User login
Rash with weakness
The FP diagnosed dermatomyositis based on the patient’s proximal muscle weakness along with the typical shawl sign (erythema and scale over the shawl distribution) seen in the top image and the Gottron papules (erythematous and scaling papules over the dorsum of the fingers) and holster sign (erythema and scale over the lateral hip region) seen in the bottom image.
The FP started the patient on prednisone 60 mg/d and topical steroids for the affected areas. Laboratory exams showed an elevated creatinine kinase and mildly elevated antinuclear antibodies (typical for dermatomyositis). The FP also started the patient on oral prednisone 40 mg/d while putting in referrals for Dermatology and Rheumatology.
Two weeks later, the patient felt stronger and the rash had faded. Dermatology saw her first and started her on a steroid-sparing agent, methotrexate, with plans to taper her prednisone to lower doses over time. As underlying malignancy may precipitate dermatomyositis, the patient was screened for internal cancers—especially ovarian cancer. Fortunately, the mammogram, Pap smear, colonoscopy, and thoracic, abdominal, and pelvic computed tomography scans all were normal.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Buckley J, Burks M, Allred A, Usatine R. Dermatomyositis. In: Usatine R, Smith M, Mayeaux EJ, et al. eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1194-1203.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the 3rd edition of the Color Atlas and Synopsis of Family Medicine as an app by clicking on this link: https://usatinemedia.com/app/color-atlas-of-family-medicine/
The FP diagnosed dermatomyositis based on the patient’s proximal muscle weakness along with the typical shawl sign (erythema and scale over the shawl distribution) seen in the top image and the Gottron papules (erythematous and scaling papules over the dorsum of the fingers) and holster sign (erythema and scale over the lateral hip region) seen in the bottom image.
The FP started the patient on prednisone 60 mg/d and topical steroids for the affected areas. Laboratory exams showed an elevated creatinine kinase and mildly elevated antinuclear antibodies (typical for dermatomyositis). The FP also started the patient on oral prednisone 40 mg/d while putting in referrals for Dermatology and Rheumatology.
Two weeks later, the patient felt stronger and the rash had faded. Dermatology saw her first and started her on a steroid-sparing agent, methotrexate, with plans to taper her prednisone to lower doses over time. As underlying malignancy may precipitate dermatomyositis, the patient was screened for internal cancers—especially ovarian cancer. Fortunately, the mammogram, Pap smear, colonoscopy, and thoracic, abdominal, and pelvic computed tomography scans all were normal.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Buckley J, Burks M, Allred A, Usatine R. Dermatomyositis. In: Usatine R, Smith M, Mayeaux EJ, et al. eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1194-1203.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the 3rd edition of the Color Atlas and Synopsis of Family Medicine as an app by clicking on this link: https://usatinemedia.com/app/color-atlas-of-family-medicine/
The FP diagnosed dermatomyositis based on the patient’s proximal muscle weakness along with the typical shawl sign (erythema and scale over the shawl distribution) seen in the top image and the Gottron papules (erythematous and scaling papules over the dorsum of the fingers) and holster sign (erythema and scale over the lateral hip region) seen in the bottom image.
The FP started the patient on prednisone 60 mg/d and topical steroids for the affected areas. Laboratory exams showed an elevated creatinine kinase and mildly elevated antinuclear antibodies (typical for dermatomyositis). The FP also started the patient on oral prednisone 40 mg/d while putting in referrals for Dermatology and Rheumatology.
Two weeks later, the patient felt stronger and the rash had faded. Dermatology saw her first and started her on a steroid-sparing agent, methotrexate, with plans to taper her prednisone to lower doses over time. As underlying malignancy may precipitate dermatomyositis, the patient was screened for internal cancers—especially ovarian cancer. Fortunately, the mammogram, Pap smear, colonoscopy, and thoracic, abdominal, and pelvic computed tomography scans all were normal.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Buckley J, Burks M, Allred A, Usatine R. Dermatomyositis. In: Usatine R, Smith M, Mayeaux EJ, et al. eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1194-1203.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the 3rd edition of the Color Atlas and Synopsis of Family Medicine as an app by clicking on this link: https://usatinemedia.com/app/color-atlas-of-family-medicine/
Supine sleep in late pregnancy may promote low birth weight
Data from previous studies suggest that impaired uteroplacental flow can affect fetal growth, wrote Ngaire H. Anderson, PhD, of the University of Auckland, N.Z., and colleagues.
“The initial going-to-sleep position is the sleep position that women maintain for the longest duration throughout the night; therefore, going-to-sleep position is likely to have the greatest impact on blood flow to the developing fetus,” they said.
In a study published in JAMA Network Open, the researchers interviewed women with ongoing pregnancies at 28 weeks’ gestation or later to determine their sleeping positions. The mean age of the participants was 30 years. Of the 1,760 women, 3% reported that they usually slept supine during the past 1-4 weeks.
The adjusted mean birth weight was 3,410 g among supine sleepers and 3,554 g among nonsupine sleepers. The primary outcome was an adjusted mean difference in birth weight between infants of supine sleepers and nonsupine sleepers, which was a statistically significant 144 g (P = .009).
The study findings were limited by several factors including the small number of women who were reported supine sleepers, as well as the reliance on self-reports of sleep position, the researchers said.
However, women who had going-to-sleep data for the previous night and the previous month suggest that most women are consistent in their going-to-sleep position, they noted. “It is also biologically plausible that the association of decreased maternal blood flow on birth size with supine maternal position is cumulative over time,” but the researchers were not able to investigate how the duration of supine sleeping might further affect birth weight.
Although it might make additional studies more difficult, a public health campaign to encourage pregnant women to sleep on their side during the third trimester is a safe and easy opportunity to potentially optimize birth weight, they added.
The study was important because of the limited number of high-quality studies on the effects of maternal sleep on perinatal outcomes, Martina Badell, MD of Emory University in Atlanta said in an interview.
“The overall findings suggested a possible small increased risk of small-for-gestational-age babies with supine maternal sleeping, however, the absolute gram difference of 144 grams at term may not be clinically relevant,” she said. In addition, the relatively small number of women who reported supine sleep in late pregnancy suggests that broad public health campaigns or recommendations may not be indicated at this time.
“Also, the percentage of women who are supine sleepers at term is only approximately 3%, and this study didn’t assess reasons for supine sleeping in this small subset of women,” she said. “Further research is needed to assess whether there are specific maternal factors associated with supine sleeping, such as GI symptoms or respiratory difficulties, which could contribute to smaller fetal size rather than the sleep position itself.”
The study was supported by a Trans-Tasman Research Funding Grant by Cure Kids and Red Nose Australia. Six coauthors reported receiving numerous grants from a variety of organizations. Dr. Anderson and the remaining coauthors had no financial conflicts to disclose. Dr. Badell had no relevant financial disclosures.
SOURCE: Anderson NH et al. JAMA Network Open. 2019 Oct 2. doi: 10.1001/jamanetworkopen.2019.12614.
Data from previous studies suggest that impaired uteroplacental flow can affect fetal growth, wrote Ngaire H. Anderson, PhD, of the University of Auckland, N.Z., and colleagues.
“The initial going-to-sleep position is the sleep position that women maintain for the longest duration throughout the night; therefore, going-to-sleep position is likely to have the greatest impact on blood flow to the developing fetus,” they said.
In a study published in JAMA Network Open, the researchers interviewed women with ongoing pregnancies at 28 weeks’ gestation or later to determine their sleeping positions. The mean age of the participants was 30 years. Of the 1,760 women, 3% reported that they usually slept supine during the past 1-4 weeks.
The adjusted mean birth weight was 3,410 g among supine sleepers and 3,554 g among nonsupine sleepers. The primary outcome was an adjusted mean difference in birth weight between infants of supine sleepers and nonsupine sleepers, which was a statistically significant 144 g (P = .009).
The study findings were limited by several factors including the small number of women who were reported supine sleepers, as well as the reliance on self-reports of sleep position, the researchers said.
However, women who had going-to-sleep data for the previous night and the previous month suggest that most women are consistent in their going-to-sleep position, they noted. “It is also biologically plausible that the association of decreased maternal blood flow on birth size with supine maternal position is cumulative over time,” but the researchers were not able to investigate how the duration of supine sleeping might further affect birth weight.
Although it might make additional studies more difficult, a public health campaign to encourage pregnant women to sleep on their side during the third trimester is a safe and easy opportunity to potentially optimize birth weight, they added.
The study was important because of the limited number of high-quality studies on the effects of maternal sleep on perinatal outcomes, Martina Badell, MD of Emory University in Atlanta said in an interview.
“The overall findings suggested a possible small increased risk of small-for-gestational-age babies with supine maternal sleeping, however, the absolute gram difference of 144 grams at term may not be clinically relevant,” she said. In addition, the relatively small number of women who reported supine sleep in late pregnancy suggests that broad public health campaigns or recommendations may not be indicated at this time.
“Also, the percentage of women who are supine sleepers at term is only approximately 3%, and this study didn’t assess reasons for supine sleeping in this small subset of women,” she said. “Further research is needed to assess whether there are specific maternal factors associated with supine sleeping, such as GI symptoms or respiratory difficulties, which could contribute to smaller fetal size rather than the sleep position itself.”
The study was supported by a Trans-Tasman Research Funding Grant by Cure Kids and Red Nose Australia. Six coauthors reported receiving numerous grants from a variety of organizations. Dr. Anderson and the remaining coauthors had no financial conflicts to disclose. Dr. Badell had no relevant financial disclosures.
SOURCE: Anderson NH et al. JAMA Network Open. 2019 Oct 2. doi: 10.1001/jamanetworkopen.2019.12614.
Data from previous studies suggest that impaired uteroplacental flow can affect fetal growth, wrote Ngaire H. Anderson, PhD, of the University of Auckland, N.Z., and colleagues.
“The initial going-to-sleep position is the sleep position that women maintain for the longest duration throughout the night; therefore, going-to-sleep position is likely to have the greatest impact on blood flow to the developing fetus,” they said.
In a study published in JAMA Network Open, the researchers interviewed women with ongoing pregnancies at 28 weeks’ gestation or later to determine their sleeping positions. The mean age of the participants was 30 years. Of the 1,760 women, 3% reported that they usually slept supine during the past 1-4 weeks.
The adjusted mean birth weight was 3,410 g among supine sleepers and 3,554 g among nonsupine sleepers. The primary outcome was an adjusted mean difference in birth weight between infants of supine sleepers and nonsupine sleepers, which was a statistically significant 144 g (P = .009).
The study findings were limited by several factors including the small number of women who were reported supine sleepers, as well as the reliance on self-reports of sleep position, the researchers said.
However, women who had going-to-sleep data for the previous night and the previous month suggest that most women are consistent in their going-to-sleep position, they noted. “It is also biologically plausible that the association of decreased maternal blood flow on birth size with supine maternal position is cumulative over time,” but the researchers were not able to investigate how the duration of supine sleeping might further affect birth weight.
Although it might make additional studies more difficult, a public health campaign to encourage pregnant women to sleep on their side during the third trimester is a safe and easy opportunity to potentially optimize birth weight, they added.
The study was important because of the limited number of high-quality studies on the effects of maternal sleep on perinatal outcomes, Martina Badell, MD of Emory University in Atlanta said in an interview.
“The overall findings suggested a possible small increased risk of small-for-gestational-age babies with supine maternal sleeping, however, the absolute gram difference of 144 grams at term may not be clinically relevant,” she said. In addition, the relatively small number of women who reported supine sleep in late pregnancy suggests that broad public health campaigns or recommendations may not be indicated at this time.
“Also, the percentage of women who are supine sleepers at term is only approximately 3%, and this study didn’t assess reasons for supine sleeping in this small subset of women,” she said. “Further research is needed to assess whether there are specific maternal factors associated with supine sleeping, such as GI symptoms or respiratory difficulties, which could contribute to smaller fetal size rather than the sleep position itself.”
The study was supported by a Trans-Tasman Research Funding Grant by Cure Kids and Red Nose Australia. Six coauthors reported receiving numerous grants from a variety of organizations. Dr. Anderson and the remaining coauthors had no financial conflicts to disclose. Dr. Badell had no relevant financial disclosures.
SOURCE: Anderson NH et al. JAMA Network Open. 2019 Oct 2. doi: 10.1001/jamanetworkopen.2019.12614.
FROM JAMA NETWORK OPEN
Neanderthal otitis media and why you can’t chillax
Dude, just chill out and relax ... or not
It’s been a tough week. You’ve struggled to get all your work done on time, you’ve had to put in long hours, you’re exhausted and stressed out, and you know that next week will be just as tough. But for now, it’s the weekend. Time to relax, right?
According to research from Penn State University published in the Journal of Affective Disorders, if you have anxiety disorder, not only will you have difficulty relaxing (hence the anxiety disorder), you may actually actively resist it, experiencing something called “relaxation-induced anxiety.”
The researchers recruited a group of students, some with anxiety disorder, some with major depressive disorder, and a control group, and administered a series of relaxation exercises both before and after watching a series of potentially upsetting videos. The people with anxiety disorders were more likely to experience spikes of negative emotion after the second relaxation exercise than the other two groups; these spikes were linked to a feeling of anxiety during relaxation exercise.
The researchers theorized that people with anxiety disorder were attempting to avoid large jumps in their stress level by remaining stressed at all times. But the investigators also noted that experiencing a range of emotions is natural and far healthier.
So, as annoying as it is to suffer through constant “stop worrying, just live in the moment” speeches from that one dudebro acquaintance who spends all his free time partying, he does have a point. We don’t recommend participating in the Edward Fortyhands game, though. Leave that to your “friend.” He’s used to it.
A salty surgeon general’s warning
Grab a pack of Marlboro Reds at the corner convenience store, and you’ll find the iconic red and white box adorned with dire warnings from the surgeon general.
Grab a salt shaker at the corner diner, and you’ll find ... salt. In a shaker. Perhaps adorned with the red residue from a prior diner’s ketchup addiction.
The World Hypertension League would like to make that salt shaker look a lot more like those Marlboros.
In a position statement in the Journal of Clinical Hypertension, the league outlined the case for giving sodium chloride the cancer-stick treatment. Exhibit A: “Unhealthy diets are a leading cause of death globally, and excess salt consumption is the biggest culprit, estimated to cause over 3 million deaths globally in 2017.”
Despite that tobacco-rivaling body count, the league says no country has demanded that salt containers wear warning labels.
But isn’t it enough to list sodium levels on food labels? Well, when’s the last time you studied the salty facts before binging on that entire party-size bag of Cheetos, Chester? (You’ll be hotboxing 4,500 mg of sodium, by the way.) The league rests its case.
What’s needed is a message that stops you mid fistful. It’s time to add warning labels to all salt packaging, implores the league. Even to that communal salt shaker. Helpfully, the league’s offering suggested wording for that harbinger-of-doom missive: “Excess sodium can cause high blood pressure and promote stomach cancer. Limit your use.”
Catchy, right? But we at the Bureau of LOTME believe a picture is worth a thousand words of warning. Which is why we’ve taped a simple biohazard logo to our office Cheetos stash. Because of the sodium, you ask? Hardly. But just imagine that much optic-orange food coloring finding its way into the groundwater.
The anatomy of extinction
Barely a day goes by without a new theory about What Killed the Dinosaurs. A meteor killed the dinosaurs. Volcanoes killed the dinosaurs. Donald Trump asked the Ukrainians to kill the dinosaurs. Hilary Clinton’s emails killed the dinosaurs. Donald Trump asked the Australians to say that Robert Mueller killed the dinosaurs. The liberal media are covering up the existence of dinosaurs.
Enough already. What about the primates? We humans are still around – at least for the time being. But when was the last time you heard a good theory about what killed the Neanderthals?
Well, hang on to your earmuffs, because here comes one now.
Researchers have reconstructed the Neanderthal Eustachian tubes and determined that those early rivals of Homo sapiens were done in by … chronic ear infections.
The Neanderthal Eustachian tubes were very similar to those of human infants, and “middle ear infections are nearly ubiquitous among infants because the flat angle of an infant’s Eustachian tubes is prone to retain the otitis media bacteria that cause these infections – the same flat angle we found in Neanderthals,” coauthor Samuel Márquez, PhD, of the State University of New York said in a statement.
Unlike modern humans, however, the Neanderthal eustachian tube did not change with age, so middle ear infections were a lifelong threat.
“It’s not just the threat of dying of an infection,” said Dr. Márquez. “If you are constantly ill, you would not be as fit and effective in competing with your Homo sapiens cousins for food and other resources. In a world of survival of the fittest, it is no wonder that modern man, not Neanderthal, prevailed.”
In other words, it wasn’t brains that beat the big, bad Neanderthals; it was their own baby ears.
H. sapiens, raise a glass: Ears to you, Charles Darwin.
Dude, just chill out and relax ... or not
It’s been a tough week. You’ve struggled to get all your work done on time, you’ve had to put in long hours, you’re exhausted and stressed out, and you know that next week will be just as tough. But for now, it’s the weekend. Time to relax, right?
According to research from Penn State University published in the Journal of Affective Disorders, if you have anxiety disorder, not only will you have difficulty relaxing (hence the anxiety disorder), you may actually actively resist it, experiencing something called “relaxation-induced anxiety.”
The researchers recruited a group of students, some with anxiety disorder, some with major depressive disorder, and a control group, and administered a series of relaxation exercises both before and after watching a series of potentially upsetting videos. The people with anxiety disorders were more likely to experience spikes of negative emotion after the second relaxation exercise than the other two groups; these spikes were linked to a feeling of anxiety during relaxation exercise.
The researchers theorized that people with anxiety disorder were attempting to avoid large jumps in their stress level by remaining stressed at all times. But the investigators also noted that experiencing a range of emotions is natural and far healthier.
So, as annoying as it is to suffer through constant “stop worrying, just live in the moment” speeches from that one dudebro acquaintance who spends all his free time partying, he does have a point. We don’t recommend participating in the Edward Fortyhands game, though. Leave that to your “friend.” He’s used to it.
A salty surgeon general’s warning
Grab a pack of Marlboro Reds at the corner convenience store, and you’ll find the iconic red and white box adorned with dire warnings from the surgeon general.
Grab a salt shaker at the corner diner, and you’ll find ... salt. In a shaker. Perhaps adorned with the red residue from a prior diner’s ketchup addiction.
The World Hypertension League would like to make that salt shaker look a lot more like those Marlboros.
In a position statement in the Journal of Clinical Hypertension, the league outlined the case for giving sodium chloride the cancer-stick treatment. Exhibit A: “Unhealthy diets are a leading cause of death globally, and excess salt consumption is the biggest culprit, estimated to cause over 3 million deaths globally in 2017.”
Despite that tobacco-rivaling body count, the league says no country has demanded that salt containers wear warning labels.
But isn’t it enough to list sodium levels on food labels? Well, when’s the last time you studied the salty facts before binging on that entire party-size bag of Cheetos, Chester? (You’ll be hotboxing 4,500 mg of sodium, by the way.) The league rests its case.
What’s needed is a message that stops you mid fistful. It’s time to add warning labels to all salt packaging, implores the league. Even to that communal salt shaker. Helpfully, the league’s offering suggested wording for that harbinger-of-doom missive: “Excess sodium can cause high blood pressure and promote stomach cancer. Limit your use.”
Catchy, right? But we at the Bureau of LOTME believe a picture is worth a thousand words of warning. Which is why we’ve taped a simple biohazard logo to our office Cheetos stash. Because of the sodium, you ask? Hardly. But just imagine that much optic-orange food coloring finding its way into the groundwater.
The anatomy of extinction
Barely a day goes by without a new theory about What Killed the Dinosaurs. A meteor killed the dinosaurs. Volcanoes killed the dinosaurs. Donald Trump asked the Ukrainians to kill the dinosaurs. Hilary Clinton’s emails killed the dinosaurs. Donald Trump asked the Australians to say that Robert Mueller killed the dinosaurs. The liberal media are covering up the existence of dinosaurs.
Enough already. What about the primates? We humans are still around – at least for the time being. But when was the last time you heard a good theory about what killed the Neanderthals?
Well, hang on to your earmuffs, because here comes one now.
Researchers have reconstructed the Neanderthal Eustachian tubes and determined that those early rivals of Homo sapiens were done in by … chronic ear infections.
The Neanderthal Eustachian tubes were very similar to those of human infants, and “middle ear infections are nearly ubiquitous among infants because the flat angle of an infant’s Eustachian tubes is prone to retain the otitis media bacteria that cause these infections – the same flat angle we found in Neanderthals,” coauthor Samuel Márquez, PhD, of the State University of New York said in a statement.
Unlike modern humans, however, the Neanderthal eustachian tube did not change with age, so middle ear infections were a lifelong threat.
“It’s not just the threat of dying of an infection,” said Dr. Márquez. “If you are constantly ill, you would not be as fit and effective in competing with your Homo sapiens cousins for food and other resources. In a world of survival of the fittest, it is no wonder that modern man, not Neanderthal, prevailed.”
In other words, it wasn’t brains that beat the big, bad Neanderthals; it was their own baby ears.
H. sapiens, raise a glass: Ears to you, Charles Darwin.
Dude, just chill out and relax ... or not
It’s been a tough week. You’ve struggled to get all your work done on time, you’ve had to put in long hours, you’re exhausted and stressed out, and you know that next week will be just as tough. But for now, it’s the weekend. Time to relax, right?
According to research from Penn State University published in the Journal of Affective Disorders, if you have anxiety disorder, not only will you have difficulty relaxing (hence the anxiety disorder), you may actually actively resist it, experiencing something called “relaxation-induced anxiety.”
The researchers recruited a group of students, some with anxiety disorder, some with major depressive disorder, and a control group, and administered a series of relaxation exercises both before and after watching a series of potentially upsetting videos. The people with anxiety disorders were more likely to experience spikes of negative emotion after the second relaxation exercise than the other two groups; these spikes were linked to a feeling of anxiety during relaxation exercise.
The researchers theorized that people with anxiety disorder were attempting to avoid large jumps in their stress level by remaining stressed at all times. But the investigators also noted that experiencing a range of emotions is natural and far healthier.
So, as annoying as it is to suffer through constant “stop worrying, just live in the moment” speeches from that one dudebro acquaintance who spends all his free time partying, he does have a point. We don’t recommend participating in the Edward Fortyhands game, though. Leave that to your “friend.” He’s used to it.
A salty surgeon general’s warning
Grab a pack of Marlboro Reds at the corner convenience store, and you’ll find the iconic red and white box adorned with dire warnings from the surgeon general.
Grab a salt shaker at the corner diner, and you’ll find ... salt. In a shaker. Perhaps adorned with the red residue from a prior diner’s ketchup addiction.
The World Hypertension League would like to make that salt shaker look a lot more like those Marlboros.
In a position statement in the Journal of Clinical Hypertension, the league outlined the case for giving sodium chloride the cancer-stick treatment. Exhibit A: “Unhealthy diets are a leading cause of death globally, and excess salt consumption is the biggest culprit, estimated to cause over 3 million deaths globally in 2017.”
Despite that tobacco-rivaling body count, the league says no country has demanded that salt containers wear warning labels.
But isn’t it enough to list sodium levels on food labels? Well, when’s the last time you studied the salty facts before binging on that entire party-size bag of Cheetos, Chester? (You’ll be hotboxing 4,500 mg of sodium, by the way.) The league rests its case.
What’s needed is a message that stops you mid fistful. It’s time to add warning labels to all salt packaging, implores the league. Even to that communal salt shaker. Helpfully, the league’s offering suggested wording for that harbinger-of-doom missive: “Excess sodium can cause high blood pressure and promote stomach cancer. Limit your use.”
Catchy, right? But we at the Bureau of LOTME believe a picture is worth a thousand words of warning. Which is why we’ve taped a simple biohazard logo to our office Cheetos stash. Because of the sodium, you ask? Hardly. But just imagine that much optic-orange food coloring finding its way into the groundwater.
The anatomy of extinction
Barely a day goes by without a new theory about What Killed the Dinosaurs. A meteor killed the dinosaurs. Volcanoes killed the dinosaurs. Donald Trump asked the Ukrainians to kill the dinosaurs. Hilary Clinton’s emails killed the dinosaurs. Donald Trump asked the Australians to say that Robert Mueller killed the dinosaurs. The liberal media are covering up the existence of dinosaurs.
Enough already. What about the primates? We humans are still around – at least for the time being. But when was the last time you heard a good theory about what killed the Neanderthals?
Well, hang on to your earmuffs, because here comes one now.
Researchers have reconstructed the Neanderthal Eustachian tubes and determined that those early rivals of Homo sapiens were done in by … chronic ear infections.
The Neanderthal Eustachian tubes were very similar to those of human infants, and “middle ear infections are nearly ubiquitous among infants because the flat angle of an infant’s Eustachian tubes is prone to retain the otitis media bacteria that cause these infections – the same flat angle we found in Neanderthals,” coauthor Samuel Márquez, PhD, of the State University of New York said in a statement.
Unlike modern humans, however, the Neanderthal eustachian tube did not change with age, so middle ear infections were a lifelong threat.
“It’s not just the threat of dying of an infection,” said Dr. Márquez. “If you are constantly ill, you would not be as fit and effective in competing with your Homo sapiens cousins for food and other resources. In a world of survival of the fittest, it is no wonder that modern man, not Neanderthal, prevailed.”
In other words, it wasn’t brains that beat the big, bad Neanderthals; it was their own baby ears.
H. sapiens, raise a glass: Ears to you, Charles Darwin.
I have seen the future
Many patients have seen their long-term physicians retire. When I ask how they like their new doctors, they say: “She’s okay, I guess. Quite efficient. Seems thorough. But it’s not the same. It’s just business. Nothing personal.”
Sometimes you have to look backward to look forward. So it’s perhaps fitting that I glimpsed the future at my last colonoscopy.
In recent years, I’ve had such procedures at a local suburban surgicenter. Easy access, plenty of parking.
The woman who checks me in is all business. She scans my insurance cards and hands me a clipboard with a medical history form. Have I ever had cancer? A hernia? Am I pregnant? I wonder whether anyone reads these.
A different young woman brings me inside, the first of many new faces. Their roles are murky.
In a curtained cubby, yet another staff person asks me to pack my clothes in a plastic bag and put on a johnny. Then an older man enters, initiating furious multitasking. A different nursing assistant asks me to confirm my name and date of birth, then inserts an intravenous line in one arm, while the old doctor hands me an anesthesia consent form to sign with the other hand. I check many answers very fast, ignore the small-print boilerplate, and sign.
I am handed two more consent forms to sign, one from each side. The staff makes no pretense of explaining them or even telling me what they are for, and I make none of reading them.
They depart, replaced by still another person, who rolls me into the next room. He confirms my name and date of birth, and which procedure I am there for. The purpose of these multiple checks is clear, along with dispiriting depersonalization. One could mitigate this with some light banter, but no one bothers. No time.
My physician – whom I actually know – enters, says hello, and exchanges pleasantries. The last guy asks me to turn onto my left side. Intravenous sedation flows into my veins. The rest is silence.
Sometime later I wake up, greeted by another staff person. She asks if I am okay and offers me water or juice and saltines. Noting her Boston Red Sox sweatshirt, I say, “Great game last night,” but she does not know what I am talking about. She cares only for football and plans to fly to Nashville, Tenn., to watch her favorites.
Curtains are closed, and I am asked to dress. Another assistant directs me to a chair, where I will await my ride home. Through I try to walk alone, she takes my arm. “We assist everyone,” she explains.
As the sedation wears off, I observe. All around me I see movement, brisk and purposeful. Staff members crisscross before me from all angles, striding from one task to another, from prep room A to cubby D, walking with or pushing patients from procedure room M to holding area 8H. No one I’ve just met recognizes me, or acknowledges having met me before.
At last, the final staff member approaches. She flashes a kind smile as she takes my arm to walk me to the door. I take this for a personal touch, until she explains that she must make sure I don’t fall and that I get into the right car. As we pass, no one in the waiting room, neither staff nor patients, takes any notice.
My wife is outside, idling in the correct car. She’s brought coffee and a chocolate croissant, which – almost – makes last night’s prep worthwhile. She confirms neither my name nor date of birth.
Altogether, I have been in and out in 90 minutes. In the car, I peruse the handout that had been given to me as I exited. Drinking my coffee, I read the postcare instructions and enjoy its full-color pictures. Seldom has my cecum looked more radiant.
In “The Checklist Manifesto,” Atul Gawande described the outcome improvement that systematized practice can achieve. Data analysis confirms the measurably superior efficacy of such a method.
As for me, I feel like output from one of today’s cataract factories: like a car just extruded from an automated wash, with a photo on its front seat of the shiny, Simonized hubcaps included with the premium service package.
Just business, though. Nothing personal.
Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at [email protected].
Many patients have seen their long-term physicians retire. When I ask how they like their new doctors, they say: “She’s okay, I guess. Quite efficient. Seems thorough. But it’s not the same. It’s just business. Nothing personal.”
Sometimes you have to look backward to look forward. So it’s perhaps fitting that I glimpsed the future at my last colonoscopy.
In recent years, I’ve had such procedures at a local suburban surgicenter. Easy access, plenty of parking.
The woman who checks me in is all business. She scans my insurance cards and hands me a clipboard with a medical history form. Have I ever had cancer? A hernia? Am I pregnant? I wonder whether anyone reads these.
A different young woman brings me inside, the first of many new faces. Their roles are murky.
In a curtained cubby, yet another staff person asks me to pack my clothes in a plastic bag and put on a johnny. Then an older man enters, initiating furious multitasking. A different nursing assistant asks me to confirm my name and date of birth, then inserts an intravenous line in one arm, while the old doctor hands me an anesthesia consent form to sign with the other hand. I check many answers very fast, ignore the small-print boilerplate, and sign.
I am handed two more consent forms to sign, one from each side. The staff makes no pretense of explaining them or even telling me what they are for, and I make none of reading them.
They depart, replaced by still another person, who rolls me into the next room. He confirms my name and date of birth, and which procedure I am there for. The purpose of these multiple checks is clear, along with dispiriting depersonalization. One could mitigate this with some light banter, but no one bothers. No time.
My physician – whom I actually know – enters, says hello, and exchanges pleasantries. The last guy asks me to turn onto my left side. Intravenous sedation flows into my veins. The rest is silence.
Sometime later I wake up, greeted by another staff person. She asks if I am okay and offers me water or juice and saltines. Noting her Boston Red Sox sweatshirt, I say, “Great game last night,” but she does not know what I am talking about. She cares only for football and plans to fly to Nashville, Tenn., to watch her favorites.
Curtains are closed, and I am asked to dress. Another assistant directs me to a chair, where I will await my ride home. Through I try to walk alone, she takes my arm. “We assist everyone,” she explains.
As the sedation wears off, I observe. All around me I see movement, brisk and purposeful. Staff members crisscross before me from all angles, striding from one task to another, from prep room A to cubby D, walking with or pushing patients from procedure room M to holding area 8H. No one I’ve just met recognizes me, or acknowledges having met me before.
At last, the final staff member approaches. She flashes a kind smile as she takes my arm to walk me to the door. I take this for a personal touch, until she explains that she must make sure I don’t fall and that I get into the right car. As we pass, no one in the waiting room, neither staff nor patients, takes any notice.
My wife is outside, idling in the correct car. She’s brought coffee and a chocolate croissant, which – almost – makes last night’s prep worthwhile. She confirms neither my name nor date of birth.
Altogether, I have been in and out in 90 minutes. In the car, I peruse the handout that had been given to me as I exited. Drinking my coffee, I read the postcare instructions and enjoy its full-color pictures. Seldom has my cecum looked more radiant.
In “The Checklist Manifesto,” Atul Gawande described the outcome improvement that systematized practice can achieve. Data analysis confirms the measurably superior efficacy of such a method.
As for me, I feel like output from one of today’s cataract factories: like a car just extruded from an automated wash, with a photo on its front seat of the shiny, Simonized hubcaps included with the premium service package.
Just business, though. Nothing personal.
Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at [email protected].
Many patients have seen their long-term physicians retire. When I ask how they like their new doctors, they say: “She’s okay, I guess. Quite efficient. Seems thorough. But it’s not the same. It’s just business. Nothing personal.”
Sometimes you have to look backward to look forward. So it’s perhaps fitting that I glimpsed the future at my last colonoscopy.
In recent years, I’ve had such procedures at a local suburban surgicenter. Easy access, plenty of parking.
The woman who checks me in is all business. She scans my insurance cards and hands me a clipboard with a medical history form. Have I ever had cancer? A hernia? Am I pregnant? I wonder whether anyone reads these.
A different young woman brings me inside, the first of many new faces. Their roles are murky.
In a curtained cubby, yet another staff person asks me to pack my clothes in a plastic bag and put on a johnny. Then an older man enters, initiating furious multitasking. A different nursing assistant asks me to confirm my name and date of birth, then inserts an intravenous line in one arm, while the old doctor hands me an anesthesia consent form to sign with the other hand. I check many answers very fast, ignore the small-print boilerplate, and sign.
I am handed two more consent forms to sign, one from each side. The staff makes no pretense of explaining them or even telling me what they are for, and I make none of reading them.
They depart, replaced by still another person, who rolls me into the next room. He confirms my name and date of birth, and which procedure I am there for. The purpose of these multiple checks is clear, along with dispiriting depersonalization. One could mitigate this with some light banter, but no one bothers. No time.
My physician – whom I actually know – enters, says hello, and exchanges pleasantries. The last guy asks me to turn onto my left side. Intravenous sedation flows into my veins. The rest is silence.
Sometime later I wake up, greeted by another staff person. She asks if I am okay and offers me water or juice and saltines. Noting her Boston Red Sox sweatshirt, I say, “Great game last night,” but she does not know what I am talking about. She cares only for football and plans to fly to Nashville, Tenn., to watch her favorites.
Curtains are closed, and I am asked to dress. Another assistant directs me to a chair, where I will await my ride home. Through I try to walk alone, she takes my arm. “We assist everyone,” she explains.
As the sedation wears off, I observe. All around me I see movement, brisk and purposeful. Staff members crisscross before me from all angles, striding from one task to another, from prep room A to cubby D, walking with or pushing patients from procedure room M to holding area 8H. No one I’ve just met recognizes me, or acknowledges having met me before.
At last, the final staff member approaches. She flashes a kind smile as she takes my arm to walk me to the door. I take this for a personal touch, until she explains that she must make sure I don’t fall and that I get into the right car. As we pass, no one in the waiting room, neither staff nor patients, takes any notice.
My wife is outside, idling in the correct car. She’s brought coffee and a chocolate croissant, which – almost – makes last night’s prep worthwhile. She confirms neither my name nor date of birth.
Altogether, I have been in and out in 90 minutes. In the car, I peruse the handout that had been given to me as I exited. Drinking my coffee, I read the postcare instructions and enjoy its full-color pictures. Seldom has my cecum looked more radiant.
In “The Checklist Manifesto,” Atul Gawande described the outcome improvement that systematized practice can achieve. Data analysis confirms the measurably superior efficacy of such a method.
As for me, I feel like output from one of today’s cataract factories: like a car just extruded from an automated wash, with a photo on its front seat of the shiny, Simonized hubcaps included with the premium service package.
Just business, though. Nothing personal.
Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at [email protected].
Central centrifugal cicatricial alopecia called epidemic in skin of color
NEW YORK – For unclear reasons, the prevalence of , creating an urgent need for early diagnosis and treatment, according to an expert who described this phenomenon at the Skin of Color Update 2019.
“CCCA has reached epidemic proportions,” contended Susan Taylor, MD, director of diversity, department of dermatology, Penn Medicine, Philadelphia.
Published data place prevalence rates of CCCA somewhere in the range of 3% to 6% among black women, but Dr. Taylor reported that she believes the condition is underdiagnosed. “I am seeing far more patients now than I was 30 years ago,” she maintained.
Others participating in the Skin of Color Update 2019 agreed. Heather Woolery-Lloyd, MD, director of ethnic skin care, department of dermatology and cutaneous surgery, University of Miami, also called the rising incidence of CCCA “an epidemic.” She, like Dr. Taylor, emphasized the critical importance of early diagnosis and treatment.
“I tell patients that if we can prevent hair loss over the next 10 years, this is a treatment success,” Dr. Woolery-Lloyd said. Although hair regrowth can be achieved in a minority of patients with treatments such as minoxidil, “the first goal is to prevent hair loss.”
Upon diagnosis, Dr. Woolery-Lloyd recommends treatment with intralesional triamcinolone and topical steroids immediately, adding other agents, such as oral antibiotics, if needed. Even in cases where CCCA has been identified before hair loss is visible, Dr. Woolery-Lloyd advised immediate therapy. Given that CCCA is a disease of reversible hair loss, she said, “do not take a wait-and-see approach.”
One potential obstacle for early diagnosis of CCCA, shared by other types of alopecia that are common in skin of color, is the failure of many clinicians to employ a standardized diagnosis in this patient population.
“If you do not have tightly coiled hair, it does not mean you cannot understand tightly coiled hair, but you have to learn, and you have to let patients know that you understand and have experience,” said Dr. Taylor, emphasizing the role of reassuring patients so they can be confident in the clinical recommendations.
Part of this reassurance will be derived from “interacting with patients in a culturally competent manner,” Dr. Taylor said. Clinicians must develop comfort and confidence in physically examining the hair and scalp, in asking patients to remove weaves or braids for a thorough inspection, and in avoiding comments that might be misinterpreted. Among these, she advised tactful questions about shampooing to avoid any implication that the clinician is implying inadequate hygiene.
When CCCA is suspected, a “biopsy is important” even in circumstances when the diagnosis seems straightforward. For one reason, a substantial proportion of patients may have a concomitant diagnosis. Dr. Taylor cited data from one study in which nearly 20% of CCCA patients also had traction alopecia and more than 10% had androgenic alopecia. Other coexisting problems identified on biopsy, including infection or seborrheic dermatitis, can help clinicians tailor a more effective intervention.
The initial signs of CCCA are typically hair breakage in the vertex of the scalp, which then expands in a central centrifugal pattern, according to Dr. Taylor. Although not all patients have signs of inflammation, such as itching and pustules, inhibition of inflammation represents the first line of therapy.
Relative to hair in the white population, the hair of black individuals grows more slowly and is more fragile, with greater amounts of breakage, said Dr. Taylor, citing published studies that support these differences. To improve early diagnosis of CCCA, understanding the hair in the black population is the first step for spotting problems in routine physical examinations. It may be this lack of familiarity that is contributing to underdiagnosis of CCCA.
“Almost 70% of African-American patients feel that physicians do not understand their hair,” Dr. Taylor said. “Let’s begin to change that.”
Cautioning that it is too often assumed that hairstyles and hair care, such as relaxants or hot combs, are the source of hair loss in black women, Dr. Taylor advised not to jump to conclusions. As an example, she described a case where weaves, braids, and other strategies were employed to mask alopecia after CCCA developed, not before.
“CCCA is the most important cause of scarring alopecia in African-American women,” Dr. Taylor said. Reiterating that hair loss can be prevented or modified with treatment, she added that this places the emphasis on first obtaining an accurate diagnosis.
Dr. Taylor has a financial relationship with Biersdorf; Dr. Woolery-Lloyd has financial relationships with Allergan, Galderma, Ortho Diagnostics, Pfizer, and Somabella Laboratories.
NEW YORK – For unclear reasons, the prevalence of , creating an urgent need for early diagnosis and treatment, according to an expert who described this phenomenon at the Skin of Color Update 2019.
“CCCA has reached epidemic proportions,” contended Susan Taylor, MD, director of diversity, department of dermatology, Penn Medicine, Philadelphia.
Published data place prevalence rates of CCCA somewhere in the range of 3% to 6% among black women, but Dr. Taylor reported that she believes the condition is underdiagnosed. “I am seeing far more patients now than I was 30 years ago,” she maintained.
Others participating in the Skin of Color Update 2019 agreed. Heather Woolery-Lloyd, MD, director of ethnic skin care, department of dermatology and cutaneous surgery, University of Miami, also called the rising incidence of CCCA “an epidemic.” She, like Dr. Taylor, emphasized the critical importance of early diagnosis and treatment.
“I tell patients that if we can prevent hair loss over the next 10 years, this is a treatment success,” Dr. Woolery-Lloyd said. Although hair regrowth can be achieved in a minority of patients with treatments such as minoxidil, “the first goal is to prevent hair loss.”
Upon diagnosis, Dr. Woolery-Lloyd recommends treatment with intralesional triamcinolone and topical steroids immediately, adding other agents, such as oral antibiotics, if needed. Even in cases where CCCA has been identified before hair loss is visible, Dr. Woolery-Lloyd advised immediate therapy. Given that CCCA is a disease of reversible hair loss, she said, “do not take a wait-and-see approach.”
One potential obstacle for early diagnosis of CCCA, shared by other types of alopecia that are common in skin of color, is the failure of many clinicians to employ a standardized diagnosis in this patient population.
“If you do not have tightly coiled hair, it does not mean you cannot understand tightly coiled hair, but you have to learn, and you have to let patients know that you understand and have experience,” said Dr. Taylor, emphasizing the role of reassuring patients so they can be confident in the clinical recommendations.
Part of this reassurance will be derived from “interacting with patients in a culturally competent manner,” Dr. Taylor said. Clinicians must develop comfort and confidence in physically examining the hair and scalp, in asking patients to remove weaves or braids for a thorough inspection, and in avoiding comments that might be misinterpreted. Among these, she advised tactful questions about shampooing to avoid any implication that the clinician is implying inadequate hygiene.
When CCCA is suspected, a “biopsy is important” even in circumstances when the diagnosis seems straightforward. For one reason, a substantial proportion of patients may have a concomitant diagnosis. Dr. Taylor cited data from one study in which nearly 20% of CCCA patients also had traction alopecia and more than 10% had androgenic alopecia. Other coexisting problems identified on biopsy, including infection or seborrheic dermatitis, can help clinicians tailor a more effective intervention.
The initial signs of CCCA are typically hair breakage in the vertex of the scalp, which then expands in a central centrifugal pattern, according to Dr. Taylor. Although not all patients have signs of inflammation, such as itching and pustules, inhibition of inflammation represents the first line of therapy.
Relative to hair in the white population, the hair of black individuals grows more slowly and is more fragile, with greater amounts of breakage, said Dr. Taylor, citing published studies that support these differences. To improve early diagnosis of CCCA, understanding the hair in the black population is the first step for spotting problems in routine physical examinations. It may be this lack of familiarity that is contributing to underdiagnosis of CCCA.
“Almost 70% of African-American patients feel that physicians do not understand their hair,” Dr. Taylor said. “Let’s begin to change that.”
Cautioning that it is too often assumed that hairstyles and hair care, such as relaxants or hot combs, are the source of hair loss in black women, Dr. Taylor advised not to jump to conclusions. As an example, she described a case where weaves, braids, and other strategies were employed to mask alopecia after CCCA developed, not before.
“CCCA is the most important cause of scarring alopecia in African-American women,” Dr. Taylor said. Reiterating that hair loss can be prevented or modified with treatment, she added that this places the emphasis on first obtaining an accurate diagnosis.
Dr. Taylor has a financial relationship with Biersdorf; Dr. Woolery-Lloyd has financial relationships with Allergan, Galderma, Ortho Diagnostics, Pfizer, and Somabella Laboratories.
NEW YORK – For unclear reasons, the prevalence of , creating an urgent need for early diagnosis and treatment, according to an expert who described this phenomenon at the Skin of Color Update 2019.
“CCCA has reached epidemic proportions,” contended Susan Taylor, MD, director of diversity, department of dermatology, Penn Medicine, Philadelphia.
Published data place prevalence rates of CCCA somewhere in the range of 3% to 6% among black women, but Dr. Taylor reported that she believes the condition is underdiagnosed. “I am seeing far more patients now than I was 30 years ago,” she maintained.
Others participating in the Skin of Color Update 2019 agreed. Heather Woolery-Lloyd, MD, director of ethnic skin care, department of dermatology and cutaneous surgery, University of Miami, also called the rising incidence of CCCA “an epidemic.” She, like Dr. Taylor, emphasized the critical importance of early diagnosis and treatment.
“I tell patients that if we can prevent hair loss over the next 10 years, this is a treatment success,” Dr. Woolery-Lloyd said. Although hair regrowth can be achieved in a minority of patients with treatments such as minoxidil, “the first goal is to prevent hair loss.”
Upon diagnosis, Dr. Woolery-Lloyd recommends treatment with intralesional triamcinolone and topical steroids immediately, adding other agents, such as oral antibiotics, if needed. Even in cases where CCCA has been identified before hair loss is visible, Dr. Woolery-Lloyd advised immediate therapy. Given that CCCA is a disease of reversible hair loss, she said, “do not take a wait-and-see approach.”
One potential obstacle for early diagnosis of CCCA, shared by other types of alopecia that are common in skin of color, is the failure of many clinicians to employ a standardized diagnosis in this patient population.
“If you do not have tightly coiled hair, it does not mean you cannot understand tightly coiled hair, but you have to learn, and you have to let patients know that you understand and have experience,” said Dr. Taylor, emphasizing the role of reassuring patients so they can be confident in the clinical recommendations.
Part of this reassurance will be derived from “interacting with patients in a culturally competent manner,” Dr. Taylor said. Clinicians must develop comfort and confidence in physically examining the hair and scalp, in asking patients to remove weaves or braids for a thorough inspection, and in avoiding comments that might be misinterpreted. Among these, she advised tactful questions about shampooing to avoid any implication that the clinician is implying inadequate hygiene.
When CCCA is suspected, a “biopsy is important” even in circumstances when the diagnosis seems straightforward. For one reason, a substantial proportion of patients may have a concomitant diagnosis. Dr. Taylor cited data from one study in which nearly 20% of CCCA patients also had traction alopecia and more than 10% had androgenic alopecia. Other coexisting problems identified on biopsy, including infection or seborrheic dermatitis, can help clinicians tailor a more effective intervention.
The initial signs of CCCA are typically hair breakage in the vertex of the scalp, which then expands in a central centrifugal pattern, according to Dr. Taylor. Although not all patients have signs of inflammation, such as itching and pustules, inhibition of inflammation represents the first line of therapy.
Relative to hair in the white population, the hair of black individuals grows more slowly and is more fragile, with greater amounts of breakage, said Dr. Taylor, citing published studies that support these differences. To improve early diagnosis of CCCA, understanding the hair in the black population is the first step for spotting problems in routine physical examinations. It may be this lack of familiarity that is contributing to underdiagnosis of CCCA.
“Almost 70% of African-American patients feel that physicians do not understand their hair,” Dr. Taylor said. “Let’s begin to change that.”
Cautioning that it is too often assumed that hairstyles and hair care, such as relaxants or hot combs, are the source of hair loss in black women, Dr. Taylor advised not to jump to conclusions. As an example, she described a case where weaves, braids, and other strategies were employed to mask alopecia after CCCA developed, not before.
“CCCA is the most important cause of scarring alopecia in African-American women,” Dr. Taylor said. Reiterating that hair loss can be prevented or modified with treatment, she added that this places the emphasis on first obtaining an accurate diagnosis.
Dr. Taylor has a financial relationship with Biersdorf; Dr. Woolery-Lloyd has financial relationships with Allergan, Galderma, Ortho Diagnostics, Pfizer, and Somabella Laboratories.
REPORTING FROM SOC 2019
Twitter Chat: Skin Cancer
Join us on Tuesday, October 8, 2019, at 8:00 pm EST on Twitter at #MDedgeChats as we discuss skin cancer, and what’s new in sunscreen, skin of color, and melanoma.
Special guests include physicians with expertise in dermatology and skin cancer, Anthony Rossi, MD (@DrAnthonyRossi), Julie Amthor Croley, MD, 15k followers on IG (@Drskinandsmiles), and Candrice Heath, MD (@DrCandriceHeath). Background information about the chat can be found below.
What will the conversation cover?
Q1: What are the most common types of skin cancer?
Q2: What recent research findings can better inform patients about skin cancer risks?
Q3: What’s the difference between melanoma in fair skin vs. darker skin?
Q4: How does the risk of skin cancer differ in people with darker skin?
Q5: Why should sunscreen be used even in the fall and winter?
Follow us here: @MDedgeDerm | @MDedgeTweets | #MDedgeChats
About Dr. Rossi:
Dr. Anthony Rossi (@DrAnthonyRossi) is a board-certified dermatologist with fellowship training in Mohs micrographic surgery, cosmetic and laser surgery, and advanced cutaneous oncology at the Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College program, both in New York. He specializes in skin cancer surgery, cosmetic dermatologic surgery, and laser surgery.
His research includes quality of life in cancer survivors, the use of noninvasive imaging of the skin, and nonsurgical treatments of skin cancer. Additionally, Dr. Rossi is active in dermatologic organizations and advocacy for medicine.
Research and Publications by Dr. Rossi
About Dr. Heath:
Dr. Candrice Heath (@DrCandriceHeath) is Assistant Professor of Dermatology at the Lewis Katz School of Medicine at Temple University in Philadelphia, Pennsylvania with fellowship training in pediatric dermatology at Johns Hopkins University in Baltimore, Maryland. Dr. Heath is triple board certified in pediatrics, dermatology, and pediatric dermatology. She specializes in adult and pediatric dermatology, skin of color, acne, and eczema. Dr. Heath also enjoys educating primary care physicians on the front lines of health care and delivering easy to understand information to consumers.
Research and publications by Dr. Heath
Guest host of MDedge podcast: A sunscreen update with Dr. Vincent DeLeo.
About Dr. Croley:
Dr. Julie Amthor Croley (@Drskinandsmiles) also known as “Dr. Skin and Smiles” has 15,000 followers on Instagram, and is a Chief Dermatology Resident at the University of Texas Medical Branch in Galveston, Texas. She has a special interest in skin cancer and dermatological surgery and hopes to complete a fellowship in Mohs micrographic surgery after residency. In her free time, Dr. Croley enjoys spending time with her husband (an orthopedic surgeon), running and competing in marathons, and spending time on the beach.
Cutaneous melanoma is the most fatal form of skin cancer and is a considerable public health concern in the United States. Early detection and management of skin cancer can lead to decreased morbidity and mortality from skin cancer. As a result, the American Academy of Dermatology Association supports safe sun-protective practices and diligent self-screening for changing lesions.
Sunscreen use is an essential component of sun protection. New regulations from the US Food and Drug Administration (FDA) have left consumers concerned about the safety of sunscreens. According to a recent Cutis editorial from Vincent A. DeLeo, MD, “There is no question that, as physicians, we want to ‘first, do no harm,’ so we should all be interested in assuring our patients that our sunscreen recommendations are safe and we support the FDA proposal for additional data.”
Patients with skin of color experience disproportionately higher morbidity and mortality when diagnosed with melanoma. “Poor prognosis in patients with skin of color is multifactorial and may be due to poor use of sun protection, misconceptions about melanoma risk, atypical clinical presentation, impaired access to care, and delay in diagnosis,” according to a recent Cutis article.
Population-based skin cancer screening performed exclusively by dermatologists is not practical. Primary care physicians and other experts in melanoma and public health need to be involved in reducing melanoma mortality.
In this chat, we will provide expert recommendations on the diagnosis of skin cancer, preventive measures, and the latest research discussed among physicians.
- “Doctor, Do I Need a Skin Check?”
- Assessing the effectiveness of knowledge-based interventions in skin of color populations.
- Melanoma in US Hispanics
- Podcast: Sunscreen update from Dr. Vincent DeLeo
- Windshield and UV exposure
- Racial, ethnic minorities often don’t practice sun-protective behaviors.
- Sunscreen regulations and advice for your patients.
Join us on Tuesday, October 8, 2019, at 8:00 pm EST on Twitter at #MDedgeChats as we discuss skin cancer, and what’s new in sunscreen, skin of color, and melanoma.
Special guests include physicians with expertise in dermatology and skin cancer, Anthony Rossi, MD (@DrAnthonyRossi), Julie Amthor Croley, MD, 15k followers on IG (@Drskinandsmiles), and Candrice Heath, MD (@DrCandriceHeath). Background information about the chat can be found below.
What will the conversation cover?
Q1: What are the most common types of skin cancer?
Q2: What recent research findings can better inform patients about skin cancer risks?
Q3: What’s the difference between melanoma in fair skin vs. darker skin?
Q4: How does the risk of skin cancer differ in people with darker skin?
Q5: Why should sunscreen be used even in the fall and winter?
Follow us here: @MDedgeDerm | @MDedgeTweets | #MDedgeChats
About Dr. Rossi:
Dr. Anthony Rossi (@DrAnthonyRossi) is a board-certified dermatologist with fellowship training in Mohs micrographic surgery, cosmetic and laser surgery, and advanced cutaneous oncology at the Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College program, both in New York. He specializes in skin cancer surgery, cosmetic dermatologic surgery, and laser surgery.
His research includes quality of life in cancer survivors, the use of noninvasive imaging of the skin, and nonsurgical treatments of skin cancer. Additionally, Dr. Rossi is active in dermatologic organizations and advocacy for medicine.
Research and Publications by Dr. Rossi
About Dr. Heath:
Dr. Candrice Heath (@DrCandriceHeath) is Assistant Professor of Dermatology at the Lewis Katz School of Medicine at Temple University in Philadelphia, Pennsylvania with fellowship training in pediatric dermatology at Johns Hopkins University in Baltimore, Maryland. Dr. Heath is triple board certified in pediatrics, dermatology, and pediatric dermatology. She specializes in adult and pediatric dermatology, skin of color, acne, and eczema. Dr. Heath also enjoys educating primary care physicians on the front lines of health care and delivering easy to understand information to consumers.
Research and publications by Dr. Heath
Guest host of MDedge podcast: A sunscreen update with Dr. Vincent DeLeo.
About Dr. Croley:
Dr. Julie Amthor Croley (@Drskinandsmiles) also known as “Dr. Skin and Smiles” has 15,000 followers on Instagram, and is a Chief Dermatology Resident at the University of Texas Medical Branch in Galveston, Texas. She has a special interest in skin cancer and dermatological surgery and hopes to complete a fellowship in Mohs micrographic surgery after residency. In her free time, Dr. Croley enjoys spending time with her husband (an orthopedic surgeon), running and competing in marathons, and spending time on the beach.
Cutaneous melanoma is the most fatal form of skin cancer and is a considerable public health concern in the United States. Early detection and management of skin cancer can lead to decreased morbidity and mortality from skin cancer. As a result, the American Academy of Dermatology Association supports safe sun-protective practices and diligent self-screening for changing lesions.
Sunscreen use is an essential component of sun protection. New regulations from the US Food and Drug Administration (FDA) have left consumers concerned about the safety of sunscreens. According to a recent Cutis editorial from Vincent A. DeLeo, MD, “There is no question that, as physicians, we want to ‘first, do no harm,’ so we should all be interested in assuring our patients that our sunscreen recommendations are safe and we support the FDA proposal for additional data.”
Patients with skin of color experience disproportionately higher morbidity and mortality when diagnosed with melanoma. “Poor prognosis in patients with skin of color is multifactorial and may be due to poor use of sun protection, misconceptions about melanoma risk, atypical clinical presentation, impaired access to care, and delay in diagnosis,” according to a recent Cutis article.
Population-based skin cancer screening performed exclusively by dermatologists is not practical. Primary care physicians and other experts in melanoma and public health need to be involved in reducing melanoma mortality.
In this chat, we will provide expert recommendations on the diagnosis of skin cancer, preventive measures, and the latest research discussed among physicians.
- “Doctor, Do I Need a Skin Check?”
- Assessing the effectiveness of knowledge-based interventions in skin of color populations.
- Melanoma in US Hispanics
- Podcast: Sunscreen update from Dr. Vincent DeLeo
- Windshield and UV exposure
- Racial, ethnic minorities often don’t practice sun-protective behaviors.
- Sunscreen regulations and advice for your patients.
Join us on Tuesday, October 8, 2019, at 8:00 pm EST on Twitter at #MDedgeChats as we discuss skin cancer, and what’s new in sunscreen, skin of color, and melanoma.
Special guests include physicians with expertise in dermatology and skin cancer, Anthony Rossi, MD (@DrAnthonyRossi), Julie Amthor Croley, MD, 15k followers on IG (@Drskinandsmiles), and Candrice Heath, MD (@DrCandriceHeath). Background information about the chat can be found below.
What will the conversation cover?
Q1: What are the most common types of skin cancer?
Q2: What recent research findings can better inform patients about skin cancer risks?
Q3: What’s the difference between melanoma in fair skin vs. darker skin?
Q4: How does the risk of skin cancer differ in people with darker skin?
Q5: Why should sunscreen be used even in the fall and winter?
Follow us here: @MDedgeDerm | @MDedgeTweets | #MDedgeChats
About Dr. Rossi:
Dr. Anthony Rossi (@DrAnthonyRossi) is a board-certified dermatologist with fellowship training in Mohs micrographic surgery, cosmetic and laser surgery, and advanced cutaneous oncology at the Memorial Sloan Kettering Cancer Center and Weill Cornell Medical College program, both in New York. He specializes in skin cancer surgery, cosmetic dermatologic surgery, and laser surgery.
His research includes quality of life in cancer survivors, the use of noninvasive imaging of the skin, and nonsurgical treatments of skin cancer. Additionally, Dr. Rossi is active in dermatologic organizations and advocacy for medicine.
Research and Publications by Dr. Rossi
About Dr. Heath:
Dr. Candrice Heath (@DrCandriceHeath) is Assistant Professor of Dermatology at the Lewis Katz School of Medicine at Temple University in Philadelphia, Pennsylvania with fellowship training in pediatric dermatology at Johns Hopkins University in Baltimore, Maryland. Dr. Heath is triple board certified in pediatrics, dermatology, and pediatric dermatology. She specializes in adult and pediatric dermatology, skin of color, acne, and eczema. Dr. Heath also enjoys educating primary care physicians on the front lines of health care and delivering easy to understand information to consumers.
Research and publications by Dr. Heath
Guest host of MDedge podcast: A sunscreen update with Dr. Vincent DeLeo.
About Dr. Croley:
Dr. Julie Amthor Croley (@Drskinandsmiles) also known as “Dr. Skin and Smiles” has 15,000 followers on Instagram, and is a Chief Dermatology Resident at the University of Texas Medical Branch in Galveston, Texas. She has a special interest in skin cancer and dermatological surgery and hopes to complete a fellowship in Mohs micrographic surgery after residency. In her free time, Dr. Croley enjoys spending time with her husband (an orthopedic surgeon), running and competing in marathons, and spending time on the beach.
Cutaneous melanoma is the most fatal form of skin cancer and is a considerable public health concern in the United States. Early detection and management of skin cancer can lead to decreased morbidity and mortality from skin cancer. As a result, the American Academy of Dermatology Association supports safe sun-protective practices and diligent self-screening for changing lesions.
Sunscreen use is an essential component of sun protection. New regulations from the US Food and Drug Administration (FDA) have left consumers concerned about the safety of sunscreens. According to a recent Cutis editorial from Vincent A. DeLeo, MD, “There is no question that, as physicians, we want to ‘first, do no harm,’ so we should all be interested in assuring our patients that our sunscreen recommendations are safe and we support the FDA proposal for additional data.”
Patients with skin of color experience disproportionately higher morbidity and mortality when diagnosed with melanoma. “Poor prognosis in patients with skin of color is multifactorial and may be due to poor use of sun protection, misconceptions about melanoma risk, atypical clinical presentation, impaired access to care, and delay in diagnosis,” according to a recent Cutis article.
Population-based skin cancer screening performed exclusively by dermatologists is not practical. Primary care physicians and other experts in melanoma and public health need to be involved in reducing melanoma mortality.
In this chat, we will provide expert recommendations on the diagnosis of skin cancer, preventive measures, and the latest research discussed among physicians.
- “Doctor, Do I Need a Skin Check?”
- Assessing the effectiveness of knowledge-based interventions in skin of color populations.
- Melanoma in US Hispanics
- Podcast: Sunscreen update from Dr. Vincent DeLeo
- Windshield and UV exposure
- Racial, ethnic minorities often don’t practice sun-protective behaviors.
- Sunscreen regulations and advice for your patients.
TAVR, SAVR share same infective endocarditis risk
PARIS – The risk of infective endocarditis following transcatheter aortic valve replacement (TAVR) for the treatment of severe aortic stenosis proved to be the same as after surgical replacement in a French national propensity score–matched study.
This finding from what is believed to be the largest-ever study of infective endocarditis following TAVR will come as a surprise to many physicians. It’s easy to mistakenly assume the risk of this feared complication is lower – and perhaps even negligible – in TAVR patients since the procedure doesn’t involve a significant surgical wound, it’s briefer, the hospital length of stay is shorter, and recovery time is markedly less than with surgical aortic valve replacement (SAVR).
Not so, Laurent Fauchier, MD, PhD, said in presenting the study findings at the annual congress of the European Society of Cardiology.
“Do not think there is a lower risk of infective endocarditis. Be aware, be careful, and provide appropriate antibiotic prophylaxis, just as surgeons do in SAVR. Don’t think, as I did, that with TAVR with no pacemaker implantation there is no risk of infective endocarditis. The TAVR valve is a device, it’s a prosthesis, and the risk is very similar to that of surgery,” advised Dr. Fauchier, a cardiologist at Francois Rabelais University in Tours, France.
He presented a study of all of the nearly 108,000 patients who underwent isolated TAVR or SAVR in France during 2010-2018. The data source was the French national administrative hospital discharge record system. Since the TAVR patients were overall markedly older and sicker than the SAVR patients, especially during the first years of the study, he and his coinvestigators performed propensity score matching using 30 variables, which enabled them to narrow the field of inquiry down to a carefully selected study population of 16,291 TAVR patients and an equal number of closely similar SAVR patients.
A total of 1,070 cases of infective endocarditis occurred during a mean follow-up of just over 2 years. The rate of hospital admission for this complication was 1.89% per year in the TAVR group and similar at 1.71% per year in the SAVR cohort.
Of note, all-cause mortality in TAVR patients who developed infective endocarditis was 1.32-fold greater than it was in SAVR patients with infective endocarditis, a statistically significant difference. The explanation for the increased mortality risk in the TAVR group probably has to do at least in part with an inability on the part of the investigators to fully capture and control for the TAVR group’s greater frailty, according to the cardiologist.
Risk factors for infective endocarditis shared in common by TAVR and SAVR patients included male gender, a higher Charlson Comorbidity Index score, and a greater frailty index. The main predictors unique to the TAVR patients were atrial fibrillation, anemia, and tricuspid regurgitation. And although pacemaker and defibrillator implantation were risk factors for infective endocarditis in the SAVR patients, it wasn’t predictive of increased risk in the TAVR population. Dr. Fauchier called this finding “quite reassuring” given that roughly 20% of the TAVR group received a pacemaker.
The causative microorganisms for infective endocarditis were essentially the same in the TAVR and SAVR groups, simplifying antimicrobial prophylaxis decision making.
Dr. Fauchier reported having no financial conflicts regarding the study, conducted free of commercial support. He serves as a consultant to and/or on speakers’ bureaus for Bayer, BMS Pfizer, Boehringer Ingelheim, Medtronic, and Novartis.
PARIS – The risk of infective endocarditis following transcatheter aortic valve replacement (TAVR) for the treatment of severe aortic stenosis proved to be the same as after surgical replacement in a French national propensity score–matched study.
This finding from what is believed to be the largest-ever study of infective endocarditis following TAVR will come as a surprise to many physicians. It’s easy to mistakenly assume the risk of this feared complication is lower – and perhaps even negligible – in TAVR patients since the procedure doesn’t involve a significant surgical wound, it’s briefer, the hospital length of stay is shorter, and recovery time is markedly less than with surgical aortic valve replacement (SAVR).
Not so, Laurent Fauchier, MD, PhD, said in presenting the study findings at the annual congress of the European Society of Cardiology.
“Do not think there is a lower risk of infective endocarditis. Be aware, be careful, and provide appropriate antibiotic prophylaxis, just as surgeons do in SAVR. Don’t think, as I did, that with TAVR with no pacemaker implantation there is no risk of infective endocarditis. The TAVR valve is a device, it’s a prosthesis, and the risk is very similar to that of surgery,” advised Dr. Fauchier, a cardiologist at Francois Rabelais University in Tours, France.
He presented a study of all of the nearly 108,000 patients who underwent isolated TAVR or SAVR in France during 2010-2018. The data source was the French national administrative hospital discharge record system. Since the TAVR patients were overall markedly older and sicker than the SAVR patients, especially during the first years of the study, he and his coinvestigators performed propensity score matching using 30 variables, which enabled them to narrow the field of inquiry down to a carefully selected study population of 16,291 TAVR patients and an equal number of closely similar SAVR patients.
A total of 1,070 cases of infective endocarditis occurred during a mean follow-up of just over 2 years. The rate of hospital admission for this complication was 1.89% per year in the TAVR group and similar at 1.71% per year in the SAVR cohort.
Of note, all-cause mortality in TAVR patients who developed infective endocarditis was 1.32-fold greater than it was in SAVR patients with infective endocarditis, a statistically significant difference. The explanation for the increased mortality risk in the TAVR group probably has to do at least in part with an inability on the part of the investigators to fully capture and control for the TAVR group’s greater frailty, according to the cardiologist.
Risk factors for infective endocarditis shared in common by TAVR and SAVR patients included male gender, a higher Charlson Comorbidity Index score, and a greater frailty index. The main predictors unique to the TAVR patients were atrial fibrillation, anemia, and tricuspid regurgitation. And although pacemaker and defibrillator implantation were risk factors for infective endocarditis in the SAVR patients, it wasn’t predictive of increased risk in the TAVR population. Dr. Fauchier called this finding “quite reassuring” given that roughly 20% of the TAVR group received a pacemaker.
The causative microorganisms for infective endocarditis were essentially the same in the TAVR and SAVR groups, simplifying antimicrobial prophylaxis decision making.
Dr. Fauchier reported having no financial conflicts regarding the study, conducted free of commercial support. He serves as a consultant to and/or on speakers’ bureaus for Bayer, BMS Pfizer, Boehringer Ingelheim, Medtronic, and Novartis.
PARIS – The risk of infective endocarditis following transcatheter aortic valve replacement (TAVR) for the treatment of severe aortic stenosis proved to be the same as after surgical replacement in a French national propensity score–matched study.
This finding from what is believed to be the largest-ever study of infective endocarditis following TAVR will come as a surprise to many physicians. It’s easy to mistakenly assume the risk of this feared complication is lower – and perhaps even negligible – in TAVR patients since the procedure doesn’t involve a significant surgical wound, it’s briefer, the hospital length of stay is shorter, and recovery time is markedly less than with surgical aortic valve replacement (SAVR).
Not so, Laurent Fauchier, MD, PhD, said in presenting the study findings at the annual congress of the European Society of Cardiology.
“Do not think there is a lower risk of infective endocarditis. Be aware, be careful, and provide appropriate antibiotic prophylaxis, just as surgeons do in SAVR. Don’t think, as I did, that with TAVR with no pacemaker implantation there is no risk of infective endocarditis. The TAVR valve is a device, it’s a prosthesis, and the risk is very similar to that of surgery,” advised Dr. Fauchier, a cardiologist at Francois Rabelais University in Tours, France.
He presented a study of all of the nearly 108,000 patients who underwent isolated TAVR or SAVR in France during 2010-2018. The data source was the French national administrative hospital discharge record system. Since the TAVR patients were overall markedly older and sicker than the SAVR patients, especially during the first years of the study, he and his coinvestigators performed propensity score matching using 30 variables, which enabled them to narrow the field of inquiry down to a carefully selected study population of 16,291 TAVR patients and an equal number of closely similar SAVR patients.
A total of 1,070 cases of infective endocarditis occurred during a mean follow-up of just over 2 years. The rate of hospital admission for this complication was 1.89% per year in the TAVR group and similar at 1.71% per year in the SAVR cohort.
Of note, all-cause mortality in TAVR patients who developed infective endocarditis was 1.32-fold greater than it was in SAVR patients with infective endocarditis, a statistically significant difference. The explanation for the increased mortality risk in the TAVR group probably has to do at least in part with an inability on the part of the investigators to fully capture and control for the TAVR group’s greater frailty, according to the cardiologist.
Risk factors for infective endocarditis shared in common by TAVR and SAVR patients included male gender, a higher Charlson Comorbidity Index score, and a greater frailty index. The main predictors unique to the TAVR patients were atrial fibrillation, anemia, and tricuspid regurgitation. And although pacemaker and defibrillator implantation were risk factors for infective endocarditis in the SAVR patients, it wasn’t predictive of increased risk in the TAVR population. Dr. Fauchier called this finding “quite reassuring” given that roughly 20% of the TAVR group received a pacemaker.
The causative microorganisms for infective endocarditis were essentially the same in the TAVR and SAVR groups, simplifying antimicrobial prophylaxis decision making.
Dr. Fauchier reported having no financial conflicts regarding the study, conducted free of commercial support. He serves as a consultant to and/or on speakers’ bureaus for Bayer, BMS Pfizer, Boehringer Ingelheim, Medtronic, and Novartis.
REPORTING FROM THE ESC CONGRESS 2019
Scars and color changes on face
The FP recognized the scarring, skin atrophy, erythema and hyperpigmentation in the malar distribution as discoid lupus erythematosus (DLE). Upon examination, the FP noted similar patterns (with the addition of hypopigmentation) in the conchal bowls of both pinna. This was confirmatory for the DLE diagnosis (AKA chronic cutaneous lupus). (If in doubt, a 4-mm punch biopsy could be performed on the lesions of the face.) Without the lesions in the ears, sarcoidosis might have been considered as part of the differential diagnosis.
DLE lesions are characterized by discrete, erythematous, slightly infiltrated papules or plaques. Hypopigmentation develops in the central area and hyperpigmentation develops at the active border. Resolution of the active lesion results in atrophy and scarring.
In this case, the FP explained the diagnosis of DLE to the patient and ordered testing for antinuclear antibodies (ANA), a complete blood count, and comprehensive metabolic panel. All the labs were normal, and the ANA was negative, which confirmed that this was not a case of systemic lupus erythematosus. Patients with only DLE generally have negative or low-titer ANA titers.
DLE therapy includes corticosteroids (topical or intralesional) and oral antimalarials, such as hydroxychloroquine. The FP in this case started the patient on hydroxychloroquine 200 mg bid and topical triamcinolone 0.1% applied twice daily to the erythematous portions of the cheeks for 2 weeks. At the 2-week follow-up, the patient’s skin looked less red and inflamed and she was happy with the improved appearance of her skin. Patients on hydroxychloroquine need a baseline eye exam by an ophthalmologist and then yearly exams after 5 years of therapy to detect any retinal or visual field problems.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Pye A, Mayeaux, EJ, Mishra V, et al. Lupus. In: Usatine R, Smith M, Mayeaux EJ, et al. eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1183-1193.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the 3rd edition of the Color Atlas and Synopsis of Family Medicine as an app by clicking on this link: https://usatinemedia.com/app/color-atlas-of-family-medicine/
The FP recognized the scarring, skin atrophy, erythema and hyperpigmentation in the malar distribution as discoid lupus erythematosus (DLE). Upon examination, the FP noted similar patterns (with the addition of hypopigmentation) in the conchal bowls of both pinna. This was confirmatory for the DLE diagnosis (AKA chronic cutaneous lupus). (If in doubt, a 4-mm punch biopsy could be performed on the lesions of the face.) Without the lesions in the ears, sarcoidosis might have been considered as part of the differential diagnosis.
DLE lesions are characterized by discrete, erythematous, slightly infiltrated papules or plaques. Hypopigmentation develops in the central area and hyperpigmentation develops at the active border. Resolution of the active lesion results in atrophy and scarring.
In this case, the FP explained the diagnosis of DLE to the patient and ordered testing for antinuclear antibodies (ANA), a complete blood count, and comprehensive metabolic panel. All the labs were normal, and the ANA was negative, which confirmed that this was not a case of systemic lupus erythematosus. Patients with only DLE generally have negative or low-titer ANA titers.
DLE therapy includes corticosteroids (topical or intralesional) and oral antimalarials, such as hydroxychloroquine. The FP in this case started the patient on hydroxychloroquine 200 mg bid and topical triamcinolone 0.1% applied twice daily to the erythematous portions of the cheeks for 2 weeks. At the 2-week follow-up, the patient’s skin looked less red and inflamed and she was happy with the improved appearance of her skin. Patients on hydroxychloroquine need a baseline eye exam by an ophthalmologist and then yearly exams after 5 years of therapy to detect any retinal or visual field problems.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Pye A, Mayeaux, EJ, Mishra V, et al. Lupus. In: Usatine R, Smith M, Mayeaux EJ, et al. eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1183-1193.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the 3rd edition of the Color Atlas and Synopsis of Family Medicine as an app by clicking on this link: https://usatinemedia.com/app/color-atlas-of-family-medicine/
The FP recognized the scarring, skin atrophy, erythema and hyperpigmentation in the malar distribution as discoid lupus erythematosus (DLE). Upon examination, the FP noted similar patterns (with the addition of hypopigmentation) in the conchal bowls of both pinna. This was confirmatory for the DLE diagnosis (AKA chronic cutaneous lupus). (If in doubt, a 4-mm punch biopsy could be performed on the lesions of the face.) Without the lesions in the ears, sarcoidosis might have been considered as part of the differential diagnosis.
DLE lesions are characterized by discrete, erythematous, slightly infiltrated papules or plaques. Hypopigmentation develops in the central area and hyperpigmentation develops at the active border. Resolution of the active lesion results in atrophy and scarring.
In this case, the FP explained the diagnosis of DLE to the patient and ordered testing for antinuclear antibodies (ANA), a complete blood count, and comprehensive metabolic panel. All the labs were normal, and the ANA was negative, which confirmed that this was not a case of systemic lupus erythematosus. Patients with only DLE generally have negative or low-titer ANA titers.
DLE therapy includes corticosteroids (topical or intralesional) and oral antimalarials, such as hydroxychloroquine. The FP in this case started the patient on hydroxychloroquine 200 mg bid and topical triamcinolone 0.1% applied twice daily to the erythematous portions of the cheeks for 2 weeks. At the 2-week follow-up, the patient’s skin looked less red and inflamed and she was happy with the improved appearance of her skin. Patients on hydroxychloroquine need a baseline eye exam by an ophthalmologist and then yearly exams after 5 years of therapy to detect any retinal or visual field problems.
Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Pye A, Mayeaux, EJ, Mishra V, et al. Lupus. In: Usatine R, Smith M, Mayeaux EJ, et al. eds. Color Atlas and Synopsis of Family Medicine. 3rd ed. New York, NY: McGraw-Hill; 2019:1183-1193.
To learn more about the newest 3rd edition of the Color Atlas and Synopsis of Family Medicine, see: https://www.amazon.com/Color-Atlas-Synopsis-Family-Medicine/dp/1259862046/
You can get the 3rd edition of the Color Atlas and Synopsis of Family Medicine as an app by clicking on this link: https://usatinemedia.com/app/color-atlas-of-family-medicine/
IPD in children may be a signal of immunodeficiency
according to a systematic review published in JAMA Pediatrics.
Coen Butters, BMed, DCH, of the Royal Children’s Hospital in Melbourne, and coauthors wrote that, even with optimal vaccine coverage, there is still a group of children with increased susceptibility to invasive pneumococcal disease (IPD), and this could be a potential marker of primary immunodeficiency.
They conducted a systematic review of 17 studies of 6,002 children to examine the evidence on the incidence of primary immunodeficiency in children who presented with IPD but without any other risk factors or predisposing conditions.
Overall, the frequency of primary immunodeficiency in children presenting with IPD who did not have any other predisposing condition ranged from 1% to 26%.
One study of 162 children with IPD, which had an overall frequency of primary immunodeficiency of 10%, found that children older than 2 years were significantly more likely to have primary immunodeficiency than those aged under 2 years (26% vs. 3%; P less than .001).
Primary antibody deficiency was the most commonly diagnosed immunodeficiency in these children with IPD, accounting for 71% of cases. These deficiencies presented as hypogammaglobulinemia, specific pneumococcal antibody deficiency, X-linked agammaglobulinemia, and IgG2 deficiency.
The review also included four studies that looked at the frequency of mannose-binding lectin deficiency in 1,493 children with primary IPD. Two of these studies reported a prevalence of mannose-binding lectin deficiency ranging from 31% in children aged younger than 2 years to 41% in children younger than 1 year.
Five studies looked at the rate of primary immunodeficiency in children presenting with recurrent IPD. In addition to other predisposing conditions such as sickle cell disease, cancer, and anatomical breach in the blood-brain barrier, the three studies that screened for primary immunodeficiency found rates ranging from 10% to 67%. The most common conditions were complement deficiency, pneumococcal antibody deficiency, and a single case of TLR-signaling defect.
In a study of 162 children with primary IPD, screening for asplenia identified a single case of congenital asplenia. In another study of 2,498 cases of IPD, 22 patients had asplenia at presentation, half of whom died at presentation.
Dr. Butters and associates concluded that “this review’s findings suggests that existing data support the immune evaluation of children older than 2 years without a known predisposing condition who present with their first episode of Streptococcus pneumoniae meningitis, pneumonia, or recurrent IPD. Immune evaluation should include assessment for immunoglobulin deficiency, pneumococcal antibody deficiency, complement disorders, and asplenia.”
In an accompanying editorial, Stephen I. Pelton, MD, of the Maxwell Finland Laboratory for Infectious Diseases at Boston Medical Center, and coauthors wrote that in children with recurrent episodes of IPD caused by nonvaccine serotypes – particularly those aged over 5 years – evaluation for primary immunodeficiencies could uncover immune defects.
“Once identified, direct and indirect protection, penicillin prophylaxis, or a combination of these offers great potential for disease prevention and reduction of mortality and morbidity in children with [primary immunodeficiency],” they wrote.
No funding or conflicts of interest were declared for the study. Two of the editorialists declared research funding or honoraria from the pharmaceutical sector.
SOURCES: Butters C et al. JAMA Pediatr. 2019 Sep 30. doi: 10.1001/jamapediatrics.2019.3203; Pelton SI et al. JAMA Pediatr. 2019 Sep 30. doi: 10.1001/jamapediatrics.2019.3185.
according to a systematic review published in JAMA Pediatrics.
Coen Butters, BMed, DCH, of the Royal Children’s Hospital in Melbourne, and coauthors wrote that, even with optimal vaccine coverage, there is still a group of children with increased susceptibility to invasive pneumococcal disease (IPD), and this could be a potential marker of primary immunodeficiency.
They conducted a systematic review of 17 studies of 6,002 children to examine the evidence on the incidence of primary immunodeficiency in children who presented with IPD but without any other risk factors or predisposing conditions.
Overall, the frequency of primary immunodeficiency in children presenting with IPD who did not have any other predisposing condition ranged from 1% to 26%.
One study of 162 children with IPD, which had an overall frequency of primary immunodeficiency of 10%, found that children older than 2 years were significantly more likely to have primary immunodeficiency than those aged under 2 years (26% vs. 3%; P less than .001).
Primary antibody deficiency was the most commonly diagnosed immunodeficiency in these children with IPD, accounting for 71% of cases. These deficiencies presented as hypogammaglobulinemia, specific pneumococcal antibody deficiency, X-linked agammaglobulinemia, and IgG2 deficiency.
The review also included four studies that looked at the frequency of mannose-binding lectin deficiency in 1,493 children with primary IPD. Two of these studies reported a prevalence of mannose-binding lectin deficiency ranging from 31% in children aged younger than 2 years to 41% in children younger than 1 year.
Five studies looked at the rate of primary immunodeficiency in children presenting with recurrent IPD. In addition to other predisposing conditions such as sickle cell disease, cancer, and anatomical breach in the blood-brain barrier, the three studies that screened for primary immunodeficiency found rates ranging from 10% to 67%. The most common conditions were complement deficiency, pneumococcal antibody deficiency, and a single case of TLR-signaling defect.
In a study of 162 children with primary IPD, screening for asplenia identified a single case of congenital asplenia. In another study of 2,498 cases of IPD, 22 patients had asplenia at presentation, half of whom died at presentation.
Dr. Butters and associates concluded that “this review’s findings suggests that existing data support the immune evaluation of children older than 2 years without a known predisposing condition who present with their first episode of Streptococcus pneumoniae meningitis, pneumonia, or recurrent IPD. Immune evaluation should include assessment for immunoglobulin deficiency, pneumococcal antibody deficiency, complement disorders, and asplenia.”
In an accompanying editorial, Stephen I. Pelton, MD, of the Maxwell Finland Laboratory for Infectious Diseases at Boston Medical Center, and coauthors wrote that in children with recurrent episodes of IPD caused by nonvaccine serotypes – particularly those aged over 5 years – evaluation for primary immunodeficiencies could uncover immune defects.
“Once identified, direct and indirect protection, penicillin prophylaxis, or a combination of these offers great potential for disease prevention and reduction of mortality and morbidity in children with [primary immunodeficiency],” they wrote.
No funding or conflicts of interest were declared for the study. Two of the editorialists declared research funding or honoraria from the pharmaceutical sector.
SOURCES: Butters C et al. JAMA Pediatr. 2019 Sep 30. doi: 10.1001/jamapediatrics.2019.3203; Pelton SI et al. JAMA Pediatr. 2019 Sep 30. doi: 10.1001/jamapediatrics.2019.3185.
according to a systematic review published in JAMA Pediatrics.
Coen Butters, BMed, DCH, of the Royal Children’s Hospital in Melbourne, and coauthors wrote that, even with optimal vaccine coverage, there is still a group of children with increased susceptibility to invasive pneumococcal disease (IPD), and this could be a potential marker of primary immunodeficiency.
They conducted a systematic review of 17 studies of 6,002 children to examine the evidence on the incidence of primary immunodeficiency in children who presented with IPD but without any other risk factors or predisposing conditions.
Overall, the frequency of primary immunodeficiency in children presenting with IPD who did not have any other predisposing condition ranged from 1% to 26%.
One study of 162 children with IPD, which had an overall frequency of primary immunodeficiency of 10%, found that children older than 2 years were significantly more likely to have primary immunodeficiency than those aged under 2 years (26% vs. 3%; P less than .001).
Primary antibody deficiency was the most commonly diagnosed immunodeficiency in these children with IPD, accounting for 71% of cases. These deficiencies presented as hypogammaglobulinemia, specific pneumococcal antibody deficiency, X-linked agammaglobulinemia, and IgG2 deficiency.
The review also included four studies that looked at the frequency of mannose-binding lectin deficiency in 1,493 children with primary IPD. Two of these studies reported a prevalence of mannose-binding lectin deficiency ranging from 31% in children aged younger than 2 years to 41% in children younger than 1 year.
Five studies looked at the rate of primary immunodeficiency in children presenting with recurrent IPD. In addition to other predisposing conditions such as sickle cell disease, cancer, and anatomical breach in the blood-brain barrier, the three studies that screened for primary immunodeficiency found rates ranging from 10% to 67%. The most common conditions were complement deficiency, pneumococcal antibody deficiency, and a single case of TLR-signaling defect.
In a study of 162 children with primary IPD, screening for asplenia identified a single case of congenital asplenia. In another study of 2,498 cases of IPD, 22 patients had asplenia at presentation, half of whom died at presentation.
Dr. Butters and associates concluded that “this review’s findings suggests that existing data support the immune evaluation of children older than 2 years without a known predisposing condition who present with their first episode of Streptococcus pneumoniae meningitis, pneumonia, or recurrent IPD. Immune evaluation should include assessment for immunoglobulin deficiency, pneumococcal antibody deficiency, complement disorders, and asplenia.”
In an accompanying editorial, Stephen I. Pelton, MD, of the Maxwell Finland Laboratory for Infectious Diseases at Boston Medical Center, and coauthors wrote that in children with recurrent episodes of IPD caused by nonvaccine serotypes – particularly those aged over 5 years – evaluation for primary immunodeficiencies could uncover immune defects.
“Once identified, direct and indirect protection, penicillin prophylaxis, or a combination of these offers great potential for disease prevention and reduction of mortality and morbidity in children with [primary immunodeficiency],” they wrote.
No funding or conflicts of interest were declared for the study. Two of the editorialists declared research funding or honoraria from the pharmaceutical sector.
SOURCES: Butters C et al. JAMA Pediatr. 2019 Sep 30. doi: 10.1001/jamapediatrics.2019.3203; Pelton SI et al. JAMA Pediatr. 2019 Sep 30. doi: 10.1001/jamapediatrics.2019.3185.
FROM JAMA PEDIATRICS
Targeted agents vs. chemoimmunotherapy as first-line treatment of CLL
SAN FRANCISCO – Should targeted agents replace chemoimmunotherapy (CIT) as first-line treatment for chronic lymphocytic leukemia (CLL)? A recent debate suggests there’s no consensus. 
William G. Wierda, MD, PhD, of The University of Texas MD Anderson Cancer Center in Houston, and Jennifer R. Brown, MD, PhD, of Dana-Farber Cancer Institute in Boston, debated the topic at the National Comprehensive Cancer Network Hematologic Malignancies Annual Congress.
Dr. Wierda argued that CLL patients should receive a BTK inhibitor or BCL2 inhibitor, with or without obinutuzumab, as first-line therapy because these targeted agents have been shown to provide better progression-free survival (PFS) than CIT, and the targeted therapies may prolong overall survival (OS) as well.
Dr. Brown countered that targeted agents don’t improve PFS for all CLL patients, improved PFS doesn’t always translate to improved OS, and targeted agents cost more than CIT.
No role for CIT as first-line treatment
“We have two approaches right now, with nonchemoimmunotherapy-based treatment,” Dr. Wierda said. “One approach, with small-molecule inhibitors, is to have a sustained and durable period of disease control, particularly with BTK inhibitors. The other strategy that has emerged is deep remissions with fixed-duration treatment with BCL2 small-molecule inhibitor-based therapy, which, I would argue, is better than being exposed to genotoxic chemoimmunotherapy.”
Dr. Wierda went on to explain that the BTK inhibitor ibrutinib has been shown to improve PFS, compared with CIT, in phase 3 trials.
In the iLLUMINATE trial, researchers compared ibrutinib plus obinutuzumab to chlorambucil plus obinutuzumab as first-line treatment in CLL. At a median follow-up of 31.3 months, the median PFS was not reached in the ibrutinib arm and was 19 months in the chlorambucil arm (P less than .0001; Lancet Oncol. 2019 Jan;20[1]:43-56).
In the A041202 study, researchers compared ibrutinib alone (Ib) or in combination with rituximab (Ib-R) to bendamustine plus rituximab (BR) in untreated, older patients with CLL. The 2-year PFS estimates were 74% in the BR arm, 87% in the Ib arm, and 88% in the Ib-R arm (P less than .001 for BR vs. Ib or Ib-R; N Engl J Med. 2018; 379:2517-28).
In the E1912 trial, researchers compared Ib-R to fludarabine, cyclophosphamide, and rituximab (FCR) in younger, untreated CLL patients. The 3-year PFS was 89.4% with Ib-R and 72.9% with FCR (P less than .001; N Engl J Med. 2019 Aug 1;381:432-43).
Dr. Wierda noted that the E1912 trial also showed superior OS with Ib-R. The 3-year OS rate was 98.8% with Ib-R and 91.5% with FCR (P less than .001). However, there was no significant difference in OS between the treatment arms in the A041202 trial or the iLLUMINATE trial.
“But I would argue that is, in part, because of short follow-up,” Dr. Wierda said. “The trials were all designed to look at progression-free survival, not overall survival. With longer follow-up, we may see differences in overall survival emerging.”
Dr. Wierda went on to say that fixed‐duration treatment with the BCL2 inhibitor venetoclax can improve PFS over CIT.
In the phase 3 CLL14 trial, researchers compared fixed-duration treatment with venetoclax plus obinutuzumab to chlorambucil plus obinutuzumab in previously untreated CLL patients with comorbidities. The estimated PFS at 2 years was 88.2% in the venetoclax group and 64.1% in the chlorambucil group (P less than .001; N Engl J Med. 2019; 380:2225-36).
“[There was] no difference in overall survival,” Dr. Wierda noted. “But, again, I would argue ... that follow-up is relatively limited. We may ultimately see a difference in overall survival.”
Based on these findings, Dr. Wierda made the following treatment recommendations:
- Any CLL patient with del(17p) or TP53 mutation, and older, unfit patients with unmutated IGHV should receive a BTK inhibitor, with or without obinutuzumab.
- All young, fit patients, and older, unfit patients with mutated IGHV should receive a BCL2 inhibitor plus obinutuzumab.
Dr. Wierda also noted that ibrutinib and venetoclax in combination have shown early promise for patients with previously untreated CLL (N Engl J Med. 2019; 380:2095-2103).
CIT still has a role as first-line treatment
Dr. Brown suggested that a PFS benefit may not be enough to recommend targeted agents over CIT. For one thing, the PFS benefit doesn’t apply to all patients, as the IGHV-mutated subgroup does equally well with CIT and targeted agents.
In the IGHV-mutated group from the E1912 trial, the 3-year PFS was 88% for patients who received Ib-R and those who received FCR (N Engl J Med. 2019 Aug 1;381:432-43). In the A041202 study, the 2-year PFS among IGHV-mutated patients was 87% in the BR arm, 86% in the Ib arm, and 88% in the Ib-R arm (N Engl J Med. 2018; 379:2517-28).
In the CLL14 trial, PFS rates were similar among IGHV-mutated patients who received chlorambucil plus obinutuzumab and IGHV-mutated or unmutated patients who received venetoclax and obinutuzumab (N Engl J Med. 2019; 380:2225-36).
Dr. Brown also noted that the overall improvement in PFS observed with ibrutinib and venetoclax doesn’t always translate to improved OS.
In the A041202 study, there was no significant difference in OS between the Ib, Ib-R, and BR arms (N Engl J Med. 2018; 379:2517-28). There was no significant difference in OS between the ibrutinib and chlorambucil arms in the iLLUMINATE trial (Lancet Oncol. 2019 Jan;20[1]:43-56). And there was no significant difference in OS between the venetoclax and chlorambucil arms in the CLL14 trial (N Engl J Med. 2019; 380:2225-36).
However, in the RESONATE-2 trial, ibrutinib provided an OS benefit over chlorambucil. The 2-year OS was 95% and 84%, respectively (P = .0145; Haematologica. Sept 2018;103:1502-10). Dr. Brown said the OS advantage in this study was due to the “very poor comparator of chlorambucil and very limited crossover.”
As Dr. Wierda mentioned, the OS rate was higher with Ib-R than with FCR in the E1912 trial. The 3-year OS rate was 98.8% and 91.5%, respectively (P less than .001; N Engl J Med. 2019 Aug 1;381:432-43). Dr. Brown noted, however, that there were few deaths in this study, and many of them “were not clearly related to the disease or its treatment.”
Dr. Brown also pointed out that FCR has been shown to have curative potential in IGHV-mutated CLL in both the FCR300 trial (Blood. 2016 127:303-9) and the CLL8 trial (Blood. 2016 127:208-15).
Another factor to consider is the greater cost of targeted agents. One analysis suggested the per-patient lifetime cost of CLL treatment in the United States will increase from $147,000 to $604,000 as targeted therapies overtake CIT as first-line treatment (J Clin Oncol. 2017 Jan 10;35[2]:166-174).
“Given all of the above, chemoimmunotherapy is going to remain part of the treatment repertoire for CLL,” Dr. Brown said. “It’s our only known potential cure for the fit, mutated patients ... and can also result in prolonged treatment-free intervals for patients who are older. As we manage CLL as a chronic disease over a lifetime, we need to continue to have this in our armamentarium.”
Specifically, Dr. Brown said CIT is appropriate for patients who don’t have del(17p) or mutated TP53. FCR should be given to young, fit patients with IGHV-mutated CLL, and FCR or BR should be given to older patients and young, fit patients with IGHV-unmutated CLL.
Dr. Brown and Dr. Wierda reported financial ties to multiple pharmaceutical companies, including makers of CLL treatments.
SAN FRANCISCO – Should targeted agents replace chemoimmunotherapy (CIT) as first-line treatment for chronic lymphocytic leukemia (CLL)? A recent debate suggests there’s no consensus.
William G. Wierda, MD, PhD, of The University of Texas MD Anderson Cancer Center in Houston, and Jennifer R. Brown, MD, PhD, of Dana-Farber Cancer Institute in Boston, debated the topic at the National Comprehensive Cancer Network Hematologic Malignancies Annual Congress.
Dr. Wierda argued that CLL patients should receive a BTK inhibitor or BCL2 inhibitor, with or without obinutuzumab, as first-line therapy because these targeted agents have been shown to provide better progression-free survival (PFS) than CIT, and the targeted therapies may prolong overall survival (OS) as well.
Dr. Brown countered that targeted agents don’t improve PFS for all CLL patients, improved PFS doesn’t always translate to improved OS, and targeted agents cost more than CIT.
No role for CIT as first-line treatment
“We have two approaches right now, with nonchemoimmunotherapy-based treatment,” Dr. Wierda said. “One approach, with small-molecule inhibitors, is to have a sustained and durable period of disease control, particularly with BTK inhibitors. The other strategy that has emerged is deep remissions with fixed-duration treatment with BCL2 small-molecule inhibitor-based therapy, which, I would argue, is better than being exposed to genotoxic chemoimmunotherapy.”
Dr. Wierda went on to explain that the BTK inhibitor ibrutinib has been shown to improve PFS, compared with CIT, in phase 3 trials.
In the iLLUMINATE trial, researchers compared ibrutinib plus obinutuzumab to chlorambucil plus obinutuzumab as first-line treatment in CLL. At a median follow-up of 31.3 months, the median PFS was not reached in the ibrutinib arm and was 19 months in the chlorambucil arm (P less than .0001; Lancet Oncol. 2019 Jan;20[1]:43-56).
In the A041202 study, researchers compared ibrutinib alone (Ib) or in combination with rituximab (Ib-R) to bendamustine plus rituximab (BR) in untreated, older patients with CLL. The 2-year PFS estimates were 74% in the BR arm, 87% in the Ib arm, and 88% in the Ib-R arm (P less than .001 for BR vs. Ib or Ib-R; N Engl J Med. 2018; 379:2517-28).
In the E1912 trial, researchers compared Ib-R to fludarabine, cyclophosphamide, and rituximab (FCR) in younger, untreated CLL patients. The 3-year PFS was 89.4% with Ib-R and 72.9% with FCR (P less than .001; N Engl J Med. 2019 Aug 1;381:432-43).
Dr. Wierda noted that the E1912 trial also showed superior OS with Ib-R. The 3-year OS rate was 98.8% with Ib-R and 91.5% with FCR (P less than .001). However, there was no significant difference in OS between the treatment arms in the A041202 trial or the iLLUMINATE trial.
“But I would argue that is, in part, because of short follow-up,” Dr. Wierda said. “The trials were all designed to look at progression-free survival, not overall survival. With longer follow-up, we may see differences in overall survival emerging.”
Dr. Wierda went on to say that fixed‐duration treatment with the BCL2 inhibitor venetoclax can improve PFS over CIT.
In the phase 3 CLL14 trial, researchers compared fixed-duration treatment with venetoclax plus obinutuzumab to chlorambucil plus obinutuzumab in previously untreated CLL patients with comorbidities. The estimated PFS at 2 years was 88.2% in the venetoclax group and 64.1% in the chlorambucil group (P less than .001; N Engl J Med. 2019; 380:2225-36).
“[There was] no difference in overall survival,” Dr. Wierda noted. “But, again, I would argue ... that follow-up is relatively limited. We may ultimately see a difference in overall survival.”
Based on these findings, Dr. Wierda made the following treatment recommendations:
- Any CLL patient with del(17p) or TP53 mutation, and older, unfit patients with unmutated IGHV should receive a BTK inhibitor, with or without obinutuzumab.
- All young, fit patients, and older, unfit patients with mutated IGHV should receive a BCL2 inhibitor plus obinutuzumab.
Dr. Wierda also noted that ibrutinib and venetoclax in combination have shown early promise for patients with previously untreated CLL (N Engl J Med. 2019; 380:2095-2103).
CIT still has a role as first-line treatment
Dr. Brown suggested that a PFS benefit may not be enough to recommend targeted agents over CIT. For one thing, the PFS benefit doesn’t apply to all patients, as the IGHV-mutated subgroup does equally well with CIT and targeted agents.
In the IGHV-mutated group from the E1912 trial, the 3-year PFS was 88% for patients who received Ib-R and those who received FCR (N Engl J Med. 2019 Aug 1;381:432-43). In the A041202 study, the 2-year PFS among IGHV-mutated patients was 87% in the BR arm, 86% in the Ib arm, and 88% in the Ib-R arm (N Engl J Med. 2018; 379:2517-28).
In the CLL14 trial, PFS rates were similar among IGHV-mutated patients who received chlorambucil plus obinutuzumab and IGHV-mutated or unmutated patients who received venetoclax and obinutuzumab (N Engl J Med. 2019; 380:2225-36).
Dr. Brown also noted that the overall improvement in PFS observed with ibrutinib and venetoclax doesn’t always translate to improved OS.
In the A041202 study, there was no significant difference in OS between the Ib, Ib-R, and BR arms (N Engl J Med. 2018; 379:2517-28). There was no significant difference in OS between the ibrutinib and chlorambucil arms in the iLLUMINATE trial (Lancet Oncol. 2019 Jan;20[1]:43-56). And there was no significant difference in OS between the venetoclax and chlorambucil arms in the CLL14 trial (N Engl J Med. 2019; 380:2225-36).
However, in the RESONATE-2 trial, ibrutinib provided an OS benefit over chlorambucil. The 2-year OS was 95% and 84%, respectively (P = .0145; Haematologica. Sept 2018;103:1502-10). Dr. Brown said the OS advantage in this study was due to the “very poor comparator of chlorambucil and very limited crossover.”
As Dr. Wierda mentioned, the OS rate was higher with Ib-R than with FCR in the E1912 trial. The 3-year OS rate was 98.8% and 91.5%, respectively (P less than .001; N Engl J Med. 2019 Aug 1;381:432-43). Dr. Brown noted, however, that there were few deaths in this study, and many of them “were not clearly related to the disease or its treatment.”
Dr. Brown also pointed out that FCR has been shown to have curative potential in IGHV-mutated CLL in both the FCR300 trial (Blood. 2016 127:303-9) and the CLL8 trial (Blood. 2016 127:208-15).
Another factor to consider is the greater cost of targeted agents. One analysis suggested the per-patient lifetime cost of CLL treatment in the United States will increase from $147,000 to $604,000 as targeted therapies overtake CIT as first-line treatment (J Clin Oncol. 2017 Jan 10;35[2]:166-174).
“Given all of the above, chemoimmunotherapy is going to remain part of the treatment repertoire for CLL,” Dr. Brown said. “It’s our only known potential cure for the fit, mutated patients ... and can also result in prolonged treatment-free intervals for patients who are older. As we manage CLL as a chronic disease over a lifetime, we need to continue to have this in our armamentarium.”
Specifically, Dr. Brown said CIT is appropriate for patients who don’t have del(17p) or mutated TP53. FCR should be given to young, fit patients with IGHV-mutated CLL, and FCR or BR should be given to older patients and young, fit patients with IGHV-unmutated CLL.
Dr. Brown and Dr. Wierda reported financial ties to multiple pharmaceutical companies, including makers of CLL treatments.
SAN FRANCISCO – Should targeted agents replace chemoimmunotherapy (CIT) as first-line treatment for chronic lymphocytic leukemia (CLL)? A recent debate suggests there’s no consensus.
William G. Wierda, MD, PhD, of The University of Texas MD Anderson Cancer Center in Houston, and Jennifer R. Brown, MD, PhD, of Dana-Farber Cancer Institute in Boston, debated the topic at the National Comprehensive Cancer Network Hematologic Malignancies Annual Congress.
Dr. Wierda argued that CLL patients should receive a BTK inhibitor or BCL2 inhibitor, with or without obinutuzumab, as first-line therapy because these targeted agents have been shown to provide better progression-free survival (PFS) than CIT, and the targeted therapies may prolong overall survival (OS) as well.
Dr. Brown countered that targeted agents don’t improve PFS for all CLL patients, improved PFS doesn’t always translate to improved OS, and targeted agents cost more than CIT.
No role for CIT as first-line treatment
“We have two approaches right now, with nonchemoimmunotherapy-based treatment,” Dr. Wierda said. “One approach, with small-molecule inhibitors, is to have a sustained and durable period of disease control, particularly with BTK inhibitors. The other strategy that has emerged is deep remissions with fixed-duration treatment with BCL2 small-molecule inhibitor-based therapy, which, I would argue, is better than being exposed to genotoxic chemoimmunotherapy.”
Dr. Wierda went on to explain that the BTK inhibitor ibrutinib has been shown to improve PFS, compared with CIT, in phase 3 trials.
In the iLLUMINATE trial, researchers compared ibrutinib plus obinutuzumab to chlorambucil plus obinutuzumab as first-line treatment in CLL. At a median follow-up of 31.3 months, the median PFS was not reached in the ibrutinib arm and was 19 months in the chlorambucil arm (P less than .0001; Lancet Oncol. 2019 Jan;20[1]:43-56).
In the A041202 study, researchers compared ibrutinib alone (Ib) or in combination with rituximab (Ib-R) to bendamustine plus rituximab (BR) in untreated, older patients with CLL. The 2-year PFS estimates were 74% in the BR arm, 87% in the Ib arm, and 88% in the Ib-R arm (P less than .001 for BR vs. Ib or Ib-R; N Engl J Med. 2018; 379:2517-28).
In the E1912 trial, researchers compared Ib-R to fludarabine, cyclophosphamide, and rituximab (FCR) in younger, untreated CLL patients. The 3-year PFS was 89.4% with Ib-R and 72.9% with FCR (P less than .001; N Engl J Med. 2019 Aug 1;381:432-43).
Dr. Wierda noted that the E1912 trial also showed superior OS with Ib-R. The 3-year OS rate was 98.8% with Ib-R and 91.5% with FCR (P less than .001). However, there was no significant difference in OS between the treatment arms in the A041202 trial or the iLLUMINATE trial.
“But I would argue that is, in part, because of short follow-up,” Dr. Wierda said. “The trials were all designed to look at progression-free survival, not overall survival. With longer follow-up, we may see differences in overall survival emerging.”
Dr. Wierda went on to say that fixed‐duration treatment with the BCL2 inhibitor venetoclax can improve PFS over CIT.
In the phase 3 CLL14 trial, researchers compared fixed-duration treatment with venetoclax plus obinutuzumab to chlorambucil plus obinutuzumab in previously untreated CLL patients with comorbidities. The estimated PFS at 2 years was 88.2% in the venetoclax group and 64.1% in the chlorambucil group (P less than .001; N Engl J Med. 2019; 380:2225-36).
“[There was] no difference in overall survival,” Dr. Wierda noted. “But, again, I would argue ... that follow-up is relatively limited. We may ultimately see a difference in overall survival.”
Based on these findings, Dr. Wierda made the following treatment recommendations:
- Any CLL patient with del(17p) or TP53 mutation, and older, unfit patients with unmutated IGHV should receive a BTK inhibitor, with or without obinutuzumab.
- All young, fit patients, and older, unfit patients with mutated IGHV should receive a BCL2 inhibitor plus obinutuzumab.
Dr. Wierda also noted that ibrutinib and venetoclax in combination have shown early promise for patients with previously untreated CLL (N Engl J Med. 2019; 380:2095-2103).
CIT still has a role as first-line treatment
Dr. Brown suggested that a PFS benefit may not be enough to recommend targeted agents over CIT. For one thing, the PFS benefit doesn’t apply to all patients, as the IGHV-mutated subgroup does equally well with CIT and targeted agents.
In the IGHV-mutated group from the E1912 trial, the 3-year PFS was 88% for patients who received Ib-R and those who received FCR (N Engl J Med. 2019 Aug 1;381:432-43). In the A041202 study, the 2-year PFS among IGHV-mutated patients was 87% in the BR arm, 86% in the Ib arm, and 88% in the Ib-R arm (N Engl J Med. 2018; 379:2517-28).
In the CLL14 trial, PFS rates were similar among IGHV-mutated patients who received chlorambucil plus obinutuzumab and IGHV-mutated or unmutated patients who received venetoclax and obinutuzumab (N Engl J Med. 2019; 380:2225-36).
Dr. Brown also noted that the overall improvement in PFS observed with ibrutinib and venetoclax doesn’t always translate to improved OS.
In the A041202 study, there was no significant difference in OS between the Ib, Ib-R, and BR arms (N Engl J Med. 2018; 379:2517-28). There was no significant difference in OS between the ibrutinib and chlorambucil arms in the iLLUMINATE trial (Lancet Oncol. 2019 Jan;20[1]:43-56). And there was no significant difference in OS between the venetoclax and chlorambucil arms in the CLL14 trial (N Engl J Med. 2019; 380:2225-36).
However, in the RESONATE-2 trial, ibrutinib provided an OS benefit over chlorambucil. The 2-year OS was 95% and 84%, respectively (P = .0145; Haematologica. Sept 2018;103:1502-10). Dr. Brown said the OS advantage in this study was due to the “very poor comparator of chlorambucil and very limited crossover.”
As Dr. Wierda mentioned, the OS rate was higher with Ib-R than with FCR in the E1912 trial. The 3-year OS rate was 98.8% and 91.5%, respectively (P less than .001; N Engl J Med. 2019 Aug 1;381:432-43). Dr. Brown noted, however, that there were few deaths in this study, and many of them “were not clearly related to the disease or its treatment.”
Dr. Brown also pointed out that FCR has been shown to have curative potential in IGHV-mutated CLL in both the FCR300 trial (Blood. 2016 127:303-9) and the CLL8 trial (Blood. 2016 127:208-15).
Another factor to consider is the greater cost of targeted agents. One analysis suggested the per-patient lifetime cost of CLL treatment in the United States will increase from $147,000 to $604,000 as targeted therapies overtake CIT as first-line treatment (J Clin Oncol. 2017 Jan 10;35[2]:166-174).
“Given all of the above, chemoimmunotherapy is going to remain part of the treatment repertoire for CLL,” Dr. Brown said. “It’s our only known potential cure for the fit, mutated patients ... and can also result in prolonged treatment-free intervals for patients who are older. As we manage CLL as a chronic disease over a lifetime, we need to continue to have this in our armamentarium.”
Specifically, Dr. Brown said CIT is appropriate for patients who don’t have del(17p) or mutated TP53. FCR should be given to young, fit patients with IGHV-mutated CLL, and FCR or BR should be given to older patients and young, fit patients with IGHV-unmutated CLL.
Dr. Brown and Dr. Wierda reported financial ties to multiple pharmaceutical companies, including makers of CLL treatments.
REPORTING FROM NCCN HEMATOLOGIC MALIGNANCIES