sit without discomfort, if they can’t go and perform the daily activities that bring them joy and belonging. We have to really work with our toolbox in a biopsychosocial manner to help our patients. I often use the incredible rehabilitation specialists called pelvic floor physical therapists.
Remember, we’re talking about libido, arousal, orgasm, and pain. Sex is important to us as a species. It’s important to our patients. Ask nonjudgmental and open-ended questions. You actually may be the only doctor to ever do so.
Dr. Rubin is an assistant clinical professor, department of urology, Georgetown University, Washington. She reported conflicts of interest with Sprout, Maternal Medical, Absorption Pharmaceuticals, GSK, and Endo.
A version of this article first appeared on Medscape.com.
New and emerging options for treating recurrent C. difficile
This transcript has been edited for clarity.
Clostridioides difficile is a toxin-based infection that takes up residence in the colon due to disturbed normal bowel flora, usually after antibiotics.
Recurrent C. difficile can happen in up to a quarter of patients who receive oral vancomycin as a treatment for their infection. It can also occur with treatment with the newer agent, fidaxomicin, although possibly in fewer patients. In general, relapses are indeed common.
When I trained at Johns Hopkins under John Bartlett, he took the approach that after the second – and always after the third – relapse, an extended course of oral therapy with vancomycin could help get patients out of trouble. He used the so-called extended pulse method, where patients would take the drug for approximately 4-6 weeks and gradually reduce the dose.
This approach can also be done with fidaxomicin. However, I’m not sure it works much better than vancomycin, and there are often hurdles to using fidaxomicin because of insurers not approving it because of the expense.
What other therapies are there?
There is bezlotoxumab, which is a human monoclonal antibody targeting C. difficile toxin B. I’ve used it a few times. It is given as a one-time infusion, and there are challenges regarding cost, the logistics of setting up the infusion, and insurance approval.
Fecal microbiota transplant
In recent years, fecal microbiota transplants (FMT) have received a lot of attention as a different avenue of treatment that could lower the potential for relapses, with success rates usually around 80%-90%. However, in the past few years, there have been some serious safety signals because of possible transmission of dangerous pathogens, often with drug resistance, with FMT.
I’m therefore pleased to say that newer fecal microbiota products are coming in fast and furious. I thought I’d spend a few minutes speaking about these.
OpenBiome, an organization dedicated to microbiome research, offers an investigational product from screened donors that has not received Food and Drug Administration approval. It’s been around for some time. It can be used in either upper or lower GI applications, and the organization cites about an 84% success rate using this product.
There are also two new FDA-approved products I think are worth knowing about. They’ve just been approved recently and we’re a little uncertain of where they’re going to end up in the treatment landscape.
The first is from Ferring, and it goes by fecal microbiota, live-jslm (Rebyota). This is a product from qualified and screened donors, the main component of which is Bacteroides, which is given as a single dose by enema.
The company did a phase 3 trial with a Bayesian primary analysis, which I think convinced the FDA to approve this product. The success rate in people with multiple relapses was 70.6%, compared with 57.5% with placebo. The estimated treatment effect was 13.1%. Of those who did respond, over 90% were kept free of relapse over a 6-month period.
The other product, also FDA approved, is from Seres. It was previously called SER-109, and is now called fecal microbiota spores, live-brpk (Vowst). Unlike the previous product, this is orally administered, with patients taking four capsules daily for 3 days. Again, these donor-derived firmicutes have been appropriately screened and are free of potential pathogens.
The phase 3 randomized clinical trial results were published in the New England Journal of Medicine. They showed that 12% of those taking this product had a relapse, compared with 40% of those taking placebo, which is about the range we tend to see in people who have had multiple relapses. The safety profile was similar to placebo.
So, how will people use these treatments?
I think the FDA imprimatur will be attractive to people, but the products, I believe, will be priced fairly expensively, in the under $10,000 range. The first (Rebyota) is a rectal infusion; it is a one-and-done treatment but creates logistical issues. Interestingly, it could be a billable procedure for infectious disease clinicians. The ease of oral administration for Vowst, no doubt, will be very appealing. Both of these are given after completing a course of treatment with vancomycin or fidaxomicin so as not to interfere with the microbiome product.
I’ll also briefly mention a paper published in JAMA on yet another microbiome product, called VE303. This product was based on eight commensal strains of Clostridia and was given orally in a phase 2 trial. Interestingly, this worked about the same as the oral product that is already FDA approved. The study showed a recurrence rate of 13.8% in the high-dose group, compared with 45.5% in the placebo group.
I think this is exciting. And, of course, there is the expense.
But anything that can be done to help improve these patients is welcome, as once they get into the multiple-relapse phase, it is challenging to turn around. These commercialized products will hopefully become a bit more mainstream. Certainly, we’ll see how these will be utilized in the coming months and over the next few years.
Dr. Auwaerter is Clinical Director, Division of Infectious Diseases, Johns Hopkins University, Baltimore. He reported conflicts of interest with Gilead, Shionogi, and Medscape.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Clostridioides difficile is a toxin-based infection that takes up residence in the colon due to disturbed normal bowel flora, usually after antibiotics.
Recurrent C. difficile can happen in up to a quarter of patients who receive oral vancomycin as a treatment for their infection. It can also occur with treatment with the newer agent, fidaxomicin, although possibly in fewer patients. In general, relapses are indeed common.
When I trained at Johns Hopkins under John Bartlett, he took the approach that after the second – and always after the third – relapse, an extended course of oral therapy with vancomycin could help get patients out of trouble. He used the so-called extended pulse method, where patients would take the drug for approximately 4-6 weeks and gradually reduce the dose.
This approach can also be done with fidaxomicin. However, I’m not sure it works much better than vancomycin, and there are often hurdles to using fidaxomicin because of insurers not approving it because of the expense.
What other therapies are there?
There is bezlotoxumab, which is a human monoclonal antibody targeting C. difficile toxin B. I’ve used it a few times. It is given as a one-time infusion, and there are challenges regarding cost, the logistics of setting up the infusion, and insurance approval.
Fecal microbiota transplant
In recent years, fecal microbiota transplants (FMT) have received a lot of attention as a different avenue of treatment that could lower the potential for relapses, with success rates usually around 80%-90%. However, in the past few years, there have been some serious safety signals because of possible transmission of dangerous pathogens, often with drug resistance, with FMT.
I’m therefore pleased to say that newer fecal microbiota products are coming in fast and furious. I thought I’d spend a few minutes speaking about these.
OpenBiome, an organization dedicated to microbiome research, offers an investigational product from screened donors that has not received Food and Drug Administration approval. It’s been around for some time. It can be used in either upper or lower GI applications, and the organization cites about an 84% success rate using this product.
There are also two new FDA-approved products I think are worth knowing about. They’ve just been approved recently and we’re a little uncertain of where they’re going to end up in the treatment landscape.
The first is from Ferring, and it goes by fecal microbiota, live-jslm (Rebyota). This is a product from qualified and screened donors, the main component of which is Bacteroides, which is given as a single dose by enema.
The company did a phase 3 trial with a Bayesian primary analysis, which I think convinced the FDA to approve this product. The success rate in people with multiple relapses was 70.6%, compared with 57.5% with placebo. The estimated treatment effect was 13.1%. Of those who did respond, over 90% were kept free of relapse over a 6-month period.
The other product, also FDA approved, is from Seres. It was previously called SER-109, and is now called fecal microbiota spores, live-brpk (Vowst). Unlike the previous product, this is orally administered, with patients taking four capsules daily for 3 days. Again, these donor-derived firmicutes have been appropriately screened and are free of potential pathogens.
The phase 3 randomized clinical trial results were published in the New England Journal of Medicine. They showed that 12% of those taking this product had a relapse, compared with 40% of those taking placebo, which is about the range we tend to see in people who have had multiple relapses. The safety profile was similar to placebo.
So, how will people use these treatments?
I think the FDA imprimatur will be attractive to people, but the products, I believe, will be priced fairly expensively, in the under $10,000 range. The first (Rebyota) is a rectal infusion; it is a one-and-done treatment but creates logistical issues. Interestingly, it could be a billable procedure for infectious disease clinicians. The ease of oral administration for Vowst, no doubt, will be very appealing. Both of these are given after completing a course of treatment with vancomycin or fidaxomicin so as not to interfere with the microbiome product.
I’ll also briefly mention a paper published in JAMA on yet another microbiome product, called VE303. This product was based on eight commensal strains of Clostridia and was given orally in a phase 2 trial. Interestingly, this worked about the same as the oral product that is already FDA approved. The study showed a recurrence rate of 13.8% in the high-dose group, compared with 45.5% in the placebo group.
I think this is exciting. And, of course, there is the expense.
But anything that can be done to help improve these patients is welcome, as once they get into the multiple-relapse phase, it is challenging to turn around. These commercialized products will hopefully become a bit more mainstream. Certainly, we’ll see how these will be utilized in the coming months and over the next few years.
Dr. Auwaerter is Clinical Director, Division of Infectious Diseases, Johns Hopkins University, Baltimore. He reported conflicts of interest with Gilead, Shionogi, and Medscape.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Clostridioides difficile is a toxin-based infection that takes up residence in the colon due to disturbed normal bowel flora, usually after antibiotics.
Recurrent C. difficile can happen in up to a quarter of patients who receive oral vancomycin as a treatment for their infection. It can also occur with treatment with the newer agent, fidaxomicin, although possibly in fewer patients. In general, relapses are indeed common.
When I trained at Johns Hopkins under John Bartlett, he took the approach that after the second – and always after the third – relapse, an extended course of oral therapy with vancomycin could help get patients out of trouble. He used the so-called extended pulse method, where patients would take the drug for approximately 4-6 weeks and gradually reduce the dose.
This approach can also be done with fidaxomicin. However, I’m not sure it works much better than vancomycin, and there are often hurdles to using fidaxomicin because of insurers not approving it because of the expense.
What other therapies are there?
There is bezlotoxumab, which is a human monoclonal antibody targeting C. difficile toxin B. I’ve used it a few times. It is given as a one-time infusion, and there are challenges regarding cost, the logistics of setting up the infusion, and insurance approval.
Fecal microbiota transplant
In recent years, fecal microbiota transplants (FMT) have received a lot of attention as a different avenue of treatment that could lower the potential for relapses, with success rates usually around 80%-90%. However, in the past few years, there have been some serious safety signals because of possible transmission of dangerous pathogens, often with drug resistance, with FMT.
I’m therefore pleased to say that newer fecal microbiota products are coming in fast and furious. I thought I’d spend a few minutes speaking about these.
OpenBiome, an organization dedicated to microbiome research, offers an investigational product from screened donors that has not received Food and Drug Administration approval. It’s been around for some time. It can be used in either upper or lower GI applications, and the organization cites about an 84% success rate using this product.
There are also two new FDA-approved products I think are worth knowing about. They’ve just been approved recently and we’re a little uncertain of where they’re going to end up in the treatment landscape.
The first is from Ferring, and it goes by fecal microbiota, live-jslm (Rebyota). This is a product from qualified and screened donors, the main component of which is Bacteroides, which is given as a single dose by enema.
The company did a phase 3 trial with a Bayesian primary analysis, which I think convinced the FDA to approve this product. The success rate in people with multiple relapses was 70.6%, compared with 57.5% with placebo. The estimated treatment effect was 13.1%. Of those who did respond, over 90% were kept free of relapse over a 6-month period.
The other product, also FDA approved, is from Seres. It was previously called SER-109, and is now called fecal microbiota spores, live-brpk (Vowst). Unlike the previous product, this is orally administered, with patients taking four capsules daily for 3 days. Again, these donor-derived firmicutes have been appropriately screened and are free of potential pathogens.
The phase 3 randomized clinical trial results were published in the New England Journal of Medicine. They showed that 12% of those taking this product had a relapse, compared with 40% of those taking placebo, which is about the range we tend to see in people who have had multiple relapses. The safety profile was similar to placebo.
So, how will people use these treatments?
I think the FDA imprimatur will be attractive to people, but the products, I believe, will be priced fairly expensively, in the under $10,000 range. The first (Rebyota) is a rectal infusion; it is a one-and-done treatment but creates logistical issues. Interestingly, it could be a billable procedure for infectious disease clinicians. The ease of oral administration for Vowst, no doubt, will be very appealing. Both of these are given after completing a course of treatment with vancomycin or fidaxomicin so as not to interfere with the microbiome product.
I’ll also briefly mention a paper published in JAMA on yet another microbiome product, called VE303. This product was based on eight commensal strains of Clostridia and was given orally in a phase 2 trial. Interestingly, this worked about the same as the oral product that is already FDA approved. The study showed a recurrence rate of 13.8% in the high-dose group, compared with 45.5% in the placebo group.
I think this is exciting. And, of course, there is the expense.
But anything that can be done to help improve these patients is welcome, as once they get into the multiple-relapse phase, it is challenging to turn around. These commercialized products will hopefully become a bit more mainstream. Certainly, we’ll see how these will be utilized in the coming months and over the next few years.
Dr. Auwaerter is Clinical Director, Division of Infectious Diseases, Johns Hopkins University, Baltimore. He reported conflicts of interest with Gilead, Shionogi, and Medscape.
A version of this article first appeared on Medscape.com.
Brain damage from recurrent relapses of bipolar mania: A call for early LAI use
Bipolar disorder (BD) is a psychotic mood disorder. Like schizophrenia, it has been shown to be associated with significant degeneration and structural brain abnormalities with multiple relapses.1,2
Just as I have always advocated preventing recurrences in schizophrenia by using long-acting injectable (LAI) antipsychotic formulations immediately after the first episode to prevent psychotic relapses and progressive brain damage,3 I strongly recommend using LAIs right after hospital discharge from the first manic episode. It is the most rational management approach for bipolar mania given the grave consequences of multiple episodes, which are so common in this psychotic mood disorder due to poor medication adherence.
In contrast to the depressive episodes of BD I, where patients have insight into their depression and seek psychiatric treatment, during a manic episode patients often have no insight (anosognosia) that they suffer from a serious brain disorder, and refuse treatment.4 In addition, young patients with BD I frequently discontinue their oral mood stabilizer or second-generation antipsychotic (which are approved for mania) because they miss the blissful euphoria and the buoyant physical and mental energy of their manic episodes. They are completely oblivious to (and uninformed about) the grave neurobiological damage of further manic episodes, which can condemn them to clinical, functional, and cognitive deterioration. These patients are also likely to become treatment-resistant, which has been labeled as “the malignant transformation of bipolar disorder.”5
The evidence for progressive brain tissue loss, clinical deterioration, functional decline, and treatment resistance is abundant.6 I was the lead investigator of the first study to report ventricular dilatation (which is a proxy for cortical atrophy) in bipolar mania,7 a discovery that was subsequently replicated by 2 dozen researchers. This was followed by numerous neuroimaging studies reporting a loss of volume across multiple brain regions, including the frontal lobe, temporal lobe, cerebellum, thalamus, hippocampus, and basal ganglia. BD is heterogeneous8 with 4 stages (Table 19), and patients experience progressively worse brain structure and function with each stage.
Many patients with bipolar mania end up with poor clinical and functional outcomes, even when they respond well to initial treatment with lithium, anticonvulsant mood stabilizers, or second-generation antipsychotics. With their intentional nonadherence to oral medications leading to multiple recurrent relapses, these patients are at serious risk for neuroprogression and brain atrophic changes driven by multiple factors: inflammatory cytokines, increased cortical steroids, decreased neurotrophins, deceased neurogenesis, increased oxidative stress, and mitochondrial energy dysfunction. The consequences include progressive shortening of the interval between episodes with every relapse and loss of responsiveness to pharmacotherapy as the illness progresses.6,10 Predictors of a downhill progression include genetic vulnerability, perinatal complication during fetal life, childhood trauma (physical, sexual, emotional, or neglect), substance use, stress, psychiatric/medial comorbidities, and especially the number of episodes.9,11
Biomarkers have been reported in both the early and late stages of BD (Table 212) as well as in postmortem studies (Table 38,13). They reflect the progressive neurodegenerative nature of recurrent BD I episodes as the disorder moves to the advanced stages. I summarize these stages in Table 19 and Table 212 for the benefit of psychiatric clinicians who do not have access to the neuroscience journals where such findings are usually published.
BD I is also believed to be associated with accelerated aging14,15 and an increased risk for dementia16 or cognitive deterioration.17 There is also an emerging hypothesis that neuroprogression and treatment resistance in BD is frequently associated with insulin resistance,18 peripheral inflammation,19 and blood-brain barrier permeability dysfunction.20
The bottom line is that like patients with schizophrenia, where relapses lead to devastating consequences,21 those with BD are at a similar high risk for neuroprogression, which includes atrophy in several brain regions, treatment resistance, and functional disability. This underscores the urgency for implementing LAI therapy early in the illness, when the first manic episode (Stage 2) emerges after the prodrome (Stage 1). This is the best strategy to preserve brain health in persons with BD22 and to allow them to remain functional with their many intellectual gifts, such as eloquence, poetry, artistic talents, humor, and social skills. It is unfortunate that the combination of patients’ and clinicians’ reluctance to use an LAI early in the illness dooms many patients with BD to a potentially avoidable malignant outcome.
1. Strakowski SM, DelBello MP, Adler CM. The functional neuroanatomy of bipolar disorder: a review of neuroimaging findings. Mol Psychiatry. 2005;10(1):105-106.
2. Kapezinski NS, Mwangi B, Cassidy RM, et al. Neuroprogression and illness trajectories in bipolar disorder. Expert Rev Neurother. 2017;17(3):277-285.
3. Nasrallah HA. Errors of omission and commission in psychiatric practice. Current Psychiatry. 2017;16(11):4,6,8.
4. Nasrallah HA. Is anosognosia a delusion, a negative symptom, or a cognitive deficit? Current Psychiatry. 2022;21(1):6-8,14.
5. Post RM. Preventing the malignant transformation of bipolar disorder. JAMA. 2018;319(12):1197-1198.
6. Berk M, Kapczinski F, Andreazza AC, et al. Pathways underlying neuroprogression in bipolar disorder: focus on inflammation, oxidative stress and neurotrophic factors. Neurosci Biobehav Rev. 2011;35(3):804-817.
7. Nasrallah HA, McCalley-Whitters M, Jacoby CG. Cerebral ventricular enlargement in young manic males. A controlled CT study. J Affective Dis. 1982;4(1):15-19.
8. Maletic V, Raison C. Integrated neurobiology of bipolar disorder. Front Psychiatry. 2014;5:98.
9. Berk M. Neuroprogression: pathways to progressive brain changes in bipolar disorder. Int J Neuropsychopharmacol. 2009;12(4):441-445.
10. Berk M, Conus P, Kapczinski F, et al. From neuroprogression to neuroprotection: implications for clinical care. Med J Aust. 2010;193(S4):S36-S40.
11. Passos IC, Mwangi B, Vieta E, et al. Areas of controversy in neuroprogression in bipolar disorder. Acta Psychiatr Scand. 2016;134(2):91-103.
12. Fries GR, Pfaffenseller B, Stertz L, et al. Staging and neuroprogression in bipolar disorder. Curr Psychiatry Rep. 2012;14(6):667-675.
13. Manji HK, Drevets WC, Charney DS. The cellular neurobiology of depression. Nat Med. 2001;7(5):541-547.
14. Fries GR, Zamzow MJ, Andrews T, et al. Accelerated aging in bipolar disorder: a comprehensive review of molecular findings and their clinical implications. Neurosci Biobehav Rev. 2020;112:107-116.
15. Fries GR, Bauer IE, Scaini G, et al. Accelerated hippocampal biological aging in bipolar disorder. Bipolar Dis. 2020;22(5):498-507.
16. Diniz BS, Teixeira AL, Cao F, et al. History of bipolar disorder and the risk of dementia: a systematic review and meta-analysis. Am J Geriatr Psychiatry. 2017;25(4):357-362.
17. Bauer IE, Ouyang A, Mwangi B, et al. Reduced white matter integrity and verbal fluency impairment in young adults with bipolar disorder: a diffusion tensor imaging study. J Psychiatr Res. 2015;62:115-122.
18. Calkin CV. Insulin resistance takes center stage: a new paradigm in the progression of bipolar disorder. Ann Med. 2019;51(5-6):281-293.
19. Grewal S, McKinlay S, Kapczinski F, et al. Biomarkers of neuroprogression and late staging in bipolar disorder: a systematic review. Aust N Z J Psychiatry. 2023;57(3):328-343.
20. Calkin C, McClelland C, Cairns K, et al. Insulin resistance and blood-brain barrier dysfunction underlie neuroprogression in bipolar disorder. Front Psychiatry. 2021;12:636174.
21. Nasrallah HA. 10 devastating consequences of psychotic relapses. Current Psychiatry. 2021;20(5):9-12.
22. Berk M, Hallam K, Malhi GS, et al. Evidence and implications for early intervention in bipolar disorder. J Ment Health. 2010;19(2):113-126.
Bipolar disorder (BD) is a psychotic mood disorder. Like schizophrenia, it has been shown to be associated with significant degeneration and structural brain abnormalities with multiple relapses.1,2
Just as I have always advocated preventing recurrences in schizophrenia by using long-acting injectable (LAI) antipsychotic formulations immediately after the first episode to prevent psychotic relapses and progressive brain damage,3 I strongly recommend using LAIs right after hospital discharge from the first manic episode. It is the most rational management approach for bipolar mania given the grave consequences of multiple episodes, which are so common in this psychotic mood disorder due to poor medication adherence.
In contrast to the depressive episodes of BD I, where patients have insight into their depression and seek psychiatric treatment, during a manic episode patients often have no insight (anosognosia) that they suffer from a serious brain disorder, and refuse treatment.4 In addition, young patients with BD I frequently discontinue their oral mood stabilizer or second-generation antipsychotic (which are approved for mania) because they miss the blissful euphoria and the buoyant physical and mental energy of their manic episodes. They are completely oblivious to (and uninformed about) the grave neurobiological damage of further manic episodes, which can condemn them to clinical, functional, and cognitive deterioration. These patients are also likely to become treatment-resistant, which has been labeled as “the malignant transformation of bipolar disorder.”5
The evidence for progressive brain tissue loss, clinical deterioration, functional decline, and treatment resistance is abundant.6 I was the lead investigator of the first study to report ventricular dilatation (which is a proxy for cortical atrophy) in bipolar mania,7 a discovery that was subsequently replicated by 2 dozen researchers. This was followed by numerous neuroimaging studies reporting a loss of volume across multiple brain regions, including the frontal lobe, temporal lobe, cerebellum, thalamus, hippocampus, and basal ganglia. BD is heterogeneous8 with 4 stages (Table 19), and patients experience progressively worse brain structure and function with each stage.
Many patients with bipolar mania end up with poor clinical and functional outcomes, even when they respond well to initial treatment with lithium, anticonvulsant mood stabilizers, or second-generation antipsychotics. With their intentional nonadherence to oral medications leading to multiple recurrent relapses, these patients are at serious risk for neuroprogression and brain atrophic changes driven by multiple factors: inflammatory cytokines, increased cortical steroids, decreased neurotrophins, deceased neurogenesis, increased oxidative stress, and mitochondrial energy dysfunction. The consequences include progressive shortening of the interval between episodes with every relapse and loss of responsiveness to pharmacotherapy as the illness progresses.6,10 Predictors of a downhill progression include genetic vulnerability, perinatal complication during fetal life, childhood trauma (physical, sexual, emotional, or neglect), substance use, stress, psychiatric/medial comorbidities, and especially the number of episodes.9,11
Biomarkers have been reported in both the early and late stages of BD (Table 212) as well as in postmortem studies (Table 38,13). They reflect the progressive neurodegenerative nature of recurrent BD I episodes as the disorder moves to the advanced stages. I summarize these stages in Table 19 and Table 212 for the benefit of psychiatric clinicians who do not have access to the neuroscience journals where such findings are usually published.
BD I is also believed to be associated with accelerated aging14,15 and an increased risk for dementia16 or cognitive deterioration.17 There is also an emerging hypothesis that neuroprogression and treatment resistance in BD is frequently associated with insulin resistance,18 peripheral inflammation,19 and blood-brain barrier permeability dysfunction.20
The bottom line is that like patients with schizophrenia, where relapses lead to devastating consequences,21 those with BD are at a similar high risk for neuroprogression, which includes atrophy in several brain regions, treatment resistance, and functional disability. This underscores the urgency for implementing LAI therapy early in the illness, when the first manic episode (Stage 2) emerges after the prodrome (Stage 1). This is the best strategy to preserve brain health in persons with BD22 and to allow them to remain functional with their many intellectual gifts, such as eloquence, poetry, artistic talents, humor, and social skills. It is unfortunate that the combination of patients’ and clinicians’ reluctance to use an LAI early in the illness dooms many patients with BD to a potentially avoidable malignant outcome.
Bipolar disorder (BD) is a psychotic mood disorder. Like schizophrenia, it has been shown to be associated with significant degeneration and structural brain abnormalities with multiple relapses.1,2
Just as I have always advocated preventing recurrences in schizophrenia by using long-acting injectable (LAI) antipsychotic formulations immediately after the first episode to prevent psychotic relapses and progressive brain damage,3 I strongly recommend using LAIs right after hospital discharge from the first manic episode. It is the most rational management approach for bipolar mania given the grave consequences of multiple episodes, which are so common in this psychotic mood disorder due to poor medication adherence.
In contrast to the depressive episodes of BD I, where patients have insight into their depression and seek psychiatric treatment, during a manic episode patients often have no insight (anosognosia) that they suffer from a serious brain disorder, and refuse treatment.4 In addition, young patients with BD I frequently discontinue their oral mood stabilizer or second-generation antipsychotic (which are approved for mania) because they miss the blissful euphoria and the buoyant physical and mental energy of their manic episodes. They are completely oblivious to (and uninformed about) the grave neurobiological damage of further manic episodes, which can condemn them to clinical, functional, and cognitive deterioration. These patients are also likely to become treatment-resistant, which has been labeled as “the malignant transformation of bipolar disorder.”5
The evidence for progressive brain tissue loss, clinical deterioration, functional decline, and treatment resistance is abundant.6 I was the lead investigator of the first study to report ventricular dilatation (which is a proxy for cortical atrophy) in bipolar mania,7 a discovery that was subsequently replicated by 2 dozen researchers. This was followed by numerous neuroimaging studies reporting a loss of volume across multiple brain regions, including the frontal lobe, temporal lobe, cerebellum, thalamus, hippocampus, and basal ganglia. BD is heterogeneous8 with 4 stages (Table 19), and patients experience progressively worse brain structure and function with each stage.
Many patients with bipolar mania end up with poor clinical and functional outcomes, even when they respond well to initial treatment with lithium, anticonvulsant mood stabilizers, or second-generation antipsychotics. With their intentional nonadherence to oral medications leading to multiple recurrent relapses, these patients are at serious risk for neuroprogression and brain atrophic changes driven by multiple factors: inflammatory cytokines, increased cortical steroids, decreased neurotrophins, deceased neurogenesis, increased oxidative stress, and mitochondrial energy dysfunction. The consequences include progressive shortening of the interval between episodes with every relapse and loss of responsiveness to pharmacotherapy as the illness progresses.6,10 Predictors of a downhill progression include genetic vulnerability, perinatal complication during fetal life, childhood trauma (physical, sexual, emotional, or neglect), substance use, stress, psychiatric/medial comorbidities, and especially the number of episodes.9,11
Biomarkers have been reported in both the early and late stages of BD (Table 212) as well as in postmortem studies (Table 38,13). They reflect the progressive neurodegenerative nature of recurrent BD I episodes as the disorder moves to the advanced stages. I summarize these stages in Table 19 and Table 212 for the benefit of psychiatric clinicians who do not have access to the neuroscience journals where such findings are usually published.
BD I is also believed to be associated with accelerated aging14,15 and an increased risk for dementia16 or cognitive deterioration.17 There is also an emerging hypothesis that neuroprogression and treatment resistance in BD is frequently associated with insulin resistance,18 peripheral inflammation,19 and blood-brain barrier permeability dysfunction.20
The bottom line is that like patients with schizophrenia, where relapses lead to devastating consequences,21 those with BD are at a similar high risk for neuroprogression, which includes atrophy in several brain regions, treatment resistance, and functional disability. This underscores the urgency for implementing LAI therapy early in the illness, when the first manic episode (Stage 2) emerges after the prodrome (Stage 1). This is the best strategy to preserve brain health in persons with BD22 and to allow them to remain functional with their many intellectual gifts, such as eloquence, poetry, artistic talents, humor, and social skills. It is unfortunate that the combination of patients’ and clinicians’ reluctance to use an LAI early in the illness dooms many patients with BD to a potentially avoidable malignant outcome.
1. Strakowski SM, DelBello MP, Adler CM. The functional neuroanatomy of bipolar disorder: a review of neuroimaging findings. Mol Psychiatry. 2005;10(1):105-106.
2. Kapezinski NS, Mwangi B, Cassidy RM, et al. Neuroprogression and illness trajectories in bipolar disorder. Expert Rev Neurother. 2017;17(3):277-285.
3. Nasrallah HA. Errors of omission and commission in psychiatric practice. Current Psychiatry. 2017;16(11):4,6,8.
4. Nasrallah HA. Is anosognosia a delusion, a negative symptom, or a cognitive deficit? Current Psychiatry. 2022;21(1):6-8,14.
5. Post RM. Preventing the malignant transformation of bipolar disorder. JAMA. 2018;319(12):1197-1198.
6. Berk M, Kapczinski F, Andreazza AC, et al. Pathways underlying neuroprogression in bipolar disorder: focus on inflammation, oxidative stress and neurotrophic factors. Neurosci Biobehav Rev. 2011;35(3):804-817.
7. Nasrallah HA, McCalley-Whitters M, Jacoby CG. Cerebral ventricular enlargement in young manic males. A controlled CT study. J Affective Dis. 1982;4(1):15-19.
8. Maletic V, Raison C. Integrated neurobiology of bipolar disorder. Front Psychiatry. 2014;5:98.
9. Berk M. Neuroprogression: pathways to progressive brain changes in bipolar disorder. Int J Neuropsychopharmacol. 2009;12(4):441-445.
10. Berk M, Conus P, Kapczinski F, et al. From neuroprogression to neuroprotection: implications for clinical care. Med J Aust. 2010;193(S4):S36-S40.
11. Passos IC, Mwangi B, Vieta E, et al. Areas of controversy in neuroprogression in bipolar disorder. Acta Psychiatr Scand. 2016;134(2):91-103.
12. Fries GR, Pfaffenseller B, Stertz L, et al. Staging and neuroprogression in bipolar disorder. Curr Psychiatry Rep. 2012;14(6):667-675.
13. Manji HK, Drevets WC, Charney DS. The cellular neurobiology of depression. Nat Med. 2001;7(5):541-547.
14. Fries GR, Zamzow MJ, Andrews T, et al. Accelerated aging in bipolar disorder: a comprehensive review of molecular findings and their clinical implications. Neurosci Biobehav Rev. 2020;112:107-116.
15. Fries GR, Bauer IE, Scaini G, et al. Accelerated hippocampal biological aging in bipolar disorder. Bipolar Dis. 2020;22(5):498-507.
16. Diniz BS, Teixeira AL, Cao F, et al. History of bipolar disorder and the risk of dementia: a systematic review and meta-analysis. Am J Geriatr Psychiatry. 2017;25(4):357-362.
17. Bauer IE, Ouyang A, Mwangi B, et al. Reduced white matter integrity and verbal fluency impairment in young adults with bipolar disorder: a diffusion tensor imaging study. J Psychiatr Res. 2015;62:115-122.
18. Calkin CV. Insulin resistance takes center stage: a new paradigm in the progression of bipolar disorder. Ann Med. 2019;51(5-6):281-293.
19. Grewal S, McKinlay S, Kapczinski F, et al. Biomarkers of neuroprogression and late staging in bipolar disorder: a systematic review. Aust N Z J Psychiatry. 2023;57(3):328-343.
20. Calkin C, McClelland C, Cairns K, et al. Insulin resistance and blood-brain barrier dysfunction underlie neuroprogression in bipolar disorder. Front Psychiatry. 2021;12:636174.
21. Nasrallah HA. 10 devastating consequences of psychotic relapses. Current Psychiatry. 2021;20(5):9-12.
22. Berk M, Hallam K, Malhi GS, et al. Evidence and implications for early intervention in bipolar disorder. J Ment Health. 2010;19(2):113-126.
1. Strakowski SM, DelBello MP, Adler CM. The functional neuroanatomy of bipolar disorder: a review of neuroimaging findings. Mol Psychiatry. 2005;10(1):105-106.
2. Kapezinski NS, Mwangi B, Cassidy RM, et al. Neuroprogression and illness trajectories in bipolar disorder. Expert Rev Neurother. 2017;17(3):277-285.
3. Nasrallah HA. Errors of omission and commission in psychiatric practice. Current Psychiatry. 2017;16(11):4,6,8.
4. Nasrallah HA. Is anosognosia a delusion, a negative symptom, or a cognitive deficit? Current Psychiatry. 2022;21(1):6-8,14.
5. Post RM. Preventing the malignant transformation of bipolar disorder. JAMA. 2018;319(12):1197-1198.
6. Berk M, Kapczinski F, Andreazza AC, et al. Pathways underlying neuroprogression in bipolar disorder: focus on inflammation, oxidative stress and neurotrophic factors. Neurosci Biobehav Rev. 2011;35(3):804-817.
7. Nasrallah HA, McCalley-Whitters M, Jacoby CG. Cerebral ventricular enlargement in young manic males. A controlled CT study. J Affective Dis. 1982;4(1):15-19.
8. Maletic V, Raison C. Integrated neurobiology of bipolar disorder. Front Psychiatry. 2014;5:98.
9. Berk M. Neuroprogression: pathways to progressive brain changes in bipolar disorder. Int J Neuropsychopharmacol. 2009;12(4):441-445.
10. Berk M, Conus P, Kapczinski F, et al. From neuroprogression to neuroprotection: implications for clinical care. Med J Aust. 2010;193(S4):S36-S40.
11. Passos IC, Mwangi B, Vieta E, et al. Areas of controversy in neuroprogression in bipolar disorder. Acta Psychiatr Scand. 2016;134(2):91-103.
12. Fries GR, Pfaffenseller B, Stertz L, et al. Staging and neuroprogression in bipolar disorder. Curr Psychiatry Rep. 2012;14(6):667-675.
13. Manji HK, Drevets WC, Charney DS. The cellular neurobiology of depression. Nat Med. 2001;7(5):541-547.
14. Fries GR, Zamzow MJ, Andrews T, et al. Accelerated aging in bipolar disorder: a comprehensive review of molecular findings and their clinical implications. Neurosci Biobehav Rev. 2020;112:107-116.
15. Fries GR, Bauer IE, Scaini G, et al. Accelerated hippocampal biological aging in bipolar disorder. Bipolar Dis. 2020;22(5):498-507.
16. Diniz BS, Teixeira AL, Cao F, et al. History of bipolar disorder and the risk of dementia: a systematic review and meta-analysis. Am J Geriatr Psychiatry. 2017;25(4):357-362.
17. Bauer IE, Ouyang A, Mwangi B, et al. Reduced white matter integrity and verbal fluency impairment in young adults with bipolar disorder: a diffusion tensor imaging study. J Psychiatr Res. 2015;62:115-122.
18. Calkin CV. Insulin resistance takes center stage: a new paradigm in the progression of bipolar disorder. Ann Med. 2019;51(5-6):281-293.
19. Grewal S, McKinlay S, Kapczinski F, et al. Biomarkers of neuroprogression and late staging in bipolar disorder: a systematic review. Aust N Z J Psychiatry. 2023;57(3):328-343.
20. Calkin C, McClelland C, Cairns K, et al. Insulin resistance and blood-brain barrier dysfunction underlie neuroprogression in bipolar disorder. Front Psychiatry. 2021;12:636174.
21. Nasrallah HA. 10 devastating consequences of psychotic relapses. Current Psychiatry. 2021;20(5):9-12.
22. Berk M, Hallam K, Malhi GS, et al. Evidence and implications for early intervention in bipolar disorder. J Ment Health. 2010;19(2):113-126.
Extended-release injectable naltrexone for opioid use disorder
We appreciate the important review by Gluck et al (“Managing patients with comorbid opioid and alcohol use disorders,”
XR-NTX should be considered an equal OUD treatment alternative to buprenorphine-naloxone, especially for patients who prefer an opioid-free option.1,2 It has the added advantage of being FDA-approved for both AUD and OUD.
One obstacle to the success of XR-NTX is the induction period. The National Institute on Drug Abuse Clinical Trials Network X:BOT trial found that once the induction hurdle was surmounted, XR-NTX and buprenorphine were equally effective in a population of approximately 80% heroin users and two-thirds injection drug users.2 Patient variables that predict successful induction include young age, baseline preference for XR-NTX, fewer drug complications, and fewer family/social complications.3 If the length of the induction (usually 7 to 10 days) is a deterrent, a study supported the feasibility of a 5-day outpatient XR-NTX induction.4 Further research is needed to improve successful induction for XR-NTX.
Ashmeer Ogbuchi, MD
Karen Drexler, MD
Atlanta, Georgia
References
1. Tanum L, Solli KK, Latif Z, et al. Effectiveness of injectable extended-release naltrexone vs daily buprenorphine-naloxone for opioid dependence. JAMA Psychiatry. 2017;74(12):1197-1205. doi:10.1001/ jamapsychiatry.2017.3206
2. Lee JD, Nunes EV Jr, Novo P, et al. Comparative effectiveness of extended-release naltrexone versus buprenorphine-naloxone for opioid relapse prevention (X:BOT): a multicentre, open-label, randomised controlled trial. Lancet. 2018;391(10118):309-318. doi:10.1016/s0140-6736(17)32812-x
3. Murphy SM, Jeng PJ, McCollister KE, et al. Cost‐effectiveness implications of increasing the efficiency of the extended‐release naltrexone induction process for the treatment of opioid use disorder: a secondary analysis. Addiction. 2021;116(12)3444-3453. doi:10.1111/add.15531
4. Sibai M, Mishlen K, Nunes EV, et al. A week-long outpatient induction onto XR-naltrexone in patients with opioid use disorder. Am J Drug Alcohol Abuse. 2020;46(3):289-296. doi:10.1080/00952990.2019.1700265
Continue to: The authors respond
The authors respond
We appreciate Drs. Ogbuchi and Drexler for their thoughtful attention to our review. They proposed amending our original algorithm, recommending that XR-NTX be considered as another first-line option for patients with OUD. We agree with this suggestion, particularly for inpatients. However, we have some reservations about applying this suggestion to outpatient treatment. Though research evidence from Lee et al1 indicates that once initiation is completed, both medications are equally safe and effective, the initial attrition rate in the XR-NTX group was much higher (28% vs 6%, P < .0001), which suggests lower acceptability/tolerability compared with buprenorphine. Notably, the initiation of both medications in Lee et al1 was done in an inpatient setting. Moreover, although some medications are endorsed as “first-line,” the actual utilization rate is often influenced by many factors, including the ease of treatment initiation. Wakeman et al2 found the most common treatment modality received by patients with OUD was nonintensive behavioral health (59.5%), followed by inpatient withdrawal management and residential treatment (15.2%). Among all patients in the Wakeman study,2 only 12.5% received buprenorphine or methadone, and 2.4% received naltrexone.
Data from our clinic corroborate this trend. Currently, in our clinic approximately 300 patients with OUD are receiving medications, including approximately 250 on buprenorphine (including 5 to 10 on the long-acting injectable formulation), 50 on methadone, and only 1 or 2 on XR-NTX. Though this disparity may reflect bias in our clinicians’ prescribing practices, in the past few years we have had many unsuccessful attempts at initiating XR-NTX. To our disappointment, a theoretically excellent medication has not translated clinically. The recent surge in fentanyl use further complicates XR-NTX initiation for OUD, because the length of induction may be longer.
In conclusion, we agree that XR-NTX is a potential treatment option for patients with OUD, but clinicians should be cognizant of the potential barriers; inform patients of the advantages, expectations, and challenges; and respect patients’ informed decisions.
Rachel Gluck, MD
Karen Hochman, MD
Yi-lang Tang, MD, PhD
Atlanta, Georgia
References
1. Lee JD, Nunes EV Jr, Novo P, et al. Comparative effectiveness of extended-release naltrexone versus buprenorphine-naloxone for opioid relapse prevention (X:BOT): a multicentre, open-label, randomised controlled trial. Lancet. 2018;391(10118):309-318. doi:10.1016/s0140-6736(17)32812-x
2. Wakeman SE, Larochelle MR, Ameli O, et al. Comparative effectiveness of different treatment pathways for opioid use disorder. JAMA Netw Open. 2020;3(2):e1920622. doi:10.1001/jamanetworkopen.2019.20622
We appreciate the important review by Gluck et al (“Managing patients with comorbid opioid and alcohol use disorders,”
XR-NTX should be considered an equal OUD treatment alternative to buprenorphine-naloxone, especially for patients who prefer an opioid-free option.1,2 It has the added advantage of being FDA-approved for both AUD and OUD.
One obstacle to the success of XR-NTX is the induction period. The National Institute on Drug Abuse Clinical Trials Network X:BOT trial found that once the induction hurdle was surmounted, XR-NTX and buprenorphine were equally effective in a population of approximately 80% heroin users and two-thirds injection drug users.2 Patient variables that predict successful induction include young age, baseline preference for XR-NTX, fewer drug complications, and fewer family/social complications.3 If the length of the induction (usually 7 to 10 days) is a deterrent, a study supported the feasibility of a 5-day outpatient XR-NTX induction.4 Further research is needed to improve successful induction for XR-NTX.
Ashmeer Ogbuchi, MD
Karen Drexler, MD
Atlanta, Georgia
References
1. Tanum L, Solli KK, Latif Z, et al. Effectiveness of injectable extended-release naltrexone vs daily buprenorphine-naloxone for opioid dependence. JAMA Psychiatry. 2017;74(12):1197-1205. doi:10.1001/ jamapsychiatry.2017.3206
2. Lee JD, Nunes EV Jr, Novo P, et al. Comparative effectiveness of extended-release naltrexone versus buprenorphine-naloxone for opioid relapse prevention (X:BOT): a multicentre, open-label, randomised controlled trial. Lancet. 2018;391(10118):309-318. doi:10.1016/s0140-6736(17)32812-x
3. Murphy SM, Jeng PJ, McCollister KE, et al. Cost‐effectiveness implications of increasing the efficiency of the extended‐release naltrexone induction process for the treatment of opioid use disorder: a secondary analysis. Addiction. 2021;116(12)3444-3453. doi:10.1111/add.15531
4. Sibai M, Mishlen K, Nunes EV, et al. A week-long outpatient induction onto XR-naltrexone in patients with opioid use disorder. Am J Drug Alcohol Abuse. 2020;46(3):289-296. doi:10.1080/00952990.2019.1700265
Continue to: The authors respond
The authors respond
We appreciate Drs. Ogbuchi and Drexler for their thoughtful attention to our review. They proposed amending our original algorithm, recommending that XR-NTX be considered as another first-line option for patients with OUD. We agree with this suggestion, particularly for inpatients. However, we have some reservations about applying this suggestion to outpatient treatment. Though research evidence from Lee et al1 indicates that once initiation is completed, both medications are equally safe and effective, the initial attrition rate in the XR-NTX group was much higher (28% vs 6%, P < .0001), which suggests lower acceptability/tolerability compared with buprenorphine. Notably, the initiation of both medications in Lee et al1 was done in an inpatient setting. Moreover, although some medications are endorsed as “first-line,” the actual utilization rate is often influenced by many factors, including the ease of treatment initiation. Wakeman et al2 found the most common treatment modality received by patients with OUD was nonintensive behavioral health (59.5%), followed by inpatient withdrawal management and residential treatment (15.2%). Among all patients in the Wakeman study,2 only 12.5% received buprenorphine or methadone, and 2.4% received naltrexone.
Data from our clinic corroborate this trend. Currently, in our clinic approximately 300 patients with OUD are receiving medications, including approximately 250 on buprenorphine (including 5 to 10 on the long-acting injectable formulation), 50 on methadone, and only 1 or 2 on XR-NTX. Though this disparity may reflect bias in our clinicians’ prescribing practices, in the past few years we have had many unsuccessful attempts at initiating XR-NTX. To our disappointment, a theoretically excellent medication has not translated clinically. The recent surge in fentanyl use further complicates XR-NTX initiation for OUD, because the length of induction may be longer.
In conclusion, we agree that XR-NTX is a potential treatment option for patients with OUD, but clinicians should be cognizant of the potential barriers; inform patients of the advantages, expectations, and challenges; and respect patients’ informed decisions.
Rachel Gluck, MD
Karen Hochman, MD
Yi-lang Tang, MD, PhD
Atlanta, Georgia
References
1. Lee JD, Nunes EV Jr, Novo P, et al. Comparative effectiveness of extended-release naltrexone versus buprenorphine-naloxone for opioid relapse prevention (X:BOT): a multicentre, open-label, randomised controlled trial. Lancet. 2018;391(10118):309-318. doi:10.1016/s0140-6736(17)32812-x
2. Wakeman SE, Larochelle MR, Ameli O, et al. Comparative effectiveness of different treatment pathways for opioid use disorder. JAMA Netw Open. 2020;3(2):e1920622. doi:10.1001/jamanetworkopen.2019.20622
We appreciate the important review by Gluck et al (“Managing patients with comorbid opioid and alcohol use disorders,”
XR-NTX should be considered an equal OUD treatment alternative to buprenorphine-naloxone, especially for patients who prefer an opioid-free option.1,2 It has the added advantage of being FDA-approved for both AUD and OUD.
One obstacle to the success of XR-NTX is the induction period. The National Institute on Drug Abuse Clinical Trials Network X:BOT trial found that once the induction hurdle was surmounted, XR-NTX and buprenorphine were equally effective in a population of approximately 80% heroin users and two-thirds injection drug users.2 Patient variables that predict successful induction include young age, baseline preference for XR-NTX, fewer drug complications, and fewer family/social complications.3 If the length of the induction (usually 7 to 10 days) is a deterrent, a study supported the feasibility of a 5-day outpatient XR-NTX induction.4 Further research is needed to improve successful induction for XR-NTX.
Ashmeer Ogbuchi, MD
Karen Drexler, MD
Atlanta, Georgia
References
1. Tanum L, Solli KK, Latif Z, et al. Effectiveness of injectable extended-release naltrexone vs daily buprenorphine-naloxone for opioid dependence. JAMA Psychiatry. 2017;74(12):1197-1205. doi:10.1001/ jamapsychiatry.2017.3206
2. Lee JD, Nunes EV Jr, Novo P, et al. Comparative effectiveness of extended-release naltrexone versus buprenorphine-naloxone for opioid relapse prevention (X:BOT): a multicentre, open-label, randomised controlled trial. Lancet. 2018;391(10118):309-318. doi:10.1016/s0140-6736(17)32812-x
3. Murphy SM, Jeng PJ, McCollister KE, et al. Cost‐effectiveness implications of increasing the efficiency of the extended‐release naltrexone induction process for the treatment of opioid use disorder: a secondary analysis. Addiction. 2021;116(12)3444-3453. doi:10.1111/add.15531
4. Sibai M, Mishlen K, Nunes EV, et al. A week-long outpatient induction onto XR-naltrexone in patients with opioid use disorder. Am J Drug Alcohol Abuse. 2020;46(3):289-296. doi:10.1080/00952990.2019.1700265
Continue to: The authors respond
The authors respond
We appreciate Drs. Ogbuchi and Drexler for their thoughtful attention to our review. They proposed amending our original algorithm, recommending that XR-NTX be considered as another first-line option for patients with OUD. We agree with this suggestion, particularly for inpatients. However, we have some reservations about applying this suggestion to outpatient treatment. Though research evidence from Lee et al1 indicates that once initiation is completed, both medications are equally safe and effective, the initial attrition rate in the XR-NTX group was much higher (28% vs 6%, P < .0001), which suggests lower acceptability/tolerability compared with buprenorphine. Notably, the initiation of both medications in Lee et al1 was done in an inpatient setting. Moreover, although some medications are endorsed as “first-line,” the actual utilization rate is often influenced by many factors, including the ease of treatment initiation. Wakeman et al2 found the most common treatment modality received by patients with OUD was nonintensive behavioral health (59.5%), followed by inpatient withdrawal management and residential treatment (15.2%). Among all patients in the Wakeman study,2 only 12.5% received buprenorphine or methadone, and 2.4% received naltrexone.
Data from our clinic corroborate this trend. Currently, in our clinic approximately 300 patients with OUD are receiving medications, including approximately 250 on buprenorphine (including 5 to 10 on the long-acting injectable formulation), 50 on methadone, and only 1 or 2 on XR-NTX. Though this disparity may reflect bias in our clinicians’ prescribing practices, in the past few years we have had many unsuccessful attempts at initiating XR-NTX. To our disappointment, a theoretically excellent medication has not translated clinically. The recent surge in fentanyl use further complicates XR-NTX initiation for OUD, because the length of induction may be longer.
In conclusion, we agree that XR-NTX is a potential treatment option for patients with OUD, but clinicians should be cognizant of the potential barriers; inform patients of the advantages, expectations, and challenges; and respect patients’ informed decisions.
Rachel Gluck, MD
Karen Hochman, MD
Yi-lang Tang, MD, PhD
Atlanta, Georgia
References
1. Lee JD, Nunes EV Jr, Novo P, et al. Comparative effectiveness of extended-release naltrexone versus buprenorphine-naloxone for opioid relapse prevention (X:BOT): a multicentre, open-label, randomised controlled trial. Lancet. 2018;391(10118):309-318. doi:10.1016/s0140-6736(17)32812-x
2. Wakeman SE, Larochelle MR, Ameli O, et al. Comparative effectiveness of different treatment pathways for opioid use disorder. JAMA Netw Open. 2020;3(2):e1920622. doi:10.1001/jamanetworkopen.2019.20622
