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The dermatologic tourist
I’m not much of a traveler. I like to see the world through the adventures of my patients.
This is especially nice in the winter, such as during school vacation week. Within the past 24 hours, I’ve gotten messages from patients in Hawaii, Arizona, and Orlando.
Writing from Hawaii, Melvin showed me a photo of a small white spot that appeared on the outer aspect of his arm. I couldn’t make much of it except to tell him that it doesn’t look like anything that warrants a 9-hour flight to show it to me, at least not until he gets back to town.
Finally, Svetlana forwarded a photograph of a rash on her foot that she said had “just come yesterday.” This was the nicest case of cutaneous larva migrans that I’ve seen in quite some time, although I am fairly sure it has been there for more than a day. I tried not to sound too excited about her diagnosis, of course (“You’ve got the coolest parasite!”), and just suggested that she come in to see me on her return next week.
North, South, West. I’ve been all over, without leaving the chair facing my computer screen. (Nobody seems to have gotten a volcanic eruption in Iceland this year.) All this with no packing, no waiting in airports, no TSA lines. Who says traveling can’t be a pleasure?
Practice dermatology – see the world!
* * * * * * * * * * * * * * * * * * * * * * *
Brian was delighted. The fungal infection on his calf, treated for weeks with a topical steroid that had produced only intolerable itch, was subsiding nicely with oral terbinafine and topical ketoconazole.
“Can I drink when I take this medicine?” he asked. “The Internet says I shouldn’t.”
“It’s only another week, Brian,” I said. “Best to hold off ‘till then.”
“Because I really needed a drink last week,” he said.
“Why was that?”
“I was on a vacation with my father.”
“I see.”
“It was my father and his 70-year-old girlfriend.”
“Oh.”
“We were at a nudist colony.”
“You know, Brian,” I said. “Just hearing about that makes me want a drink myself.”
Practice can take you places you never went, places you’ll never get to, places you never want to get to.
* * * * * * * * * * * * * * * * * * * * * * *
Although I have patients fill out the usual consent form on oral isotretinoin, on which they promise to contact me if they become depressed, I rarely find anyone who does. Instead, people tend to become rather happy once their acne improves.
Since I’m not a psychiatrist, I try to do an amateur job of assessing mood when patients come in for their monthly follow-up. I pass on my technique for any of you might find it useful.
“Hello, Peter, are you having any problems?”
“No.”
“Do you get headaches?”
“No.”
“Nosebleeds?”
“No.”
“Any aches and pains in your muscles?”
“No.”
“Are you depressed?”
“No.”
“Are you always this negative?”
If the patient smiles while saying, “No,” you’re in good shape. If not, consider suggesting a therapist.
Better still, send the patient to the Caribbean. Then propose that you go come along yourself as a consultant, just to keep an eye on things.
And bring sunscreen. For the two of you.
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 new book “Act Like a Doctor, Think Like a Patient” is now available at amazon.com and barnesandnoble.com. This is his second book. Write to him at [email protected].
I’m not much of a traveler. I like to see the world through the adventures of my patients.
This is especially nice in the winter, such as during school vacation week. Within the past 24 hours, I’ve gotten messages from patients in Hawaii, Arizona, and Orlando.
Writing from Hawaii, Melvin showed me a photo of a small white spot that appeared on the outer aspect of his arm. I couldn’t make much of it except to tell him that it doesn’t look like anything that warrants a 9-hour flight to show it to me, at least not until he gets back to town.
Finally, Svetlana forwarded a photograph of a rash on her foot that she said had “just come yesterday.” This was the nicest case of cutaneous larva migrans that I’ve seen in quite some time, although I am fairly sure it has been there for more than a day. I tried not to sound too excited about her diagnosis, of course (“You’ve got the coolest parasite!”), and just suggested that she come in to see me on her return next week.
North, South, West. I’ve been all over, without leaving the chair facing my computer screen. (Nobody seems to have gotten a volcanic eruption in Iceland this year.) All this with no packing, no waiting in airports, no TSA lines. Who says traveling can’t be a pleasure?
Practice dermatology – see the world!
* * * * * * * * * * * * * * * * * * * * * * *
Brian was delighted. The fungal infection on his calf, treated for weeks with a topical steroid that had produced only intolerable itch, was subsiding nicely with oral terbinafine and topical ketoconazole.
“Can I drink when I take this medicine?” he asked. “The Internet says I shouldn’t.”
“It’s only another week, Brian,” I said. “Best to hold off ‘till then.”
“Because I really needed a drink last week,” he said.
“Why was that?”
“I was on a vacation with my father.”
“I see.”
“It was my father and his 70-year-old girlfriend.”
“Oh.”
“We were at a nudist colony.”
“You know, Brian,” I said. “Just hearing about that makes me want a drink myself.”
Practice can take you places you never went, places you’ll never get to, places you never want to get to.
* * * * * * * * * * * * * * * * * * * * * * *
Although I have patients fill out the usual consent form on oral isotretinoin, on which they promise to contact me if they become depressed, I rarely find anyone who does. Instead, people tend to become rather happy once their acne improves.
Since I’m not a psychiatrist, I try to do an amateur job of assessing mood when patients come in for their monthly follow-up. I pass on my technique for any of you might find it useful.
“Hello, Peter, are you having any problems?”
“No.”
“Do you get headaches?”
“No.”
“Nosebleeds?”
“No.”
“Any aches and pains in your muscles?”
“No.”
“Are you depressed?”
“No.”
“Are you always this negative?”
If the patient smiles while saying, “No,” you’re in good shape. If not, consider suggesting a therapist.
Better still, send the patient to the Caribbean. Then propose that you go come along yourself as a consultant, just to keep an eye on things.
And bring sunscreen. For the two of you.
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 new book “Act Like a Doctor, Think Like a Patient” is now available at amazon.com and barnesandnoble.com. This is his second book. Write to him at [email protected].
I’m not much of a traveler. I like to see the world through the adventures of my patients.
This is especially nice in the winter, such as during school vacation week. Within the past 24 hours, I’ve gotten messages from patients in Hawaii, Arizona, and Orlando.
Writing from Hawaii, Melvin showed me a photo of a small white spot that appeared on the outer aspect of his arm. I couldn’t make much of it except to tell him that it doesn’t look like anything that warrants a 9-hour flight to show it to me, at least not until he gets back to town.
Finally, Svetlana forwarded a photograph of a rash on her foot that she said had “just come yesterday.” This was the nicest case of cutaneous larva migrans that I’ve seen in quite some time, although I am fairly sure it has been there for more than a day. I tried not to sound too excited about her diagnosis, of course (“You’ve got the coolest parasite!”), and just suggested that she come in to see me on her return next week.
North, South, West. I’ve been all over, without leaving the chair facing my computer screen. (Nobody seems to have gotten a volcanic eruption in Iceland this year.) All this with no packing, no waiting in airports, no TSA lines. Who says traveling can’t be a pleasure?
Practice dermatology – see the world!
* * * * * * * * * * * * * * * * * * * * * * *
Brian was delighted. The fungal infection on his calf, treated for weeks with a topical steroid that had produced only intolerable itch, was subsiding nicely with oral terbinafine and topical ketoconazole.
“Can I drink when I take this medicine?” he asked. “The Internet says I shouldn’t.”
“It’s only another week, Brian,” I said. “Best to hold off ‘till then.”
“Because I really needed a drink last week,” he said.
“Why was that?”
“I was on a vacation with my father.”
“I see.”
“It was my father and his 70-year-old girlfriend.”
“Oh.”
“We were at a nudist colony.”
“You know, Brian,” I said. “Just hearing about that makes me want a drink myself.”
Practice can take you places you never went, places you’ll never get to, places you never want to get to.
* * * * * * * * * * * * * * * * * * * * * * *
Although I have patients fill out the usual consent form on oral isotretinoin, on which they promise to contact me if they become depressed, I rarely find anyone who does. Instead, people tend to become rather happy once their acne improves.
Since I’m not a psychiatrist, I try to do an amateur job of assessing mood when patients come in for their monthly follow-up. I pass on my technique for any of you might find it useful.
“Hello, Peter, are you having any problems?”
“No.”
“Do you get headaches?”
“No.”
“Nosebleeds?”
“No.”
“Any aches and pains in your muscles?”
“No.”
“Are you depressed?”
“No.”
“Are you always this negative?”
If the patient smiles while saying, “No,” you’re in good shape. If not, consider suggesting a therapist.
Better still, send the patient to the Caribbean. Then propose that you go come along yourself as a consultant, just to keep an eye on things.
And bring sunscreen. For the two of you.
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 new book “Act Like a Doctor, Think Like a Patient” is now available at amazon.com and barnesandnoble.com. This is his second book. Write to him at [email protected].
Surveillance
A few weeks ago I received an email from a pediatrician thanking me for supporting her decision to quit work so that she could be home when her teenage son came home from school. She felt that by being home during her son’s adolescence, not only had she provided him a secure base but she also had helped protect him from a drug-dominated culture that permeated the community where they lived. While I hadn’t touched on it in my column, “Perfect Attendance” (Pediatric News, March 2017), this pediatrician’s experience highlights another benefit of a parental presence during those potentially stormy adolescent years.
In a recent article in the New York Times (“Teenagers Do Dumb Things, but There Are Ways to Limit Recklessness,” by Lisa Damour, March 8, 2017), Dr. Laurence Steinberg, a psychology professor at Temple University, is quoted as saying that “the context in which kids grow up must matter a great deal, and that recklessness isn’t the inevitable byproduct of the period’s biology.”
As writer Lisa Damour cogently states in her article, “For teenagers to find trouble, temptation must meet opportunity.”
Here in Brunswick, high school students finish their school day at 2:10 pm. If the student doesn’t play on a sports team and even if his or her home is at the end of the longest bus route, he or she is going to be home before 3 p.m. ... probably unsupervised. And stuff happens.
Although I may have been unsupervised, I was – or at least I believed that I was – always under constant surveillance. In the 1950s and 1960s, the population of Pleasantville, N.Y. was 5,000 and my mother had me convinced that she knew 4,000 of them. She recounted enough little things she had heard to make me believe that I was being watched by 8,000 eyes. She and the other mothers in town were masters of information sharing long before anyone had heard of networking.
These were not helicopter mothers hovering over every shady corner of our lives. They were simply concerned parents and fellow citizens going about their daily business who were not afraid to say something if they saw something. My mother’s apparent omniscience was a powerful deterrent to my adolescent recklessness. Only after I could afford to buy a car did I feel I could escape her surveillance network. And even then I wasn’t always sure.
The Internet has opened opportunities for mischief that are several orders of magnitude greater than the ones my friends and I sought to exploit in the 1950s and 1960s. However, parents today do have tools with which they can create a surveillance network to protect adolescents from their biologically predetermined urges. They simply need to have to courage to use them and not be afraid to say something if they see something.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
A few weeks ago I received an email from a pediatrician thanking me for supporting her decision to quit work so that she could be home when her teenage son came home from school. She felt that by being home during her son’s adolescence, not only had she provided him a secure base but she also had helped protect him from a drug-dominated culture that permeated the community where they lived. While I hadn’t touched on it in my column, “Perfect Attendance” (Pediatric News, March 2017), this pediatrician’s experience highlights another benefit of a parental presence during those potentially stormy adolescent years.
In a recent article in the New York Times (“Teenagers Do Dumb Things, but There Are Ways to Limit Recklessness,” by Lisa Damour, March 8, 2017), Dr. Laurence Steinberg, a psychology professor at Temple University, is quoted as saying that “the context in which kids grow up must matter a great deal, and that recklessness isn’t the inevitable byproduct of the period’s biology.”
As writer Lisa Damour cogently states in her article, “For teenagers to find trouble, temptation must meet opportunity.”
Here in Brunswick, high school students finish their school day at 2:10 pm. If the student doesn’t play on a sports team and even if his or her home is at the end of the longest bus route, he or she is going to be home before 3 p.m. ... probably unsupervised. And stuff happens.
Although I may have been unsupervised, I was – or at least I believed that I was – always under constant surveillance. In the 1950s and 1960s, the population of Pleasantville, N.Y. was 5,000 and my mother had me convinced that she knew 4,000 of them. She recounted enough little things she had heard to make me believe that I was being watched by 8,000 eyes. She and the other mothers in town were masters of information sharing long before anyone had heard of networking.
These were not helicopter mothers hovering over every shady corner of our lives. They were simply concerned parents and fellow citizens going about their daily business who were not afraid to say something if they saw something. My mother’s apparent omniscience was a powerful deterrent to my adolescent recklessness. Only after I could afford to buy a car did I feel I could escape her surveillance network. And even then I wasn’t always sure.
The Internet has opened opportunities for mischief that are several orders of magnitude greater than the ones my friends and I sought to exploit in the 1950s and 1960s. However, parents today do have tools with which they can create a surveillance network to protect adolescents from their biologically predetermined urges. They simply need to have to courage to use them and not be afraid to say something if they see something.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
A few weeks ago I received an email from a pediatrician thanking me for supporting her decision to quit work so that she could be home when her teenage son came home from school. She felt that by being home during her son’s adolescence, not only had she provided him a secure base but she also had helped protect him from a drug-dominated culture that permeated the community where they lived. While I hadn’t touched on it in my column, “Perfect Attendance” (Pediatric News, March 2017), this pediatrician’s experience highlights another benefit of a parental presence during those potentially stormy adolescent years.
In a recent article in the New York Times (“Teenagers Do Dumb Things, but There Are Ways to Limit Recklessness,” by Lisa Damour, March 8, 2017), Dr. Laurence Steinberg, a psychology professor at Temple University, is quoted as saying that “the context in which kids grow up must matter a great deal, and that recklessness isn’t the inevitable byproduct of the period’s biology.”
As writer Lisa Damour cogently states in her article, “For teenagers to find trouble, temptation must meet opportunity.”
Here in Brunswick, high school students finish their school day at 2:10 pm. If the student doesn’t play on a sports team and even if his or her home is at the end of the longest bus route, he or she is going to be home before 3 p.m. ... probably unsupervised. And stuff happens.
Although I may have been unsupervised, I was – or at least I believed that I was – always under constant surveillance. In the 1950s and 1960s, the population of Pleasantville, N.Y. was 5,000 and my mother had me convinced that she knew 4,000 of them. She recounted enough little things she had heard to make me believe that I was being watched by 8,000 eyes. She and the other mothers in town were masters of information sharing long before anyone had heard of networking.
These were not helicopter mothers hovering over every shady corner of our lives. They were simply concerned parents and fellow citizens going about their daily business who were not afraid to say something if they saw something. My mother’s apparent omniscience was a powerful deterrent to my adolescent recklessness. Only after I could afford to buy a car did I feel I could escape her surveillance network. And even then I wasn’t always sure.
The Internet has opened opportunities for mischief that are several orders of magnitude greater than the ones my friends and I sought to exploit in the 1950s and 1960s. However, parents today do have tools with which they can create a surveillance network to protect adolescents from their biologically predetermined urges. They simply need to have to courage to use them and not be afraid to say something if they see something.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
On vacation, my patients go with me
I’m in the process of planning our family vacations for the summer. I do something different from most when on the road: I take my patients with me.
Well, obviously not physically, but I do cover everything, no matter where I am.
Yes, it takes time. In a ritual my family is used to, two to three times a day I’ll call my staff and go over a list of calls that came in, refills needed, and test results. We go back and forth for a bit. For more complicated questions, I may have to wait until I have my laptop, with the charts on it. If there’s an emergency they’ll call me, and if I can’t be reached, they’ll dial up my call partners.
• I know my patients. I think we all feel that way. I’m more comfortable, and I hope they are too, with the doc who knows them making the decisions.
• My call partners don’t know them. We’re all in solo practice. They don’t have access to my charts any more than I do to theirs. That’s an okay arrangement for a weekend call, but not 2 weeks.
• No surprises. I know that I’m not going to be coming home to a pile of MRI and lab reports that I need to review and act on. If my patient was in the ER or admitted, I spoke to the physician handling it.
A long time ago, when I first started out, I asked another neurologist in my building to cover for me when I was leaving town. I didn’t know him very well, but I was still learning the ropes. He said fine.
When I came home, I found he’d actually “poached” several who’d called, having them come in and convincing them to switch doctors. He’d also changed medications on well-controlled epilepsy and migraine patients who’d needed refills, leaving me to deal with the complications of it when I returned.
Granted, I’ve since learned that he was unusual in that degree, but it really rattled me. I decided I’d rather handle things on my own from then on.
This isn’t an easy decision, but I’m glad I do it. I come home to an office with no surprises, no test results piled up to review, no medication changes that I look at and wonder about.
Does it ruin my vacation? Not at all. Yes, it’s 30-60 minutes out of each day that I have to spend with my office, but I think it’s worth it. It’s peace of mind for me, my staff, and my patients, at least as much as you can ever have in this field.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
[polldaddy:9696724]
I’m in the process of planning our family vacations for the summer. I do something different from most when on the road: I take my patients with me.
Well, obviously not physically, but I do cover everything, no matter where I am.
Yes, it takes time. In a ritual my family is used to, two to three times a day I’ll call my staff and go over a list of calls that came in, refills needed, and test results. We go back and forth for a bit. For more complicated questions, I may have to wait until I have my laptop, with the charts on it. If there’s an emergency they’ll call me, and if I can’t be reached, they’ll dial up my call partners.
• I know my patients. I think we all feel that way. I’m more comfortable, and I hope they are too, with the doc who knows them making the decisions.
• My call partners don’t know them. We’re all in solo practice. They don’t have access to my charts any more than I do to theirs. That’s an okay arrangement for a weekend call, but not 2 weeks.
• No surprises. I know that I’m not going to be coming home to a pile of MRI and lab reports that I need to review and act on. If my patient was in the ER or admitted, I spoke to the physician handling it.
A long time ago, when I first started out, I asked another neurologist in my building to cover for me when I was leaving town. I didn’t know him very well, but I was still learning the ropes. He said fine.
When I came home, I found he’d actually “poached” several who’d called, having them come in and convincing them to switch doctors. He’d also changed medications on well-controlled epilepsy and migraine patients who’d needed refills, leaving me to deal with the complications of it when I returned.
Granted, I’ve since learned that he was unusual in that degree, but it really rattled me. I decided I’d rather handle things on my own from then on.
This isn’t an easy decision, but I’m glad I do it. I come home to an office with no surprises, no test results piled up to review, no medication changes that I look at and wonder about.
Does it ruin my vacation? Not at all. Yes, it’s 30-60 minutes out of each day that I have to spend with my office, but I think it’s worth it. It’s peace of mind for me, my staff, and my patients, at least as much as you can ever have in this field.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
[polldaddy:9696724]
I’m in the process of planning our family vacations for the summer. I do something different from most when on the road: I take my patients with me.
Well, obviously not physically, but I do cover everything, no matter where I am.
Yes, it takes time. In a ritual my family is used to, two to three times a day I’ll call my staff and go over a list of calls that came in, refills needed, and test results. We go back and forth for a bit. For more complicated questions, I may have to wait until I have my laptop, with the charts on it. If there’s an emergency they’ll call me, and if I can’t be reached, they’ll dial up my call partners.
• I know my patients. I think we all feel that way. I’m more comfortable, and I hope they are too, with the doc who knows them making the decisions.
• My call partners don’t know them. We’re all in solo practice. They don’t have access to my charts any more than I do to theirs. That’s an okay arrangement for a weekend call, but not 2 weeks.
• No surprises. I know that I’m not going to be coming home to a pile of MRI and lab reports that I need to review and act on. If my patient was in the ER or admitted, I spoke to the physician handling it.
A long time ago, when I first started out, I asked another neurologist in my building to cover for me when I was leaving town. I didn’t know him very well, but I was still learning the ropes. He said fine.
When I came home, I found he’d actually “poached” several who’d called, having them come in and convincing them to switch doctors. He’d also changed medications on well-controlled epilepsy and migraine patients who’d needed refills, leaving me to deal with the complications of it when I returned.
Granted, I’ve since learned that he was unusual in that degree, but it really rattled me. I decided I’d rather handle things on my own from then on.
This isn’t an easy decision, but I’m glad I do it. I come home to an office with no surprises, no test results piled up to review, no medication changes that I look at and wonder about.
Does it ruin my vacation? Not at all. Yes, it’s 30-60 minutes out of each day that I have to spend with my office, but I think it’s worth it. It’s peace of mind for me, my staff, and my patients, at least as much as you can ever have in this field.
Dr. Block has a solo neurology practice in Scottsdale, Ariz.
[polldaddy:9696724]
Ursolic acid
Ursolic acid (3beta-hydroxy-urs-12-en-28-oic acid) is a pentacyclic triterpenoid found naturally in apples, waxy berries, rosemary, oregano, and several other plants and herbs used in medicine and the diet.1,2 It is known to have significant antioxidant, anti-inflammatory, and antiproliferative properties, and has also been associated with a wider range of biologic activities, including anticancer, antimicrobial, antitumor, antiwrinkle, anti-HIV, cytotoxic, and hepatoprotective.3,4 In addition, ursolic acid is the focus of human clinical trials for potential uses in cancer and skin wrinkles.4 While this triterpenoid is known to suppress tumor formation and viability in various kinds of cancer, including skin cancer, several forms of cancer are resistant to ursolic acid.
Anti-inflammatory activity
In a 2013 study of the antibacterial and anti-inflammatory effects of Syzygium jambos on acne, Sharma et al. found that ursolic acid was one of the constituents of the leaf extracts that contributed to a significant suppression of the release of inflammatory cytokines interleukin (IL)-8 and tumor necrosis factor-alpha.5
In 2010, Yang et al. identified ursolic acid as a key constituent of Acanthopanax koreanum fruit, a popular fruit in Jeju Island, South Korea, extracts of which they found to exhibit significant anti-inflammatory activity and suitability as a topical agent.6
Yasukawa et al. conducted an in vivo two-stage carcinogenesis test in mice in 2009 in which extracts of the branches of Hippophae rhamnoides displayed significant antitumor activity after initiation with 7,12-dimethylbenz[a]anthracene (DMBA) and promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA). Ursolic acid and (-)-epigallocatechin were the constituents found to have the greatest inhibitory effects on TPA-induced inflammation.7
A 2002 study by Chattopadhyay et al. revealed that the ursolic acid present in Mallotus peltatus extract (long used in traditional folk medicine to treat skin infections and intestinal disorders) may partially account for the broad anti-inflammatory and antimicrobial activity of the plant.9
In 1997, Máñez et al. noted that ursolic acid was among two of the four selected natural triterpenoids tested and found to be significantly effective against inflammation in a TPA multiple-dose model of chronic skin inflammation.10
Anticancer activity
In 2015, Cho et al. reported on the inhibitory effects on skin tumor promotion from the topical application of ursolic acid, resveratrol, or the combination of the two prior to TPA treatment on mouse skin. The combination of the two botanical agents yielded the strongest suppression of TPA-induced epidermal hyperproliferation, skin inflammation, inflammatory gene expression, and skin tumor promotion.11
In another study that year buttressing the combination of the two botanical agents, Junco et al. demonstrated that chloroquine could be used to sensitize B16F10 metastatic mouse melanoma to the anticancer activities of ursolic acid and resveratrol. The investigators concluded that the combination of ursolic acid or resveratrol with chloroquine has potential for inclusion in melanoma treatment in humans.12 Previously, Junco et al. observed that the anti–skin cancer effects of ursolic acid are augmented by P-glycoprotein inhibitors, and that ursolic acid and the stilbene resveratrol, a potent antioxidant, work synergistically, although not by blocking P-glycoprotein. The investigators suggested that ursolic acid along with resveratrol and/or P-glycoprotein inhibitors have potential as effective anti–skin cancer regimens.
In 2014, Lee et al. showed that ursolic acid can differentially modulate apoptosis in cutaneous melanoma and retinal pigment epithelial cells exposed to ultraviolet to visible broadband radiation, exhibiting the potential to protect normal cells while sensitizing melanoma cells to the effects of UV radiation.13 These findings supported earlier work by the team showing that pretreatment of human cells derived from a malignant skin melanoma markedly enhanced the sensitivity of melanoma cells to UV radiation, while providing some photoprotection to retinal pigment epithelium.
Also that year, Soica et al. demonstrated, using in vitro tests and in vivo skin cancer models, that the mixture of oleanolic and ursolic acids and in complex with cyclodextrin rendered a synergistic antitumor activity.14
A year earlier, Kowalczyk et al. showed that the combined action of phytochemicals – dietary calcium D-glucarate and topical ursolic acid and resveratrol – was effective in suppressing the initiation (with 7,12-dimethylbenz[a]anthracene [DMBA]) and promotion (with TPA) of skin tumorigenesis in SENCAR mice. Ursolic acid alone or in combination with calcium D-glucarate significantly diminished epidermal hyperplasia when applied during promotion. All of the antipromotion protocols led to significant decreases in cyclooxygenase-2 and interleukin (IL)-6 expression. The researchers concluded that ursolic acid strongly inhibits skin tumor promotion and inflammatory signaling, and warrants attention as a potential preventive agent against skin and other epithelial cancers.15 Kowalczyk et al. had previously found that ursolic acid and other phytochemicals displayed significant in vitro and in vivo antioxidant and antitumorigenic activity, inhibiting murine skin carcinogenesis by blunting tumor initiation and tumor promotion/progression.16
In 2006, beta-ursolic acid isolated from Salvia officinalis was found by Jedinák et al. to be effective in suppressing lung colonization of beta16 mouse melanoma cells in vivo.17
Huang et al. showed in 1994 that extracts of the leaves of Rosmarinus officinalis (rosemary) were effective in suppressing tumor initiation and promotion in a two-stage skin tumorigenesis mouse model. Topically applied ursolic acid isolated from the leaves was found to hinder TPA-induced ear inflammation, ornithine decarboxylase activity, and tumor promotion. The number of tumors per mouse also declined significantly due to the topical application of ursolic acid concurrent with twice weekly application of the tumor-promoter TPA in DMBA-initiated mice.18
Antiaging and other activities
In 2015, Herndon et al. conducted an open-label clinical trial in 37 females (aged 35-60 years) to ascertain the effectiveness of an anti-aging moisturizer containing Astragalus membranaceus root extract, a peptide blend including palmitoyl tripeptide-38, standardized rosemary leaf extract (ursolic acid), tetrahexyldecyl ascorbate (THD ascorbate), and ubiquinone (coenzyme Q10). Subjects were instructed to apply the moisturizer once in the morning and once in the evening, and were assessed at baseline, and after 4, 8, and 12 weeks of twice daily application. Clinical evaluations after 8 weeks revealed a statistically significant improvement in all grading parameters (fine lines and wrinkles, clarity/brightness, visual roughness, tactile roughness, redness, hyperpigmentation, and overall appearance), with even more pronounced improvement at 12 weeks. The product was found to be mild and well tolerated, and digital photography reinforced clinical assessments and self-evaluations.19
Lee et al. reported in 2012 on in vitro results suggesting that ursolic acid was effective as an inhibitor of matrix metalloproteinase (MMP)-1 after UVB exposure and was more effective than retinoic acid.20
Based on studies with hairless mice, Lim et al. found in 2007 that ursolic and oleanolic acids can enhance the recovery of skin barrier function and, via peroxisome proliferator-activated receptor-alpha, spur epidermal keratinocyte differentiation. They concluded that both acids have potential for use as agents to promote epidermal permeability barrier function.21
In 2003, Soo et al. observed that pretreatment with ursolic acid inhibited UVA-induced oxidative stress and activation and expression of MMP-2 in HaCaT human keratinocytes. They concluded that ursolic acid may merit attention for the prevention of UVA-induced photoaging.22
Three years earlier, Yarosh et al. showed that liposomes containing ursolic acid augmented ceramide content in cultured normal human epidermal keratinocytes and collagen content in cultured normal human dermal fibroblasts. Over an 11-day period, clinical tests with the ursolic acid–containing liposome (Merotaine) revealed increases in the ceramide content in human skin.23 Two years later, many of the same researchers duplicated their results. This new study also demonstrated that ursolic acid liposomes raise ceramide levels in normal human epidermal keratinocytes, in contrast to the effects of retinoic acid, earlier shown to reduce such levels. They concluded that ursolic acid liposomes show promise for use alone or in combination to replenish or maintain cutaneous ceramide and collagen levels.24 Notably, ursolic acid is incorporated into topical oils and creams intended to confer rejuvenating effects to the skin.
Conclusion
Ursolic acid is a compelling ingredient. I especially will be interested in the results of ongoing human clinical trials of this triterpenoid for treating cancer and skin wrinkles. As it is, ursolic acid is known to exert significant inhibitory activity against tumor formation and tumor cell viability in the laboratory. Given its wide range of biologic activity, and some promising cutaneous results, there is reason to believe that ursolic acid has the potential to play an increasingly useful role in topical skin care agents and dermatologic practice.
References
1. J Dermatol. 2007 Sep;34(9):625-34.
2. Folia Histochem Cytobiol. 2011;49(4):664-9.
3. J Cosmet Dermatol. 2004 Jan;3(1):26-34.
4. J Enzyme Inhib Med Chem. 2011 Oct;26(5):616-42.
5. BMC Complement Altern Med. 2013 Oct 29;13:292.
6. J Biomed Biotechnol. 2010;2010:715739.
7. Fitoterapia. 2009 Apr;80(3):164-7.
8. Biosci Biotechnol Biochem. 2004 Jan;68(1):85-90.
9. J Ethnopharmacol. 2002 Oct;82(2-3):229-37.
10. Eur J Pharmacol. 1997 Sep 3;334(1):103-5.
11. Cancer Prev Res (Phila). 2015 Sep;8(9):817-25.
12. Melanoma Res. 2015 Apr;25(2):103-12.
13. Apoptosis. 2014 May;19(5):816-28.
14. Molecules. 2014 Apr 17;19(4):4924-40.
15. Int J Oncol. 2013 Sep;43(3):911-8.
16. Carcinogenesis. 2009 Jun;30(6):1008-15.
17. Z Naturforsch C. 2006 Nov-Dec;61(11-12):777-82.
18. Cancer Res. 1994 Feb 1;54(3):701-8.
19. J Drugs Dermatol. 2015 Jul;14(7):699-704.
20. Bioorg Khim. 2012 May-Jun;38(3):374-81.
21. J Dermatol. 2007;34(9):625-34.
22. Eur J Pharmacol. 2003 Aug 29;476(3):173-8.
23. Horm Res. 2000;54(5-6):318-21.
24. Arch Dermatol Res. 2002 Jan;293(11):569-75.
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever. Dr. Baumann also developed and owns the Baumann Skin Type Solution skin typing systems and related products.
Ursolic acid (3beta-hydroxy-urs-12-en-28-oic acid) is a pentacyclic triterpenoid found naturally in apples, waxy berries, rosemary, oregano, and several other plants and herbs used in medicine and the diet.1,2 It is known to have significant antioxidant, anti-inflammatory, and antiproliferative properties, and has also been associated with a wider range of biologic activities, including anticancer, antimicrobial, antitumor, antiwrinkle, anti-HIV, cytotoxic, and hepatoprotective.3,4 In addition, ursolic acid is the focus of human clinical trials for potential uses in cancer and skin wrinkles.4 While this triterpenoid is known to suppress tumor formation and viability in various kinds of cancer, including skin cancer, several forms of cancer are resistant to ursolic acid.
Anti-inflammatory activity
In a 2013 study of the antibacterial and anti-inflammatory effects of Syzygium jambos on acne, Sharma et al. found that ursolic acid was one of the constituents of the leaf extracts that contributed to a significant suppression of the release of inflammatory cytokines interleukin (IL)-8 and tumor necrosis factor-alpha.5
In 2010, Yang et al. identified ursolic acid as a key constituent of Acanthopanax koreanum fruit, a popular fruit in Jeju Island, South Korea, extracts of which they found to exhibit significant anti-inflammatory activity and suitability as a topical agent.6
Yasukawa et al. conducted an in vivo two-stage carcinogenesis test in mice in 2009 in which extracts of the branches of Hippophae rhamnoides displayed significant antitumor activity after initiation with 7,12-dimethylbenz[a]anthracene (DMBA) and promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA). Ursolic acid and (-)-epigallocatechin were the constituents found to have the greatest inhibitory effects on TPA-induced inflammation.7
A 2002 study by Chattopadhyay et al. revealed that the ursolic acid present in Mallotus peltatus extract (long used in traditional folk medicine to treat skin infections and intestinal disorders) may partially account for the broad anti-inflammatory and antimicrobial activity of the plant.9
In 1997, Máñez et al. noted that ursolic acid was among two of the four selected natural triterpenoids tested and found to be significantly effective against inflammation in a TPA multiple-dose model of chronic skin inflammation.10
Anticancer activity
In 2015, Cho et al. reported on the inhibitory effects on skin tumor promotion from the topical application of ursolic acid, resveratrol, or the combination of the two prior to TPA treatment on mouse skin. The combination of the two botanical agents yielded the strongest suppression of TPA-induced epidermal hyperproliferation, skin inflammation, inflammatory gene expression, and skin tumor promotion.11
In another study that year buttressing the combination of the two botanical agents, Junco et al. demonstrated that chloroquine could be used to sensitize B16F10 metastatic mouse melanoma to the anticancer activities of ursolic acid and resveratrol. The investigators concluded that the combination of ursolic acid or resveratrol with chloroquine has potential for inclusion in melanoma treatment in humans.12 Previously, Junco et al. observed that the anti–skin cancer effects of ursolic acid are augmented by P-glycoprotein inhibitors, and that ursolic acid and the stilbene resveratrol, a potent antioxidant, work synergistically, although not by blocking P-glycoprotein. The investigators suggested that ursolic acid along with resveratrol and/or P-glycoprotein inhibitors have potential as effective anti–skin cancer regimens.
In 2014, Lee et al. showed that ursolic acid can differentially modulate apoptosis in cutaneous melanoma and retinal pigment epithelial cells exposed to ultraviolet to visible broadband radiation, exhibiting the potential to protect normal cells while sensitizing melanoma cells to the effects of UV radiation.13 These findings supported earlier work by the team showing that pretreatment of human cells derived from a malignant skin melanoma markedly enhanced the sensitivity of melanoma cells to UV radiation, while providing some photoprotection to retinal pigment epithelium.
Also that year, Soica et al. demonstrated, using in vitro tests and in vivo skin cancer models, that the mixture of oleanolic and ursolic acids and in complex with cyclodextrin rendered a synergistic antitumor activity.14
A year earlier, Kowalczyk et al. showed that the combined action of phytochemicals – dietary calcium D-glucarate and topical ursolic acid and resveratrol – was effective in suppressing the initiation (with 7,12-dimethylbenz[a]anthracene [DMBA]) and promotion (with TPA) of skin tumorigenesis in SENCAR mice. Ursolic acid alone or in combination with calcium D-glucarate significantly diminished epidermal hyperplasia when applied during promotion. All of the antipromotion protocols led to significant decreases in cyclooxygenase-2 and interleukin (IL)-6 expression. The researchers concluded that ursolic acid strongly inhibits skin tumor promotion and inflammatory signaling, and warrants attention as a potential preventive agent against skin and other epithelial cancers.15 Kowalczyk et al. had previously found that ursolic acid and other phytochemicals displayed significant in vitro and in vivo antioxidant and antitumorigenic activity, inhibiting murine skin carcinogenesis by blunting tumor initiation and tumor promotion/progression.16
In 2006, beta-ursolic acid isolated from Salvia officinalis was found by Jedinák et al. to be effective in suppressing lung colonization of beta16 mouse melanoma cells in vivo.17
Huang et al. showed in 1994 that extracts of the leaves of Rosmarinus officinalis (rosemary) were effective in suppressing tumor initiation and promotion in a two-stage skin tumorigenesis mouse model. Topically applied ursolic acid isolated from the leaves was found to hinder TPA-induced ear inflammation, ornithine decarboxylase activity, and tumor promotion. The number of tumors per mouse also declined significantly due to the topical application of ursolic acid concurrent with twice weekly application of the tumor-promoter TPA in DMBA-initiated mice.18
Antiaging and other activities
In 2015, Herndon et al. conducted an open-label clinical trial in 37 females (aged 35-60 years) to ascertain the effectiveness of an anti-aging moisturizer containing Astragalus membranaceus root extract, a peptide blend including palmitoyl tripeptide-38, standardized rosemary leaf extract (ursolic acid), tetrahexyldecyl ascorbate (THD ascorbate), and ubiquinone (coenzyme Q10). Subjects were instructed to apply the moisturizer once in the morning and once in the evening, and were assessed at baseline, and after 4, 8, and 12 weeks of twice daily application. Clinical evaluations after 8 weeks revealed a statistically significant improvement in all grading parameters (fine lines and wrinkles, clarity/brightness, visual roughness, tactile roughness, redness, hyperpigmentation, and overall appearance), with even more pronounced improvement at 12 weeks. The product was found to be mild and well tolerated, and digital photography reinforced clinical assessments and self-evaluations.19
Lee et al. reported in 2012 on in vitro results suggesting that ursolic acid was effective as an inhibitor of matrix metalloproteinase (MMP)-1 after UVB exposure and was more effective than retinoic acid.20
Based on studies with hairless mice, Lim et al. found in 2007 that ursolic and oleanolic acids can enhance the recovery of skin barrier function and, via peroxisome proliferator-activated receptor-alpha, spur epidermal keratinocyte differentiation. They concluded that both acids have potential for use as agents to promote epidermal permeability barrier function.21
In 2003, Soo et al. observed that pretreatment with ursolic acid inhibited UVA-induced oxidative stress and activation and expression of MMP-2 in HaCaT human keratinocytes. They concluded that ursolic acid may merit attention for the prevention of UVA-induced photoaging.22
Three years earlier, Yarosh et al. showed that liposomes containing ursolic acid augmented ceramide content in cultured normal human epidermal keratinocytes and collagen content in cultured normal human dermal fibroblasts. Over an 11-day period, clinical tests with the ursolic acid–containing liposome (Merotaine) revealed increases in the ceramide content in human skin.23 Two years later, many of the same researchers duplicated their results. This new study also demonstrated that ursolic acid liposomes raise ceramide levels in normal human epidermal keratinocytes, in contrast to the effects of retinoic acid, earlier shown to reduce such levels. They concluded that ursolic acid liposomes show promise for use alone or in combination to replenish or maintain cutaneous ceramide and collagen levels.24 Notably, ursolic acid is incorporated into topical oils and creams intended to confer rejuvenating effects to the skin.
Conclusion
Ursolic acid is a compelling ingredient. I especially will be interested in the results of ongoing human clinical trials of this triterpenoid for treating cancer and skin wrinkles. As it is, ursolic acid is known to exert significant inhibitory activity against tumor formation and tumor cell viability in the laboratory. Given its wide range of biologic activity, and some promising cutaneous results, there is reason to believe that ursolic acid has the potential to play an increasingly useful role in topical skin care agents and dermatologic practice.
References
1. J Dermatol. 2007 Sep;34(9):625-34.
2. Folia Histochem Cytobiol. 2011;49(4):664-9.
3. J Cosmet Dermatol. 2004 Jan;3(1):26-34.
4. J Enzyme Inhib Med Chem. 2011 Oct;26(5):616-42.
5. BMC Complement Altern Med. 2013 Oct 29;13:292.
6. J Biomed Biotechnol. 2010;2010:715739.
7. Fitoterapia. 2009 Apr;80(3):164-7.
8. Biosci Biotechnol Biochem. 2004 Jan;68(1):85-90.
9. J Ethnopharmacol. 2002 Oct;82(2-3):229-37.
10. Eur J Pharmacol. 1997 Sep 3;334(1):103-5.
11. Cancer Prev Res (Phila). 2015 Sep;8(9):817-25.
12. Melanoma Res. 2015 Apr;25(2):103-12.
13. Apoptosis. 2014 May;19(5):816-28.
14. Molecules. 2014 Apr 17;19(4):4924-40.
15. Int J Oncol. 2013 Sep;43(3):911-8.
16. Carcinogenesis. 2009 Jun;30(6):1008-15.
17. Z Naturforsch C. 2006 Nov-Dec;61(11-12):777-82.
18. Cancer Res. 1994 Feb 1;54(3):701-8.
19. J Drugs Dermatol. 2015 Jul;14(7):699-704.
20. Bioorg Khim. 2012 May-Jun;38(3):374-81.
21. J Dermatol. 2007;34(9):625-34.
22. Eur J Pharmacol. 2003 Aug 29;476(3):173-8.
23. Horm Res. 2000;54(5-6):318-21.
24. Arch Dermatol Res. 2002 Jan;293(11):569-75.
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever. Dr. Baumann also developed and owns the Baumann Skin Type Solution skin typing systems and related products.
Ursolic acid (3beta-hydroxy-urs-12-en-28-oic acid) is a pentacyclic triterpenoid found naturally in apples, waxy berries, rosemary, oregano, and several other plants and herbs used in medicine and the diet.1,2 It is known to have significant antioxidant, anti-inflammatory, and antiproliferative properties, and has also been associated with a wider range of biologic activities, including anticancer, antimicrobial, antitumor, antiwrinkle, anti-HIV, cytotoxic, and hepatoprotective.3,4 In addition, ursolic acid is the focus of human clinical trials for potential uses in cancer and skin wrinkles.4 While this triterpenoid is known to suppress tumor formation and viability in various kinds of cancer, including skin cancer, several forms of cancer are resistant to ursolic acid.
Anti-inflammatory activity
In a 2013 study of the antibacterial and anti-inflammatory effects of Syzygium jambos on acne, Sharma et al. found that ursolic acid was one of the constituents of the leaf extracts that contributed to a significant suppression of the release of inflammatory cytokines interleukin (IL)-8 and tumor necrosis factor-alpha.5
In 2010, Yang et al. identified ursolic acid as a key constituent of Acanthopanax koreanum fruit, a popular fruit in Jeju Island, South Korea, extracts of which they found to exhibit significant anti-inflammatory activity and suitability as a topical agent.6
Yasukawa et al. conducted an in vivo two-stage carcinogenesis test in mice in 2009 in which extracts of the branches of Hippophae rhamnoides displayed significant antitumor activity after initiation with 7,12-dimethylbenz[a]anthracene (DMBA) and promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA). Ursolic acid and (-)-epigallocatechin were the constituents found to have the greatest inhibitory effects on TPA-induced inflammation.7
A 2002 study by Chattopadhyay et al. revealed that the ursolic acid present in Mallotus peltatus extract (long used in traditional folk medicine to treat skin infections and intestinal disorders) may partially account for the broad anti-inflammatory and antimicrobial activity of the plant.9
In 1997, Máñez et al. noted that ursolic acid was among two of the four selected natural triterpenoids tested and found to be significantly effective against inflammation in a TPA multiple-dose model of chronic skin inflammation.10
Anticancer activity
In 2015, Cho et al. reported on the inhibitory effects on skin tumor promotion from the topical application of ursolic acid, resveratrol, or the combination of the two prior to TPA treatment on mouse skin. The combination of the two botanical agents yielded the strongest suppression of TPA-induced epidermal hyperproliferation, skin inflammation, inflammatory gene expression, and skin tumor promotion.11
In another study that year buttressing the combination of the two botanical agents, Junco et al. demonstrated that chloroquine could be used to sensitize B16F10 metastatic mouse melanoma to the anticancer activities of ursolic acid and resveratrol. The investigators concluded that the combination of ursolic acid or resveratrol with chloroquine has potential for inclusion in melanoma treatment in humans.12 Previously, Junco et al. observed that the anti–skin cancer effects of ursolic acid are augmented by P-glycoprotein inhibitors, and that ursolic acid and the stilbene resveratrol, a potent antioxidant, work synergistically, although not by blocking P-glycoprotein. The investigators suggested that ursolic acid along with resveratrol and/or P-glycoprotein inhibitors have potential as effective anti–skin cancer regimens.
In 2014, Lee et al. showed that ursolic acid can differentially modulate apoptosis in cutaneous melanoma and retinal pigment epithelial cells exposed to ultraviolet to visible broadband radiation, exhibiting the potential to protect normal cells while sensitizing melanoma cells to the effects of UV radiation.13 These findings supported earlier work by the team showing that pretreatment of human cells derived from a malignant skin melanoma markedly enhanced the sensitivity of melanoma cells to UV radiation, while providing some photoprotection to retinal pigment epithelium.
Also that year, Soica et al. demonstrated, using in vitro tests and in vivo skin cancer models, that the mixture of oleanolic and ursolic acids and in complex with cyclodextrin rendered a synergistic antitumor activity.14
A year earlier, Kowalczyk et al. showed that the combined action of phytochemicals – dietary calcium D-glucarate and topical ursolic acid and resveratrol – was effective in suppressing the initiation (with 7,12-dimethylbenz[a]anthracene [DMBA]) and promotion (with TPA) of skin tumorigenesis in SENCAR mice. Ursolic acid alone or in combination with calcium D-glucarate significantly diminished epidermal hyperplasia when applied during promotion. All of the antipromotion protocols led to significant decreases in cyclooxygenase-2 and interleukin (IL)-6 expression. The researchers concluded that ursolic acid strongly inhibits skin tumor promotion and inflammatory signaling, and warrants attention as a potential preventive agent against skin and other epithelial cancers.15 Kowalczyk et al. had previously found that ursolic acid and other phytochemicals displayed significant in vitro and in vivo antioxidant and antitumorigenic activity, inhibiting murine skin carcinogenesis by blunting tumor initiation and tumor promotion/progression.16
In 2006, beta-ursolic acid isolated from Salvia officinalis was found by Jedinák et al. to be effective in suppressing lung colonization of beta16 mouse melanoma cells in vivo.17
Huang et al. showed in 1994 that extracts of the leaves of Rosmarinus officinalis (rosemary) were effective in suppressing tumor initiation and promotion in a two-stage skin tumorigenesis mouse model. Topically applied ursolic acid isolated from the leaves was found to hinder TPA-induced ear inflammation, ornithine decarboxylase activity, and tumor promotion. The number of tumors per mouse also declined significantly due to the topical application of ursolic acid concurrent with twice weekly application of the tumor-promoter TPA in DMBA-initiated mice.18
Antiaging and other activities
In 2015, Herndon et al. conducted an open-label clinical trial in 37 females (aged 35-60 years) to ascertain the effectiveness of an anti-aging moisturizer containing Astragalus membranaceus root extract, a peptide blend including palmitoyl tripeptide-38, standardized rosemary leaf extract (ursolic acid), tetrahexyldecyl ascorbate (THD ascorbate), and ubiquinone (coenzyme Q10). Subjects were instructed to apply the moisturizer once in the morning and once in the evening, and were assessed at baseline, and after 4, 8, and 12 weeks of twice daily application. Clinical evaluations after 8 weeks revealed a statistically significant improvement in all grading parameters (fine lines and wrinkles, clarity/brightness, visual roughness, tactile roughness, redness, hyperpigmentation, and overall appearance), with even more pronounced improvement at 12 weeks. The product was found to be mild and well tolerated, and digital photography reinforced clinical assessments and self-evaluations.19
Lee et al. reported in 2012 on in vitro results suggesting that ursolic acid was effective as an inhibitor of matrix metalloproteinase (MMP)-1 after UVB exposure and was more effective than retinoic acid.20
Based on studies with hairless mice, Lim et al. found in 2007 that ursolic and oleanolic acids can enhance the recovery of skin barrier function and, via peroxisome proliferator-activated receptor-alpha, spur epidermal keratinocyte differentiation. They concluded that both acids have potential for use as agents to promote epidermal permeability barrier function.21
In 2003, Soo et al. observed that pretreatment with ursolic acid inhibited UVA-induced oxidative stress and activation and expression of MMP-2 in HaCaT human keratinocytes. They concluded that ursolic acid may merit attention for the prevention of UVA-induced photoaging.22
Three years earlier, Yarosh et al. showed that liposomes containing ursolic acid augmented ceramide content in cultured normal human epidermal keratinocytes and collagen content in cultured normal human dermal fibroblasts. Over an 11-day period, clinical tests with the ursolic acid–containing liposome (Merotaine) revealed increases in the ceramide content in human skin.23 Two years later, many of the same researchers duplicated their results. This new study also demonstrated that ursolic acid liposomes raise ceramide levels in normal human epidermal keratinocytes, in contrast to the effects of retinoic acid, earlier shown to reduce such levels. They concluded that ursolic acid liposomes show promise for use alone or in combination to replenish or maintain cutaneous ceramide and collagen levels.24 Notably, ursolic acid is incorporated into topical oils and creams intended to confer rejuvenating effects to the skin.
Conclusion
Ursolic acid is a compelling ingredient. I especially will be interested in the results of ongoing human clinical trials of this triterpenoid for treating cancer and skin wrinkles. As it is, ursolic acid is known to exert significant inhibitory activity against tumor formation and tumor cell viability in the laboratory. Given its wide range of biologic activity, and some promising cutaneous results, there is reason to believe that ursolic acid has the potential to play an increasingly useful role in topical skin care agents and dermatologic practice.
References
1. J Dermatol. 2007 Sep;34(9):625-34.
2. Folia Histochem Cytobiol. 2011;49(4):664-9.
3. J Cosmet Dermatol. 2004 Jan;3(1):26-34.
4. J Enzyme Inhib Med Chem. 2011 Oct;26(5):616-42.
5. BMC Complement Altern Med. 2013 Oct 29;13:292.
6. J Biomed Biotechnol. 2010;2010:715739.
7. Fitoterapia. 2009 Apr;80(3):164-7.
8. Biosci Biotechnol Biochem. 2004 Jan;68(1):85-90.
9. J Ethnopharmacol. 2002 Oct;82(2-3):229-37.
10. Eur J Pharmacol. 1997 Sep 3;334(1):103-5.
11. Cancer Prev Res (Phila). 2015 Sep;8(9):817-25.
12. Melanoma Res. 2015 Apr;25(2):103-12.
13. Apoptosis. 2014 May;19(5):816-28.
14. Molecules. 2014 Apr 17;19(4):4924-40.
15. Int J Oncol. 2013 Sep;43(3):911-8.
16. Carcinogenesis. 2009 Jun;30(6):1008-15.
17. Z Naturforsch C. 2006 Nov-Dec;61(11-12):777-82.
18. Cancer Res. 1994 Feb 1;54(3):701-8.
19. J Drugs Dermatol. 2015 Jul;14(7):699-704.
20. Bioorg Khim. 2012 May-Jun;38(3):374-81.
21. J Dermatol. 2007;34(9):625-34.
22. Eur J Pharmacol. 2003 Aug 29;476(3):173-8.
23. Horm Res. 2000;54(5-6):318-21.
24. Arch Dermatol Res. 2002 Jan;293(11):569-75.
Dr. Baumann is chief executive officer of the Baumann Cosmetic & Research Institute in the Design District in Miami. She founded the Cosmetic Dermatology Center at the University of Miami in 1997. Dr. Baumann wrote the textbook “Cosmetic Dermatology: Principles and Practice” (New York: McGraw-Hill, 2002), and a book for consumers, “The Skin Type Solution” (New York: Bantam Dell, 2006). Her latest book, “Cosmeceuticals and Cosmetic Ingredients,” was published in November 2014. Dr. Baumann has received funding for clinical grants from Allergan, Aveeno, Avon Products, Evolus, Galderma, GlaxoSmithKline, Kythera Biopharmaceuticals, Mary Kay, Medicis Pharmaceuticals, Neutrogena, Philosophy, Topix Pharmaceuticals, and Unilever. Dr. Baumann also developed and owns the Baumann Skin Type Solution skin typing systems and related products.
Five-day treatment of ear infections
In December 2016, the results of a randomized, controlled trial of 5-day vs. 10-day amoxicillin/clavulanate treatment of acute otitis media (AOM) in children aged 6-23 months was reported by Hoberman et al. in the New England Journal of Medicine (NEJM).1 Predefined criteria for clinical failure were used that considered both symptoms and signs of AOM, assessed on days 12-14 after start of treatment with 5 vs. 10 days of treatment with the antibiotic. The conclusion reached was clear: The clinical failure rate for the 5-day regimen was 34% vs. 16% in the 10-day group, supporting a preference for the 10-day treatment.
I was surprised. The clinical failure rate for the 5-day regimen seemed very high for treatment with amoxicillin/clavulanate. If it is 34% with amoxicillin/clavulanate, then what would it have been with amoxicillin, as recommended by the American Academy of Pediatrics?
So, why did the systematic review conclude that there was a minimal difference between shortened treatments and the standard 10-day when the NEJM study reported such a striking difference?
In Rochester, N.Y., we have been conducting a longitudinal, prospective study of AOM that is NIH-sponsored to better understand the immune response to AOM, especially in otitis-prone children.3,4 In that study we are treating all children aged 6-23 months with amoxicillin/clavulanate using the same dose as used in the study by Hoberman et al. We have two exceptions: If the child has a second AOM within 30 days of a prior episode or they have an eardrum rupture, we treat for 10 days.5 Our clinical failure rate is 6%. Why is the failure rate in Rochester so much lower than that in Pittsburgh and Bardstown, Ky., where the Hoberman et al. study was done?
One possibility is an important difference in our study design, compared with that of the NEJM study. All the children in our prospective study have a tympanocentesis to confirm the clinical diagnosis, and our research has shown that tympanocentesis results in immediate relief of ear pain and reduces the frequency of antibiotic treatment failure about twofold, compared with children diagnosed and treated by the same physicians in the same clinic practice.6 So, if the tympanocentesis is factored out of the equation, the Rochester clinical failure comes out to 14% for 5-day treatment. Why would the children in Rochester not getting a tympanocentesis, being treated with the same antibiotic, same dose, and same definition of clinical failure, during the same time frame, and having the same bacteria with the same antibiotic resistance rates have a clinical failure rate of 14%, compared with the 34% in the NEJM study?
Next question: How does a clinical failure rate of 34% fit according to past studies of shortened course antibiotic treatment of AOM? Besides the systematic review and meta-analysis noted above, in many countries outside the United States the 5-day regimen is standard, so, if health care providers were seeing a 34% failure rate, that would have been noticeable for sure.8 So, if health care providers were seeing a 34% failure rate, would that not have been noticeable? And would not a 16% failure rate, nearly 1 of 5 cases, be noticeable for children treated for 10 days?
Was there something different about the children who were in the Hoberman et al. study and the children treated in countries outside the United States and in our practice in Rochester? My group has collaborated and published on studies of AOM with the Pittsburgh and Kentucky groups, and we have not found significant site to site differences in outcomes, demonstrating that a population difference is unlikely.9-11
Next question: How does a clinical failure rate of 16% fit according to past studies of 10 days’ antibiotic treatment of AOM? It is on target with the meta-analysis and two other recent studies in the NEJM.12,13 However, if the failure rate was 16% with amoxicillin/clavulanate (which is effective against beta-lactamase–producing Haemophilus influenzae and Moraxella catarrhalis, whereas amoxicillin is not), then the predicted failure rate with amoxicillin for 10 days should be double (34%) or triple (51%) had amoxicillin been used as recommended by the AAP in light of the bacterial resistance of otopathogens. That calculation is based on the prevalence of beta-lactamase–producing H. influenzae and M. catarrhalis in the Pittsburgh and Kentucky populations, the same prevalence seen in the Rochester population.” 14
So, I conclude that this wonderful study does not convince me to change my practice from standard use of 5-day amoxicillin/clavulanate treatment of AOM. Besides, outside of a study setting, most parents don’t give the full 10-day treatment. They stop when their child seems normal (a few days after starting treatment) and save the remainder of the medicine in the refrigerator for the next illness to save a trip to the doctor. Plus, in this column, I did not even get into the issue of disturbing the microbiome with longer courses of antibiotic treatment, a topic for a future discussion.
References
1. N Engl J Med. 2016 Dec 22;375(25):2446-56.
2. Cochrane Database Syst Rev. 2010 Sep 8;(9):CD001095.
3. Pediatr Infect Dis J. 2016 Sep;35(9):1027-32.
4. Pediatr Infect Dis J. 2016 Sep;35(9):1033-9.
5. Otolaryngol Head Neck Surg. 2001 Apr;124(4):381-7.
6. Pediatr Infect Dis J. 2013 May;32(5):473-8.
7. Pediatr Infect Dis J. 2006 Mar;25(3):211-8.
8. Pediatr Infect Dis J. 2000 Sep;19(9):929-37.
9. Pediatr Infect Dis J. 1999 Aug;18(8):741-4.
10. Clin Pediatr (Phila). 2008 Nov;47(9):901-6.
11. Drugs. 2012 Oct 22;72(15):1991-7.
12. N Engl J Med. 2011 Jan 13;364(2):105-15.
13. N Engl J Med. 2011 Jan 13;364(2):116-26.
14. Pediatr Infect Dis J. 2016 Aug;35(8):901-6.
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. He has no disclosures.
In December 2016, the results of a randomized, controlled trial of 5-day vs. 10-day amoxicillin/clavulanate treatment of acute otitis media (AOM) in children aged 6-23 months was reported by Hoberman et al. in the New England Journal of Medicine (NEJM).1 Predefined criteria for clinical failure were used that considered both symptoms and signs of AOM, assessed on days 12-14 after start of treatment with 5 vs. 10 days of treatment with the antibiotic. The conclusion reached was clear: The clinical failure rate for the 5-day regimen was 34% vs. 16% in the 10-day group, supporting a preference for the 10-day treatment.
I was surprised. The clinical failure rate for the 5-day regimen seemed very high for treatment with amoxicillin/clavulanate. If it is 34% with amoxicillin/clavulanate, then what would it have been with amoxicillin, as recommended by the American Academy of Pediatrics?
So, why did the systematic review conclude that there was a minimal difference between shortened treatments and the standard 10-day when the NEJM study reported such a striking difference?
In Rochester, N.Y., we have been conducting a longitudinal, prospective study of AOM that is NIH-sponsored to better understand the immune response to AOM, especially in otitis-prone children.3,4 In that study we are treating all children aged 6-23 months with amoxicillin/clavulanate using the same dose as used in the study by Hoberman et al. We have two exceptions: If the child has a second AOM within 30 days of a prior episode or they have an eardrum rupture, we treat for 10 days.5 Our clinical failure rate is 6%. Why is the failure rate in Rochester so much lower than that in Pittsburgh and Bardstown, Ky., where the Hoberman et al. study was done?
One possibility is an important difference in our study design, compared with that of the NEJM study. All the children in our prospective study have a tympanocentesis to confirm the clinical diagnosis, and our research has shown that tympanocentesis results in immediate relief of ear pain and reduces the frequency of antibiotic treatment failure about twofold, compared with children diagnosed and treated by the same physicians in the same clinic practice.6 So, if the tympanocentesis is factored out of the equation, the Rochester clinical failure comes out to 14% for 5-day treatment. Why would the children in Rochester not getting a tympanocentesis, being treated with the same antibiotic, same dose, and same definition of clinical failure, during the same time frame, and having the same bacteria with the same antibiotic resistance rates have a clinical failure rate of 14%, compared with the 34% in the NEJM study?
Next question: How does a clinical failure rate of 34% fit according to past studies of shortened course antibiotic treatment of AOM? Besides the systematic review and meta-analysis noted above, in many countries outside the United States the 5-day regimen is standard, so, if health care providers were seeing a 34% failure rate, that would have been noticeable for sure.8 So, if health care providers were seeing a 34% failure rate, would that not have been noticeable? And would not a 16% failure rate, nearly 1 of 5 cases, be noticeable for children treated for 10 days?
Was there something different about the children who were in the Hoberman et al. study and the children treated in countries outside the United States and in our practice in Rochester? My group has collaborated and published on studies of AOM with the Pittsburgh and Kentucky groups, and we have not found significant site to site differences in outcomes, demonstrating that a population difference is unlikely.9-11
Next question: How does a clinical failure rate of 16% fit according to past studies of 10 days’ antibiotic treatment of AOM? It is on target with the meta-analysis and two other recent studies in the NEJM.12,13 However, if the failure rate was 16% with amoxicillin/clavulanate (which is effective against beta-lactamase–producing Haemophilus influenzae and Moraxella catarrhalis, whereas amoxicillin is not), then the predicted failure rate with amoxicillin for 10 days should be double (34%) or triple (51%) had amoxicillin been used as recommended by the AAP in light of the bacterial resistance of otopathogens. That calculation is based on the prevalence of beta-lactamase–producing H. influenzae and M. catarrhalis in the Pittsburgh and Kentucky populations, the same prevalence seen in the Rochester population.” 14
So, I conclude that this wonderful study does not convince me to change my practice from standard use of 5-day amoxicillin/clavulanate treatment of AOM. Besides, outside of a study setting, most parents don’t give the full 10-day treatment. They stop when their child seems normal (a few days after starting treatment) and save the remainder of the medicine in the refrigerator for the next illness to save a trip to the doctor. Plus, in this column, I did not even get into the issue of disturbing the microbiome with longer courses of antibiotic treatment, a topic for a future discussion.
References
1. N Engl J Med. 2016 Dec 22;375(25):2446-56.
2. Cochrane Database Syst Rev. 2010 Sep 8;(9):CD001095.
3. Pediatr Infect Dis J. 2016 Sep;35(9):1027-32.
4. Pediatr Infect Dis J. 2016 Sep;35(9):1033-9.
5. Otolaryngol Head Neck Surg. 2001 Apr;124(4):381-7.
6. Pediatr Infect Dis J. 2013 May;32(5):473-8.
7. Pediatr Infect Dis J. 2006 Mar;25(3):211-8.
8. Pediatr Infect Dis J. 2000 Sep;19(9):929-37.
9. Pediatr Infect Dis J. 1999 Aug;18(8):741-4.
10. Clin Pediatr (Phila). 2008 Nov;47(9):901-6.
11. Drugs. 2012 Oct 22;72(15):1991-7.
12. N Engl J Med. 2011 Jan 13;364(2):105-15.
13. N Engl J Med. 2011 Jan 13;364(2):116-26.
14. Pediatr Infect Dis J. 2016 Aug;35(8):901-6.
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. He has no disclosures.
In December 2016, the results of a randomized, controlled trial of 5-day vs. 10-day amoxicillin/clavulanate treatment of acute otitis media (AOM) in children aged 6-23 months was reported by Hoberman et al. in the New England Journal of Medicine (NEJM).1 Predefined criteria for clinical failure were used that considered both symptoms and signs of AOM, assessed on days 12-14 after start of treatment with 5 vs. 10 days of treatment with the antibiotic. The conclusion reached was clear: The clinical failure rate for the 5-day regimen was 34% vs. 16% in the 10-day group, supporting a preference for the 10-day treatment.
I was surprised. The clinical failure rate for the 5-day regimen seemed very high for treatment with amoxicillin/clavulanate. If it is 34% with amoxicillin/clavulanate, then what would it have been with amoxicillin, as recommended by the American Academy of Pediatrics?
So, why did the systematic review conclude that there was a minimal difference between shortened treatments and the standard 10-day when the NEJM study reported such a striking difference?
In Rochester, N.Y., we have been conducting a longitudinal, prospective study of AOM that is NIH-sponsored to better understand the immune response to AOM, especially in otitis-prone children.3,4 In that study we are treating all children aged 6-23 months with amoxicillin/clavulanate using the same dose as used in the study by Hoberman et al. We have two exceptions: If the child has a second AOM within 30 days of a prior episode or they have an eardrum rupture, we treat for 10 days.5 Our clinical failure rate is 6%. Why is the failure rate in Rochester so much lower than that in Pittsburgh and Bardstown, Ky., where the Hoberman et al. study was done?
One possibility is an important difference in our study design, compared with that of the NEJM study. All the children in our prospective study have a tympanocentesis to confirm the clinical diagnosis, and our research has shown that tympanocentesis results in immediate relief of ear pain and reduces the frequency of antibiotic treatment failure about twofold, compared with children diagnosed and treated by the same physicians in the same clinic practice.6 So, if the tympanocentesis is factored out of the equation, the Rochester clinical failure comes out to 14% for 5-day treatment. Why would the children in Rochester not getting a tympanocentesis, being treated with the same antibiotic, same dose, and same definition of clinical failure, during the same time frame, and having the same bacteria with the same antibiotic resistance rates have a clinical failure rate of 14%, compared with the 34% in the NEJM study?
Next question: How does a clinical failure rate of 34% fit according to past studies of shortened course antibiotic treatment of AOM? Besides the systematic review and meta-analysis noted above, in many countries outside the United States the 5-day regimen is standard, so, if health care providers were seeing a 34% failure rate, that would have been noticeable for sure.8 So, if health care providers were seeing a 34% failure rate, would that not have been noticeable? And would not a 16% failure rate, nearly 1 of 5 cases, be noticeable for children treated for 10 days?
Was there something different about the children who were in the Hoberman et al. study and the children treated in countries outside the United States and in our practice in Rochester? My group has collaborated and published on studies of AOM with the Pittsburgh and Kentucky groups, and we have not found significant site to site differences in outcomes, demonstrating that a population difference is unlikely.9-11
Next question: How does a clinical failure rate of 16% fit according to past studies of 10 days’ antibiotic treatment of AOM? It is on target with the meta-analysis and two other recent studies in the NEJM.12,13 However, if the failure rate was 16% with amoxicillin/clavulanate (which is effective against beta-lactamase–producing Haemophilus influenzae and Moraxella catarrhalis, whereas amoxicillin is not), then the predicted failure rate with amoxicillin for 10 days should be double (34%) or triple (51%) had amoxicillin been used as recommended by the AAP in light of the bacterial resistance of otopathogens. That calculation is based on the prevalence of beta-lactamase–producing H. influenzae and M. catarrhalis in the Pittsburgh and Kentucky populations, the same prevalence seen in the Rochester population.” 14
So, I conclude that this wonderful study does not convince me to change my practice from standard use of 5-day amoxicillin/clavulanate treatment of AOM. Besides, outside of a study setting, most parents don’t give the full 10-day treatment. They stop when their child seems normal (a few days after starting treatment) and save the remainder of the medicine in the refrigerator for the next illness to save a trip to the doctor. Plus, in this column, I did not even get into the issue of disturbing the microbiome with longer courses of antibiotic treatment, a topic for a future discussion.
References
1. N Engl J Med. 2016 Dec 22;375(25):2446-56.
2. Cochrane Database Syst Rev. 2010 Sep 8;(9):CD001095.
3. Pediatr Infect Dis J. 2016 Sep;35(9):1027-32.
4. Pediatr Infect Dis J. 2016 Sep;35(9):1033-9.
5. Otolaryngol Head Neck Surg. 2001 Apr;124(4):381-7.
6. Pediatr Infect Dis J. 2013 May;32(5):473-8.
7. Pediatr Infect Dis J. 2006 Mar;25(3):211-8.
8. Pediatr Infect Dis J. 2000 Sep;19(9):929-37.
9. Pediatr Infect Dis J. 1999 Aug;18(8):741-4.
10. Clin Pediatr (Phila). 2008 Nov;47(9):901-6.
11. Drugs. 2012 Oct 22;72(15):1991-7.
12. N Engl J Med. 2011 Jan 13;364(2):105-15.
13. N Engl J Med. 2011 Jan 13;364(2):116-26.
14. Pediatr Infect Dis J. 2016 Aug;35(8):901-6.
Dr. Pichichero, a specialist in pediatric infectious diseases, is director of the Research Institute, Rochester (N.Y.) General Hospital. He is also a pediatrician at Legacy Pediatrics in Rochester. He has no disclosures.
Book Review: Psychiatrist rejects ‘physician as cog’ model of care
The title of the book, “Passion for Patients,” by Lee H. Beecher, MD, DLFAPA, FASAM, with writer Dave Racer, MLitt (St. Paul, Minn., Alethos Press, 2017), clearly represents Dr. Beecher’s approach to his professional life: His focal interest has been his patients ever since he went to medical school and started a very long and successful practice.
Dr. Beecher’s years of practice encompass many of the changes that the practice of medicine has seen in the last 50 years.
He attended medical school when an office was the place where a physician and his patients would get together to exchange thoughts, feelings, ideas, and plans so that they would eventually work together directly and unencumbered on the same concepts that they share and that they considered crucial to their relationship.
Shortly after Dr. Beecher graduated, Medicaid and Medicare came into medical practice, together with progressive limitations, threats, and a great many unwelcome interlopers, whose mission drastically changed the doctor-patient relationship. No matter how one examines the actions of the numerous new participants – be they auditors, insurance companies, employers, or money managers – one of their main missions was to modify, qualify, re-identify, and limit the interaction between the doctor and the patient.
“What is amazing – and contrary to truth – about the current evolution of medical care reform is its manifold references to safeguarding the best interests of the patient,” Dr. Beecher wrote. “On the contrary, the medical care reformers in current vogue see the physician as but one cog in the production of a specified medical care outcome – a cog that must be greased by evidence-based medicine and managed by analytical applications derived from data, cured in the crucible of number crunching, and controlled by payment systems.”
We live in an age when forces other than medical thinking and practice are trying to define what psychiatrists do, how we do it, and whether our effort is worth being paid for. This has created lack of satisfaction in the exercise of psychiatry, early retirements, and lack of growth in many quarters. When one considers that practically all psychiatric endeavors can be traced to the efforts of devoted practitioners interested in improving the profession, one can see that the future might look bleak because people other than psychiatrists define, quantify, and evaluate the practice of our specialty.
“I escaped from managed care into the practice model that had served so well for decades prior to HMOs, [preferred provider organizations], and other externally controlled practice models,” he wrote. “My patients paid me directly.”
Dr. Beecher is a witness and protester, as well as a thinking innovator, coming to defend patients and physicians at a time when they are under attack from precisely the same forces that were supposed to help and support them.
Throughout his book, Dr. Beecher tells us the story of his many points of disagreement with the intruders and his many arguments in favor of patients and doctors, going back to the beginning of the forces that are controlling and destroying their relationship at this time and advocating principled resistance and a careful search for independence. The reader easily accompanies the author to the points when independence blends with excellence – accepting that neither one exists without the other.
Dr. Muñoz, a former president of the American Psychiatric Association, has written eight books and more than 200 articles about various aspects of psychiatry. He is a professor of psychiatry at the University of California, San Diego, and has a private practice. Dr. Muñoz and Dr. Beecher serve on the Editorial Advisory Board of Clinical Psychiatry News.
The title of the book, “Passion for Patients,” by Lee H. Beecher, MD, DLFAPA, FASAM, with writer Dave Racer, MLitt (St. Paul, Minn., Alethos Press, 2017), clearly represents Dr. Beecher’s approach to his professional life: His focal interest has been his patients ever since he went to medical school and started a very long and successful practice.
Dr. Beecher’s years of practice encompass many of the changes that the practice of medicine has seen in the last 50 years.
He attended medical school when an office was the place where a physician and his patients would get together to exchange thoughts, feelings, ideas, and plans so that they would eventually work together directly and unencumbered on the same concepts that they share and that they considered crucial to their relationship.
Shortly after Dr. Beecher graduated, Medicaid and Medicare came into medical practice, together with progressive limitations, threats, and a great many unwelcome interlopers, whose mission drastically changed the doctor-patient relationship. No matter how one examines the actions of the numerous new participants – be they auditors, insurance companies, employers, or money managers – one of their main missions was to modify, qualify, re-identify, and limit the interaction between the doctor and the patient.
“What is amazing – and contrary to truth – about the current evolution of medical care reform is its manifold references to safeguarding the best interests of the patient,” Dr. Beecher wrote. “On the contrary, the medical care reformers in current vogue see the physician as but one cog in the production of a specified medical care outcome – a cog that must be greased by evidence-based medicine and managed by analytical applications derived from data, cured in the crucible of number crunching, and controlled by payment systems.”
We live in an age when forces other than medical thinking and practice are trying to define what psychiatrists do, how we do it, and whether our effort is worth being paid for. This has created lack of satisfaction in the exercise of psychiatry, early retirements, and lack of growth in many quarters. When one considers that practically all psychiatric endeavors can be traced to the efforts of devoted practitioners interested in improving the profession, one can see that the future might look bleak because people other than psychiatrists define, quantify, and evaluate the practice of our specialty.
“I escaped from managed care into the practice model that had served so well for decades prior to HMOs, [preferred provider organizations], and other externally controlled practice models,” he wrote. “My patients paid me directly.”
Dr. Beecher is a witness and protester, as well as a thinking innovator, coming to defend patients and physicians at a time when they are under attack from precisely the same forces that were supposed to help and support them.
Throughout his book, Dr. Beecher tells us the story of his many points of disagreement with the intruders and his many arguments in favor of patients and doctors, going back to the beginning of the forces that are controlling and destroying their relationship at this time and advocating principled resistance and a careful search for independence. The reader easily accompanies the author to the points when independence blends with excellence – accepting that neither one exists without the other.
Dr. Muñoz, a former president of the American Psychiatric Association, has written eight books and more than 200 articles about various aspects of psychiatry. He is a professor of psychiatry at the University of California, San Diego, and has a private practice. Dr. Muñoz and Dr. Beecher serve on the Editorial Advisory Board of Clinical Psychiatry News.
The title of the book, “Passion for Patients,” by Lee H. Beecher, MD, DLFAPA, FASAM, with writer Dave Racer, MLitt (St. Paul, Minn., Alethos Press, 2017), clearly represents Dr. Beecher’s approach to his professional life: His focal interest has been his patients ever since he went to medical school and started a very long and successful practice.
Dr. Beecher’s years of practice encompass many of the changes that the practice of medicine has seen in the last 50 years.
He attended medical school when an office was the place where a physician and his patients would get together to exchange thoughts, feelings, ideas, and plans so that they would eventually work together directly and unencumbered on the same concepts that they share and that they considered crucial to their relationship.
Shortly after Dr. Beecher graduated, Medicaid and Medicare came into medical practice, together with progressive limitations, threats, and a great many unwelcome interlopers, whose mission drastically changed the doctor-patient relationship. No matter how one examines the actions of the numerous new participants – be they auditors, insurance companies, employers, or money managers – one of their main missions was to modify, qualify, re-identify, and limit the interaction between the doctor and the patient.
“What is amazing – and contrary to truth – about the current evolution of medical care reform is its manifold references to safeguarding the best interests of the patient,” Dr. Beecher wrote. “On the contrary, the medical care reformers in current vogue see the physician as but one cog in the production of a specified medical care outcome – a cog that must be greased by evidence-based medicine and managed by analytical applications derived from data, cured in the crucible of number crunching, and controlled by payment systems.”
We live in an age when forces other than medical thinking and practice are trying to define what psychiatrists do, how we do it, and whether our effort is worth being paid for. This has created lack of satisfaction in the exercise of psychiatry, early retirements, and lack of growth in many quarters. When one considers that practically all psychiatric endeavors can be traced to the efforts of devoted practitioners interested in improving the profession, one can see that the future might look bleak because people other than psychiatrists define, quantify, and evaluate the practice of our specialty.
“I escaped from managed care into the practice model that had served so well for decades prior to HMOs, [preferred provider organizations], and other externally controlled practice models,” he wrote. “My patients paid me directly.”
Dr. Beecher is a witness and protester, as well as a thinking innovator, coming to defend patients and physicians at a time when they are under attack from precisely the same forces that were supposed to help and support them.
Throughout his book, Dr. Beecher tells us the story of his many points of disagreement with the intruders and his many arguments in favor of patients and doctors, going back to the beginning of the forces that are controlling and destroying their relationship at this time and advocating principled resistance and a careful search for independence. The reader easily accompanies the author to the points when independence blends with excellence – accepting that neither one exists without the other.
Dr. Muñoz, a former president of the American Psychiatric Association, has written eight books and more than 200 articles about various aspects of psychiatry. He is a professor of psychiatry at the University of California, San Diego, and has a private practice. Dr. Muñoz and Dr. Beecher serve on the Editorial Advisory Board of Clinical Psychiatry News.
Wired to win
In 1929, an industrialist in Philadelphia whose factories had been plagued by vandalism sought to curtail the problem by organizing the boys in the community into athletic teams. Within a few years, his effort became Pop Warner Football. A few years later, a group of parents in Williamsport, Pa., started what was to become Little League Baseball.
Prior to the development of these two programs, kids organized their own games using shared equipment, if any at all. They drew foul lines and cobbled together goals in the bare dirt and the stubbly weeds of vacant lots and backyards. Kids shared equipment with each other. They picked teams in a manner that reflected the sometimes painful reality that some kids were proven winners and others were not. Rules were adjusted to fit the situation. Disagreements were settled without referees, or the game dissolved and a lesson was learned.
From its start in the 1930’s, the model of adult-organized and miniaturized versions of professional sports has spread from baseball and football to almost every team sport, including soccer, hockey, and lacrosse. Children may have been deprived of some self-organizing and negotiating skills, but, when one considers the electronically dominated sedentary alternatives, for the most part, adult-organized team youth sports have been a positive.
Of course, there have been some growing pains because an adult sport that has simply been miniaturized doesn’t necessarily fit well with young minds and bodies that are still developing. In some sports, adult/parent coaches now are required to undergo rigorous training in hopes of making the sport more child appropriate. However, the truth remains that, when teams compete, there are going to be winners and losers.
I recently read a newspaper article that included references to a few recent studies that suggest humans are hard wired to win (Sapolsky, Robert. “The Grim Truth Behind the ‘Winner Effect.’ ”The Wall Street Journal. Feb. 24, 2017). Well, not to win exactly but to be more likely to win again once they have been victorious, a phenomenon known as the “winner effect.”
A mouse that has been allowed to win a fixed fight with another mouse is more likely to win his next fight. Other studies on a variety of species, including humans, have found that winning can elevate testosterone levels and suppress stress-mediating hormones – winning boosts confidence and risk taking. More recent studies on zebra fish have demonstrated that a region of the habenula, a portion of the brain, seems to be critical for controlling these behaviors and chemical mediators.
Of course, the problem is that, when there are winners, there have to be losers. From time to time, the adult organizers have struggled with how to compensate for this unfortunate reality in the structure of their youth sports programs. One response has been to give every participant a trophy. Except when the children are so young that they don’t know which goal is theirs, however, awarding trophies to all is a transparent and foolish charade. The winners know who they are and so do the losers. Skillful and compassionate coaches of both winning and losing teams can cooperate to soften the cutting edge of competition, but it will never disappear. It should be fun to play, but it is always going to be more fun to win.
If there is a solution, it falls on the shoulders of parents, educators, and sometimes pediatricians to help the losers find environments and activities in which their skills and aptitudes will give them the greatest chance of enjoying the benefits of the “winner effect.” Winning isn’t everything, but it feels a lot better than losing. If we can help a child to win once – whether it is on the athletic field or in a classroom – it is more likely he or she will do it again.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
In 1929, an industrialist in Philadelphia whose factories had been plagued by vandalism sought to curtail the problem by organizing the boys in the community into athletic teams. Within a few years, his effort became Pop Warner Football. A few years later, a group of parents in Williamsport, Pa., started what was to become Little League Baseball.
Prior to the development of these two programs, kids organized their own games using shared equipment, if any at all. They drew foul lines and cobbled together goals in the bare dirt and the stubbly weeds of vacant lots and backyards. Kids shared equipment with each other. They picked teams in a manner that reflected the sometimes painful reality that some kids were proven winners and others were not. Rules were adjusted to fit the situation. Disagreements were settled without referees, or the game dissolved and a lesson was learned.
From its start in the 1930’s, the model of adult-organized and miniaturized versions of professional sports has spread from baseball and football to almost every team sport, including soccer, hockey, and lacrosse. Children may have been deprived of some self-organizing and negotiating skills, but, when one considers the electronically dominated sedentary alternatives, for the most part, adult-organized team youth sports have been a positive.
Of course, there have been some growing pains because an adult sport that has simply been miniaturized doesn’t necessarily fit well with young minds and bodies that are still developing. In some sports, adult/parent coaches now are required to undergo rigorous training in hopes of making the sport more child appropriate. However, the truth remains that, when teams compete, there are going to be winners and losers.
I recently read a newspaper article that included references to a few recent studies that suggest humans are hard wired to win (Sapolsky, Robert. “The Grim Truth Behind the ‘Winner Effect.’ ”The Wall Street Journal. Feb. 24, 2017). Well, not to win exactly but to be more likely to win again once they have been victorious, a phenomenon known as the “winner effect.”
A mouse that has been allowed to win a fixed fight with another mouse is more likely to win his next fight. Other studies on a variety of species, including humans, have found that winning can elevate testosterone levels and suppress stress-mediating hormones – winning boosts confidence and risk taking. More recent studies on zebra fish have demonstrated that a region of the habenula, a portion of the brain, seems to be critical for controlling these behaviors and chemical mediators.
Of course, the problem is that, when there are winners, there have to be losers. From time to time, the adult organizers have struggled with how to compensate for this unfortunate reality in the structure of their youth sports programs. One response has been to give every participant a trophy. Except when the children are so young that they don’t know which goal is theirs, however, awarding trophies to all is a transparent and foolish charade. The winners know who they are and so do the losers. Skillful and compassionate coaches of both winning and losing teams can cooperate to soften the cutting edge of competition, but it will never disappear. It should be fun to play, but it is always going to be more fun to win.
If there is a solution, it falls on the shoulders of parents, educators, and sometimes pediatricians to help the losers find environments and activities in which their skills and aptitudes will give them the greatest chance of enjoying the benefits of the “winner effect.” Winning isn’t everything, but it feels a lot better than losing. If we can help a child to win once – whether it is on the athletic field or in a classroom – it is more likely he or she will do it again.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
In 1929, an industrialist in Philadelphia whose factories had been plagued by vandalism sought to curtail the problem by organizing the boys in the community into athletic teams. Within a few years, his effort became Pop Warner Football. A few years later, a group of parents in Williamsport, Pa., started what was to become Little League Baseball.
Prior to the development of these two programs, kids organized their own games using shared equipment, if any at all. They drew foul lines and cobbled together goals in the bare dirt and the stubbly weeds of vacant lots and backyards. Kids shared equipment with each other. They picked teams in a manner that reflected the sometimes painful reality that some kids were proven winners and others were not. Rules were adjusted to fit the situation. Disagreements were settled without referees, or the game dissolved and a lesson was learned.
From its start in the 1930’s, the model of adult-organized and miniaturized versions of professional sports has spread from baseball and football to almost every team sport, including soccer, hockey, and lacrosse. Children may have been deprived of some self-organizing and negotiating skills, but, when one considers the electronically dominated sedentary alternatives, for the most part, adult-organized team youth sports have been a positive.
Of course, there have been some growing pains because an adult sport that has simply been miniaturized doesn’t necessarily fit well with young minds and bodies that are still developing. In some sports, adult/parent coaches now are required to undergo rigorous training in hopes of making the sport more child appropriate. However, the truth remains that, when teams compete, there are going to be winners and losers.
I recently read a newspaper article that included references to a few recent studies that suggest humans are hard wired to win (Sapolsky, Robert. “The Grim Truth Behind the ‘Winner Effect.’ ”The Wall Street Journal. Feb. 24, 2017). Well, not to win exactly but to be more likely to win again once they have been victorious, a phenomenon known as the “winner effect.”
A mouse that has been allowed to win a fixed fight with another mouse is more likely to win his next fight. Other studies on a variety of species, including humans, have found that winning can elevate testosterone levels and suppress stress-mediating hormones – winning boosts confidence and risk taking. More recent studies on zebra fish have demonstrated that a region of the habenula, a portion of the brain, seems to be critical for controlling these behaviors and chemical mediators.
Of course, the problem is that, when there are winners, there have to be losers. From time to time, the adult organizers have struggled with how to compensate for this unfortunate reality in the structure of their youth sports programs. One response has been to give every participant a trophy. Except when the children are so young that they don’t know which goal is theirs, however, awarding trophies to all is a transparent and foolish charade. The winners know who they are and so do the losers. Skillful and compassionate coaches of both winning and losing teams can cooperate to soften the cutting edge of competition, but it will never disappear. It should be fun to play, but it is always going to be more fun to win.
If there is a solution, it falls on the shoulders of parents, educators, and sometimes pediatricians to help the losers find environments and activities in which their skills and aptitudes will give them the greatest chance of enjoying the benefits of the “winner effect.” Winning isn’t everything, but it feels a lot better than losing. If we can help a child to win once – whether it is on the athletic field or in a classroom – it is more likely he or she will do it again.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].
Two boys, a dog, and our electronic health records
“Speak clearly, if you speak at all; carve every word before you let it fall.” – Oliver Wendell Holmes Sr.
One of our favorite stories is that of two boys talking to one another with a dog sitting nearby. One boy says to the other, “I taught my dog how to whistle.” Skeptically, the other boy responds, “Really? I don’t hear him whistling.” The first boys then replies, “I said I taught him. I didn’t say he learned!”
We spend a lot of time as physicians going over information with our patients, yet, according to the best data available, they retain only a small portion of what we tell them. Medication adherence rates for chronic disease range from 30% to 70%, showing that many doses of important medications are missed. Patients often don’t even remember the last instructions we give them as they are walking out of the office. This raises questions about both the way we explain information and how we can use the tools at our disposal to enhance the communication so vital to patient outcomes.
Obviously, we need to consider our words carefully and focus on teaching, not just speaking. What sets teaching apart from speaking is consideration of the learner. The better we understand our patients’ perspectives, the better the knowledge transfer will be. A simple way to address this may be better eye contact.
We have all heard the expression “the eyes are a window to the soul.” Yet, we now have computers that acts as a virtual shades, covering that window and drawing our gaze away from our patients. These shades can blind us to important clues, impeding communication and leading to misunderstanding, missed opportunity, and even patient harm. This is why some practices have chosen to use scribes to handle documentation, freeing up physicians’ eyes and addressing another obstacle to communication: time.
One of the most cited complaints from physicians is lack of time. There is an ever-growing demand on us to see more patients, manage more data, and “check off more boxes” to meet bureaucratic requirements. It should come as no surprise that these impede good patient care. We are thankful that attempts to modernize payment models are recognizing this problem. For example, the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) helps to blaze the trail by focusing on care quality, practice improvement, and patient satisfaction for incentive payments. While these are early steps, they certainly point to a future more concerned with value than with volume.
As we move toward that future, we need to acknowledge that information technology can be both the problem and the answer. The current state of health IT is far from perfect. The tools we use have been designed, seemingly, around financial performance or developed to meet government requirements. It appears that neither physicians nor patients were consulted to ensure their usability or utility. Step No. 1 was getting EHRs out there. Steps 2-10 will be making them useful to clinicians, patients, and health care systems. Part of that utility will come in their ability to enhance communication.
Take patient portals, for example. The “meaningful use program” set as a requirement the ability for patients to “view, download, or transmit” their health information through electronic means. EHR vendors complied with this request but seem to have missed the intent of the measure. Patients accessing the information often are confronted with a morass of technical jargon and unfamiliar medical terms, which may even be offensive. For example, we recently spoke to a parent of a teenager with moderate intellectual disabilities. A hold-out ICD-9 code on the teen’s chart translated to her portal as “318.0 – Imbecile.” Her mother was appropriately upset, and she decided to leave the practice.
As we begin to understand technology’s advantages – and learn its pitfalls – we believe EHR vendors must enhance their offerings while engaging both providers and patients in the process of improvement. We also believe physicians need to leverage the entire care team to realize the software’s full potential. This approach may present new challenges in communication, but it also presents new opportunities. We hope that this collaborative approach will allow physicians to have more time to spend connecting with patients, leading to enhanced understanding and satisfaction.
Our knowledge of human health and disease is growing more sophisticated and so is the challenge of imparting that knowledge to patients. It is critical to find ways to do so that are relevant and understandable and give patients the tools they need to reinforce and remember what we say. This is one of the promises that we are just beginning to see fulfilled by modern EHR technology. Unlike the boy who was trying to teach his dog to whistle, our words have deep impact, and our roles as educators have never been more important.
This article was updated 3/24/17.
Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is associate director of the family medicine residency program at Abington Memorial Hospital and professor of family and community medicine at Temple University in Philadelphia.
“Speak clearly, if you speak at all; carve every word before you let it fall.” – Oliver Wendell Holmes Sr.
One of our favorite stories is that of two boys talking to one another with a dog sitting nearby. One boy says to the other, “I taught my dog how to whistle.” Skeptically, the other boy responds, “Really? I don’t hear him whistling.” The first boys then replies, “I said I taught him. I didn’t say he learned!”
We spend a lot of time as physicians going over information with our patients, yet, according to the best data available, they retain only a small portion of what we tell them. Medication adherence rates for chronic disease range from 30% to 70%, showing that many doses of important medications are missed. Patients often don’t even remember the last instructions we give them as they are walking out of the office. This raises questions about both the way we explain information and how we can use the tools at our disposal to enhance the communication so vital to patient outcomes.
Obviously, we need to consider our words carefully and focus on teaching, not just speaking. What sets teaching apart from speaking is consideration of the learner. The better we understand our patients’ perspectives, the better the knowledge transfer will be. A simple way to address this may be better eye contact.
We have all heard the expression “the eyes are a window to the soul.” Yet, we now have computers that acts as a virtual shades, covering that window and drawing our gaze away from our patients. These shades can blind us to important clues, impeding communication and leading to misunderstanding, missed opportunity, and even patient harm. This is why some practices have chosen to use scribes to handle documentation, freeing up physicians’ eyes and addressing another obstacle to communication: time.
One of the most cited complaints from physicians is lack of time. There is an ever-growing demand on us to see more patients, manage more data, and “check off more boxes” to meet bureaucratic requirements. It should come as no surprise that these impede good patient care. We are thankful that attempts to modernize payment models are recognizing this problem. For example, the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) helps to blaze the trail by focusing on care quality, practice improvement, and patient satisfaction for incentive payments. While these are early steps, they certainly point to a future more concerned with value than with volume.
As we move toward that future, we need to acknowledge that information technology can be both the problem and the answer. The current state of health IT is far from perfect. The tools we use have been designed, seemingly, around financial performance or developed to meet government requirements. It appears that neither physicians nor patients were consulted to ensure their usability or utility. Step No. 1 was getting EHRs out there. Steps 2-10 will be making them useful to clinicians, patients, and health care systems. Part of that utility will come in their ability to enhance communication.
Take patient portals, for example. The “meaningful use program” set as a requirement the ability for patients to “view, download, or transmit” their health information through electronic means. EHR vendors complied with this request but seem to have missed the intent of the measure. Patients accessing the information often are confronted with a morass of technical jargon and unfamiliar medical terms, which may even be offensive. For example, we recently spoke to a parent of a teenager with moderate intellectual disabilities. A hold-out ICD-9 code on the teen’s chart translated to her portal as “318.0 – Imbecile.” Her mother was appropriately upset, and she decided to leave the practice.
As we begin to understand technology’s advantages – and learn its pitfalls – we believe EHR vendors must enhance their offerings while engaging both providers and patients in the process of improvement. We also believe physicians need to leverage the entire care team to realize the software’s full potential. This approach may present new challenges in communication, but it also presents new opportunities. We hope that this collaborative approach will allow physicians to have more time to spend connecting with patients, leading to enhanced understanding and satisfaction.
Our knowledge of human health and disease is growing more sophisticated and so is the challenge of imparting that knowledge to patients. It is critical to find ways to do so that are relevant and understandable and give patients the tools they need to reinforce and remember what we say. This is one of the promises that we are just beginning to see fulfilled by modern EHR technology. Unlike the boy who was trying to teach his dog to whistle, our words have deep impact, and our roles as educators have never been more important.
This article was updated 3/24/17.
Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is associate director of the family medicine residency program at Abington Memorial Hospital and professor of family and community medicine at Temple University in Philadelphia.
“Speak clearly, if you speak at all; carve every word before you let it fall.” – Oliver Wendell Holmes Sr.
One of our favorite stories is that of two boys talking to one another with a dog sitting nearby. One boy says to the other, “I taught my dog how to whistle.” Skeptically, the other boy responds, “Really? I don’t hear him whistling.” The first boys then replies, “I said I taught him. I didn’t say he learned!”
We spend a lot of time as physicians going over information with our patients, yet, according to the best data available, they retain only a small portion of what we tell them. Medication adherence rates for chronic disease range from 30% to 70%, showing that many doses of important medications are missed. Patients often don’t even remember the last instructions we give them as they are walking out of the office. This raises questions about both the way we explain information and how we can use the tools at our disposal to enhance the communication so vital to patient outcomes.
Obviously, we need to consider our words carefully and focus on teaching, not just speaking. What sets teaching apart from speaking is consideration of the learner. The better we understand our patients’ perspectives, the better the knowledge transfer will be. A simple way to address this may be better eye contact.
We have all heard the expression “the eyes are a window to the soul.” Yet, we now have computers that acts as a virtual shades, covering that window and drawing our gaze away from our patients. These shades can blind us to important clues, impeding communication and leading to misunderstanding, missed opportunity, and even patient harm. This is why some practices have chosen to use scribes to handle documentation, freeing up physicians’ eyes and addressing another obstacle to communication: time.
One of the most cited complaints from physicians is lack of time. There is an ever-growing demand on us to see more patients, manage more data, and “check off more boxes” to meet bureaucratic requirements. It should come as no surprise that these impede good patient care. We are thankful that attempts to modernize payment models are recognizing this problem. For example, the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) helps to blaze the trail by focusing on care quality, practice improvement, and patient satisfaction for incentive payments. While these are early steps, they certainly point to a future more concerned with value than with volume.
As we move toward that future, we need to acknowledge that information technology can be both the problem and the answer. The current state of health IT is far from perfect. The tools we use have been designed, seemingly, around financial performance or developed to meet government requirements. It appears that neither physicians nor patients were consulted to ensure their usability or utility. Step No. 1 was getting EHRs out there. Steps 2-10 will be making them useful to clinicians, patients, and health care systems. Part of that utility will come in their ability to enhance communication.
Take patient portals, for example. The “meaningful use program” set as a requirement the ability for patients to “view, download, or transmit” their health information through electronic means. EHR vendors complied with this request but seem to have missed the intent of the measure. Patients accessing the information often are confronted with a morass of technical jargon and unfamiliar medical terms, which may even be offensive. For example, we recently spoke to a parent of a teenager with moderate intellectual disabilities. A hold-out ICD-9 code on the teen’s chart translated to her portal as “318.0 – Imbecile.” Her mother was appropriately upset, and she decided to leave the practice.
As we begin to understand technology’s advantages – and learn its pitfalls – we believe EHR vendors must enhance their offerings while engaging both providers and patients in the process of improvement. We also believe physicians need to leverage the entire care team to realize the software’s full potential. This approach may present new challenges in communication, but it also presents new opportunities. We hope that this collaborative approach will allow physicians to have more time to spend connecting with patients, leading to enhanced understanding and satisfaction.
Our knowledge of human health and disease is growing more sophisticated and so is the challenge of imparting that knowledge to patients. It is critical to find ways to do so that are relevant and understandable and give patients the tools they need to reinforce and remember what we say. This is one of the promises that we are just beginning to see fulfilled by modern EHR technology. Unlike the boy who was trying to teach his dog to whistle, our words have deep impact, and our roles as educators have never been more important.
This article was updated 3/24/17.
Dr. Notte is a family physician and clinical informaticist for Abington (Pa.) Memorial Hospital. He is a partner in EHR Practice Consultants, a firm that aids physicians in adopting electronic health records. Dr. Skolnik is associate director of the family medicine residency program at Abington Memorial Hospital and professor of family and community medicine at Temple University in Philadelphia.
Depression and deep brain stimulation: ‘Furor therapeuticus redux’
Looking back after a long and distinguished career, Leon Eisenberg, MD, invoked the term “furor therapeuticus” to describe overzealous treatment by doctors who became frustrated with therapeutic limitations or motivated by professional enthusiasm.1
With this in mind, Dr. Eisenberg criticized expansive marketing and prescribing of psychotropic drugs in an editorial published exactly 10 years ago. He might also have questioned the current interest in deep brain stimulation (DBS) as a treatment for depression and a growing list of behavioral disorders. Initial studies of DBS in depression were promising, but recent setbacks have brought research to a scientific and ethical crossroads that compels broader discussion.
Besides uncertainties over the right targets to stimulate, identification of the right candidates for DBS treatment can be difficult. Trials of DBS recruited highly selected depressed subjects with no consensus on symptoms or biomarkers that could be used to predict who might respond. Doctors still rely on clinical symptoms to distinguish patients with melancholic depression, who respond to medications or electroconvulsive therapy and might also respond to DBS, from patients with depressed mood because of psychosocial problems, who respond to psychotherapy or social interventions.
Evidence on the efficacy and safety of DBS in depression is mixed. Initial open trials were promising, with dramatic and sustained recovery in some patients, but they were limited by small numbers of subjects and a lack of randomized controls and standardized methods.4,5
DBS is not without serious side effects, and substantial maintenance costs are not always covered by insurance. So, two recent industry trials were eagerly anticipated but showed no significant differences between active and sham stimulations in depression.6,7 These disappointing results prompted soul-searching among investigators, who presented ingenious ideas for correcting shortcomings that could be tested in future trials but also raised doubts as to the prospects of DBS in depression.4,5
Given that DBS devices already are marketed for neurological disorders, regulation of practice is crucial to prevent off-label misuse in behavioral disorders.8 Federal agencies enforce rules governing DBS devices but rely on investigators and local review boards in research and on voluntary postmarketing reports by individual practitioners to monitor compliance and safety. Unscrupulous commercial interests could expand the market for these devices, as demonstrated by the proliferation of psychotropic drug prescribing decried by Dr. Eisenberg. DBS also must be restricted to specialized teams and medical centers to prevent inappropriate implantation by poorly trained providers.
Because behavioral disorders exact an enormous toll on patients, families, and society, better access to effective care and the search for better treatments must remain public health priorities.
Transformative, breakthrough discoveries in brain research will undoubtedly lead to improvements in treatment, including surgical devices in some cases, but, DBS is at risk of being exaggerated and oversold. Adverse consequences of misuse could provoke a public backlash that would have a chilling effect on vital brain research.
One possible way to prevent this is the risk evaluation and mitigation strategy established by the Food and Drug Administration to manage high-risk pharmaceuticals. The FDA mandates that certain high-risk drugs can be prescribed only if doctors are certified and only if patients are enrolled in a national registry where eligibility, course, and outcome are monitored. A similar mechanism should apply to high-risk surgical devices when used for behavioral disorders.9,10
People with behavioral disorders deserve the right to volunteer for experimental programs that offer hope of recovery for themselves and future generations, but they also deserve to be treated with the utmost scientific rigor and protection that society can provide.
Dr. Caroff is emeritus professor of psychiatry at the University of Pennsylvania, Philadelphia. He has received research grant funding from Sunovion Pharmaceuticals and serves as a consultant to Neurocrine Biosciences and TEVA.
References
1. Am J Psychiatry. 2007;164(4):552-5
2. Curr Behav Neurosci Rep. 2014;1(2):55-63
3. J Affect Disord. 2014;156:1-7
4. JAMA Psychiatry. 2016;739(5):439-40
5. Biol Psychiatry. 2016;79(4):e9-10
6. Stereotact Funct Neurosurg. 2015;93:366-9
7. Neurotherapeutics. 2014;11(3):475-84
8. J Neurol Neurosurg Psychiatry. 2014;85(9):1003-8
9. Brain Stimul. 2012;5(4):653-5
10. Fed Reg. 1977 May 23;42(99):26318-32
Looking back after a long and distinguished career, Leon Eisenberg, MD, invoked the term “furor therapeuticus” to describe overzealous treatment by doctors who became frustrated with therapeutic limitations or motivated by professional enthusiasm.1
With this in mind, Dr. Eisenberg criticized expansive marketing and prescribing of psychotropic drugs in an editorial published exactly 10 years ago. He might also have questioned the current interest in deep brain stimulation (DBS) as a treatment for depression and a growing list of behavioral disorders. Initial studies of DBS in depression were promising, but recent setbacks have brought research to a scientific and ethical crossroads that compels broader discussion.
Besides uncertainties over the right targets to stimulate, identification of the right candidates for DBS treatment can be difficult. Trials of DBS recruited highly selected depressed subjects with no consensus on symptoms or biomarkers that could be used to predict who might respond. Doctors still rely on clinical symptoms to distinguish patients with melancholic depression, who respond to medications or electroconvulsive therapy and might also respond to DBS, from patients with depressed mood because of psychosocial problems, who respond to psychotherapy or social interventions.
Evidence on the efficacy and safety of DBS in depression is mixed. Initial open trials were promising, with dramatic and sustained recovery in some patients, but they were limited by small numbers of subjects and a lack of randomized controls and standardized methods.4,5
DBS is not without serious side effects, and substantial maintenance costs are not always covered by insurance. So, two recent industry trials were eagerly anticipated but showed no significant differences between active and sham stimulations in depression.6,7 These disappointing results prompted soul-searching among investigators, who presented ingenious ideas for correcting shortcomings that could be tested in future trials but also raised doubts as to the prospects of DBS in depression.4,5
Given that DBS devices already are marketed for neurological disorders, regulation of practice is crucial to prevent off-label misuse in behavioral disorders.8 Federal agencies enforce rules governing DBS devices but rely on investigators and local review boards in research and on voluntary postmarketing reports by individual practitioners to monitor compliance and safety. Unscrupulous commercial interests could expand the market for these devices, as demonstrated by the proliferation of psychotropic drug prescribing decried by Dr. Eisenberg. DBS also must be restricted to specialized teams and medical centers to prevent inappropriate implantation by poorly trained providers.
Because behavioral disorders exact an enormous toll on patients, families, and society, better access to effective care and the search for better treatments must remain public health priorities.
Transformative, breakthrough discoveries in brain research will undoubtedly lead to improvements in treatment, including surgical devices in some cases, but, DBS is at risk of being exaggerated and oversold. Adverse consequences of misuse could provoke a public backlash that would have a chilling effect on vital brain research.
One possible way to prevent this is the risk evaluation and mitigation strategy established by the Food and Drug Administration to manage high-risk pharmaceuticals. The FDA mandates that certain high-risk drugs can be prescribed only if doctors are certified and only if patients are enrolled in a national registry where eligibility, course, and outcome are monitored. A similar mechanism should apply to high-risk surgical devices when used for behavioral disorders.9,10
People with behavioral disorders deserve the right to volunteer for experimental programs that offer hope of recovery for themselves and future generations, but they also deserve to be treated with the utmost scientific rigor and protection that society can provide.
Dr. Caroff is emeritus professor of psychiatry at the University of Pennsylvania, Philadelphia. He has received research grant funding from Sunovion Pharmaceuticals and serves as a consultant to Neurocrine Biosciences and TEVA.
References
1. Am J Psychiatry. 2007;164(4):552-5
2. Curr Behav Neurosci Rep. 2014;1(2):55-63
3. J Affect Disord. 2014;156:1-7
4. JAMA Psychiatry. 2016;739(5):439-40
5. Biol Psychiatry. 2016;79(4):e9-10
6. Stereotact Funct Neurosurg. 2015;93:366-9
7. Neurotherapeutics. 2014;11(3):475-84
8. J Neurol Neurosurg Psychiatry. 2014;85(9):1003-8
9. Brain Stimul. 2012;5(4):653-5
10. Fed Reg. 1977 May 23;42(99):26318-32
Looking back after a long and distinguished career, Leon Eisenberg, MD, invoked the term “furor therapeuticus” to describe overzealous treatment by doctors who became frustrated with therapeutic limitations or motivated by professional enthusiasm.1
With this in mind, Dr. Eisenberg criticized expansive marketing and prescribing of psychotropic drugs in an editorial published exactly 10 years ago. He might also have questioned the current interest in deep brain stimulation (DBS) as a treatment for depression and a growing list of behavioral disorders. Initial studies of DBS in depression were promising, but recent setbacks have brought research to a scientific and ethical crossroads that compels broader discussion.
Besides uncertainties over the right targets to stimulate, identification of the right candidates for DBS treatment can be difficult. Trials of DBS recruited highly selected depressed subjects with no consensus on symptoms or biomarkers that could be used to predict who might respond. Doctors still rely on clinical symptoms to distinguish patients with melancholic depression, who respond to medications or electroconvulsive therapy and might also respond to DBS, from patients with depressed mood because of psychosocial problems, who respond to psychotherapy or social interventions.
Evidence on the efficacy and safety of DBS in depression is mixed. Initial open trials were promising, with dramatic and sustained recovery in some patients, but they were limited by small numbers of subjects and a lack of randomized controls and standardized methods.4,5
DBS is not without serious side effects, and substantial maintenance costs are not always covered by insurance. So, two recent industry trials were eagerly anticipated but showed no significant differences between active and sham stimulations in depression.6,7 These disappointing results prompted soul-searching among investigators, who presented ingenious ideas for correcting shortcomings that could be tested in future trials but also raised doubts as to the prospects of DBS in depression.4,5
Given that DBS devices already are marketed for neurological disorders, regulation of practice is crucial to prevent off-label misuse in behavioral disorders.8 Federal agencies enforce rules governing DBS devices but rely on investigators and local review boards in research and on voluntary postmarketing reports by individual practitioners to monitor compliance and safety. Unscrupulous commercial interests could expand the market for these devices, as demonstrated by the proliferation of psychotropic drug prescribing decried by Dr. Eisenberg. DBS also must be restricted to specialized teams and medical centers to prevent inappropriate implantation by poorly trained providers.
Because behavioral disorders exact an enormous toll on patients, families, and society, better access to effective care and the search for better treatments must remain public health priorities.
Transformative, breakthrough discoveries in brain research will undoubtedly lead to improvements in treatment, including surgical devices in some cases, but, DBS is at risk of being exaggerated and oversold. Adverse consequences of misuse could provoke a public backlash that would have a chilling effect on vital brain research.
One possible way to prevent this is the risk evaluation and mitigation strategy established by the Food and Drug Administration to manage high-risk pharmaceuticals. The FDA mandates that certain high-risk drugs can be prescribed only if doctors are certified and only if patients are enrolled in a national registry where eligibility, course, and outcome are monitored. A similar mechanism should apply to high-risk surgical devices when used for behavioral disorders.9,10
People with behavioral disorders deserve the right to volunteer for experimental programs that offer hope of recovery for themselves and future generations, but they also deserve to be treated with the utmost scientific rigor and protection that society can provide.
Dr. Caroff is emeritus professor of psychiatry at the University of Pennsylvania, Philadelphia. He has received research grant funding from Sunovion Pharmaceuticals and serves as a consultant to Neurocrine Biosciences and TEVA.
References
1. Am J Psychiatry. 2007;164(4):552-5
2. Curr Behav Neurosci Rep. 2014;1(2):55-63
3. J Affect Disord. 2014;156:1-7
4. JAMA Psychiatry. 2016;739(5):439-40
5. Biol Psychiatry. 2016;79(4):e9-10
6. Stereotact Funct Neurosurg. 2015;93:366-9
7. Neurotherapeutics. 2014;11(3):475-84
8. J Neurol Neurosurg Psychiatry. 2014;85(9):1003-8
9. Brain Stimul. 2012;5(4):653-5
10. Fed Reg. 1977 May 23;42(99):26318-32
Acute Department Syndrome
In this issue of Emergency Medicine, Greg Weingart, MD, and Shravan Kumar, MD, guide readers through the diagnosis, monitoring, and treatment of acute compartment syndrome, a relatively uncommon but devastating injury that may affect an extremity following a long bone fracture, deep vein thrombosis, or rhabdomyolysis from crush injuries or high-intensity exercising. Compartment syndrome occurs when increased pressure within a limited anatomic space compresses the circulation and tissue within that space until function becomes impossible. Even with heightened awareness of the disastrous sequelae, and with very early pressure monitoring of the injured compartment, physicians are at a loss to effectively intervene to prevent the continuing rise in pressure until a fasciotomy is required.
The disastrous consequences of rising pressure in a closed space suggests what can occur in the severely overcrowded EDs that now are common in every city in this country—EDs with too many patients waiting for treatment and inpatient beds.
Pressure on the nation’s ED capacity has been steadily increasing for the past three decades. Hospital/ED closings, demand for preadmission testing by managed care and primary care physicians, increasing numbers of documented and undocumented people seeking care, a rapidly aging population with more comorbidities, and increased numbers of patients seeking care under the Affordable Care Act have not been met with a commensurate increase in ED capacity. Between 1990 and 2010, the country’s urban and suburban areas lost one quarter of their hospital EDs (Hsia RY et al. JAMA. 2011;305[19]:1978-1985). In that same period, New York City lost 20 hospitals and about 5,000 inpatient beds; after 2010, when the state stopped bailing out financially failing hospitals, four more hospitals closed and were replaced by three freestanding EDs (FSEDs). Though FSEDs may partially fulfill the need for 24/7 emergency care at their former hospital sites, when patients in FSEDs require admission, they must compete with patients in hospital-based EDs for inpatient beds.
Despite the many and varied sources of increasing numbers of patients arriving in EDs, by all accounts this influx in and of itself is not the major driver of ED overcrowding. Trained, competent EPs, supported by skilled and highly motivated RNs, NPs, and PAs, are capable of efficiently managing even frequent surges in patient volume—as long as the “outflow” is not blocked. In many cases, this means having adequate, timely outpatient follow-up available to allow for safe discharge. But overwhelmingly, it means having adequate numbers of inpatient beds.
The discomfort and loss of privacy that patients experience from spending many hours or days on hallway stretchers are bad enough, but eventually patient safety also becomes a concern. With some creative approaches varying by location and circumstances, EPs have generally been able to successfully address the safety issues—so far. For example, many years ago, we began holding in reserve a small portion of our fee-for-service EM revenue available to supplement the hospital-provided base salaries. By frequently monitoring conditions throughout the day, taking into account rate of registration in the ED, day of the week, OR schedules, etc, we were able to decide before noon whether there was a need to offer 4, 6, or 8 evening/night hours at double the hourly sessional rate to the first EPs, PAs, and NPs in our group who responded to the e-mails. The hours worked did not earn these “first responders” any additional “RVU” credits as, for the most part, they were working closely with the inpatient services to moni
In this issue of Emergency Medicine, Greg Weingart, MD, and Shravan Kumar, MD, guide readers through the diagnosis, monitoring, and treatment of acute compartment syndrome, a relatively uncommon but devastating injury that may affect an extremity following a long bone fracture, deep vein thrombosis, or rhabdomyolysis from crush injuries or high-intensity exercising. Compartment syndrome occurs when increased pressure within a limited anatomic space compresses the circulation and tissue within that space until function becomes impossible. Even with heightened awareness of the disastrous sequelae, and with very early pressure monitoring of the injured compartment, physicians are at a loss to effectively intervene to prevent the continuing rise in pressure until a fasciotomy is required.
The disastrous consequences of rising pressure in a closed space suggests what can occur in the severely overcrowded EDs that now are common in every city in this country—EDs with too many patients waiting for treatment and inpatient beds.
Pressure on the nation’s ED capacity has been steadily increasing for the past three decades. Hospital/ED closings, demand for preadmission testing by managed care and primary care physicians, increasing numbers of documented and undocumented people seeking care, a rapidly aging population with more comorbidities, and increased numbers of patients seeking care under the Affordable Care Act have not been met with a commensurate increase in ED capacity. Between 1990 and 2010, the country’s urban and suburban areas lost one quarter of their hospital EDs (Hsia RY et al. JAMA. 2011;305[19]:1978-1985). In that same period, New York City lost 20 hospitals and about 5,000 inpatient beds; after 2010, when the state stopped bailing out financially failing hospitals, four more hospitals closed and were replaced by three freestanding EDs (FSEDs). Though FSEDs may partially fulfill the need for 24/7 emergency care at their former hospital sites, when patients in FSEDs require admission, they must compete with patients in hospital-based EDs for inpatient beds.
Despite the many and varied sources of increasing numbers of patients arriving in EDs, by all accounts this influx in and of itself is not the major driver of ED overcrowding. Trained, competent EPs, supported by skilled and highly motivated RNs, NPs, and PAs, are capable of efficiently managing even frequent surges in patient volume—as long as the “outflow” is not blocked. In many cases, this means having adequate, timely outpatient follow-up available to allow for safe discharge. But overwhelmingly, it means having adequate numbers of inpatient beds.
The discomfort and loss of privacy that patients experience from spending many hours or days on hallway stretchers are bad enough, but eventually patient safety also becomes a concern. With some creative approaches varying by location and circumstances, EPs have generally been able to successfully address the safety issues—so far. For example, many years ago, we began holding in reserve a small portion of our fee-for-service EM revenue available to supplement the hospital-provided base salaries. By frequently monitoring conditions throughout the day, taking into account rate of registration in the ED, day of the week, OR schedules, etc, we were able to decide before noon whether there was a need to offer 4, 6, or 8 evening/night hours at double the hourly sessional rate to the first EPs, PAs, and NPs in our group who responded to the e-mails. The hours worked did not earn these “first responders” any additional “RVU” credits as, for the most part, they were working closely with the inpatient services to moni
In this issue of Emergency Medicine, Greg Weingart, MD, and Shravan Kumar, MD, guide readers through the diagnosis, monitoring, and treatment of acute compartment syndrome, a relatively uncommon but devastating injury that may affect an extremity following a long bone fracture, deep vein thrombosis, or rhabdomyolysis from crush injuries or high-intensity exercising. Compartment syndrome occurs when increased pressure within a limited anatomic space compresses the circulation and tissue within that space until function becomes impossible. Even with heightened awareness of the disastrous sequelae, and with very early pressure monitoring of the injured compartment, physicians are at a loss to effectively intervene to prevent the continuing rise in pressure until a fasciotomy is required.
The disastrous consequences of rising pressure in a closed space suggests what can occur in the severely overcrowded EDs that now are common in every city in this country—EDs with too many patients waiting for treatment and inpatient beds.
Pressure on the nation’s ED capacity has been steadily increasing for the past three decades. Hospital/ED closings, demand for preadmission testing by managed care and primary care physicians, increasing numbers of documented and undocumented people seeking care, a rapidly aging population with more comorbidities, and increased numbers of patients seeking care under the Affordable Care Act have not been met with a commensurate increase in ED capacity. Between 1990 and 2010, the country’s urban and suburban areas lost one quarter of their hospital EDs (Hsia RY et al. JAMA. 2011;305[19]:1978-1985). In that same period, New York City lost 20 hospitals and about 5,000 inpatient beds; after 2010, when the state stopped bailing out financially failing hospitals, four more hospitals closed and were replaced by three freestanding EDs (FSEDs). Though FSEDs may partially fulfill the need for 24/7 emergency care at their former hospital sites, when patients in FSEDs require admission, they must compete with patients in hospital-based EDs for inpatient beds.
Despite the many and varied sources of increasing numbers of patients arriving in EDs, by all accounts this influx in and of itself is not the major driver of ED overcrowding. Trained, competent EPs, supported by skilled and highly motivated RNs, NPs, and PAs, are capable of efficiently managing even frequent surges in patient volume—as long as the “outflow” is not blocked. In many cases, this means having adequate, timely outpatient follow-up available to allow for safe discharge. But overwhelmingly, it means having adequate numbers of inpatient beds.
The discomfort and loss of privacy that patients experience from spending many hours or days on hallway stretchers are bad enough, but eventually patient safety also becomes a concern. With some creative approaches varying by location and circumstances, EPs have generally been able to successfully address the safety issues—so far. For example, many years ago, we began holding in reserve a small portion of our fee-for-service EM revenue available to supplement the hospital-provided base salaries. By frequently monitoring conditions throughout the day, taking into account rate of registration in the ED, day of the week, OR schedules, etc, we were able to decide before noon whether there was a need to offer 4, 6, or 8 evening/night hours at double the hourly sessional rate to the first EPs, PAs, and NPs in our group who responded to the e-mails. The hours worked did not earn these “first responders” any additional “RVU” credits as, for the most part, they were working closely with the inpatient services to moni
