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Europe Is Facing a Pancreatic Cancer Emergency
“It’s a health emergency for society, with mortality rates at over 90%,” warned Professor Alfredo Carrato, MD, PhD, the chairperson of Pancreatic Cancer Europe.
There are many challenges with pancreatic cancer: Lack of awareness, difficult to diagnose, no screening programs for the general population, poor survival rate, and limited treatment options.
Life expectancy at the time of diagnosis is just 4.6 months. Only 3% of people diagnosed with pancreatic cancer will survive for 5 years.
A 2024 systematic analysis in The Lancet suggested that people living in Western Europe are more likely to develop pancreatic cancer than those living anywhere else in the world.
Dr. Carrato, emeritus professor of medical oncology at the University of Alcalá, Madrid, Spain, wasn’t surprised. He told this news organization: “I think the lifestyle in Europe plays a part. We have all of the risk factors in society like obesity, our sedentary behavior, too much red meat consumption, and excess alcohol intake.”
Other risk factors include smoking, diabetes, chronic pancreatitis, and a family history.
The incidence of pancreatic cancer increases with age, so the longer life expectancy in Western Europe could also contribute to the region’s high rates.
A Silent Killer
Pancreatic cancer is difficult to identify. It is often asymptomatic. Symptoms that do show themselves, like back pain, weight loss, and nausea, are nonspecific and make early diagnosis challenging.
Professor Mattias Löhr from the Karolinska Institutet, Stockholm, Sweden, told this news organization: “It’s a dismal disease. It’s not accessible for any easy screening or surveillance. Even early diagnosis is too late with pancreatic cancer.”
There have been few advancements in patient outcomes over the past few decades.
Only about 20% of patients are suitable candidates for surgery that could prolong their lives.
Also, cancer reoccurs in two thirds of surgical candidates, said Dr. Carrato, and oncologists don’t know how to identify them in advance. “I have patients who survive 3 months and others who survive 4 or 5 years, so there’s a need to identify these subtypes at a molecular level for personalized, clinical, and translational research and therapies.”
Dr. Löhr agreed: “All of the medical therapies are not really working well enough for pancreatic cancer in sharp contrast to other cancers.”
How Can Rates Be Reduced?
“Pancreatic Cancer Europe is working in every EU state to try to raise awareness,” said Dr. Carrato. “We should have primary prevention programs to modify lifestyle risks. We also need funds for translational and clinical research. Secondary prevention isn’t possible yet as we haven’t identified the higher-risk population who would be the target for screening.”
Screening programs are available for the 10% of people who have a family history of pancreatic cancer. But, for the vast majority, there are no tests or screenings that allow for earlier detection.
“We need blood or stool tests that have high specificity and sensitivity that are cost-effective,” said Dr. Carrato.
“It’s a type of cancer with a particular and very aggressive biology. There is a lack of pancreatic tumor tissue for research, as many patients are diagnosed by fine-needle aspiration cytology. It’s a challenge for researchers. We have no biomarkers available to direct our decisions; no precision oncology,” he added.
Still, there are some encouraging developments.
The European PANCAID project (pancreatic cancer initial detection via liquid biopsy) is trying to find biomarkers to screen at-risk groups for earlier diagnosis via a blood test.
Also, the European Union (EU)-funded PANCAIM project (pancreatic cancer artificial intelligence [AI] for genomics and personalized medicine) has developed an AI algorithm that detects small cancers in CT scans that even experienced radiologists might easily overlook.
The project’s head, Henkjan Huisman, is professor of medical imaging AI at Radboud University Medical Center, Nijmegen, the Netherlands. He told this news organization: “It’s an extremely important step, as 20% of people with pancreas cancer have the ability to undergo surgery, which means they might live substantially longer. We believe if the tumors are found earlier, thanks to the algorithm, they are smaller and more contained, and so substantially more than 20% of patients would be suitable for surgery, which would be a breakthrough.”
Dr. Löhr added that a messenger RNA vaccine is being developed in the United States to prevent pancreatic cancer from returning after surgery and is demonstrating encouraging results in its early trials.
The Road Toward Better Care
To improve cancer care in Europe, Dr. Carrato said: “Reference centers should be a requirement in health policy programs because the outcomes are much better than in centers which only perform fewer surgeries, and Pancreatic Cancer Europe is working with the EU in this direction.”
Finland is a country that appears to have succeeded in this regard. Its 2005 Health Care Act, for example, ensures that cancer patients are able to receive care in one of its five specialized hospitals.
More research funding is also needed. According to Pancreatic Cancer Europe, only 2% of EU funding on cancer is spent on pancreatic cancer.
The American Cancer Society’s Cancer Facts & Figures 2024 makes room for some optimism, with the 5-year survival rate in the United States jumping to 13% from 6% in the society’s 2014 report, as a result of earlier diagnoses and more personalized treatment. But, even with potentially longer survival rates, said Dr. Löhr, “we are still on the trajectory of pancreatic cancer being number two for cancer deaths by 2030.”
“We need more money on research, centralized surgery, and networking between European countries,” said Dr. Carrato. “This networking would need more money for prevention, better diagnosis, and treatment. The problem is pancreatic cancer incidence is increasing and mortality is also in parallel, and we are not making real progress in this scenario.”
A version of this article appeared on Medscape.com.
“It’s a health emergency for society, with mortality rates at over 90%,” warned Professor Alfredo Carrato, MD, PhD, the chairperson of Pancreatic Cancer Europe.
There are many challenges with pancreatic cancer: Lack of awareness, difficult to diagnose, no screening programs for the general population, poor survival rate, and limited treatment options.
Life expectancy at the time of diagnosis is just 4.6 months. Only 3% of people diagnosed with pancreatic cancer will survive for 5 years.
A 2024 systematic analysis in The Lancet suggested that people living in Western Europe are more likely to develop pancreatic cancer than those living anywhere else in the world.
Dr. Carrato, emeritus professor of medical oncology at the University of Alcalá, Madrid, Spain, wasn’t surprised. He told this news organization: “I think the lifestyle in Europe plays a part. We have all of the risk factors in society like obesity, our sedentary behavior, too much red meat consumption, and excess alcohol intake.”
Other risk factors include smoking, diabetes, chronic pancreatitis, and a family history.
The incidence of pancreatic cancer increases with age, so the longer life expectancy in Western Europe could also contribute to the region’s high rates.
A Silent Killer
Pancreatic cancer is difficult to identify. It is often asymptomatic. Symptoms that do show themselves, like back pain, weight loss, and nausea, are nonspecific and make early diagnosis challenging.
Professor Mattias Löhr from the Karolinska Institutet, Stockholm, Sweden, told this news organization: “It’s a dismal disease. It’s not accessible for any easy screening or surveillance. Even early diagnosis is too late with pancreatic cancer.”
There have been few advancements in patient outcomes over the past few decades.
Only about 20% of patients are suitable candidates for surgery that could prolong their lives.
Also, cancer reoccurs in two thirds of surgical candidates, said Dr. Carrato, and oncologists don’t know how to identify them in advance. “I have patients who survive 3 months and others who survive 4 or 5 years, so there’s a need to identify these subtypes at a molecular level for personalized, clinical, and translational research and therapies.”
Dr. Löhr agreed: “All of the medical therapies are not really working well enough for pancreatic cancer in sharp contrast to other cancers.”
How Can Rates Be Reduced?
“Pancreatic Cancer Europe is working in every EU state to try to raise awareness,” said Dr. Carrato. “We should have primary prevention programs to modify lifestyle risks. We also need funds for translational and clinical research. Secondary prevention isn’t possible yet as we haven’t identified the higher-risk population who would be the target for screening.”
Screening programs are available for the 10% of people who have a family history of pancreatic cancer. But, for the vast majority, there are no tests or screenings that allow for earlier detection.
“We need blood or stool tests that have high specificity and sensitivity that are cost-effective,” said Dr. Carrato.
“It’s a type of cancer with a particular and very aggressive biology. There is a lack of pancreatic tumor tissue for research, as many patients are diagnosed by fine-needle aspiration cytology. It’s a challenge for researchers. We have no biomarkers available to direct our decisions; no precision oncology,” he added.
Still, there are some encouraging developments.
The European PANCAID project (pancreatic cancer initial detection via liquid biopsy) is trying to find biomarkers to screen at-risk groups for earlier diagnosis via a blood test.
Also, the European Union (EU)-funded PANCAIM project (pancreatic cancer artificial intelligence [AI] for genomics and personalized medicine) has developed an AI algorithm that detects small cancers in CT scans that even experienced radiologists might easily overlook.
The project’s head, Henkjan Huisman, is professor of medical imaging AI at Radboud University Medical Center, Nijmegen, the Netherlands. He told this news organization: “It’s an extremely important step, as 20% of people with pancreas cancer have the ability to undergo surgery, which means they might live substantially longer. We believe if the tumors are found earlier, thanks to the algorithm, they are smaller and more contained, and so substantially more than 20% of patients would be suitable for surgery, which would be a breakthrough.”
Dr. Löhr added that a messenger RNA vaccine is being developed in the United States to prevent pancreatic cancer from returning after surgery and is demonstrating encouraging results in its early trials.
The Road Toward Better Care
To improve cancer care in Europe, Dr. Carrato said: “Reference centers should be a requirement in health policy programs because the outcomes are much better than in centers which only perform fewer surgeries, and Pancreatic Cancer Europe is working with the EU in this direction.”
Finland is a country that appears to have succeeded in this regard. Its 2005 Health Care Act, for example, ensures that cancer patients are able to receive care in one of its five specialized hospitals.
More research funding is also needed. According to Pancreatic Cancer Europe, only 2% of EU funding on cancer is spent on pancreatic cancer.
The American Cancer Society’s Cancer Facts & Figures 2024 makes room for some optimism, with the 5-year survival rate in the United States jumping to 13% from 6% in the society’s 2014 report, as a result of earlier diagnoses and more personalized treatment. But, even with potentially longer survival rates, said Dr. Löhr, “we are still on the trajectory of pancreatic cancer being number two for cancer deaths by 2030.”
“We need more money on research, centralized surgery, and networking between European countries,” said Dr. Carrato. “This networking would need more money for prevention, better diagnosis, and treatment. The problem is pancreatic cancer incidence is increasing and mortality is also in parallel, and we are not making real progress in this scenario.”
A version of this article appeared on Medscape.com.
“It’s a health emergency for society, with mortality rates at over 90%,” warned Professor Alfredo Carrato, MD, PhD, the chairperson of Pancreatic Cancer Europe.
There are many challenges with pancreatic cancer: Lack of awareness, difficult to diagnose, no screening programs for the general population, poor survival rate, and limited treatment options.
Life expectancy at the time of diagnosis is just 4.6 months. Only 3% of people diagnosed with pancreatic cancer will survive for 5 years.
A 2024 systematic analysis in The Lancet suggested that people living in Western Europe are more likely to develop pancreatic cancer than those living anywhere else in the world.
Dr. Carrato, emeritus professor of medical oncology at the University of Alcalá, Madrid, Spain, wasn’t surprised. He told this news organization: “I think the lifestyle in Europe plays a part. We have all of the risk factors in society like obesity, our sedentary behavior, too much red meat consumption, and excess alcohol intake.”
Other risk factors include smoking, diabetes, chronic pancreatitis, and a family history.
The incidence of pancreatic cancer increases with age, so the longer life expectancy in Western Europe could also contribute to the region’s high rates.
A Silent Killer
Pancreatic cancer is difficult to identify. It is often asymptomatic. Symptoms that do show themselves, like back pain, weight loss, and nausea, are nonspecific and make early diagnosis challenging.
Professor Mattias Löhr from the Karolinska Institutet, Stockholm, Sweden, told this news organization: “It’s a dismal disease. It’s not accessible for any easy screening or surveillance. Even early diagnosis is too late with pancreatic cancer.”
There have been few advancements in patient outcomes over the past few decades.
Only about 20% of patients are suitable candidates for surgery that could prolong their lives.
Also, cancer reoccurs in two thirds of surgical candidates, said Dr. Carrato, and oncologists don’t know how to identify them in advance. “I have patients who survive 3 months and others who survive 4 or 5 years, so there’s a need to identify these subtypes at a molecular level for personalized, clinical, and translational research and therapies.”
Dr. Löhr agreed: “All of the medical therapies are not really working well enough for pancreatic cancer in sharp contrast to other cancers.”
How Can Rates Be Reduced?
“Pancreatic Cancer Europe is working in every EU state to try to raise awareness,” said Dr. Carrato. “We should have primary prevention programs to modify lifestyle risks. We also need funds for translational and clinical research. Secondary prevention isn’t possible yet as we haven’t identified the higher-risk population who would be the target for screening.”
Screening programs are available for the 10% of people who have a family history of pancreatic cancer. But, for the vast majority, there are no tests or screenings that allow for earlier detection.
“We need blood or stool tests that have high specificity and sensitivity that are cost-effective,” said Dr. Carrato.
“It’s a type of cancer with a particular and very aggressive biology. There is a lack of pancreatic tumor tissue for research, as many patients are diagnosed by fine-needle aspiration cytology. It’s a challenge for researchers. We have no biomarkers available to direct our decisions; no precision oncology,” he added.
Still, there are some encouraging developments.
The European PANCAID project (pancreatic cancer initial detection via liquid biopsy) is trying to find biomarkers to screen at-risk groups for earlier diagnosis via a blood test.
Also, the European Union (EU)-funded PANCAIM project (pancreatic cancer artificial intelligence [AI] for genomics and personalized medicine) has developed an AI algorithm that detects small cancers in CT scans that even experienced radiologists might easily overlook.
The project’s head, Henkjan Huisman, is professor of medical imaging AI at Radboud University Medical Center, Nijmegen, the Netherlands. He told this news organization: “It’s an extremely important step, as 20% of people with pancreas cancer have the ability to undergo surgery, which means they might live substantially longer. We believe if the tumors are found earlier, thanks to the algorithm, they are smaller and more contained, and so substantially more than 20% of patients would be suitable for surgery, which would be a breakthrough.”
Dr. Löhr added that a messenger RNA vaccine is being developed in the United States to prevent pancreatic cancer from returning after surgery and is demonstrating encouraging results in its early trials.
The Road Toward Better Care
To improve cancer care in Europe, Dr. Carrato said: “Reference centers should be a requirement in health policy programs because the outcomes are much better than in centers which only perform fewer surgeries, and Pancreatic Cancer Europe is working with the EU in this direction.”
Finland is a country that appears to have succeeded in this regard. Its 2005 Health Care Act, for example, ensures that cancer patients are able to receive care in one of its five specialized hospitals.
More research funding is also needed. According to Pancreatic Cancer Europe, only 2% of EU funding on cancer is spent on pancreatic cancer.
The American Cancer Society’s Cancer Facts & Figures 2024 makes room for some optimism, with the 5-year survival rate in the United States jumping to 13% from 6% in the society’s 2014 report, as a result of earlier diagnoses and more personalized treatment. But, even with potentially longer survival rates, said Dr. Löhr, “we are still on the trajectory of pancreatic cancer being number two for cancer deaths by 2030.”
“We need more money on research, centralized surgery, and networking between European countries,” said Dr. Carrato. “This networking would need more money for prevention, better diagnosis, and treatment. The problem is pancreatic cancer incidence is increasing and mortality is also in parallel, and we are not making real progress in this scenario.”
A version of this article appeared on Medscape.com.
Think Outside the Traditional Toolbox to Treat Itch
ORLANDO — “Itch may not be as sexy as Mohs surgery or aesthetic procedures,” but treating it is important and meaningful to patients, particularly those who’ve found little relief previously, Shawn G. Kwatra, MD, said at the annual ODAC Dermatology, Aesthetic & Surgery Conference.
In doctors’ defense, it can be highly challenging to know which approach is optimal for each individual with pruritus, added Dr. Kwatra, associate professor of dermatology at Johns Hopkins University, Baltimore, Maryland.
Cooling agents, topical capsaicin, topical anesthetics like pramoxine 1%, various forms of lidocaine, strontium, opioid modulators like naltrexone, oral Janus kinase inhibitor (JAK) inhibitors, and medical marijuana are among some of the “outside the box” tools in Dr. Kwatra’s itch toolbox.
Often a Medical Puzzle
Frequently, patients come to the dermatologist complaining of itch, “but you don’t see much on their skin.” After a trial of antihistamines, and some topical steroids, the doctor might put up their hands and think: I tried, but I don’t know what else to do. “This actually happens a lot,” said Dr. Kwatra, who is also director of the Johns Hopkins Itch Center.
This means itch can frustrate providers as well. But for patients, the impact on their quality of life can be on the same level as recovering from a stroke or living with heart failure, Dr. Kwatra said. Finding relief for their itch is where “we can make a big difference for patients.”
Consider Cooling Agents
Many of these therapies are inexpensive and widely available. Cooling agents like menthol, camphor, or calamine can reduce activity of the transient receptor potential (TRP) channels in the skin associated with itch. This ion channel also senses temperature, pressure, and other sensations.
Another option is topical capsaicin, which works through the same ion channels. It binds to the TRPV1 receptors in sensory nerve fibers and causes desensitization. Initially, four to six applications a day are required to reduce itch. After that, patients can apply the medication less frequently. “You have to tell folks we know it’s going to work, but it’s going to burn a lot initially,” Dr. Kwatra said. “In real world practice, I’m not using it often.”
A 1.8% capsaicin patch, approved for treating postherpetic neuralgia, can be used to treat pruritus as well. “You put the patch on for one hour and you can have a true clinical response,” he noted.
Another option for itch relief, the topical anesthetic pramoxine 1%, “is probably underutilized for our patients,” Dr. Kwatra said. Pramoxine 1% works fast — as quickly as 2 minutes — and lasts up to 8 hours and is well-tolerated with low toxicity, he added. The agent is applied three to four times a day and relieves itch by reducing the transmembrane permeability of sodium ions on the skin. “This is something widely available and cheap.”
Lidocaine, another topical anesthetic, is available compounded, over the counter, and as a spray or patch. “I would be careful before you use high doses, like 10%” because of tolerability issues, Dr. Kwatra cautioned. He generally starts with lower concentrations.
Topical strontium is really interesting as a strategy, Dr. Kwatra said. Strontium is a soft, white metal that competes with calcium for receptor binding. There are over-the-counter formulations available as a scalp solution or lotion, which, he said, “are ways to go with more episodic itching.”
Topical oatmeal can also relieve itch in some patients. “There is actually some good scientific evidence for topical oatmeal preparations,” he said.
Steroid-Sparing Novel Topicals
Topical ruxolitinib (a JAK inhibitor approved for atopic dermatitis and vitiligo); topical roflumilast (a phosphodiesterase-4 inhibitor) and topical tapinarof (an aryl hydrocarbon receptor agonist), both approved for treating psoriasis; and the atopic dermatitis drug crisaborole fall into this category of topicals with potential for treating itch, he said, noting that use for treating itch is off label.
Off-label use of biologic agents are also possible treatment options for itch, dupilumab and tralokinumab, both US Food and Drug Administration (FDA)–approved for treating atopic dermatitis. Emerging agents that may prove useful for treating itch include lebrikizumab, nemolizumab, amlitelimab, and rocatinlimab, he said.
In terms of oral therapies, the FDA has approved two oral JAK inhibitors for atopic dermatitis, abrocitinib and upadacitinib, which could prove useful for itch as an off-label indication, according to Dr. Kwatra.
Naltrexone Off Label
An emerging therapeutic concept for treating itch is using an opioid antagonist like naltrexone. Morphine causes more itch, so the theory is a reversal agent might help reduce it. The challenge is that naltrexone only comes as a 50 mg tablet, “and I find the high dose makes people nauseous and vomit,” he added.
Don’t Forget Devices
He referred to a “great paper” that he said has been “totally overlooked,” published in 2001, which evaluated a device that stimulates C fibers in the skin to reduce itch. In the study, 19 patients used the device to treat local areas 20 minutes daily for 5 weeks. Punch biopsies of the affected areas were taken at baseline and after treatment. Mean itch ratings decreased from 78% to 42%, and the number of immunoreactive nerve fibers in the epidermis decreased by 40% at the end of treatment.
“Electrical neurostimulation is better for localized pruritus. There is limited case series evidence, but it’s something to think about,” Dr. Kwatra said.
He and his colleagues also have a case study in press that explored the use of injected botulinum toxin to relieve recalcitrant, chronic itch in a 65-year-old man “who failed everything.”
Dr. Kwatra is a consultant or advisory board member for AbbVie, Amgen, Arcutis Biotherapeutics, ASLAN Pharmaceuticals, Cara Therapeutics, Castle Biosciences, Celldex Therapeutics, Galderma, Incyte Corporation, Johnson & Johnson, LEO Pharma, Novartis, Pfizer, Regeneron, and Sanofi.
A version of this article appeared on Medscape.com.
ORLANDO — “Itch may not be as sexy as Mohs surgery or aesthetic procedures,” but treating it is important and meaningful to patients, particularly those who’ve found little relief previously, Shawn G. Kwatra, MD, said at the annual ODAC Dermatology, Aesthetic & Surgery Conference.
In doctors’ defense, it can be highly challenging to know which approach is optimal for each individual with pruritus, added Dr. Kwatra, associate professor of dermatology at Johns Hopkins University, Baltimore, Maryland.
Cooling agents, topical capsaicin, topical anesthetics like pramoxine 1%, various forms of lidocaine, strontium, opioid modulators like naltrexone, oral Janus kinase inhibitor (JAK) inhibitors, and medical marijuana are among some of the “outside the box” tools in Dr. Kwatra’s itch toolbox.
Often a Medical Puzzle
Frequently, patients come to the dermatologist complaining of itch, “but you don’t see much on their skin.” After a trial of antihistamines, and some topical steroids, the doctor might put up their hands and think: I tried, but I don’t know what else to do. “This actually happens a lot,” said Dr. Kwatra, who is also director of the Johns Hopkins Itch Center.
This means itch can frustrate providers as well. But for patients, the impact on their quality of life can be on the same level as recovering from a stroke or living with heart failure, Dr. Kwatra said. Finding relief for their itch is where “we can make a big difference for patients.”
Consider Cooling Agents
Many of these therapies are inexpensive and widely available. Cooling agents like menthol, camphor, or calamine can reduce activity of the transient receptor potential (TRP) channels in the skin associated with itch. This ion channel also senses temperature, pressure, and other sensations.
Another option is topical capsaicin, which works through the same ion channels. It binds to the TRPV1 receptors in sensory nerve fibers and causes desensitization. Initially, four to six applications a day are required to reduce itch. After that, patients can apply the medication less frequently. “You have to tell folks we know it’s going to work, but it’s going to burn a lot initially,” Dr. Kwatra said. “In real world practice, I’m not using it often.”
A 1.8% capsaicin patch, approved for treating postherpetic neuralgia, can be used to treat pruritus as well. “You put the patch on for one hour and you can have a true clinical response,” he noted.
Another option for itch relief, the topical anesthetic pramoxine 1%, “is probably underutilized for our patients,” Dr. Kwatra said. Pramoxine 1% works fast — as quickly as 2 minutes — and lasts up to 8 hours and is well-tolerated with low toxicity, he added. The agent is applied three to four times a day and relieves itch by reducing the transmembrane permeability of sodium ions on the skin. “This is something widely available and cheap.”
Lidocaine, another topical anesthetic, is available compounded, over the counter, and as a spray or patch. “I would be careful before you use high doses, like 10%” because of tolerability issues, Dr. Kwatra cautioned. He generally starts with lower concentrations.
Topical strontium is really interesting as a strategy, Dr. Kwatra said. Strontium is a soft, white metal that competes with calcium for receptor binding. There are over-the-counter formulations available as a scalp solution or lotion, which, he said, “are ways to go with more episodic itching.”
Topical oatmeal can also relieve itch in some patients. “There is actually some good scientific evidence for topical oatmeal preparations,” he said.
Steroid-Sparing Novel Topicals
Topical ruxolitinib (a JAK inhibitor approved for atopic dermatitis and vitiligo); topical roflumilast (a phosphodiesterase-4 inhibitor) and topical tapinarof (an aryl hydrocarbon receptor agonist), both approved for treating psoriasis; and the atopic dermatitis drug crisaborole fall into this category of topicals with potential for treating itch, he said, noting that use for treating itch is off label.
Off-label use of biologic agents are also possible treatment options for itch, dupilumab and tralokinumab, both US Food and Drug Administration (FDA)–approved for treating atopic dermatitis. Emerging agents that may prove useful for treating itch include lebrikizumab, nemolizumab, amlitelimab, and rocatinlimab, he said.
In terms of oral therapies, the FDA has approved two oral JAK inhibitors for atopic dermatitis, abrocitinib and upadacitinib, which could prove useful for itch as an off-label indication, according to Dr. Kwatra.
Naltrexone Off Label
An emerging therapeutic concept for treating itch is using an opioid antagonist like naltrexone. Morphine causes more itch, so the theory is a reversal agent might help reduce it. The challenge is that naltrexone only comes as a 50 mg tablet, “and I find the high dose makes people nauseous and vomit,” he added.
Don’t Forget Devices
He referred to a “great paper” that he said has been “totally overlooked,” published in 2001, which evaluated a device that stimulates C fibers in the skin to reduce itch. In the study, 19 patients used the device to treat local areas 20 minutes daily for 5 weeks. Punch biopsies of the affected areas were taken at baseline and after treatment. Mean itch ratings decreased from 78% to 42%, and the number of immunoreactive nerve fibers in the epidermis decreased by 40% at the end of treatment.
“Electrical neurostimulation is better for localized pruritus. There is limited case series evidence, but it’s something to think about,” Dr. Kwatra said.
He and his colleagues also have a case study in press that explored the use of injected botulinum toxin to relieve recalcitrant, chronic itch in a 65-year-old man “who failed everything.”
Dr. Kwatra is a consultant or advisory board member for AbbVie, Amgen, Arcutis Biotherapeutics, ASLAN Pharmaceuticals, Cara Therapeutics, Castle Biosciences, Celldex Therapeutics, Galderma, Incyte Corporation, Johnson & Johnson, LEO Pharma, Novartis, Pfizer, Regeneron, and Sanofi.
A version of this article appeared on Medscape.com.
ORLANDO — “Itch may not be as sexy as Mohs surgery or aesthetic procedures,” but treating it is important and meaningful to patients, particularly those who’ve found little relief previously, Shawn G. Kwatra, MD, said at the annual ODAC Dermatology, Aesthetic & Surgery Conference.
In doctors’ defense, it can be highly challenging to know which approach is optimal for each individual with pruritus, added Dr. Kwatra, associate professor of dermatology at Johns Hopkins University, Baltimore, Maryland.
Cooling agents, topical capsaicin, topical anesthetics like pramoxine 1%, various forms of lidocaine, strontium, opioid modulators like naltrexone, oral Janus kinase inhibitor (JAK) inhibitors, and medical marijuana are among some of the “outside the box” tools in Dr. Kwatra’s itch toolbox.
Often a Medical Puzzle
Frequently, patients come to the dermatologist complaining of itch, “but you don’t see much on their skin.” After a trial of antihistamines, and some topical steroids, the doctor might put up their hands and think: I tried, but I don’t know what else to do. “This actually happens a lot,” said Dr. Kwatra, who is also director of the Johns Hopkins Itch Center.
This means itch can frustrate providers as well. But for patients, the impact on their quality of life can be on the same level as recovering from a stroke or living with heart failure, Dr. Kwatra said. Finding relief for their itch is where “we can make a big difference for patients.”
Consider Cooling Agents
Many of these therapies are inexpensive and widely available. Cooling agents like menthol, camphor, or calamine can reduce activity of the transient receptor potential (TRP) channels in the skin associated with itch. This ion channel also senses temperature, pressure, and other sensations.
Another option is topical capsaicin, which works through the same ion channels. It binds to the TRPV1 receptors in sensory nerve fibers and causes desensitization. Initially, four to six applications a day are required to reduce itch. After that, patients can apply the medication less frequently. “You have to tell folks we know it’s going to work, but it’s going to burn a lot initially,” Dr. Kwatra said. “In real world practice, I’m not using it often.”
A 1.8% capsaicin patch, approved for treating postherpetic neuralgia, can be used to treat pruritus as well. “You put the patch on for one hour and you can have a true clinical response,” he noted.
Another option for itch relief, the topical anesthetic pramoxine 1%, “is probably underutilized for our patients,” Dr. Kwatra said. Pramoxine 1% works fast — as quickly as 2 minutes — and lasts up to 8 hours and is well-tolerated with low toxicity, he added. The agent is applied three to four times a day and relieves itch by reducing the transmembrane permeability of sodium ions on the skin. “This is something widely available and cheap.”
Lidocaine, another topical anesthetic, is available compounded, over the counter, and as a spray or patch. “I would be careful before you use high doses, like 10%” because of tolerability issues, Dr. Kwatra cautioned. He generally starts with lower concentrations.
Topical strontium is really interesting as a strategy, Dr. Kwatra said. Strontium is a soft, white metal that competes with calcium for receptor binding. There are over-the-counter formulations available as a scalp solution or lotion, which, he said, “are ways to go with more episodic itching.”
Topical oatmeal can also relieve itch in some patients. “There is actually some good scientific evidence for topical oatmeal preparations,” he said.
Steroid-Sparing Novel Topicals
Topical ruxolitinib (a JAK inhibitor approved for atopic dermatitis and vitiligo); topical roflumilast (a phosphodiesterase-4 inhibitor) and topical tapinarof (an aryl hydrocarbon receptor agonist), both approved for treating psoriasis; and the atopic dermatitis drug crisaborole fall into this category of topicals with potential for treating itch, he said, noting that use for treating itch is off label.
Off-label use of biologic agents are also possible treatment options for itch, dupilumab and tralokinumab, both US Food and Drug Administration (FDA)–approved for treating atopic dermatitis. Emerging agents that may prove useful for treating itch include lebrikizumab, nemolizumab, amlitelimab, and rocatinlimab, he said.
In terms of oral therapies, the FDA has approved two oral JAK inhibitors for atopic dermatitis, abrocitinib and upadacitinib, which could prove useful for itch as an off-label indication, according to Dr. Kwatra.
Naltrexone Off Label
An emerging therapeutic concept for treating itch is using an opioid antagonist like naltrexone. Morphine causes more itch, so the theory is a reversal agent might help reduce it. The challenge is that naltrexone only comes as a 50 mg tablet, “and I find the high dose makes people nauseous and vomit,” he added.
Don’t Forget Devices
He referred to a “great paper” that he said has been “totally overlooked,” published in 2001, which evaluated a device that stimulates C fibers in the skin to reduce itch. In the study, 19 patients used the device to treat local areas 20 minutes daily for 5 weeks. Punch biopsies of the affected areas were taken at baseline and after treatment. Mean itch ratings decreased from 78% to 42%, and the number of immunoreactive nerve fibers in the epidermis decreased by 40% at the end of treatment.
“Electrical neurostimulation is better for localized pruritus. There is limited case series evidence, but it’s something to think about,” Dr. Kwatra said.
He and his colleagues also have a case study in press that explored the use of injected botulinum toxin to relieve recalcitrant, chronic itch in a 65-year-old man “who failed everything.”
Dr. Kwatra is a consultant or advisory board member for AbbVie, Amgen, Arcutis Biotherapeutics, ASLAN Pharmaceuticals, Cara Therapeutics, Castle Biosciences, Celldex Therapeutics, Galderma, Incyte Corporation, Johnson & Johnson, LEO Pharma, Novartis, Pfizer, Regeneron, and Sanofi.
A version of this article appeared on Medscape.com.
FROM ODAC 2024
Cancer Identified as a New Cardiovascular Risk Factor
A history of cancer is an independent predictor of major cardiovascular events in patients undergoing coronary angioplasty. Cancer should be considered a new cardiovascular risk factor in primary and secondary prevention, according to a study presented at the 2023 American Heart Association Congress in Philadelphia.
, for example, equating it to the situation of a patient with diabetes or chronic renal failure,” said lead author Renzo Melchiori, MD, a cardiologist at the University Hospital Austral in Pilar, Argentina.
The researchers also advocate for intensifying cardiovascular control measures in secondary prevention for these patients, reconsidering goals, and ensuring compliance with prescribed pharmacological regimens and healthy lifestyle habits.
“Previously, when a patient had oncological pathology, thinking about associated cardiovascular risk seemed somewhat superfluous. But today, oncological diseases are treated so effectively, increasing survival and life expectancy, that we begin to focus on what happens with the arteries of these patients after treatment,” said Dr. Melchiori.
Higher Incidence Density
The retrospective analysis included 937 patients of both sexes aged 18 years and older who underwent coronary angioplasty for acute coronary syndrome between 2008 and 2022 at a university hospital. Of these participants, 89 (9.5%) had a history of cancer, with a median time since oncologic diagnosis of around 2 years for solid and hematologic tumors. Most participants had treated and resolved cancer.
Over a median follow-up of 45 months (range, 14-72 months), the cumulative incidence rates of a major cardiovascular event (nonfatal stroke, nonfatal acute myocardial infarction, cardiovascular death, or new angioplasty) were 22.2% (155/698) and 28.4% (25/88) in the groups without and with a history of cancer, respectively. The incidence density was significantly higher in the group with an oncologic history than in the group without such a history: 0.78 events/100 patients/month vs 0.48 events/100 patients/month (P = .01).
Kaplan-Meier analysis showed a higher probability of a major cardiovascular event in the group of patients with cancer or a history of cancer (P = .0086). In multivariate Cox regression analysis, cancer history was an independent predictor of major cardiovascular events adjusted for other risk factors such as age, hypertension, diabetes, smoking, sedentary lifestyle, and family history (hazard ratio, 1.66; P = .025).
Dr. Melchiori clarified that the increased incidence of cardiovascular events in patients with cancer or a history of cancer cannot be attributed to differences in percutaneous intervention or the indication or compliance of post-treatment pharmacological therapy.
In addition, the specialist acknowledged that due to the sample size, discrimination by cancer type, disease stage, or therapeutic strategies couldn’t be performed. A subanalysis, which has not been presented, indicated that the effect could not be explained solely by the application of radiotherapy or chemotherapy in the 90 days before angioplasty — two factors that cause arterial inflammation.
Intensifying Prevention Measures
Two independent experts told this news organization that the new study is "interesting" and reinforces the close connection between oncologic and cardiovascular pathology.
Andrés Daniele, MD, cardiologist and president of the Argentine Cardio-Oncology Association, a local chapter of the International Cardio-Oncology Society, emphasized that the study “reiterates an observation seen in other works: A higher rate of atherosclerotic pathology and cardiovascular events in patients with a history of cancer. And that has a reason to be: Both pathologies present common risk factors, and on the other hand, there is greater endothelial dysfunction secondary to the inflammatory syndrome and oncologic therapies.”
“There needs to be a continuum in the intensification of measures in primary and secondary cardiovascular prevention in cancer survivors, whether in remission or with chronic disease. We need to be very aggressive in managing risk factors and insist that patients who have had a cardiovascular event enter cardiovascular rehabilitation therapies,” said Dr. Daniele, who also heads the Cardio-Oncology Department at the centenary Roffo Institute of Oncology at the University of Buenos Aires, Argentina.
The study provides a valuable contribution because “we need to understand the epidemiology and natural history of patients with cancer at risk of developing cardiovascular complications to implement personalized cardiovascular prevention strategies,” said Teresa López Fernández, MD, cardiologist, coordinator of the Cardio-Oncology Program at La Paz University Hospital in Madrid, member of the Cardio-Oncology Working Group of the Spanish Society of Cardiology, member of the board of the International Cardio-Oncology Society, and cochair of the first clinical practice guidelines in cardio-oncology of the European Society of Cardiology.
“We have to be aware that perhaps we should not guide ourselves in these patients with the usual risk stratification scores as cancer or cardiotoxic treatment are not included as variables. However, they require our attention and effort to improve their quality and quantity of life, avoiding potentially preventable cardiovascular events that could negatively impact the survival achieved thanks to advances in cancer treatments,” said Dr. López Fernández.
Dr. Melchiori and Dr. Daniele declared no relevant economic conflicts of interest. Dr. López Fernández reported relationships with Daiichi Sankyo, Almirall España, Janssen-Cilag, Bayer, Roche, Philips, and Incyte.
This article was translated from the Medscape Spanish edition. A version of this article appeared on Medscape.com.
A history of cancer is an independent predictor of major cardiovascular events in patients undergoing coronary angioplasty. Cancer should be considered a new cardiovascular risk factor in primary and secondary prevention, according to a study presented at the 2023 American Heart Association Congress in Philadelphia.
, for example, equating it to the situation of a patient with diabetes or chronic renal failure,” said lead author Renzo Melchiori, MD, a cardiologist at the University Hospital Austral in Pilar, Argentina.
The researchers also advocate for intensifying cardiovascular control measures in secondary prevention for these patients, reconsidering goals, and ensuring compliance with prescribed pharmacological regimens and healthy lifestyle habits.
“Previously, when a patient had oncological pathology, thinking about associated cardiovascular risk seemed somewhat superfluous. But today, oncological diseases are treated so effectively, increasing survival and life expectancy, that we begin to focus on what happens with the arteries of these patients after treatment,” said Dr. Melchiori.
Higher Incidence Density
The retrospective analysis included 937 patients of both sexes aged 18 years and older who underwent coronary angioplasty for acute coronary syndrome between 2008 and 2022 at a university hospital. Of these participants, 89 (9.5%) had a history of cancer, with a median time since oncologic diagnosis of around 2 years for solid and hematologic tumors. Most participants had treated and resolved cancer.
Over a median follow-up of 45 months (range, 14-72 months), the cumulative incidence rates of a major cardiovascular event (nonfatal stroke, nonfatal acute myocardial infarction, cardiovascular death, or new angioplasty) were 22.2% (155/698) and 28.4% (25/88) in the groups without and with a history of cancer, respectively. The incidence density was significantly higher in the group with an oncologic history than in the group without such a history: 0.78 events/100 patients/month vs 0.48 events/100 patients/month (P = .01).
Kaplan-Meier analysis showed a higher probability of a major cardiovascular event in the group of patients with cancer or a history of cancer (P = .0086). In multivariate Cox regression analysis, cancer history was an independent predictor of major cardiovascular events adjusted for other risk factors such as age, hypertension, diabetes, smoking, sedentary lifestyle, and family history (hazard ratio, 1.66; P = .025).
Dr. Melchiori clarified that the increased incidence of cardiovascular events in patients with cancer or a history of cancer cannot be attributed to differences in percutaneous intervention or the indication or compliance of post-treatment pharmacological therapy.
In addition, the specialist acknowledged that due to the sample size, discrimination by cancer type, disease stage, or therapeutic strategies couldn’t be performed. A subanalysis, which has not been presented, indicated that the effect could not be explained solely by the application of radiotherapy or chemotherapy in the 90 days before angioplasty — two factors that cause arterial inflammation.
Intensifying Prevention Measures
Two independent experts told this news organization that the new study is "interesting" and reinforces the close connection between oncologic and cardiovascular pathology.
Andrés Daniele, MD, cardiologist and president of the Argentine Cardio-Oncology Association, a local chapter of the International Cardio-Oncology Society, emphasized that the study “reiterates an observation seen in other works: A higher rate of atherosclerotic pathology and cardiovascular events in patients with a history of cancer. And that has a reason to be: Both pathologies present common risk factors, and on the other hand, there is greater endothelial dysfunction secondary to the inflammatory syndrome and oncologic therapies.”
“There needs to be a continuum in the intensification of measures in primary and secondary cardiovascular prevention in cancer survivors, whether in remission or with chronic disease. We need to be very aggressive in managing risk factors and insist that patients who have had a cardiovascular event enter cardiovascular rehabilitation therapies,” said Dr. Daniele, who also heads the Cardio-Oncology Department at the centenary Roffo Institute of Oncology at the University of Buenos Aires, Argentina.
The study provides a valuable contribution because “we need to understand the epidemiology and natural history of patients with cancer at risk of developing cardiovascular complications to implement personalized cardiovascular prevention strategies,” said Teresa López Fernández, MD, cardiologist, coordinator of the Cardio-Oncology Program at La Paz University Hospital in Madrid, member of the Cardio-Oncology Working Group of the Spanish Society of Cardiology, member of the board of the International Cardio-Oncology Society, and cochair of the first clinical practice guidelines in cardio-oncology of the European Society of Cardiology.
“We have to be aware that perhaps we should not guide ourselves in these patients with the usual risk stratification scores as cancer or cardiotoxic treatment are not included as variables. However, they require our attention and effort to improve their quality and quantity of life, avoiding potentially preventable cardiovascular events that could negatively impact the survival achieved thanks to advances in cancer treatments,” said Dr. López Fernández.
Dr. Melchiori and Dr. Daniele declared no relevant economic conflicts of interest. Dr. López Fernández reported relationships with Daiichi Sankyo, Almirall España, Janssen-Cilag, Bayer, Roche, Philips, and Incyte.
This article was translated from the Medscape Spanish edition. A version of this article appeared on Medscape.com.
A history of cancer is an independent predictor of major cardiovascular events in patients undergoing coronary angioplasty. Cancer should be considered a new cardiovascular risk factor in primary and secondary prevention, according to a study presented at the 2023 American Heart Association Congress in Philadelphia.
, for example, equating it to the situation of a patient with diabetes or chronic renal failure,” said lead author Renzo Melchiori, MD, a cardiologist at the University Hospital Austral in Pilar, Argentina.
The researchers also advocate for intensifying cardiovascular control measures in secondary prevention for these patients, reconsidering goals, and ensuring compliance with prescribed pharmacological regimens and healthy lifestyle habits.
“Previously, when a patient had oncological pathology, thinking about associated cardiovascular risk seemed somewhat superfluous. But today, oncological diseases are treated so effectively, increasing survival and life expectancy, that we begin to focus on what happens with the arteries of these patients after treatment,” said Dr. Melchiori.
Higher Incidence Density
The retrospective analysis included 937 patients of both sexes aged 18 years and older who underwent coronary angioplasty for acute coronary syndrome between 2008 and 2022 at a university hospital. Of these participants, 89 (9.5%) had a history of cancer, with a median time since oncologic diagnosis of around 2 years for solid and hematologic tumors. Most participants had treated and resolved cancer.
Over a median follow-up of 45 months (range, 14-72 months), the cumulative incidence rates of a major cardiovascular event (nonfatal stroke, nonfatal acute myocardial infarction, cardiovascular death, or new angioplasty) were 22.2% (155/698) and 28.4% (25/88) in the groups without and with a history of cancer, respectively. The incidence density was significantly higher in the group with an oncologic history than in the group without such a history: 0.78 events/100 patients/month vs 0.48 events/100 patients/month (P = .01).
Kaplan-Meier analysis showed a higher probability of a major cardiovascular event in the group of patients with cancer or a history of cancer (P = .0086). In multivariate Cox regression analysis, cancer history was an independent predictor of major cardiovascular events adjusted for other risk factors such as age, hypertension, diabetes, smoking, sedentary lifestyle, and family history (hazard ratio, 1.66; P = .025).
Dr. Melchiori clarified that the increased incidence of cardiovascular events in patients with cancer or a history of cancer cannot be attributed to differences in percutaneous intervention or the indication or compliance of post-treatment pharmacological therapy.
In addition, the specialist acknowledged that due to the sample size, discrimination by cancer type, disease stage, or therapeutic strategies couldn’t be performed. A subanalysis, which has not been presented, indicated that the effect could not be explained solely by the application of radiotherapy or chemotherapy in the 90 days before angioplasty — two factors that cause arterial inflammation.
Intensifying Prevention Measures
Two independent experts told this news organization that the new study is "interesting" and reinforces the close connection between oncologic and cardiovascular pathology.
Andrés Daniele, MD, cardiologist and president of the Argentine Cardio-Oncology Association, a local chapter of the International Cardio-Oncology Society, emphasized that the study “reiterates an observation seen in other works: A higher rate of atherosclerotic pathology and cardiovascular events in patients with a history of cancer. And that has a reason to be: Both pathologies present common risk factors, and on the other hand, there is greater endothelial dysfunction secondary to the inflammatory syndrome and oncologic therapies.”
“There needs to be a continuum in the intensification of measures in primary and secondary cardiovascular prevention in cancer survivors, whether in remission or with chronic disease. We need to be very aggressive in managing risk factors and insist that patients who have had a cardiovascular event enter cardiovascular rehabilitation therapies,” said Dr. Daniele, who also heads the Cardio-Oncology Department at the centenary Roffo Institute of Oncology at the University of Buenos Aires, Argentina.
The study provides a valuable contribution because “we need to understand the epidemiology and natural history of patients with cancer at risk of developing cardiovascular complications to implement personalized cardiovascular prevention strategies,” said Teresa López Fernández, MD, cardiologist, coordinator of the Cardio-Oncology Program at La Paz University Hospital in Madrid, member of the Cardio-Oncology Working Group of the Spanish Society of Cardiology, member of the board of the International Cardio-Oncology Society, and cochair of the first clinical practice guidelines in cardio-oncology of the European Society of Cardiology.
“We have to be aware that perhaps we should not guide ourselves in these patients with the usual risk stratification scores as cancer or cardiotoxic treatment are not included as variables. However, they require our attention and effort to improve their quality and quantity of life, avoiding potentially preventable cardiovascular events that could negatively impact the survival achieved thanks to advances in cancer treatments,” said Dr. López Fernández.
Dr. Melchiori and Dr. Daniele declared no relevant economic conflicts of interest. Dr. López Fernández reported relationships with Daiichi Sankyo, Almirall España, Janssen-Cilag, Bayer, Roche, Philips, and Incyte.
This article was translated from the Medscape Spanish edition. A version of this article appeared on Medscape.com.
Even Intentional Weight Loss Linked With Cancer
This transcript has been edited for clarity.
As anyone who has been through medical training will tell you, some little scenes just stick with you. I had been seeing a patient in our resident clinic in West Philly for a couple of years. She was in her mid-60s with diabetes and hypertension and a distant smoking history. She was overweight and had been trying to improve her diet and lose weight since I started seeing her. One day she came in and was delighted to report that she had finally started shedding some pounds — about 15 in the past 2 months.
I enthusiastically told my preceptor that my careful dietary counseling had finally done the job. She looked through the chart for a moment and asked, “Is she up to date on her cancer screening?” A workup revealed adenocarcinoma of the lung. The patient did well, actually, but the story stuck with me.
The textbooks call it “unintentional weight loss,” often in big, scary letters, and every doctor will go just a bit pale if a patient tells them that, despite efforts not to, they are losing weight. But true unintentional weight loss is not that common. After all, most of us are at least half-heartedly trying to lose weight all the time. Should doctors be worried when we are successful?
A new study suggests that perhaps they should. We’re talking about this study, appearing in JAMA, which combined participants from two long-running observational cohorts: 120,000 women from the Nurses’ Health Study, and 50,000 men from the Health Professionals Follow-Up Study. (These cohorts started in the 1970s and 1980s, so we’ll give them a pass on the gender-specific study designs.)
The rationale of enrolling healthcare providers in these cohort studies is that they would be reliable witnesses of their own health status. If a nurse or doctor says they have pancreatic cancer, it’s likely that they truly have pancreatic cancer. Detailed health surveys were distributed to the participants every other year, and the average follow-up was more than a decade.
Participants recorded their weight — as an aside, a nested study found that self-reported rate was extremely well correlated with professionally measured weight — and whether they had received a cancer diagnosis since the last survey.
This allowed researchers to look at the phenomenon described above. Would weight loss precede a new diagnosis of cancer? And, more interestingly, would intentional weight loss precede a new diagnosis of cancer.
I don’t think it will surprise you to hear that individuals in the highest category of weight loss, those who lost more than 10% of their body weight over a 2-year period, had a larger risk of being diagnosed with cancer in the next year. That’s the yellow line in this graph. In fact, they had about a 40% higher risk than those who did not lose weight.
Increased risk was found across multiple cancer types, though cancers of the gastrointestinal tract, not surprisingly, were most strongly associated with antecedent weight loss.
What about intentionality of weight loss? Unfortunately, the surveys did not ask participants whether they were trying to lose weight. Rather, the surveys asked about exercise and dietary habits. The researchers leveraged these responses to create three categories of participants: those who seemed to be trying to lose weight (defined as people who had increased their exercise and dietary quality); those who didn’t seem to be trying to lose weight (they changed neither exercise nor dietary behaviors); and a middle group, which changed one or the other of these behaviors but not both.
Let’s look at those who really seemed to be trying to lose weight. Over 2 years, they got more exercise and improved their diet.
If they succeeded in losing 10% or more of their body weight, they still had a higher risk for cancer than those who had not lost weight — about 30% higher, which is not that different from the 40% increased risk when you include those folks who weren’t changing their lifestyle.
This is why this study is important. The classic teaching is that unintentional weight loss is a bad thing and needs a workup. That’s fine. But we live in a world where perhaps the majority of people are, at any given time, trying to lose weight.
We need to be careful here. I am not by any means trying to say that people who have successfully lost weight have cancer. Both of the following statements can be true:
Significant weight loss, whether intentional or not, is associated with a higher risk for cancer.
Most people with significant weight loss will not have cancer.
Both of these can be true because cancer is, fortunately, rare. Of people who lose weight, the vast majority will lose weight because they are engaging in healthier behaviors. A small number may lose weight because something else is wrong. It’s just hard to tell the two apart.
Out of the nearly 200,000 people in this study, only around 16,000 developed cancer during follow-up. Again, although the chance of having cancer is slightly higher if someone has experienced weight loss, the chance is still very low.
We also need to avoid suggesting that weight loss causes cancer. Some people lose weight because of an existing, as of yet undiagnosed cancer and its metabolic effects. This is borne out if you look at the risk of being diagnosed with cancer as you move further away from the interval of weight loss.
The further you get from the year of that 10% weight loss, the less likely you are to be diagnosed with cancer. Most of these cancers are diagnosed within a year of losing weight. In other words, if you’re reading this and getting worried that you lost weight 10 years ago, you’re probably out of the woods. That was, most likely, just you getting healthier.
Last thing: We have methods for weight loss now that are way more effective than diet or exercise. I’m looking at you, Ozempic. But aside from the weight loss wonder drugs, we have surgery and other interventions. This study did not capture any of that data. Ozempic wasn’t even on the market during this study, so we can’t say anything about the relationship between weight loss and cancer among people using nonlifestyle mechanisms to lose weight.
It’s a complicated system. But the clinically actionable point here is to notice if patients have lost weight. If they’ve lost it without trying, further workup is reasonable. If they’ve lost it but were trying to lose it, tell them “good job.” And consider a workup anyway.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
As anyone who has been through medical training will tell you, some little scenes just stick with you. I had been seeing a patient in our resident clinic in West Philly for a couple of years. She was in her mid-60s with diabetes and hypertension and a distant smoking history. She was overweight and had been trying to improve her diet and lose weight since I started seeing her. One day she came in and was delighted to report that she had finally started shedding some pounds — about 15 in the past 2 months.
I enthusiastically told my preceptor that my careful dietary counseling had finally done the job. She looked through the chart for a moment and asked, “Is she up to date on her cancer screening?” A workup revealed adenocarcinoma of the lung. The patient did well, actually, but the story stuck with me.
The textbooks call it “unintentional weight loss,” often in big, scary letters, and every doctor will go just a bit pale if a patient tells them that, despite efforts not to, they are losing weight. But true unintentional weight loss is not that common. After all, most of us are at least half-heartedly trying to lose weight all the time. Should doctors be worried when we are successful?
A new study suggests that perhaps they should. We’re talking about this study, appearing in JAMA, which combined participants from two long-running observational cohorts: 120,000 women from the Nurses’ Health Study, and 50,000 men from the Health Professionals Follow-Up Study. (These cohorts started in the 1970s and 1980s, so we’ll give them a pass on the gender-specific study designs.)
The rationale of enrolling healthcare providers in these cohort studies is that they would be reliable witnesses of their own health status. If a nurse or doctor says they have pancreatic cancer, it’s likely that they truly have pancreatic cancer. Detailed health surveys were distributed to the participants every other year, and the average follow-up was more than a decade.
Participants recorded their weight — as an aside, a nested study found that self-reported rate was extremely well correlated with professionally measured weight — and whether they had received a cancer diagnosis since the last survey.
This allowed researchers to look at the phenomenon described above. Would weight loss precede a new diagnosis of cancer? And, more interestingly, would intentional weight loss precede a new diagnosis of cancer.
I don’t think it will surprise you to hear that individuals in the highest category of weight loss, those who lost more than 10% of their body weight over a 2-year period, had a larger risk of being diagnosed with cancer in the next year. That’s the yellow line in this graph. In fact, they had about a 40% higher risk than those who did not lose weight.
Increased risk was found across multiple cancer types, though cancers of the gastrointestinal tract, not surprisingly, were most strongly associated with antecedent weight loss.
What about intentionality of weight loss? Unfortunately, the surveys did not ask participants whether they were trying to lose weight. Rather, the surveys asked about exercise and dietary habits. The researchers leveraged these responses to create three categories of participants: those who seemed to be trying to lose weight (defined as people who had increased their exercise and dietary quality); those who didn’t seem to be trying to lose weight (they changed neither exercise nor dietary behaviors); and a middle group, which changed one or the other of these behaviors but not both.
Let’s look at those who really seemed to be trying to lose weight. Over 2 years, they got more exercise and improved their diet.
If they succeeded in losing 10% or more of their body weight, they still had a higher risk for cancer than those who had not lost weight — about 30% higher, which is not that different from the 40% increased risk when you include those folks who weren’t changing their lifestyle.
This is why this study is important. The classic teaching is that unintentional weight loss is a bad thing and needs a workup. That’s fine. But we live in a world where perhaps the majority of people are, at any given time, trying to lose weight.
We need to be careful here. I am not by any means trying to say that people who have successfully lost weight have cancer. Both of the following statements can be true:
Significant weight loss, whether intentional or not, is associated with a higher risk for cancer.
Most people with significant weight loss will not have cancer.
Both of these can be true because cancer is, fortunately, rare. Of people who lose weight, the vast majority will lose weight because they are engaging in healthier behaviors. A small number may lose weight because something else is wrong. It’s just hard to tell the two apart.
Out of the nearly 200,000 people in this study, only around 16,000 developed cancer during follow-up. Again, although the chance of having cancer is slightly higher if someone has experienced weight loss, the chance is still very low.
We also need to avoid suggesting that weight loss causes cancer. Some people lose weight because of an existing, as of yet undiagnosed cancer and its metabolic effects. This is borne out if you look at the risk of being diagnosed with cancer as you move further away from the interval of weight loss.
The further you get from the year of that 10% weight loss, the less likely you are to be diagnosed with cancer. Most of these cancers are diagnosed within a year of losing weight. In other words, if you’re reading this and getting worried that you lost weight 10 years ago, you’re probably out of the woods. That was, most likely, just you getting healthier.
Last thing: We have methods for weight loss now that are way more effective than diet or exercise. I’m looking at you, Ozempic. But aside from the weight loss wonder drugs, we have surgery and other interventions. This study did not capture any of that data. Ozempic wasn’t even on the market during this study, so we can’t say anything about the relationship between weight loss and cancer among people using nonlifestyle mechanisms to lose weight.
It’s a complicated system. But the clinically actionable point here is to notice if patients have lost weight. If they’ve lost it without trying, further workup is reasonable. If they’ve lost it but were trying to lose it, tell them “good job.” And consider a workup anyway.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
As anyone who has been through medical training will tell you, some little scenes just stick with you. I had been seeing a patient in our resident clinic in West Philly for a couple of years. She was in her mid-60s with diabetes and hypertension and a distant smoking history. She was overweight and had been trying to improve her diet and lose weight since I started seeing her. One day she came in and was delighted to report that she had finally started shedding some pounds — about 15 in the past 2 months.
I enthusiastically told my preceptor that my careful dietary counseling had finally done the job. She looked through the chart for a moment and asked, “Is she up to date on her cancer screening?” A workup revealed adenocarcinoma of the lung. The patient did well, actually, but the story stuck with me.
The textbooks call it “unintentional weight loss,” often in big, scary letters, and every doctor will go just a bit pale if a patient tells them that, despite efforts not to, they are losing weight. But true unintentional weight loss is not that common. After all, most of us are at least half-heartedly trying to lose weight all the time. Should doctors be worried when we are successful?
A new study suggests that perhaps they should. We’re talking about this study, appearing in JAMA, which combined participants from two long-running observational cohorts: 120,000 women from the Nurses’ Health Study, and 50,000 men from the Health Professionals Follow-Up Study. (These cohorts started in the 1970s and 1980s, so we’ll give them a pass on the gender-specific study designs.)
The rationale of enrolling healthcare providers in these cohort studies is that they would be reliable witnesses of their own health status. If a nurse or doctor says they have pancreatic cancer, it’s likely that they truly have pancreatic cancer. Detailed health surveys were distributed to the participants every other year, and the average follow-up was more than a decade.
Participants recorded their weight — as an aside, a nested study found that self-reported rate was extremely well correlated with professionally measured weight — and whether they had received a cancer diagnosis since the last survey.
This allowed researchers to look at the phenomenon described above. Would weight loss precede a new diagnosis of cancer? And, more interestingly, would intentional weight loss precede a new diagnosis of cancer.
I don’t think it will surprise you to hear that individuals in the highest category of weight loss, those who lost more than 10% of their body weight over a 2-year period, had a larger risk of being diagnosed with cancer in the next year. That’s the yellow line in this graph. In fact, they had about a 40% higher risk than those who did not lose weight.
Increased risk was found across multiple cancer types, though cancers of the gastrointestinal tract, not surprisingly, were most strongly associated with antecedent weight loss.
What about intentionality of weight loss? Unfortunately, the surveys did not ask participants whether they were trying to lose weight. Rather, the surveys asked about exercise and dietary habits. The researchers leveraged these responses to create three categories of participants: those who seemed to be trying to lose weight (defined as people who had increased their exercise and dietary quality); those who didn’t seem to be trying to lose weight (they changed neither exercise nor dietary behaviors); and a middle group, which changed one or the other of these behaviors but not both.
Let’s look at those who really seemed to be trying to lose weight. Over 2 years, they got more exercise and improved their diet.
If they succeeded in losing 10% or more of their body weight, they still had a higher risk for cancer than those who had not lost weight — about 30% higher, which is not that different from the 40% increased risk when you include those folks who weren’t changing their lifestyle.
This is why this study is important. The classic teaching is that unintentional weight loss is a bad thing and needs a workup. That’s fine. But we live in a world where perhaps the majority of people are, at any given time, trying to lose weight.
We need to be careful here. I am not by any means trying to say that people who have successfully lost weight have cancer. Both of the following statements can be true:
Significant weight loss, whether intentional or not, is associated with a higher risk for cancer.
Most people with significant weight loss will not have cancer.
Both of these can be true because cancer is, fortunately, rare. Of people who lose weight, the vast majority will lose weight because they are engaging in healthier behaviors. A small number may lose weight because something else is wrong. It’s just hard to tell the two apart.
Out of the nearly 200,000 people in this study, only around 16,000 developed cancer during follow-up. Again, although the chance of having cancer is slightly higher if someone has experienced weight loss, the chance is still very low.
We also need to avoid suggesting that weight loss causes cancer. Some people lose weight because of an existing, as of yet undiagnosed cancer and its metabolic effects. This is borne out if you look at the risk of being diagnosed with cancer as you move further away from the interval of weight loss.
The further you get from the year of that 10% weight loss, the less likely you are to be diagnosed with cancer. Most of these cancers are diagnosed within a year of losing weight. In other words, if you’re reading this and getting worried that you lost weight 10 years ago, you’re probably out of the woods. That was, most likely, just you getting healthier.
Last thing: We have methods for weight loss now that are way more effective than diet or exercise. I’m looking at you, Ozempic. But aside from the weight loss wonder drugs, we have surgery and other interventions. This study did not capture any of that data. Ozempic wasn’t even on the market during this study, so we can’t say anything about the relationship between weight loss and cancer among people using nonlifestyle mechanisms to lose weight.
It’s a complicated system. But the clinically actionable point here is to notice if patients have lost weight. If they’ve lost it without trying, further workup is reasonable. If they’ve lost it but were trying to lose it, tell them “good job.” And consider a workup anyway.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Magnetic System May Improve Kidney Stone Removal
Kidney stones afflict approximately one in nine individuals, causing intense pain and serious infections. With over 1.3 million emergency room visits and healthcare expenditures exceeding $5 billion annually in the United States, they pose a significant health burden. Small, hard-to-extract fragments are often left behind, risking natural elimination. While technologies like focused ultrasound, fragment adhesion with biopolymers, and negative pressure aspiration have been explored, they face limitations, especially with standard ureteroscope channel sizes.
Magnetizing Renal Calculus Fragments
A published study introduced the Magnetic System for Total Nephrolith Extraction, a system designed to enhance the efficiency of renal calculus fragment removal. In this system, the stones are coated with a magnetic hydrogel and retrieved using a magnetic guidewire compatible with standard ureteroscopes.
In vitro, laser-obtained renal calculus fragments were separated by size and coated with either ferumoxytol alone or combined with chitosan (Hydrogel CF). Treated fragments were then subjected to a magnetic wire for fragment removal assessment. Additional tests included scanning electron microscopy and cell culture with human urothelial cells to evaluate the cytotoxicity of the magnetic hydrogel components. The hydrogel and its components underwent safety and efficacy evaluations in in vitro studies, human tissue samples, and murine models to assess their impact on urothelium and antibacterial properties.
Safe Fragment Removal
The Hydrogel CF, composed of ferumoxytol and chitosan, demonstrated 100% effectiveness in eliminating all tested fragments, even those measuring up to 4 mm, across various stone compositions. Particle tracing simulations indicated that small-sized stones (1 and 3 mm) could be captured several millimeters away. Scanning electron microscopy confirmed the binding of ferumoxytol and Hydrogel CF to the surface of calcium oxalate stones.
The components of Hydrogel CF did not induce significant cytotoxicity on human urothelial cells, even after a 4-hour exposure. Moreover, live mouse studies showed that Hydrogel CF caused less bladder urothelium exfoliation compared with chitosan, and the urothelium returned to normal within 12 hours. In addition, these components exhibited antibacterial properties, inhibiting the growth of uropathogenic bacteria such as Escherichia coli and Proteus mirabilis, comparable to that of ciprofloxacin.
The ability to eliminate lithiasic fragments, the absence of significant urothelial toxicity, and antibacterial activity suggest that the use of magnetic hydrogel could be integrated into laser treatments for renal stones through ureteroscopy without immediate complications. The antibacterial properties could offer potential postoperative benefits while reducing procedural time. Further animal studies are underway to assess the safety of Hydrogel CF before proceeding to human clinical trials.
This article was translated from JIM, which is part of the Medscape Professional Network. A version of this article appeared on Medscape.com.
Kidney stones afflict approximately one in nine individuals, causing intense pain and serious infections. With over 1.3 million emergency room visits and healthcare expenditures exceeding $5 billion annually in the United States, they pose a significant health burden. Small, hard-to-extract fragments are often left behind, risking natural elimination. While technologies like focused ultrasound, fragment adhesion with biopolymers, and negative pressure aspiration have been explored, they face limitations, especially with standard ureteroscope channel sizes.
Magnetizing Renal Calculus Fragments
A published study introduced the Magnetic System for Total Nephrolith Extraction, a system designed to enhance the efficiency of renal calculus fragment removal. In this system, the stones are coated with a magnetic hydrogel and retrieved using a magnetic guidewire compatible with standard ureteroscopes.
In vitro, laser-obtained renal calculus fragments were separated by size and coated with either ferumoxytol alone or combined with chitosan (Hydrogel CF). Treated fragments were then subjected to a magnetic wire for fragment removal assessment. Additional tests included scanning electron microscopy and cell culture with human urothelial cells to evaluate the cytotoxicity of the magnetic hydrogel components. The hydrogel and its components underwent safety and efficacy evaluations in in vitro studies, human tissue samples, and murine models to assess their impact on urothelium and antibacterial properties.
Safe Fragment Removal
The Hydrogel CF, composed of ferumoxytol and chitosan, demonstrated 100% effectiveness in eliminating all tested fragments, even those measuring up to 4 mm, across various stone compositions. Particle tracing simulations indicated that small-sized stones (1 and 3 mm) could be captured several millimeters away. Scanning electron microscopy confirmed the binding of ferumoxytol and Hydrogel CF to the surface of calcium oxalate stones.
The components of Hydrogel CF did not induce significant cytotoxicity on human urothelial cells, even after a 4-hour exposure. Moreover, live mouse studies showed that Hydrogel CF caused less bladder urothelium exfoliation compared with chitosan, and the urothelium returned to normal within 12 hours. In addition, these components exhibited antibacterial properties, inhibiting the growth of uropathogenic bacteria such as Escherichia coli and Proteus mirabilis, comparable to that of ciprofloxacin.
The ability to eliminate lithiasic fragments, the absence of significant urothelial toxicity, and antibacterial activity suggest that the use of magnetic hydrogel could be integrated into laser treatments for renal stones through ureteroscopy without immediate complications. The antibacterial properties could offer potential postoperative benefits while reducing procedural time. Further animal studies are underway to assess the safety of Hydrogel CF before proceeding to human clinical trials.
This article was translated from JIM, which is part of the Medscape Professional Network. A version of this article appeared on Medscape.com.
Kidney stones afflict approximately one in nine individuals, causing intense pain and serious infections. With over 1.3 million emergency room visits and healthcare expenditures exceeding $5 billion annually in the United States, they pose a significant health burden. Small, hard-to-extract fragments are often left behind, risking natural elimination. While technologies like focused ultrasound, fragment adhesion with biopolymers, and negative pressure aspiration have been explored, they face limitations, especially with standard ureteroscope channel sizes.
Magnetizing Renal Calculus Fragments
A published study introduced the Magnetic System for Total Nephrolith Extraction, a system designed to enhance the efficiency of renal calculus fragment removal. In this system, the stones are coated with a magnetic hydrogel and retrieved using a magnetic guidewire compatible with standard ureteroscopes.
In vitro, laser-obtained renal calculus fragments were separated by size and coated with either ferumoxytol alone or combined with chitosan (Hydrogel CF). Treated fragments were then subjected to a magnetic wire for fragment removal assessment. Additional tests included scanning electron microscopy and cell culture with human urothelial cells to evaluate the cytotoxicity of the magnetic hydrogel components. The hydrogel and its components underwent safety and efficacy evaluations in in vitro studies, human tissue samples, and murine models to assess their impact on urothelium and antibacterial properties.
Safe Fragment Removal
The Hydrogel CF, composed of ferumoxytol and chitosan, demonstrated 100% effectiveness in eliminating all tested fragments, even those measuring up to 4 mm, across various stone compositions. Particle tracing simulations indicated that small-sized stones (1 and 3 mm) could be captured several millimeters away. Scanning electron microscopy confirmed the binding of ferumoxytol and Hydrogel CF to the surface of calcium oxalate stones.
The components of Hydrogel CF did not induce significant cytotoxicity on human urothelial cells, even after a 4-hour exposure. Moreover, live mouse studies showed that Hydrogel CF caused less bladder urothelium exfoliation compared with chitosan, and the urothelium returned to normal within 12 hours. In addition, these components exhibited antibacterial properties, inhibiting the growth of uropathogenic bacteria such as Escherichia coli and Proteus mirabilis, comparable to that of ciprofloxacin.
The ability to eliminate lithiasic fragments, the absence of significant urothelial toxicity, and antibacterial activity suggest that the use of magnetic hydrogel could be integrated into laser treatments for renal stones through ureteroscopy without immediate complications. The antibacterial properties could offer potential postoperative benefits while reducing procedural time. Further animal studies are underway to assess the safety of Hydrogel CF before proceeding to human clinical trials.
This article was translated from JIM, which is part of the Medscape Professional Network. A version of this article appeared on Medscape.com.
Deaths Linked to Substance Use, CVD on the Rise
TOPLINE:
, with the most pronounced rise among women, American Indians, younger people, rural residents, and users of cannabis and psychostimulants, results of new research suggest.
METHODOLOGY:
- From the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) database and using International Classification of Diseases (ICD) codes, researchers collected data on deaths within the United States where both SU and CVD (SU+CVD) were a contributing or an underlying cause and gathered information on location of death (medical facility, home, hospice, nursing home/long-term care facility), demographics (sex, race/ethnicity, age), and region (urban-rural, state).
- Researchers determined crude and age-adjusted mortality rates (AAMRs) per 100,000 population, identified trends in AAMR using annual percent change (APC) and calculated the weighted average of APCs (AAPCs).
- Between 1999 and 2019, there were 636,572 deaths related to CVD+SU, 75.6% of which were among men and 70.6% among non-Hispanic White individuals, with 65% related to alcohol, and where location of death was available, 47.7% occurred in medical facilities.
TAKEAWAY:
- The overall SU+CVD-related AAMR from 1999 to 2019 was 14.3 (95% CI, 14.3-14.3) per 100,000 individuals, with the rate being higher in men (22.5) than in women (6.8) and highest in American Indians or Alaska Natives (37.7) compared with other races/ethnicities.
- Rural areas had higher SU+CVD-related AAMR (15.2; 95% CI, 15.1-15.3) than urban areas, with the District of Columbia having the highest AAMR geographically (25.4), individuals aged 55-69 years having the highest rate agewise (25.1), and alcohol accounting for the highest rate (9.09) among substance types.
- Temporal trends show that the overall SU+CVD-related AAMR increased from 9.9 in 1999 to 21.4 in 2019, a rate that started accelerating in 2012, with an AAPC of 4.0% (95% CI, 3.7-4.3); increases were across all ethnicities and age groups and were particularly pronounced among women (4.8%; 95% CI, 4.5-5.1).
- Cannabis had the highest AAPC of all substances (12.7%), but stimulants had an APC of 21.4 (95% CI, 20.0-22.8) from 2009 to 2019, a period during which stimulants were the fastest-growing substance abuse category.
IN PRACTICE:
These new results identify high-risk groups, which “is crucial for prioritizing preventive measures aiming to reduce substance use and cardiovascular disease-related mortality in these populations,” the researchers wrote.
SOURCE:
Abdul Mannan Khan Minhas, MD, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, and Jakrin Kewcharoen, MD, Division of Cardiology, Loma Linda University Medical Center, Loma Linda, California, were co-first authors of the study, which was published online in the Journal of the American Heart Association.
A version of this article first appeared on Medscape.com.
TOPLINE:
, with the most pronounced rise among women, American Indians, younger people, rural residents, and users of cannabis and psychostimulants, results of new research suggest.
METHODOLOGY:
- From the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) database and using International Classification of Diseases (ICD) codes, researchers collected data on deaths within the United States where both SU and CVD (SU+CVD) were a contributing or an underlying cause and gathered information on location of death (medical facility, home, hospice, nursing home/long-term care facility), demographics (sex, race/ethnicity, age), and region (urban-rural, state).
- Researchers determined crude and age-adjusted mortality rates (AAMRs) per 100,000 population, identified trends in AAMR using annual percent change (APC) and calculated the weighted average of APCs (AAPCs).
- Between 1999 and 2019, there were 636,572 deaths related to CVD+SU, 75.6% of which were among men and 70.6% among non-Hispanic White individuals, with 65% related to alcohol, and where location of death was available, 47.7% occurred in medical facilities.
TAKEAWAY:
- The overall SU+CVD-related AAMR from 1999 to 2019 was 14.3 (95% CI, 14.3-14.3) per 100,000 individuals, with the rate being higher in men (22.5) than in women (6.8) and highest in American Indians or Alaska Natives (37.7) compared with other races/ethnicities.
- Rural areas had higher SU+CVD-related AAMR (15.2; 95% CI, 15.1-15.3) than urban areas, with the District of Columbia having the highest AAMR geographically (25.4), individuals aged 55-69 years having the highest rate agewise (25.1), and alcohol accounting for the highest rate (9.09) among substance types.
- Temporal trends show that the overall SU+CVD-related AAMR increased from 9.9 in 1999 to 21.4 in 2019, a rate that started accelerating in 2012, with an AAPC of 4.0% (95% CI, 3.7-4.3); increases were across all ethnicities and age groups and were particularly pronounced among women (4.8%; 95% CI, 4.5-5.1).
- Cannabis had the highest AAPC of all substances (12.7%), but stimulants had an APC of 21.4 (95% CI, 20.0-22.8) from 2009 to 2019, a period during which stimulants were the fastest-growing substance abuse category.
IN PRACTICE:
These new results identify high-risk groups, which “is crucial for prioritizing preventive measures aiming to reduce substance use and cardiovascular disease-related mortality in these populations,” the researchers wrote.
SOURCE:
Abdul Mannan Khan Minhas, MD, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, and Jakrin Kewcharoen, MD, Division of Cardiology, Loma Linda University Medical Center, Loma Linda, California, were co-first authors of the study, which was published online in the Journal of the American Heart Association.
A version of this article first appeared on Medscape.com.
TOPLINE:
, with the most pronounced rise among women, American Indians, younger people, rural residents, and users of cannabis and psychostimulants, results of new research suggest.
METHODOLOGY:
- From the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) database and using International Classification of Diseases (ICD) codes, researchers collected data on deaths within the United States where both SU and CVD (SU+CVD) were a contributing or an underlying cause and gathered information on location of death (medical facility, home, hospice, nursing home/long-term care facility), demographics (sex, race/ethnicity, age), and region (urban-rural, state).
- Researchers determined crude and age-adjusted mortality rates (AAMRs) per 100,000 population, identified trends in AAMR using annual percent change (APC) and calculated the weighted average of APCs (AAPCs).
- Between 1999 and 2019, there were 636,572 deaths related to CVD+SU, 75.6% of which were among men and 70.6% among non-Hispanic White individuals, with 65% related to alcohol, and where location of death was available, 47.7% occurred in medical facilities.
TAKEAWAY:
- The overall SU+CVD-related AAMR from 1999 to 2019 was 14.3 (95% CI, 14.3-14.3) per 100,000 individuals, with the rate being higher in men (22.5) than in women (6.8) and highest in American Indians or Alaska Natives (37.7) compared with other races/ethnicities.
- Rural areas had higher SU+CVD-related AAMR (15.2; 95% CI, 15.1-15.3) than urban areas, with the District of Columbia having the highest AAMR geographically (25.4), individuals aged 55-69 years having the highest rate agewise (25.1), and alcohol accounting for the highest rate (9.09) among substance types.
- Temporal trends show that the overall SU+CVD-related AAMR increased from 9.9 in 1999 to 21.4 in 2019, a rate that started accelerating in 2012, with an AAPC of 4.0% (95% CI, 3.7-4.3); increases were across all ethnicities and age groups and were particularly pronounced among women (4.8%; 95% CI, 4.5-5.1).
- Cannabis had the highest AAPC of all substances (12.7%), but stimulants had an APC of 21.4 (95% CI, 20.0-22.8) from 2009 to 2019, a period during which stimulants were the fastest-growing substance abuse category.
IN PRACTICE:
These new results identify high-risk groups, which “is crucial for prioritizing preventive measures aiming to reduce substance use and cardiovascular disease-related mortality in these populations,” the researchers wrote.
SOURCE:
Abdul Mannan Khan Minhas, MD, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, and Jakrin Kewcharoen, MD, Division of Cardiology, Loma Linda University Medical Center, Loma Linda, California, were co-first authors of the study, which was published online in the Journal of the American Heart Association.
A version of this article first appeared on Medscape.com.
Researchers Uncover Nanoplastics in Water Bottles
Using an advanced microscopic technique, American researchers have detected 100,000 nanoplastic molecules per liter of water in plastic bottles. Because of their small size, these particles can enter the bloodstream, cells, and the brain, thus posing potential health risks. The study, recently published in the Proceedings of the National Academy of Sciences, raises concerns about the impact of these nanoparticles.
An Unknown Realm
Formed as plastics break down into increasingly small pieces, these particles are consumed by humans and other organisms, with unknown effects on health and ecosystems. Whereas macroplastics have been found in various organs, including the lungs and liver, the study marks a unique exploration into the world of nanoplastics.
Concerns about nanoplastic presence in humans intensified when a 2018 study revealed contamination signs in 93% of 259 examined bottles from nine countries.
The novelty of this research lies in its focus, using a refined spectrometry method, on the poorly understood world of nanoplastics, which derive from the decomposition of microplastics. For the first time, American researchers, including biophysicists and chemists, counted and identified these tiny particles in bottled water. On average, they found around 240,000 detectable plastic fragments per liter, which is 10-100 times more than previous estimates based on larger sizes.
Microplastics are defined as fragments ranging from 5 mm to 1 µm, whereas nanoplastics, particles < 1 µm, are measured in billionths of a meter.
In contrast to microplastics, nanoplastics are so small that they can traverse the intestines and lungs and move directly into the bloodstream, reaching organs such as the heart or brain or even the fetus via the placenta.
“This was previously an obscure, unexplored area. Toxicity studies could only speculate about what was in there,” said Beizhan Yan, PhD, coauthor of the study and environmental chemist at the Lamont–Doherty Earth Observatory of Columbia University, New York. “This study opens a window for us to observe a world we were not exposed to before.”
90% Nanoplastics Found
The new study employed a technique called stimulated Raman scattering microscopy, which was invented by study coauthor Wei Min, a biophysicist at Columbia. This method involves probing samples simultaneously with two lasers tuned to resonate specific molecules.
Researchers tested three bottled water brands that are popular in the United States, analyzing plastic particles up to 100 nm in size. They identified 110,000-370,000 plastic particles per liter. About 90% were nanoplastics — which are invisible by standard imaging techniques — and the rest were microplastics. The study also identified the seven plastics involved.
The most common is polyamide, a type of nylon, likely from plastic filters purportedly used to purify water before bottling. Next is polyethylene terephthalate, which is commonly used for water bottles and other food containers. Researchers also found other common plastics, including polystyrene, polyvinyl chloride, and methyl methacrylate, used in various industrial processes.
Not Size But Quantity
What’s more concerning is that the seven types of plastics accounted for only about 10% of all nanoparticles found in the samples. Researchers have no idea about the composition of the remaining 90%. If these are all nanoparticles, their number could reach tens of millions per liter, representing the complex composition of seemingly simple water samples, as noted by the authors.
Researchers now plan to expand beyond bottled water, exploring the vast realm of nanoplastics. They emphasize that, in terms of mass, nanoplastics are far smaller than microplastics, but “it’s not about size. It’s about the numbers as smaller things can easily penetrate us.”
The team aims to study tap water, which also contains microplastics but in much smaller proportions than bottled water.
This article was translated from the Medscape French edition.
Using an advanced microscopic technique, American researchers have detected 100,000 nanoplastic molecules per liter of water in plastic bottles. Because of their small size, these particles can enter the bloodstream, cells, and the brain, thus posing potential health risks. The study, recently published in the Proceedings of the National Academy of Sciences, raises concerns about the impact of these nanoparticles.
An Unknown Realm
Formed as plastics break down into increasingly small pieces, these particles are consumed by humans and other organisms, with unknown effects on health and ecosystems. Whereas macroplastics have been found in various organs, including the lungs and liver, the study marks a unique exploration into the world of nanoplastics.
Concerns about nanoplastic presence in humans intensified when a 2018 study revealed contamination signs in 93% of 259 examined bottles from nine countries.
The novelty of this research lies in its focus, using a refined spectrometry method, on the poorly understood world of nanoplastics, which derive from the decomposition of microplastics. For the first time, American researchers, including biophysicists and chemists, counted and identified these tiny particles in bottled water. On average, they found around 240,000 detectable plastic fragments per liter, which is 10-100 times more than previous estimates based on larger sizes.
Microplastics are defined as fragments ranging from 5 mm to 1 µm, whereas nanoplastics, particles < 1 µm, are measured in billionths of a meter.
In contrast to microplastics, nanoplastics are so small that they can traverse the intestines and lungs and move directly into the bloodstream, reaching organs such as the heart or brain or even the fetus via the placenta.
“This was previously an obscure, unexplored area. Toxicity studies could only speculate about what was in there,” said Beizhan Yan, PhD, coauthor of the study and environmental chemist at the Lamont–Doherty Earth Observatory of Columbia University, New York. “This study opens a window for us to observe a world we were not exposed to before.”
90% Nanoplastics Found
The new study employed a technique called stimulated Raman scattering microscopy, which was invented by study coauthor Wei Min, a biophysicist at Columbia. This method involves probing samples simultaneously with two lasers tuned to resonate specific molecules.
Researchers tested three bottled water brands that are popular in the United States, analyzing plastic particles up to 100 nm in size. They identified 110,000-370,000 plastic particles per liter. About 90% were nanoplastics — which are invisible by standard imaging techniques — and the rest were microplastics. The study also identified the seven plastics involved.
The most common is polyamide, a type of nylon, likely from plastic filters purportedly used to purify water before bottling. Next is polyethylene terephthalate, which is commonly used for water bottles and other food containers. Researchers also found other common plastics, including polystyrene, polyvinyl chloride, and methyl methacrylate, used in various industrial processes.
Not Size But Quantity
What’s more concerning is that the seven types of plastics accounted for only about 10% of all nanoparticles found in the samples. Researchers have no idea about the composition of the remaining 90%. If these are all nanoparticles, their number could reach tens of millions per liter, representing the complex composition of seemingly simple water samples, as noted by the authors.
Researchers now plan to expand beyond bottled water, exploring the vast realm of nanoplastics. They emphasize that, in terms of mass, nanoplastics are far smaller than microplastics, but “it’s not about size. It’s about the numbers as smaller things can easily penetrate us.”
The team aims to study tap water, which also contains microplastics but in much smaller proportions than bottled water.
This article was translated from the Medscape French edition.
Using an advanced microscopic technique, American researchers have detected 100,000 nanoplastic molecules per liter of water in plastic bottles. Because of their small size, these particles can enter the bloodstream, cells, and the brain, thus posing potential health risks. The study, recently published in the Proceedings of the National Academy of Sciences, raises concerns about the impact of these nanoparticles.
An Unknown Realm
Formed as plastics break down into increasingly small pieces, these particles are consumed by humans and other organisms, with unknown effects on health and ecosystems. Whereas macroplastics have been found in various organs, including the lungs and liver, the study marks a unique exploration into the world of nanoplastics.
Concerns about nanoplastic presence in humans intensified when a 2018 study revealed contamination signs in 93% of 259 examined bottles from nine countries.
The novelty of this research lies in its focus, using a refined spectrometry method, on the poorly understood world of nanoplastics, which derive from the decomposition of microplastics. For the first time, American researchers, including biophysicists and chemists, counted and identified these tiny particles in bottled water. On average, they found around 240,000 detectable plastic fragments per liter, which is 10-100 times more than previous estimates based on larger sizes.
Microplastics are defined as fragments ranging from 5 mm to 1 µm, whereas nanoplastics, particles < 1 µm, are measured in billionths of a meter.
In contrast to microplastics, nanoplastics are so small that they can traverse the intestines and lungs and move directly into the bloodstream, reaching organs such as the heart or brain or even the fetus via the placenta.
“This was previously an obscure, unexplored area. Toxicity studies could only speculate about what was in there,” said Beizhan Yan, PhD, coauthor of the study and environmental chemist at the Lamont–Doherty Earth Observatory of Columbia University, New York. “This study opens a window for us to observe a world we were not exposed to before.”
90% Nanoplastics Found
The new study employed a technique called stimulated Raman scattering microscopy, which was invented by study coauthor Wei Min, a biophysicist at Columbia. This method involves probing samples simultaneously with two lasers tuned to resonate specific molecules.
Researchers tested three bottled water brands that are popular in the United States, analyzing plastic particles up to 100 nm in size. They identified 110,000-370,000 plastic particles per liter. About 90% were nanoplastics — which are invisible by standard imaging techniques — and the rest were microplastics. The study also identified the seven plastics involved.
The most common is polyamide, a type of nylon, likely from plastic filters purportedly used to purify water before bottling. Next is polyethylene terephthalate, which is commonly used for water bottles and other food containers. Researchers also found other common plastics, including polystyrene, polyvinyl chloride, and methyl methacrylate, used in various industrial processes.
Not Size But Quantity
What’s more concerning is that the seven types of plastics accounted for only about 10% of all nanoparticles found in the samples. Researchers have no idea about the composition of the remaining 90%. If these are all nanoparticles, their number could reach tens of millions per liter, representing the complex composition of seemingly simple water samples, as noted by the authors.
Researchers now plan to expand beyond bottled water, exploring the vast realm of nanoplastics. They emphasize that, in terms of mass, nanoplastics are far smaller than microplastics, but “it’s not about size. It’s about the numbers as smaller things can easily penetrate us.”
The team aims to study tap water, which also contains microplastics but in much smaller proportions than bottled water.
This article was translated from the Medscape French edition.
FROM THE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES
Testosterone Replacement May Cause ... Fracture?
This transcript has been edited for clarity.
I am showing you a graph without any labels.
What could this line represent? The stock price of some company that made a big splash but failed to live up to expectations? An outbreak curve charting the introduction of a new infectious agent to a population? The performance of a viral tweet?
I’ll tell you what it is in a moment, but I wanted you to recognize that there is something inherently wistful in this shape, something that speaks of past glory and inevitable declines. It’s a graph that induces a feeling of resistance — no, do not go gently into that good night.
The graph actually represents (roughly) the normal level of serum testosterone in otherwise-healthy men as they age.
A caveat here: These numbers are not as well defined as I made them seem on this graph, particularly for those older than 65 years. But it is clear that testosterone levels decline with time, and the idea to supplement testosterone is hardly new. Like all treatments, testosterone supplementation has risks and benefits. Some risks are predictable, like exacerbating the symptoms of benign prostatic hyperplasia. Some risks seem to come completely out of left field. That’s what we have today, in a study suggesting that testosterone supplementation increases the risk for bone fractures.
Let me set the stage here by saying that nearly all prior research into the effects of testosterone supplementation has suggested that it is pretty good for bone health. It increases bone mineral density, bone strength, and improves bone architecture.
So if you were to do a randomized trial of testosterone supplementation and look at fracture risk in the testosterone group compared with the placebo group, you would expect the fracture risk would be much lower in those getting supplemented. Of course, this is why we actually do studies instead of assuming we know the answer already — because in this case, you’d be wrong.
I’m talking about this study, appearing in The New England Journal of Medicine.
It’s a prespecified secondary analysis of a randomized trial known as the TRAVERSE trial, which randomly assigned 5246 men with low testosterone levels to transdermal testosterone gel vs placebo. The primary goal of that trial was to assess the cardiovascular risk associated with testosterone supplementation, and the major take-home was that there was no difference in cardiovascular event rates between the testosterone and placebo groups.
This secondary analysis looked at fracture incidence. Researchers contacted participants multiple times in the first year of the study and yearly thereafter. Each time, they asked whether the participant had sustained a fracture. If they answered in the affirmative, a request for medical records was made and the researchers, still blinded to randomization status, adjudicated whether there was indeed a fracture or not, along with some details as to location, situation, and so on.
This was a big study, though, and that translates to just a 3.5% fracture rate in testosterone vs 2.5% in control, but the difference was statistically significant.
This difference persisted across various fracture types (non–high-impact fractures, for example) after excluding the small percentage of men taking osteoporosis medication.
How does a drug that increases bone mineral density and bone strength increase the risk for fracture?
Well, one clue — and this was pointed out in a nice editorial by Matthis Grossman and Bradley Anawalt — is that the increased risk for fracture occurs quite soon after starting treatment, which is not consistent with direct bone effects. Rather, this might represent behavioral differences. Testosterone supplementation seems to increase energy levels; might it lead men to engage in activities that put them at higher risk for fracture?
Regardless of the cause, this adds to our knowledge about the rather complex mix of risks and benefits of testosterone supplementation and probably puts a bit more weight on the risks side. The truth is that testosterone levels do decline with age, as do many things, and it may not be appropriate to try to fight against that in all people. It’s worth noting that all of these studies use low levels of total serum testosterone as an entry criterion. But total testosterone is not what your body “sees.” It sees free testosterone, the portion not bound to sex hormone–binding globulin. And that binding protein is affected by lots of stuff — diabetes and obesity lower it, for example — making total testosterone levels seem low when free testosterone might be just fine.
In other words, testosterone supplementation is probably not terrible, but it is definitely not the cure for aging. In situations like this, we need better data to guide exactly who will benefit from the therapy and who will only be exposed to the risks.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I am showing you a graph without any labels.
What could this line represent? The stock price of some company that made a big splash but failed to live up to expectations? An outbreak curve charting the introduction of a new infectious agent to a population? The performance of a viral tweet?
I’ll tell you what it is in a moment, but I wanted you to recognize that there is something inherently wistful in this shape, something that speaks of past glory and inevitable declines. It’s a graph that induces a feeling of resistance — no, do not go gently into that good night.
The graph actually represents (roughly) the normal level of serum testosterone in otherwise-healthy men as they age.
A caveat here: These numbers are not as well defined as I made them seem on this graph, particularly for those older than 65 years. But it is clear that testosterone levels decline with time, and the idea to supplement testosterone is hardly new. Like all treatments, testosterone supplementation has risks and benefits. Some risks are predictable, like exacerbating the symptoms of benign prostatic hyperplasia. Some risks seem to come completely out of left field. That’s what we have today, in a study suggesting that testosterone supplementation increases the risk for bone fractures.
Let me set the stage here by saying that nearly all prior research into the effects of testosterone supplementation has suggested that it is pretty good for bone health. It increases bone mineral density, bone strength, and improves bone architecture.
So if you were to do a randomized trial of testosterone supplementation and look at fracture risk in the testosterone group compared with the placebo group, you would expect the fracture risk would be much lower in those getting supplemented. Of course, this is why we actually do studies instead of assuming we know the answer already — because in this case, you’d be wrong.
I’m talking about this study, appearing in The New England Journal of Medicine.
It’s a prespecified secondary analysis of a randomized trial known as the TRAVERSE trial, which randomly assigned 5246 men with low testosterone levels to transdermal testosterone gel vs placebo. The primary goal of that trial was to assess the cardiovascular risk associated with testosterone supplementation, and the major take-home was that there was no difference in cardiovascular event rates between the testosterone and placebo groups.
This secondary analysis looked at fracture incidence. Researchers contacted participants multiple times in the first year of the study and yearly thereafter. Each time, they asked whether the participant had sustained a fracture. If they answered in the affirmative, a request for medical records was made and the researchers, still blinded to randomization status, adjudicated whether there was indeed a fracture or not, along with some details as to location, situation, and so on.
This was a big study, though, and that translates to just a 3.5% fracture rate in testosterone vs 2.5% in control, but the difference was statistically significant.
This difference persisted across various fracture types (non–high-impact fractures, for example) after excluding the small percentage of men taking osteoporosis medication.
How does a drug that increases bone mineral density and bone strength increase the risk for fracture?
Well, one clue — and this was pointed out in a nice editorial by Matthis Grossman and Bradley Anawalt — is that the increased risk for fracture occurs quite soon after starting treatment, which is not consistent with direct bone effects. Rather, this might represent behavioral differences. Testosterone supplementation seems to increase energy levels; might it lead men to engage in activities that put them at higher risk for fracture?
Regardless of the cause, this adds to our knowledge about the rather complex mix of risks and benefits of testosterone supplementation and probably puts a bit more weight on the risks side. The truth is that testosterone levels do decline with age, as do many things, and it may not be appropriate to try to fight against that in all people. It’s worth noting that all of these studies use low levels of total serum testosterone as an entry criterion. But total testosterone is not what your body “sees.” It sees free testosterone, the portion not bound to sex hormone–binding globulin. And that binding protein is affected by lots of stuff — diabetes and obesity lower it, for example — making total testosterone levels seem low when free testosterone might be just fine.
In other words, testosterone supplementation is probably not terrible, but it is definitely not the cure for aging. In situations like this, we need better data to guide exactly who will benefit from the therapy and who will only be exposed to the risks.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
I am showing you a graph without any labels.
What could this line represent? The stock price of some company that made a big splash but failed to live up to expectations? An outbreak curve charting the introduction of a new infectious agent to a population? The performance of a viral tweet?
I’ll tell you what it is in a moment, but I wanted you to recognize that there is something inherently wistful in this shape, something that speaks of past glory and inevitable declines. It’s a graph that induces a feeling of resistance — no, do not go gently into that good night.
The graph actually represents (roughly) the normal level of serum testosterone in otherwise-healthy men as they age.
A caveat here: These numbers are not as well defined as I made them seem on this graph, particularly for those older than 65 years. But it is clear that testosterone levels decline with time, and the idea to supplement testosterone is hardly new. Like all treatments, testosterone supplementation has risks and benefits. Some risks are predictable, like exacerbating the symptoms of benign prostatic hyperplasia. Some risks seem to come completely out of left field. That’s what we have today, in a study suggesting that testosterone supplementation increases the risk for bone fractures.
Let me set the stage here by saying that nearly all prior research into the effects of testosterone supplementation has suggested that it is pretty good for bone health. It increases bone mineral density, bone strength, and improves bone architecture.
So if you were to do a randomized trial of testosterone supplementation and look at fracture risk in the testosterone group compared with the placebo group, you would expect the fracture risk would be much lower in those getting supplemented. Of course, this is why we actually do studies instead of assuming we know the answer already — because in this case, you’d be wrong.
I’m talking about this study, appearing in The New England Journal of Medicine.
It’s a prespecified secondary analysis of a randomized trial known as the TRAVERSE trial, which randomly assigned 5246 men with low testosterone levels to transdermal testosterone gel vs placebo. The primary goal of that trial was to assess the cardiovascular risk associated with testosterone supplementation, and the major take-home was that there was no difference in cardiovascular event rates between the testosterone and placebo groups.
This secondary analysis looked at fracture incidence. Researchers contacted participants multiple times in the first year of the study and yearly thereafter. Each time, they asked whether the participant had sustained a fracture. If they answered in the affirmative, a request for medical records was made and the researchers, still blinded to randomization status, adjudicated whether there was indeed a fracture or not, along with some details as to location, situation, and so on.
This was a big study, though, and that translates to just a 3.5% fracture rate in testosterone vs 2.5% in control, but the difference was statistically significant.
This difference persisted across various fracture types (non–high-impact fractures, for example) after excluding the small percentage of men taking osteoporosis medication.
How does a drug that increases bone mineral density and bone strength increase the risk for fracture?
Well, one clue — and this was pointed out in a nice editorial by Matthis Grossman and Bradley Anawalt — is that the increased risk for fracture occurs quite soon after starting treatment, which is not consistent with direct bone effects. Rather, this might represent behavioral differences. Testosterone supplementation seems to increase energy levels; might it lead men to engage in activities that put them at higher risk for fracture?
Regardless of the cause, this adds to our knowledge about the rather complex mix of risks and benefits of testosterone supplementation and probably puts a bit more weight on the risks side. The truth is that testosterone levels do decline with age, as do many things, and it may not be appropriate to try to fight against that in all people. It’s worth noting that all of these studies use low levels of total serum testosterone as an entry criterion. But total testosterone is not what your body “sees.” It sees free testosterone, the portion not bound to sex hormone–binding globulin. And that binding protein is affected by lots of stuff — diabetes and obesity lower it, for example — making total testosterone levels seem low when free testosterone might be just fine.
In other words, testosterone supplementation is probably not terrible, but it is definitely not the cure for aging. In situations like this, we need better data to guide exactly who will benefit from the therapy and who will only be exposed to the risks.
Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Smoking Associated With Increased Risk for Hair Loss Among Men
, according to a new study.
In addition, the odds of developing AGA are higher among those who smoke at least 10 cigarettes per day than among those who smoke less, the study authors found.
“Men who smoke are more likely to develop and experience progression of male pattern hair loss,” lead author Aditya Gupta, MD, PhD, professor of medicine at the University of Toronto, Toronto, and director of clinical research at Mediprobe Research Inc., London, Ontario, Canada, told this news organization.
“Our patients with male pattern baldness need to be educated about the negative effects of smoking, given that this condition can have a profound negative psychological impact on those who suffer from it,” he said.
The study was published online in the Journal of Cosmetic Dermatology.
Analyzing Smoking’s Effects
Smoking generally has been accepted as a risk factor for the development and progression of AGA or the most common form of hair loss. The research evidence on this association has been inconsistent, however, the authors wrote.
The investigators conducted a review and meta-analysis of eight observational studies to understand the links between smoking and AGA. Ever-smokers were defined as current and former smokers.
Overall, based on six studies, men who have ever smoked are 1.8 times more likely (P < .05) to develop AGA.
Based on two studies, men who smoke 10 or more cigarettes daily are about twice as likely (P < .05) to develop AGA than those who smoke up to 10 cigarettes per day.
Based on four studies, ever smoking is associated with 1.3 times higher odds of AGA progressing from mild (ie, Norwood-Hamilton stages I-III) to more severe (stages IV-VII) than among those who have never smoked.
Based on two studies, there’s no association between AGA progression and smoking intensity (as defined as smoking up to 20 cigarettes daily vs smoking 20 or more cigarettes per day).
“Though our pooled analysis found no significant association between smoking intensity and severity of male AGA, a positive correlation may exist and be detected through an analysis that is statistically better powered,” said Dr. Gupta.
The investigators noted the limitations of their analysis, such as its reliance on observational studies and its lack of data about nicotine levels, smoking intensity, and smoking cessation among study participants.
Additional studies are needed to better understand the links between smoking and hair loss, said Dr. Gupta, as well as the effects of smoking cessation.
Improving Practice and Research
Commenting on the findings for this news organization, Arash Babadjouni, MD, a dermatologist at Midwestern University, Glendale, Arizona, said, “Smoking is not only a preventable cause of significant systemic disease but also affects the follicular growth cycle and fiber pigmentation. The prevalence of hair loss and premature hair graying is higher in smokers than nonsmokers.”
Dr. Babadjouni, who wasn’t involved with this study, has researched the associations between smoking and hair loss and premature hair graying.
“Evidence of this association can be used to clinically promote smoking cessation and emphasize the consequences of smoking on hair,” he said. “Smoking status should be assessed in patients who are presenting to their dermatologist and physicians alike for evaluation of alopecia and premature hair graying.”
The study was conducted without outside funding, and the authors declared no conflicts of interest. Dr. Babadjouni reported no relevant disclosures.
A version of this article appeared on Medscape.com.
, according to a new study.
In addition, the odds of developing AGA are higher among those who smoke at least 10 cigarettes per day than among those who smoke less, the study authors found.
“Men who smoke are more likely to develop and experience progression of male pattern hair loss,” lead author Aditya Gupta, MD, PhD, professor of medicine at the University of Toronto, Toronto, and director of clinical research at Mediprobe Research Inc., London, Ontario, Canada, told this news organization.
“Our patients with male pattern baldness need to be educated about the negative effects of smoking, given that this condition can have a profound negative psychological impact on those who suffer from it,” he said.
The study was published online in the Journal of Cosmetic Dermatology.
Analyzing Smoking’s Effects
Smoking generally has been accepted as a risk factor for the development and progression of AGA or the most common form of hair loss. The research evidence on this association has been inconsistent, however, the authors wrote.
The investigators conducted a review and meta-analysis of eight observational studies to understand the links between smoking and AGA. Ever-smokers were defined as current and former smokers.
Overall, based on six studies, men who have ever smoked are 1.8 times more likely (P < .05) to develop AGA.
Based on two studies, men who smoke 10 or more cigarettes daily are about twice as likely (P < .05) to develop AGA than those who smoke up to 10 cigarettes per day.
Based on four studies, ever smoking is associated with 1.3 times higher odds of AGA progressing from mild (ie, Norwood-Hamilton stages I-III) to more severe (stages IV-VII) than among those who have never smoked.
Based on two studies, there’s no association between AGA progression and smoking intensity (as defined as smoking up to 20 cigarettes daily vs smoking 20 or more cigarettes per day).
“Though our pooled analysis found no significant association between smoking intensity and severity of male AGA, a positive correlation may exist and be detected through an analysis that is statistically better powered,” said Dr. Gupta.
The investigators noted the limitations of their analysis, such as its reliance on observational studies and its lack of data about nicotine levels, smoking intensity, and smoking cessation among study participants.
Additional studies are needed to better understand the links between smoking and hair loss, said Dr. Gupta, as well as the effects of smoking cessation.
Improving Practice and Research
Commenting on the findings for this news organization, Arash Babadjouni, MD, a dermatologist at Midwestern University, Glendale, Arizona, said, “Smoking is not only a preventable cause of significant systemic disease but also affects the follicular growth cycle and fiber pigmentation. The prevalence of hair loss and premature hair graying is higher in smokers than nonsmokers.”
Dr. Babadjouni, who wasn’t involved with this study, has researched the associations between smoking and hair loss and premature hair graying.
“Evidence of this association can be used to clinically promote smoking cessation and emphasize the consequences of smoking on hair,” he said. “Smoking status should be assessed in patients who are presenting to their dermatologist and physicians alike for evaluation of alopecia and premature hair graying.”
The study was conducted without outside funding, and the authors declared no conflicts of interest. Dr. Babadjouni reported no relevant disclosures.
A version of this article appeared on Medscape.com.
, according to a new study.
In addition, the odds of developing AGA are higher among those who smoke at least 10 cigarettes per day than among those who smoke less, the study authors found.
“Men who smoke are more likely to develop and experience progression of male pattern hair loss,” lead author Aditya Gupta, MD, PhD, professor of medicine at the University of Toronto, Toronto, and director of clinical research at Mediprobe Research Inc., London, Ontario, Canada, told this news organization.
“Our patients with male pattern baldness need to be educated about the negative effects of smoking, given that this condition can have a profound negative psychological impact on those who suffer from it,” he said.
The study was published online in the Journal of Cosmetic Dermatology.
Analyzing Smoking’s Effects
Smoking generally has been accepted as a risk factor for the development and progression of AGA or the most common form of hair loss. The research evidence on this association has been inconsistent, however, the authors wrote.
The investigators conducted a review and meta-analysis of eight observational studies to understand the links between smoking and AGA. Ever-smokers were defined as current and former smokers.
Overall, based on six studies, men who have ever smoked are 1.8 times more likely (P < .05) to develop AGA.
Based on two studies, men who smoke 10 or more cigarettes daily are about twice as likely (P < .05) to develop AGA than those who smoke up to 10 cigarettes per day.
Based on four studies, ever smoking is associated with 1.3 times higher odds of AGA progressing from mild (ie, Norwood-Hamilton stages I-III) to more severe (stages IV-VII) than among those who have never smoked.
Based on two studies, there’s no association between AGA progression and smoking intensity (as defined as smoking up to 20 cigarettes daily vs smoking 20 or more cigarettes per day).
“Though our pooled analysis found no significant association between smoking intensity and severity of male AGA, a positive correlation may exist and be detected through an analysis that is statistically better powered,” said Dr. Gupta.
The investigators noted the limitations of their analysis, such as its reliance on observational studies and its lack of data about nicotine levels, smoking intensity, and smoking cessation among study participants.
Additional studies are needed to better understand the links between smoking and hair loss, said Dr. Gupta, as well as the effects of smoking cessation.
Improving Practice and Research
Commenting on the findings for this news organization, Arash Babadjouni, MD, a dermatologist at Midwestern University, Glendale, Arizona, said, “Smoking is not only a preventable cause of significant systemic disease but also affects the follicular growth cycle and fiber pigmentation. The prevalence of hair loss and premature hair graying is higher in smokers than nonsmokers.”
Dr. Babadjouni, who wasn’t involved with this study, has researched the associations between smoking and hair loss and premature hair graying.
“Evidence of this association can be used to clinically promote smoking cessation and emphasize the consequences of smoking on hair,” he said. “Smoking status should be assessed in patients who are presenting to their dermatologist and physicians alike for evaluation of alopecia and premature hair graying.”
The study was conducted without outside funding, and the authors declared no conflicts of interest. Dr. Babadjouni reported no relevant disclosures.
A version of this article appeared on Medscape.com.
FROM THE JOURNAL OF COSMETIC DERMATOLOGY
Prostate Risks Similar for Testosterone Therapy and Placebo
TOPLINE:
including cancer.
METHODOLOGY:
- Uncertainty and concern exist about a link between prostate cancer risk and testosterone levels. Most professional society guidelines recommend against TRT in men with a history of or an increased risk for prostate cancer.
- The Testosterone Replacement Therapy for Assessment of Long-Term Vascular Events and Efficacy Response in Hypogonadal Men included 5204 men (ages 45-80, 17% Black, 80% White), randomly assigned to receive testosterone gel or placebo.
- Men with a history of cardiovascular disease or increased cardiovascular risk were evaluated to exclude those at increased prostate cancer risk (fasting testosterone < 300 ng/dL, ≥ 1 hypogonadal symptoms).
- The primary prostate safety endpoint was high-grade prostate cancer incidence (Gleason score, ≥ 4 + 3).
- Secondary endpoints were incidences of any prostate cancer, acute urinary retention, invasive procedure for benign prostatic hyperplasia, prostate biopsy, and new pharmacologic treatment for lower urinary tract symptoms.
TAKEAWAY:
- During 14,304 person-years of follow-up, high-grade prostate cancer incidence did not differ significantly between the TRT and placebo (0.19% vs 0.12%; P = .51) groups.
- The incidences of prostate cancer, acute urinary retention, invasive procedures for benign prostatic hyperplasia, prostate biopsy, and new pharmacologic treatment for lower urinary tract symptoms were also similar between the groups.
- TRT did not lead to an increase in lower urinary tract symptoms.
- The increase in prostate-specific antigen (PSA) levels was higher in the TRT group than in the placebo group (P < .001). However, the between-group difference did not widen after 12 months.
IN PRACTICE:
For “clinicians and patients who are considering testosterone replacement therapy for hypogonadism,” wrote the authors, “the study’s findings will facilitate a more informed appraisal of the potential prostate risks of testosterone replacement therapy.”
SOURCE:
Shalender Bhasin, MB, BS, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, led the study. It was published online in JAMA Network Open.
LIMITATIONS:
- The study findings do not apply to men with known prostate cancer or higher PSA values or those without confirmed hypogonadism.
- Although the TRAVERSE study was longer than many contemporary trials, carcinogens may require many years to induce malignant neoplasms.
- The trial’s structured evaluation of men after PSA testing did not include prostate imaging or other biomarker tests, which could affect the decision to perform a biopsy.
DISCLOSURES:
This study was funded by a consortium of testosterone manufacturers led by AbbVie Inc with additional financial support from Endo Pharmaceuticals, Acerus Pharmaceuticals Corp, and Upsher-Smith Laboratories. Mr. Bhasin and two coauthors declared receiving grants, consulting and personal fees, and other ties with pharmaceutical and device companies and other sources.
A version of this article appeared on Medscape.com.
TOPLINE:
including cancer.
METHODOLOGY:
- Uncertainty and concern exist about a link between prostate cancer risk and testosterone levels. Most professional society guidelines recommend against TRT in men with a history of or an increased risk for prostate cancer.
- The Testosterone Replacement Therapy for Assessment of Long-Term Vascular Events and Efficacy Response in Hypogonadal Men included 5204 men (ages 45-80, 17% Black, 80% White), randomly assigned to receive testosterone gel or placebo.
- Men with a history of cardiovascular disease or increased cardiovascular risk were evaluated to exclude those at increased prostate cancer risk (fasting testosterone < 300 ng/dL, ≥ 1 hypogonadal symptoms).
- The primary prostate safety endpoint was high-grade prostate cancer incidence (Gleason score, ≥ 4 + 3).
- Secondary endpoints were incidences of any prostate cancer, acute urinary retention, invasive procedure for benign prostatic hyperplasia, prostate biopsy, and new pharmacologic treatment for lower urinary tract symptoms.
TAKEAWAY:
- During 14,304 person-years of follow-up, high-grade prostate cancer incidence did not differ significantly between the TRT and placebo (0.19% vs 0.12%; P = .51) groups.
- The incidences of prostate cancer, acute urinary retention, invasive procedures for benign prostatic hyperplasia, prostate biopsy, and new pharmacologic treatment for lower urinary tract symptoms were also similar between the groups.
- TRT did not lead to an increase in lower urinary tract symptoms.
- The increase in prostate-specific antigen (PSA) levels was higher in the TRT group than in the placebo group (P < .001). However, the between-group difference did not widen after 12 months.
IN PRACTICE:
For “clinicians and patients who are considering testosterone replacement therapy for hypogonadism,” wrote the authors, “the study’s findings will facilitate a more informed appraisal of the potential prostate risks of testosterone replacement therapy.”
SOURCE:
Shalender Bhasin, MB, BS, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, led the study. It was published online in JAMA Network Open.
LIMITATIONS:
- The study findings do not apply to men with known prostate cancer or higher PSA values or those without confirmed hypogonadism.
- Although the TRAVERSE study was longer than many contemporary trials, carcinogens may require many years to induce malignant neoplasms.
- The trial’s structured evaluation of men after PSA testing did not include prostate imaging or other biomarker tests, which could affect the decision to perform a biopsy.
DISCLOSURES:
This study was funded by a consortium of testosterone manufacturers led by AbbVie Inc with additional financial support from Endo Pharmaceuticals, Acerus Pharmaceuticals Corp, and Upsher-Smith Laboratories. Mr. Bhasin and two coauthors declared receiving grants, consulting and personal fees, and other ties with pharmaceutical and device companies and other sources.
A version of this article appeared on Medscape.com.
TOPLINE:
including cancer.
METHODOLOGY:
- Uncertainty and concern exist about a link between prostate cancer risk and testosterone levels. Most professional society guidelines recommend against TRT in men with a history of or an increased risk for prostate cancer.
- The Testosterone Replacement Therapy for Assessment of Long-Term Vascular Events and Efficacy Response in Hypogonadal Men included 5204 men (ages 45-80, 17% Black, 80% White), randomly assigned to receive testosterone gel or placebo.
- Men with a history of cardiovascular disease or increased cardiovascular risk were evaluated to exclude those at increased prostate cancer risk (fasting testosterone < 300 ng/dL, ≥ 1 hypogonadal symptoms).
- The primary prostate safety endpoint was high-grade prostate cancer incidence (Gleason score, ≥ 4 + 3).
- Secondary endpoints were incidences of any prostate cancer, acute urinary retention, invasive procedure for benign prostatic hyperplasia, prostate biopsy, and new pharmacologic treatment for lower urinary tract symptoms.
TAKEAWAY:
- During 14,304 person-years of follow-up, high-grade prostate cancer incidence did not differ significantly between the TRT and placebo (0.19% vs 0.12%; P = .51) groups.
- The incidences of prostate cancer, acute urinary retention, invasive procedures for benign prostatic hyperplasia, prostate biopsy, and new pharmacologic treatment for lower urinary tract symptoms were also similar between the groups.
- TRT did not lead to an increase in lower urinary tract symptoms.
- The increase in prostate-specific antigen (PSA) levels was higher in the TRT group than in the placebo group (P < .001). However, the between-group difference did not widen after 12 months.
IN PRACTICE:
For “clinicians and patients who are considering testosterone replacement therapy for hypogonadism,” wrote the authors, “the study’s findings will facilitate a more informed appraisal of the potential prostate risks of testosterone replacement therapy.”
SOURCE:
Shalender Bhasin, MB, BS, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, led the study. It was published online in JAMA Network Open.
LIMITATIONS:
- The study findings do not apply to men with known prostate cancer or higher PSA values or those without confirmed hypogonadism.
- Although the TRAVERSE study was longer than many contemporary trials, carcinogens may require many years to induce malignant neoplasms.
- The trial’s structured evaluation of men after PSA testing did not include prostate imaging or other biomarker tests, which could affect the decision to perform a biopsy.
DISCLOSURES:
This study was funded by a consortium of testosterone manufacturers led by AbbVie Inc with additional financial support from Endo Pharmaceuticals, Acerus Pharmaceuticals Corp, and Upsher-Smith Laboratories. Mr. Bhasin and two coauthors declared receiving grants, consulting and personal fees, and other ties with pharmaceutical and device companies and other sources.
A version of this article appeared on Medscape.com.