Robert Finn

Major Finding: Women who are current smokers are 3 times as likely to report problems with urinary frequency and 2.7 times as likely to report problems with urinary urgency as women who do not smoke.

Data Source: Population-based study of a representative sample of 1,790 Finnish women.

Disclosures: Dr. Tikkinen said that he had no conflicts. Pirkanmaa Hospital District and Pfizer funded the study through unrestricted grants.

SAN FRANCISCO — A Finnish study has found a strong association between tobacco smoking and urinary storage symptoms in women.

Women who smoke are 3 times as likely to report abnormal urinary frequency and 2.7 times as likely to report abnormal urinary urgency, compared with nonsmokers, Dr. Kari A.O. Tikkinen of Helsinki University Central Hospital said at the meeting.

The study involved survey responses from a nationally representative sample of 1,790 Finnish women aged 18-79 years (mean age 42 years). Investigators assessed urinary symptoms from responses to questions on the American Urological Association Symptom Index and the Danish Prostatic Symptom Score questionnaires.

In addition to urinary frequency and urgency, the women were asked about nocturia, stress incontinence, and urgency incontinence. The researchers found that only frequency and urgency were significantly associated with smoking.

They defined urinary frequency as abnormal if the women reported their longest interval between each urination was less than 2 hours. They defined abnormal urgency as often or always experiencing an imperative urge to urinate, nocturia as two or more voids per night, stress incontinence as often or always experiencing leakage of urine when physically active, and urgency incontinence as often or always experiencing an urge so strong that urine starts to flow before reaching the toilet.

In the multivariate analysis, the researchers controlled for a large number of potential confounders. These included 33 different physician-diagnosed medical conditions, 26 different classes of prescription medications, lifestyle and social demographic factors such as education and income, and anthropometric and reproductive factors such as body mass index and menopausal status.

About half of the women had never smoked, a quarter were current smokers, and a quarter were former smokers. The former smokers also had a significantly higher risk of abnormal urinary frequency and urgency than the never smokers, although not to the extent of current smokers. They were 70% more likely to experience abnormal frequency and 80% more likely to experience abnormal urgency than never smokers.

The researchers also found a dose-response effect. Compared with light smokers (1-10 cigarettes per day), heavy smokers (10 or more cigarettes per day) were 2.2 times as likely to experience abnormal frequency and 2.1 times as likely to experience abnormal urgency.

Studies such as this can only show association, not causation, but Dr. Tikkinen said at a press briefing the fact that the reasearchers controlled for so many potential confounders strengthens the case for causation.

Major Finding: Women who are current smokers are 3 times as likely to report problems with urinary frequency and 2.7 times as likely to report problems with urinary urgency as women who do not smoke.

Data Source: Population-based study of a representative sample of 1,790 Finnish women.

Disclosures: Dr. Tikkinen said that he had no conflicts. Pirkanmaa Hospital District and Pfizer funded the study through unrestricted grants.

SAN FRANCISCO — A Finnish study has found a strong association between tobacco smoking and urinary storage symptoms in women.

Women who smoke are 3 times as likely to report abnormal urinary frequency and 2.7 times as likely to report abnormal urinary urgency, compared with nonsmokers, Dr. Kari A.O. Tikkinen of Helsinki University Central Hospital said at the meeting.

The study involved survey responses from a nationally representative sample of 1,790 Finnish women aged 18-79 years (mean age 42 years). Investigators assessed urinary symptoms from responses to questions on the American Urological Association Symptom Index and the Danish Prostatic Symptom Score questionnaires.

In addition to urinary frequency and urgency, the women were asked about nocturia, stress incontinence, and urgency incontinence. The researchers found that only frequency and urgency were significantly associated with smoking.

They defined urinary frequency as abnormal if the women reported their longest interval between each urination was less than 2 hours. They defined abnormal urgency as often or always experiencing an imperative urge to urinate, nocturia as two or more voids per night, stress incontinence as often or always experiencing leakage of urine when physically active, and urgency incontinence as often or always experiencing an urge so strong that urine starts to flow before reaching the toilet.

In the multivariate analysis, the researchers controlled for a large number of potential confounders. These included 33 different physician-diagnosed medical conditions, 26 different classes of prescription medications, lifestyle and social demographic factors such as education and income, and anthropometric and reproductive factors such as body mass index and menopausal status.

About half of the women had never smoked, a quarter were current smokers, and a quarter were former smokers. The former smokers also had a significantly higher risk of abnormal urinary frequency and urgency than the never smokers, although not to the extent of current smokers. They were 70% more likely to experience abnormal frequency and 80% more likely to experience abnormal urgency than never smokers.

The researchers also found a dose-response effect. Compared with light smokers (1-10 cigarettes per day), heavy smokers (10 or more cigarettes per day) were 2.2 times as likely to experience abnormal frequency and 2.1 times as likely to experience abnormal urgency.

Studies such as this can only show association, not causation, but Dr. Tikkinen said at a press briefing the fact that the reasearchers controlled for so many potential confounders strengthens the case for causation.

Major Finding: Women who are current smokers are 3 times as likely to report problems with urinary frequency and 2.7 times as likely to report problems with urinary urgency as women who do not smoke.

Data Source: Population-based study of a representative sample of 1,790 Finnish women.

Disclosures: Dr. Tikkinen said that he had no conflicts. Pirkanmaa Hospital District and Pfizer funded the study through unrestricted grants.

SAN FRANCISCO — A Finnish study has found a strong association between tobacco smoking and urinary storage symptoms in women.

Women who smoke are 3 times as likely to report abnormal urinary frequency and 2.7 times as likely to report abnormal urinary urgency, compared with nonsmokers, Dr. Kari A.O. Tikkinen of Helsinki University Central Hospital said at the meeting.

The study involved survey responses from a nationally representative sample of 1,790 Finnish women aged 18-79 years (mean age 42 years). Investigators assessed urinary symptoms from responses to questions on the American Urological Association Symptom Index and the Danish Prostatic Symptom Score questionnaires.

In addition to urinary frequency and urgency, the women were asked about nocturia, stress incontinence, and urgency incontinence. The researchers found that only frequency and urgency were significantly associated with smoking.

They defined urinary frequency as abnormal if the women reported their longest interval between each urination was less than 2 hours. They defined abnormal urgency as often or always experiencing an imperative urge to urinate, nocturia as two or more voids per night, stress incontinence as often or always experiencing leakage of urine when physically active, and urgency incontinence as often or always experiencing an urge so strong that urine starts to flow before reaching the toilet.

In the multivariate analysis, the researchers controlled for a large number of potential confounders. These included 33 different physician-diagnosed medical conditions, 26 different classes of prescription medications, lifestyle and social demographic factors such as education and income, and anthropometric and reproductive factors such as body mass index and menopausal status.

About half of the women had never smoked, a quarter were current smokers, and a quarter were former smokers. The former smokers also had a significantly higher risk of abnormal urinary frequency and urgency than the never smokers, although not to the extent of current smokers. They were 70% more likely to experience abnormal frequency and 80% more likely to experience abnormal urgency than never smokers.

The researchers also found a dose-response effect. Compared with light smokers (1-10 cigarettes per day), heavy smokers (10 or more cigarettes per day) were 2.2 times as likely to experience abnormal frequency and 2.1 times as likely to experience abnormal urgency.

Studies such as this can only show association, not causation, but Dr. Tikkinen said at a press briefing the fact that the reasearchers controlled for so many potential confounders strengthens the case for causation.

Major Finding: Survival rate after cardiac arrest was 12.5% with chest compression alone and 11.0% with chest compression plus rescue breathing in a U.S./British study; corresponding survival rates were 8.7% and 7.0% in a Swedish study.

Data Source: Two randomized, controlled trials with a total of 3,217 patients.

Disclosures: The Laerdal Foundation for Acute Medicine funded the U.S./British study. The Stockholm County Council, SOS Alarm, and the Swedish Heart-Lung Foundation funded the Swedish study.

Two independent, randomized, controlled trials found no statistically significant differences in survival between patients in cardiac arrest who are given standard cardiopulmonary resuscitation with chest compression and rescue breathing, compared with those given chest compression alone.

Both studies showed that, when performed by laypeople, CPR with compression alone was at least as effective as compressions plus rescue breathing, while being simpler to teach and perform.

In 2008, modifying previous CPR recommendations that had stood for decades, the American Heart Association introduced the concept of “hands-only CPR.” Citing numerous animal and human studies, the AHA announced that chest compressions alone were acceptable and potentially lifesaving when performed by people not trained in conventional CPR or those who are unable or unwilling to perform rescue breathing in addition to chest compressions.

The newly published randomized, controlled trials confirm and extend the conclusions of the earlier studies. In one of the new studies, dispatchers in London and in two counties in the state of Washington randomly delivered compression-only or standard CPR instructions to 911 callers (999 in London).

That study, led by Dr. Thomas D. Rea of the University of Washington, Seattle, eventually enrolled 1,941 patients, of whom 981 received chest compression alone and 960 received chest compression plus rescue breathing. Among those patients, 12.5% who received chest compression alone and 11.0% who received compression plus rescue breathing survived to hospital discharge. The difference was not statistically significant (N. Engl. J. Med. 2010;363:423-33).

The investigators, reasoning that the two techniques might have different neurologic consequences, also investigated the proportion of patients who survived with favorable neurologic status. No significant difference was seen on that measure either.

One difference between the two groups approached—but did not reach—statistical significance. Patients who had a cardiac cause of arrest were somewhat more likely to survive to discharge if they received compressions alone (15.5% vs. 12.3%, P = .09).

In the other new study, investigators randomized 1,276 patients who were the subjects of emergency calls to the 18 emergency medical dispatch centers in Sweden. At the direction of dispatchers, 620 received compression-only CPR and 656 received standard CPR. Dr. Leif Svensson of the Karolinska Institute, Stockholm, and his colleagues found that the rate of 30-day survival was 8.7% in the compression-only group and 7.0% in the group receiving standard CPR (N. Engl. J. Med. 2010;363:434-42).

Several planned subgroup analyses in that study also failed to reveal significant group differences. In particular, the survival rates did not differ significantly with age, with the interval between the call and the first emergency medical services response, or with the interval between the call and the first cardiac rhythm.

Citing earlier studies, the investigators wrote, “Complete occlusion of the airways does not reduce the chances of survival if reasonable circulation is provided by chest compression.”

My Take

With CPR, Less May Be Better

The straightforward conclusion from the primary analyses of these studies is that continuous chest compression without active ventilation, which is simpler to teach and perform, results in a survival rate similar to that with chest compression with rescue breathing. Equally straightforward is the message that advocating continuous chest compression without ventilation should increase the frequency of bystanders effectively performing CPR and therefore increase the chances of survival after cardiac arrest. One suggestion made by [the U.S./British researchers] deserves some attention: that mouth-to-mouth ventilation is performed so poorly by bystanders that this periodic interruption for “ventilation” succeeds solely in diminishing coronary flow. Nonetheless, CPR courses should teach rescue breathing, since it is important in cases of cardiac arrest from obvious respiratory failure, which include most cardiac arrests in children and some in adults.

Excerpted from an editorial by MYRON L. WEISFELDT, M.D., of Johns Hopkins Medicine, Baltimore (N. Engl. J. Med. 2010;363:481-3). He had no relevant conflicts of interest.

Major Finding: Survival rate after cardiac arrest was 12.5% with chest compression alone and 11.0% with chest compression plus rescue breathing in a U.S./British study; corresponding survival rates were 8.7% and 7.0% in a Swedish study.

Data Source: Two randomized, controlled trials with a total of 3,217 patients.

Disclosures: The Laerdal Foundation for Acute Medicine funded the U.S./British study. The Stockholm County Council, SOS Alarm, and the Swedish Heart-Lung Foundation funded the Swedish study.

Two independent, randomized, controlled trials found no statistically significant differences in survival between patients in cardiac arrest who are given standard cardiopulmonary resuscitation with chest compression and rescue breathing, compared with those given chest compression alone.

Both studies showed that, when performed by laypeople, CPR with compression alone was at least as effective as compressions plus rescue breathing, while being simpler to teach and perform.

In 2008, modifying previous CPR recommendations that had stood for decades, the American Heart Association introduced the concept of “hands-only CPR.” Citing numerous animal and human studies, the AHA announced that chest compressions alone were acceptable and potentially lifesaving when performed by people not trained in conventional CPR or those who are unable or unwilling to perform rescue breathing in addition to chest compressions.

The newly published randomized, controlled trials confirm and extend the conclusions of the earlier studies. In one of the new studies, dispatchers in London and in two counties in the state of Washington randomly delivered compression-only or standard CPR instructions to 911 callers (999 in London).

That study, led by Dr. Thomas D. Rea of the University of Washington, Seattle, eventually enrolled 1,941 patients, of whom 981 received chest compression alone and 960 received chest compression plus rescue breathing. Among those patients, 12.5% who received chest compression alone and 11.0% who received compression plus rescue breathing survived to hospital discharge. The difference was not statistically significant (N. Engl. J. Med. 2010;363:423-33).

The investigators, reasoning that the two techniques might have different neurologic consequences, also investigated the proportion of patients who survived with favorable neurologic status. No significant difference was seen on that measure either.

One difference between the two groups approached—but did not reach—statistical significance. Patients who had a cardiac cause of arrest were somewhat more likely to survive to discharge if they received compressions alone (15.5% vs. 12.3%, P = .09).

In the other new study, investigators randomized 1,276 patients who were the subjects of emergency calls to the 18 emergency medical dispatch centers in Sweden. At the direction of dispatchers, 620 received compression-only CPR and 656 received standard CPR. Dr. Leif Svensson of the Karolinska Institute, Stockholm, and his colleagues found that the rate of 30-day survival was 8.7% in the compression-only group and 7.0% in the group receiving standard CPR (N. Engl. J. Med. 2010;363:434-42).

Several planned subgroup analyses in that study also failed to reveal significant group differences. In particular, the survival rates did not differ significantly with age, with the interval between the call and the first emergency medical services response, or with the interval between the call and the first cardiac rhythm.

Citing earlier studies, the investigators wrote, “Complete occlusion of the airways does not reduce the chances of survival if reasonable circulation is provided by chest compression.”

My Take

With CPR, Less May Be Better

The straightforward conclusion from the primary analyses of these studies is that continuous chest compression without active ventilation, which is simpler to teach and perform, results in a survival rate similar to that with chest compression with rescue breathing. Equally straightforward is the message that advocating continuous chest compression without ventilation should increase the frequency of bystanders effectively performing CPR and therefore increase the chances of survival after cardiac arrest. One suggestion made by [the U.S./British researchers] deserves some attention: that mouth-to-mouth ventilation is performed so poorly by bystanders that this periodic interruption for “ventilation” succeeds solely in diminishing coronary flow. Nonetheless, CPR courses should teach rescue breathing, since it is important in cases of cardiac arrest from obvious respiratory failure, which include most cardiac arrests in children and some in adults.

Excerpted from an editorial by MYRON L. WEISFELDT, M.D., of Johns Hopkins Medicine, Baltimore (N. Engl. J. Med. 2010;363:481-3). He had no relevant conflicts of interest.

Major Finding: Survival rate after cardiac arrest was 12.5% with chest compression alone and 11.0% with chest compression plus rescue breathing in a U.S./British study; corresponding survival rates were 8.7% and 7.0% in a Swedish study.

Data Source: Two randomized, controlled trials with a total of 3,217 patients.

Disclosures: The Laerdal Foundation for Acute Medicine funded the U.S./British study. The Stockholm County Council, SOS Alarm, and the Swedish Heart-Lung Foundation funded the Swedish study.

Two independent, randomized, controlled trials found no statistically significant differences in survival between patients in cardiac arrest who are given standard cardiopulmonary resuscitation with chest compression and rescue breathing, compared with those given chest compression alone.

Both studies showed that, when performed by laypeople, CPR with compression alone was at least as effective as compressions plus rescue breathing, while being simpler to teach and perform.

In 2008, modifying previous CPR recommendations that had stood for decades, the American Heart Association introduced the concept of “hands-only CPR.” Citing numerous animal and human studies, the AHA announced that chest compressions alone were acceptable and potentially lifesaving when performed by people not trained in conventional CPR or those who are unable or unwilling to perform rescue breathing in addition to chest compressions.

The newly published randomized, controlled trials confirm and extend the conclusions of the earlier studies. In one of the new studies, dispatchers in London and in two counties in the state of Washington randomly delivered compression-only or standard CPR instructions to 911 callers (999 in London).

That study, led by Dr. Thomas D. Rea of the University of Washington, Seattle, eventually enrolled 1,941 patients, of whom 981 received chest compression alone and 960 received chest compression plus rescue breathing. Among those patients, 12.5% who received chest compression alone and 11.0% who received compression plus rescue breathing survived to hospital discharge. The difference was not statistically significant (N. Engl. J. Med. 2010;363:423-33).

The investigators, reasoning that the two techniques might have different neurologic consequences, also investigated the proportion of patients who survived with favorable neurologic status. No significant difference was seen on that measure either.

One difference between the two groups approached—but did not reach—statistical significance. Patients who had a cardiac cause of arrest were somewhat more likely to survive to discharge if they received compressions alone (15.5% vs. 12.3%, P = .09).

In the other new study, investigators randomized 1,276 patients who were the subjects of emergency calls to the 18 emergency medical dispatch centers in Sweden. At the direction of dispatchers, 620 received compression-only CPR and 656 received standard CPR. Dr. Leif Svensson of the Karolinska Institute, Stockholm, and his colleagues found that the rate of 30-day survival was 8.7% in the compression-only group and 7.0% in the group receiving standard CPR (N. Engl. J. Med. 2010;363:434-42).

Several planned subgroup analyses in that study also failed to reveal significant group differences. In particular, the survival rates did not differ significantly with age, with the interval between the call and the first emergency medical services response, or with the interval between the call and the first cardiac rhythm.

Citing earlier studies, the investigators wrote, “Complete occlusion of the airways does not reduce the chances of survival if reasonable circulation is provided by chest compression.”

My Take

With CPR, Less May Be Better

The straightforward conclusion from the primary analyses of these studies is that continuous chest compression without active ventilation, which is simpler to teach and perform, results in a survival rate similar to that with chest compression with rescue breathing. Equally straightforward is the message that advocating continuous chest compression without ventilation should increase the frequency of bystanders effectively performing CPR and therefore increase the chances of survival after cardiac arrest. One suggestion made by [the U.S./British researchers] deserves some attention: that mouth-to-mouth ventilation is performed so poorly by bystanders that this periodic interruption for “ventilation” succeeds solely in diminishing coronary flow. Nonetheless, CPR courses should teach rescue breathing, since it is important in cases of cardiac arrest from obvious respiratory failure, which include most cardiac arrests in children and some in adults.

Excerpted from an editorial by MYRON L. WEISFELDT, M.D., of Johns Hopkins Medicine, Baltimore (N. Engl. J. Med. 2010;363:481-3). He had no relevant conflicts of interest.

Major Finding: No human studies suggest that retinyl palmitate causes skin cancer. Although some animal studies suggest an association, an analysis of results from one study showed a significant increase in neoplasms only at the highest dose tested (0.5%) and only at intermediate solar intensities (6.75 mJ/cm

Data Source: Analysis of published and unpublished human and animal studies, including one study of 430 SKH-1 hairless mice.

Disclosures: The authors stated they had no conflicts of interest.

In spite of an alarming report earlier this year by the Environmental Working Group, an analysis of human and animal studies found little support for the assertion that sunscreens containing retinyl palmitate cause skin cancer.

In a commentary published online, Dr. Steven Q. Wang of Memorial Sloan-Kettering Cancer Center, New York, and his colleagues evaluated the compound from several points of view, and concluded that “there is no convincing evidence” that retinyl palmitate, a form of vitamin A, is carcinogenic in sunscreens (J. Amer. Acad. Dermatol. 2010 [doi:10.1016/j.jaad.2010.07.015]).

“In fact, clinical observations spanning over decades suggest that retinoids are helpful in skin cancer chemoprevention,” the authors wrote. “Correcting this false impression is an important and necessary step to ensure that the public continues to use sunscreen as a component of photoprotective strategy.”

The suggestion by the Environmental Working Group, a nonprofit public health research and advocacy organization, that retinyl palmitate in sunscreens may cause skin cancer garnered widespread media attention, because 41% of sunscreens on the market contain this compound. Retinyl palmitate, an antioxidant, does not directly provide sun protection, but instead is added as a cosmetic ingredient.

Dr. Wang and his colleagues noted that retinyl palmitate and other closely related compounds are natural components of human skin. In 2000, the compound was referred to the National Institutes of Health's National Toxicology Program (NTP) for phototoxicity and photocarcinogenicity testing, along with many other common ingredients such as alpha- and beta-hydroxy acids, aloe vera, and nanoscale titanium dioxide and zinc oxide.

Between 2002 and 2009, the FDA published eight in vitro studies and three animal studies of retinyl palmitate. Several of these studies showed that the combination of retinyl palmitate and UV light induced reactive oxygen species. In addition, an NTP study involving 430 SKH-1 hairless mice examined two concentrations of retinyl palmitate and placebo at three levels of solar radiation.

This study has not been subject to peer review, but some of the data are available online, and Dr. Wang and his colleagues analyzed them. The only statistically significant results were an apparent increase in neoplasms in animals given the higher concentrations (0.5%) of retinyl palmitate at an intermediate level of simulated solar radiation (6.75 mJ/cm

In addition, that study had several limitations, including the fact that the SKH-1 strain of hairless mice is highly susceptible to the development of skin cancer after UV exposure. In fact, at the higher level of solar radiation, 82% of the mice developed malignant skin lesions when given the placebo.

Although no similar studies in humans have been published, Dr. Wang and his colleagues noted that dermatologists have been prescribing topical retinoidstfor more than 40 years, and. ave published no evidence suggesting thattopese compounds increase cancer risk.

Major Finding: No human studies suggest that retinyl palmitate causes skin cancer. Although some animal studies suggest an association, an analysis of results from one study showed a significant increase in neoplasms only at the highest dose tested (0.5%) and only at intermediate solar intensities (6.75 mJ/cm

Data Source: Analysis of published and unpublished human and animal studies, including one study of 430 SKH-1 hairless mice.

Disclosures: The authors stated they had no conflicts of interest.

In spite of an alarming report earlier this year by the Environmental Working Group, an analysis of human and animal studies found little support for the assertion that sunscreens containing retinyl palmitate cause skin cancer.

In a commentary published online, Dr. Steven Q. Wang of Memorial Sloan-Kettering Cancer Center, New York, and his colleagues evaluated the compound from several points of view, and concluded that “there is no convincing evidence” that retinyl palmitate, a form of vitamin A, is carcinogenic in sunscreens (J. Amer. Acad. Dermatol. 2010 [doi:10.1016/j.jaad.2010.07.015]).

“In fact, clinical observations spanning over decades suggest that retinoids are helpful in skin cancer chemoprevention,” the authors wrote. “Correcting this false impression is an important and necessary step to ensure that the public continues to use sunscreen as a component of photoprotective strategy.”

The suggestion by the Environmental Working Group, a nonprofit public health research and advocacy organization, that retinyl palmitate in sunscreens may cause skin cancer garnered widespread media attention, because 41% of sunscreens on the market contain this compound. Retinyl palmitate, an antioxidant, does not directly provide sun protection, but instead is added as a cosmetic ingredient.

Dr. Wang and his colleagues noted that retinyl palmitate and other closely related compounds are natural components of human skin. In 2000, the compound was referred to the National Institutes of Health's National Toxicology Program (NTP) for phototoxicity and photocarcinogenicity testing, along with many other common ingredients such as alpha- and beta-hydroxy acids, aloe vera, and nanoscale titanium dioxide and zinc oxide.

Between 2002 and 2009, the FDA published eight in vitro studies and three animal studies of retinyl palmitate. Several of these studies showed that the combination of retinyl palmitate and UV light induced reactive oxygen species. In addition, an NTP study involving 430 SKH-1 hairless mice examined two concentrations of retinyl palmitate and placebo at three levels of solar radiation.

This study has not been subject to peer review, but some of the data are available online, and Dr. Wang and his colleagues analyzed them. The only statistically significant results were an apparent increase in neoplasms in animals given the higher concentrations (0.5%) of retinyl palmitate at an intermediate level of simulated solar radiation (6.75 mJ/cm

In addition, that study had several limitations, including the fact that the SKH-1 strain of hairless mice is highly susceptible to the development of skin cancer after UV exposure. In fact, at the higher level of solar radiation, 82% of the mice developed malignant skin lesions when given the placebo.

Although no similar studies in humans have been published, Dr. Wang and his colleagues noted that dermatologists have been prescribing topical retinoidstfor more than 40 years, and. ave published no evidence suggesting thattopese compounds increase cancer risk.

Major Finding: No human studies suggest that retinyl palmitate causes skin cancer. Although some animal studies suggest an association, an analysis of results from one study showed a significant increase in neoplasms only at the highest dose tested (0.5%) and only at intermediate solar intensities (6.75 mJ/cm

Data Source: Analysis of published and unpublished human and animal studies, including one study of 430 SKH-1 hairless mice.

Disclosures: The authors stated they had no conflicts of interest.

In spite of an alarming report earlier this year by the Environmental Working Group, an analysis of human and animal studies found little support for the assertion that sunscreens containing retinyl palmitate cause skin cancer.

In a commentary published online, Dr. Steven Q. Wang of Memorial Sloan-Kettering Cancer Center, New York, and his colleagues evaluated the compound from several points of view, and concluded that “there is no convincing evidence” that retinyl palmitate, a form of vitamin A, is carcinogenic in sunscreens (J. Amer. Acad. Dermatol. 2010 [doi:10.1016/j.jaad.2010.07.015]).

“In fact, clinical observations spanning over decades suggest that retinoids are helpful in skin cancer chemoprevention,” the authors wrote. “Correcting this false impression is an important and necessary step to ensure that the public continues to use sunscreen as a component of photoprotective strategy.”

The suggestion by the Environmental Working Group, a nonprofit public health research and advocacy organization, that retinyl palmitate in sunscreens may cause skin cancer garnered widespread media attention, because 41% of sunscreens on the market contain this compound. Retinyl palmitate, an antioxidant, does not directly provide sun protection, but instead is added as a cosmetic ingredient.

Dr. Wang and his colleagues noted that retinyl palmitate and other closely related compounds are natural components of human skin. In 2000, the compound was referred to the National Institutes of Health's National Toxicology Program (NTP) for phototoxicity and photocarcinogenicity testing, along with many other common ingredients such as alpha- and beta-hydroxy acids, aloe vera, and nanoscale titanium dioxide and zinc oxide.

Between 2002 and 2009, the FDA published eight in vitro studies and three animal studies of retinyl palmitate. Several of these studies showed that the combination of retinyl palmitate and UV light induced reactive oxygen species. In addition, an NTP study involving 430 SKH-1 hairless mice examined two concentrations of retinyl palmitate and placebo at three levels of solar radiation.

This study has not been subject to peer review, but some of the data are available online, and Dr. Wang and his colleagues analyzed them. The only statistically significant results were an apparent increase in neoplasms in animals given the higher concentrations (0.5%) of retinyl palmitate at an intermediate level of simulated solar radiation (6.75 mJ/cm

In addition, that study had several limitations, including the fact that the SKH-1 strain of hairless mice is highly susceptible to the development of skin cancer after UV exposure. In fact, at the higher level of solar radiation, 82% of the mice developed malignant skin lesions when given the placebo.

Although no similar studies in humans have been published, Dr. Wang and his colleagues noted that dermatologists have been prescribing topical retinoidstfor more than 40 years, and. ave published no evidence suggesting thattopese compounds increase cancer risk.

Major Finding: In patients with treatment-resistant bipolar depression, an infusion of 0.5 mg/kg of ketamine significantly relieved depression within 40 minutes, an effect that lasted at least 3 days.

Data Source: Randomized, placebo-controlled, double-blind, crossover study involving 18 patients.

Disclosures: The National Institute of Mental Health and the National Alliance for Research on Schizophrenia and Depression funded the study. A patent application for the use of ketamine for depression has been submitted, listing two of the investigators among the inventors; they have assigned their rights on the patent to the U.S. government.

A single infusion of ketamine relieved bipolar depression within 40 minutes in patients with treatment-resistant bipolar disorder, according to a randomized, placebo-controlled, double-blind, crossover study involving 18 patients.

The effect lasted at least 3 days, wrote Dr. Nancy Diazgranados and her colleagues from the National Institute of Mental Health.

The participants in the study were an average of 48 years old, had suffered from bipolar I or bipolar II depression for an average of 28 years, and had failed an average of seven antidepressant treatments before the ketamine study. Fifty-five percent of the participants had failed to respond to electroconvulsive therapy. Two-thirds of participants were on psychiatric disability, and all but one were unemployed (Arch. Gen. Psychiatry 2010;67:793-802).

The investigators randomly assigned the patients to receive an infusion of 0.5 mg/kg of ketamine or placebo. Two weeks later, the patients who had been given ketamine were given placebo and vice versa.

Of the 17 patients who completed the ketamine phase of the study, 12 (71%) responded to ketamine. In contrast, of the 16 patients who completed the placebo phase of the study, only 1 (6%) responded to placebo.

The investigators assessed the patients at baseline using several rating scales, including the Montgomery-Åsberg Depression Rating Scale, the Hamilton Scale for Depression, and the Beck Depression Inventory.

Patients showed statistically significant improvements in depression with ketamine, compared with those who were on placebo on all three scales beginning at 40 minutes after ketamine infusion and continuing for at least 3 days. The mean scores on the rating scales did not differ from placebo on days 7, 10, and 14.

Within 40 minutes, 9 of 16 patients receiving ketamine (56%) responded and an additional 2 (13%) experienced complete remission of their depression. One day after the infusion of ketamine, 44% of the patients had responded and 31% had remitted.

None of the patients experienced serious adverse events during the study. Among the adverse events associated with ketamine and experienced by at least 10% of the patients were disassociation; feeling strange, weird, or bizarre; dry mouth; tachycardia; and increased blood pressure.

Ketamine has been used in human and veterinary medicine since 1962, most commonly for inducing and maintaining general anesthesia, sedation in intensive care, analgesia, and treatment of bronchospasm.

When used for general anesthesia, the initial dose of intravenous ketamine is typically 1.5-4.5 mg/kg, which is substantially higher than the level used in this study.

Ketamine is thought to act as a noncompetitive inhibitor of the N-methyl-d-aspartate (NMDA) receptor, which is part of the glutaminergic neurotransmitter system.

Several lines of evidence have implicated the glutaminergic system in bipolar disorder.

Major Finding: In patients with treatment-resistant bipolar depression, an infusion of 0.5 mg/kg of ketamine significantly relieved depression within 40 minutes, an effect that lasted at least 3 days.

Data Source: Randomized, placebo-controlled, double-blind, crossover study involving 18 patients.

Disclosures: The National Institute of Mental Health and the National Alliance for Research on Schizophrenia and Depression funded the study. A patent application for the use of ketamine for depression has been submitted, listing two of the investigators among the inventors; they have assigned their rights on the patent to the U.S. government.

A single infusion of ketamine relieved bipolar depression within 40 minutes in patients with treatment-resistant bipolar disorder, according to a randomized, placebo-controlled, double-blind, crossover study involving 18 patients.

The effect lasted at least 3 days, wrote Dr. Nancy Diazgranados and her colleagues from the National Institute of Mental Health.

The participants in the study were an average of 48 years old, had suffered from bipolar I or bipolar II depression for an average of 28 years, and had failed an average of seven antidepressant treatments before the ketamine study. Fifty-five percent of the participants had failed to respond to electroconvulsive therapy. Two-thirds of participants were on psychiatric disability, and all but one were unemployed (Arch. Gen. Psychiatry 2010;67:793-802).

The investigators randomly assigned the patients to receive an infusion of 0.5 mg/kg of ketamine or placebo. Two weeks later, the patients who had been given ketamine were given placebo and vice versa.

Of the 17 patients who completed the ketamine phase of the study, 12 (71%) responded to ketamine. In contrast, of the 16 patients who completed the placebo phase of the study, only 1 (6%) responded to placebo.

The investigators assessed the patients at baseline using several rating scales, including the Montgomery-Åsberg Depression Rating Scale, the Hamilton Scale for Depression, and the Beck Depression Inventory.

Patients showed statistically significant improvements in depression with ketamine, compared with those who were on placebo on all three scales beginning at 40 minutes after ketamine infusion and continuing for at least 3 days. The mean scores on the rating scales did not differ from placebo on days 7, 10, and 14.

Within 40 minutes, 9 of 16 patients receiving ketamine (56%) responded and an additional 2 (13%) experienced complete remission of their depression. One day after the infusion of ketamine, 44% of the patients had responded and 31% had remitted.

None of the patients experienced serious adverse events during the study. Among the adverse events associated with ketamine and experienced by at least 10% of the patients were disassociation; feeling strange, weird, or bizarre; dry mouth; tachycardia; and increased blood pressure.

Ketamine has been used in human and veterinary medicine since 1962, most commonly for inducing and maintaining general anesthesia, sedation in intensive care, analgesia, and treatment of bronchospasm.

When used for general anesthesia, the initial dose of intravenous ketamine is typically 1.5-4.5 mg/kg, which is substantially higher than the level used in this study.

Ketamine is thought to act as a noncompetitive inhibitor of the N-methyl-d-aspartate (NMDA) receptor, which is part of the glutaminergic neurotransmitter system.

Several lines of evidence have implicated the glutaminergic system in bipolar disorder.

Major Finding: In patients with treatment-resistant bipolar depression, an infusion of 0.5 mg/kg of ketamine significantly relieved depression within 40 minutes, an effect that lasted at least 3 days.

Data Source: Randomized, placebo-controlled, double-blind, crossover study involving 18 patients.

Disclosures: The National Institute of Mental Health and the National Alliance for Research on Schizophrenia and Depression funded the study. A patent application for the use of ketamine for depression has been submitted, listing two of the investigators among the inventors; they have assigned their rights on the patent to the U.S. government.

A single infusion of ketamine relieved bipolar depression within 40 minutes in patients with treatment-resistant bipolar disorder, according to a randomized, placebo-controlled, double-blind, crossover study involving 18 patients.

The effect lasted at least 3 days, wrote Dr. Nancy Diazgranados and her colleagues from the National Institute of Mental Health.

The participants in the study were an average of 48 years old, had suffered from bipolar I or bipolar II depression for an average of 28 years, and had failed an average of seven antidepressant treatments before the ketamine study. Fifty-five percent of the participants had failed to respond to electroconvulsive therapy. Two-thirds of participants were on psychiatric disability, and all but one were unemployed (Arch. Gen. Psychiatry 2010;67:793-802).

The investigators randomly assigned the patients to receive an infusion of 0.5 mg/kg of ketamine or placebo. Two weeks later, the patients who had been given ketamine were given placebo and vice versa.

Of the 17 patients who completed the ketamine phase of the study, 12 (71%) responded to ketamine. In contrast, of the 16 patients who completed the placebo phase of the study, only 1 (6%) responded to placebo.

The investigators assessed the patients at baseline using several rating scales, including the Montgomery-Åsberg Depression Rating Scale, the Hamilton Scale for Depression, and the Beck Depression Inventory.

Patients showed statistically significant improvements in depression with ketamine, compared with those who were on placebo on all three scales beginning at 40 minutes after ketamine infusion and continuing for at least 3 days. The mean scores on the rating scales did not differ from placebo on days 7, 10, and 14.

Within 40 minutes, 9 of 16 patients receiving ketamine (56%) responded and an additional 2 (13%) experienced complete remission of their depression. One day after the infusion of ketamine, 44% of the patients had responded and 31% had remitted.

None of the patients experienced serious adverse events during the study. Among the adverse events associated with ketamine and experienced by at least 10% of the patients were disassociation; feeling strange, weird, or bizarre; dry mouth; tachycardia; and increased blood pressure.

Ketamine has been used in human and veterinary medicine since 1962, most commonly for inducing and maintaining general anesthesia, sedation in intensive care, analgesia, and treatment of bronchospasm.

When used for general anesthesia, the initial dose of intravenous ketamine is typically 1.5-4.5 mg/kg, which is substantially higher than the level used in this study.

Ketamine is thought to act as a noncompetitive inhibitor of the N-methyl-d-aspartate (NMDA) receptor, which is part of the glutaminergic neurotransmitter system.

Several lines of evidence have implicated the glutaminergic system in bipolar disorder.

Major Findings: At 27-32 weeks of treatment, 82% of adolescents achieved remission, compared with 76% of adults at week 26 and 79% of adults at week 52.

Source of Data: A post hoc analysis of trials involving 202 adolescents aged 13-17 years and 853 adults aged 18-65 years.

Disclosures: The studies were supported by funding from Bristol-Myers Squibb and Otsuka Pharmaceutical Co. Dr. Correll acknowledged serving as a consultant to or receiving honoraria from several pharmaceutical companies, including Bristol-Myers Squibb and Otsuka Pharmaceutical. He also has served on the speakers bureaus of those two companies and several others. Several of the coauthors in each of the studies were employees of Bristol-Myers or Otsuka.

HONOLULU – Adolescents with schizophrenia respond to treatment with aripiprazole as well as adults do, according to two poster presentations at the meeting.

As in adults, an early response to aripiprazole predicted future treatment success in adolescents with schizophrenia, wrote Dr. Christoph U. Correll, medical director of the Recognition and Prevention Program at Zucker Hillside Hospital Glen Oaks, N.Y., and his colleagues.

And both adults and adolescents saw about 40-point improvements in total Positive and Negative Syndrome Scale (PANSS) scores at 32 weeks of treatment, wrote Dr. Margaretta Nyilas, director of clinical development at Otsuka Pharmaceutical Development and Commercialization Inc., Princeton, N.J., and her colleagues.

While aripiprazole is approved for the acute and maintenance treatment of schizophrenia in both adolescents and adults, relatively few studies have been performed in adolescents–especially on long-term treatment.

In addition, few studies directly address the question of whether adolescents and adults respond similarly to aripiprazole treatment.

In the early-response study, investigators conducted a post-hoc analysis of data from a 6-week randomized, double-blind, placebo-controlled trial of aripiprazole (10 or 30 mg per day) in 294 adolescents aged 13-17 years.

An early response at week 3 proved highl y sensitive and specific in predicting an even larger reduction in PANSS scores at week 6. Investigators defined early response as a 20% reduction in baseline PANSS scores. That early reduction predicted week 6 responses with a sensitivity of 88%, a specificity of 83%, a positive predictive value of 84%, and a negative predictive value of 87%.

“This is the first confirmation that, like in adults, the majority of response occurs early in adolescents with schizophrenia,” the investigators wrote. “Moreover, those who responded early are likely to maintain that status at 6 weeks.”

The investigators noted that predicting response or nonresponse early in treatment can save both time and resources.

The long-term study also found comparable remission rates between adolescents and adults.

Major Findings: At 27-32 weeks of treatment, 82% of adolescents achieved remission, compared with 76% of adults at week 26 and 79% of adults at week 52.

Source of Data: A post hoc analysis of trials involving 202 adolescents aged 13-17 years and 853 adults aged 18-65 years.

Disclosures: The studies were supported by funding from Bristol-Myers Squibb and Otsuka Pharmaceutical Co. Dr. Correll acknowledged serving as a consultant to or receiving honoraria from several pharmaceutical companies, including Bristol-Myers Squibb and Otsuka Pharmaceutical. He also has served on the speakers bureaus of those two companies and several others. Several of the coauthors in each of the studies were employees of Bristol-Myers or Otsuka.

HONOLULU – Adolescents with schizophrenia respond to treatment with aripiprazole as well as adults do, according to two poster presentations at the meeting.

As in adults, an early response to aripiprazole predicted future treatment success in adolescents with schizophrenia, wrote Dr. Christoph U. Correll, medical director of the Recognition and Prevention Program at Zucker Hillside Hospital Glen Oaks, N.Y., and his colleagues.

And both adults and adolescents saw about 40-point improvements in total Positive and Negative Syndrome Scale (PANSS) scores at 32 weeks of treatment, wrote Dr. Margaretta Nyilas, director of clinical development at Otsuka Pharmaceutical Development and Commercialization Inc., Princeton, N.J., and her colleagues.

While aripiprazole is approved for the acute and maintenance treatment of schizophrenia in both adolescents and adults, relatively few studies have been performed in adolescents–especially on long-term treatment.

In addition, few studies directly address the question of whether adolescents and adults respond similarly to aripiprazole treatment.

In the early-response study, investigators conducted a post-hoc analysis of data from a 6-week randomized, double-blind, placebo-controlled trial of aripiprazole (10 or 30 mg per day) in 294 adolescents aged 13-17 years.

An early response at week 3 proved highl y sensitive and specific in predicting an even larger reduction in PANSS scores at week 6. Investigators defined early response as a 20% reduction in baseline PANSS scores. That early reduction predicted week 6 responses with a sensitivity of 88%, a specificity of 83%, a positive predictive value of 84%, and a negative predictive value of 87%.

“This is the first confirmation that, like in adults, the majority of response occurs early in adolescents with schizophrenia,” the investigators wrote. “Moreover, those who responded early are likely to maintain that status at 6 weeks.”

The investigators noted that predicting response or nonresponse early in treatment can save both time and resources.

The long-term study also found comparable remission rates between adolescents and adults.

Major Findings: At 27-32 weeks of treatment, 82% of adolescents achieved remission, compared with 76% of adults at week 26 and 79% of adults at week 52.

Source of Data: A post hoc analysis of trials involving 202 adolescents aged 13-17 years and 853 adults aged 18-65 years.

Disclosures: The studies were supported by funding from Bristol-Myers Squibb and Otsuka Pharmaceutical Co. Dr. Correll acknowledged serving as a consultant to or receiving honoraria from several pharmaceutical companies, including Bristol-Myers Squibb and Otsuka Pharmaceutical. He also has served on the speakers bureaus of those two companies and several others. Several of the coauthors in each of the studies were employees of Bristol-Myers or Otsuka.

HONOLULU – Adolescents with schizophrenia respond to treatment with aripiprazole as well as adults do, according to two poster presentations at the meeting.

As in adults, an early response to aripiprazole predicted future treatment success in adolescents with schizophrenia, wrote Dr. Christoph U. Correll, medical director of the Recognition and Prevention Program at Zucker Hillside Hospital Glen Oaks, N.Y., and his colleagues.

And both adults and adolescents saw about 40-point improvements in total Positive and Negative Syndrome Scale (PANSS) scores at 32 weeks of treatment, wrote Dr. Margaretta Nyilas, director of clinical development at Otsuka Pharmaceutical Development and Commercialization Inc., Princeton, N.J., and her colleagues.

While aripiprazole is approved for the acute and maintenance treatment of schizophrenia in both adolescents and adults, relatively few studies have been performed in adolescents–especially on long-term treatment.

In addition, few studies directly address the question of whether adolescents and adults respond similarly to aripiprazole treatment.

In the early-response study, investigators conducted a post-hoc analysis of data from a 6-week randomized, double-blind, placebo-controlled trial of aripiprazole (10 or 30 mg per day) in 294 adolescents aged 13-17 years.

An early response at week 3 proved highl y sensitive and specific in predicting an even larger reduction in PANSS scores at week 6. Investigators defined early response as a 20% reduction in baseline PANSS scores. That early reduction predicted week 6 responses with a sensitivity of 88%, a specificity of 83%, a positive predictive value of 84%, and a negative predictive value of 87%.

“This is the first confirmation that, like in adults, the majority of response occurs early in adolescents with schizophrenia,” the investigators wrote. “Moreover, those who responded early are likely to maintain that status at 6 weeks.”

The investigators noted that predicting response or nonresponse early in treatment can save both time and resources.

The long-term study also found comparable remission rates between adolescents and adults.

In spite of an alarming report earlier this year by the Environmental Working Group, an analysis of human and animal studies found little support for the assertion that sunscreens containing retinyl palmitate cause skin cancer.

In a commentary published online in the Journal of the American Academy of Dermatology, Dr. Steven Q. Wang of Memorial Sloan-Kettering Cancer Center, New York, and his colleagues evaluated the compound from several points of view, and concluded that “there is no convincing evidence” that retinyl palmitate, a form of vitamin A, is carcinogenic in sunscreens (J. Amer. Acad. Dermatol. 2010 [doi:10.1016/j.jaad.2010.07.015]).

“In fact, clinical observations spanning over decades suggest that retinoids are helpful in skin cancer chemoprevention,” the authors wrote. “Correcting this false impression is an important and necessary step to ensure that the public continues to use sunscreen as a component of photoprotective strategy.”

The suggestion by the Environmental Working Group, a nonprofit public health research and advocacy organization, that retinyl palmitate in sunscreens may cause skin cancer garnered widespread media attention, because 41% of sunscreens on the market contain this compound. Retinyl palmitate, an antioxidant, does not directly provide sun protection, but instead is added as a cosmetic ingredient.

Dr. Wang and his colleagues noted that retinyl palmitate and other closely related compounds are natural components of human skin. In 2000, the compound was referred to the National Institutes of Health’s National Toxicology Program (NTP) for phototoxicity and photocarcinogenicity testing, along with many other common ingredients such as alpha- and beta-hydroxy acids, aloe vera, and nanoscale titanium dioxide and zinc oxide.

Between 2002 and 2009, the Food and Drug Administration published eight in vitro studies and three animal studies of retinyl palmitate. Several of these studies showed that the combination of retinyl palmitate and UV light induced reactive oxygen species. In addition, an NTP study involving 430 SKH-1 hairless mice examined two concentrations of retinyl palmitate and placebo at three levels of solar radiation.

This study has not been subject to peer review, but some of the data are available online, and Dr. Wang and his colleagues analyzed them. The only statistically significant results were an apparent increase in neoplasms in animals given the higher concentrations (0.5%) of retinyl palmitate at an intermediate level of simulated solar radiation (6.75 mJ/cm2). Higher levels of solar radiation resulted in no significant increase in neoplasms, so the authors concluded that the study failed to provide conclusive evidence indicating that the combination of retinyl palmitate and UV radiation is carcinogenic.

In addition, that study had several limitations, including the fact that the SKH-1 strain of hairless mice is highly susceptible to the development of skin cancer after UV exposure. In fact, at the higher level of solar radiation, 82% of the mice developed malignant skin lesions when given the placebo.

Although no similar studies in humans have been published, Dr. Wang and his colleagues noted that dermatologists have been prescribing various forms of topical retinoids to manage a variety of skin conditions for more than 40 years. While millions of patients have received these compounds, dermatologists have published no evidence suggesting that topical retinoids increase cancer risk.

The authors declared that they had no financial conflicts of interest.

In spite of an alarming report earlier this year by the Environmental Working Group, an analysis of human and animal studies found little support for the assertion that sunscreens containing retinyl palmitate cause skin cancer.

In a commentary published online in the Journal of the American Academy of Dermatology, Dr. Steven Q. Wang of Memorial Sloan-Kettering Cancer Center, New York, and his colleagues evaluated the compound from several points of view, and concluded that “there is no convincing evidence” that retinyl palmitate, a form of vitamin A, is carcinogenic in sunscreens (J. Amer. Acad. Dermatol. 2010 [doi:10.1016/j.jaad.2010.07.015]).

“In fact, clinical observations spanning over decades suggest that retinoids are helpful in skin cancer chemoprevention,” the authors wrote. “Correcting this false impression is an important and necessary step to ensure that the public continues to use sunscreen as a component of photoprotective strategy.”

The suggestion by the Environmental Working Group, a nonprofit public health research and advocacy organization, that retinyl palmitate in sunscreens may cause skin cancer garnered widespread media attention, because 41% of sunscreens on the market contain this compound. Retinyl palmitate, an antioxidant, does not directly provide sun protection, but instead is added as a cosmetic ingredient.

Dr. Wang and his colleagues noted that retinyl palmitate and other closely related compounds are natural components of human skin. In 2000, the compound was referred to the National Institutes of Health’s National Toxicology Program (NTP) for phototoxicity and photocarcinogenicity testing, along with many other common ingredients such as alpha- and beta-hydroxy acids, aloe vera, and nanoscale titanium dioxide and zinc oxide.

Between 2002 and 2009, the Food and Drug Administration published eight in vitro studies and three animal studies of retinyl palmitate. Several of these studies showed that the combination of retinyl palmitate and UV light induced reactive oxygen species. In addition, an NTP study involving 430 SKH-1 hairless mice examined two concentrations of retinyl palmitate and placebo at three levels of solar radiation.

This study has not been subject to peer review, but some of the data are available online, and Dr. Wang and his colleagues analyzed them. The only statistically significant results were an apparent increase in neoplasms in animals given the higher concentrations (0.5%) of retinyl palmitate at an intermediate level of simulated solar radiation (6.75 mJ/cm2). Higher levels of solar radiation resulted in no significant increase in neoplasms, so the authors concluded that the study failed to provide conclusive evidence indicating that the combination of retinyl palmitate and UV radiation is carcinogenic.

In addition, that study had several limitations, including the fact that the SKH-1 strain of hairless mice is highly susceptible to the development of skin cancer after UV exposure. In fact, at the higher level of solar radiation, 82% of the mice developed malignant skin lesions when given the placebo.

Although no similar studies in humans have been published, Dr. Wang and his colleagues noted that dermatologists have been prescribing various forms of topical retinoids to manage a variety of skin conditions for more than 40 years. While millions of patients have received these compounds, dermatologists have published no evidence suggesting that topical retinoids increase cancer risk.

The authors declared that they had no financial conflicts of interest.

In spite of an alarming report earlier this year by the Environmental Working Group, an analysis of human and animal studies found little support for the assertion that sunscreens containing retinyl palmitate cause skin cancer.

In a commentary published online in the Journal of the American Academy of Dermatology, Dr. Steven Q. Wang of Memorial Sloan-Kettering Cancer Center, New York, and his colleagues evaluated the compound from several points of view, and concluded that “there is no convincing evidence” that retinyl palmitate, a form of vitamin A, is carcinogenic in sunscreens (J. Amer. Acad. Dermatol. 2010 [doi:10.1016/j.jaad.2010.07.015]).

“In fact, clinical observations spanning over decades suggest that retinoids are helpful in skin cancer chemoprevention,” the authors wrote. “Correcting this false impression is an important and necessary step to ensure that the public continues to use sunscreen as a component of photoprotective strategy.”

The suggestion by the Environmental Working Group, a nonprofit public health research and advocacy organization, that retinyl palmitate in sunscreens may cause skin cancer garnered widespread media attention, because 41% of sunscreens on the market contain this compound. Retinyl palmitate, an antioxidant, does not directly provide sun protection, but instead is added as a cosmetic ingredient.

Dr. Wang and his colleagues noted that retinyl palmitate and other closely related compounds are natural components of human skin. In 2000, the compound was referred to the National Institutes of Health’s National Toxicology Program (NTP) for phototoxicity and photocarcinogenicity testing, along with many other common ingredients such as alpha- and beta-hydroxy acids, aloe vera, and nanoscale titanium dioxide and zinc oxide.

Between 2002 and 2009, the Food and Drug Administration published eight in vitro studies and three animal studies of retinyl palmitate. Several of these studies showed that the combination of retinyl palmitate and UV light induced reactive oxygen species. In addition, an NTP study involving 430 SKH-1 hairless mice examined two concentrations of retinyl palmitate and placebo at three levels of solar radiation.

This study has not been subject to peer review, but some of the data are available online, and Dr. Wang and his colleagues analyzed them. The only statistically significant results were an apparent increase in neoplasms in animals given the higher concentrations (0.5%) of retinyl palmitate at an intermediate level of simulated solar radiation (6.75 mJ/cm2). Higher levels of solar radiation resulted in no significant increase in neoplasms, so the authors concluded that the study failed to provide conclusive evidence indicating that the combination of retinyl palmitate and UV radiation is carcinogenic.

In addition, that study had several limitations, including the fact that the SKH-1 strain of hairless mice is highly susceptible to the development of skin cancer after UV exposure. In fact, at the higher level of solar radiation, 82% of the mice developed malignant skin lesions when given the placebo.

Although no similar studies in humans have been published, Dr. Wang and his colleagues noted that dermatologists have been prescribing various forms of topical retinoids to manage a variety of skin conditions for more than 40 years. While millions of patients have received these compounds, dermatologists have published no evidence suggesting that topical retinoids increase cancer risk.

The authors declared that they had no financial conflicts of interest.

Patients newly diagnosed with prostate cancer who have a prostate specific antigen levels of 4.0 ng/mL or below tend to receive aggressive therapy despite having a low risk of disease, according to a retrospective study of 123,934 men in the July 26 issue of the Archives of Internal Medicine.

In a multivariate analysis correcting for age, race, and year of diagnosis, men with screen-detected prostate cancer and prostate specific antigen (PSA) values of 4.0 ng/mL or below were 49% more likely to undergo radical prostatectomy and 39% more likely to undergo radiation therapy than were men with non–screen detected prostate cancer, according to Yu-Hsuan Shao, Ph.D., of the Cancer Institute of New Jersey, New Brunswick, and her colleagues.

Although 54% of men diagnosed with prostate cancer with low PSA levels harbor low-risk disease, 77% of them underwent radical prostatectomy or radiotherapy. Men with low PSA levels and screen-detected prostate cancer were 33% less likely to have high-grade disease than were men with non–screen detected prostate cancer, the investigators said.

“The finding that men in low-risk groups were treated intensively raises the concern of overtreatment, especially among older patients,” the authors wrote.

Investigators used the Surveillance, Epidemiology, and End Results (SEER) database, covering approximately 26% of the U.S. population, to identify men newly diagnosed with prostate cancer between 2004 and 2006. They excluded men under the age of 24 years, those with missing PSA values, or those with missing Gleason scores and clinical stage.

The men in the study were divided into four groups based on PSA values. A total of 14% of the men had PSA values of 4.0 ng/mL or less, 57.6% had values between 4.1-10.0 ng/mL, 15.9% had values between 10.1-20.0 ng/mL, and 12.5% had values above 20 ng/mL (Arch. Int. Med. 2010;170:1256-61).

Of the men with the lowest PSA values, 44% underwent radical prostatectomy, 33% underwent radiation therapy, and 23% were treated with conservative management. In contrast, of the men with the highest PSA levels, 12.5% underwent radical prostatectomy, 31.5% underwent radiation therapy, and 56% were treated with conservative management.

One of the study’s authors acknowledged receiving clinical research funding from the Ohl Foundation, the New Jersey Commission on Cancer Research, and the Agency for Healthcare Research and Quality. Another author acknowledged receiving clinical research funding from Sanofi-Aventis and consultation fees from Blue Cross/Blue Shield. The study was supported by the National Cancer Institute, the Cancer Institute of New Jersey, and the Robert Wood Johnson Foundation.

Patients newly diagnosed with prostate cancer who have a prostate specific antigen levels of 4.0 ng/mL or below tend to receive aggressive therapy despite having a low risk of disease, according to a retrospective study of 123,934 men in the July 26 issue of the Archives of Internal Medicine.

In a multivariate analysis correcting for age, race, and year of diagnosis, men with screen-detected prostate cancer and prostate specific antigen (PSA) values of 4.0 ng/mL or below were 49% more likely to undergo radical prostatectomy and 39% more likely to undergo radiation therapy than were men with non–screen detected prostate cancer, according to Yu-Hsuan Shao, Ph.D., of the Cancer Institute of New Jersey, New Brunswick, and her colleagues.

Although 54% of men diagnosed with prostate cancer with low PSA levels harbor low-risk disease, 77% of them underwent radical prostatectomy or radiotherapy. Men with low PSA levels and screen-detected prostate cancer were 33% less likely to have high-grade disease than were men with non–screen detected prostate cancer, the investigators said.

“The finding that men in low-risk groups were treated intensively raises the concern of overtreatment, especially among older patients,” the authors wrote.

Investigators used the Surveillance, Epidemiology, and End Results (SEER) database, covering approximately 26% of the U.S. population, to identify men newly diagnosed with prostate cancer between 2004 and 2006. They excluded men under the age of 24 years, those with missing PSA values, or those with missing Gleason scores and clinical stage.

The men in the study were divided into four groups based on PSA values. A total of 14% of the men had PSA values of 4.0 ng/mL or less, 57.6% had values between 4.1-10.0 ng/mL, 15.9% had values between 10.1-20.0 ng/mL, and 12.5% had values above 20 ng/mL (Arch. Int. Med. 2010;170:1256-61).

Of the men with the lowest PSA values, 44% underwent radical prostatectomy, 33% underwent radiation therapy, and 23% were treated with conservative management. In contrast, of the men with the highest PSA levels, 12.5% underwent radical prostatectomy, 31.5% underwent radiation therapy, and 56% were treated with conservative management.

One of the study’s authors acknowledged receiving clinical research funding from the Ohl Foundation, the New Jersey Commission on Cancer Research, and the Agency for Healthcare Research and Quality. Another author acknowledged receiving clinical research funding from Sanofi-Aventis and consultation fees from Blue Cross/Blue Shield. The study was supported by the National Cancer Institute, the Cancer Institute of New Jersey, and the Robert Wood Johnson Foundation.

Patients newly diagnosed with prostate cancer who have a prostate specific antigen levels of 4.0 ng/mL or below tend to receive aggressive therapy despite having a low risk of disease, according to a retrospective study of 123,934 men in the July 26 issue of the Archives of Internal Medicine.

In a multivariate analysis correcting for age, race, and year of diagnosis, men with screen-detected prostate cancer and prostate specific antigen (PSA) values of 4.0 ng/mL or below were 49% more likely to undergo radical prostatectomy and 39% more likely to undergo radiation therapy than were men with non–screen detected prostate cancer, according to Yu-Hsuan Shao, Ph.D., of the Cancer Institute of New Jersey, New Brunswick, and her colleagues.

Although 54% of men diagnosed with prostate cancer with low PSA levels harbor low-risk disease, 77% of them underwent radical prostatectomy or radiotherapy. Men with low PSA levels and screen-detected prostate cancer were 33% less likely to have high-grade disease than were men with non–screen detected prostate cancer, the investigators said.

“The finding that men in low-risk groups were treated intensively raises the concern of overtreatment, especially among older patients,” the authors wrote.

Investigators used the Surveillance, Epidemiology, and End Results (SEER) database, covering approximately 26% of the U.S. population, to identify men newly diagnosed with prostate cancer between 2004 and 2006. They excluded men under the age of 24 years, those with missing PSA values, or those with missing Gleason scores and clinical stage.

The men in the study were divided into four groups based on PSA values. A total of 14% of the men had PSA values of 4.0 ng/mL or less, 57.6% had values between 4.1-10.0 ng/mL, 15.9% had values between 10.1-20.0 ng/mL, and 12.5% had values above 20 ng/mL (Arch. Int. Med. 2010;170:1256-61).

Of the men with the lowest PSA values, 44% underwent radical prostatectomy, 33% underwent radiation therapy, and 23% were treated with conservative management. In contrast, of the men with the highest PSA levels, 12.5% underwent radical prostatectomy, 31.5% underwent radiation therapy, and 56% were treated with conservative management.

One of the study’s authors acknowledged receiving clinical research funding from the Ohl Foundation, the New Jersey Commission on Cancer Research, and the Agency for Healthcare Research and Quality. Another author acknowledged receiving clinical research funding from Sanofi-Aventis and consultation fees from Blue Cross/Blue Shield. The study was supported by the National Cancer Institute, the Cancer Institute of New Jersey, and the Robert Wood Johnson Foundation.

A prospective observational study that began following more than 50,000 California teachers in 1995 has confirmed reports linking hormone replacement therapy to breast cancer, but suggests obesity may offer some protection.

Data from 56,867 women enrolled in the California Teachers Study indicate that women who used estrogen therapy for at least 15 years had a 19% increase in the risk of breast cancer, and women who used combined estrogen-progestin therapy had an 83% increase in breast cancer risk.

The increase in risk was confined to tumors that were positive for both estrogen and progesterone receptors, wrote Tanmei Saxena of the University of Southern California, Los Angeles, and her coauthors. It was also more pronounced in women with low body mass index (BMI).

Ms. Saxena is an M.D./Ph.D. student at USC’s Keck School of Medicine. The study is published in the September issue of the journal Cancer Epidemiology, Biomarkers and Prevention.

“These findings, taken in context of the larger literature on this topic, continue to underscore the need to personalize risk-benefit discussions for women contemplating the use of [hormone therapy],” wrote the investigators (Cancer Epidemiol. Biomarkers Prev. 2010;19:OF1-13).

The California Teachers Study is a prospective cohort study of 133,479 women who were enrolled in 1995. For the purposes of this study, the investigators excluded women who were not California residents, who had a previous or unknown history of breast cancer, who were older than 80 years at baseline, who were premenopausal or of unknown menopausal status, or who had an unknown history of hormone therapy.

Of the remaining 56,867 perimenopausal and postmenopausal teachers, 2,857 women (5%) were diagnosed with pathologically confirmed invasive breast cancer through December 2006, after a mean follow-up of 9.8 years. The average age at diagnosis was 67.1 years.

In a multivariate analysis, the investigators adjusted for race/ethnicity, first-degree family history of breast cancer, BMI, smoking history, alcohol consumption during the year prior to baseline, mammographic screening over the prior 2 years, parity and age at first full-term pregnancy, age at menarche, age at menopause, and history of breast biopsy.

Compared with women who never used any hormone therapy, those who did had a statistically significant 40% increase in the risk of breast cancer. The increase in risk was 19% for women who reported at least 15 years of estrogen-alone therapy, and 83% in women who reported at least 15 years of combined estrogen-progestin therapy.

Current use of hormonal therapy was associated with higher risk than past use. The greatest increase in risk – 69% – was among women who were using estrogen-progestin therapy currently and had never used any other formulation. The investigators noted that duration of use tended to be shorter among former users.

The longer the women used hormone therapy, the greater the risk. The increase associated with duration of use was statistically significant for all forms of hormone therapy. For example, women using estrogen-progestin therapy for less than 2 years at baseline had a 12% increase in the risk of breast cancer, compared with women who never used hormone therapy. The increase in risk was 42% for those using estrogen-progestin therapy for 3-5 years, 50% at 6-9 years, 67% at 10-14 years, 79% at 15-19 years, and 92% at 20 years or more.

Among current users of hormonal therapy, the association with breast cancer risk was statistically significant only for tumors that were both estrogen receptor–positive and progesterone receptor–positive, with increased risks of 33% in women who had 15 or more years of estrogen therapy and 84% in those who had been on estrogen and progestin for 15 years or more. The risks were even higher for women whose tumors were also HER2 positive, but the investigators suggested this might be a statistical fluke because of the small numbers involved. No association was seen between long duration of hormone use and triple-negative tumors.

BMI seemed to modify the risk associated with hormonal therapy, the investigators reported. Among women with a BMI of 25 or less, the relative risk of breast cancer was 2.1 in current long-term users of estrogen and progestin, compared with women who had never used hormone therapy (P less than .0001). In women with a BMI of 25-30, the relative risk was 1.9 in current long-term users of estrogen and progestin (P less than .0001). However, the effect was not statistically significant in women with a BMI higher than 30 (RR 1.2, P = .11).

The National Cancer Institute and the California Breast Cancer Research Fund sponsored the study. A coauthor disclosed serving as an expert witness for plaintiffs pursuing Prempro litigation.

A prospective observational study that began following more than 50,000 California teachers in 1995 has confirmed reports linking hormone replacement therapy to breast cancer, but suggests obesity may offer some protection.

Data from 56,867 women enrolled in the California Teachers Study indicate that women who used estrogen therapy for at least 15 years had a 19% increase in the risk of breast cancer, and women who used combined estrogen-progestin therapy had an 83% increase in breast cancer risk.

The increase in risk was confined to tumors that were positive for both estrogen and progesterone receptors, wrote Tanmei Saxena of the University of Southern California, Los Angeles, and her coauthors. It was also more pronounced in women with low body mass index (BMI).

Ms. Saxena is an M.D./Ph.D. student at USC’s Keck School of Medicine. The study is published in the September issue of the journal Cancer Epidemiology, Biomarkers and Prevention.

“These findings, taken in context of the larger literature on this topic, continue to underscore the need to personalize risk-benefit discussions for women contemplating the use of [hormone therapy],” wrote the investigators (Cancer Epidemiol. Biomarkers Prev. 2010;19:OF1-13).

The California Teachers Study is a prospective cohort study of 133,479 women who were enrolled in 1995. For the purposes of this study, the investigators excluded women who were not California residents, who had a previous or unknown history of breast cancer, who were older than 80 years at baseline, who were premenopausal or of unknown menopausal status, or who had an unknown history of hormone therapy.

Of the remaining 56,867 perimenopausal and postmenopausal teachers, 2,857 women (5%) were diagnosed with pathologically confirmed invasive breast cancer through December 2006, after a mean follow-up of 9.8 years. The average age at diagnosis was 67.1 years.

In a multivariate analysis, the investigators adjusted for race/ethnicity, first-degree family history of breast cancer, BMI, smoking history, alcohol consumption during the year prior to baseline, mammographic screening over the prior 2 years, parity and age at first full-term pregnancy, age at menarche, age at menopause, and history of breast biopsy.

Compared with women who never used any hormone therapy, those who did had a statistically significant 40% increase in the risk of breast cancer. The increase in risk was 19% for women who reported at least 15 years of estrogen-alone therapy, and 83% in women who reported at least 15 years of combined estrogen-progestin therapy.

Current use of hormonal therapy was associated with higher risk than past use. The greatest increase in risk – 69% – was among women who were using estrogen-progestin therapy currently and had never used any other formulation. The investigators noted that duration of use tended to be shorter among former users.

The longer the women used hormone therapy, the greater the risk. The increase associated with duration of use was statistically significant for all forms of hormone therapy. For example, women using estrogen-progestin therapy for less than 2 years at baseline had a 12% increase in the risk of breast cancer, compared with women who never used hormone therapy. The increase in risk was 42% for those using estrogen-progestin therapy for 3-5 years, 50% at 6-9 years, 67% at 10-14 years, 79% at 15-19 years, and 92% at 20 years or more.

Among current users of hormonal therapy, the association with breast cancer risk was statistically significant only for tumors that were both estrogen receptor–positive and progesterone receptor–positive, with increased risks of 33% in women who had 15 or more years of estrogen therapy and 84% in those who had been on estrogen and progestin for 15 years or more. The risks were even higher for women whose tumors were also HER2 positive, but the investigators suggested this might be a statistical fluke because of the small numbers involved. No association was seen between long duration of hormone use and triple-negative tumors.

BMI seemed to modify the risk associated with hormonal therapy, the investigators reported. Among women with a BMI of 25 or less, the relative risk of breast cancer was 2.1 in current long-term users of estrogen and progestin, compared with women who had never used hormone therapy (P less than .0001). In women with a BMI of 25-30, the relative risk was 1.9 in current long-term users of estrogen and progestin (P less than .0001). However, the effect was not statistically significant in women with a BMI higher than 30 (RR 1.2, P = .11).

The National Cancer Institute and the California Breast Cancer Research Fund sponsored the study. A coauthor disclosed serving as an expert witness for plaintiffs pursuing Prempro litigation.

A prospective observational study that began following more than 50,000 California teachers in 1995 has confirmed reports linking hormone replacement therapy to breast cancer, but suggests obesity may offer some protection.

Data from 56,867 women enrolled in the California Teachers Study indicate that women who used estrogen therapy for at least 15 years had a 19% increase in the risk of breast cancer, and women who used combined estrogen-progestin therapy had an 83% increase in breast cancer risk.

The increase in risk was confined to tumors that were positive for both estrogen and progesterone receptors, wrote Tanmei Saxena of the University of Southern California, Los Angeles, and her coauthors. It was also more pronounced in women with low body mass index (BMI).

Ms. Saxena is an M.D./Ph.D. student at USC’s Keck School of Medicine. The study is published in the September issue of the journal Cancer Epidemiology, Biomarkers and Prevention.

“These findings, taken in context of the larger literature on this topic, continue to underscore the need to personalize risk-benefit discussions for women contemplating the use of [hormone therapy],” wrote the investigators (Cancer Epidemiol. Biomarkers Prev. 2010;19:OF1-13).

The California Teachers Study is a prospective cohort study of 133,479 women who were enrolled in 1995. For the purposes of this study, the investigators excluded women who were not California residents, who had a previous or unknown history of breast cancer, who were older than 80 years at baseline, who were premenopausal or of unknown menopausal status, or who had an unknown history of hormone therapy.

Of the remaining 56,867 perimenopausal and postmenopausal teachers, 2,857 women (5%) were diagnosed with pathologically confirmed invasive breast cancer through December 2006, after a mean follow-up of 9.8 years. The average age at diagnosis was 67.1 years.

In a multivariate analysis, the investigators adjusted for race/ethnicity, first-degree family history of breast cancer, BMI, smoking history, alcohol consumption during the year prior to baseline, mammographic screening over the prior 2 years, parity and age at first full-term pregnancy, age at menarche, age at menopause, and history of breast biopsy.

Compared with women who never used any hormone therapy, those who did had a statistically significant 40% increase in the risk of breast cancer. The increase in risk was 19% for women who reported at least 15 years of estrogen-alone therapy, and 83% in women who reported at least 15 years of combined estrogen-progestin therapy.

Current use of hormonal therapy was associated with higher risk than past use. The greatest increase in risk – 69% – was among women who were using estrogen-progestin therapy currently and had never used any other formulation. The investigators noted that duration of use tended to be shorter among former users.

The longer the women used hormone therapy, the greater the risk. The increase associated with duration of use was statistically significant for all forms of hormone therapy. For example, women using estrogen-progestin therapy for less than 2 years at baseline had a 12% increase in the risk of breast cancer, compared with women who never used hormone therapy. The increase in risk was 42% for those using estrogen-progestin therapy for 3-5 years, 50% at 6-9 years, 67% at 10-14 years, 79% at 15-19 years, and 92% at 20 years or more.

Among current users of hormonal therapy, the association with breast cancer risk was statistically significant only for tumors that were both estrogen receptor–positive and progesterone receptor–positive, with increased risks of 33% in women who had 15 or more years of estrogen therapy and 84% in those who had been on estrogen and progestin for 15 years or more. The risks were even higher for women whose tumors were also HER2 positive, but the investigators suggested this might be a statistical fluke because of the small numbers involved. No association was seen between long duration of hormone use and triple-negative tumors.

BMI seemed to modify the risk associated with hormonal therapy, the investigators reported. Among women with a BMI of 25 or less, the relative risk of breast cancer was 2.1 in current long-term users of estrogen and progestin, compared with women who had never used hormone therapy (P less than .0001). In women with a BMI of 25-30, the relative risk was 1.9 in current long-term users of estrogen and progestin (P less than .0001). However, the effect was not statistically significant in women with a BMI higher than 30 (RR 1.2, P = .11).

The National Cancer Institute and the California Breast Cancer Research Fund sponsored the study. A coauthor disclosed serving as an expert witness for plaintiffs pursuing Prempro litigation.

Two independent, randomized, controlled trials found no statistically significant differences in survival between patients in cardiac arrest who are given standard cardiopulmonary resuscitation with chest compression and rescue breathing, compared with those given chest compression alone.

The studies both concluded that when performed by laypeople, CPR with chest compression alone was at least as effective as compressions plus rescue breathing, while also being simpler to teach and to perform. Both studies appear in the July 29, 2010, issue of the New England Journal of Medicine.

In 2008, modifying previous CPR recommendations that had stood for decades, the American Heart Association introduced the concept of “hands-only CPR.” Citing numerous animal and human studies, the AHA announced that chest compressions alone were acceptable and potentially lifesaving when performed by people not trained in conventional CPR or those who are unable or unwilling to perform rescue breathing in addition to chest compressions.

The newly published randomized, controlled trials confirm and extend the conclusions of the earlier studies. In one of the new studies, dispatchers in London and in two counties in the state of Washington randomly delivered compression-only or standard CPR instructions to 911 callers (999 in London). That study, led by Dr. Thomas D. Rea of the University of Washington, Seattle, eventually enrolled 1,941 patients, of whom 981 received chest compression alone and 960 received chest compression plus rescue breathing. Among those patients, 12.5% who received chest compression alone and 11.0% who received compression plus rescue breathing survived to hospital discharge. The difference was not statistically significant (N. Engl. J. Med. 2010;363:423-33).

The investigators, reasoning that the two techniques might have different neurologic consequences, also investigated the proportion of patients who survived with favorable neurologic status. No significant difference was seen on that measure either.

One difference between the two groups approached – but did not reach – statistical significance. Patients who had a cardiac cause of arrest were somewhat more likely to survive to discharge if they received compressions alone (15.5% vs. 12.3%, P = .09). Conversely, the survival rate among patients with noncardiac causes of arrest was 5.0% with compressions alone and 7.2% with chest compressions plus rescue breathing, but this difference was even farther from statistical significance (P = .29).

In the other new study, investigators randomized 1,276 patients who were the subjects of emergency calls to the 18 emergency medical dispatch centers in Sweden. At the direction of dispatchers, 620 received compression-only CPR and 656 received standard CPR. Dr. Leif Svensson of the Karolinska Institute, Stockholm, and his colleagues found that the rate of 30-day survival was 8.7% in the compression-only group and 7.0% in the group receiving standard CPR (N. Engl. J. Med. 2010;363:434-42).

Several planned subgroup analyses in that study also failed to reveal significant group differences. In particular, the survival rates did not differ significantly with age, with the interval between the call and the first emergency medical services response, or with the interval between the call and the first cardiac rhythm.

Citing earlier studies, Dr. Svensson and his colleagues wrote, “Complete occlusion of the airways does not reduce the chances of survival if reasonable circulation is provided by chest compression.”

They also pointed to studies demonstrating that laypeople have difficulty providing adequate ventilation using rescue breaths. Standard CPR guidelines call for the two breaths after each set of 15 chest compressions to take 1.5-2 seconds/breath. But in one study, people not trained in CPR took 16 seconds on average to deliver the two breaths.

“Overall, the study lends further support to the hypothesis that compression-only CPR, which is easier to learn and to perform, should be considered the preferred method for CPR performed by bystanders in patients with cardiac arrest,” Dr. Svensson and his colleagues wrote.

The U.S./British study was funded by the Laerdal Foundation for Acute Medicine. Two of the investigators acknowledged receiving defibrillators and funding from Philips Medical Systems and Physio-Control, and disclosed that their institutions received funding from the Medtronic Foundation. The Swedish study received funding from Stockholm County Council, SOS Alarm, and the Swedish Heart-Lung Foundation. The investigators stated that they had no other conflicts of interest.

Two independent, randomized, controlled trials found no statistically significant differences in survival between patients in cardiac arrest who are given standard cardiopulmonary resuscitation with chest compression and rescue breathing, compared with those given chest compression alone.

The studies both concluded that when performed by laypeople, CPR with chest compression alone was at least as effective as compressions plus rescue breathing, while also being simpler to teach and to perform. Both studies appear in the July 29, 2010, issue of the New England Journal of Medicine.

In 2008, modifying previous CPR recommendations that had stood for decades, the American Heart Association introduced the concept of “hands-only CPR.” Citing numerous animal and human studies, the AHA announced that chest compressions alone were acceptable and potentially lifesaving when performed by people not trained in conventional CPR or those who are unable or unwilling to perform rescue breathing in addition to chest compressions.

The newly published randomized, controlled trials confirm and extend the conclusions of the earlier studies. In one of the new studies, dispatchers in London and in two counties in the state of Washington randomly delivered compression-only or standard CPR instructions to 911 callers (999 in London). That study, led by Dr. Thomas D. Rea of the University of Washington, Seattle, eventually enrolled 1,941 patients, of whom 981 received chest compression alone and 960 received chest compression plus rescue breathing. Among those patients, 12.5% who received chest compression alone and 11.0% who received compression plus rescue breathing survived to hospital discharge. The difference was not statistically significant (N. Engl. J. Med. 2010;363:423-33).

The investigators, reasoning that the two techniques might have different neurologic consequences, also investigated the proportion of patients who survived with favorable neurologic status. No significant difference was seen on that measure either.

One difference between the two groups approached – but did not reach – statistical significance. Patients who had a cardiac cause of arrest were somewhat more likely to survive to discharge if they received compressions alone (15.5% vs. 12.3%, P = .09). Conversely, the survival rate among patients with noncardiac causes of arrest was 5.0% with compressions alone and 7.2% with chest compressions plus rescue breathing, but this difference was even farther from statistical significance (P = .29).

In the other new study, investigators randomized 1,276 patients who were the subjects of emergency calls to the 18 emergency medical dispatch centers in Sweden. At the direction of dispatchers, 620 received compression-only CPR and 656 received standard CPR. Dr. Leif Svensson of the Karolinska Institute, Stockholm, and his colleagues found that the rate of 30-day survival was 8.7% in the compression-only group and 7.0% in the group receiving standard CPR (N. Engl. J. Med. 2010;363:434-42).

Several planned subgroup analyses in that study also failed to reveal significant group differences. In particular, the survival rates did not differ significantly with age, with the interval between the call and the first emergency medical services response, or with the interval between the call and the first cardiac rhythm.

Citing earlier studies, Dr. Svensson and his colleagues wrote, “Complete occlusion of the airways does not reduce the chances of survival if reasonable circulation is provided by chest compression.”

They also pointed to studies demonstrating that laypeople have difficulty providing adequate ventilation using rescue breaths. Standard CPR guidelines call for the two breaths after each set of 15 chest compressions to take 1.5-2 seconds/breath. But in one study, people not trained in CPR took 16 seconds on average to deliver the two breaths.

“Overall, the study lends further support to the hypothesis that compression-only CPR, which is easier to learn and to perform, should be considered the preferred method for CPR performed by bystanders in patients with cardiac arrest,” Dr. Svensson and his colleagues wrote.

The U.S./British study was funded by the Laerdal Foundation for Acute Medicine. Two of the investigators acknowledged receiving defibrillators and funding from Philips Medical Systems and Physio-Control, and disclosed that their institutions received funding from the Medtronic Foundation. The Swedish study received funding from Stockholm County Council, SOS Alarm, and the Swedish Heart-Lung Foundation. The investigators stated that they had no other conflicts of interest.

Two independent, randomized, controlled trials found no statistically significant differences in survival between patients in cardiac arrest who are given standard cardiopulmonary resuscitation with chest compression and rescue breathing, compared with those given chest compression alone.

The studies both concluded that when performed by laypeople, CPR with chest compression alone was at least as effective as compressions plus rescue breathing, while also being simpler to teach and to perform. Both studies appear in the July 29, 2010, issue of the New England Journal of Medicine.

In 2008, modifying previous CPR recommendations that had stood for decades, the American Heart Association introduced the concept of “hands-only CPR.” Citing numerous animal and human studies, the AHA announced that chest compressions alone were acceptable and potentially lifesaving when performed by people not trained in conventional CPR or those who are unable or unwilling to perform rescue breathing in addition to chest compressions.

The newly published randomized, controlled trials confirm and extend the conclusions of the earlier studies. In one of the new studies, dispatchers in London and in two counties in the state of Washington randomly delivered compression-only or standard CPR instructions to 911 callers (999 in London). That study, led by Dr. Thomas D. Rea of the University of Washington, Seattle, eventually enrolled 1,941 patients, of whom 981 received chest compression alone and 960 received chest compression plus rescue breathing. Among those patients, 12.5% who received chest compression alone and 11.0% who received compression plus rescue breathing survived to hospital discharge. The difference was not statistically significant (N. Engl. J. Med. 2010;363:423-33).

The investigators, reasoning that the two techniques might have different neurologic consequences, also investigated the proportion of patients who survived with favorable neurologic status. No significant difference was seen on that measure either.

One difference between the two groups approached – but did not reach – statistical significance. Patients who had a cardiac cause of arrest were somewhat more likely to survive to discharge if they received compressions alone (15.5% vs. 12.3%, P = .09). Conversely, the survival rate among patients with noncardiac causes of arrest was 5.0% with compressions alone and 7.2% with chest compressions plus rescue breathing, but this difference was even farther from statistical significance (P = .29).

In the other new study, investigators randomized 1,276 patients who were the subjects of emergency calls to the 18 emergency medical dispatch centers in Sweden. At the direction of dispatchers, 620 received compression-only CPR and 656 received standard CPR. Dr. Leif Svensson of the Karolinska Institute, Stockholm, and his colleagues found that the rate of 30-day survival was 8.7% in the compression-only group and 7.0% in the group receiving standard CPR (N. Engl. J. Med. 2010;363:434-42).

Several planned subgroup analyses in that study also failed to reveal significant group differences. In particular, the survival rates did not differ significantly with age, with the interval between the call and the first emergency medical services response, or with the interval between the call and the first cardiac rhythm.

Citing earlier studies, Dr. Svensson and his colleagues wrote, “Complete occlusion of the airways does not reduce the chances of survival if reasonable circulation is provided by chest compression.”

They also pointed to studies demonstrating that laypeople have difficulty providing adequate ventilation using rescue breaths. Standard CPR guidelines call for the two breaths after each set of 15 chest compressions to take 1.5-2 seconds/breath. But in one study, people not trained in CPR took 16 seconds on average to deliver the two breaths.

“Overall, the study lends further support to the hypothesis that compression-only CPR, which is easier to learn and to perform, should be considered the preferred method for CPR performed by bystanders in patients with cardiac arrest,” Dr. Svensson and his colleagues wrote.

The U.S./British study was funded by the Laerdal Foundation for Acute Medicine. Two of the investigators acknowledged receiving defibrillators and funding from Philips Medical Systems and Physio-Control, and disclosed that their institutions received funding from the Medtronic Foundation. The Swedish study received funding from Stockholm County Council, SOS Alarm, and the Swedish Heart-Lung Foundation. The investigators stated that they had no other conflicts of interest.

An intervention intended to increase empowerment among Chinese female victims of intimate partner violence failed to decrease depression appreciably more than did usual community services, according to a randomized, controlled trial published Aug. 4 in JAMA.

Women in both the experimental and control groups achieved substantial reduction in depression scores, as measured by the Chinese version of the Beck Depression Inventory II (C-BDI-II). Mean scores of 38-39 placed the women in the “severe depression” category at baseline. At the end of the 12-week intervention, mean scores declined to 24-26 in both groups, corresponding to “moderate depression.” Six months later, mean scores declined to 16-18, corresponding to “mild depression” (JAMA 2010;304:536-43).

After the researchers adjusted for differences in baseline scores, Agnes Tiwari, Ph.D., of the University of Hong Kong, and her colleagues found a 2.7-point difference between the groups in C-BDI-II scores at the final follow-up. Although that difference achieved statistical significance, it did not achieve the 5-point difference needed for meaningful clinical significance.

The study involved 200 women, aged 18 years and older, who screened positive for intimate partner violence (IPV) at a community center in Hong Kong between 2007 and 2009. They were randomly assigned to experimental and control groups. Participants in the control group received usual community services, including childcare, health care, health promotion, and recreation.

Women in the experimental group received an intervention consisting of two components: empowerment and social support. The empowerment component, delivered by a research assistant in a 30-minute one-to-one interview, aimed to increase women’s safety through recognition of danger and use of a safety plan. They learned about the cycle of violence, facts and options, community resources, and legal interventions. The social support component consisted of 12 weekly telephone calls with a research assistant and 24-hour access to a hotline.

None of the women were lost to follow-up during the course of the 9-month study. A total of 88 of the 100 women in the experimental group received all 12 weeks of telephone support, and the remaining 12 all received 10 or 11 weeks, indicating a very high level of adherence to the experimental protocol.

While the differences in depression scores between the groups were not clinically meaningful, women in the experimental group were significantly more likely than were controls to say that the intervention was “useful to extremely useful” in improving their intimate relationships (94% vs. 82%) and in helping them resolve conflicts with their intimate partners (98% vs. 84%).

The study was supported by the Food and Health Bureau of the Hong Kong Government. The authors of the study said they had no financial relationships to disclose.

An intervention intended to increase empowerment among Chinese female victims of intimate partner violence failed to decrease depression appreciably more than did usual community services, according to a randomized, controlled trial published Aug. 4 in JAMA.

Women in both the experimental and control groups achieved substantial reduction in depression scores, as measured by the Chinese version of the Beck Depression Inventory II (C-BDI-II). Mean scores of 38-39 placed the women in the “severe depression” category at baseline. At the end of the 12-week intervention, mean scores declined to 24-26 in both groups, corresponding to “moderate depression.” Six months later, mean scores declined to 16-18, corresponding to “mild depression” (JAMA 2010;304:536-43).

After the researchers adjusted for differences in baseline scores, Agnes Tiwari, Ph.D., of the University of Hong Kong, and her colleagues found a 2.7-point difference between the groups in C-BDI-II scores at the final follow-up. Although that difference achieved statistical significance, it did not achieve the 5-point difference needed for meaningful clinical significance.

The study involved 200 women, aged 18 years and older, who screened positive for intimate partner violence (IPV) at a community center in Hong Kong between 2007 and 2009. They were randomly assigned to experimental and control groups. Participants in the control group received usual community services, including childcare, health care, health promotion, and recreation.

Women in the experimental group received an intervention consisting of two components: empowerment and social support. The empowerment component, delivered by a research assistant in a 30-minute one-to-one interview, aimed to increase women’s safety through recognition of danger and use of a safety plan. They learned about the cycle of violence, facts and options, community resources, and legal interventions. The social support component consisted of 12 weekly telephone calls with a research assistant and 24-hour access to a hotline.

None of the women were lost to follow-up during the course of the 9-month study. A total of 88 of the 100 women in the experimental group received all 12 weeks of telephone support, and the remaining 12 all received 10 or 11 weeks, indicating a very high level of adherence to the experimental protocol.

While the differences in depression scores between the groups were not clinically meaningful, women in the experimental group were significantly more likely than were controls to say that the intervention was “useful to extremely useful” in improving their intimate relationships (94% vs. 82%) and in helping them resolve conflicts with their intimate partners (98% vs. 84%).

The study was supported by the Food and Health Bureau of the Hong Kong Government. The authors of the study said they had no financial relationships to disclose.

An intervention intended to increase empowerment among Chinese female victims of intimate partner violence failed to decrease depression appreciably more than did usual community services, according to a randomized, controlled trial published Aug. 4 in JAMA.

Women in both the experimental and control groups achieved substantial reduction in depression scores, as measured by the Chinese version of the Beck Depression Inventory II (C-BDI-II). Mean scores of 38-39 placed the women in the “severe depression” category at baseline. At the end of the 12-week intervention, mean scores declined to 24-26 in both groups, corresponding to “moderate depression.” Six months later, mean scores declined to 16-18, corresponding to “mild depression” (JAMA 2010;304:536-43).

After the researchers adjusted for differences in baseline scores, Agnes Tiwari, Ph.D., of the University of Hong Kong, and her colleagues found a 2.7-point difference between the groups in C-BDI-II scores at the final follow-up. Although that difference achieved statistical significance, it did not achieve the 5-point difference needed for meaningful clinical significance.

The study involved 200 women, aged 18 years and older, who screened positive for intimate partner violence (IPV) at a community center in Hong Kong between 2007 and 2009. They were randomly assigned to experimental and control groups. Participants in the control group received usual community services, including childcare, health care, health promotion, and recreation.

Women in the experimental group received an intervention consisting of two components: empowerment and social support. The empowerment component, delivered by a research assistant in a 30-minute one-to-one interview, aimed to increase women’s safety through recognition of danger and use of a safety plan. They learned about the cycle of violence, facts and options, community resources, and legal interventions. The social support component consisted of 12 weekly telephone calls with a research assistant and 24-hour access to a hotline.

None of the women were lost to follow-up during the course of the 9-month study. A total of 88 of the 100 women in the experimental group received all 12 weeks of telephone support, and the remaining 12 all received 10 or 11 weeks, indicating a very high level of adherence to the experimental protocol.

While the differences in depression scores between the groups were not clinically meaningful, women in the experimental group were significantly more likely than were controls to say that the intervention was “useful to extremely useful” in improving their intimate relationships (94% vs. 82%) and in helping them resolve conflicts with their intimate partners (98% vs. 84%).

The study was supported by the Food and Health Bureau of the Hong Kong Government. The authors of the study said they had no financial relationships to disclose.