This 4-part video series is moderated by Jeffrey M. Weinberg, MD, and features discussion among dermatologists on this chronic inflammatory condition that has a significant impact on the quality of life of patients. Moderated by Jeffrey M. Weinberg, MD, this series covers pathogenesis, comorbidities, diagnosis, treatment, and patient education.

This video roundtable was produced by the Custom Programs division of Frontline Medical Communications. The editorial staff of Dermatology News was not involved in developing  the video roundtable.

Participants include:

• Robert G. Micheletti, MD
• George Han, MD, PhD
• Mary Ruth Buchness, MD

Disclosure: The faculty received modest honoraria from Frontline Medical Communications for their time participating in this roundtable, and maintained complete editorial control over all content presented.

Dr. Weinberg discloses that he has received honoraria from AbbVie Inc.

Dr. Buchness discloses that she is on the speakers’ bureau for AbbVie Inc.

Dr. Micheletti and Dr. Han have nothing to disclose.

This 4-part video series is moderated by Jeffrey M. Weinberg, MD, and features discussion among dermatologists on this chronic inflammatory condition that has a significant impact on the quality of life of patients. Moderated by Jeffrey M. Weinberg, MD, this series covers pathogenesis, comorbidities, diagnosis, treatment, and patient education.

This video roundtable was produced by the Custom Programs division of Frontline Medical Communications. The editorial staff of Dermatology News was not involved in developing  the video roundtable.

Participants include:

• Robert G. Micheletti, MD
• George Han, MD, PhD
• Mary Ruth Buchness, MD

Disclosure: The faculty received modest honoraria from Frontline Medical Communications for their time participating in this roundtable, and maintained complete editorial control over all content presented.

Dr. Weinberg discloses that he has received honoraria from AbbVie Inc.

Dr. Buchness discloses that she is on the speakers’ bureau for AbbVie Inc.

Dr. Micheletti and Dr. Han have nothing to disclose.

This 4-part video series is moderated by Jeffrey M. Weinberg, MD, and features discussion among dermatologists on this chronic inflammatory condition that has a significant impact on the quality of life of patients. Moderated by Jeffrey M. Weinberg, MD, this series covers pathogenesis, comorbidities, diagnosis, treatment, and patient education.

This video roundtable was produced by the Custom Programs division of Frontline Medical Communications. The editorial staff of Dermatology News was not involved in developing  the video roundtable.

Participants include:

• Robert G. Micheletti, MD
• George Han, MD, PhD
• Mary Ruth Buchness, MD

Disclosure: The faculty received modest honoraria from Frontline Medical Communications for their time participating in this roundtable, and maintained complete editorial control over all content presented.

Dr. Weinberg discloses that he has received honoraria from AbbVie Inc.

Dr. Buchness discloses that she is on the speakers’ bureau for AbbVie Inc.

Dr. Micheletti and Dr. Han have nothing to disclose.

The U.S. Supreme Court has refused to decide whether pharmacists with strongly held religious beliefs can be forced to dispense emergency contraception to patients.

Justices did not explain their June 28 denial of Stormans, Inc. vs. Wiesman, but the decision was made over the objection of Chief Justice John G. Roberts Jr., Associate Justice Samuel Alito Jr., and Associate Justice Clarence Thomas. In his dissent, Associate Justice Alito wrote the court should have heard the case to ensure that novel and concededly “unnecessary burden on religious objectors” does not trample fundamental rights.

©jsmith/iStockphoto

“If this is a sign of how religious liberty claims will be treated in the years ahead, those who value religious freedom have cause for great concern,” he wrote in his dissent.

At issue in the case is a 2007 rule by Washington state that a family-owned pharmacy in Olympia must provide Plan B contraception to patients. The “delivery rule” creates “a duty for pharmacists to deliver lawfully prescribed drugs or devices in a timely manner and does not allow for conscience-based decisions not to dispense the drug. The Stormans family, who own Ralph’s Thriftway, sued the state over the regulation, alleging violations of the free exercise, equal protection, and due process clauses of the Constitution. The business owners equate emergency contraception to abortion, and they argue that dispensing the medication violates their religious beliefs.

The 9th U.S. Circuit Court of Appeals sided with the state, calling the regulations “neutral and generally applicable.” The plaintiffs appealed to the Supreme Court. The denial by the high court allows the 9th Circuit decision to stand.

Nearly 20 court briefs were issued to the Supreme Court in the case, including briefs by the American Association of Pro-Life Obstetricians and Gynecologists and 4,609 individual health care professionals in support of the pharmacy.

“By effectively prohibiting exemptions for religious reasons, the state of Washington’s regulations depart radically from widely established norms within the health care industry protecting the individual conscience rights of health care professionals,” the health care professionals wrote in their brief. “Such norms favoring the freedom of conscience are particularly well established where, as here, the practitioner’s right to decline care applies to particular treatments, not to individual patients or classes of persons; and where, as here, declining treatment for reasons of religious conscience has no practical impact on quality or availability of care.”

[email protected]

On Twitter @legal_med

The U.S. Supreme Court has refused to decide whether pharmacists with strongly held religious beliefs can be forced to dispense emergency contraception to patients.

Justices did not explain their June 28 denial of Stormans, Inc. vs. Wiesman, but the decision was made over the objection of Chief Justice John G. Roberts Jr., Associate Justice Samuel Alito Jr., and Associate Justice Clarence Thomas. In his dissent, Associate Justice Alito wrote the court should have heard the case to ensure that novel and concededly “unnecessary burden on religious objectors” does not trample fundamental rights.

©jsmith/iStockphoto

“If this is a sign of how religious liberty claims will be treated in the years ahead, those who value religious freedom have cause for great concern,” he wrote in his dissent.

At issue in the case is a 2007 rule by Washington state that a family-owned pharmacy in Olympia must provide Plan B contraception to patients. The “delivery rule” creates “a duty for pharmacists to deliver lawfully prescribed drugs or devices in a timely manner and does not allow for conscience-based decisions not to dispense the drug. The Stormans family, who own Ralph’s Thriftway, sued the state over the regulation, alleging violations of the free exercise, equal protection, and due process clauses of the Constitution. The business owners equate emergency contraception to abortion, and they argue that dispensing the medication violates their religious beliefs.

The 9th U.S. Circuit Court of Appeals sided with the state, calling the regulations “neutral and generally applicable.” The plaintiffs appealed to the Supreme Court. The denial by the high court allows the 9th Circuit decision to stand.

Nearly 20 court briefs were issued to the Supreme Court in the case, including briefs by the American Association of Pro-Life Obstetricians and Gynecologists and 4,609 individual health care professionals in support of the pharmacy.

“By effectively prohibiting exemptions for religious reasons, the state of Washington’s regulations depart radically from widely established norms within the health care industry protecting the individual conscience rights of health care professionals,” the health care professionals wrote in their brief. “Such norms favoring the freedom of conscience are particularly well established where, as here, the practitioner’s right to decline care applies to particular treatments, not to individual patients or classes of persons; and where, as here, declining treatment for reasons of religious conscience has no practical impact on quality or availability of care.”

[email protected]

On Twitter @legal_med

The U.S. Supreme Court has refused to decide whether pharmacists with strongly held religious beliefs can be forced to dispense emergency contraception to patients.

Justices did not explain their June 28 denial of Stormans, Inc. vs. Wiesman, but the decision was made over the objection of Chief Justice John G. Roberts Jr., Associate Justice Samuel Alito Jr., and Associate Justice Clarence Thomas. In his dissent, Associate Justice Alito wrote the court should have heard the case to ensure that novel and concededly “unnecessary burden on religious objectors” does not trample fundamental rights.

©jsmith/iStockphoto

“If this is a sign of how religious liberty claims will be treated in the years ahead, those who value religious freedom have cause for great concern,” he wrote in his dissent.

At issue in the case is a 2007 rule by Washington state that a family-owned pharmacy in Olympia must provide Plan B contraception to patients. The “delivery rule” creates “a duty for pharmacists to deliver lawfully prescribed drugs or devices in a timely manner and does not allow for conscience-based decisions not to dispense the drug. The Stormans family, who own Ralph’s Thriftway, sued the state over the regulation, alleging violations of the free exercise, equal protection, and due process clauses of the Constitution. The business owners equate emergency contraception to abortion, and they argue that dispensing the medication violates their religious beliefs.

The 9th U.S. Circuit Court of Appeals sided with the state, calling the regulations “neutral and generally applicable.” The plaintiffs appealed to the Supreme Court. The denial by the high court allows the 9th Circuit decision to stand.

Nearly 20 court briefs were issued to the Supreme Court in the case, including briefs by the American Association of Pro-Life Obstetricians and Gynecologists and 4,609 individual health care professionals in support of the pharmacy.

“By effectively prohibiting exemptions for religious reasons, the state of Washington’s regulations depart radically from widely established norms within the health care industry protecting the individual conscience rights of health care professionals,” the health care professionals wrote in their brief. “Such norms favoring the freedom of conscience are particularly well established where, as here, the practitioner’s right to decline care applies to particular treatments, not to individual patients or classes of persons; and where, as here, declining treatment for reasons of religious conscience has no practical impact on quality or availability of care.”

[email protected]

On Twitter @legal_med

WASHINGTON - U.S. House of Representatives Speaker Paul Ryan unveiled a Republican healthcare agenda on Wednesday that would repeal Obamacare but keep some of its more popular provisions.

The proposal is part of Ryan's blueprint, titled "A Better Way," which offers a Republican alternative to the Democratic Party on policy issues ahead of the Nov. 8 election.

Earlier this month, Ryan, the country's highest-ranking elected Republican, released initiatives on national security and combating poverty. Proposals on regulation, tax reform and constitutional authority are expected in the coming weeks.

Republicans have challenged President Barack Obama's signature healthcare law, the Affordable Care Act, since it was enacted in 2010 after a bitter fight in Congress.

"Obamacare has limited choices for patients, driven up costs for consumers, and buried employers and health care providers under thousands of new regulations," a draft of the Ryan plan said. "This law cannot be fixed."

But Ryan's proposal would keep some popular aspects of the law, including not allowing people with pre-existing conditions to be denied coverage and permitting children to stay on their parents' coverage until age 26.

The Obama administration says some 20 million Americans have become insured as a result of the Affordable Care Act.

The Ryan plan recycles long-held Republican proposals like allowing consumers to buy health insurance across state lines, expanding the use of health savings accounts and giving states block grants to run the Medicaid program for the poor.

For people who do not get insurance through their jobs, the Republican plan would establish a refundable tax credit. Obamacare, by contrast, provides subsidies to some lower-income people to buy insurance if they do not qualify for Medicaid.

The Republican proposal would gradually increase the Medicare eligibility age, which currently is 65, to match that of the Social Security pension plan, which is 67 for people born in 1960 or later.

Like Obamacare's so-called Cadillac tax on expensive healthcare plans offered by employers, the Republican proposal would cap the tax deductibility of employer-based plans.

The Republican plan includes medical liability reform that would put a cap on non-economic damages awarded in lawsuits, a measure aimed at cutting overall healthcare costs.

Under Obamacare, many states expanded the number of people eligible for Medicaid. The Republican plan would allow states that decided to expand Medicaid before this year to keep the expansion, while preventing any new states from doing so.

WASHINGTON - U.S. House of Representatives Speaker Paul Ryan unveiled a Republican healthcare agenda on Wednesday that would repeal Obamacare but keep some of its more popular provisions.

The proposal is part of Ryan's blueprint, titled "A Better Way," which offers a Republican alternative to the Democratic Party on policy issues ahead of the Nov. 8 election.

Earlier this month, Ryan, the country's highest-ranking elected Republican, released initiatives on national security and combating poverty. Proposals on regulation, tax reform and constitutional authority are expected in the coming weeks.

Republicans have challenged President Barack Obama's signature healthcare law, the Affordable Care Act, since it was enacted in 2010 after a bitter fight in Congress.

"Obamacare has limited choices for patients, driven up costs for consumers, and buried employers and health care providers under thousands of new regulations," a draft of the Ryan plan said. "This law cannot be fixed."

But Ryan's proposal would keep some popular aspects of the law, including not allowing people with pre-existing conditions to be denied coverage and permitting children to stay on their parents' coverage until age 26.

The Obama administration says some 20 million Americans have become insured as a result of the Affordable Care Act.

The Ryan plan recycles long-held Republican proposals like allowing consumers to buy health insurance across state lines, expanding the use of health savings accounts and giving states block grants to run the Medicaid program for the poor.

For people who do not get insurance through their jobs, the Republican plan would establish a refundable tax credit. Obamacare, by contrast, provides subsidies to some lower-income people to buy insurance if they do not qualify for Medicaid.

The Republican proposal would gradually increase the Medicare eligibility age, which currently is 65, to match that of the Social Security pension plan, which is 67 for people born in 1960 or later.

Like Obamacare's so-called Cadillac tax on expensive healthcare plans offered by employers, the Republican proposal would cap the tax deductibility of employer-based plans.

The Republican plan includes medical liability reform that would put a cap on non-economic damages awarded in lawsuits, a measure aimed at cutting overall healthcare costs.

Under Obamacare, many states expanded the number of people eligible for Medicaid. The Republican plan would allow states that decided to expand Medicaid before this year to keep the expansion, while preventing any new states from doing so.

WASHINGTON - U.S. House of Representatives Speaker Paul Ryan unveiled a Republican healthcare agenda on Wednesday that would repeal Obamacare but keep some of its more popular provisions.

The proposal is part of Ryan's blueprint, titled "A Better Way," which offers a Republican alternative to the Democratic Party on policy issues ahead of the Nov. 8 election.

Earlier this month, Ryan, the country's highest-ranking elected Republican, released initiatives on national security and combating poverty. Proposals on regulation, tax reform and constitutional authority are expected in the coming weeks.

Republicans have challenged President Barack Obama's signature healthcare law, the Affordable Care Act, since it was enacted in 2010 after a bitter fight in Congress.

"Obamacare has limited choices for patients, driven up costs for consumers, and buried employers and health care providers under thousands of new regulations," a draft of the Ryan plan said. "This law cannot be fixed."

But Ryan's proposal would keep some popular aspects of the law, including not allowing people with pre-existing conditions to be denied coverage and permitting children to stay on their parents' coverage until age 26.

The Obama administration says some 20 million Americans have become insured as a result of the Affordable Care Act.

The Ryan plan recycles long-held Republican proposals like allowing consumers to buy health insurance across state lines, expanding the use of health savings accounts and giving states block grants to run the Medicaid program for the poor.

For people who do not get insurance through their jobs, the Republican plan would establish a refundable tax credit. Obamacare, by contrast, provides subsidies to some lower-income people to buy insurance if they do not qualify for Medicaid.

The Republican proposal would gradually increase the Medicare eligibility age, which currently is 65, to match that of the Social Security pension plan, which is 67 for people born in 1960 or later.

Like Obamacare's so-called Cadillac tax on expensive healthcare plans offered by employers, the Republican proposal would cap the tax deductibility of employer-based plans.

The Republican plan includes medical liability reform that would put a cap on non-economic damages awarded in lawsuits, a measure aimed at cutting overall healthcare costs.

Under Obamacare, many states expanded the number of people eligible for Medicaid. The Republican plan would allow states that decided to expand Medicaid before this year to keep the expansion, while preventing any new states from doing so.

In male patients with adult-onset germ cell tumors, cisplatin-based chemotherapy may be associated with hearing loss, according to the results of the large, multicenter Platinum Study.

For every 100-mg/m² increase in cumulative cisplatin dose, a 3.2-dB decline in overall hearing threshold occurred, Robert Frisina, PhD, of the University of South Florida, Tampa, and his associates reported (J Clin Oncol. 2016 Jun. doi: 10.1200/JCO.2016.66.8822).

©monkeybusinessimages/thinkstockphotos.com

A total of 488 men with adult-onset germ cell tumors who were treated with cisplatin-based chemotherapy were consented into this study, and completed questionnaires concerning neurotoxic symptoms, lifestyle habits, and medication use. Each patient underwent bone-conduction and speech-conducting threshold testing. Pure-tone air conduction thresholds were obtained bilaterally at speech frequency range (0.25 to 12 kHz). Classification of hearing loss and assessment of severity followed standardized criteria as defined by the American Speech-Language-Hearing Association. Median age at cancer diagnosis was 31 years; the median interval between chemotherapy and audiometric testing was 4.25 years. Median cumulative cisplatin dose was 400 mg/m². Increasing cumulative cisplatin dose was associated with increasing (worse) hearing thresholds at 4 kHz (P = .021), 6 kHz (P = .0017), 8 kHz (P less than .001), 10 kHz (P less than .001), and 12 kHz (P = .0013) after correcting for age.

Cumulative cisplatin doses above 300 mg/m² were associated with more severe hearing loss, compared with doses less than 300 mg/m² (odds ratio, 1.59; 95% confidence interval, 1.14-2.21; P = .0066).

Conductive hearing loss in the middle ear was not associated with drug exposure dosage levels. Hypertension was identified as a risk factor for hearing loss as impaired overall hearing threshold was significantly associated with hypertension when correcting for age and cisplatin dose (n = 60, P = .0066).

“Because alterations in the highly successful [germ cell tumor] regimens are unlikely, our results point to the importance of ongoing research aimed at the identification of genetic variants associated with cisplatin-related ototoxicity,” investigators wrote. They also suggested that cancer patients treated with cisplatin should be careful to avoid noise exposure, ototoxic drugs, and other factors that could further increase damage.

This study was funded by the National Cancer Institute. Dr. Frisina reported holding patents related to hearing loss products. Six other investigators reported serving in advisory roles, receiving financial compensation or honoraria from multiple pharmaceutical and biomedical companies.

[email protected]

On Twitter @jessnicolecraig

In male patients with adult-onset germ cell tumors, cisplatin-based chemotherapy may be associated with hearing loss, according to the results of the large, multicenter Platinum Study.

For every 100-mg/m² increase in cumulative cisplatin dose, a 3.2-dB decline in overall hearing threshold occurred, Robert Frisina, PhD, of the University of South Florida, Tampa, and his associates reported (J Clin Oncol. 2016 Jun. doi: 10.1200/JCO.2016.66.8822).

©monkeybusinessimages/thinkstockphotos.com

A total of 488 men with adult-onset germ cell tumors who were treated with cisplatin-based chemotherapy were consented into this study, and completed questionnaires concerning neurotoxic symptoms, lifestyle habits, and medication use. Each patient underwent bone-conduction and speech-conducting threshold testing. Pure-tone air conduction thresholds were obtained bilaterally at speech frequency range (0.25 to 12 kHz). Classification of hearing loss and assessment of severity followed standardized criteria as defined by the American Speech-Language-Hearing Association. Median age at cancer diagnosis was 31 years; the median interval between chemotherapy and audiometric testing was 4.25 years. Median cumulative cisplatin dose was 400 mg/m². Increasing cumulative cisplatin dose was associated with increasing (worse) hearing thresholds at 4 kHz (P = .021), 6 kHz (P = .0017), 8 kHz (P less than .001), 10 kHz (P less than .001), and 12 kHz (P = .0013) after correcting for age.

Cumulative cisplatin doses above 300 mg/m² were associated with more severe hearing loss, compared with doses less than 300 mg/m² (odds ratio, 1.59; 95% confidence interval, 1.14-2.21; P = .0066).

Conductive hearing loss in the middle ear was not associated with drug exposure dosage levels. Hypertension was identified as a risk factor for hearing loss as impaired overall hearing threshold was significantly associated with hypertension when correcting for age and cisplatin dose (n = 60, P = .0066).

“Because alterations in the highly successful [germ cell tumor] regimens are unlikely, our results point to the importance of ongoing research aimed at the identification of genetic variants associated with cisplatin-related ototoxicity,” investigators wrote. They also suggested that cancer patients treated with cisplatin should be careful to avoid noise exposure, ototoxic drugs, and other factors that could further increase damage.

This study was funded by the National Cancer Institute. Dr. Frisina reported holding patents related to hearing loss products. Six other investigators reported serving in advisory roles, receiving financial compensation or honoraria from multiple pharmaceutical and biomedical companies.

[email protected]

On Twitter @jessnicolecraig

In male patients with adult-onset germ cell tumors, cisplatin-based chemotherapy may be associated with hearing loss, according to the results of the large, multicenter Platinum Study.

For every 100-mg/m² increase in cumulative cisplatin dose, a 3.2-dB decline in overall hearing threshold occurred, Robert Frisina, PhD, of the University of South Florida, Tampa, and his associates reported (J Clin Oncol. 2016 Jun. doi: 10.1200/JCO.2016.66.8822).

©monkeybusinessimages/thinkstockphotos.com

A total of 488 men with adult-onset germ cell tumors who were treated with cisplatin-based chemotherapy were consented into this study, and completed questionnaires concerning neurotoxic symptoms, lifestyle habits, and medication use. Each patient underwent bone-conduction and speech-conducting threshold testing. Pure-tone air conduction thresholds were obtained bilaterally at speech frequency range (0.25 to 12 kHz). Classification of hearing loss and assessment of severity followed standardized criteria as defined by the American Speech-Language-Hearing Association. Median age at cancer diagnosis was 31 years; the median interval between chemotherapy and audiometric testing was 4.25 years. Median cumulative cisplatin dose was 400 mg/m². Increasing cumulative cisplatin dose was associated with increasing (worse) hearing thresholds at 4 kHz (P = .021), 6 kHz (P = .0017), 8 kHz (P less than .001), 10 kHz (P less than .001), and 12 kHz (P = .0013) after correcting for age.

Cumulative cisplatin doses above 300 mg/m² were associated with more severe hearing loss, compared with doses less than 300 mg/m² (odds ratio, 1.59; 95% confidence interval, 1.14-2.21; P = .0066).

Conductive hearing loss in the middle ear was not associated with drug exposure dosage levels. Hypertension was identified as a risk factor for hearing loss as impaired overall hearing threshold was significantly associated with hypertension when correcting for age and cisplatin dose (n = 60, P = .0066).

“Because alterations in the highly successful [germ cell tumor] regimens are unlikely, our results point to the importance of ongoing research aimed at the identification of genetic variants associated with cisplatin-related ototoxicity,” investigators wrote. They also suggested that cancer patients treated with cisplatin should be careful to avoid noise exposure, ototoxic drugs, and other factors that could further increase damage.

This study was funded by the National Cancer Institute. Dr. Frisina reported holding patents related to hearing loss products. Six other investigators reported serving in advisory roles, receiving financial compensation or honoraria from multiple pharmaceutical and biomedical companies.

[email protected]

On Twitter @jessnicolecraig

“Sticks and stones may break my bones, but words will never hurt me.” This mantra was the retort of choice for thousands of apparently resilient premillennial children. But you and I, and just about everyone else, know that words can be very hurtful. A recent article in the journal Eating and Weight Disorders entitled, “ ‘Don’t eat so much’: How parent comments relate to female weight satisfaction” (Eat Weight Disord. 2016 Jun 6. [Epub ahead of print]) reminds us that the pain can last forever.

In a retrospective study of 501 young women aged 20-35 years, the investigators asked whether the women could recall their parents making any comments about their weight when they were young children. What the authors discovered was that even among young women who were of normal weight, those who could recall their parents making a comment about their weight were more dissatisfied with their body weight than the young women who could not recall such a comment. However, if the comment had been about eating habits and not weight, then there was no significant association with weight dissatisfaction.

Before we rush out to send all of the parents of weight-dissatisfied young women on a guilt trip, let’s remember that this was a retrospective study. Let’s consider the not unlikely explanation that there may be something built into the psyche of weight-dissatisfied young women that sharpens their memory for negative comments from friends and family.

Regardless of how we interpret the findings from this study, it is probably safe to say that telling a young girl that she is overweight doesn’t help and should be avoided. This is just another example of how poorly chosen words can be hurtful. But it is also an example of how words alone are seldom shapers of positive behaviors. You can’t talk a picky eater into eating spinach anymore than you can talk the child in the middle of a tantrum into settling down. Good manners are best learned by modeling the behavior of respected adults and not by being subjected to a series of parental lectures. Telling a child she is overweight won’t solve the problem.

So what is the parent of an obese child to do? Unfortunately, many parents of obese children don’t perceive their child as being significantly overweight. But let’s assume we have cleared that hurdle of denial. If telling the child she is overweight is the wrong thing to do, then her parents are forced into using strategies that are subliminal, applied slowly and patiently – silently.

©SolStock/iStock

These strategies could include gradually decreasing the child’s screen time, hoping that it will be replaced by calorie-burning activities; changing the food available for all the inhabitants of the home to increase the likelihood that healthier choices will dominate; and decreasing serving sizes. It is critical that these changes are done so slowly that they go unnoticed by the child. If the child questions the changes, then the response should be that they are being done to help the entire family to be healthier, and that they are not being targeted at any one individual. Of course, the big problem is getting the rest of the family to buy into the changes so that the overweight child doesn’t become a scapegoat.

Shielding the overweight child from the blame game is much easier if the parents have been careful to avoid labeling from the moment they realized or accepted that the child had a weight problem. Here is where we pediatricians can play a critical role in our choice of words, and the setting in which we discuss the child’s weight with the parents. We must point out to the parents that their words can create a hurt that may not ever go away.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

“Sticks and stones may break my bones, but words will never hurt me.” This mantra was the retort of choice for thousands of apparently resilient premillennial children. But you and I, and just about everyone else, know that words can be very hurtful. A recent article in the journal Eating and Weight Disorders entitled, “ ‘Don’t eat so much’: How parent comments relate to female weight satisfaction” (Eat Weight Disord. 2016 Jun 6. [Epub ahead of print]) reminds us that the pain can last forever.

In a retrospective study of 501 young women aged 20-35 years, the investigators asked whether the women could recall their parents making any comments about their weight when they were young children. What the authors discovered was that even among young women who were of normal weight, those who could recall their parents making a comment about their weight were more dissatisfied with their body weight than the young women who could not recall such a comment. However, if the comment had been about eating habits and not weight, then there was no significant association with weight dissatisfaction.

Before we rush out to send all of the parents of weight-dissatisfied young women on a guilt trip, let’s remember that this was a retrospective study. Let’s consider the not unlikely explanation that there may be something built into the psyche of weight-dissatisfied young women that sharpens their memory for negative comments from friends and family.

Regardless of how we interpret the findings from this study, it is probably safe to say that telling a young girl that she is overweight doesn’t help and should be avoided. This is just another example of how poorly chosen words can be hurtful. But it is also an example of how words alone are seldom shapers of positive behaviors. You can’t talk a picky eater into eating spinach anymore than you can talk the child in the middle of a tantrum into settling down. Good manners are best learned by modeling the behavior of respected adults and not by being subjected to a series of parental lectures. Telling a child she is overweight won’t solve the problem.

So what is the parent of an obese child to do? Unfortunately, many parents of obese children don’t perceive their child as being significantly overweight. But let’s assume we have cleared that hurdle of denial. If telling the child she is overweight is the wrong thing to do, then her parents are forced into using strategies that are subliminal, applied slowly and patiently – silently.

©SolStock/iStock

These strategies could include gradually decreasing the child’s screen time, hoping that it will be replaced by calorie-burning activities; changing the food available for all the inhabitants of the home to increase the likelihood that healthier choices will dominate; and decreasing serving sizes. It is critical that these changes are done so slowly that they go unnoticed by the child. If the child questions the changes, then the response should be that they are being done to help the entire family to be healthier, and that they are not being targeted at any one individual. Of course, the big problem is getting the rest of the family to buy into the changes so that the overweight child doesn’t become a scapegoat.

Shielding the overweight child from the blame game is much easier if the parents have been careful to avoid labeling from the moment they realized or accepted that the child had a weight problem. Here is where we pediatricians can play a critical role in our choice of words, and the setting in which we discuss the child’s weight with the parents. We must point out to the parents that their words can create a hurt that may not ever go away.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

“Sticks and stones may break my bones, but words will never hurt me.” This mantra was the retort of choice for thousands of apparently resilient premillennial children. But you and I, and just about everyone else, know that words can be very hurtful. A recent article in the journal Eating and Weight Disorders entitled, “ ‘Don’t eat so much’: How parent comments relate to female weight satisfaction” (Eat Weight Disord. 2016 Jun 6. [Epub ahead of print]) reminds us that the pain can last forever.

In a retrospective study of 501 young women aged 20-35 years, the investigators asked whether the women could recall their parents making any comments about their weight when they were young children. What the authors discovered was that even among young women who were of normal weight, those who could recall their parents making a comment about their weight were more dissatisfied with their body weight than the young women who could not recall such a comment. However, if the comment had been about eating habits and not weight, then there was no significant association with weight dissatisfaction.

Before we rush out to send all of the parents of weight-dissatisfied young women on a guilt trip, let’s remember that this was a retrospective study. Let’s consider the not unlikely explanation that there may be something built into the psyche of weight-dissatisfied young women that sharpens their memory for negative comments from friends and family.

Regardless of how we interpret the findings from this study, it is probably safe to say that telling a young girl that she is overweight doesn’t help and should be avoided. This is just another example of how poorly chosen words can be hurtful. But it is also an example of how words alone are seldom shapers of positive behaviors. You can’t talk a picky eater into eating spinach anymore than you can talk the child in the middle of a tantrum into settling down. Good manners are best learned by modeling the behavior of respected adults and not by being subjected to a series of parental lectures. Telling a child she is overweight won’t solve the problem.

So what is the parent of an obese child to do? Unfortunately, many parents of obese children don’t perceive their child as being significantly overweight. But let’s assume we have cleared that hurdle of denial. If telling the child she is overweight is the wrong thing to do, then her parents are forced into using strategies that are subliminal, applied slowly and patiently – silently.

©SolStock/iStock

These strategies could include gradually decreasing the child’s screen time, hoping that it will be replaced by calorie-burning activities; changing the food available for all the inhabitants of the home to increase the likelihood that healthier choices will dominate; and decreasing serving sizes. It is critical that these changes are done so slowly that they go unnoticed by the child. If the child questions the changes, then the response should be that they are being done to help the entire family to be healthier, and that they are not being targeted at any one individual. Of course, the big problem is getting the rest of the family to buy into the changes so that the overweight child doesn’t become a scapegoat.

Shielding the overweight child from the blame game is much easier if the parents have been careful to avoid labeling from the moment they realized or accepted that the child had a weight problem. Here is where we pediatricians can play a critical role in our choice of words, and the setting in which we discuss the child’s weight with the parents. We must point out to the parents that their words can create a hurt that may not ever go away.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.”

Now that the interleukin-17 inhibitor secukinumab and tumor necrosis factor inhibitors are competing options for treatment of patients with ankylosing spondylitis, the companies that make those drugs must feel pressure to find some sort of advantage for their agents.

How else to explain the remarkable pair of similar post hoc analyses presented in June at the European Congress of Rheumatology in London? One of the analyses was funded by Novartis – the company that markets secukinumab (Cosentyx) – and included several Novartis employees as coauthors. The second study, presented immediately afterward in the main session at the meeting devoted to ankylosing spondylitis (AS) treatments, had backing from AbbVie, which markets adalimumab (Humira), the largest-selling tumor necrosis factor inhibitor worldwide, and had several AbbVie employees as coauthors.

Both analyses used a “matching adjusted indirect comparison,” a fairly new way to compare the performance of interventions studied in two totally independent trials by propensity matching patients from each of the two trials. It’s purportedly a way to make a legitimate comparison in the absence of head-to-head data.

Making the two reports even more surreal was their use of essentially the same data.

The first report came from Walter P. Maksymowych, MD, an AS clinician and researcher from the University of Alberta, who with his coauthors used data collected on secukinumab in the MEASURE 1 pivotal trial and on adalimumab in the ATLAS pivotal trial. He spent much of his presentation describing the methods behind the indirect comparison, and I don’t think I can be blamed for calling the results of this Novartis-sponsored analysis predictable: overall better performance by secukinumab, compared “indirectly” with adalimumab for clinical responses and patient quality of life.

Mitchel L. Zoler/Frontline Medical News

The second report, the one sponsored by AbbVie, came from Keith A. Betts, PhD, a biostatistician who works for the Analysis Group, an international consulting firm. He also used the ATLAS database as the source for adalimumab outcomes, and differed marginally from Dr. Maksymowych by taking data on secukinumab patients from both the MEASURE 1 and MEASURE 2 pivotal trials. Although Dr. Betts also used the matching adjusted indirect comparison approach and broadened his data source modestly, his results showed a distinctly different outcome: similar efficacy for the two drugs. Dr. Betts also included a cost efficacy analysis, and in this part adalimumab showed superior performance after he factored in the cost per responding AS patient.

During the combined discussion period following the two talks, both presenters defended the legitimacy of their approaches, although Dr. Maksymowych conceded that these indirect comparisons are “hypothesis generating rather than producing a definitive answer.” But a couple of active European AS researchers rose to comment from the floor and discredit the whole process.

“These two presentations show why I am not a proponent of indirect comparisons. The statistical models squeeze the data until they confess,” said Robert Landewé, MD, an AS specialist at the University of Amsterdam. “This is now a commercial rather than a scientific clash between two important drugs. I challenge these companies to perform a head-to-head trial. Indirect comparisons are not good,” he concluded, to a round of audience applause.

“There are so many methodological issues,” said Désirée van der Heijde, MD, another Dutch AS clinician and researcher who rose to critique both studies. “The only thing you can rely on is head-to-head trials.”

I later spoke with Dr. Maksymowych, and he expressed some pessimism about the prospects for a fully-powered, head-to-head trial of an interleukin-17 inhibitor and tumor necrosis factor inhibitor because it would need to enroll so many patients. “Randomized studies of active comparators need to be huge because it’s hard to show improvements when the response rates are high,” he said. Plus, he added, it isn’t entirely about a drug’s efficacy against AS spinal symptoms anyway.

“We also have to think about the impact of treatment on other aspects of this disease, such as psoriasis and colitis, as well as radiographic disease progression,” he said. These aspects of the activity of both classes of drugs have not received much study in AS patients until now.

In other words, the battle between treatment options for AS has just begun, and seems likely to be fought on many fronts.

[email protected]

On Twitter @mitchelzoler

Now that the interleukin-17 inhibitor secukinumab and tumor necrosis factor inhibitors are competing options for treatment of patients with ankylosing spondylitis, the companies that make those drugs must feel pressure to find some sort of advantage for their agents.

How else to explain the remarkable pair of similar post hoc analyses presented in June at the European Congress of Rheumatology in London? One of the analyses was funded by Novartis – the company that markets secukinumab (Cosentyx) – and included several Novartis employees as coauthors. The second study, presented immediately afterward in the main session at the meeting devoted to ankylosing spondylitis (AS) treatments, had backing from AbbVie, which markets adalimumab (Humira), the largest-selling tumor necrosis factor inhibitor worldwide, and had several AbbVie employees as coauthors.

Both analyses used a “matching adjusted indirect comparison,” a fairly new way to compare the performance of interventions studied in two totally independent trials by propensity matching patients from each of the two trials. It’s purportedly a way to make a legitimate comparison in the absence of head-to-head data.

Making the two reports even more surreal was their use of essentially the same data.

The first report came from Walter P. Maksymowych, MD, an AS clinician and researcher from the University of Alberta, who with his coauthors used data collected on secukinumab in the MEASURE 1 pivotal trial and on adalimumab in the ATLAS pivotal trial. He spent much of his presentation describing the methods behind the indirect comparison, and I don’t think I can be blamed for calling the results of this Novartis-sponsored analysis predictable: overall better performance by secukinumab, compared “indirectly” with adalimumab for clinical responses and patient quality of life.

Mitchel L. Zoler/Frontline Medical News

The second report, the one sponsored by AbbVie, came from Keith A. Betts, PhD, a biostatistician who works for the Analysis Group, an international consulting firm. He also used the ATLAS database as the source for adalimumab outcomes, and differed marginally from Dr. Maksymowych by taking data on secukinumab patients from both the MEASURE 1 and MEASURE 2 pivotal trials. Although Dr. Betts also used the matching adjusted indirect comparison approach and broadened his data source modestly, his results showed a distinctly different outcome: similar efficacy for the two drugs. Dr. Betts also included a cost efficacy analysis, and in this part adalimumab showed superior performance after he factored in the cost per responding AS patient.

During the combined discussion period following the two talks, both presenters defended the legitimacy of their approaches, although Dr. Maksymowych conceded that these indirect comparisons are “hypothesis generating rather than producing a definitive answer.” But a couple of active European AS researchers rose to comment from the floor and discredit the whole process.

“These two presentations show why I am not a proponent of indirect comparisons. The statistical models squeeze the data until they confess,” said Robert Landewé, MD, an AS specialist at the University of Amsterdam. “This is now a commercial rather than a scientific clash between two important drugs. I challenge these companies to perform a head-to-head trial. Indirect comparisons are not good,” he concluded, to a round of audience applause.

“There are so many methodological issues,” said Désirée van der Heijde, MD, another Dutch AS clinician and researcher who rose to critique both studies. “The only thing you can rely on is head-to-head trials.”

I later spoke with Dr. Maksymowych, and he expressed some pessimism about the prospects for a fully-powered, head-to-head trial of an interleukin-17 inhibitor and tumor necrosis factor inhibitor because it would need to enroll so many patients. “Randomized studies of active comparators need to be huge because it’s hard to show improvements when the response rates are high,” he said. Plus, he added, it isn’t entirely about a drug’s efficacy against AS spinal symptoms anyway.

“We also have to think about the impact of treatment on other aspects of this disease, such as psoriasis and colitis, as well as radiographic disease progression,” he said. These aspects of the activity of both classes of drugs have not received much study in AS patients until now.

In other words, the battle between treatment options for AS has just begun, and seems likely to be fought on many fronts.

[email protected]

On Twitter @mitchelzoler

Now that the interleukin-17 inhibitor secukinumab and tumor necrosis factor inhibitors are competing options for treatment of patients with ankylosing spondylitis, the companies that make those drugs must feel pressure to find some sort of advantage for their agents.

How else to explain the remarkable pair of similar post hoc analyses presented in June at the European Congress of Rheumatology in London? One of the analyses was funded by Novartis – the company that markets secukinumab (Cosentyx) – and included several Novartis employees as coauthors. The second study, presented immediately afterward in the main session at the meeting devoted to ankylosing spondylitis (AS) treatments, had backing from AbbVie, which markets adalimumab (Humira), the largest-selling tumor necrosis factor inhibitor worldwide, and had several AbbVie employees as coauthors.

Both analyses used a “matching adjusted indirect comparison,” a fairly new way to compare the performance of interventions studied in two totally independent trials by propensity matching patients from each of the two trials. It’s purportedly a way to make a legitimate comparison in the absence of head-to-head data.

Making the two reports even more surreal was their use of essentially the same data.

The first report came from Walter P. Maksymowych, MD, an AS clinician and researcher from the University of Alberta, who with his coauthors used data collected on secukinumab in the MEASURE 1 pivotal trial and on adalimumab in the ATLAS pivotal trial. He spent much of his presentation describing the methods behind the indirect comparison, and I don’t think I can be blamed for calling the results of this Novartis-sponsored analysis predictable: overall better performance by secukinumab, compared “indirectly” with adalimumab for clinical responses and patient quality of life.

Mitchel L. Zoler/Frontline Medical News

The second report, the one sponsored by AbbVie, came from Keith A. Betts, PhD, a biostatistician who works for the Analysis Group, an international consulting firm. He also used the ATLAS database as the source for adalimumab outcomes, and differed marginally from Dr. Maksymowych by taking data on secukinumab patients from both the MEASURE 1 and MEASURE 2 pivotal trials. Although Dr. Betts also used the matching adjusted indirect comparison approach and broadened his data source modestly, his results showed a distinctly different outcome: similar efficacy for the two drugs. Dr. Betts also included a cost efficacy analysis, and in this part adalimumab showed superior performance after he factored in the cost per responding AS patient.

During the combined discussion period following the two talks, both presenters defended the legitimacy of their approaches, although Dr. Maksymowych conceded that these indirect comparisons are “hypothesis generating rather than producing a definitive answer.” But a couple of active European AS researchers rose to comment from the floor and discredit the whole process.

“These two presentations show why I am not a proponent of indirect comparisons. The statistical models squeeze the data until they confess,” said Robert Landewé, MD, an AS specialist at the University of Amsterdam. “This is now a commercial rather than a scientific clash between two important drugs. I challenge these companies to perform a head-to-head trial. Indirect comparisons are not good,” he concluded, to a round of audience applause.

“There are so many methodological issues,” said Désirée van der Heijde, MD, another Dutch AS clinician and researcher who rose to critique both studies. “The only thing you can rely on is head-to-head trials.”

I later spoke with Dr. Maksymowych, and he expressed some pessimism about the prospects for a fully-powered, head-to-head trial of an interleukin-17 inhibitor and tumor necrosis factor inhibitor because it would need to enroll so many patients. “Randomized studies of active comparators need to be huge because it’s hard to show improvements when the response rates are high,” he said. Plus, he added, it isn’t entirely about a drug’s efficacy against AS spinal symptoms anyway.

“We also have to think about the impact of treatment on other aspects of this disease, such as psoriasis and colitis, as well as radiographic disease progression,” he said. These aspects of the activity of both classes of drugs have not received much study in AS patients until now.

In other words, the battle between treatment options for AS has just begun, and seems likely to be fought on many fronts.

[email protected]

On Twitter @mitchelzoler

By Ellen S. Haddock, MBA, and Lawrence F. Eichenfield, MD

Molluscum

Molluscum typically presents as smooth, flesh-colored, flat-topped papules 2-8 mm in diameter with central whitish area, which is composed of the causative molluscum pox virus. While central depressions called umbilications are common, they may not be present in early molluscum lesions.^1,2 Lesions most often occur on the trunk and arms, but can occur anywhere.3-5 Individuals usually have multiple lesions, which may be clustered especially in areas of skin-to-skin contact.^5,6 Molluscum lesions can be itchy.

Molluscum is a benign viral skin infection caused by the molluscum contagiosum virus, which is a member of the poxvirus family. Molluscum infections are common, affecting 5%-11% of children.^5,7 Molluscum most often affects children younger than 8-years-old,⁵ with an average age of 5.8 years.⁸ The infection is spread through skin-to-skin contact with other individuals and by autoinoculation, which means that the infection can be spread from one area of an individual's skin to another when he or she scratches a lesion and then touches another area. It also can be spread by contact with fomites like towels and sponges.1 An association between public swimming pool use and molluscum infection has been reported, but this may have more to do with shared towels and equipment like kick-boards than transmission through the water itself.9 Molluscum sometimes is spread through contact sports like wrestling⁶ and between children sharing a bath.⁹ In adults, in whom molluscum is much less common because of acquired immunity,10 molluscum may be sexually transmitted or associated with HIV; however, this is rarely the case in children.¹

Children with atopic dermatitis have increased risk of molluscum infection in part because breaks in their skin and pruritus facilitate autoinoculation through scratching.¹¹ Not uncommonly, molluscum lesions become inflamed, with tenderness, erythema, and crust. In a study by Berger et al., 22% of patients had inflamed molluscum lesions.³ The appearance of inflamed molluscum lesions may raise concern about bacterial infection, but more often, the inflammation is a sign that the immune system is reacting to the viral infection and has almost "won the battle."¹⁰ After inflamed molluscum lesions develop, the total number of molluscum lesions typically declines,3 and some consider inflamed molluscum lesions to be a "beginning of the end sign," indicating that the infection may soon resolve.¹⁰ If the child is afebrile, lesions are itchy and painless, skin culture is negative, and there is no lymphangitis or spreading erythema, the inflammation is more likely a sign of impending resolution than bacterial secondary infection, and the urge to prescribe antibiotics should be resisted.¹⁰

As seen in this case, some patients with molluscum (5%) develop a diffuse, monomorphous, papular, or papulovesicular eruption that is an id reaction.3 This may appear to be eczema-like, lichenoid in appearance, or mimicking Gianotti-Crosti syndrome (papular acrodermatitis of childhood).³ It typically affects the arms and legs, is bilateral, and may be pruritic. The id reaction may occur in conjunction with inflamed molluscum, as is true in this case. The diffuse eruption can sometimes be mistaken for a sudden increase in the number of molluscum lesions, but the papular dermatitis lesions do not have the flat-topped dome-shape nor white centers.³ On average, the id reaction lasts about 6 weeks, after which both it and the primary molluscum lesions typically resolve.³ Although not seen in this case, more than a third of molluscum patients develop a pruritic, erythematous, eczematous area around molluscum lesions, termed molluscum dermatitis or eczema molluscatum, which may be more prominent than the molluscum itself.³ The eczematous patch typically surrounds molluscum lesions but also may occur at distant sites.¹² This reaction is especially common in patients with atopic dermatitis, 51% of whom develop it.³ It is considered a hypersensitivity reaction and may be asymptomatic or minimally pruritic.¹² Molluscum dermatitis suggests that the immune system has taken notice of the infection and is fighting it¹³; however, it does not necessarily indicate impending resolution.³

Differential diagnosis

The differential diagnosis for molluscum includes herpes simplex, warts, and milia.¹⁴ Like molluscum, herpes simplex lesions can have central umbilication, but the lesions are vesicular rather than solid. Warts typically have a rough, jagged surface in contrast to the smooth surface of molluscum lesions. Milia tend to be smaller and not flat topped. They are more common in infants and adults than in children and primarily affect the face.

Inflamed molluscum lesions and molluscum dermatitis can be mistaken for atopic dermatitis, and molluscum-associated id reactions may exacerbate atopic dermatitis. Inflamed molluscum and molluscum with id reaction could be confused with scabies, which may become crusted and also may be accompanied by id reaction. Presence of serpiginous linear burrows would suggest scabies rather than molluscum, and the diagnosis of scabies can be confirmed by scraping a burrow and looking for a mite or its feces under a microscope.

Prognosis and treatment

Molluscum infections typically resolve spontaneously in months to years (average duration, 13 months),¹⁴ so treatment may not be required. The goal of treatment is to accelerate the resolution of the infection, but some studies have found that common treatments may not shorten the time to resolution.¹¹ However, if there is substantial pruritus, lesions are cosmetically undesirable, or a child has atopic dermatitis and is at increased risk for autoinoculation, treatment may be warranted.¹⁵ Furthermore, molluscum lesions can scar, so prevention of autoinoculation may help minimize scarring.¹⁶

Few high-quality studies of the efficacy of molluscum treatments exist, and a 2009 Cochrane review found insufficient evidence to recommend any therapy for molluscum. The most common treatment used by pediatric dermatologists is cantharidin,¹⁷ and this treatment also is available to primary care practitioners. This option is preferred over other destructive methods such as curettage or liquid nitrogen cryotherapy because it is not painful or traumatic and is well tolerated by pediatric patients.⁸ Parent and physician satisfaction with the therapy is high; 78%-95% of parents would use cantharidin treatment again for molluscum recurrence.^4,8,18 Originally extracted from the blister beetle but now synthesized commercially,¹⁹ cantharidin causes vesiculation at the dermoepidermal junction6 by destroying intercellular connections.4 Vesiculation of the skin causes extrusion of the molluscum body, which facilitates resolution of the lesion.¹⁹ The cantharidin formulation is applied directly to molluscum lesions with the wooden end of a cotton-tipped applicator.⁴ Patients may be directed to wash it off after 4-6 hours. Blistering is an expected, desired outcome. A minority of patients may experience mild temporary pain (7%), more significant blistering (2.5%), burning (less than 1%), pruritus (less than 1%), or irritation (less than 1%).⁴ There is a risk of scarring and pigmentary changes, but these risks also exist for untreated lesions.¹⁹ Cantharidin treatment is repeated approximately every 4 weeks, and 90% of cases resolve after an average of 2.1 treatments.¹⁸ Topical retinoids can be used in an attempt to trigger an irritant response by the immune system, and they are the preferred therapy for facial lesions, but they are inconsistently effective.4 Randomized controlled trials found that imiquimod, a previously popular treatment is not effective,²⁰ and the evidence for cimetidine is contradictory.^21,22 Molluscum dermatitis and id reaction can be treated with medium strength topical steroids. 

References

1. Viral diseases of the skin, in "Hurwitz Clinical Pediatric Dermatology," 4 ed. (New York: Elsevier, 2011, pp. 348-69). .
2. Molluscum, in "Red Book Report of the Committee on Infectious Diseases," 2015.

Ms. Haddock is a medical student at the University of California, San Diego, and a research associate at Rady Children's Hospital-San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children's Hospital-San Diego and professor of dermatology and pediatrics at the University of California, San Diego. Dr. Eichenfield and Ms. Haddock state they have no relevant financial disclosures.

By Ellen S. Haddock, MBA, and Lawrence F. Eichenfield, MD

Molluscum

Molluscum typically presents as smooth, flesh-colored, flat-topped papules 2-8 mm in diameter with central whitish area, which is composed of the causative molluscum pox virus. While central depressions called umbilications are common, they may not be present in early molluscum lesions.^1,2 Lesions most often occur on the trunk and arms, but can occur anywhere.3-5 Individuals usually have multiple lesions, which may be clustered especially in areas of skin-to-skin contact.^5,6 Molluscum lesions can be itchy.

Molluscum is a benign viral skin infection caused by the molluscum contagiosum virus, which is a member of the poxvirus family. Molluscum infections are common, affecting 5%-11% of children.^5,7 Molluscum most often affects children younger than 8-years-old,⁵ with an average age of 5.8 years.⁸ The infection is spread through skin-to-skin contact with other individuals and by autoinoculation, which means that the infection can be spread from one area of an individual's skin to another when he or she scratches a lesion and then touches another area. It also can be spread by contact with fomites like towels and sponges.1 An association between public swimming pool use and molluscum infection has been reported, but this may have more to do with shared towels and equipment like kick-boards than transmission through the water itself.9 Molluscum sometimes is spread through contact sports like wrestling⁶ and between children sharing a bath.⁹ In adults, in whom molluscum is much less common because of acquired immunity,10 molluscum may be sexually transmitted or associated with HIV; however, this is rarely the case in children.¹

Children with atopic dermatitis have increased risk of molluscum infection in part because breaks in their skin and pruritus facilitate autoinoculation through scratching.¹¹ Not uncommonly, molluscum lesions become inflamed, with tenderness, erythema, and crust. In a study by Berger et al., 22% of patients had inflamed molluscum lesions.³ The appearance of inflamed molluscum lesions may raise concern about bacterial infection, but more often, the inflammation is a sign that the immune system is reacting to the viral infection and has almost "won the battle."¹⁰ After inflamed molluscum lesions develop, the total number of molluscum lesions typically declines,3 and some consider inflamed molluscum lesions to be a "beginning of the end sign," indicating that the infection may soon resolve.¹⁰ If the child is afebrile, lesions are itchy and painless, skin culture is negative, and there is no lymphangitis or spreading erythema, the inflammation is more likely a sign of impending resolution than bacterial secondary infection, and the urge to prescribe antibiotics should be resisted.¹⁰

As seen in this case, some patients with molluscum (5%) develop a diffuse, monomorphous, papular, or papulovesicular eruption that is an id reaction.3 This may appear to be eczema-like, lichenoid in appearance, or mimicking Gianotti-Crosti syndrome (papular acrodermatitis of childhood).³ It typically affects the arms and legs, is bilateral, and may be pruritic. The id reaction may occur in conjunction with inflamed molluscum, as is true in this case. The diffuse eruption can sometimes be mistaken for a sudden increase in the number of molluscum lesions, but the papular dermatitis lesions do not have the flat-topped dome-shape nor white centers.³ On average, the id reaction lasts about 6 weeks, after which both it and the primary molluscum lesions typically resolve.³ Although not seen in this case, more than a third of molluscum patients develop a pruritic, erythematous, eczematous area around molluscum lesions, termed molluscum dermatitis or eczema molluscatum, which may be more prominent than the molluscum itself.³ The eczematous patch typically surrounds molluscum lesions but also may occur at distant sites.¹² This reaction is especially common in patients with atopic dermatitis, 51% of whom develop it.³ It is considered a hypersensitivity reaction and may be asymptomatic or minimally pruritic.¹² Molluscum dermatitis suggests that the immune system has taken notice of the infection and is fighting it¹³; however, it does not necessarily indicate impending resolution.³

Differential diagnosis

The differential diagnosis for molluscum includes herpes simplex, warts, and milia.¹⁴ Like molluscum, herpes simplex lesions can have central umbilication, but the lesions are vesicular rather than solid. Warts typically have a rough, jagged surface in contrast to the smooth surface of molluscum lesions. Milia tend to be smaller and not flat topped. They are more common in infants and adults than in children and primarily affect the face.

Inflamed molluscum lesions and molluscum dermatitis can be mistaken for atopic dermatitis, and molluscum-associated id reactions may exacerbate atopic dermatitis. Inflamed molluscum and molluscum with id reaction could be confused with scabies, which may become crusted and also may be accompanied by id reaction. Presence of serpiginous linear burrows would suggest scabies rather than molluscum, and the diagnosis of scabies can be confirmed by scraping a burrow and looking for a mite or its feces under a microscope.

Prognosis and treatment

Molluscum infections typically resolve spontaneously in months to years (average duration, 13 months),¹⁴ so treatment may not be required. The goal of treatment is to accelerate the resolution of the infection, but some studies have found that common treatments may not shorten the time to resolution.¹¹ However, if there is substantial pruritus, lesions are cosmetically undesirable, or a child has atopic dermatitis and is at increased risk for autoinoculation, treatment may be warranted.¹⁵ Furthermore, molluscum lesions can scar, so prevention of autoinoculation may help minimize scarring.¹⁶

Few high-quality studies of the efficacy of molluscum treatments exist, and a 2009 Cochrane review found insufficient evidence to recommend any therapy for molluscum. The most common treatment used by pediatric dermatologists is cantharidin,¹⁷ and this treatment also is available to primary care practitioners. This option is preferred over other destructive methods such as curettage or liquid nitrogen cryotherapy because it is not painful or traumatic and is well tolerated by pediatric patients.⁸ Parent and physician satisfaction with the therapy is high; 78%-95% of parents would use cantharidin treatment again for molluscum recurrence.^4,8,18 Originally extracted from the blister beetle but now synthesized commercially,¹⁹ cantharidin causes vesiculation at the dermoepidermal junction6 by destroying intercellular connections.4 Vesiculation of the skin causes extrusion of the molluscum body, which facilitates resolution of the lesion.¹⁹ The cantharidin formulation is applied directly to molluscum lesions with the wooden end of a cotton-tipped applicator.⁴ Patients may be directed to wash it off after 4-6 hours. Blistering is an expected, desired outcome. A minority of patients may experience mild temporary pain (7%), more significant blistering (2.5%), burning (less than 1%), pruritus (less than 1%), or irritation (less than 1%).⁴ There is a risk of scarring and pigmentary changes, but these risks also exist for untreated lesions.¹⁹ Cantharidin treatment is repeated approximately every 4 weeks, and 90% of cases resolve after an average of 2.1 treatments.¹⁸ Topical retinoids can be used in an attempt to trigger an irritant response by the immune system, and they are the preferred therapy for facial lesions, but they are inconsistently effective.4 Randomized controlled trials found that imiquimod, a previously popular treatment is not effective,²⁰ and the evidence for cimetidine is contradictory.^21,22 Molluscum dermatitis and id reaction can be treated with medium strength topical steroids. 

References

1. Viral diseases of the skin, in "Hurwitz Clinical Pediatric Dermatology," 4 ed. (New York: Elsevier, 2011, pp. 348-69). .
2. Molluscum, in "Red Book Report of the Committee on Infectious Diseases," 2015.

Ms. Haddock is a medical student at the University of California, San Diego, and a research associate at Rady Children's Hospital-San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children's Hospital-San Diego and professor of dermatology and pediatrics at the University of California, San Diego. Dr. Eichenfield and Ms. Haddock state they have no relevant financial disclosures.

By Ellen S. Haddock, MBA, and Lawrence F. Eichenfield, MD

Molluscum

Molluscum typically presents as smooth, flesh-colored, flat-topped papules 2-8 mm in diameter with central whitish area, which is composed of the causative molluscum pox virus. While central depressions called umbilications are common, they may not be present in early molluscum lesions.^1,2 Lesions most often occur on the trunk and arms, but can occur anywhere.3-5 Individuals usually have multiple lesions, which may be clustered especially in areas of skin-to-skin contact.^5,6 Molluscum lesions can be itchy.

Molluscum is a benign viral skin infection caused by the molluscum contagiosum virus, which is a member of the poxvirus family. Molluscum infections are common, affecting 5%-11% of children.^5,7 Molluscum most often affects children younger than 8-years-old,⁵ with an average age of 5.8 years.⁸ The infection is spread through skin-to-skin contact with other individuals and by autoinoculation, which means that the infection can be spread from one area of an individual's skin to another when he or she scratches a lesion and then touches another area. It also can be spread by contact with fomites like towels and sponges.1 An association between public swimming pool use and molluscum infection has been reported, but this may have more to do with shared towels and equipment like kick-boards than transmission through the water itself.9 Molluscum sometimes is spread through contact sports like wrestling⁶ and between children sharing a bath.⁹ In adults, in whom molluscum is much less common because of acquired immunity,10 molluscum may be sexually transmitted or associated with HIV; however, this is rarely the case in children.¹

Children with atopic dermatitis have increased risk of molluscum infection in part because breaks in their skin and pruritus facilitate autoinoculation through scratching.¹¹ Not uncommonly, molluscum lesions become inflamed, with tenderness, erythema, and crust. In a study by Berger et al., 22% of patients had inflamed molluscum lesions.³ The appearance of inflamed molluscum lesions may raise concern about bacterial infection, but more often, the inflammation is a sign that the immune system is reacting to the viral infection and has almost "won the battle."¹⁰ After inflamed molluscum lesions develop, the total number of molluscum lesions typically declines,3 and some consider inflamed molluscum lesions to be a "beginning of the end sign," indicating that the infection may soon resolve.¹⁰ If the child is afebrile, lesions are itchy and painless, skin culture is negative, and there is no lymphangitis or spreading erythema, the inflammation is more likely a sign of impending resolution than bacterial secondary infection, and the urge to prescribe antibiotics should be resisted.¹⁰

As seen in this case, some patients with molluscum (5%) develop a diffuse, monomorphous, papular, or papulovesicular eruption that is an id reaction.3 This may appear to be eczema-like, lichenoid in appearance, or mimicking Gianotti-Crosti syndrome (papular acrodermatitis of childhood).³ It typically affects the arms and legs, is bilateral, and may be pruritic. The id reaction may occur in conjunction with inflamed molluscum, as is true in this case. The diffuse eruption can sometimes be mistaken for a sudden increase in the number of molluscum lesions, but the papular dermatitis lesions do not have the flat-topped dome-shape nor white centers.³ On average, the id reaction lasts about 6 weeks, after which both it and the primary molluscum lesions typically resolve.³ Although not seen in this case, more than a third of molluscum patients develop a pruritic, erythematous, eczematous area around molluscum lesions, termed molluscum dermatitis or eczema molluscatum, which may be more prominent than the molluscum itself.³ The eczematous patch typically surrounds molluscum lesions but also may occur at distant sites.¹² This reaction is especially common in patients with atopic dermatitis, 51% of whom develop it.³ It is considered a hypersensitivity reaction and may be asymptomatic or minimally pruritic.¹² Molluscum dermatitis suggests that the immune system has taken notice of the infection and is fighting it¹³; however, it does not necessarily indicate impending resolution.³

Differential diagnosis

The differential diagnosis for molluscum includes herpes simplex, warts, and milia.¹⁴ Like molluscum, herpes simplex lesions can have central umbilication, but the lesions are vesicular rather than solid. Warts typically have a rough, jagged surface in contrast to the smooth surface of molluscum lesions. Milia tend to be smaller and not flat topped. They are more common in infants and adults than in children and primarily affect the face.

Inflamed molluscum lesions and molluscum dermatitis can be mistaken for atopic dermatitis, and molluscum-associated id reactions may exacerbate atopic dermatitis. Inflamed molluscum and molluscum with id reaction could be confused with scabies, which may become crusted and also may be accompanied by id reaction. Presence of serpiginous linear burrows would suggest scabies rather than molluscum, and the diagnosis of scabies can be confirmed by scraping a burrow and looking for a mite or its feces under a microscope.

Prognosis and treatment

Molluscum infections typically resolve spontaneously in months to years (average duration, 13 months),¹⁴ so treatment may not be required. The goal of treatment is to accelerate the resolution of the infection, but some studies have found that common treatments may not shorten the time to resolution.¹¹ However, if there is substantial pruritus, lesions are cosmetically undesirable, or a child has atopic dermatitis and is at increased risk for autoinoculation, treatment may be warranted.¹⁵ Furthermore, molluscum lesions can scar, so prevention of autoinoculation may help minimize scarring.¹⁶

Few high-quality studies of the efficacy of molluscum treatments exist, and a 2009 Cochrane review found insufficient evidence to recommend any therapy for molluscum. The most common treatment used by pediatric dermatologists is cantharidin,¹⁷ and this treatment also is available to primary care practitioners. This option is preferred over other destructive methods such as curettage or liquid nitrogen cryotherapy because it is not painful or traumatic and is well tolerated by pediatric patients.⁸ Parent and physician satisfaction with the therapy is high; 78%-95% of parents would use cantharidin treatment again for molluscum recurrence.^4,8,18 Originally extracted from the blister beetle but now synthesized commercially,¹⁹ cantharidin causes vesiculation at the dermoepidermal junction6 by destroying intercellular connections.4 Vesiculation of the skin causes extrusion of the molluscum body, which facilitates resolution of the lesion.¹⁹ The cantharidin formulation is applied directly to molluscum lesions with the wooden end of a cotton-tipped applicator.⁴ Patients may be directed to wash it off after 4-6 hours. Blistering is an expected, desired outcome. A minority of patients may experience mild temporary pain (7%), more significant blistering (2.5%), burning (less than 1%), pruritus (less than 1%), or irritation (less than 1%).⁴ There is a risk of scarring and pigmentary changes, but these risks also exist for untreated lesions.¹⁹ Cantharidin treatment is repeated approximately every 4 weeks, and 90% of cases resolve after an average of 2.1 treatments.¹⁸ Topical retinoids can be used in an attempt to trigger an irritant response by the immune system, and they are the preferred therapy for facial lesions, but they are inconsistently effective.4 Randomized controlled trials found that imiquimod, a previously popular treatment is not effective,²⁰ and the evidence for cimetidine is contradictory.^21,22 Molluscum dermatitis and id reaction can be treated with medium strength topical steroids. 

References

1. Viral diseases of the skin, in "Hurwitz Clinical Pediatric Dermatology," 4 ed. (New York: Elsevier, 2011, pp. 348-69). .
2. Molluscum, in "Red Book Report of the Committee on Infectious Diseases," 2015.

Ms. Haddock is a medical student at the University of California, San Diego, and a research associate at Rady Children's Hospital-San Diego. Dr. Eichenfield is chief of pediatric and adolescent dermatology at Rady Children's Hospital-San Diego and professor of dermatology and pediatrics at the University of California, San Diego. Dr. Eichenfield and Ms. Haddock state they have no relevant financial disclosures.

WASHINGTON – Challenging patients with depression to stay engaged in their recovery while rigorously monitoring and measuring their treatment response can mean the difference between remission or resistance, according to an expert.

“We all wish for better treatments, but we really don’t have any coming available to us in the near future, so our task is to do as well as we can with what we have,” Michael E. Thase, MD, professor of psychiatry at the University of Pennsylvania, Philadelphia, said at Summit in Neurology & Psychiatry.

“We know far too well that there is a large gap between what we might be able to accomplish and what actually happens in clinical practice,” Dr. Thase said.

To close that gap, start with evaluating what can be done to combat patient nonadherence. A 2007 study indicated that just under 20% of patients adhere to antidepressant medication guidelines (Prim Care Companion J Clin Psychiatry. 2007;9[2]:91-9.), and according to Dr. Thase, less than 10% of patients being seen for depression in primary care actually fill their prescriptions.

“Don’t delude yourself that these patients drop out of treatment because they no longer need it. They drop out mostly because they have gotten disgusted, disappointed, or discouraged,” said Dr. Thase, attributing the high rate of nonadherence to the nature of depression itself.

“Depression is a state of pessimism, low confidence, and of not really feeling capable.”

Helping patients overcome their reluctance to follow treatment guidelines begins with accurately assessing their symptom severity. Patients who rate 4 or less on the Patient Health Questionnaire–9 (PHQ-9), which is based on the DSM-IV, are considered in remission or not to have severe depression. Similarly, patients who score 5 or less on the Quick Inventory of Depressive Symptomatology (QIDS) are not considered in the danger zone.

The severity ratings included in the DSM-5 can help clinicians pinpoint the level of depression a patient is experiencing, as can a therapeutic relationship with the patient and the family, Dr. Thase said at the summit, held by Global Academy for Medical Education.

He urged clinicians to monitor adherence routinely by asking patients whether or not they have filled or refilled their prescriptions. It is helpful to ask patients about missing doses and whether they are feeling any improvement, he said.

“It’s a very simple process: You keep track of the patients. Chase after them if they don’t follow through. If you’re not keeping track, the patients think [what they do] doesn’t matter,” Dr. Thase said.

A 2010 study of chronic depression treatment in primary care practices showed that compared with regular care, aggressive monitoring of patient adherence and outcomes in 728 adults with depression resulted in better remission rates across 18 months of treatment. At 6 months 43.4% of patients who had been contacted regularly by nursing and social worker staff were in remission, compared with 33.3% of the 78 who had received regular care (P = .11). At 12 months, the results were 52% vs. 33.9% (P = .012), and at 18 months remission was reported in 49.2% vs. 27.3% (P = .004) (Ann Fam Med. 2010 Sep;8[5]:387-96).

By being alert to side effects, using a rating scale to measure symptom reduction, and not staying “locked” into the idea that all treatments require 6-8 weeks before patients see any improvement, clinicians can boost chances for adherence – and thus for remission – since patients who don’t improve in the first 2 weeks have just a 15% chance for improvement, Dr. Thase said. “You need 6-8 weeks to get to the maximum titration. That old 8-week rule applies mostly to patients who are showing improvement by week 2.”

If by week 2, the patient is not tolerating the medication’s side effects and has no symptom reduction, then move on to the next medication, Dr. Thase said, emphasizing the importance of seeing patients at least twice monthly. “If we’re only seeing a patient once a month, we’ve already fallen behind in the up-titration part, and we’ve missed the opportunity for early intervention if the patient is having side effects.”

Algorithms for choosing depression treatments should be a “fact of life,” he said. Start with the safest, easiest to tolerate, and least expensive of the available antidepressants, such as escitalopram and fluoxetine before working through the second- and third-line therapies and adjunctive therapies, all of which have greater risk profiles as you move through them. This algorithmic approach has been shown to result in patients scoring at least 10 points higher on a depression rating scale (JAMA Psychiatry. 2004;61:[7]669-80), which Dr. Thase said is equivalent to about a 30% higher chance of remission. “Don’t go over and over with the simple treatments that aren’t [evoking] a response. Move briskly on to the more complex treatments until patients respond.”

Treatment algorithms can include psychotherapies, either in combination with pharmacotherapy or as monotherapy. He encouraged clinicians to refer to the American Psychiatric Association (APA) practice guideline for depression for more details. The absence of depressive symptoms alone is not indicative of remission, according to the guideline, which Dr. Thase coauthored. The presence of positive emotions and resilience, along with a sense of control over emotions and hope for the future, indicates remission.

If after applying those methods a patient remains depressed and has been negatively screened for bipolar disorder, the use of tricyclics or monoamine oxidase inhibitors (MAOIs) may be appropriate. “MAOIs account for less than 1 in every 1,000 prescriptions for antidepressants, yet for people who don’t respond to modern antidepressants, they still can carry a 30%-40% response rate. So, if you don’t prescribe them yourself, please get access to someone who does,” Dr. Thase said.

The tenets of measurement-based care are essentially the lessons learned from the landmark Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial, which sought to address how pharmacologic care for depression could be delivered based on adequate dosing, attenuation of symptoms, fewer side effects, and other factors (Am J Psychiatry. 2006;163:1905-17).

Now,10 years later, measurement-based treatment is still finding its way into practice, Dr. Thase said in an interview. “But, there’s no reason to be unduly pessimistic. Ten years ago, depression screening was in the same position, and now it is both considered to be the standard of care and is widely done.”

Dr. Thase reported having extensive industry relationships, noting that he has been involved in the development of nearly every drug for the treatment of mood disorders. Global Academy and this news organization are owned by the same company.

[email protected]

On Twitter @whitneymcknight

WASHINGTON – Challenging patients with depression to stay engaged in their recovery while rigorously monitoring and measuring their treatment response can mean the difference between remission or resistance, according to an expert.

“We all wish for better treatments, but we really don’t have any coming available to us in the near future, so our task is to do as well as we can with what we have,” Michael E. Thase, MD, professor of psychiatry at the University of Pennsylvania, Philadelphia, said at Summit in Neurology & Psychiatry.

“We know far too well that there is a large gap between what we might be able to accomplish and what actually happens in clinical practice,” Dr. Thase said.

To close that gap, start with evaluating what can be done to combat patient nonadherence. A 2007 study indicated that just under 20% of patients adhere to antidepressant medication guidelines (Prim Care Companion J Clin Psychiatry. 2007;9[2]:91-9.), and according to Dr. Thase, less than 10% of patients being seen for depression in primary care actually fill their prescriptions.

“Don’t delude yourself that these patients drop out of treatment because they no longer need it. They drop out mostly because they have gotten disgusted, disappointed, or discouraged,” said Dr. Thase, attributing the high rate of nonadherence to the nature of depression itself.

“Depression is a state of pessimism, low confidence, and of not really feeling capable.”

Helping patients overcome their reluctance to follow treatment guidelines begins with accurately assessing their symptom severity. Patients who rate 4 or less on the Patient Health Questionnaire–9 (PHQ-9), which is based on the DSM-IV, are considered in remission or not to have severe depression. Similarly, patients who score 5 or less on the Quick Inventory of Depressive Symptomatology (QIDS) are not considered in the danger zone.

The severity ratings included in the DSM-5 can help clinicians pinpoint the level of depression a patient is experiencing, as can a therapeutic relationship with the patient and the family, Dr. Thase said at the summit, held by Global Academy for Medical Education.

He urged clinicians to monitor adherence routinely by asking patients whether or not they have filled or refilled their prescriptions. It is helpful to ask patients about missing doses and whether they are feeling any improvement, he said.

“It’s a very simple process: You keep track of the patients. Chase after them if they don’t follow through. If you’re not keeping track, the patients think [what they do] doesn’t matter,” Dr. Thase said.

A 2010 study of chronic depression treatment in primary care practices showed that compared with regular care, aggressive monitoring of patient adherence and outcomes in 728 adults with depression resulted in better remission rates across 18 months of treatment. At 6 months 43.4% of patients who had been contacted regularly by nursing and social worker staff were in remission, compared with 33.3% of the 78 who had received regular care (P = .11). At 12 months, the results were 52% vs. 33.9% (P = .012), and at 18 months remission was reported in 49.2% vs. 27.3% (P = .004) (Ann Fam Med. 2010 Sep;8[5]:387-96).

By being alert to side effects, using a rating scale to measure symptom reduction, and not staying “locked” into the idea that all treatments require 6-8 weeks before patients see any improvement, clinicians can boost chances for adherence – and thus for remission – since patients who don’t improve in the first 2 weeks have just a 15% chance for improvement, Dr. Thase said. “You need 6-8 weeks to get to the maximum titration. That old 8-week rule applies mostly to patients who are showing improvement by week 2.”

If by week 2, the patient is not tolerating the medication’s side effects and has no symptom reduction, then move on to the next medication, Dr. Thase said, emphasizing the importance of seeing patients at least twice monthly. “If we’re only seeing a patient once a month, we’ve already fallen behind in the up-titration part, and we’ve missed the opportunity for early intervention if the patient is having side effects.”

Algorithms for choosing depression treatments should be a “fact of life,” he said. Start with the safest, easiest to tolerate, and least expensive of the available antidepressants, such as escitalopram and fluoxetine before working through the second- and third-line therapies and adjunctive therapies, all of which have greater risk profiles as you move through them. This algorithmic approach has been shown to result in patients scoring at least 10 points higher on a depression rating scale (JAMA Psychiatry. 2004;61:[7]669-80), which Dr. Thase said is equivalent to about a 30% higher chance of remission. “Don’t go over and over with the simple treatments that aren’t [evoking] a response. Move briskly on to the more complex treatments until patients respond.”

Treatment algorithms can include psychotherapies, either in combination with pharmacotherapy or as monotherapy. He encouraged clinicians to refer to the American Psychiatric Association (APA) practice guideline for depression for more details. The absence of depressive symptoms alone is not indicative of remission, according to the guideline, which Dr. Thase coauthored. The presence of positive emotions and resilience, along with a sense of control over emotions and hope for the future, indicates remission.

If after applying those methods a patient remains depressed and has been negatively screened for bipolar disorder, the use of tricyclics or monoamine oxidase inhibitors (MAOIs) may be appropriate. “MAOIs account for less than 1 in every 1,000 prescriptions for antidepressants, yet for people who don’t respond to modern antidepressants, they still can carry a 30%-40% response rate. So, if you don’t prescribe them yourself, please get access to someone who does,” Dr. Thase said.

The tenets of measurement-based care are essentially the lessons learned from the landmark Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial, which sought to address how pharmacologic care for depression could be delivered based on adequate dosing, attenuation of symptoms, fewer side effects, and other factors (Am J Psychiatry. 2006;163:1905-17).

Now,10 years later, measurement-based treatment is still finding its way into practice, Dr. Thase said in an interview. “But, there’s no reason to be unduly pessimistic. Ten years ago, depression screening was in the same position, and now it is both considered to be the standard of care and is widely done.”

Dr. Thase reported having extensive industry relationships, noting that he has been involved in the development of nearly every drug for the treatment of mood disorders. Global Academy and this news organization are owned by the same company.

[email protected]

On Twitter @whitneymcknight

WASHINGTON – Challenging patients with depression to stay engaged in their recovery while rigorously monitoring and measuring their treatment response can mean the difference between remission or resistance, according to an expert.

“We all wish for better treatments, but we really don’t have any coming available to us in the near future, so our task is to do as well as we can with what we have,” Michael E. Thase, MD, professor of psychiatry at the University of Pennsylvania, Philadelphia, said at Summit in Neurology & Psychiatry.

“We know far too well that there is a large gap between what we might be able to accomplish and what actually happens in clinical practice,” Dr. Thase said.

To close that gap, start with evaluating what can be done to combat patient nonadherence. A 2007 study indicated that just under 20% of patients adhere to antidepressant medication guidelines (Prim Care Companion J Clin Psychiatry. 2007;9[2]:91-9.), and according to Dr. Thase, less than 10% of patients being seen for depression in primary care actually fill their prescriptions.

“Don’t delude yourself that these patients drop out of treatment because they no longer need it. They drop out mostly because they have gotten disgusted, disappointed, or discouraged,” said Dr. Thase, attributing the high rate of nonadherence to the nature of depression itself.

“Depression is a state of pessimism, low confidence, and of not really feeling capable.”

Helping patients overcome their reluctance to follow treatment guidelines begins with accurately assessing their symptom severity. Patients who rate 4 or less on the Patient Health Questionnaire–9 (PHQ-9), which is based on the DSM-IV, are considered in remission or not to have severe depression. Similarly, patients who score 5 or less on the Quick Inventory of Depressive Symptomatology (QIDS) are not considered in the danger zone.

The severity ratings included in the DSM-5 can help clinicians pinpoint the level of depression a patient is experiencing, as can a therapeutic relationship with the patient and the family, Dr. Thase said at the summit, held by Global Academy for Medical Education.

He urged clinicians to monitor adherence routinely by asking patients whether or not they have filled or refilled their prescriptions. It is helpful to ask patients about missing doses and whether they are feeling any improvement, he said.

“It’s a very simple process: You keep track of the patients. Chase after them if they don’t follow through. If you’re not keeping track, the patients think [what they do] doesn’t matter,” Dr. Thase said.

A 2010 study of chronic depression treatment in primary care practices showed that compared with regular care, aggressive monitoring of patient adherence and outcomes in 728 adults with depression resulted in better remission rates across 18 months of treatment. At 6 months 43.4% of patients who had been contacted regularly by nursing and social worker staff were in remission, compared with 33.3% of the 78 who had received regular care (P = .11). At 12 months, the results were 52% vs. 33.9% (P = .012), and at 18 months remission was reported in 49.2% vs. 27.3% (P = .004) (Ann Fam Med. 2010 Sep;8[5]:387-96).

By being alert to side effects, using a rating scale to measure symptom reduction, and not staying “locked” into the idea that all treatments require 6-8 weeks before patients see any improvement, clinicians can boost chances for adherence – and thus for remission – since patients who don’t improve in the first 2 weeks have just a 15% chance for improvement, Dr. Thase said. “You need 6-8 weeks to get to the maximum titration. That old 8-week rule applies mostly to patients who are showing improvement by week 2.”

If by week 2, the patient is not tolerating the medication’s side effects and has no symptom reduction, then move on to the next medication, Dr. Thase said, emphasizing the importance of seeing patients at least twice monthly. “If we’re only seeing a patient once a month, we’ve already fallen behind in the up-titration part, and we’ve missed the opportunity for early intervention if the patient is having side effects.”

Algorithms for choosing depression treatments should be a “fact of life,” he said. Start with the safest, easiest to tolerate, and least expensive of the available antidepressants, such as escitalopram and fluoxetine before working through the second- and third-line therapies and adjunctive therapies, all of which have greater risk profiles as you move through them. This algorithmic approach has been shown to result in patients scoring at least 10 points higher on a depression rating scale (JAMA Psychiatry. 2004;61:[7]669-80), which Dr. Thase said is equivalent to about a 30% higher chance of remission. “Don’t go over and over with the simple treatments that aren’t [evoking] a response. Move briskly on to the more complex treatments until patients respond.”

Treatment algorithms can include psychotherapies, either in combination with pharmacotherapy or as monotherapy. He encouraged clinicians to refer to the American Psychiatric Association (APA) practice guideline for depression for more details. The absence of depressive symptoms alone is not indicative of remission, according to the guideline, which Dr. Thase coauthored. The presence of positive emotions and resilience, along with a sense of control over emotions and hope for the future, indicates remission.

If after applying those methods a patient remains depressed and has been negatively screened for bipolar disorder, the use of tricyclics or monoamine oxidase inhibitors (MAOIs) may be appropriate. “MAOIs account for less than 1 in every 1,000 prescriptions for antidepressants, yet for people who don’t respond to modern antidepressants, they still can carry a 30%-40% response rate. So, if you don’t prescribe them yourself, please get access to someone who does,” Dr. Thase said.

The tenets of measurement-based care are essentially the lessons learned from the landmark Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial, which sought to address how pharmacologic care for depression could be delivered based on adequate dosing, attenuation of symptoms, fewer side effects, and other factors (Am J Psychiatry. 2006;163:1905-17).

Now,10 years later, measurement-based treatment is still finding its way into practice, Dr. Thase said in an interview. “But, there’s no reason to be unduly pessimistic. Ten years ago, depression screening was in the same position, and now it is both considered to be the standard of care and is widely done.”

Dr. Thase reported having extensive industry relationships, noting that he has been involved in the development of nearly every drug for the treatment of mood disorders. Global Academy and this news organization are owned by the same company.

[email protected]

On Twitter @whitneymcknight

Inundating our popular and academic media circles is information regarding the Zika virus. A recent article by Farahnik et al in the Journal of the American Academy of Dermatology (2016;74:1286-1287) briefly outlines what is known about Zika infection thus far and its dermatologic manifestations. Pairing this article with Centers for Disease Control and Prevention guidelines on the topic, we are presented with an evolving introduction to this new entity. Here’s what we know:

What’s the issue?

As with any new outbreak, the applicability to the general population and true risks remain to be seen. Each of our clinics recalls the stark changes in patient intake and screening questions with infections as ubiquitous as methicillin-resistant Staphylococcus aureus to much rarer exposures such as Ebola virus, each with progressive understanding of risk groups, disease manifestations, and eradication and prevention measures.

By mid-June 2016, 30 hits on PubMed addressing Zika had already been cited just within the month, outlining various aspects of the infection, and many specialties, particularly neurology, obstetrics, primary care, infectious disease, and dermatology, are weighing in. Unfortunately, the majority of cases of primary Zika infection do not manifest with skin or systemic symptoms, and even cases that do are nonspecific, exanthematous, and flulike.

Vague as it may be so far, it is nonetheless imperative that clinicians be familiar with what is concretely known about Zika virus and acquaint ourselves with the travel distribution and restrictions, disease risk factors, known sequelae, testing availability and limitations, and reporting guidelines. From personal experience, as I traveled to Belize earlier this year during my first trimester of pregnancy before the travel restrictions were outlined, even obstetricians are not wholly familiar with the manner in which to order testing and the appropriate window to do so. I have been asymptomatic, my blood was drawn in a period of time that exceeded the interval for accurate results (as outlined above) and was therefore inappropriately recommended/ordered, and now serial fetal ultrasonography is being implemented every few weeks.

With lack of ubiquitous knowledge about the infection, clinicians are not universally certain of the appropriate next steps when a patient presents with Zika risk factors, and therefore anxiety remains high for pregnant patients and their contacts. The Centers for Disease Control and Prevention website is the official home base, and we should review it and await their further evolving specific recommendations as more cases unfortunately accumulate.

Have you encountered any patients this year with exposure to or symptoms of Zika infection, and what, if anything, have you outlined for them?

We want to know your views! Tell us what you think.

Inundating our popular and academic media circles is information regarding the Zika virus. A recent article by Farahnik et al in the Journal of the American Academy of Dermatology (2016;74:1286-1287) briefly outlines what is known about Zika infection thus far and its dermatologic manifestations. Pairing this article with Centers for Disease Control and Prevention guidelines on the topic, we are presented with an evolving introduction to this new entity. Here’s what we know:

What’s the issue?

As with any new outbreak, the applicability to the general population and true risks remain to be seen. Each of our clinics recalls the stark changes in patient intake and screening questions with infections as ubiquitous as methicillin-resistant Staphylococcus aureus to much rarer exposures such as Ebola virus, each with progressive understanding of risk groups, disease manifestations, and eradication and prevention measures.

By mid-June 2016, 30 hits on PubMed addressing Zika had already been cited just within the month, outlining various aspects of the infection, and many specialties, particularly neurology, obstetrics, primary care, infectious disease, and dermatology, are weighing in. Unfortunately, the majority of cases of primary Zika infection do not manifest with skin or systemic symptoms, and even cases that do are nonspecific, exanthematous, and flulike.

Vague as it may be so far, it is nonetheless imperative that clinicians be familiar with what is concretely known about Zika virus and acquaint ourselves with the travel distribution and restrictions, disease risk factors, known sequelae, testing availability and limitations, and reporting guidelines. From personal experience, as I traveled to Belize earlier this year during my first trimester of pregnancy before the travel restrictions were outlined, even obstetricians are not wholly familiar with the manner in which to order testing and the appropriate window to do so. I have been asymptomatic, my blood was drawn in a period of time that exceeded the interval for accurate results (as outlined above) and was therefore inappropriately recommended/ordered, and now serial fetal ultrasonography is being implemented every few weeks.

With lack of ubiquitous knowledge about the infection, clinicians are not universally certain of the appropriate next steps when a patient presents with Zika risk factors, and therefore anxiety remains high for pregnant patients and their contacts. The Centers for Disease Control and Prevention website is the official home base, and we should review it and await their further evolving specific recommendations as more cases unfortunately accumulate.

Have you encountered any patients this year with exposure to or symptoms of Zika infection, and what, if anything, have you outlined for them?

We want to know your views! Tell us what you think.

Inundating our popular and academic media circles is information regarding the Zika virus. A recent article by Farahnik et al in the Journal of the American Academy of Dermatology (2016;74:1286-1287) briefly outlines what is known about Zika infection thus far and its dermatologic manifestations. Pairing this article with Centers for Disease Control and Prevention guidelines on the topic, we are presented with an evolving introduction to this new entity. Here’s what we know:

What’s the issue?

As with any new outbreak, the applicability to the general population and true risks remain to be seen. Each of our clinics recalls the stark changes in patient intake and screening questions with infections as ubiquitous as methicillin-resistant Staphylococcus aureus to much rarer exposures such as Ebola virus, each with progressive understanding of risk groups, disease manifestations, and eradication and prevention measures.

By mid-June 2016, 30 hits on PubMed addressing Zika had already been cited just within the month, outlining various aspects of the infection, and many specialties, particularly neurology, obstetrics, primary care, infectious disease, and dermatology, are weighing in. Unfortunately, the majority of cases of primary Zika infection do not manifest with skin or systemic symptoms, and even cases that do are nonspecific, exanthematous, and flulike.

Vague as it may be so far, it is nonetheless imperative that clinicians be familiar with what is concretely known about Zika virus and acquaint ourselves with the travel distribution and restrictions, disease risk factors, known sequelae, testing availability and limitations, and reporting guidelines. From personal experience, as I traveled to Belize earlier this year during my first trimester of pregnancy before the travel restrictions were outlined, even obstetricians are not wholly familiar with the manner in which to order testing and the appropriate window to do so. I have been asymptomatic, my blood was drawn in a period of time that exceeded the interval for accurate results (as outlined above) and was therefore inappropriately recommended/ordered, and now serial fetal ultrasonography is being implemented every few weeks.

With lack of ubiquitous knowledge about the infection, clinicians are not universally certain of the appropriate next steps when a patient presents with Zika risk factors, and therefore anxiety remains high for pregnant patients and their contacts. The Centers for Disease Control and Prevention website is the official home base, and we should review it and await their further evolving specific recommendations as more cases unfortunately accumulate.

Have you encountered any patients this year with exposure to or symptoms of Zika infection, and what, if anything, have you outlined for them?

We want to know your views! Tell us what you think.

Most authorities recommend that, following delivery, all women should receive a uterotonic medication to reduce the risk of postpartum hemorrhage (PPH).¹ In the United States, the preferred uterotonic for this preventive effort is oxytocin—a low-cost, highly effective agent that typically is administered as an intravenous (IV) infusion or intramuscular (IM) injection. Unfortunately, even with the universal administration of oxytocin in the third stage of labor, PPH occurs in about 3% of vaginal deliveries.

A key decision in treating a PPH due to uterine atony is treatment with an optimal uterotonic. The options include:

Many obstetricians choose rectal misoprostol alone or in combination with oxytocin as the preferred treatment of PPH. However, evidence from clinical trials and pharmacokinetic studies suggest that rectal misoprostol is not an optimal choice if parenteral uterotonics are available. Here I pre-sent this evidence and urge you to stop the practice of using rectal misoprostol in efforts to manage PPH.

RCTs do not support the use of rectal misoprostolRandomized clinical trials (RCTs) have not demonstrated that misoprostol is superior to oxytocin for the treatment of PPH caused by uterine atony.² For example, Blum and colleagues studied 31,055 women who received oxytocin (by IV or IM route) at vaginal delivery and observed that 809 (3%) developed a PPH.³ The women who developed PPH were randomly assigned to treatment with misoprostol 800 µg sublingual or oxytocin 40 U in 1,000 mL as an IV infusion over 15 minutes.

Both oxytocin and misoprostol had similar efficacy for controlling bleeding within 20 minutes (90% and 89%, respectively). Fewer women had blood loss of 1,000 mL or greater when treated with oxytocin compared with misoprostol (1% vs 3%, respectively; P = .062). In addition, oxytocin was associated with fewer temperature elevations of 38°C (100.4°F) or above (15% vs 22% for misoprostol, P = .007) and fewer temperature elevations of 40°C (104°F) or above (0.2% vs 1.2% for misoprostol, P = .11).

In another trial, women with a vaginal delivery who were not treated with a uterotonic in the third stage were monitored for the development of a PPH.⁴ PPH did develop in 1,422 women, who were then randomly assigned to receive oxytocin (10 U IV or IM) plus a placebo tablet or oxytocin plus misoprostol (600 µg sublingual).

Comparing oxytocin alone versus oxytocin plus misoprostol, there was no difference in blood loss of 500 mL or greater after treatment initiation (14% vs 14%). However, 90 minutes following treatment, temperature elevations occurred much more often in the women who received oxytocin plus misoprostol compared with the women who received oxytocin alone (temperature ≥38°C: 58% vs 19%; temperature ≥40°C: 6.8% vs 0.4%).

Bottom line: If you have access to oxytocin, there is no advantage to using misoprostol to treat a PPH due to uterine atony.⁵

Rectal misoprostol does not achieve optimal circulating concentrations of the drugMisoprostol tablets are formulated for oral administration, not rectal administration. The studies in the TABLE show that rectal administration of misoprostol results in lower circulating concentration of the medication compared to oral, buccal, or vaginal administration.⁶⁻⁸ After rectal administration it takes about 60 minutes to reach the peak circulating concentration of misoprostol.^6,7 By contrast, parenteral oxytocin, methylergonovine, and carboprost tromethamine reach peak serum concentration much more quickly after administration.

In a study of misoprostol stimulation of uterine contractility as measured by an intrauterine pressure catheter, buccal administration resulted in higher peak uterine tone than rectal administration (49 vs 31 mm Hg).⁸ In addition, time to onset of uterine contractility was 41 minutes and 103 minutes, respectively, for buccal and rectal administration.

These studies show that rectal misoprostol is associated with lower serum concentrations, longer time to onset of uterine contraction, and less contractility than buccal administration. The one advantage of rectal administration is that it has a longer duration of action than the oral, buccal, or sublingual routes. In pharmacokinetic comparisons of buccal versus sublingual administration of misoprostol, the sublingual route results in greater peak concentration, which may cause more adverse effects.^9,10

Prioritize oxytocin, methergine, and carboprost tromethamineWhen treating PPH, administration of oxytocin, methylergonovine, or carboprost tromethamine rapidly provides therapeutic concentration of medication. For oxytocin, 40 U in 1 L, administered at a rate sufficient to control atony, or 10 U IM injection are often effective in controlling bleeding due to atony. Carboprost tromethamine 0.25 mg administered intramuscularly every 15 minutes up to 8 doses provides an excellent second-line agent. Carboprost tromethamine is contraindicated for women with asthma.

Methylergonovine 0.2 mg administered intramuscularly only can be given every 2 to 4 hours. Consequently, because time is of the essence in managing a severe PPH, it is unusual to be able to administer more than one dose of the agent during the course of treatment. Methylergonovine is contraindicated for women with hypertension.

There is scant evidence that misoprostol is more effective than oxytocin, and misoprostol clearly causes a higher rate of elevated temperature than any of the parenteral uterotonic agents. In your practice stop using rectal misoprostol for the treatment of PPH caused by uterine atony, and prioritize the use of parenteral uterotonics.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Most authorities recommend that, following delivery, all women should receive a uterotonic medication to reduce the risk of postpartum hemorrhage (PPH).¹ In the United States, the preferred uterotonic for this preventive effort is oxytocin—a low-cost, highly effective agent that typically is administered as an intravenous (IV) infusion or intramuscular (IM) injection. Unfortunately, even with the universal administration of oxytocin in the third stage of labor, PPH occurs in about 3% of vaginal deliveries.

A key decision in treating a PPH due to uterine atony is treatment with an optimal uterotonic. The options include:

Many obstetricians choose rectal misoprostol alone or in combination with oxytocin as the preferred treatment of PPH. However, evidence from clinical trials and pharmacokinetic studies suggest that rectal misoprostol is not an optimal choice if parenteral uterotonics are available. Here I pre-sent this evidence and urge you to stop the practice of using rectal misoprostol in efforts to manage PPH.

RCTs do not support the use of rectal misoprostolRandomized clinical trials (RCTs) have not demonstrated that misoprostol is superior to oxytocin for the treatment of PPH caused by uterine atony.² For example, Blum and colleagues studied 31,055 women who received oxytocin (by IV or IM route) at vaginal delivery and observed that 809 (3%) developed a PPH.³ The women who developed PPH were randomly assigned to treatment with misoprostol 800 µg sublingual or oxytocin 40 U in 1,000 mL as an IV infusion over 15 minutes.

Both oxytocin and misoprostol had similar efficacy for controlling bleeding within 20 minutes (90% and 89%, respectively). Fewer women had blood loss of 1,000 mL or greater when treated with oxytocin compared with misoprostol (1% vs 3%, respectively; P = .062). In addition, oxytocin was associated with fewer temperature elevations of 38°C (100.4°F) or above (15% vs 22% for misoprostol, P = .007) and fewer temperature elevations of 40°C (104°F) or above (0.2% vs 1.2% for misoprostol, P = .11).

In another trial, women with a vaginal delivery who were not treated with a uterotonic in the third stage were monitored for the development of a PPH.⁴ PPH did develop in 1,422 women, who were then randomly assigned to receive oxytocin (10 U IV or IM) plus a placebo tablet or oxytocin plus misoprostol (600 µg sublingual).

Comparing oxytocin alone versus oxytocin plus misoprostol, there was no difference in blood loss of 500 mL or greater after treatment initiation (14% vs 14%). However, 90 minutes following treatment, temperature elevations occurred much more often in the women who received oxytocin plus misoprostol compared with the women who received oxytocin alone (temperature ≥38°C: 58% vs 19%; temperature ≥40°C: 6.8% vs 0.4%).

Bottom line: If you have access to oxytocin, there is no advantage to using misoprostol to treat a PPH due to uterine atony.⁵

Rectal misoprostol does not achieve optimal circulating concentrations of the drugMisoprostol tablets are formulated for oral administration, not rectal administration. The studies in the TABLE show that rectal administration of misoprostol results in lower circulating concentration of the medication compared to oral, buccal, or vaginal administration.⁶⁻⁸ After rectal administration it takes about 60 minutes to reach the peak circulating concentration of misoprostol.^6,7 By contrast, parenteral oxytocin, methylergonovine, and carboprost tromethamine reach peak serum concentration much more quickly after administration.

In a study of misoprostol stimulation of uterine contractility as measured by an intrauterine pressure catheter, buccal administration resulted in higher peak uterine tone than rectal administration (49 vs 31 mm Hg).⁸ In addition, time to onset of uterine contractility was 41 minutes and 103 minutes, respectively, for buccal and rectal administration.

These studies show that rectal misoprostol is associated with lower serum concentrations, longer time to onset of uterine contraction, and less contractility than buccal administration. The one advantage of rectal administration is that it has a longer duration of action than the oral, buccal, or sublingual routes. In pharmacokinetic comparisons of buccal versus sublingual administration of misoprostol, the sublingual route results in greater peak concentration, which may cause more adverse effects.^9,10

Prioritize oxytocin, methergine, and carboprost tromethamineWhen treating PPH, administration of oxytocin, methylergonovine, or carboprost tromethamine rapidly provides therapeutic concentration of medication. For oxytocin, 40 U in 1 L, administered at a rate sufficient to control atony, or 10 U IM injection are often effective in controlling bleeding due to atony. Carboprost tromethamine 0.25 mg administered intramuscularly every 15 minutes up to 8 doses provides an excellent second-line agent. Carboprost tromethamine is contraindicated for women with asthma.

Methylergonovine 0.2 mg administered intramuscularly only can be given every 2 to 4 hours. Consequently, because time is of the essence in managing a severe PPH, it is unusual to be able to administer more than one dose of the agent during the course of treatment. Methylergonovine is contraindicated for women with hypertension.

There is scant evidence that misoprostol is more effective than oxytocin, and misoprostol clearly causes a higher rate of elevated temperature than any of the parenteral uterotonic agents. In your practice stop using rectal misoprostol for the treatment of PPH caused by uterine atony, and prioritize the use of parenteral uterotonics.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Most authorities recommend that, following delivery, all women should receive a uterotonic medication to reduce the risk of postpartum hemorrhage (PPH).¹ In the United States, the preferred uterotonic for this preventive effort is oxytocin—a low-cost, highly effective agent that typically is administered as an intravenous (IV) infusion or intramuscular (IM) injection. Unfortunately, even with the universal administration of oxytocin in the third stage of labor, PPH occurs in about 3% of vaginal deliveries.

A key decision in treating a PPH due to uterine atony is treatment with an optimal uterotonic. The options include:

Many obstetricians choose rectal misoprostol alone or in combination with oxytocin as the preferred treatment of PPH. However, evidence from clinical trials and pharmacokinetic studies suggest that rectal misoprostol is not an optimal choice if parenteral uterotonics are available. Here I pre-sent this evidence and urge you to stop the practice of using rectal misoprostol in efforts to manage PPH.

RCTs do not support the use of rectal misoprostolRandomized clinical trials (RCTs) have not demonstrated that misoprostol is superior to oxytocin for the treatment of PPH caused by uterine atony.² For example, Blum and colleagues studied 31,055 women who received oxytocin (by IV or IM route) at vaginal delivery and observed that 809 (3%) developed a PPH.³ The women who developed PPH were randomly assigned to treatment with misoprostol 800 µg sublingual or oxytocin 40 U in 1,000 mL as an IV infusion over 15 minutes.

Both oxytocin and misoprostol had similar efficacy for controlling bleeding within 20 minutes (90% and 89%, respectively). Fewer women had blood loss of 1,000 mL or greater when treated with oxytocin compared with misoprostol (1% vs 3%, respectively; P = .062). In addition, oxytocin was associated with fewer temperature elevations of 38°C (100.4°F) or above (15% vs 22% for misoprostol, P = .007) and fewer temperature elevations of 40°C (104°F) or above (0.2% vs 1.2% for misoprostol, P = .11).

In another trial, women with a vaginal delivery who were not treated with a uterotonic in the third stage were monitored for the development of a PPH.⁴ PPH did develop in 1,422 women, who were then randomly assigned to receive oxytocin (10 U IV or IM) plus a placebo tablet or oxytocin plus misoprostol (600 µg sublingual).

Comparing oxytocin alone versus oxytocin plus misoprostol, there was no difference in blood loss of 500 mL or greater after treatment initiation (14% vs 14%). However, 90 minutes following treatment, temperature elevations occurred much more often in the women who received oxytocin plus misoprostol compared with the women who received oxytocin alone (temperature ≥38°C: 58% vs 19%; temperature ≥40°C: 6.8% vs 0.4%).

Bottom line: If you have access to oxytocin, there is no advantage to using misoprostol to treat a PPH due to uterine atony.⁵

Rectal misoprostol does not achieve optimal circulating concentrations of the drugMisoprostol tablets are formulated for oral administration, not rectal administration. The studies in the TABLE show that rectal administration of misoprostol results in lower circulating concentration of the medication compared to oral, buccal, or vaginal administration.⁶⁻⁸ After rectal administration it takes about 60 minutes to reach the peak circulating concentration of misoprostol.^6,7 By contrast, parenteral oxytocin, methylergonovine, and carboprost tromethamine reach peak serum concentration much more quickly after administration.

In a study of misoprostol stimulation of uterine contractility as measured by an intrauterine pressure catheter, buccal administration resulted in higher peak uterine tone than rectal administration (49 vs 31 mm Hg).⁸ In addition, time to onset of uterine contractility was 41 minutes and 103 minutes, respectively, for buccal and rectal administration.

These studies show that rectal misoprostol is associated with lower serum concentrations, longer time to onset of uterine contraction, and less contractility than buccal administration. The one advantage of rectal administration is that it has a longer duration of action than the oral, buccal, or sublingual routes. In pharmacokinetic comparisons of buccal versus sublingual administration of misoprostol, the sublingual route results in greater peak concentration, which may cause more adverse effects.^9,10

Prioritize oxytocin, methergine, and carboprost tromethamineWhen treating PPH, administration of oxytocin, methylergonovine, or carboprost tromethamine rapidly provides therapeutic concentration of medication. For oxytocin, 40 U in 1 L, administered at a rate sufficient to control atony, or 10 U IM injection are often effective in controlling bleeding due to atony. Carboprost tromethamine 0.25 mg administered intramuscularly every 15 minutes up to 8 doses provides an excellent second-line agent. Carboprost tromethamine is contraindicated for women with asthma.

Methylergonovine 0.2 mg administered intramuscularly only can be given every 2 to 4 hours. Consequently, because time is of the essence in managing a severe PPH, it is unusual to be able to administer more than one dose of the agent during the course of treatment. Methylergonovine is contraindicated for women with hypertension.

There is scant evidence that misoprostol is more effective than oxytocin, and misoprostol clearly causes a higher rate of elevated temperature than any of the parenteral uterotonic agents. In your practice stop using rectal misoprostol for the treatment of PPH caused by uterine atony, and prioritize the use of parenteral uterotonics.

Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.