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MedPAC to look at physician prescribing tools as a way to control drug spending
WASHINGTON – The Medicare Payment Advisory Commission is going to look at physician prescribing tools as part of a broader examination of how to rein in Medicare drug spending.
Members acknowledged during the Sept. 11, 2015, meeting that when it comes to the prices of drugs in the Medicare programs, the tools are limited to keep the prices low. Between statutory requirements for coverage of drugs in protected classes and a prohibition against the secretary of Health and Human Services negotiating prices for the Part D prescription drug benefit and other statutory requirements, even for intermediaries such as plan providers and hospital groups, leverage in price negotiations is very limited.
However, commission member Dr. Craig Samitt, former partner at Oliver Wyman of Paradise Valley, Ariz., suggested that the focus should be more on what leverage providers might have when it comes to utilization.
“So if we feel that neither CMS nor the intermediaries have sufficient leverage, well then who has significant leverage? The prescribing clinician,” Dr. Samitt said. “How well have we aligned interests around utilization in particular, not so much price, with the clinicians?”
Dr. Samitt noted that on the commercial side, there is a focus on utilization as a more effective driver of price, rather than simply targeting price first in the negotiation process, and suggested there might be room in Medicare for that kind of focus.
He also suggested that perhaps including drug utilization within the context of accountable care organizations could result in “additional focus on more effective prescribing patterns.”
The conversation occurred against a backdrop of examination of drug spending in general. MedPAC staff noted that Medicare is becoming a more prominent payer for drugs in the wake of Part D’s launch.
MedPAC staff estimates that in 2013, retail drugs made up 13% of Medicare spending, versus 9% of national health expenditures. Additionally, of the $574 billion spent by Medicare in that year, 19% was drugs and pharmacy, with the majority of drug spending (57%) coming from Part D.
The discussion was just the first on the subject as the group will look at other aspects of drug pricing and spending in future meetings. A specific timetable for offering policy recommendations was not discussed.
Dr. William Hall, professor at the University of Rochester (N.Y.) School of Medicine, added that it is not the price of the drug per se, but its value that needs to be focused on. He noted that the prices of the latest hepatitis C drugs might be high, but the value they have to the health care system is much greater and needs to be taken into consideration.
“One of the big differences from 2004 is we know a great deal more about the efficacy of drugs,” Dr. Hall said, suggesting that more needs to be done to educate clinicians on the proper use of medications as part of finding the right way to use physician prescribing patterns as leverage in price negotiations.
WASHINGTON – The Medicare Payment Advisory Commission is going to look at physician prescribing tools as part of a broader examination of how to rein in Medicare drug spending.
Members acknowledged during the Sept. 11, 2015, meeting that when it comes to the prices of drugs in the Medicare programs, the tools are limited to keep the prices low. Between statutory requirements for coverage of drugs in protected classes and a prohibition against the secretary of Health and Human Services negotiating prices for the Part D prescription drug benefit and other statutory requirements, even for intermediaries such as plan providers and hospital groups, leverage in price negotiations is very limited.
However, commission member Dr. Craig Samitt, former partner at Oliver Wyman of Paradise Valley, Ariz., suggested that the focus should be more on what leverage providers might have when it comes to utilization.
“So if we feel that neither CMS nor the intermediaries have sufficient leverage, well then who has significant leverage? The prescribing clinician,” Dr. Samitt said. “How well have we aligned interests around utilization in particular, not so much price, with the clinicians?”
Dr. Samitt noted that on the commercial side, there is a focus on utilization as a more effective driver of price, rather than simply targeting price first in the negotiation process, and suggested there might be room in Medicare for that kind of focus.
He also suggested that perhaps including drug utilization within the context of accountable care organizations could result in “additional focus on more effective prescribing patterns.”
The conversation occurred against a backdrop of examination of drug spending in general. MedPAC staff noted that Medicare is becoming a more prominent payer for drugs in the wake of Part D’s launch.
MedPAC staff estimates that in 2013, retail drugs made up 13% of Medicare spending, versus 9% of national health expenditures. Additionally, of the $574 billion spent by Medicare in that year, 19% was drugs and pharmacy, with the majority of drug spending (57%) coming from Part D.
The discussion was just the first on the subject as the group will look at other aspects of drug pricing and spending in future meetings. A specific timetable for offering policy recommendations was not discussed.
Dr. William Hall, professor at the University of Rochester (N.Y.) School of Medicine, added that it is not the price of the drug per se, but its value that needs to be focused on. He noted that the prices of the latest hepatitis C drugs might be high, but the value they have to the health care system is much greater and needs to be taken into consideration.
“One of the big differences from 2004 is we know a great deal more about the efficacy of drugs,” Dr. Hall said, suggesting that more needs to be done to educate clinicians on the proper use of medications as part of finding the right way to use physician prescribing patterns as leverage in price negotiations.
WASHINGTON – The Medicare Payment Advisory Commission is going to look at physician prescribing tools as part of a broader examination of how to rein in Medicare drug spending.
Members acknowledged during the Sept. 11, 2015, meeting that when it comes to the prices of drugs in the Medicare programs, the tools are limited to keep the prices low. Between statutory requirements for coverage of drugs in protected classes and a prohibition against the secretary of Health and Human Services negotiating prices for the Part D prescription drug benefit and other statutory requirements, even for intermediaries such as plan providers and hospital groups, leverage in price negotiations is very limited.
However, commission member Dr. Craig Samitt, former partner at Oliver Wyman of Paradise Valley, Ariz., suggested that the focus should be more on what leverage providers might have when it comes to utilization.
“So if we feel that neither CMS nor the intermediaries have sufficient leverage, well then who has significant leverage? The prescribing clinician,” Dr. Samitt said. “How well have we aligned interests around utilization in particular, not so much price, with the clinicians?”
Dr. Samitt noted that on the commercial side, there is a focus on utilization as a more effective driver of price, rather than simply targeting price first in the negotiation process, and suggested there might be room in Medicare for that kind of focus.
He also suggested that perhaps including drug utilization within the context of accountable care organizations could result in “additional focus on more effective prescribing patterns.”
The conversation occurred against a backdrop of examination of drug spending in general. MedPAC staff noted that Medicare is becoming a more prominent payer for drugs in the wake of Part D’s launch.
MedPAC staff estimates that in 2013, retail drugs made up 13% of Medicare spending, versus 9% of national health expenditures. Additionally, of the $574 billion spent by Medicare in that year, 19% was drugs and pharmacy, with the majority of drug spending (57%) coming from Part D.
The discussion was just the first on the subject as the group will look at other aspects of drug pricing and spending in future meetings. A specific timetable for offering policy recommendations was not discussed.
Dr. William Hall, professor at the University of Rochester (N.Y.) School of Medicine, added that it is not the price of the drug per se, but its value that needs to be focused on. He noted that the prices of the latest hepatitis C drugs might be high, but the value they have to the health care system is much greater and needs to be taken into consideration.
“One of the big differences from 2004 is we know a great deal more about the efficacy of drugs,” Dr. Hall said, suggesting that more needs to be done to educate clinicians on the proper use of medications as part of finding the right way to use physician prescribing patterns as leverage in price negotiations.
AT A MEETING OF THE MEDICARE PAYMENT ADVISORY COMMISSION
Metronidazole and alcohol
A 32-year-old man develops diarrhea after receiving amoxicillin/clavulanate to treat an infection following a dog bite. He is diagnosed with Clostridium difficile and prescribed a 10-day course of metronidazole. He has no other medical problems. He will be the best man at his brother’s wedding tomorrow. What advice should you give him about alcohol use at the reception?
A. Do not take metronidazole the day of the wedding if you will be drinking alcohol.
B. Take metronidazole, do not drink alcohol.
C. It’s okay to drink alcohol.
For years, we have advised patients to not use alcohol if they are taking metronidazole because of concern for a disulfiram-like reaction between alcohol and metronidazole. This has been a standard warning given by physicians and appears as a contraindication in the prescribing information. It has been well accepted as a true, proven reaction.
Is it true?
As early as the 1960s, case reports and an uncontrolled study suggested that combining metronidazole with alcohol produced a disulfiram-like reaction, with case reports of severe reactions, including death.1, 2, 3 This was initially considered an area that might be therapeutic in the treatment of alcoholism, but several studies showed no benefit.4, 5
Caroline S. Williams and Dr. Kevin R. Woodcock reviewed the case reports for evidence of proof of a true interaction between metronidazole and ethanol.6 The case reports referenced textbooks to substantiate the interaction, but they did not present clear evidence of an interaction as the cause of elevated acetaldehyde levels.
Researchers have shown in a rat model that metronidazole can increase intracolonic, but not blood, acetaldehyde levels in rats that have received a combination of ethanol and metronidazole.7 Metronidazole did not have any inhibitory effect on hepatic or colonic alcohol dehydrogenase or aldehyde dehydrogenase. What was found was that rats treated with metronidazole had increased growth of Enterobacteriaceae, an alcohol dehydrogenase–containing aerobe, which could be the cause of the higher intracolonic acetaldehyde levels.
Jukka-Pekka Visapää and his colleagues studied the effect of coadministration of metronidazole and ethanol in young, healthy male volunteers.8 The study was a placebo-controlled, randomized trial. The study was small, with 12 participants. One-half of the study participants received metronidazole three times a day for 5 days; the other half received placebo. All participants then received ethanol 0.4g/kg, with blood testing being done every 20 minutes for the next 4 hours. Blood was tested for ethanol concentrations and for acetaldehyde levels. The study participants also had blood pressure, pulse, skin temperature, and symptoms monitored during the study.
There was no difference in blood acetaldehyde levels, vital signs, or symptoms between patients who received metronidazole or placebo. None of the subjects in the study had any measurable symptoms.
Metronidazole has many side effects, including nausea, vomiting, headache, dizziness, and seizures. These symptoms have a great deal of overlap with the symptoms of alcohol-disulfiram interaction. It has been assumed in early case reports that metronidazole caused a similar interaction with alcohol and raised acetaldehyde levels by interfering with aldehyde dehydrogenase.
Animal models and the human study do not show this to be the case. It is possible that metronidazole side effects alone were the cause of the symptoms in case reports. The one human study done was on healthy male volunteers, so projecting the results to a population with liver disease or other serious illness is a bit of a stretch. I think that if a problem exists with alcohol and metronidazole, it is uncommon and unlikely to occur in healthy individuals.
So, what would I advise the patient in the case about whether he can drink alcohol? I think that the risk would be minimal and that it would be safe for him to drink alcohol.
References
1. Br J Clin Pract. 1985 Jul;39(7):292-3.
2. Psychiatr Neurol. 1966;152:395-401.
3. Am J Forensic Med Pathol. 1996 Dec;17(4):343-6.
4. Q J Stud Alcohol. 1972 Sep;33: 734-40.
5. Q J Stud Ethanol. 1969 Mar;30: 140-51.
6. Ann Pharmacother. 2000 Feb;34(2):255-7.
7. Alcohol Clin Exp Res. 2000 Apr;24(4):570-5.
8. Ann Pharmacother. 2002 Jun;36(6):971-4.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.
A 32-year-old man develops diarrhea after receiving amoxicillin/clavulanate to treat an infection following a dog bite. He is diagnosed with Clostridium difficile and prescribed a 10-day course of metronidazole. He has no other medical problems. He will be the best man at his brother’s wedding tomorrow. What advice should you give him about alcohol use at the reception?
A. Do not take metronidazole the day of the wedding if you will be drinking alcohol.
B. Take metronidazole, do not drink alcohol.
C. It’s okay to drink alcohol.
For years, we have advised patients to not use alcohol if they are taking metronidazole because of concern for a disulfiram-like reaction between alcohol and metronidazole. This has been a standard warning given by physicians and appears as a contraindication in the prescribing information. It has been well accepted as a true, proven reaction.
Is it true?
As early as the 1960s, case reports and an uncontrolled study suggested that combining metronidazole with alcohol produced a disulfiram-like reaction, with case reports of severe reactions, including death.1, 2, 3 This was initially considered an area that might be therapeutic in the treatment of alcoholism, but several studies showed no benefit.4, 5
Caroline S. Williams and Dr. Kevin R. Woodcock reviewed the case reports for evidence of proof of a true interaction between metronidazole and ethanol.6 The case reports referenced textbooks to substantiate the interaction, but they did not present clear evidence of an interaction as the cause of elevated acetaldehyde levels.
Researchers have shown in a rat model that metronidazole can increase intracolonic, but not blood, acetaldehyde levels in rats that have received a combination of ethanol and metronidazole.7 Metronidazole did not have any inhibitory effect on hepatic or colonic alcohol dehydrogenase or aldehyde dehydrogenase. What was found was that rats treated with metronidazole had increased growth of Enterobacteriaceae, an alcohol dehydrogenase–containing aerobe, which could be the cause of the higher intracolonic acetaldehyde levels.
Jukka-Pekka Visapää and his colleagues studied the effect of coadministration of metronidazole and ethanol in young, healthy male volunteers.8 The study was a placebo-controlled, randomized trial. The study was small, with 12 participants. One-half of the study participants received metronidazole three times a day for 5 days; the other half received placebo. All participants then received ethanol 0.4g/kg, with blood testing being done every 20 minutes for the next 4 hours. Blood was tested for ethanol concentrations and for acetaldehyde levels. The study participants also had blood pressure, pulse, skin temperature, and symptoms monitored during the study.
There was no difference in blood acetaldehyde levels, vital signs, or symptoms between patients who received metronidazole or placebo. None of the subjects in the study had any measurable symptoms.
Metronidazole has many side effects, including nausea, vomiting, headache, dizziness, and seizures. These symptoms have a great deal of overlap with the symptoms of alcohol-disulfiram interaction. It has been assumed in early case reports that metronidazole caused a similar interaction with alcohol and raised acetaldehyde levels by interfering with aldehyde dehydrogenase.
Animal models and the human study do not show this to be the case. It is possible that metronidazole side effects alone were the cause of the symptoms in case reports. The one human study done was on healthy male volunteers, so projecting the results to a population with liver disease or other serious illness is a bit of a stretch. I think that if a problem exists with alcohol and metronidazole, it is uncommon and unlikely to occur in healthy individuals.
So, what would I advise the patient in the case about whether he can drink alcohol? I think that the risk would be minimal and that it would be safe for him to drink alcohol.
References
1. Br J Clin Pract. 1985 Jul;39(7):292-3.
2. Psychiatr Neurol. 1966;152:395-401.
3. Am J Forensic Med Pathol. 1996 Dec;17(4):343-6.
4. Q J Stud Alcohol. 1972 Sep;33: 734-40.
5. Q J Stud Ethanol. 1969 Mar;30: 140-51.
6. Ann Pharmacother. 2000 Feb;34(2):255-7.
7. Alcohol Clin Exp Res. 2000 Apr;24(4):570-5.
8. Ann Pharmacother. 2002 Jun;36(6):971-4.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.
A 32-year-old man develops diarrhea after receiving amoxicillin/clavulanate to treat an infection following a dog bite. He is diagnosed with Clostridium difficile and prescribed a 10-day course of metronidazole. He has no other medical problems. He will be the best man at his brother’s wedding tomorrow. What advice should you give him about alcohol use at the reception?
A. Do not take metronidazole the day of the wedding if you will be drinking alcohol.
B. Take metronidazole, do not drink alcohol.
C. It’s okay to drink alcohol.
For years, we have advised patients to not use alcohol if they are taking metronidazole because of concern for a disulfiram-like reaction between alcohol and metronidazole. This has been a standard warning given by physicians and appears as a contraindication in the prescribing information. It has been well accepted as a true, proven reaction.
Is it true?
As early as the 1960s, case reports and an uncontrolled study suggested that combining metronidazole with alcohol produced a disulfiram-like reaction, with case reports of severe reactions, including death.1, 2, 3 This was initially considered an area that might be therapeutic in the treatment of alcoholism, but several studies showed no benefit.4, 5
Caroline S. Williams and Dr. Kevin R. Woodcock reviewed the case reports for evidence of proof of a true interaction between metronidazole and ethanol.6 The case reports referenced textbooks to substantiate the interaction, but they did not present clear evidence of an interaction as the cause of elevated acetaldehyde levels.
Researchers have shown in a rat model that metronidazole can increase intracolonic, but not blood, acetaldehyde levels in rats that have received a combination of ethanol and metronidazole.7 Metronidazole did not have any inhibitory effect on hepatic or colonic alcohol dehydrogenase or aldehyde dehydrogenase. What was found was that rats treated with metronidazole had increased growth of Enterobacteriaceae, an alcohol dehydrogenase–containing aerobe, which could be the cause of the higher intracolonic acetaldehyde levels.
Jukka-Pekka Visapää and his colleagues studied the effect of coadministration of metronidazole and ethanol in young, healthy male volunteers.8 The study was a placebo-controlled, randomized trial. The study was small, with 12 participants. One-half of the study participants received metronidazole three times a day for 5 days; the other half received placebo. All participants then received ethanol 0.4g/kg, with blood testing being done every 20 minutes for the next 4 hours. Blood was tested for ethanol concentrations and for acetaldehyde levels. The study participants also had blood pressure, pulse, skin temperature, and symptoms monitored during the study.
There was no difference in blood acetaldehyde levels, vital signs, or symptoms between patients who received metronidazole or placebo. None of the subjects in the study had any measurable symptoms.
Metronidazole has many side effects, including nausea, vomiting, headache, dizziness, and seizures. These symptoms have a great deal of overlap with the symptoms of alcohol-disulfiram interaction. It has been assumed in early case reports that metronidazole caused a similar interaction with alcohol and raised acetaldehyde levels by interfering with aldehyde dehydrogenase.
Animal models and the human study do not show this to be the case. It is possible that metronidazole side effects alone were the cause of the symptoms in case reports. The one human study done was on healthy male volunteers, so projecting the results to a population with liver disease or other serious illness is a bit of a stretch. I think that if a problem exists with alcohol and metronidazole, it is uncommon and unlikely to occur in healthy individuals.
So, what would I advise the patient in the case about whether he can drink alcohol? I think that the risk would be minimal and that it would be safe for him to drink alcohol.
References
1. Br J Clin Pract. 1985 Jul;39(7):292-3.
2. Psychiatr Neurol. 1966;152:395-401.
3. Am J Forensic Med Pathol. 1996 Dec;17(4):343-6.
4. Q J Stud Alcohol. 1972 Sep;33: 734-40.
5. Q J Stud Ethanol. 1969 Mar;30: 140-51.
6. Ann Pharmacother. 2000 Feb;34(2):255-7.
7. Alcohol Clin Exp Res. 2000 Apr;24(4):570-5.
8. Ann Pharmacother. 2002 Jun;36(6):971-4.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.
E-cigarette Smokers Less Exposed to Carbon Monoxide
NEW YORK—Smokers who switch to e-cigarettes - even if only some of the time - may dramatically reduce their exposure to air pollutants including carbon monoxide and acrolein, a British study suggests.
Researchers gave e-cigarettes to 40 smokers who said they wanted to quit. After four weeks, the 16 participants using only e-cigarettes had about an 80% drop in exposure both to carbon monoxide and to acrolein, a harmful breakdown product that is also in some e-cigarettes' vapor. Acrolein is known to irritate exposed tissues and can destroy cilia.
The 17 participants who swapped some regular cigarettes for the electronic version had a 52% decline in carbon monoxide exposure and a 60% decline for acrolein, according to a report online September 3 in Cancer Prevention Research.
To get the most benefit from switching to e-cigarettes, smokers need to completely give up traditional cigarettes, lead study author Dr. Hayden McRobbie, of the Wolfson Institute of Preventive Medicine at Queen Mary University of London, said by email.
"Smokers may get some encouragement from the finding that there is some potential health benefit as soon as they start the process," Dr. McRobbie said.
While tobacco control advocates fear that e-cigarettes may give rise to a new generation of nicotine addicts who eventually transition to conventional cigarettes, the current study adds to a small but growing body of evidence suggesting the devices might benefit the health of people who already smoke.
An international analysis of published research by the Cochrane Review in December concluded the devices could help smokers quit but said much of the existing research on e-cigarettes was thin.
Even though the current study points to another potential benefit of e-cigarettes, more evidence is still needed from longer and larger trials before scientists can draw firm conclusions about any safety advantages, Dr. Nancy Rigotti, director of tobacco research at Massachusetts General Hospital in Boston, said by email.
"It is exactly the type of incremental, careful work that is needed but it is not yet a definitive study," Rigotti, who wasn't involved in the study, said.
Study participants were typically in their 40s and had attempted to quit at least twice before joining the trial. All of them were offered the same type of e-cigarette and encouraged to completely abandon traditional cigarettes.
Researchers measured carbon monoxide in participants' breath one week before switching to e-cigarettes, on the day they switched, and again four weeks later. They followed the same schedule for testing urine for exposure to acrolein.
A limitation of the study, the authors acknowledged, is that it only included people with a desire to quit smoking, making it possible the results would be different for smokers with no intention of quitting. It's also possible that the specific model of e-cigarette used in the study might not be representative of other devices.
Still, the findings suggest smokers should be told e-cigarettes may curb their exposure to toxic chemicals, Dr. Riccardo Polosa, head of the tobacco research center at the University of Catania in Italy, said by email.
"This study adds to the evidence that e-cigarettes are much less harmful compared to conventional cigarettes," said Polosa, who wasn't involved in the study.
NEW YORK—Smokers who switch to e-cigarettes - even if only some of the time - may dramatically reduce their exposure to air pollutants including carbon monoxide and acrolein, a British study suggests.
Researchers gave e-cigarettes to 40 smokers who said they wanted to quit. After four weeks, the 16 participants using only e-cigarettes had about an 80% drop in exposure both to carbon monoxide and to acrolein, a harmful breakdown product that is also in some e-cigarettes' vapor. Acrolein is known to irritate exposed tissues and can destroy cilia.
The 17 participants who swapped some regular cigarettes for the electronic version had a 52% decline in carbon monoxide exposure and a 60% decline for acrolein, according to a report online September 3 in Cancer Prevention Research.
To get the most benefit from switching to e-cigarettes, smokers need to completely give up traditional cigarettes, lead study author Dr. Hayden McRobbie, of the Wolfson Institute of Preventive Medicine at Queen Mary University of London, said by email.
"Smokers may get some encouragement from the finding that there is some potential health benefit as soon as they start the process," Dr. McRobbie said.
While tobacco control advocates fear that e-cigarettes may give rise to a new generation of nicotine addicts who eventually transition to conventional cigarettes, the current study adds to a small but growing body of evidence suggesting the devices might benefit the health of people who already smoke.
An international analysis of published research by the Cochrane Review in December concluded the devices could help smokers quit but said much of the existing research on e-cigarettes was thin.
Even though the current study points to another potential benefit of e-cigarettes, more evidence is still needed from longer and larger trials before scientists can draw firm conclusions about any safety advantages, Dr. Nancy Rigotti, director of tobacco research at Massachusetts General Hospital in Boston, said by email.
"It is exactly the type of incremental, careful work that is needed but it is not yet a definitive study," Rigotti, who wasn't involved in the study, said.
Study participants were typically in their 40s and had attempted to quit at least twice before joining the trial. All of them were offered the same type of e-cigarette and encouraged to completely abandon traditional cigarettes.
Researchers measured carbon monoxide in participants' breath one week before switching to e-cigarettes, on the day they switched, and again four weeks later. They followed the same schedule for testing urine for exposure to acrolein.
A limitation of the study, the authors acknowledged, is that it only included people with a desire to quit smoking, making it possible the results would be different for smokers with no intention of quitting. It's also possible that the specific model of e-cigarette used in the study might not be representative of other devices.
Still, the findings suggest smokers should be told e-cigarettes may curb their exposure to toxic chemicals, Dr. Riccardo Polosa, head of the tobacco research center at the University of Catania in Italy, said by email.
"This study adds to the evidence that e-cigarettes are much less harmful compared to conventional cigarettes," said Polosa, who wasn't involved in the study.
NEW YORK—Smokers who switch to e-cigarettes - even if only some of the time - may dramatically reduce their exposure to air pollutants including carbon monoxide and acrolein, a British study suggests.
Researchers gave e-cigarettes to 40 smokers who said they wanted to quit. After four weeks, the 16 participants using only e-cigarettes had about an 80% drop in exposure both to carbon monoxide and to acrolein, a harmful breakdown product that is also in some e-cigarettes' vapor. Acrolein is known to irritate exposed tissues and can destroy cilia.
The 17 participants who swapped some regular cigarettes for the electronic version had a 52% decline in carbon monoxide exposure and a 60% decline for acrolein, according to a report online September 3 in Cancer Prevention Research.
To get the most benefit from switching to e-cigarettes, smokers need to completely give up traditional cigarettes, lead study author Dr. Hayden McRobbie, of the Wolfson Institute of Preventive Medicine at Queen Mary University of London, said by email.
"Smokers may get some encouragement from the finding that there is some potential health benefit as soon as they start the process," Dr. McRobbie said.
While tobacco control advocates fear that e-cigarettes may give rise to a new generation of nicotine addicts who eventually transition to conventional cigarettes, the current study adds to a small but growing body of evidence suggesting the devices might benefit the health of people who already smoke.
An international analysis of published research by the Cochrane Review in December concluded the devices could help smokers quit but said much of the existing research on e-cigarettes was thin.
Even though the current study points to another potential benefit of e-cigarettes, more evidence is still needed from longer and larger trials before scientists can draw firm conclusions about any safety advantages, Dr. Nancy Rigotti, director of tobacco research at Massachusetts General Hospital in Boston, said by email.
"It is exactly the type of incremental, careful work that is needed but it is not yet a definitive study," Rigotti, who wasn't involved in the study, said.
Study participants were typically in their 40s and had attempted to quit at least twice before joining the trial. All of them were offered the same type of e-cigarette and encouraged to completely abandon traditional cigarettes.
Researchers measured carbon monoxide in participants' breath one week before switching to e-cigarettes, on the day they switched, and again four weeks later. They followed the same schedule for testing urine for exposure to acrolein.
A limitation of the study, the authors acknowledged, is that it only included people with a desire to quit smoking, making it possible the results would be different for smokers with no intention of quitting. It's also possible that the specific model of e-cigarette used in the study might not be representative of other devices.
Still, the findings suggest smokers should be told e-cigarettes may curb their exposure to toxic chemicals, Dr. Riccardo Polosa, head of the tobacco research center at the University of Catania in Italy, said by email.
"This study adds to the evidence that e-cigarettes are much less harmful compared to conventional cigarettes," said Polosa, who wasn't involved in the study.
Social factors may impact survival in AML
Photo by Rhoda Baer
A new study indicates that certain social factors may impact survival in adults with acute myelogenous leukemia (AML) who are under 65.
The research showed associations between patient survival and insurance status, marital status, and county-level income.
“We believe these 3 factors indicate lack of material and social support preventing young patients from successfully walking the long and difficult road towards a cure,” said Uma Borate, MD, of the University of Alabama at Birmingham.
To conduct this study, Dr Borate and her colleagues analyzed data on 5541 patients, ages 19 to 64, who were diagnosed with AML between 2007 and 2011.
The team reported their findings in Cancer.
Multivariable analysis showed that AML subtype, age, and sex were independently associated with patients’ survival. And the non-biological factors independently associated with survival were insurance status, marital status, and county-level median household income.
Specifically, there was a significantly increased risk of premature death among patients who were uninsured (P=0.005) or Medicaid beneficiaries (P<0.001), compared to patients with private insurance.
Single (P<0.001) or divorced (P=0.011) patients had a significantly higher risk of premature death than married patients. But there was no significant difference between married and widowed patients (P=0.206).
And patients who lived in areas with lower income—the lowest 3 of 5 income groups—had a significantly increased risk of premature death.
Compared to patients in the fifth income quintile ($58.3K-$79.9K), there was an increased risk of death in the first quintile ($16.2K-$38.8K, P=0.001), second quintile ($38.8K-$42.2K, P<0.001), and third quintile ($42.2K-$47.9K, P<0.001).
Early and late mortality
The researchers wanted to determine if the impact of non-biological factors on survival was related to early mortality (a possible surrogate for access to care or late presentation) or late mortality (a possible surrogate for access to post-remission therapy and hematopoietic stem cell transplant).
So they conducted an exploratory analysis of factors influencing the risk of death within the first 2 months of diagnosis.
Being a Medicaid beneficiary (P=0.01) or uninsured (P<0.001) was independently associated with an increased risk of death within the first 2 months.
The same was true for patients belonging to the first income quartile (P=0.001), second quartile (P=0.003), third quartile (P=0.02), and fourth quartile (P=0.028).
On the other hand, there was no significant difference in early death according to marital status.
The researchers also performed a landmark survival analysis including only patients who survived at least 2 months from diagnosis.
In this analysis, marital status (P<0.001), insurance status (P=0.001), and income (P=0.021) were all independent predictors of survival.
Implications
“As physicians, we often emphasize more of the biology of the cancer, especially with the recent focus on personalized medicine,” said study author Luciano Jose Costa, MD, PhD, also of the University of Alabama at Birmingham.
“But we need to pay the same attention to resources available to our patients, as this greatly impacts their chances to survive leukemia.”
The researchers believe this will be especially important as the US transitions to a healthcare system that ties physician and hospital payments to patient outcomes.
“Taking from the results of this study, factors that have nothing to do with quality of care need to be accounted for when comparing predicted with actual outcomes,” Dr Borate said. “Otherwise, we will create a disincentive for hospitals and doctors to care for less privileged patients.” 
Photo by Rhoda Baer
A new study indicates that certain social factors may impact survival in adults with acute myelogenous leukemia (AML) who are under 65.
The research showed associations between patient survival and insurance status, marital status, and county-level income.
“We believe these 3 factors indicate lack of material and social support preventing young patients from successfully walking the long and difficult road towards a cure,” said Uma Borate, MD, of the University of Alabama at Birmingham.
To conduct this study, Dr Borate and her colleagues analyzed data on 5541 patients, ages 19 to 64, who were diagnosed with AML between 2007 and 2011.
The team reported their findings in Cancer.
Multivariable analysis showed that AML subtype, age, and sex were independently associated with patients’ survival. And the non-biological factors independently associated with survival were insurance status, marital status, and county-level median household income.
Specifically, there was a significantly increased risk of premature death among patients who were uninsured (P=0.005) or Medicaid beneficiaries (P<0.001), compared to patients with private insurance.
Single (P<0.001) or divorced (P=0.011) patients had a significantly higher risk of premature death than married patients. But there was no significant difference between married and widowed patients (P=0.206).
And patients who lived in areas with lower income—the lowest 3 of 5 income groups—had a significantly increased risk of premature death.
Compared to patients in the fifth income quintile ($58.3K-$79.9K), there was an increased risk of death in the first quintile ($16.2K-$38.8K, P=0.001), second quintile ($38.8K-$42.2K, P<0.001), and third quintile ($42.2K-$47.9K, P<0.001).
Early and late mortality
The researchers wanted to determine if the impact of non-biological factors on survival was related to early mortality (a possible surrogate for access to care or late presentation) or late mortality (a possible surrogate for access to post-remission therapy and hematopoietic stem cell transplant).
So they conducted an exploratory analysis of factors influencing the risk of death within the first 2 months of diagnosis.
Being a Medicaid beneficiary (P=0.01) or uninsured (P<0.001) was independently associated with an increased risk of death within the first 2 months.
The same was true for patients belonging to the first income quartile (P=0.001), second quartile (P=0.003), third quartile (P=0.02), and fourth quartile (P=0.028).
On the other hand, there was no significant difference in early death according to marital status.
The researchers also performed a landmark survival analysis including only patients who survived at least 2 months from diagnosis.
In this analysis, marital status (P<0.001), insurance status (P=0.001), and income (P=0.021) were all independent predictors of survival.
Implications
“As physicians, we often emphasize more of the biology of the cancer, especially with the recent focus on personalized medicine,” said study author Luciano Jose Costa, MD, PhD, also of the University of Alabama at Birmingham.
“But we need to pay the same attention to resources available to our patients, as this greatly impacts their chances to survive leukemia.”
The researchers believe this will be especially important as the US transitions to a healthcare system that ties physician and hospital payments to patient outcomes.
“Taking from the results of this study, factors that have nothing to do with quality of care need to be accounted for when comparing predicted with actual outcomes,” Dr Borate said. “Otherwise, we will create a disincentive for hospitals and doctors to care for less privileged patients.”
Photo by Rhoda Baer
A new study indicates that certain social factors may impact survival in adults with acute myelogenous leukemia (AML) who are under 65.
The research showed associations between patient survival and insurance status, marital status, and county-level income.
“We believe these 3 factors indicate lack of material and social support preventing young patients from successfully walking the long and difficult road towards a cure,” said Uma Borate, MD, of the University of Alabama at Birmingham.
To conduct this study, Dr Borate and her colleagues analyzed data on 5541 patients, ages 19 to 64, who were diagnosed with AML between 2007 and 2011.
The team reported their findings in Cancer.
Multivariable analysis showed that AML subtype, age, and sex were independently associated with patients’ survival. And the non-biological factors independently associated with survival were insurance status, marital status, and county-level median household income.
Specifically, there was a significantly increased risk of premature death among patients who were uninsured (P=0.005) or Medicaid beneficiaries (P<0.001), compared to patients with private insurance.
Single (P<0.001) or divorced (P=0.011) patients had a significantly higher risk of premature death than married patients. But there was no significant difference between married and widowed patients (P=0.206).
And patients who lived in areas with lower income—the lowest 3 of 5 income groups—had a significantly increased risk of premature death.
Compared to patients in the fifth income quintile ($58.3K-$79.9K), there was an increased risk of death in the first quintile ($16.2K-$38.8K, P=0.001), second quintile ($38.8K-$42.2K, P<0.001), and third quintile ($42.2K-$47.9K, P<0.001).
Early and late mortality
The researchers wanted to determine if the impact of non-biological factors on survival was related to early mortality (a possible surrogate for access to care or late presentation) or late mortality (a possible surrogate for access to post-remission therapy and hematopoietic stem cell transplant).
So they conducted an exploratory analysis of factors influencing the risk of death within the first 2 months of diagnosis.
Being a Medicaid beneficiary (P=0.01) or uninsured (P<0.001) was independently associated with an increased risk of death within the first 2 months.
The same was true for patients belonging to the first income quartile (P=0.001), second quartile (P=0.003), third quartile (P=0.02), and fourth quartile (P=0.028).
On the other hand, there was no significant difference in early death according to marital status.
The researchers also performed a landmark survival analysis including only patients who survived at least 2 months from diagnosis.
In this analysis, marital status (P<0.001), insurance status (P=0.001), and income (P=0.021) were all independent predictors of survival.
Implications
“As physicians, we often emphasize more of the biology of the cancer, especially with the recent focus on personalized medicine,” said study author Luciano Jose Costa, MD, PhD, also of the University of Alabama at Birmingham.
“But we need to pay the same attention to resources available to our patients, as this greatly impacts their chances to survive leukemia.”
The researchers believe this will be especially important as the US transitions to a healthcare system that ties physician and hospital payments to patient outcomes.
“Taking from the results of this study, factors that have nothing to do with quality of care need to be accounted for when comparing predicted with actual outcomes,” Dr Borate said. “Otherwise, we will create a disincentive for hospitals and doctors to care for less privileged patients.”
EMA recommends orphan designation for LJPC-401
red blood cells
Image by Graham Beards
The European Medicines Agency’s (EMA’s) Committee for Orphan Medicinal Products (COMP) has adopted a positive opinion recommending that LJPC-401, a novel formulation of hepcidin, receive orphan designation to treat chronic iron overload requiring chelation therapy.
Chronic iron overload occurs in patients suffering from beta thalassemia, sickle cell disease, and hereditary hemochromatosis.
The COMP’s opinion, which is subject to review and approval by the European Commission, may include all or a subset of these conditions.
About LJPC-401
LJPC-401 is a novel formulation of hepcidin, an endogenous peptide hormone that is the body’s naturally occurring regulator of iron absorption and distribution. Hepcidin prevents excessive iron accumulation in tissues, such as the liver and heart, where it can cause significant damage and even result in death.
La Jolla Pharmaceutical Company is developing LJPC-401 for the treatment of iron overload occurring as a results of hereditary hemochromatosis, beta thalassemia, and sickle cell disease.
LJPC-401 has been shown to be effective in reducing serum iron in preclinical testing, according to La Jolla. The company said it expects to release preliminary results from a phase 1 trial of LJPC-401 by the end of this year.
About orphan designation
The EMA’s COMP adopts an opinion on the granting of orphan drug designation, and that opinion is submitted to the European Commission for endorsement.
In the European Union, orphan designation is granted to therapies intended to treat a life-threatening or chronically debilitating condition that affects no more than 5 in 10,000 persons and where no satisfactory treatment is available.
Companies that obtain orphan designation for a drug benefit from a number of incentives, including protocol assistance, a type of scientific advice specific for designated orphan medicines, and 10 years of market exclusivity if the medicine is approved. Fee reductions are also available, depending on the status of the sponsor and the type of service required.
red blood cells
Image by Graham Beards
The European Medicines Agency’s (EMA’s) Committee for Orphan Medicinal Products (COMP) has adopted a positive opinion recommending that LJPC-401, a novel formulation of hepcidin, receive orphan designation to treat chronic iron overload requiring chelation therapy.
Chronic iron overload occurs in patients suffering from beta thalassemia, sickle cell disease, and hereditary hemochromatosis.
The COMP’s opinion, which is subject to review and approval by the European Commission, may include all or a subset of these conditions.
About LJPC-401
LJPC-401 is a novel formulation of hepcidin, an endogenous peptide hormone that is the body’s naturally occurring regulator of iron absorption and distribution. Hepcidin prevents excessive iron accumulation in tissues, such as the liver and heart, where it can cause significant damage and even result in death.
La Jolla Pharmaceutical Company is developing LJPC-401 for the treatment of iron overload occurring as a results of hereditary hemochromatosis, beta thalassemia, and sickle cell disease.
LJPC-401 has been shown to be effective in reducing serum iron in preclinical testing, according to La Jolla. The company said it expects to release preliminary results from a phase 1 trial of LJPC-401 by the end of this year.
About orphan designation
The EMA’s COMP adopts an opinion on the granting of orphan drug designation, and that opinion is submitted to the European Commission for endorsement.
In the European Union, orphan designation is granted to therapies intended to treat a life-threatening or chronically debilitating condition that affects no more than 5 in 10,000 persons and where no satisfactory treatment is available.
Companies that obtain orphan designation for a drug benefit from a number of incentives, including protocol assistance, a type of scientific advice specific for designated orphan medicines, and 10 years of market exclusivity if the medicine is approved. Fee reductions are also available, depending on the status of the sponsor and the type of service required.
red blood cells
Image by Graham Beards
The European Medicines Agency’s (EMA’s) Committee for Orphan Medicinal Products (COMP) has adopted a positive opinion recommending that LJPC-401, a novel formulation of hepcidin, receive orphan designation to treat chronic iron overload requiring chelation therapy.
Chronic iron overload occurs in patients suffering from beta thalassemia, sickle cell disease, and hereditary hemochromatosis.
The COMP’s opinion, which is subject to review and approval by the European Commission, may include all or a subset of these conditions.
About LJPC-401
LJPC-401 is a novel formulation of hepcidin, an endogenous peptide hormone that is the body’s naturally occurring regulator of iron absorption and distribution. Hepcidin prevents excessive iron accumulation in tissues, such as the liver and heart, where it can cause significant damage and even result in death.
La Jolla Pharmaceutical Company is developing LJPC-401 for the treatment of iron overload occurring as a results of hereditary hemochromatosis, beta thalassemia, and sickle cell disease.
LJPC-401 has been shown to be effective in reducing serum iron in preclinical testing, according to La Jolla. The company said it expects to release preliminary results from a phase 1 trial of LJPC-401 by the end of this year.
About orphan designation
The EMA’s COMP adopts an opinion on the granting of orphan drug designation, and that opinion is submitted to the European Commission for endorsement.
In the European Union, orphan designation is granted to therapies intended to treat a life-threatening or chronically debilitating condition that affects no more than 5 in 10,000 persons and where no satisfactory treatment is available.
Companies that obtain orphan designation for a drug benefit from a number of incentives, including protocol assistance, a type of scientific advice specific for designated orphan medicines, and 10 years of market exclusivity if the medicine is approved. Fee reductions are also available, depending on the status of the sponsor and the type of service required.
Communication key to helping kids after disasters
Posttraumatic stress disorder can be hard to spot in kids after natural or manmade disasters.
They may not understand that intrusive thoughts, panic attacks, and other symptoms are problems that can be addressed, and are unlikely to mention them.
As a result, parents, teachers, and others often underestimate children’s distress levels and overestimate their resilience. One way around the problem is to ask children how they’re doing, and probe for signs of trouble. It helps to let them know that PTSD and adjustment problems are normal after a frightening event, and to teach them how to anticipate and cope with PTSD triggers.
That’s just a small fraction of the useful advice in new guidance from the American Academy of Pediatrics on the psychosocial support of children and families after disasters, published online Sept. 14 (Pediatrics. 2015 Sept. 14. doi:10.1542/peds.2015-2861).
“Children are particularly vulnerable to the effects of disasters and other traumatic events because of a lack of experience, skills, and resources to be able to independently meet their developmental, socioemotional, mental, and behavioral health needs,” said the authors, led by Dr. David Schonfeld of St. Christopher’s Hospital for Children, and Thomas Demaria, Ph.D., of Long Island (N.Y.) University.
Mental health triage should come right after medical stabilization. Dissociative symptoms; extreme confusion or inability to concentrate or make even simple decisions; intense fear, anxiety, panic, helplessness, or horror; depression at the time of the event; uncontrollable and intense grief; suicidal ideation; and marked somatization are among the warning signs that kids are in trouble.
Psychiatric medications to blunt such reactions are usually the wrong call. “Children need to develop an understanding of the event and learn to express and cope with their reactions.” If medication does seem necessary, its best to let an expert in childhood trauma make the decision, the authors said.
Dismissing children’s concerns is a mistake. “In reality, if children feel worried, then they are worried. Telling them that they should not be worried is usually ineffective.” It’s also a mistake to avoid talking about grief for fear of making it worse. Children’s “distress is caused by the reaction to the death itself, rather than any question or invitation to talk. Talking may provide some relief if not coerced. Avoiding discussion is rarely helpful and often isolates children at a time when they are most in need of support and assistance,” they said.
Simple, basic facts about the event – as long as they’re not graphic or overwhelming – will help children make sense of what they’ve been through, and reassurance that things will eventually be okay can be healing. Kids also have to know that the situation isn’t their fault, and how to cope with it.
Parents can share how they’re upset about losing their home, for instance, but then discuss how talking to another trusted adult, getting exercise, meditating, and helping others makes them feel better. Pediatricians can boost spirits by saying something like “the tornado created a big mess, but we are pulling together as a community” or “living in a shelter with all the other children in the neighborhood must have been a real adventure,” the authors said.
Having children contribute to food drives or draw hopeful pictures for victims in the hospital can help them regain a sense of control and usefulness. Resuming their routines as soon as possible will also help bring back a sense of normalcy.
Bereavement counseling is in order when children are struggling with the loss of a loved one, and cognitive behavioral therapy for kids with PTSD.
Posttraumatic stress disorder can be hard to spot in kids after natural or manmade disasters.
They may not understand that intrusive thoughts, panic attacks, and other symptoms are problems that can be addressed, and are unlikely to mention them.
As a result, parents, teachers, and others often underestimate children’s distress levels and overestimate their resilience. One way around the problem is to ask children how they’re doing, and probe for signs of trouble. It helps to let them know that PTSD and adjustment problems are normal after a frightening event, and to teach them how to anticipate and cope with PTSD triggers.
That’s just a small fraction of the useful advice in new guidance from the American Academy of Pediatrics on the psychosocial support of children and families after disasters, published online Sept. 14 (Pediatrics. 2015 Sept. 14. doi:10.1542/peds.2015-2861).
“Children are particularly vulnerable to the effects of disasters and other traumatic events because of a lack of experience, skills, and resources to be able to independently meet their developmental, socioemotional, mental, and behavioral health needs,” said the authors, led by Dr. David Schonfeld of St. Christopher’s Hospital for Children, and Thomas Demaria, Ph.D., of Long Island (N.Y.) University.
Mental health triage should come right after medical stabilization. Dissociative symptoms; extreme confusion or inability to concentrate or make even simple decisions; intense fear, anxiety, panic, helplessness, or horror; depression at the time of the event; uncontrollable and intense grief; suicidal ideation; and marked somatization are among the warning signs that kids are in trouble.
Psychiatric medications to blunt such reactions are usually the wrong call. “Children need to develop an understanding of the event and learn to express and cope with their reactions.” If medication does seem necessary, its best to let an expert in childhood trauma make the decision, the authors said.
Dismissing children’s concerns is a mistake. “In reality, if children feel worried, then they are worried. Telling them that they should not be worried is usually ineffective.” It’s also a mistake to avoid talking about grief for fear of making it worse. Children’s “distress is caused by the reaction to the death itself, rather than any question or invitation to talk. Talking may provide some relief if not coerced. Avoiding discussion is rarely helpful and often isolates children at a time when they are most in need of support and assistance,” they said.
Simple, basic facts about the event – as long as they’re not graphic or overwhelming – will help children make sense of what they’ve been through, and reassurance that things will eventually be okay can be healing. Kids also have to know that the situation isn’t their fault, and how to cope with it.
Parents can share how they’re upset about losing their home, for instance, but then discuss how talking to another trusted adult, getting exercise, meditating, and helping others makes them feel better. Pediatricians can boost spirits by saying something like “the tornado created a big mess, but we are pulling together as a community” or “living in a shelter with all the other children in the neighborhood must have been a real adventure,” the authors said.
Having children contribute to food drives or draw hopeful pictures for victims in the hospital can help them regain a sense of control and usefulness. Resuming their routines as soon as possible will also help bring back a sense of normalcy.
Bereavement counseling is in order when children are struggling with the loss of a loved one, and cognitive behavioral therapy for kids with PTSD.
Posttraumatic stress disorder can be hard to spot in kids after natural or manmade disasters.
They may not understand that intrusive thoughts, panic attacks, and other symptoms are problems that can be addressed, and are unlikely to mention them.
As a result, parents, teachers, and others often underestimate children’s distress levels and overestimate their resilience. One way around the problem is to ask children how they’re doing, and probe for signs of trouble. It helps to let them know that PTSD and adjustment problems are normal after a frightening event, and to teach them how to anticipate and cope with PTSD triggers.
That’s just a small fraction of the useful advice in new guidance from the American Academy of Pediatrics on the psychosocial support of children and families after disasters, published online Sept. 14 (Pediatrics. 2015 Sept. 14. doi:10.1542/peds.2015-2861).
“Children are particularly vulnerable to the effects of disasters and other traumatic events because of a lack of experience, skills, and resources to be able to independently meet their developmental, socioemotional, mental, and behavioral health needs,” said the authors, led by Dr. David Schonfeld of St. Christopher’s Hospital for Children, and Thomas Demaria, Ph.D., of Long Island (N.Y.) University.
Mental health triage should come right after medical stabilization. Dissociative symptoms; extreme confusion or inability to concentrate or make even simple decisions; intense fear, anxiety, panic, helplessness, or horror; depression at the time of the event; uncontrollable and intense grief; suicidal ideation; and marked somatization are among the warning signs that kids are in trouble.
Psychiatric medications to blunt such reactions are usually the wrong call. “Children need to develop an understanding of the event and learn to express and cope with their reactions.” If medication does seem necessary, its best to let an expert in childhood trauma make the decision, the authors said.
Dismissing children’s concerns is a mistake. “In reality, if children feel worried, then they are worried. Telling them that they should not be worried is usually ineffective.” It’s also a mistake to avoid talking about grief for fear of making it worse. Children’s “distress is caused by the reaction to the death itself, rather than any question or invitation to talk. Talking may provide some relief if not coerced. Avoiding discussion is rarely helpful and often isolates children at a time when they are most in need of support and assistance,” they said.
Simple, basic facts about the event – as long as they’re not graphic or overwhelming – will help children make sense of what they’ve been through, and reassurance that things will eventually be okay can be healing. Kids also have to know that the situation isn’t their fault, and how to cope with it.
Parents can share how they’re upset about losing their home, for instance, but then discuss how talking to another trusted adult, getting exercise, meditating, and helping others makes them feel better. Pediatricians can boost spirits by saying something like “the tornado created a big mess, but we are pulling together as a community” or “living in a shelter with all the other children in the neighborhood must have been a real adventure,” the authors said.
Having children contribute to food drives or draw hopeful pictures for victims in the hospital can help them regain a sense of control and usefulness. Resuming their routines as soon as possible will also help bring back a sense of normalcy.
Bereavement counseling is in order when children are struggling with the loss of a loved one, and cognitive behavioral therapy for kids with PTSD.
FROM PEDIATRICS
Product News: 09 2015
Cyclosporine A
Immune Pharmaceuticals acquires a nanoparticle topical formulation of cyclosporine A for the treatment of psoriasis, atopic dermatitis, pemphigus vulgaris, and other severe inflammatory dermatoses. Researchers have incorporated cyclosporine A into biodegradable nanocapsules and have developed stable topical formulations that are able to achieve therapeutic cyclosporine A levels in the targeted skin layers. This topical treatment provides a potential alternative to oral cyclosporine A and other topical immunosuppressive drugs. For more information, visit www.immunepharmaceuticals.com.
Picato Gel Warning
The US Food and Drug Administration (FDA) issues a warning about reports of severe allergic reactions and herpes zoster associated with the use of Picato Gel (ingenol mebutate) for the treatment of actinic keratosis. The allergic reaction may include throat tightness, difficulty breathing, feeling faint, or swelling of the lips or tongue. The FDA received reports of cases involving severe eye injuries associated with Picato Gel not being used according to the instructions for use on the label. Changes to the labeling have been requested by the FDA to warn about these new safety risks. Patients should not use Picato Gel for a longer period or on an area of skin larger than instructed on the drug label. Patients also should avoid application in, near, and around the mouth, lips, and eye area. For more information, visit www.fda.gov/MedWatch.
Ximino Extended-Release Capsules
Sun Pharmaceutical Industries Ltd announces US Food and Drug Administration approval of the Supplemental New Drug Application for Ximino (minocycline hydrochloride) extended-release capsules (45, 90, and 135 mg). Ximino extended-release capsules are indicated for the treatment of inflammatory lesions of nonnodular moderate to severe acne vulgaris in patients 12 years and older. Ximino extended-release capsules are expected to be available for patients during the fourth quarter of 2015. For more information, visit www.sunpharma.com.
If you would like your product included in Product News, please e-mail a press release to the Editorial Office at cutis@frontlinemedcom.com.
Cyclosporine A
Immune Pharmaceuticals acquires a nanoparticle topical formulation of cyclosporine A for the treatment of psoriasis, atopic dermatitis, pemphigus vulgaris, and other severe inflammatory dermatoses. Researchers have incorporated cyclosporine A into biodegradable nanocapsules and have developed stable topical formulations that are able to achieve therapeutic cyclosporine A levels in the targeted skin layers. This topical treatment provides a potential alternative to oral cyclosporine A and other topical immunosuppressive drugs. For more information, visit www.immunepharmaceuticals.com.
Picato Gel Warning
The US Food and Drug Administration (FDA) issues a warning about reports of severe allergic reactions and herpes zoster associated with the use of Picato Gel (ingenol mebutate) for the treatment of actinic keratosis. The allergic reaction may include throat tightness, difficulty breathing, feeling faint, or swelling of the lips or tongue. The FDA received reports of cases involving severe eye injuries associated with Picato Gel not being used according to the instructions for use on the label. Changes to the labeling have been requested by the FDA to warn about these new safety risks. Patients should not use Picato Gel for a longer period or on an area of skin larger than instructed on the drug label. Patients also should avoid application in, near, and around the mouth, lips, and eye area. For more information, visit www.fda.gov/MedWatch.
Ximino Extended-Release Capsules
Sun Pharmaceutical Industries Ltd announces US Food and Drug Administration approval of the Supplemental New Drug Application for Ximino (minocycline hydrochloride) extended-release capsules (45, 90, and 135 mg). Ximino extended-release capsules are indicated for the treatment of inflammatory lesions of nonnodular moderate to severe acne vulgaris in patients 12 years and older. Ximino extended-release capsules are expected to be available for patients during the fourth quarter of 2015. For more information, visit www.sunpharma.com.
If you would like your product included in Product News, please e-mail a press release to the Editorial Office at cutis@frontlinemedcom.com.
Cyclosporine A
Immune Pharmaceuticals acquires a nanoparticle topical formulation of cyclosporine A for the treatment of psoriasis, atopic dermatitis, pemphigus vulgaris, and other severe inflammatory dermatoses. Researchers have incorporated cyclosporine A into biodegradable nanocapsules and have developed stable topical formulations that are able to achieve therapeutic cyclosporine A levels in the targeted skin layers. This topical treatment provides a potential alternative to oral cyclosporine A and other topical immunosuppressive drugs. For more information, visit www.immunepharmaceuticals.com.
Picato Gel Warning
The US Food and Drug Administration (FDA) issues a warning about reports of severe allergic reactions and herpes zoster associated with the use of Picato Gel (ingenol mebutate) for the treatment of actinic keratosis. The allergic reaction may include throat tightness, difficulty breathing, feeling faint, or swelling of the lips or tongue. The FDA received reports of cases involving severe eye injuries associated with Picato Gel not being used according to the instructions for use on the label. Changes to the labeling have been requested by the FDA to warn about these new safety risks. Patients should not use Picato Gel for a longer period or on an area of skin larger than instructed on the drug label. Patients also should avoid application in, near, and around the mouth, lips, and eye area. For more information, visit www.fda.gov/MedWatch.
Ximino Extended-Release Capsules
Sun Pharmaceutical Industries Ltd announces US Food and Drug Administration approval of the Supplemental New Drug Application for Ximino (minocycline hydrochloride) extended-release capsules (45, 90, and 135 mg). Ximino extended-release capsules are indicated for the treatment of inflammatory lesions of nonnodular moderate to severe acne vulgaris in patients 12 years and older. Ximino extended-release capsules are expected to be available for patients during the fourth quarter of 2015. For more information, visit www.sunpharma.com.
If you would like your product included in Product News, please e-mail a press release to the Editorial Office at cutis@frontlinemedcom.com.
Erratum (Cutis. 2015;95:47-51)
Due to a submission error, the article “Reduced Degree of Irritation During a Second Cycle of Ingenol Mebutate Gel 0.015% for the Treatment of Actinic Keratosis” (Cutis. 2015;95:47-51) contained the incorrect scale for local skin reactions (LSRs). The text in the Methods should have stated:
Using standardized photographic guides, 6 individual LSRs—erythema, flaking/scaling, crusting, swelling, vesiculation/pustulation, and erosion/ulceration—were assessed on a scale of 0 (none) to 4 (severe), with higher numbers indicating more severe reactions.
The staff of Cutis® makes every possible effort to ensure accuracy in its articles and apologizes for the mistake.
Due to a submission error, the article “Reduced Degree of Irritation During a Second Cycle of Ingenol Mebutate Gel 0.015% for the Treatment of Actinic Keratosis” (Cutis. 2015;95:47-51) contained the incorrect scale for local skin reactions (LSRs). The text in the Methods should have stated:
Using standardized photographic guides, 6 individual LSRs—erythema, flaking/scaling, crusting, swelling, vesiculation/pustulation, and erosion/ulceration—were assessed on a scale of 0 (none) to 4 (severe), with higher numbers indicating more severe reactions.
The staff of Cutis® makes every possible effort to ensure accuracy in its articles and apologizes for the mistake.
Due to a submission error, the article “Reduced Degree of Irritation During a Second Cycle of Ingenol Mebutate Gel 0.015% for the Treatment of Actinic Keratosis” (Cutis. 2015;95:47-51) contained the incorrect scale for local skin reactions (LSRs). The text in the Methods should have stated:
Using standardized photographic guides, 6 individual LSRs—erythema, flaking/scaling, crusting, swelling, vesiculation/pustulation, and erosion/ulceration—were assessed on a scale of 0 (none) to 4 (severe), with higher numbers indicating more severe reactions.
The staff of Cutis® makes every possible effort to ensure accuracy in its articles and apologizes for the mistake.
What Is Your Diagnosis? Idiopathic Guttate Hypomelanosis
The Diagnosis: Idiopathic Guttate Hypomelanosis
A biopsy of the largest lesion from the left leg superior to the lateral malleolus was performed. Histopathologic examination revealed solar elastosis, diminished number of focal melanocytes and pigment within keratinocytes compared to uninvolved skin, and presence of hyperkeratosis with flattening of rete ridges. The clinical presentation along with histopathologic analysis confirmed a diagnosis of idiopathic guttate hypomelanosis (IGH). The lesions were treated with short-exposure cryotherapy, which resulted in partial repigmentation after several treatments.
Idiopathic guttate hypomelanosis is a common but underreported condition in elderly patients that usually presents with small, discrete, asymptomatic, hypopigmented macules. The frequency of IGH increases with age.1 Frequency of the condition is much lower in patients aged 21 to 30 years and does not exceed 7%. Lesions of IGH have a predilection for sun-exposed areas such as the arms and legs but rarely can be seen on the face and trunk. Facial lesions of IGH are more frequently reported in women.1 The size of lesions can be up to 1.5 cm in diameter. The condition generally is self-limited, but some patients may express aesthetic concerns. Rare cases of IGH in children have been associated with prolonged sun exposure.2
The etiology of IGH is unknown but an association with sun exposure has been noted. Patients with IGH frequently show other signs of photoaging, such as numerous seborrheic keratoses, solar lentigines, xeroses, freckles, and actinic keratoses.1 Short-term exposure to UVB radiation and psoralen plus UVA therapy has been shown to cause IGH in patients with chronic diseases such as mycosis fungoides.3-5 One small study that examined renal transplant recipients determined an association between HLA-DQ3 antigens and IGH, whereas HLA-DR8 antigens were not identified in any patients with IGH, indicating it may have some advantage in preventing the development of IGH.6 Shin et al1 reported that IGH was prevalent among patients who regularly traumatized their skin by scrubbing.
Clinically, IGH should be differentiated from other conditions characterized by hypopigmentation, such as pityriasis alba, pityriasis versicolor, postinflammatory hypopigmentation, progressive macular hypomelanosis, and vitiligo. Aside from clinical examination, histopathologic studies are helpful in making a definitive diagnosis. The differential diagnosis of IGH is presented in the Table.
Histopathology of IGH lesions usually reveals slight atrophy of the epidermis with flattening of rete ridges and concomitant hyperkeratosis. A thickened stratum granulosum also has been noted in lesions of IGH.2 The diminished number of melanocytes and melanin pigment granules along with hyperkeratosis both appear to contribute to the hypopigmentation noted in IGH.7 Ultrastructural studies of lesions of IGH can confirm melanocytic degeneration and a decreased number of melanosomes in melanocytes and keratinocytes.2,8
There is no uniformly effective treatment of IGH. Topical application of tacrolimus and tretinoin have shown efficacy in repigmenting IGH lesions.8,9 Short-exposure cryotherapy with a duration of 3 to 5 seconds, localized chemical peels, and/or local dermabrasion can be helpful.10-12 CO2 lasers also have demonstrated promising results.13
- Shin MK, Jeong KH, Oh IH, et al. Clinical features of idiopathic guttate hypomelanosis in 646 subjects and association with other aspects of photoaging. Int J Dermatol. 2011;50:798-805.
- Kim SK, Kim EH, Kang HY, et al. Comprehensive understanding of idiopathic guttate hypomelanosis: clinical and histopathological correlation. Int J Dermatol. 2010;49:162-166.
- Friedland R, David M, Feinmesser M, et al. Idiopathic guttate hypomelanosis-like lesions in patients with mycosis fungoides: a new adverse effect of phototherapy. J Eur Acad Dermatol Venereol. 2010;24:1026-1030.
- Kaya TI, Yazici AC, Tursen U, et al. Idiopathic guttate hypomelanosis: idiopathic or ultraviolet induced? Photodermatol Photoimmunol Photomed. 2005;21:270-271.
- Loquai C, Metze D, Nashan D, et al. Confetti-like lesions with hyperkeratosis: a novel ultraviolet-induced hypomelanotic disorder? Br J Dermatol. 2005;153:190-193.
- Arrunategui A, Trujillo RA, Marulanda MP, et al. HLA-DQ3 is associated with idiopathic guttate hypomelanosis, whereas HLA-DR8 is not, in a group of renal transplant patients. Int J Dermatol. 2002;41:744-747.
- Wallace ML, Grichnik JM, Prieto VG, et al. Numbers and differentiation status of melanocytes in idiopathic guttate hypomelanosis. J Cutan Pathol. 1998;25:375-379.
- Ortonne JP, Perrot H. Idiopathic guttate hypomelanosis. ultrastructural study. Arch Dermatol. 1980;116:664-668.
- Rerknimitr P, Disphanurat W, Achariyakul M. Topical tacrolimus significantly promotes repigmentation in idiopathic guttate hypomelanosis: a double-blind, randomized, placebo-controlled study. J Eur Acad Dermatol Venereol. 2013;27:460-464.
- Pagnoni A, Kligman AM, Sadiq I, et al. Hypopigmented macules of photodamaged skin and their treatment with topical tretinoin. Acta Derm Venereol. 1999;79:305-310.
- Kumarasinghe SP. 3-5 second cryotherapy is effective in idiopathic guttate hypomelanosis. J Dermatol. 2004;31:457-459.
- Hexsel DM. Treatment of idiopathic guttate hypomelanosis by localized superficial dermabrasion. Dermatol Surg. 1999;25:917-918.
- Shin J, Kim M, Park SH, et al. The effect of fractional carbon dioxide lasers on idiopathic guttate hypomelanosis: a preliminary study. J Eur Acad Dermatol Venereol. 2013;27:e243-e246.
The Diagnosis: Idiopathic Guttate Hypomelanosis
A biopsy of the largest lesion from the left leg superior to the lateral malleolus was performed. Histopathologic examination revealed solar elastosis, diminished number of focal melanocytes and pigment within keratinocytes compared to uninvolved skin, and presence of hyperkeratosis with flattening of rete ridges. The clinical presentation along with histopathologic analysis confirmed a diagnosis of idiopathic guttate hypomelanosis (IGH). The lesions were treated with short-exposure cryotherapy, which resulted in partial repigmentation after several treatments.
Idiopathic guttate hypomelanosis is a common but underreported condition in elderly patients that usually presents with small, discrete, asymptomatic, hypopigmented macules. The frequency of IGH increases with age.1 Frequency of the condition is much lower in patients aged 21 to 30 years and does not exceed 7%. Lesions of IGH have a predilection for sun-exposed areas such as the arms and legs but rarely can be seen on the face and trunk. Facial lesions of IGH are more frequently reported in women.1 The size of lesions can be up to 1.5 cm in diameter. The condition generally is self-limited, but some patients may express aesthetic concerns. Rare cases of IGH in children have been associated with prolonged sun exposure.2
The etiology of IGH is unknown but an association with sun exposure has been noted. Patients with IGH frequently show other signs of photoaging, such as numerous seborrheic keratoses, solar lentigines, xeroses, freckles, and actinic keratoses.1 Short-term exposure to UVB radiation and psoralen plus UVA therapy has been shown to cause IGH in patients with chronic diseases such as mycosis fungoides.3-5 One small study that examined renal transplant recipients determined an association between HLA-DQ3 antigens and IGH, whereas HLA-DR8 antigens were not identified in any patients with IGH, indicating it may have some advantage in preventing the development of IGH.6 Shin et al1 reported that IGH was prevalent among patients who regularly traumatized their skin by scrubbing.
Clinically, IGH should be differentiated from other conditions characterized by hypopigmentation, such as pityriasis alba, pityriasis versicolor, postinflammatory hypopigmentation, progressive macular hypomelanosis, and vitiligo. Aside from clinical examination, histopathologic studies are helpful in making a definitive diagnosis. The differential diagnosis of IGH is presented in the Table.
Histopathology of IGH lesions usually reveals slight atrophy of the epidermis with flattening of rete ridges and concomitant hyperkeratosis. A thickened stratum granulosum also has been noted in lesions of IGH.2 The diminished number of melanocytes and melanin pigment granules along with hyperkeratosis both appear to contribute to the hypopigmentation noted in IGH.7 Ultrastructural studies of lesions of IGH can confirm melanocytic degeneration and a decreased number of melanosomes in melanocytes and keratinocytes.2,8
There is no uniformly effective treatment of IGH. Topical application of tacrolimus and tretinoin have shown efficacy in repigmenting IGH lesions.8,9 Short-exposure cryotherapy with a duration of 3 to 5 seconds, localized chemical peels, and/or local dermabrasion can be helpful.10-12 CO2 lasers also have demonstrated promising results.13
The Diagnosis: Idiopathic Guttate Hypomelanosis
A biopsy of the largest lesion from the left leg superior to the lateral malleolus was performed. Histopathologic examination revealed solar elastosis, diminished number of focal melanocytes and pigment within keratinocytes compared to uninvolved skin, and presence of hyperkeratosis with flattening of rete ridges. The clinical presentation along with histopathologic analysis confirmed a diagnosis of idiopathic guttate hypomelanosis (IGH). The lesions were treated with short-exposure cryotherapy, which resulted in partial repigmentation after several treatments.
Idiopathic guttate hypomelanosis is a common but underreported condition in elderly patients that usually presents with small, discrete, asymptomatic, hypopigmented macules. The frequency of IGH increases with age.1 Frequency of the condition is much lower in patients aged 21 to 30 years and does not exceed 7%. Lesions of IGH have a predilection for sun-exposed areas such as the arms and legs but rarely can be seen on the face and trunk. Facial lesions of IGH are more frequently reported in women.1 The size of lesions can be up to 1.5 cm in diameter. The condition generally is self-limited, but some patients may express aesthetic concerns. Rare cases of IGH in children have been associated with prolonged sun exposure.2
The etiology of IGH is unknown but an association with sun exposure has been noted. Patients with IGH frequently show other signs of photoaging, such as numerous seborrheic keratoses, solar lentigines, xeroses, freckles, and actinic keratoses.1 Short-term exposure to UVB radiation and psoralen plus UVA therapy has been shown to cause IGH in patients with chronic diseases such as mycosis fungoides.3-5 One small study that examined renal transplant recipients determined an association between HLA-DQ3 antigens and IGH, whereas HLA-DR8 antigens were not identified in any patients with IGH, indicating it may have some advantage in preventing the development of IGH.6 Shin et al1 reported that IGH was prevalent among patients who regularly traumatized their skin by scrubbing.
Clinically, IGH should be differentiated from other conditions characterized by hypopigmentation, such as pityriasis alba, pityriasis versicolor, postinflammatory hypopigmentation, progressive macular hypomelanosis, and vitiligo. Aside from clinical examination, histopathologic studies are helpful in making a definitive diagnosis. The differential diagnosis of IGH is presented in the Table.
Histopathology of IGH lesions usually reveals slight atrophy of the epidermis with flattening of rete ridges and concomitant hyperkeratosis. A thickened stratum granulosum also has been noted in lesions of IGH.2 The diminished number of melanocytes and melanin pigment granules along with hyperkeratosis both appear to contribute to the hypopigmentation noted in IGH.7 Ultrastructural studies of lesions of IGH can confirm melanocytic degeneration and a decreased number of melanosomes in melanocytes and keratinocytes.2,8
There is no uniformly effective treatment of IGH. Topical application of tacrolimus and tretinoin have shown efficacy in repigmenting IGH lesions.8,9 Short-exposure cryotherapy with a duration of 3 to 5 seconds, localized chemical peels, and/or local dermabrasion can be helpful.10-12 CO2 lasers also have demonstrated promising results.13
- Shin MK, Jeong KH, Oh IH, et al. Clinical features of idiopathic guttate hypomelanosis in 646 subjects and association with other aspects of photoaging. Int J Dermatol. 2011;50:798-805.
- Kim SK, Kim EH, Kang HY, et al. Comprehensive understanding of idiopathic guttate hypomelanosis: clinical and histopathological correlation. Int J Dermatol. 2010;49:162-166.
- Friedland R, David M, Feinmesser M, et al. Idiopathic guttate hypomelanosis-like lesions in patients with mycosis fungoides: a new adverse effect of phototherapy. J Eur Acad Dermatol Venereol. 2010;24:1026-1030.
- Kaya TI, Yazici AC, Tursen U, et al. Idiopathic guttate hypomelanosis: idiopathic or ultraviolet induced? Photodermatol Photoimmunol Photomed. 2005;21:270-271.
- Loquai C, Metze D, Nashan D, et al. Confetti-like lesions with hyperkeratosis: a novel ultraviolet-induced hypomelanotic disorder? Br J Dermatol. 2005;153:190-193.
- Arrunategui A, Trujillo RA, Marulanda MP, et al. HLA-DQ3 is associated with idiopathic guttate hypomelanosis, whereas HLA-DR8 is not, in a group of renal transplant patients. Int J Dermatol. 2002;41:744-747.
- Wallace ML, Grichnik JM, Prieto VG, et al. Numbers and differentiation status of melanocytes in idiopathic guttate hypomelanosis. J Cutan Pathol. 1998;25:375-379.
- Ortonne JP, Perrot H. Idiopathic guttate hypomelanosis. ultrastructural study. Arch Dermatol. 1980;116:664-668.
- Rerknimitr P, Disphanurat W, Achariyakul M. Topical tacrolimus significantly promotes repigmentation in idiopathic guttate hypomelanosis: a double-blind, randomized, placebo-controlled study. J Eur Acad Dermatol Venereol. 2013;27:460-464.
- Pagnoni A, Kligman AM, Sadiq I, et al. Hypopigmented macules of photodamaged skin and their treatment with topical tretinoin. Acta Derm Venereol. 1999;79:305-310.
- Kumarasinghe SP. 3-5 second cryotherapy is effective in idiopathic guttate hypomelanosis. J Dermatol. 2004;31:457-459.
- Hexsel DM. Treatment of idiopathic guttate hypomelanosis by localized superficial dermabrasion. Dermatol Surg. 1999;25:917-918.
- Shin J, Kim M, Park SH, et al. The effect of fractional carbon dioxide lasers on idiopathic guttate hypomelanosis: a preliminary study. J Eur Acad Dermatol Venereol. 2013;27:e243-e246.
- Shin MK, Jeong KH, Oh IH, et al. Clinical features of idiopathic guttate hypomelanosis in 646 subjects and association with other aspects of photoaging. Int J Dermatol. 2011;50:798-805.
- Kim SK, Kim EH, Kang HY, et al. Comprehensive understanding of idiopathic guttate hypomelanosis: clinical and histopathological correlation. Int J Dermatol. 2010;49:162-166.
- Friedland R, David M, Feinmesser M, et al. Idiopathic guttate hypomelanosis-like lesions in patients with mycosis fungoides: a new adverse effect of phototherapy. J Eur Acad Dermatol Venereol. 2010;24:1026-1030.
- Kaya TI, Yazici AC, Tursen U, et al. Idiopathic guttate hypomelanosis: idiopathic or ultraviolet induced? Photodermatol Photoimmunol Photomed. 2005;21:270-271.
- Loquai C, Metze D, Nashan D, et al. Confetti-like lesions with hyperkeratosis: a novel ultraviolet-induced hypomelanotic disorder? Br J Dermatol. 2005;153:190-193.
- Arrunategui A, Trujillo RA, Marulanda MP, et al. HLA-DQ3 is associated with idiopathic guttate hypomelanosis, whereas HLA-DR8 is not, in a group of renal transplant patients. Int J Dermatol. 2002;41:744-747.
- Wallace ML, Grichnik JM, Prieto VG, et al. Numbers and differentiation status of melanocytes in idiopathic guttate hypomelanosis. J Cutan Pathol. 1998;25:375-379.
- Ortonne JP, Perrot H. Idiopathic guttate hypomelanosis. ultrastructural study. Arch Dermatol. 1980;116:664-668.
- Rerknimitr P, Disphanurat W, Achariyakul M. Topical tacrolimus significantly promotes repigmentation in idiopathic guttate hypomelanosis: a double-blind, randomized, placebo-controlled study. J Eur Acad Dermatol Venereol. 2013;27:460-464.
- Pagnoni A, Kligman AM, Sadiq I, et al. Hypopigmented macules of photodamaged skin and their treatment with topical tretinoin. Acta Derm Venereol. 1999;79:305-310.
- Kumarasinghe SP. 3-5 second cryotherapy is effective in idiopathic guttate hypomelanosis. J Dermatol. 2004;31:457-459.
- Hexsel DM. Treatment of idiopathic guttate hypomelanosis by localized superficial dermabrasion. Dermatol Surg. 1999;25:917-918.
- Shin J, Kim M, Park SH, et al. The effect of fractional carbon dioxide lasers on idiopathic guttate hypomelanosis: a preliminary study. J Eur Acad Dermatol Venereol. 2013;27:e243-e246.
A 58-year-old man presented with disseminated, hypopigmented, asymptomatic lesions on the right arm (top) and left leg (bottom) that had been present for approximately 6 years. The patient reported that the lesions had become more visible and greater in number within the last year. Multiple circular hypopigmented macules of various sizes ranging from 1 to 3 mm in diameter were identified. No scaling was seen. Physical examination was otherwise unremarkable.
Syringoid Eccrine Carcinoma
Syringoid eccrine carcinoma is a rare malignant adnexal tumor with eccrine differentiation that histologically resembles a syringoma.1 Originally described as eccrine epithelioma by Freeman and Winklemann2 in 1969, syringoid eccrine carcinoma has been reported in the literature as eccrine carcinoma, eccrine syringomatous carcinoma, and sclerosing sweat duct carcinoma.3 Clinically, syringoid eccrine carcinoma most commonly presents as a tender plaque or nodule on the scalp, and histologic examination generally reveals a dermal-based lesion that rarely shows epidermal connection. It demonstrates syringomalike tadpole morphology (epithelial strands with lumen formation) composed of basaloid epithelium with uniform hyperchromatic nuclei (Figure 1). There usually is an infiltrative growth pattern to the subcutis (Figure 2 [left]) or skeletal muscle as well as remarkable perineural invasion (Figure 2 [right]). Mitotic activity is minimal to absent. The tumor cells of syringoid eccrine carcinoma typically show positive immuno-staining for high- and low-molecular-weight cytokeratin, while the lumina are highlighted by epithelial membrane antigen and carcinoembryonic antigen.4 However, immunohistochemistry often is not contributory in diagnosing primary eccrine carcinomas.
The differential diagnosis of syringoid eccrine carcinoma includes cutaneous adenoid cystic carcinoma, metastatic adenocarcinoma, sclerosing basal cell carcinoma, and syringoma. Cutaneous adenoid cystic carcinoma is a rare, slow-growing, flesh-colored tumor that consists of lobules, islands, and cords of basaloid cells with prominent cystic cribriforming (Figure 3). The tumor cells typically are small, cuboidal, and monomorphic. Metastatic adenoid cystic carcinoma, such as from a primary tumor of the salivary glands or breasts, must be excluded before rendering a diagnosis of primary cutaneous disease.
Metastatic adenocarcinoma of the skin usually presents in patients with a clinical history of preexisting disease. The breasts, colon, stomach, and ovaries are common origins of metastases. The histopathologic and immunohistochemical findings depend on the particular site of origin of the metastasis. Compared with primary eccrine carcinomas, metastatic adenocarcinomas of the skin generally are high-grade lesions with prominent atypia, mitosis, and necrosis (Figure 4).
Sclerosing basal cell carcinoma shows basaloid tumor cells with deep infiltration. Unlike syringoid eccrine carcinoma, basal cell carcinoma is an epidermal tumor that does not have true lumen formation. Furthermore, other variants of basal cell carcinoma, including nodular, micronodular, or superficial multicentric tumors, often coexist with the sclerosing variant in the same lesion and constitute a useful diagnostic clue (Figure 5). Staining for epithelial membrane antigen may be useful in identifying the absence of lumen formation, and Ber-EP4 highlights the epidermal origin of the lesion.5
Syringomas most commonly present as multiple small flesh-colored papules on the eyelids. On histology, syringomas present as small superficial dermal lesions composed of small ducts that may form tadpolelike structures in a fibrotic stroma (Figure 6). The ducts are lined by benign cuboidal cells. In contrast to syringoid eccrine carcinomas, syringomas usually present as multiple lesions that are microscopically superficial without perineural involvement.
1. Sidiropoulos M, Sade S, Al-Habeeb A, et al. Syringoid eccrine carcinoma: a clinicopathological and immunohistochemical study of four cases. J Clin Pathol. 2011;64:788-792.
2. Freeman RG, Winklemann RK. Basal cell tumor with eccrine differentiations (eccrine epithelioma). Arch Dermatol. 1969;100:234-242.
3. Nishizawa A, Nakanishi Y, Sasajima Y, et al. Syringoid carcinoma with apparently aggressive transformation: case report and review of the literature. Int J Dermatol. 2006;45:1218-1221.
4. Urso C, Bondi R, Paglierani M, et al. Carcinomas of sweat glands: report of 60 cases. Arch Pathol Lab Med. 2001;125:498-505.
5. Cassarino D. Diagnostic Pathology: Neoplastic Dermatopathology. Salt Lake City, UT: Amirsys Publishing Inc; 2012.
Syringoid eccrine carcinoma is a rare malignant adnexal tumor with eccrine differentiation that histologically resembles a syringoma.1 Originally described as eccrine epithelioma by Freeman and Winklemann2 in 1969, syringoid eccrine carcinoma has been reported in the literature as eccrine carcinoma, eccrine syringomatous carcinoma, and sclerosing sweat duct carcinoma.3 Clinically, syringoid eccrine carcinoma most commonly presents as a tender plaque or nodule on the scalp, and histologic examination generally reveals a dermal-based lesion that rarely shows epidermal connection. It demonstrates syringomalike tadpole morphology (epithelial strands with lumen formation) composed of basaloid epithelium with uniform hyperchromatic nuclei (Figure 1). There usually is an infiltrative growth pattern to the subcutis (Figure 2 [left]) or skeletal muscle as well as remarkable perineural invasion (Figure 2 [right]). Mitotic activity is minimal to absent. The tumor cells of syringoid eccrine carcinoma typically show positive immuno-staining for high- and low-molecular-weight cytokeratin, while the lumina are highlighted by epithelial membrane antigen and carcinoembryonic antigen.4 However, immunohistochemistry often is not contributory in diagnosing primary eccrine carcinomas.
The differential diagnosis of syringoid eccrine carcinoma includes cutaneous adenoid cystic carcinoma, metastatic adenocarcinoma, sclerosing basal cell carcinoma, and syringoma. Cutaneous adenoid cystic carcinoma is a rare, slow-growing, flesh-colored tumor that consists of lobules, islands, and cords of basaloid cells with prominent cystic cribriforming (Figure 3). The tumor cells typically are small, cuboidal, and monomorphic. Metastatic adenoid cystic carcinoma, such as from a primary tumor of the salivary glands or breasts, must be excluded before rendering a diagnosis of primary cutaneous disease.
Metastatic adenocarcinoma of the skin usually presents in patients with a clinical history of preexisting disease. The breasts, colon, stomach, and ovaries are common origins of metastases. The histopathologic and immunohistochemical findings depend on the particular site of origin of the metastasis. Compared with primary eccrine carcinomas, metastatic adenocarcinomas of the skin generally are high-grade lesions with prominent atypia, mitosis, and necrosis (Figure 4).
Sclerosing basal cell carcinoma shows basaloid tumor cells with deep infiltration. Unlike syringoid eccrine carcinoma, basal cell carcinoma is an epidermal tumor that does not have true lumen formation. Furthermore, other variants of basal cell carcinoma, including nodular, micronodular, or superficial multicentric tumors, often coexist with the sclerosing variant in the same lesion and constitute a useful diagnostic clue (Figure 5). Staining for epithelial membrane antigen may be useful in identifying the absence of lumen formation, and Ber-EP4 highlights the epidermal origin of the lesion.5
Syringomas most commonly present as multiple small flesh-colored papules on the eyelids. On histology, syringomas present as small superficial dermal lesions composed of small ducts that may form tadpolelike structures in a fibrotic stroma (Figure 6). The ducts are lined by benign cuboidal cells. In contrast to syringoid eccrine carcinomas, syringomas usually present as multiple lesions that are microscopically superficial without perineural involvement.
Syringoid eccrine carcinoma is a rare malignant adnexal tumor with eccrine differentiation that histologically resembles a syringoma.1 Originally described as eccrine epithelioma by Freeman and Winklemann2 in 1969, syringoid eccrine carcinoma has been reported in the literature as eccrine carcinoma, eccrine syringomatous carcinoma, and sclerosing sweat duct carcinoma.3 Clinically, syringoid eccrine carcinoma most commonly presents as a tender plaque or nodule on the scalp, and histologic examination generally reveals a dermal-based lesion that rarely shows epidermal connection. It demonstrates syringomalike tadpole morphology (epithelial strands with lumen formation) composed of basaloid epithelium with uniform hyperchromatic nuclei (Figure 1). There usually is an infiltrative growth pattern to the subcutis (Figure 2 [left]) or skeletal muscle as well as remarkable perineural invasion (Figure 2 [right]). Mitotic activity is minimal to absent. The tumor cells of syringoid eccrine carcinoma typically show positive immuno-staining for high- and low-molecular-weight cytokeratin, while the lumina are highlighted by epithelial membrane antigen and carcinoembryonic antigen.4 However, immunohistochemistry often is not contributory in diagnosing primary eccrine carcinomas.
The differential diagnosis of syringoid eccrine carcinoma includes cutaneous adenoid cystic carcinoma, metastatic adenocarcinoma, sclerosing basal cell carcinoma, and syringoma. Cutaneous adenoid cystic carcinoma is a rare, slow-growing, flesh-colored tumor that consists of lobules, islands, and cords of basaloid cells with prominent cystic cribriforming (Figure 3). The tumor cells typically are small, cuboidal, and monomorphic. Metastatic adenoid cystic carcinoma, such as from a primary tumor of the salivary glands or breasts, must be excluded before rendering a diagnosis of primary cutaneous disease.
Metastatic adenocarcinoma of the skin usually presents in patients with a clinical history of preexisting disease. The breasts, colon, stomach, and ovaries are common origins of metastases. The histopathologic and immunohistochemical findings depend on the particular site of origin of the metastasis. Compared with primary eccrine carcinomas, metastatic adenocarcinomas of the skin generally are high-grade lesions with prominent atypia, mitosis, and necrosis (Figure 4).
Sclerosing basal cell carcinoma shows basaloid tumor cells with deep infiltration. Unlike syringoid eccrine carcinoma, basal cell carcinoma is an epidermal tumor that does not have true lumen formation. Furthermore, other variants of basal cell carcinoma, including nodular, micronodular, or superficial multicentric tumors, often coexist with the sclerosing variant in the same lesion and constitute a useful diagnostic clue (Figure 5). Staining for epithelial membrane antigen may be useful in identifying the absence of lumen formation, and Ber-EP4 highlights the epidermal origin of the lesion.5
Syringomas most commonly present as multiple small flesh-colored papules on the eyelids. On histology, syringomas present as small superficial dermal lesions composed of small ducts that may form tadpolelike structures in a fibrotic stroma (Figure 6). The ducts are lined by benign cuboidal cells. In contrast to syringoid eccrine carcinomas, syringomas usually present as multiple lesions that are microscopically superficial without perineural involvement.
1. Sidiropoulos M, Sade S, Al-Habeeb A, et al. Syringoid eccrine carcinoma: a clinicopathological and immunohistochemical study of four cases. J Clin Pathol. 2011;64:788-792.
2. Freeman RG, Winklemann RK. Basal cell tumor with eccrine differentiations (eccrine epithelioma). Arch Dermatol. 1969;100:234-242.
3. Nishizawa A, Nakanishi Y, Sasajima Y, et al. Syringoid carcinoma with apparently aggressive transformation: case report and review of the literature. Int J Dermatol. 2006;45:1218-1221.
4. Urso C, Bondi R, Paglierani M, et al. Carcinomas of sweat glands: report of 60 cases. Arch Pathol Lab Med. 2001;125:498-505.
5. Cassarino D. Diagnostic Pathology: Neoplastic Dermatopathology. Salt Lake City, UT: Amirsys Publishing Inc; 2012.
1. Sidiropoulos M, Sade S, Al-Habeeb A, et al. Syringoid eccrine carcinoma: a clinicopathological and immunohistochemical study of four cases. J Clin Pathol. 2011;64:788-792.
2. Freeman RG, Winklemann RK. Basal cell tumor with eccrine differentiations (eccrine epithelioma). Arch Dermatol. 1969;100:234-242.
3. Nishizawa A, Nakanishi Y, Sasajima Y, et al. Syringoid carcinoma with apparently aggressive transformation: case report and review of the literature. Int J Dermatol. 2006;45:1218-1221.
4. Urso C, Bondi R, Paglierani M, et al. Carcinomas of sweat glands: report of 60 cases. Arch Pathol Lab Med. 2001;125:498-505.
5. Cassarino D. Diagnostic Pathology: Neoplastic Dermatopathology. Salt Lake City, UT: Amirsys Publishing Inc; 2012.
