Pelvic organ prolapse: Effective treatments

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Editor’s Note: This is the fifth installment of a six-part series that will review key concepts and articles that ob.gyns. can use to prepare for the American Board of Obstetrics and Gynecology Maintenance of Certification examination. The series is adapted from Ob/Gyn Board Master (obgynboardmaster.com), an online board review course created by Erudyte. This month’s edition of the Board Corner focuses on pelvic organ prolapse.

The American College of Obstetricians and Gynecologists’ “Practice Bulletins” are important practice management guidelines for ob.gyn. clinicians. The Practice Bulletins are rich sources of material that is often tested on board exams. Earlier this year, ACOG released a revised Practice Bulletin (#176) updating its advice on the diagnosis and management of pelvic organ prolapse (POP).1 It is a well-written document summarizing most of the landmark articles published in the field of female pelvic medicine and reconstructive surgery. We recommend you read this bulletin and review this topic carefully.

Let’s begin with a possible medical board question: Which of the following procedures is the most effective for a sexually-active patient with advanced prolapse?

A. Sacrospinous ligament suspension (SSLS)

B. Uterosacral ligament suspension (USLS)

C. Sacrocolpopexy (SCP)

D. Colpocleisis

E. Hysteropexy

Dr. Sam Siddighi
The correct answer is C.

A randomized trial comparing SSLS and USLS found the two apical procedures with native tissue repair are equally effective with comparable functional and adverse outcomes (answers A and B are incorrect). However, randomized trials comparing SCP to SSLS show that SCP with synthetic mesh has the lowest recurrence rate for prolapse. Colpocleisis is done for patients who are not sexually active (answer D is incorrect). Hysteropexy is performed for patients who desire preservation of the uterus. There is less available evidence on safety and efficacy, compared with hysterectomy at the time of prolapse repair (answer E is incorrect)

Key points

The key points to remember are:

1. SCP is the most effective prolapse repair technique.

2. USLS and SSLS fixation are equally effective when compared with one another.

3. Colpocleisis is a highly successful procedure for POP in patients who are not sexually active.

Literature summary

The lifetime risk for undergoing surgery for POP or stress incontinence is 20%. POP is the descent of one or more aspects of the vagina or uterus, which allows nearby organs to herniate into the vagina. POP should only be treated if it is symptomatic and bothersome for the patient. The pessary is an alternative to surgical treatment of prolapse.

Proven risk factors for POP are increased parity, vaginal delivery, age, obesity, chronic constipation, and certain congenital anomalies. A history should be taken to elucidate symptoms of prolapse, such as bulge, pressure, sexual dysfunction, lower urinary tract dysfunction, or defecatory dysfunction. It is also important to find out how much the POP is affecting her quality of life. A physical exam is best performed with a split speculum, with bladder empty, while the patient performs a Valsalva maneuver. We recommend using the POP-Q system to grade the severity of prolapse. The tone of the pelvic floor muscle should also be evaluated (absent, weak, normal, or strong) during pelvic exam.

The minimum testing necessary for a patient with POP is urinalysis and a postvoid residual. A stress test with a full bladder should also be done with and without reduction of the prolapse. If you’re considering surgery and the patient has advanced prolapse and/or other complicating factors – such as obstructive symptoms or significant neurologic disorder – you should consider performing urodynamic testing as well.

Native tissue, suture-based reconstructive repairs of the vagina include apical procedures, such as SSLS and USLS, in addition to anterior colporrhaphy and posterior repair. At 2-year follow-up, SSLS and USLS along with anterior colporrhaphy and posterior repair are equally effective for treatment of prolapse with comparable functional and adverse outcomes. SCP is more effective than SSLS but the abdominal procedure (not laparoscopic) may be associated with more complications. Currently, there are no published randomized trials comparing minimally-invasive SCP to USLS, but one is underway (clinicaltrials.gov).

Other procedures for POP include obliterative procedures such as colpocleisis, which is highly effective for patients who do not desire future vaginal intercourse and also has low morbidity. Preservation of the uterus by hysteropexy procedures (either transvaginal or transabdominal) are also options for women desiring to preserve their uterus, but these procedures have little safety and efficacy data. Regardless of the procedure performed, routine intraoperative cystoscopy should be done to assure ureteral patency and to rule out injury to the lower urinary tract.

Some type of prophylactic anti-incontinence procedure – retropubic or Burch – may be done at the time of vaginal prolapse repair or abdominal prolapse repair, respectively, in order to reduce the chance of postoperative stress urinary incontinence in a patient without symptoms of stress incontinence. The exception to this is in a patient who has an elevated postvoid residual or someone with a prior anti-incontinence procedure without symptoms of stress urinary incontinence.

 

 

Practice tips

Finally, here are some precautions and words of advice about the following POP procedures:

  • Neither synthetic nor biologic grafts should be used to augment posterior repairs as these do not improve outcomes.
  • Transvaginal repair of rectocele is superior to the transanal repair techniques.
  • Synthetic mesh augmentation of the anterior vaginal wall may improve anatomic outcomes, but this comes at a cost (more reoperations and higher rate of complications). Thus, surgeons performing these procedures should have specialized training and the patient should have a unique indication and must undergo proper consent as recommended by ACOG.

Dr. Siddighi is editor-in-chief of the Ob/Gyn Board Master and director of female pelvic medicine and reconstructive surgery and director of grand rounds at Loma Linda University Health in California. Ob.Gyn. News and Ob/Gyn Board Master are owned by the same parent company, Frontline Medical Communications.

Reference

1. Obstet Gynecol. 2017 Apr;129(4):e56-e72.

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Editor’s Note: This is the fifth installment of a six-part series that will review key concepts and articles that ob.gyns. can use to prepare for the American Board of Obstetrics and Gynecology Maintenance of Certification examination. The series is adapted from Ob/Gyn Board Master (obgynboardmaster.com), an online board review course created by Erudyte. This month’s edition of the Board Corner focuses on pelvic organ prolapse.

The American College of Obstetricians and Gynecologists’ “Practice Bulletins” are important practice management guidelines for ob.gyn. clinicians. The Practice Bulletins are rich sources of material that is often tested on board exams. Earlier this year, ACOG released a revised Practice Bulletin (#176) updating its advice on the diagnosis and management of pelvic organ prolapse (POP).1 It is a well-written document summarizing most of the landmark articles published in the field of female pelvic medicine and reconstructive surgery. We recommend you read this bulletin and review this topic carefully.

Let’s begin with a possible medical board question: Which of the following procedures is the most effective for a sexually-active patient with advanced prolapse?

A. Sacrospinous ligament suspension (SSLS)

B. Uterosacral ligament suspension (USLS)

C. Sacrocolpopexy (SCP)

D. Colpocleisis

E. Hysteropexy

Dr. Sam Siddighi
The correct answer is C.

A randomized trial comparing SSLS and USLS found the two apical procedures with native tissue repair are equally effective with comparable functional and adverse outcomes (answers A and B are incorrect). However, randomized trials comparing SCP to SSLS show that SCP with synthetic mesh has the lowest recurrence rate for prolapse. Colpocleisis is done for patients who are not sexually active (answer D is incorrect). Hysteropexy is performed for patients who desire preservation of the uterus. There is less available evidence on safety and efficacy, compared with hysterectomy at the time of prolapse repair (answer E is incorrect)

Key points

The key points to remember are:

1. SCP is the most effective prolapse repair technique.

2. USLS and SSLS fixation are equally effective when compared with one another.

3. Colpocleisis is a highly successful procedure for POP in patients who are not sexually active.

Literature summary

The lifetime risk for undergoing surgery for POP or stress incontinence is 20%. POP is the descent of one or more aspects of the vagina or uterus, which allows nearby organs to herniate into the vagina. POP should only be treated if it is symptomatic and bothersome for the patient. The pessary is an alternative to surgical treatment of prolapse.

Proven risk factors for POP are increased parity, vaginal delivery, age, obesity, chronic constipation, and certain congenital anomalies. A history should be taken to elucidate symptoms of prolapse, such as bulge, pressure, sexual dysfunction, lower urinary tract dysfunction, or defecatory dysfunction. It is also important to find out how much the POP is affecting her quality of life. A physical exam is best performed with a split speculum, with bladder empty, while the patient performs a Valsalva maneuver. We recommend using the POP-Q system to grade the severity of prolapse. The tone of the pelvic floor muscle should also be evaluated (absent, weak, normal, or strong) during pelvic exam.

The minimum testing necessary for a patient with POP is urinalysis and a postvoid residual. A stress test with a full bladder should also be done with and without reduction of the prolapse. If you’re considering surgery and the patient has advanced prolapse and/or other complicating factors – such as obstructive symptoms or significant neurologic disorder – you should consider performing urodynamic testing as well.

Native tissue, suture-based reconstructive repairs of the vagina include apical procedures, such as SSLS and USLS, in addition to anterior colporrhaphy and posterior repair. At 2-year follow-up, SSLS and USLS along with anterior colporrhaphy and posterior repair are equally effective for treatment of prolapse with comparable functional and adverse outcomes. SCP is more effective than SSLS but the abdominal procedure (not laparoscopic) may be associated with more complications. Currently, there are no published randomized trials comparing minimally-invasive SCP to USLS, but one is underway (clinicaltrials.gov).

Other procedures for POP include obliterative procedures such as colpocleisis, which is highly effective for patients who do not desire future vaginal intercourse and also has low morbidity. Preservation of the uterus by hysteropexy procedures (either transvaginal or transabdominal) are also options for women desiring to preserve their uterus, but these procedures have little safety and efficacy data. Regardless of the procedure performed, routine intraoperative cystoscopy should be done to assure ureteral patency and to rule out injury to the lower urinary tract.

Some type of prophylactic anti-incontinence procedure – retropubic or Burch – may be done at the time of vaginal prolapse repair or abdominal prolapse repair, respectively, in order to reduce the chance of postoperative stress urinary incontinence in a patient without symptoms of stress incontinence. The exception to this is in a patient who has an elevated postvoid residual or someone with a prior anti-incontinence procedure without symptoms of stress urinary incontinence.

 

 

Practice tips

Finally, here are some precautions and words of advice about the following POP procedures:

  • Neither synthetic nor biologic grafts should be used to augment posterior repairs as these do not improve outcomes.
  • Transvaginal repair of rectocele is superior to the transanal repair techniques.
  • Synthetic mesh augmentation of the anterior vaginal wall may improve anatomic outcomes, but this comes at a cost (more reoperations and higher rate of complications). Thus, surgeons performing these procedures should have specialized training and the patient should have a unique indication and must undergo proper consent as recommended by ACOG.

Dr. Siddighi is editor-in-chief of the Ob/Gyn Board Master and director of female pelvic medicine and reconstructive surgery and director of grand rounds at Loma Linda University Health in California. Ob.Gyn. News and Ob/Gyn Board Master are owned by the same parent company, Frontline Medical Communications.

Reference

1. Obstet Gynecol. 2017 Apr;129(4):e56-e72.

 

Editor’s Note: This is the fifth installment of a six-part series that will review key concepts and articles that ob.gyns. can use to prepare for the American Board of Obstetrics and Gynecology Maintenance of Certification examination. The series is adapted from Ob/Gyn Board Master (obgynboardmaster.com), an online board review course created by Erudyte. This month’s edition of the Board Corner focuses on pelvic organ prolapse.

The American College of Obstetricians and Gynecologists’ “Practice Bulletins” are important practice management guidelines for ob.gyn. clinicians. The Practice Bulletins are rich sources of material that is often tested on board exams. Earlier this year, ACOG released a revised Practice Bulletin (#176) updating its advice on the diagnosis and management of pelvic organ prolapse (POP).1 It is a well-written document summarizing most of the landmark articles published in the field of female pelvic medicine and reconstructive surgery. We recommend you read this bulletin and review this topic carefully.

Let’s begin with a possible medical board question: Which of the following procedures is the most effective for a sexually-active patient with advanced prolapse?

A. Sacrospinous ligament suspension (SSLS)

B. Uterosacral ligament suspension (USLS)

C. Sacrocolpopexy (SCP)

D. Colpocleisis

E. Hysteropexy

Dr. Sam Siddighi
The correct answer is C.

A randomized trial comparing SSLS and USLS found the two apical procedures with native tissue repair are equally effective with comparable functional and adverse outcomes (answers A and B are incorrect). However, randomized trials comparing SCP to SSLS show that SCP with synthetic mesh has the lowest recurrence rate for prolapse. Colpocleisis is done for patients who are not sexually active (answer D is incorrect). Hysteropexy is performed for patients who desire preservation of the uterus. There is less available evidence on safety and efficacy, compared with hysterectomy at the time of prolapse repair (answer E is incorrect)

Key points

The key points to remember are:

1. SCP is the most effective prolapse repair technique.

2. USLS and SSLS fixation are equally effective when compared with one another.

3. Colpocleisis is a highly successful procedure for POP in patients who are not sexually active.

Literature summary

The lifetime risk for undergoing surgery for POP or stress incontinence is 20%. POP is the descent of one or more aspects of the vagina or uterus, which allows nearby organs to herniate into the vagina. POP should only be treated if it is symptomatic and bothersome for the patient. The pessary is an alternative to surgical treatment of prolapse.

Proven risk factors for POP are increased parity, vaginal delivery, age, obesity, chronic constipation, and certain congenital anomalies. A history should be taken to elucidate symptoms of prolapse, such as bulge, pressure, sexual dysfunction, lower urinary tract dysfunction, or defecatory dysfunction. It is also important to find out how much the POP is affecting her quality of life. A physical exam is best performed with a split speculum, with bladder empty, while the patient performs a Valsalva maneuver. We recommend using the POP-Q system to grade the severity of prolapse. The tone of the pelvic floor muscle should also be evaluated (absent, weak, normal, or strong) during pelvic exam.

The minimum testing necessary for a patient with POP is urinalysis and a postvoid residual. A stress test with a full bladder should also be done with and without reduction of the prolapse. If you’re considering surgery and the patient has advanced prolapse and/or other complicating factors – such as obstructive symptoms or significant neurologic disorder – you should consider performing urodynamic testing as well.

Native tissue, suture-based reconstructive repairs of the vagina include apical procedures, such as SSLS and USLS, in addition to anterior colporrhaphy and posterior repair. At 2-year follow-up, SSLS and USLS along with anterior colporrhaphy and posterior repair are equally effective for treatment of prolapse with comparable functional and adverse outcomes. SCP is more effective than SSLS but the abdominal procedure (not laparoscopic) may be associated with more complications. Currently, there are no published randomized trials comparing minimally-invasive SCP to USLS, but one is underway (clinicaltrials.gov).

Other procedures for POP include obliterative procedures such as colpocleisis, which is highly effective for patients who do not desire future vaginal intercourse and also has low morbidity. Preservation of the uterus by hysteropexy procedures (either transvaginal or transabdominal) are also options for women desiring to preserve their uterus, but these procedures have little safety and efficacy data. Regardless of the procedure performed, routine intraoperative cystoscopy should be done to assure ureteral patency and to rule out injury to the lower urinary tract.

Some type of prophylactic anti-incontinence procedure – retropubic or Burch – may be done at the time of vaginal prolapse repair or abdominal prolapse repair, respectively, in order to reduce the chance of postoperative stress urinary incontinence in a patient without symptoms of stress incontinence. The exception to this is in a patient who has an elevated postvoid residual or someone with a prior anti-incontinence procedure without symptoms of stress urinary incontinence.

 

 

Practice tips

Finally, here are some precautions and words of advice about the following POP procedures:

  • Neither synthetic nor biologic grafts should be used to augment posterior repairs as these do not improve outcomes.
  • Transvaginal repair of rectocele is superior to the transanal repair techniques.
  • Synthetic mesh augmentation of the anterior vaginal wall may improve anatomic outcomes, but this comes at a cost (more reoperations and higher rate of complications). Thus, surgeons performing these procedures should have specialized training and the patient should have a unique indication and must undergo proper consent as recommended by ACOG.

Dr. Siddighi is editor-in-chief of the Ob/Gyn Board Master and director of female pelvic medicine and reconstructive surgery and director of grand rounds at Loma Linda University Health in California. Ob.Gyn. News and Ob/Gyn Board Master are owned by the same parent company, Frontline Medical Communications.

Reference

1. Obstet Gynecol. 2017 Apr;129(4):e56-e72.

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Access to ‘the little blue book’ just got a lot more expensive

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“The little blue book” has been an office standard as long as I’ve been in practice. Every practice has a dog-eared copy in a drawer somewhere that’s constantly being pulled out to look up hospitals, other doctors, and pharmacies.

As small as it is, it’s pretty useful in the daily flow of my office routine.

Dr. Allan M. Block
So I’ve never griped about my annual payment of $39.90 to get two copies of it. In a world of expensive and unused textbooks and coding guides, this little thing is indispensable. It generally seemed a lot more reliable than Google. It even became a running office gag, where when it showed up my medical assistant would yell “THE NEW BLUE BOOKS ARE HERE! THE NEW BLUE BOOKS ARE HERE!” imitating Steve Martin in “The Jerk.”

Until now.

Sadly, 2016 was apparently the year I ordered my last copies. The publisher’s marketing people inform me that the paper version has been discontinued, and I can now get the digital version for only ... $500 per year.

Thanks, but no thanks.

I have nothing against digital editions. In fact, if it was the same price as the paper one, I’d get it. If I were a big practice that needed, say, 50 copies for the staff, the $500 per practice fee is a deal, compared with the $998 I’d pay for 50 paper copies.

But for my dinky little two-person practice? The difference between $39.90 and $500 just isn’t worth all the advantages a digital version may offer. For that kind of money, I’ll use Google.

This is another part of a gradual, and disturbing, trend in medicine: ignoring small practices. Large corporate practices are worth a lot more in sales than little one-to-three doctor groups, so companies, such as “the little blue book,” have no incentive to tailor their products to us. We have become medical persona non grata.

I understand this is a business decision. It’s not specifically directed at me.

Yet ...

I’ve been in practice for almost 20 years now, and buying two copies of the LBB is something I’ve done annually, in good and bad economic years. I’ve supported the publisher because it was a good product at a fair price. Sadly, they no longer find my little practice to be worth the effort or profit margin.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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“The little blue book” has been an office standard as long as I’ve been in practice. Every practice has a dog-eared copy in a drawer somewhere that’s constantly being pulled out to look up hospitals, other doctors, and pharmacies.

As small as it is, it’s pretty useful in the daily flow of my office routine.

Dr. Allan M. Block
So I’ve never griped about my annual payment of $39.90 to get two copies of it. In a world of expensive and unused textbooks and coding guides, this little thing is indispensable. It generally seemed a lot more reliable than Google. It even became a running office gag, where when it showed up my medical assistant would yell “THE NEW BLUE BOOKS ARE HERE! THE NEW BLUE BOOKS ARE HERE!” imitating Steve Martin in “The Jerk.”

Until now.

Sadly, 2016 was apparently the year I ordered my last copies. The publisher’s marketing people inform me that the paper version has been discontinued, and I can now get the digital version for only ... $500 per year.

Thanks, but no thanks.

I have nothing against digital editions. In fact, if it was the same price as the paper one, I’d get it. If I were a big practice that needed, say, 50 copies for the staff, the $500 per practice fee is a deal, compared with the $998 I’d pay for 50 paper copies.

But for my dinky little two-person practice? The difference between $39.90 and $500 just isn’t worth all the advantages a digital version may offer. For that kind of money, I’ll use Google.

This is another part of a gradual, and disturbing, trend in medicine: ignoring small practices. Large corporate practices are worth a lot more in sales than little one-to-three doctor groups, so companies, such as “the little blue book,” have no incentive to tailor their products to us. We have become medical persona non grata.

I understand this is a business decision. It’s not specifically directed at me.

Yet ...

I’ve been in practice for almost 20 years now, and buying two copies of the LBB is something I’ve done annually, in good and bad economic years. I’ve supported the publisher because it was a good product at a fair price. Sadly, they no longer find my little practice to be worth the effort or profit margin.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

 



“The little blue book” has been an office standard as long as I’ve been in practice. Every practice has a dog-eared copy in a drawer somewhere that’s constantly being pulled out to look up hospitals, other doctors, and pharmacies.

As small as it is, it’s pretty useful in the daily flow of my office routine.

Dr. Allan M. Block
So I’ve never griped about my annual payment of $39.90 to get two copies of it. In a world of expensive and unused textbooks and coding guides, this little thing is indispensable. It generally seemed a lot more reliable than Google. It even became a running office gag, where when it showed up my medical assistant would yell “THE NEW BLUE BOOKS ARE HERE! THE NEW BLUE BOOKS ARE HERE!” imitating Steve Martin in “The Jerk.”

Until now.

Sadly, 2016 was apparently the year I ordered my last copies. The publisher’s marketing people inform me that the paper version has been discontinued, and I can now get the digital version for only ... $500 per year.

Thanks, but no thanks.

I have nothing against digital editions. In fact, if it was the same price as the paper one, I’d get it. If I were a big practice that needed, say, 50 copies for the staff, the $500 per practice fee is a deal, compared with the $998 I’d pay for 50 paper copies.

But for my dinky little two-person practice? The difference between $39.90 and $500 just isn’t worth all the advantages a digital version may offer. For that kind of money, I’ll use Google.

This is another part of a gradual, and disturbing, trend in medicine: ignoring small practices. Large corporate practices are worth a lot more in sales than little one-to-three doctor groups, so companies, such as “the little blue book,” have no incentive to tailor their products to us. We have become medical persona non grata.

I understand this is a business decision. It’s not specifically directed at me.

Yet ...

I’ve been in practice for almost 20 years now, and buying two copies of the LBB is something I’ve done annually, in good and bad economic years. I’ve supported the publisher because it was a good product at a fair price. Sadly, they no longer find my little practice to be worth the effort or profit margin.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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A case for building our leadership skills

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Let me ask you a question: When was the last time you used the Krebs cycle in the hospital?

Now another question: When did you last have to persuade your boss to give you additional resources?

My guess is that your need for additional resources comes up more frequently than the Krebs cycle. It’s interesting that we spent so much time in our training focused on biochemical pathways and next to nothing on leadership skills, such as ways to motivate our health care teams or the most effective way to provide feedback – skills that we use on a regular basis. Yet, these skills are just as critical as understanding the science behind our daily work.

Dr. Nasim Afsar
I’ll give you an example. I’ve been involved in quality improvement and operational work for a decade, so I often find myself in front of groups of health care professionals convincing them to implement new pathways and protocols.

In the past, I would present my case in the following way:

1. Highlight the importance of the ask.

2. Leverage data to prove the point.

3. Illustrate large-scale implications of the ask.

4. Make the ask.

I’ll use a project to increase DVT prophylaxis rates to illustrate this point:

1. Highlight the importance of DVT prophylaxis: I would focus on statistics that would surprise the audience, such as “Hospital acquired venous thromboembolism leads to significant morbidity and mortality, including more than 100,000 deaths.”1

2. Leverage data to prove the point: “Worldwide, only 40%-60% of patients who require DVT prophylaxis actually receive it in the hospital.2 Our performance leaves tremendous room for improvement – we’re currently at 68%.”

3. Illustrate large-scale implications of the ask: “If we do this, it enhances our reputation as a group, and it will improve hospital revenues.”

4. Make the ask: “I have an evidence-based protocol that we need to implement to achieve results.”

Through leadership courses over the past couple of years, I’ve changed my approach significantly. By leveraging concepts from behavioral economics, we can significantly improve the effect of our work. Here’s how I would conduct that same meeting:

1. Connect with the audience in a genuine way: Start off with “You are quality-minded providers who have taken on major challenges in the past and successfully delivered results, like the time you reduced the rates of catheter associated urinary tract infections.”

2. Make the ask: “I’m here to talk to you about improving our DVT prophylaxis rates. Here’s the protocol we need to implement.”

3. Leverage data to prove the point: “DVT prophylaxis rates at the hospital across town (or at another unit in the hospital) are at 82%. What do you think our numbers are? We’re actually at 68%!”

4. Illustrate large-scale implications of the ask: “We all know this. Patients under our care will die or be seriously harmed if we don’t improve our practice. The hospital will also lose money, which will ultimately impact us. So, we have two options: a) We can continue what we’ve been doing – work as hard as we can and our practice will not improve. b) Or we can decide today to pilot this new protocol and change our practice and performance.”

Let’s look at the changes above in greater detail:

Connect with the audience in a genuine way: Instead of highlighting the importance of the ask with statistics, use an attention getter to connect with the group. Highlighting the fact that the group is “quality-minded” and has surmounted challenging obstacles in the past reinforces the providers’ sense of identity.3 This helps the group think more openly about the proposal.

Make the ask: Now that you’ve captured their attention, make your ask, clearly and concisely, upfront. Remember, in today’s health care settings, we have short attention spans. You’re minutes away from someone getting paged away from the meeting or people checking their emails or the latest Facebook post. Don’t schedule the protocol review as the last item on the agenda.

Leverage data to prove your point: Data are powerful, but only if presented in the right way. Use questions to keep your audience engaged (“What do you think our numbers are?”), particularly around data, where most people decide to switch their attention to their smartphones. Based on your access to data sources, find another unit or institution with a higher performance than yours. State that upfront. It anchors,the group to a higher number, so, when you reveal your current performance, the gap is highlighted. 3,4 In the first case, when the lower national average of 40-60% is presented initially, the group will be happy that their performance is in fact better at 68%.

Illustrate large-scale implications of the ask: There are two concepts at work here: First, loss aversion.3,4 We tend to experience greater psychological burden with losses versus gains. Changing the framing from the fact that the hospital will lose money, versus making money in the first case, changes how we perceive the information. Second, active choice.3 Emphasizing that a decision has to be made today and giving the group a choice around it increases the likelihood of walking out of the meeting with a decision.

With some simple, yet thoughtful, modifications, the message takes on a more effective tone, and, based on my experience, it is significantly more impactful.

So, while I’m a fan of biochemical pathways that enable us to generate energy, I also hope we can integrate leadership lessons into our day-to-day learning and life.

 

 

Dr. Afsar is an assistant clinical professor in the departments of medicine and neurosurgery and the associate chief medical officer at UCLA Hospitals.

References

1. The Surgeon General’s Call to Action to Prevent Deep Vein Thrombosis and Pulmonary Embolism. Office of the Surgeon General (US); National Heart, Lung, and Blood Institute (US). Office of the Surgeon General (US). 2008.

2. Cohen AT, Tapson VF, Bergmann JF, et al. Venous thromboembolism risk and prophylaxis in the acute hospital care setting (ENDORSE study): A multinational cross-sectional study. Lancet. 2008;371(9610):387-94.

3. Soman D. The Last Mile. 2015.

4. Thaler RH, Sunstein CR. Nudge. 2009.

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Let me ask you a question: When was the last time you used the Krebs cycle in the hospital?

Now another question: When did you last have to persuade your boss to give you additional resources?

My guess is that your need for additional resources comes up more frequently than the Krebs cycle. It’s interesting that we spent so much time in our training focused on biochemical pathways and next to nothing on leadership skills, such as ways to motivate our health care teams or the most effective way to provide feedback – skills that we use on a regular basis. Yet, these skills are just as critical as understanding the science behind our daily work.

Dr. Nasim Afsar
I’ll give you an example. I’ve been involved in quality improvement and operational work for a decade, so I often find myself in front of groups of health care professionals convincing them to implement new pathways and protocols.

In the past, I would present my case in the following way:

1. Highlight the importance of the ask.

2. Leverage data to prove the point.

3. Illustrate large-scale implications of the ask.

4. Make the ask.

I’ll use a project to increase DVT prophylaxis rates to illustrate this point:

1. Highlight the importance of DVT prophylaxis: I would focus on statistics that would surprise the audience, such as “Hospital acquired venous thromboembolism leads to significant morbidity and mortality, including more than 100,000 deaths.”1

2. Leverage data to prove the point: “Worldwide, only 40%-60% of patients who require DVT prophylaxis actually receive it in the hospital.2 Our performance leaves tremendous room for improvement – we’re currently at 68%.”

3. Illustrate large-scale implications of the ask: “If we do this, it enhances our reputation as a group, and it will improve hospital revenues.”

4. Make the ask: “I have an evidence-based protocol that we need to implement to achieve results.”

Through leadership courses over the past couple of years, I’ve changed my approach significantly. By leveraging concepts from behavioral economics, we can significantly improve the effect of our work. Here’s how I would conduct that same meeting:

1. Connect with the audience in a genuine way: Start off with “You are quality-minded providers who have taken on major challenges in the past and successfully delivered results, like the time you reduced the rates of catheter associated urinary tract infections.”

2. Make the ask: “I’m here to talk to you about improving our DVT prophylaxis rates. Here’s the protocol we need to implement.”

3. Leverage data to prove the point: “DVT prophylaxis rates at the hospital across town (or at another unit in the hospital) are at 82%. What do you think our numbers are? We’re actually at 68%!”

4. Illustrate large-scale implications of the ask: “We all know this. Patients under our care will die or be seriously harmed if we don’t improve our practice. The hospital will also lose money, which will ultimately impact us. So, we have two options: a) We can continue what we’ve been doing – work as hard as we can and our practice will not improve. b) Or we can decide today to pilot this new protocol and change our practice and performance.”

Let’s look at the changes above in greater detail:

Connect with the audience in a genuine way: Instead of highlighting the importance of the ask with statistics, use an attention getter to connect with the group. Highlighting the fact that the group is “quality-minded” and has surmounted challenging obstacles in the past reinforces the providers’ sense of identity.3 This helps the group think more openly about the proposal.

Make the ask: Now that you’ve captured their attention, make your ask, clearly and concisely, upfront. Remember, in today’s health care settings, we have short attention spans. You’re minutes away from someone getting paged away from the meeting or people checking their emails or the latest Facebook post. Don’t schedule the protocol review as the last item on the agenda.

Leverage data to prove your point: Data are powerful, but only if presented in the right way. Use questions to keep your audience engaged (“What do you think our numbers are?”), particularly around data, where most people decide to switch their attention to their smartphones. Based on your access to data sources, find another unit or institution with a higher performance than yours. State that upfront. It anchors,the group to a higher number, so, when you reveal your current performance, the gap is highlighted. 3,4 In the first case, when the lower national average of 40-60% is presented initially, the group will be happy that their performance is in fact better at 68%.

Illustrate large-scale implications of the ask: There are two concepts at work here: First, loss aversion.3,4 We tend to experience greater psychological burden with losses versus gains. Changing the framing from the fact that the hospital will lose money, versus making money in the first case, changes how we perceive the information. Second, active choice.3 Emphasizing that a decision has to be made today and giving the group a choice around it increases the likelihood of walking out of the meeting with a decision.

With some simple, yet thoughtful, modifications, the message takes on a more effective tone, and, based on my experience, it is significantly more impactful.

So, while I’m a fan of biochemical pathways that enable us to generate energy, I also hope we can integrate leadership lessons into our day-to-day learning and life.

 

 

Dr. Afsar is an assistant clinical professor in the departments of medicine and neurosurgery and the associate chief medical officer at UCLA Hospitals.

References

1. The Surgeon General’s Call to Action to Prevent Deep Vein Thrombosis and Pulmonary Embolism. Office of the Surgeon General (US); National Heart, Lung, and Blood Institute (US). Office of the Surgeon General (US). 2008.

2. Cohen AT, Tapson VF, Bergmann JF, et al. Venous thromboembolism risk and prophylaxis in the acute hospital care setting (ENDORSE study): A multinational cross-sectional study. Lancet. 2008;371(9610):387-94.

3. Soman D. The Last Mile. 2015.

4. Thaler RH, Sunstein CR. Nudge. 2009.

 

Let me ask you a question: When was the last time you used the Krebs cycle in the hospital?

Now another question: When did you last have to persuade your boss to give you additional resources?

My guess is that your need for additional resources comes up more frequently than the Krebs cycle. It’s interesting that we spent so much time in our training focused on biochemical pathways and next to nothing on leadership skills, such as ways to motivate our health care teams or the most effective way to provide feedback – skills that we use on a regular basis. Yet, these skills are just as critical as understanding the science behind our daily work.

Dr. Nasim Afsar
I’ll give you an example. I’ve been involved in quality improvement and operational work for a decade, so I often find myself in front of groups of health care professionals convincing them to implement new pathways and protocols.

In the past, I would present my case in the following way:

1. Highlight the importance of the ask.

2. Leverage data to prove the point.

3. Illustrate large-scale implications of the ask.

4. Make the ask.

I’ll use a project to increase DVT prophylaxis rates to illustrate this point:

1. Highlight the importance of DVT prophylaxis: I would focus on statistics that would surprise the audience, such as “Hospital acquired venous thromboembolism leads to significant morbidity and mortality, including more than 100,000 deaths.”1

2. Leverage data to prove the point: “Worldwide, only 40%-60% of patients who require DVT prophylaxis actually receive it in the hospital.2 Our performance leaves tremendous room for improvement – we’re currently at 68%.”

3. Illustrate large-scale implications of the ask: “If we do this, it enhances our reputation as a group, and it will improve hospital revenues.”

4. Make the ask: “I have an evidence-based protocol that we need to implement to achieve results.”

Through leadership courses over the past couple of years, I’ve changed my approach significantly. By leveraging concepts from behavioral economics, we can significantly improve the effect of our work. Here’s how I would conduct that same meeting:

1. Connect with the audience in a genuine way: Start off with “You are quality-minded providers who have taken on major challenges in the past and successfully delivered results, like the time you reduced the rates of catheter associated urinary tract infections.”

2. Make the ask: “I’m here to talk to you about improving our DVT prophylaxis rates. Here’s the protocol we need to implement.”

3. Leverage data to prove the point: “DVT prophylaxis rates at the hospital across town (or at another unit in the hospital) are at 82%. What do you think our numbers are? We’re actually at 68%!”

4. Illustrate large-scale implications of the ask: “We all know this. Patients under our care will die or be seriously harmed if we don’t improve our practice. The hospital will also lose money, which will ultimately impact us. So, we have two options: a) We can continue what we’ve been doing – work as hard as we can and our practice will not improve. b) Or we can decide today to pilot this new protocol and change our practice and performance.”

Let’s look at the changes above in greater detail:

Connect with the audience in a genuine way: Instead of highlighting the importance of the ask with statistics, use an attention getter to connect with the group. Highlighting the fact that the group is “quality-minded” and has surmounted challenging obstacles in the past reinforces the providers’ sense of identity.3 This helps the group think more openly about the proposal.

Make the ask: Now that you’ve captured their attention, make your ask, clearly and concisely, upfront. Remember, in today’s health care settings, we have short attention spans. You’re minutes away from someone getting paged away from the meeting or people checking their emails or the latest Facebook post. Don’t schedule the protocol review as the last item on the agenda.

Leverage data to prove your point: Data are powerful, but only if presented in the right way. Use questions to keep your audience engaged (“What do you think our numbers are?”), particularly around data, where most people decide to switch their attention to their smartphones. Based on your access to data sources, find another unit or institution with a higher performance than yours. State that upfront. It anchors,the group to a higher number, so, when you reveal your current performance, the gap is highlighted. 3,4 In the first case, when the lower national average of 40-60% is presented initially, the group will be happy that their performance is in fact better at 68%.

Illustrate large-scale implications of the ask: There are two concepts at work here: First, loss aversion.3,4 We tend to experience greater psychological burden with losses versus gains. Changing the framing from the fact that the hospital will lose money, versus making money in the first case, changes how we perceive the information. Second, active choice.3 Emphasizing that a decision has to be made today and giving the group a choice around it increases the likelihood of walking out of the meeting with a decision.

With some simple, yet thoughtful, modifications, the message takes on a more effective tone, and, based on my experience, it is significantly more impactful.

So, while I’m a fan of biochemical pathways that enable us to generate energy, I also hope we can integrate leadership lessons into our day-to-day learning and life.

 

 

Dr. Afsar is an assistant clinical professor in the departments of medicine and neurosurgery and the associate chief medical officer at UCLA Hospitals.

References

1. The Surgeon General’s Call to Action to Prevent Deep Vein Thrombosis and Pulmonary Embolism. Office of the Surgeon General (US); National Heart, Lung, and Blood Institute (US). Office of the Surgeon General (US). 2008.

2. Cohen AT, Tapson VF, Bergmann JF, et al. Venous thromboembolism risk and prophylaxis in the acute hospital care setting (ENDORSE study): A multinational cross-sectional study. Lancet. 2008;371(9610):387-94.

3. Soman D. The Last Mile. 2015.

4. Thaler RH, Sunstein CR. Nudge. 2009.

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Use ProPublica

Flashback to 2012

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It’s a whole new biosimilar world. In the April 2012 issue of GI & Hepatology News (GIHN) there was a small article on the issued Food and Drug Administration guidance on how to develop biosimilars. A biosimilar molecule must be structurally similar to the reference or originator product with the expectation that the safety and efficacy will be the same. The European Medicines Agency (EMA) established a legal framework for approving biologics in the European Union in 2003 and guidelines for approval in 2005 to 2006 with the first biosimilar approved in 2006 (somatropin [Omnitrope]).

The first monoclonal antibody biosimilar approved by the EMA was CT-P13 (infliximab-dyyb) in June 2013. There are now over 23 biosimilars approved for use in Europe. In 2012 there were no biosimilars on the market in the United States. This past year (2016) has been the year of the biosimilar with two of the four approved compounds used in inflammatory bowel disease – Inflectra (infliximab-dyyb, Hospira) April 2016 and Amjevita (adalimumab-atto, Amgen) September 2016 appearing.

Dr. Kim L. Isaacs


The launch of these biosimilars raises a whole new series of questions. First and foremost for gastroenterologists – are the biosimilars truly similar in patients with inflammatory bowel disease? Adalimumab-atto was approved on the basis of two phase III studies in psoriasis and in rheumatoid arthritis and infliximab-dyyb was approved on the basis of studies in rheumatoid arthritis and ankylosing spondylitis. Other questions arise: 1. Can a patient who is doing well on the originator be safely switched to the biosimilar? 2. Can we use the same assays for drug monitoring? 3. Will use of biosimilars lead to a lower cost structure for patients and hospitals? 4. What are the regulations and guidelines for interchangeability? (GIHN March 2017) In the United States, development of biosimilars was slow to start but we expect to see an explosion in development of these agents in gastroenterology as the patents expire on the biologics currently in use.
 

Kim L. Isaacs, MD, PhD, is professor of medicine in the division of gastroenterology and hepatology at the University of North Carolina at Chapel Hill. She is codirector of the UNC Center for Inflammatory Bowel Disease. She is an Associate Editor for GI and Hepatology News.

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It’s a whole new biosimilar world. In the April 2012 issue of GI & Hepatology News (GIHN) there was a small article on the issued Food and Drug Administration guidance on how to develop biosimilars. A biosimilar molecule must be structurally similar to the reference or originator product with the expectation that the safety and efficacy will be the same. The European Medicines Agency (EMA) established a legal framework for approving biologics in the European Union in 2003 and guidelines for approval in 2005 to 2006 with the first biosimilar approved in 2006 (somatropin [Omnitrope]).

The first monoclonal antibody biosimilar approved by the EMA was CT-P13 (infliximab-dyyb) in June 2013. There are now over 23 biosimilars approved for use in Europe. In 2012 there were no biosimilars on the market in the United States. This past year (2016) has been the year of the biosimilar with two of the four approved compounds used in inflammatory bowel disease – Inflectra (infliximab-dyyb, Hospira) April 2016 and Amjevita (adalimumab-atto, Amgen) September 2016 appearing.

Dr. Kim L. Isaacs


The launch of these biosimilars raises a whole new series of questions. First and foremost for gastroenterologists – are the biosimilars truly similar in patients with inflammatory bowel disease? Adalimumab-atto was approved on the basis of two phase III studies in psoriasis and in rheumatoid arthritis and infliximab-dyyb was approved on the basis of studies in rheumatoid arthritis and ankylosing spondylitis. Other questions arise: 1. Can a patient who is doing well on the originator be safely switched to the biosimilar? 2. Can we use the same assays for drug monitoring? 3. Will use of biosimilars lead to a lower cost structure for patients and hospitals? 4. What are the regulations and guidelines for interchangeability? (GIHN March 2017) In the United States, development of biosimilars was slow to start but we expect to see an explosion in development of these agents in gastroenterology as the patents expire on the biologics currently in use.
 

Kim L. Isaacs, MD, PhD, is professor of medicine in the division of gastroenterology and hepatology at the University of North Carolina at Chapel Hill. She is codirector of the UNC Center for Inflammatory Bowel Disease. She is an Associate Editor for GI and Hepatology News.

 

It’s a whole new biosimilar world. In the April 2012 issue of GI & Hepatology News (GIHN) there was a small article on the issued Food and Drug Administration guidance on how to develop biosimilars. A biosimilar molecule must be structurally similar to the reference or originator product with the expectation that the safety and efficacy will be the same. The European Medicines Agency (EMA) established a legal framework for approving biologics in the European Union in 2003 and guidelines for approval in 2005 to 2006 with the first biosimilar approved in 2006 (somatropin [Omnitrope]).

The first monoclonal antibody biosimilar approved by the EMA was CT-P13 (infliximab-dyyb) in June 2013. There are now over 23 biosimilars approved for use in Europe. In 2012 there were no biosimilars on the market in the United States. This past year (2016) has been the year of the biosimilar with two of the four approved compounds used in inflammatory bowel disease – Inflectra (infliximab-dyyb, Hospira) April 2016 and Amjevita (adalimumab-atto, Amgen) September 2016 appearing.

Dr. Kim L. Isaacs


The launch of these biosimilars raises a whole new series of questions. First and foremost for gastroenterologists – are the biosimilars truly similar in patients with inflammatory bowel disease? Adalimumab-atto was approved on the basis of two phase III studies in psoriasis and in rheumatoid arthritis and infliximab-dyyb was approved on the basis of studies in rheumatoid arthritis and ankylosing spondylitis. Other questions arise: 1. Can a patient who is doing well on the originator be safely switched to the biosimilar? 2. Can we use the same assays for drug monitoring? 3. Will use of biosimilars lead to a lower cost structure for patients and hospitals? 4. What are the regulations and guidelines for interchangeability? (GIHN March 2017) In the United States, development of biosimilars was slow to start but we expect to see an explosion in development of these agents in gastroenterology as the patents expire on the biologics currently in use.
 

Kim L. Isaacs, MD, PhD, is professor of medicine in the division of gastroenterology and hepatology at the University of North Carolina at Chapel Hill. She is codirector of the UNC Center for Inflammatory Bowel Disease. She is an Associate Editor for GI and Hepatology News.

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Adolescent sexuality and disclosure

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Adolescence is a time of rapid growth and development both physically and emotionally. Some of the major tasks of adolescent development include developing a stable identity (this includes sexual and gender identity) and establishing independence from parents. This separation process from parents is often buffered by peer relationships. By the end of adolescence, those who are healthy and mature in their sexuality are able to:1,2,3

•  Identify and live according to their own values and take responsibility for their behavior.

•  Practice effective decision-making, and develop critical-thinking skills.

•  Affirm that human development includes sexual development, which may or may not include reproduction or sexual experience.

•  Seek further information about sexuality and reproduction as needed and make informed choices about family options and relationships.

•  Interact with all genders in respectful and appropriate ways.

•  Affirm their own gender identity and sexual orientation, and respect the gender identities and sexual orientations of others.

•  Appreciate their body and enjoy their sexuality throughout life, expressing sexuality in ways that are congruent with their values.

•  Express love and intimacy in appropriate ways.

•  Develop and maintain meaningful relationships, avoiding exploitative or manipulative relationships.

•  Exhibit skills and communication that enhance personal relationships with family, peers, and romantic partners.

Anywhere from 5% to 10% of teens identify as lesbian, gay, or bisexual (LGB).4 For these teens, the development of a sexual identity can add additional challenges to the development process, particularly if youth do not feel supported by family, peers, and their communities. Previous columns have addressed the role family acceptance can play in promoting the healthy development of sexual minority youth. Likewise, peer relationships also can play an important role in an adolescent’s development and health.

Dr. Gayathri Chelvakumar


Some factors that can promote resilience and counteract stigma that LGB youth may face include:5

•  Acceptance.

•  Competence.

•  Higher levels of self-esteem and psychological well-being.

•  Strong sense of self and self-acceptance.

•  Strong ethnic identification.

•  Strong connections to family and school.

•  Caring adult role models outside the family.

•  Community involvement.

For some youth who may not be able receive acceptance from their families, peers and trusted adults may fill in this role and serve as a “chosen family.” A chosen family is commonly understood to mean a group of people who deliberately chose one another to play significant roles in each other’s lives even though they are not biologically or legally related. These relationships may be in addition to or in place of traditional family relationships. These connections can increase a youth’s sense of acceptance and connectedness and help promote resiliency.

Adolescents often may struggle on the decision of when to “come out” or disclose their sexual orientation to friends and family, and may ask their health care providers for advice. The number one consideration when making a decision about disclosure is safety. Unfortunately, some family members and peers may not react in a supportive manner to a youth’s disclosure, and disclosure may result in being kicked out, financial coercion, bullying, physical violence, or alienation. In these cases, youth may choose to delay disclosure until they are in a more supportive environment, and health care providers can play an important role in validating and affirming patients’ identities and maintaining confidentiality as appropriate. LGB youth should be counseled to consider the when, who, and how of their disclosure. They also should plan for how they might deal with a negative or rejecting response. Some tips are included below.5



When

•  You are ready.

•  You are comfortable with your identity.

•  You want to share information with people you trust and are close to.

•  You have a plan for support if you are not accepted (particularly when coming out to family).



Who

•  Someone you know well and expect to be supportive.

•  Someone you trust, feel safe with, and who can keep information confidential if needed (may need to explore school’s privacy and confidentiality policies if disclosing to a teacher or school personnel).

•  Be clear about who else information may be shared with and who NOT to share with.



How

•  Be sure you are prepared. You may want to talk to other sexual minority youth or adults who have come out, attend LGBTQ groups/forums, or seek out Internet resources to learn about others’ coming out experiences. These sources may serve as a support for you should you experience any negative or rejecting responses.

•  Make sure you have support resources in place prior to coming out.

•  Coming out by letter allows you time to carefully word what you want to say, and allows the other person time and privacy to consider their response.

•  If coming out in person, try to choose a quiet private space, and try to choose a time when everyone is relaxed and well-rested.

•  If concerned about your safety, make sure other people are immediately accessible if needed.

•  Plan what you are going to say, how you might end the conversation, and how you may want to talk about it later.

•  Listen actively to what the other person has to say.

•  Avoid any alcohol or drugs, as these may affect your mental and emotional state and responses.

•  Avoid coming out because of pressure from others or because you are angry.

 

 

Youth should be reminded that people’s responses may not always be predictable. It is important to note that for many individuals, coming out may be a lifelong process and occur in stages, beginning with close friends or family members and progressing from there. In the age of social media, youth should be reminded that disclosures through social media may be widely accessible, are easily shared, and may be difficult to remove. For youth who do not have supportive peer groups, and may not be able to disclose their sexual identity, providing support resources can be helpful.
 

Dr. Chelvakumar is an attending physician in the division of adolescent medicine at Nationwide Children’s Hospital and an assistant professor of clinical pediatrics at the Ohio State University, both in Columbus. She has no relevant financial disclosures. Email her at pdnews@frontlinemedcom.com.

Resources for sexual minority youth and peers/families

Gay-Straight Alliance Network: gsanetwork.org

Gay Lesbian Straight Education Network: Information for Students: glsen.org/students

Sexuality Information and Education Council of the United States: www.siecus.org

The Trevor Project: Help and Suicide Prevention: www.thetrevorproject.org

It Gets Better Project: http://www.itgetsbetter.org/

Family and Ally Organization: PFLAG: https://www.pflag.org/

Advocates for Youth Parent Tips: http://www.advocatesforyouth.org/parents/173-parents

References

1. “Adolescent Sexuality,” by Michelle Forcier, MD, in Up to Date. Updated March 2017.

2. Pediatrics. 2016 Aug;138(2). pii: e20161348.

3. The Guidelines for Comprehensive Sexuality Education: Grades K-12 (Washington, D.C.: Sexuality Information and Education Council of the United States, 2004).

4. MMWR Surveillance Summaries, 2016, Aug 12;65(9):1-202.

5. “Sexual minority youth: Epidemiology and health concerns,” by Michelle Forcier, MD, and Johanna Olson-Kennedy, MD, in Up to Date.
 

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Adolescence is a time of rapid growth and development both physically and emotionally. Some of the major tasks of adolescent development include developing a stable identity (this includes sexual and gender identity) and establishing independence from parents. This separation process from parents is often buffered by peer relationships. By the end of adolescence, those who are healthy and mature in their sexuality are able to:1,2,3

•  Identify and live according to their own values and take responsibility for their behavior.

•  Practice effective decision-making, and develop critical-thinking skills.

•  Affirm that human development includes sexual development, which may or may not include reproduction or sexual experience.

•  Seek further information about sexuality and reproduction as needed and make informed choices about family options and relationships.

•  Interact with all genders in respectful and appropriate ways.

•  Affirm their own gender identity and sexual orientation, and respect the gender identities and sexual orientations of others.

•  Appreciate their body and enjoy their sexuality throughout life, expressing sexuality in ways that are congruent with their values.

•  Express love and intimacy in appropriate ways.

•  Develop and maintain meaningful relationships, avoiding exploitative or manipulative relationships.

•  Exhibit skills and communication that enhance personal relationships with family, peers, and romantic partners.

Anywhere from 5% to 10% of teens identify as lesbian, gay, or bisexual (LGB).4 For these teens, the development of a sexual identity can add additional challenges to the development process, particularly if youth do not feel supported by family, peers, and their communities. Previous columns have addressed the role family acceptance can play in promoting the healthy development of sexual minority youth. Likewise, peer relationships also can play an important role in an adolescent’s development and health.

Dr. Gayathri Chelvakumar


Some factors that can promote resilience and counteract stigma that LGB youth may face include:5

•  Acceptance.

•  Competence.

•  Higher levels of self-esteem and psychological well-being.

•  Strong sense of self and self-acceptance.

•  Strong ethnic identification.

•  Strong connections to family and school.

•  Caring adult role models outside the family.

•  Community involvement.

For some youth who may not be able receive acceptance from their families, peers and trusted adults may fill in this role and serve as a “chosen family.” A chosen family is commonly understood to mean a group of people who deliberately chose one another to play significant roles in each other’s lives even though they are not biologically or legally related. These relationships may be in addition to or in place of traditional family relationships. These connections can increase a youth’s sense of acceptance and connectedness and help promote resiliency.

Adolescents often may struggle on the decision of when to “come out” or disclose their sexual orientation to friends and family, and may ask their health care providers for advice. The number one consideration when making a decision about disclosure is safety. Unfortunately, some family members and peers may not react in a supportive manner to a youth’s disclosure, and disclosure may result in being kicked out, financial coercion, bullying, physical violence, or alienation. In these cases, youth may choose to delay disclosure until they are in a more supportive environment, and health care providers can play an important role in validating and affirming patients’ identities and maintaining confidentiality as appropriate. LGB youth should be counseled to consider the when, who, and how of their disclosure. They also should plan for how they might deal with a negative or rejecting response. Some tips are included below.5



When

•  You are ready.

•  You are comfortable with your identity.

•  You want to share information with people you trust and are close to.

•  You have a plan for support if you are not accepted (particularly when coming out to family).



Who

•  Someone you know well and expect to be supportive.

•  Someone you trust, feel safe with, and who can keep information confidential if needed (may need to explore school’s privacy and confidentiality policies if disclosing to a teacher or school personnel).

•  Be clear about who else information may be shared with and who NOT to share with.



How

•  Be sure you are prepared. You may want to talk to other sexual minority youth or adults who have come out, attend LGBTQ groups/forums, or seek out Internet resources to learn about others’ coming out experiences. These sources may serve as a support for you should you experience any negative or rejecting responses.

•  Make sure you have support resources in place prior to coming out.

•  Coming out by letter allows you time to carefully word what you want to say, and allows the other person time and privacy to consider their response.

•  If coming out in person, try to choose a quiet private space, and try to choose a time when everyone is relaxed and well-rested.

•  If concerned about your safety, make sure other people are immediately accessible if needed.

•  Plan what you are going to say, how you might end the conversation, and how you may want to talk about it later.

•  Listen actively to what the other person has to say.

•  Avoid any alcohol or drugs, as these may affect your mental and emotional state and responses.

•  Avoid coming out because of pressure from others or because you are angry.

 

 

Youth should be reminded that people’s responses may not always be predictable. It is important to note that for many individuals, coming out may be a lifelong process and occur in stages, beginning with close friends or family members and progressing from there. In the age of social media, youth should be reminded that disclosures through social media may be widely accessible, are easily shared, and may be difficult to remove. For youth who do not have supportive peer groups, and may not be able to disclose their sexual identity, providing support resources can be helpful.
 

Dr. Chelvakumar is an attending physician in the division of adolescent medicine at Nationwide Children’s Hospital and an assistant professor of clinical pediatrics at the Ohio State University, both in Columbus. She has no relevant financial disclosures. Email her at pdnews@frontlinemedcom.com.

Resources for sexual minority youth and peers/families

Gay-Straight Alliance Network: gsanetwork.org

Gay Lesbian Straight Education Network: Information for Students: glsen.org/students

Sexuality Information and Education Council of the United States: www.siecus.org

The Trevor Project: Help and Suicide Prevention: www.thetrevorproject.org

It Gets Better Project: http://www.itgetsbetter.org/

Family and Ally Organization: PFLAG: https://www.pflag.org/

Advocates for Youth Parent Tips: http://www.advocatesforyouth.org/parents/173-parents

References

1. “Adolescent Sexuality,” by Michelle Forcier, MD, in Up to Date. Updated March 2017.

2. Pediatrics. 2016 Aug;138(2). pii: e20161348.

3. The Guidelines for Comprehensive Sexuality Education: Grades K-12 (Washington, D.C.: Sexuality Information and Education Council of the United States, 2004).

4. MMWR Surveillance Summaries, 2016, Aug 12;65(9):1-202.

5. “Sexual minority youth: Epidemiology and health concerns,” by Michelle Forcier, MD, and Johanna Olson-Kennedy, MD, in Up to Date.
 

 

Adolescence is a time of rapid growth and development both physically and emotionally. Some of the major tasks of adolescent development include developing a stable identity (this includes sexual and gender identity) and establishing independence from parents. This separation process from parents is often buffered by peer relationships. By the end of adolescence, those who are healthy and mature in their sexuality are able to:1,2,3

•  Identify and live according to their own values and take responsibility for their behavior.

•  Practice effective decision-making, and develop critical-thinking skills.

•  Affirm that human development includes sexual development, which may or may not include reproduction or sexual experience.

•  Seek further information about sexuality and reproduction as needed and make informed choices about family options and relationships.

•  Interact with all genders in respectful and appropriate ways.

•  Affirm their own gender identity and sexual orientation, and respect the gender identities and sexual orientations of others.

•  Appreciate their body and enjoy their sexuality throughout life, expressing sexuality in ways that are congruent with their values.

•  Express love and intimacy in appropriate ways.

•  Develop and maintain meaningful relationships, avoiding exploitative or manipulative relationships.

•  Exhibit skills and communication that enhance personal relationships with family, peers, and romantic partners.

Anywhere from 5% to 10% of teens identify as lesbian, gay, or bisexual (LGB).4 For these teens, the development of a sexual identity can add additional challenges to the development process, particularly if youth do not feel supported by family, peers, and their communities. Previous columns have addressed the role family acceptance can play in promoting the healthy development of sexual minority youth. Likewise, peer relationships also can play an important role in an adolescent’s development and health.

Dr. Gayathri Chelvakumar


Some factors that can promote resilience and counteract stigma that LGB youth may face include:5

•  Acceptance.

•  Competence.

•  Higher levels of self-esteem and psychological well-being.

•  Strong sense of self and self-acceptance.

•  Strong ethnic identification.

•  Strong connections to family and school.

•  Caring adult role models outside the family.

•  Community involvement.

For some youth who may not be able receive acceptance from their families, peers and trusted adults may fill in this role and serve as a “chosen family.” A chosen family is commonly understood to mean a group of people who deliberately chose one another to play significant roles in each other’s lives even though they are not biologically or legally related. These relationships may be in addition to or in place of traditional family relationships. These connections can increase a youth’s sense of acceptance and connectedness and help promote resiliency.

Adolescents often may struggle on the decision of when to “come out” or disclose their sexual orientation to friends and family, and may ask their health care providers for advice. The number one consideration when making a decision about disclosure is safety. Unfortunately, some family members and peers may not react in a supportive manner to a youth’s disclosure, and disclosure may result in being kicked out, financial coercion, bullying, physical violence, or alienation. In these cases, youth may choose to delay disclosure until they are in a more supportive environment, and health care providers can play an important role in validating and affirming patients’ identities and maintaining confidentiality as appropriate. LGB youth should be counseled to consider the when, who, and how of their disclosure. They also should plan for how they might deal with a negative or rejecting response. Some tips are included below.5



When

•  You are ready.

•  You are comfortable with your identity.

•  You want to share information with people you trust and are close to.

•  You have a plan for support if you are not accepted (particularly when coming out to family).



Who

•  Someone you know well and expect to be supportive.

•  Someone you trust, feel safe with, and who can keep information confidential if needed (may need to explore school’s privacy and confidentiality policies if disclosing to a teacher or school personnel).

•  Be clear about who else information may be shared with and who NOT to share with.



How

•  Be sure you are prepared. You may want to talk to other sexual minority youth or adults who have come out, attend LGBTQ groups/forums, or seek out Internet resources to learn about others’ coming out experiences. These sources may serve as a support for you should you experience any negative or rejecting responses.

•  Make sure you have support resources in place prior to coming out.

•  Coming out by letter allows you time to carefully word what you want to say, and allows the other person time and privacy to consider their response.

•  If coming out in person, try to choose a quiet private space, and try to choose a time when everyone is relaxed and well-rested.

•  If concerned about your safety, make sure other people are immediately accessible if needed.

•  Plan what you are going to say, how you might end the conversation, and how you may want to talk about it later.

•  Listen actively to what the other person has to say.

•  Avoid any alcohol or drugs, as these may affect your mental and emotional state and responses.

•  Avoid coming out because of pressure from others or because you are angry.

 

 

Youth should be reminded that people’s responses may not always be predictable. It is important to note that for many individuals, coming out may be a lifelong process and occur in stages, beginning with close friends or family members and progressing from there. In the age of social media, youth should be reminded that disclosures through social media may be widely accessible, are easily shared, and may be difficult to remove. For youth who do not have supportive peer groups, and may not be able to disclose their sexual identity, providing support resources can be helpful.
 

Dr. Chelvakumar is an attending physician in the division of adolescent medicine at Nationwide Children’s Hospital and an assistant professor of clinical pediatrics at the Ohio State University, both in Columbus. She has no relevant financial disclosures. Email her at pdnews@frontlinemedcom.com.

Resources for sexual minority youth and peers/families

Gay-Straight Alliance Network: gsanetwork.org

Gay Lesbian Straight Education Network: Information for Students: glsen.org/students

Sexuality Information and Education Council of the United States: www.siecus.org

The Trevor Project: Help and Suicide Prevention: www.thetrevorproject.org

It Gets Better Project: http://www.itgetsbetter.org/

Family and Ally Organization: PFLAG: https://www.pflag.org/

Advocates for Youth Parent Tips: http://www.advocatesforyouth.org/parents/173-parents

References

1. “Adolescent Sexuality,” by Michelle Forcier, MD, in Up to Date. Updated March 2017.

2. Pediatrics. 2016 Aug;138(2). pii: e20161348.

3. The Guidelines for Comprehensive Sexuality Education: Grades K-12 (Washington, D.C.: Sexuality Information and Education Council of the United States, 2004).

4. MMWR Surveillance Summaries, 2016, Aug 12;65(9):1-202.

5. “Sexual minority youth: Epidemiology and health concerns,” by Michelle Forcier, MD, and Johanna Olson-Kennedy, MD, in Up to Date.
 

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Weight loss and dietary management for PCOS

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“TREATING POLYCYSTIC OVARY SYNDROME: START USING DUAL MEDICAL THERAPY”

ROBERT L. BARBIERI, MD (EDITORIAL; APRIL 2017)

Weight loss and dietary management for PCOS

I enjoyed Dr. Barbieri’s editorial on polycystic ovary syndrome (PCOS), but I feel that first-line management for PCOS should be weight loss and diet modifications that include instructions on decreasing carbohydrates and insulin spikes. A 5% to 10% weight loss should produce a return of cycles. Of course, metformin and spironolactone have a place for added treatment/prevention of acne and diabetes.

Luis Linan, MD
El Paso, Texas
 

Metformin and progesterone for PCOS-related infertility

I have been using Beyaz and Yaz for several years in my PCOS patients for the lower androgenic activity of the drospirenone based on the same assumption and its similarity to spironolactone. I have gotten great results with metformin 1,500 mg daily and, for those who desire fertility, cycling once a month for 10 days with progesterone. My own daughter was able to conceive in just 3 months of therapy. PCOS is extremely common in our region, probably due to the high obesity rate. I saw many more cases here than I ever thought I would when I was training.

Lisa Gowan, CNM, WHNP-BC
Albany, Georgia

 

Check insulin levels in PCOS patients before giving metformin?

Thank you for the very nice article regarding PCOS treatment. Does Dr. Barbieri routinely check insulin levels on patients before treating with metformin and does he require abnormal insulin levels to be present before initiating treatment? The article suggested that using the listed risk factors is sufficient. Additionally, does he perform glucose-insulin testing? If so, what is the protocol used? I have used fasting levels and 2-hour post 75-g glucose-drink testing as well. What is the best approach?

Scott A. Beckman, MD
Jasper, Indiana
 

Contraception and spironolactone

As usual, Dr. Barbieri has provided a thorough, concise, and practical overview on the medical management of PCOS. I would add just one small point. Another reason for using an oral estrogen-progestin pill concomitantly with spironolactone is due to the potential teratogenicity of this medication.

Bryan R. Hecht, MD
Cleveland, Ohio

 

Low-carb diet helps mitigate metformin side effects

Thank you for the article on PCOS. I have been treating PCOS this way for about 15 years and have been following lipids and seen dramatic improvements with that as well. I wish we as a medical community would focus on the low carbohydrate diet to help avert metformin side effects as well as treat the metabolic issues. You can get many people back on metformin by just adjusting their diet. I hope you can spread this word.

Steven Foley, MD
Lamar, Colorado

 

Appreciates Dr. Barbieri’s editorials

G’Day from Australia. I am a big fan of your editorials and opinions and enjoy reading OBG Management. Please keep it up.

Kanapathippillai Sivanesan, MD
Brisbane, Australia

 

Dr. Barbieri responds

I thank Dr. Linan, Dr. Foley, and Ms. Gowan for sharing their important insights with our readers. I agree with Dr. Linan that I should have highlighted the important guidance that women with PCOS and a body mass index (BMI) above the normal range should be encouraged to reduce their weight by 5% to 10% with diet and exercise. Dr. Foley offers a clinical pearl that a low carbohydrate diet will reduce the gastrointestinal symptoms that may occur with metformin therapy. Ms. Gowan notes that the combination of metformin plus cyclic progesterone may help to initiate more frequent ovulatory cycles in women with PCOS, thereby improving fertility. Dr. Hecht reminds us that spironolactone is a teratogen and using effective contraception can help reduce the risk of exposing a pregnancy to the medication.

Dr. Beckman raises the important clinical issue of whether it is helpful to measure insulin concentration. Measuring insulin and glucose is especially helpful in understanding the causes of hypoglycemia. An elevated insulin level at the time of an abnormally low glucose level is very worrisome. However, for women with PCOS, in whom insulin resistance is common, measuring insulin is of minimal clinical value. A normal or elevated insulin level is consistent with the diagnosis of PCOS. Assessing BMI, waist circumference, HDL-cholesterol, fasting triglyceride level, and blood pressure— components of the metabolic syndrome—are much more useful clinically. The dermatologic skin lesion acanthosis nigricans is also a sign consistent with insulin resistance. I do not measure insulin levels in my patients with PCOS. Metformin is a useful agent in the treatment of PCOS whether or not insulin resistance is present. Metformin may have direct actions on the ovary to reduce androgen production, in addition to its beneficial effects in the liver.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

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“TREATING POLYCYSTIC OVARY SYNDROME: START USING DUAL MEDICAL THERAPY”

ROBERT L. BARBIERI, MD (EDITORIAL; APRIL 2017)

Weight loss and dietary management for PCOS

I enjoyed Dr. Barbieri’s editorial on polycystic ovary syndrome (PCOS), but I feel that first-line management for PCOS should be weight loss and diet modifications that include instructions on decreasing carbohydrates and insulin spikes. A 5% to 10% weight loss should produce a return of cycles. Of course, metformin and spironolactone have a place for added treatment/prevention of acne and diabetes.

Luis Linan, MD
El Paso, Texas
 

Metformin and progesterone for PCOS-related infertility

I have been using Beyaz and Yaz for several years in my PCOS patients for the lower androgenic activity of the drospirenone based on the same assumption and its similarity to spironolactone. I have gotten great results with metformin 1,500 mg daily and, for those who desire fertility, cycling once a month for 10 days with progesterone. My own daughter was able to conceive in just 3 months of therapy. PCOS is extremely common in our region, probably due to the high obesity rate. I saw many more cases here than I ever thought I would when I was training.

Lisa Gowan, CNM, WHNP-BC
Albany, Georgia

 

Check insulin levels in PCOS patients before giving metformin?

Thank you for the very nice article regarding PCOS treatment. Does Dr. Barbieri routinely check insulin levels on patients before treating with metformin and does he require abnormal insulin levels to be present before initiating treatment? The article suggested that using the listed risk factors is sufficient. Additionally, does he perform glucose-insulin testing? If so, what is the protocol used? I have used fasting levels and 2-hour post 75-g glucose-drink testing as well. What is the best approach?

Scott A. Beckman, MD
Jasper, Indiana
 

Contraception and spironolactone

As usual, Dr. Barbieri has provided a thorough, concise, and practical overview on the medical management of PCOS. I would add just one small point. Another reason for using an oral estrogen-progestin pill concomitantly with spironolactone is due to the potential teratogenicity of this medication.

Bryan R. Hecht, MD
Cleveland, Ohio

 

Low-carb diet helps mitigate metformin side effects

Thank you for the article on PCOS. I have been treating PCOS this way for about 15 years and have been following lipids and seen dramatic improvements with that as well. I wish we as a medical community would focus on the low carbohydrate diet to help avert metformin side effects as well as treat the metabolic issues. You can get many people back on metformin by just adjusting their diet. I hope you can spread this word.

Steven Foley, MD
Lamar, Colorado

 

Appreciates Dr. Barbieri’s editorials

G’Day from Australia. I am a big fan of your editorials and opinions and enjoy reading OBG Management. Please keep it up.

Kanapathippillai Sivanesan, MD
Brisbane, Australia

 

Dr. Barbieri responds

I thank Dr. Linan, Dr. Foley, and Ms. Gowan for sharing their important insights with our readers. I agree with Dr. Linan that I should have highlighted the important guidance that women with PCOS and a body mass index (BMI) above the normal range should be encouraged to reduce their weight by 5% to 10% with diet and exercise. Dr. Foley offers a clinical pearl that a low carbohydrate diet will reduce the gastrointestinal symptoms that may occur with metformin therapy. Ms. Gowan notes that the combination of metformin plus cyclic progesterone may help to initiate more frequent ovulatory cycles in women with PCOS, thereby improving fertility. Dr. Hecht reminds us that spironolactone is a teratogen and using effective contraception can help reduce the risk of exposing a pregnancy to the medication.

Dr. Beckman raises the important clinical issue of whether it is helpful to measure insulin concentration. Measuring insulin and glucose is especially helpful in understanding the causes of hypoglycemia. An elevated insulin level at the time of an abnormally low glucose level is very worrisome. However, for women with PCOS, in whom insulin resistance is common, measuring insulin is of minimal clinical value. A normal or elevated insulin level is consistent with the diagnosis of PCOS. Assessing BMI, waist circumference, HDL-cholesterol, fasting triglyceride level, and blood pressure— components of the metabolic syndrome—are much more useful clinically. The dermatologic skin lesion acanthosis nigricans is also a sign consistent with insulin resistance. I do not measure insulin levels in my patients with PCOS. Metformin is a useful agent in the treatment of PCOS whether or not insulin resistance is present. Metformin may have direct actions on the ovary to reduce androgen production, in addition to its beneficial effects in the liver.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

“TREATING POLYCYSTIC OVARY SYNDROME: START USING DUAL MEDICAL THERAPY”

ROBERT L. BARBIERI, MD (EDITORIAL; APRIL 2017)

Weight loss and dietary management for PCOS

I enjoyed Dr. Barbieri’s editorial on polycystic ovary syndrome (PCOS), but I feel that first-line management for PCOS should be weight loss and diet modifications that include instructions on decreasing carbohydrates and insulin spikes. A 5% to 10% weight loss should produce a return of cycles. Of course, metformin and spironolactone have a place for added treatment/prevention of acne and diabetes.

Luis Linan, MD
El Paso, Texas
 

Metformin and progesterone for PCOS-related infertility

I have been using Beyaz and Yaz for several years in my PCOS patients for the lower androgenic activity of the drospirenone based on the same assumption and its similarity to spironolactone. I have gotten great results with metformin 1,500 mg daily and, for those who desire fertility, cycling once a month for 10 days with progesterone. My own daughter was able to conceive in just 3 months of therapy. PCOS is extremely common in our region, probably due to the high obesity rate. I saw many more cases here than I ever thought I would when I was training.

Lisa Gowan, CNM, WHNP-BC
Albany, Georgia

 

Check insulin levels in PCOS patients before giving metformin?

Thank you for the very nice article regarding PCOS treatment. Does Dr. Barbieri routinely check insulin levels on patients before treating with metformin and does he require abnormal insulin levels to be present before initiating treatment? The article suggested that using the listed risk factors is sufficient. Additionally, does he perform glucose-insulin testing? If so, what is the protocol used? I have used fasting levels and 2-hour post 75-g glucose-drink testing as well. What is the best approach?

Scott A. Beckman, MD
Jasper, Indiana
 

Contraception and spironolactone

As usual, Dr. Barbieri has provided a thorough, concise, and practical overview on the medical management of PCOS. I would add just one small point. Another reason for using an oral estrogen-progestin pill concomitantly with spironolactone is due to the potential teratogenicity of this medication.

Bryan R. Hecht, MD
Cleveland, Ohio

 

Low-carb diet helps mitigate metformin side effects

Thank you for the article on PCOS. I have been treating PCOS this way for about 15 years and have been following lipids and seen dramatic improvements with that as well. I wish we as a medical community would focus on the low carbohydrate diet to help avert metformin side effects as well as treat the metabolic issues. You can get many people back on metformin by just adjusting their diet. I hope you can spread this word.

Steven Foley, MD
Lamar, Colorado

 

Appreciates Dr. Barbieri’s editorials

G’Day from Australia. I am a big fan of your editorials and opinions and enjoy reading OBG Management. Please keep it up.

Kanapathippillai Sivanesan, MD
Brisbane, Australia

 

Dr. Barbieri responds

I thank Dr. Linan, Dr. Foley, and Ms. Gowan for sharing their important insights with our readers. I agree with Dr. Linan that I should have highlighted the important guidance that women with PCOS and a body mass index (BMI) above the normal range should be encouraged to reduce their weight by 5% to 10% with diet and exercise. Dr. Foley offers a clinical pearl that a low carbohydrate diet will reduce the gastrointestinal symptoms that may occur with metformin therapy. Ms. Gowan notes that the combination of metformin plus cyclic progesterone may help to initiate more frequent ovulatory cycles in women with PCOS, thereby improving fertility. Dr. Hecht reminds us that spironolactone is a teratogen and using effective contraception can help reduce the risk of exposing a pregnancy to the medication.

Dr. Beckman raises the important clinical issue of whether it is helpful to measure insulin concentration. Measuring insulin and glucose is especially helpful in understanding the causes of hypoglycemia. An elevated insulin level at the time of an abnormally low glucose level is very worrisome. However, for women with PCOS, in whom insulin resistance is common, measuring insulin is of minimal clinical value. A normal or elevated insulin level is consistent with the diagnosis of PCOS. Assessing BMI, waist circumference, HDL-cholesterol, fasting triglyceride level, and blood pressure— components of the metabolic syndrome—are much more useful clinically. The dermatologic skin lesion acanthosis nigricans is also a sign consistent with insulin resistance. I do not measure insulin levels in my patients with PCOS. Metformin is a useful agent in the treatment of PCOS whether or not insulin resistance is present. Metformin may have direct actions on the ovary to reduce androgen production, in addition to its beneficial effects in the liver.

 

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

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The ‘monster note’ in EHR systems rarely helps

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Recently, the hospital I take call at switched to Epic as its electronic health record system.

Overall, I don’t have too many complaints about it. It does some things better and some things worse than other systems I’ve used. That’s to be expected.

But with Epic has come an alarming new trend: the monster note.

Dr. Allan M. Block
The feature that automatically pastes radiology and lab results in a note has become horribly misused. I’m sure it looks good for legal purposes (“Hey, of course I read it. It’s in my note”). But what it really does is fill up a note with drivel: test results that take up space, followed by an exam that’s likely been cut and pasted from the previous day, and an impression that’s usually almost meaningless. Typically the last is along the lines of “continue current treatment” or “cardiology to see.”

Rarely does it ever give you a hint into the thought process or what’s going on that (at least to me) is so critical to medicine.

In a recent example of the insanity, one of my office patients was in the hospital overnight for a transient ischemic attack. When I went to get the discharge summary, it was 97 pages long! (Really, it was.) All of it was auto-filled in with test results, vital signs, MRI screening forms, medication administration records, and nurse, therapy, and respiratory notes. Most of it was far from the stuff that discharge summaries are supposed to contain. What part of “summary” are people not understanding anymore?

Of course, this isn’t Epic’s fault. It’s just a tool. It’s how humans use it that becomes the problem. This misuse of the system has made routine notes, as Shakespeare’s Macbeth said, “a tale told by an idiot, full of sound and fury, signifying nothing.”

For better or worse, I deliberately don’t do this. I let Epic put in the patient’s name, birthday, and most recent vital signs ... and nothing else. I’ll fill in the test results when needed, in a concise form that I can grasp. (It’s my note, after all.) To me, writing (or typing) the note is part of the thought process. As I enter results, I turn over what they mean, in a way that just seeing five paragraphs auto-pasted in doesn’t do. It also allows me to boil them down to one or two sentences.

After all, brevity is the soul of wit. And while I’m not trying to be witty in my notes, I am trying solve the problem in front of me. Taking the time write it out in my own words is essential to my thought process and letting others understand how I came to my plan. And, as a result, it is what’s best for the patient.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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Recently, the hospital I take call at switched to Epic as its electronic health record system.

Overall, I don’t have too many complaints about it. It does some things better and some things worse than other systems I’ve used. That’s to be expected.

But with Epic has come an alarming new trend: the monster note.

Dr. Allan M. Block
The feature that automatically pastes radiology and lab results in a note has become horribly misused. I’m sure it looks good for legal purposes (“Hey, of course I read it. It’s in my note”). But what it really does is fill up a note with drivel: test results that take up space, followed by an exam that’s likely been cut and pasted from the previous day, and an impression that’s usually almost meaningless. Typically the last is along the lines of “continue current treatment” or “cardiology to see.”

Rarely does it ever give you a hint into the thought process or what’s going on that (at least to me) is so critical to medicine.

In a recent example of the insanity, one of my office patients was in the hospital overnight for a transient ischemic attack. When I went to get the discharge summary, it was 97 pages long! (Really, it was.) All of it was auto-filled in with test results, vital signs, MRI screening forms, medication administration records, and nurse, therapy, and respiratory notes. Most of it was far from the stuff that discharge summaries are supposed to contain. What part of “summary” are people not understanding anymore?

Of course, this isn’t Epic’s fault. It’s just a tool. It’s how humans use it that becomes the problem. This misuse of the system has made routine notes, as Shakespeare’s Macbeth said, “a tale told by an idiot, full of sound and fury, signifying nothing.”

For better or worse, I deliberately don’t do this. I let Epic put in the patient’s name, birthday, and most recent vital signs ... and nothing else. I’ll fill in the test results when needed, in a concise form that I can grasp. (It’s my note, after all.) To me, writing (or typing) the note is part of the thought process. As I enter results, I turn over what they mean, in a way that just seeing five paragraphs auto-pasted in doesn’t do. It also allows me to boil them down to one or two sentences.

After all, brevity is the soul of wit. And while I’m not trying to be witty in my notes, I am trying solve the problem in front of me. Taking the time write it out in my own words is essential to my thought process and letting others understand how I came to my plan. And, as a result, it is what’s best for the patient.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

 

Recently, the hospital I take call at switched to Epic as its electronic health record system.

Overall, I don’t have too many complaints about it. It does some things better and some things worse than other systems I’ve used. That’s to be expected.

But with Epic has come an alarming new trend: the monster note.

Dr. Allan M. Block
The feature that automatically pastes radiology and lab results in a note has become horribly misused. I’m sure it looks good for legal purposes (“Hey, of course I read it. It’s in my note”). But what it really does is fill up a note with drivel: test results that take up space, followed by an exam that’s likely been cut and pasted from the previous day, and an impression that’s usually almost meaningless. Typically the last is along the lines of “continue current treatment” or “cardiology to see.”

Rarely does it ever give you a hint into the thought process or what’s going on that (at least to me) is so critical to medicine.

In a recent example of the insanity, one of my office patients was in the hospital overnight for a transient ischemic attack. When I went to get the discharge summary, it was 97 pages long! (Really, it was.) All of it was auto-filled in with test results, vital signs, MRI screening forms, medication administration records, and nurse, therapy, and respiratory notes. Most of it was far from the stuff that discharge summaries are supposed to contain. What part of “summary” are people not understanding anymore?

Of course, this isn’t Epic’s fault. It’s just a tool. It’s how humans use it that becomes the problem. This misuse of the system has made routine notes, as Shakespeare’s Macbeth said, “a tale told by an idiot, full of sound and fury, signifying nothing.”

For better or worse, I deliberately don’t do this. I let Epic put in the patient’s name, birthday, and most recent vital signs ... and nothing else. I’ll fill in the test results when needed, in a concise form that I can grasp. (It’s my note, after all.) To me, writing (or typing) the note is part of the thought process. As I enter results, I turn over what they mean, in a way that just seeing five paragraphs auto-pasted in doesn’t do. It also allows me to boil them down to one or two sentences.

After all, brevity is the soul of wit. And while I’m not trying to be witty in my notes, I am trying solve the problem in front of me. Taking the time write it out in my own words is essential to my thought process and letting others understand how I came to my plan. And, as a result, it is what’s best for the patient.
 

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

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My face is all red!

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My grandson is almost 3. He is, of course, very advanced in many areas, including self-awareness.

At the moment he is suffering from Fifth Disease. (See how advanced he is – he skipped right over Diseases One through Four!) Every now and then his face clouds over as he announces, to anyone and no one, “My face is all red!”

I am not worried about long-term psychic harm. A moment later his face lights up as he looks up at the sky. “It’s a helicopter!” he declares.

Dr. Alan Rockoff
So what do you think about my grandson’s observation about his complexion? Do you think he is vain? (Careful!) Would you call his concerns cosmetic?

By the way, does his behavior remind you of anyone else you’ve met? How about all your patients with rosacea or facial keratosis pilaris who stop by the office to say, “My face is all red!” If they didn’t notice this themselves, others have been happy to help. “You’re all red!” say their family, friends, and coworkers. “Are you all right?”

What about patients like those? Would you call them vain, or cosmetically oriented?

It seems to me that the behavior of little kids – too young to elaborate their psychological musings – sheds light on the way their elders behave, or the way they will themselves when they grow up. Years ago, I was about to laser the face of a woman with an old pulsed-dye unit that left deep-purple bruises. Her job was to train monkeys for the blind. “I need makeup,” she said. “When my monkeys see red spots on my face, they get very upset and start to point at me.”

“Not just monkeys,” I replied.

To take another example, many years ago I saw a little tyke about 18 months old. His parents were concerned about a mole on his palm.

He was not happy to let me examine him, and he let me know. “It’s OK,” I said, in my most condescending, clueless adult voice. “Your Mom and Dad just asked me to check your boo-boo.”

That set him off. “No boo-boo!” he shouted. “No boo-boo!”

Well, silly me, I later realized. The tyke was right: Of course it was not a boo-boo. A boo-boo is an assault on the integrity of the body: a cut, a scrape, a burn, something new, painful, hard to look at. That is why 9.8 out of 10 people whom we freeze, burn, or puncture look the other way while we do it. It’s also why kids dial their screams down to whimpers when we hide what we froze, burned, or punctured by covering it with a Band-Aid. Now the boo-boo is out of sight.

The tyke’s mole, on the other hand, is not an insult to the body but a part of it. It’s him.

Fast forward 15 years and ask a teen with a large (but not giant) hairy congenital nevus if she wants it off. She does not. “That’s me,” she explains.

Or ask an adult with what you would think is a disfiguring facial port-wine stain what growing up with that was like. “It was fine,” they reply. “Strangers sometimes commented, but my friends knew that was just how I looked.”

Or listen to folks who want their liver spots lasered off. They point to a dozen or so, then add, “But don’t take off that one! That’s always been there. That’s just me.”

If you listen for it, you can pick up how early a lot of adult behavior starts. Little ones destined to be lifetime pickers start scraping off anything that’s raised above the skin. Teens finicky about facial moles or minute perturbations in their complexion grow into fussy adults.

We grownups learn to embroider our primal responses with words, thoughts, feeling, explanations. Kids just come out and say what they think – “My face is all red!”

Soon my grandson will have overcome his Fifth Disease without, I hope, graduating to any higher numbers. His other grandfather is a retired engineer who used to design helicopters. By next year I expect that our mutual grandson will be able to identify anything flying overhead by make and model number.

As I said, he’s very advanced.

Also cute as all get-out, (temporary) red face and all.
 

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at dermnews@frontlinemedcom.com

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My grandson is almost 3. He is, of course, very advanced in many areas, including self-awareness.

At the moment he is suffering from Fifth Disease. (See how advanced he is – he skipped right over Diseases One through Four!) Every now and then his face clouds over as he announces, to anyone and no one, “My face is all red!”

I am not worried about long-term psychic harm. A moment later his face lights up as he looks up at the sky. “It’s a helicopter!” he declares.

Dr. Alan Rockoff
So what do you think about my grandson’s observation about his complexion? Do you think he is vain? (Careful!) Would you call his concerns cosmetic?

By the way, does his behavior remind you of anyone else you’ve met? How about all your patients with rosacea or facial keratosis pilaris who stop by the office to say, “My face is all red!” If they didn’t notice this themselves, others have been happy to help. “You’re all red!” say their family, friends, and coworkers. “Are you all right?”

What about patients like those? Would you call them vain, or cosmetically oriented?

It seems to me that the behavior of little kids – too young to elaborate their psychological musings – sheds light on the way their elders behave, or the way they will themselves when they grow up. Years ago, I was about to laser the face of a woman with an old pulsed-dye unit that left deep-purple bruises. Her job was to train monkeys for the blind. “I need makeup,” she said. “When my monkeys see red spots on my face, they get very upset and start to point at me.”

“Not just monkeys,” I replied.

To take another example, many years ago I saw a little tyke about 18 months old. His parents were concerned about a mole on his palm.

He was not happy to let me examine him, and he let me know. “It’s OK,” I said, in my most condescending, clueless adult voice. “Your Mom and Dad just asked me to check your boo-boo.”

That set him off. “No boo-boo!” he shouted. “No boo-boo!”

Well, silly me, I later realized. The tyke was right: Of course it was not a boo-boo. A boo-boo is an assault on the integrity of the body: a cut, a scrape, a burn, something new, painful, hard to look at. That is why 9.8 out of 10 people whom we freeze, burn, or puncture look the other way while we do it. It’s also why kids dial their screams down to whimpers when we hide what we froze, burned, or punctured by covering it with a Band-Aid. Now the boo-boo is out of sight.

The tyke’s mole, on the other hand, is not an insult to the body but a part of it. It’s him.

Fast forward 15 years and ask a teen with a large (but not giant) hairy congenital nevus if she wants it off. She does not. “That’s me,” she explains.

Or ask an adult with what you would think is a disfiguring facial port-wine stain what growing up with that was like. “It was fine,” they reply. “Strangers sometimes commented, but my friends knew that was just how I looked.”

Or listen to folks who want their liver spots lasered off. They point to a dozen or so, then add, “But don’t take off that one! That’s always been there. That’s just me.”

If you listen for it, you can pick up how early a lot of adult behavior starts. Little ones destined to be lifetime pickers start scraping off anything that’s raised above the skin. Teens finicky about facial moles or minute perturbations in their complexion grow into fussy adults.

We grownups learn to embroider our primal responses with words, thoughts, feeling, explanations. Kids just come out and say what they think – “My face is all red!”

Soon my grandson will have overcome his Fifth Disease without, I hope, graduating to any higher numbers. His other grandfather is a retired engineer who used to design helicopters. By next year I expect that our mutual grandson will be able to identify anything flying overhead by make and model number.

As I said, he’s very advanced.

Also cute as all get-out, (temporary) red face and all.
 

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at dermnews@frontlinemedcom.com

 

My grandson is almost 3. He is, of course, very advanced in many areas, including self-awareness.

At the moment he is suffering from Fifth Disease. (See how advanced he is – he skipped right over Diseases One through Four!) Every now and then his face clouds over as he announces, to anyone and no one, “My face is all red!”

I am not worried about long-term psychic harm. A moment later his face lights up as he looks up at the sky. “It’s a helicopter!” he declares.

Dr. Alan Rockoff
So what do you think about my grandson’s observation about his complexion? Do you think he is vain? (Careful!) Would you call his concerns cosmetic?

By the way, does his behavior remind you of anyone else you’ve met? How about all your patients with rosacea or facial keratosis pilaris who stop by the office to say, “My face is all red!” If they didn’t notice this themselves, others have been happy to help. “You’re all red!” say their family, friends, and coworkers. “Are you all right?”

What about patients like those? Would you call them vain, or cosmetically oriented?

It seems to me that the behavior of little kids – too young to elaborate their psychological musings – sheds light on the way their elders behave, or the way they will themselves when they grow up. Years ago, I was about to laser the face of a woman with an old pulsed-dye unit that left deep-purple bruises. Her job was to train monkeys for the blind. “I need makeup,” she said. “When my monkeys see red spots on my face, they get very upset and start to point at me.”

“Not just monkeys,” I replied.

To take another example, many years ago I saw a little tyke about 18 months old. His parents were concerned about a mole on his palm.

He was not happy to let me examine him, and he let me know. “It’s OK,” I said, in my most condescending, clueless adult voice. “Your Mom and Dad just asked me to check your boo-boo.”

That set him off. “No boo-boo!” he shouted. “No boo-boo!”

Well, silly me, I later realized. The tyke was right: Of course it was not a boo-boo. A boo-boo is an assault on the integrity of the body: a cut, a scrape, a burn, something new, painful, hard to look at. That is why 9.8 out of 10 people whom we freeze, burn, or puncture look the other way while we do it. It’s also why kids dial their screams down to whimpers when we hide what we froze, burned, or punctured by covering it with a Band-Aid. Now the boo-boo is out of sight.

The tyke’s mole, on the other hand, is not an insult to the body but a part of it. It’s him.

Fast forward 15 years and ask a teen with a large (but not giant) hairy congenital nevus if she wants it off. She does not. “That’s me,” she explains.

Or ask an adult with what you would think is a disfiguring facial port-wine stain what growing up with that was like. “It was fine,” they reply. “Strangers sometimes commented, but my friends knew that was just how I looked.”

Or listen to folks who want their liver spots lasered off. They point to a dozen or so, then add, “But don’t take off that one! That’s always been there. That’s just me.”

If you listen for it, you can pick up how early a lot of adult behavior starts. Little ones destined to be lifetime pickers start scraping off anything that’s raised above the skin. Teens finicky about facial moles or minute perturbations in their complexion grow into fussy adults.

We grownups learn to embroider our primal responses with words, thoughts, feeling, explanations. Kids just come out and say what they think – “My face is all red!”

Soon my grandson will have overcome his Fifth Disease without, I hope, graduating to any higher numbers. His other grandfather is a retired engineer who used to design helicopters. By next year I expect that our mutual grandson will be able to identify anything flying overhead by make and model number.

As I said, he’s very advanced.

Also cute as all get-out, (temporary) red face and all.
 

Dr. Rockoff practices dermatology in Brookline, Mass., and is a longtime contributor to Dermatology News. He serves on the clinical faculty at Tufts University, Boston, and has taught senior medical students and other trainees for 30 years. His second book, “Act Like a Doctor, Think Like a Patient,” is available at amazon.com and barnesandnoble.com. Write to him at dermnews@frontlinemedcom.com

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Fighting in a passive manner active against Clostridium difficile

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Infections resulting from Clostridium difficile are a major clinical challenge. In hematology and oncology, the widespread use of broad-spectrum antibiotics is essential for patients with profound neutropenia and infectious complications, which are a high-risk factor for C. difficile enteritis.

C. difficile enteritis occurs in 5%-20% of cancer patients.1 With standard of care antibiotics, oral metronidazole or oral vancomycin, high C. difficile cure rates are possible, but up to 25% of these infections recur. Recently, oral fidaxomicin was approved for treatment of C. difficile enteritis and was associated with high cure rates and, more importantly, with significantly lower recurrence rates.2

Dr. Thomas Fischer
About 40 years ago, the pathogenesis of C. difficile enteritis was described when toxin A (enterotoxin) and toxin B (cytotoxin) were identified.3 There is good evidence that, among both toxins, toxin B plays the essential role in virulence of C. difficile.4C. difficile toxin B uses eukaryotic signals for induced autoproteolysis to deliver its toxic products into the cytosol of target cells. Toxin B binds to the surface of intestinal epithelial cells, where it is internalized and catalyzes the glucosylation of cytoplasmic-rho proteins, leading to disaggregation of the cytoskeleton and cell death.5 Toxin B must be neutralized to protect against recurrent infection.6

Bezlotoxumab, a fully humanized monoclonal antibody against C. difficile toxin B, has been shown by x-ray crystallography to neutralize toxin B by blocking its ability to bind to host cells.7 Most recently, this new therapeutic approach was investigated in humans.8

Wilcox et al. used pooled data of 2655 adults treated in two double-blind, randomized, placebo-controlled phase III clinical trials (MODIFY I and MODIFY II) for primary or recurrent C. difficile enteritis. This industry-sponsored trial was conducted at 322 sites in 30 countries.

In one treatment group, patients received a single infusion of bezlotoxumab (781 patients) or placebo (773 patients) and one of the three oral standard-of-care C. difficile antibiotics. Importantly, the primary end point of this trial was recurrent infection within 12 weeks. About 28% of the patients in both the bezlotoxumab group and the placebo group previously had at least one episode of C. difficile enteritis. About 20% of the patients in both groups were immunocompromised.

Pooled data showed that recurrent infection was significantly lower (P less than 0.001) in the bezlotoxumab group (17%), compared with the placebo group (27%). The difference in recurrence rate (25% vs. 41%) was even more pronounced in patients with one or more episodes of recurrent C. difficile enteritis in the past 6 months. Furthermore, a benefit for bezlotoxumab was seen in immunocompromised patients, whose recurrence rates were 15% with bezlotoxumab, vs. 28% with placebo. After the 12 weeks of follow-up, the absolute difference in the Kaplan-Meier rates of recurrent infection was 13% (absolute rate, 21% in bezlotoxumab group vs. 34% in placebo group; P less than 0.001).

The results indicate that bezlotoxumab, which was approved in 2016 by the U.S. Food and Drug Administration, might improve the outcome of patients with C. difficile enteritis. However, bezlotoxumab is not a “magic bullet.” The number needed to treat to prevent one episode of C. difficile enteritis is 10.

It is conceivable that bezlotoxumab may find its role in high-risk patients – those older than 65 years or patients with recurrent C. difficile enteritis – since the number needed to treat is only 6 in these subgroups.8

This new agent could be an important treatment option for our high-risk patients in hematology. However, more studies concerning costs and real-life efficacy are needed.

The new approach of passive immunization for prevention of recurrent C. difficile enteritis shows the importance and the role of toxin B – not only the bacterium per se – in pathogenesis and virulence of C. difficile. This could mean that we have to renew our view on the role of antibiotics against C. difficile. However, in contrast, bezlotoxumab does not affect the efficacy of standard of care antibiotics since the initial cure rates were 80% for both the antibody and the placebo groups.8 Toxin B levels are not detectable in stool samples between days 4 and 10 of standard of care antibiotic treatment. Afterward, however, they increase again.9 Most of the patients had received bezlotoxumab 3 or more days after they began standard-of-care antibiotic treatment – in the time period when toxin B is undetectable in stool – which underlines the importance of toxin B in the pathogenesis of recurrent C. difficile enteritis.8

In summary, the introduction of bezlotoxumab in clinical care gives new and important insights and solutions not only for treatment options but also for our understanding of C. difficile pathogenesis.
 

 

Dr. Schalk is consultant of internal medicine at the department of hematology and oncology, Magdeburg University Hospital, Germany, with clinical and research focus on infectious diseases in hematology and oncology.

Dr. Fischer is professor of internal medicine, hematology and oncology, at the Otto-von-Guericke University Hospital Magdeburg, Germany. He is head of the department of hematology and oncology and a clinical/molecular researcher in myeloid neoplasms. He is a member of the editorial advisory board of Hematology News.

Contact Dr. Schalk at enrico.schalk@med.ovgu.de.

References

1. Vehreschild, MJ et al. Diagnosis and management of gastrointestinal complications in adult cancer patients: Wvidence-based guidelines of the Infectious Diseases Working Party (AGIHO) of the German Society of Hematology and Oncology (DGHO). Ann Oncol. 2013;24:1189-202

2. Cornely, OA. Current and emerging management options for Clostridium difficile infection: What is the role of fidaxomicin? Clin Microbiol Infect. 2012;18(Suppl 6):28-35.

3. Bartlett, JG et al. Antibiotic-associated pseudomembranous colitis due to toxin-producing clostridia. N Engl J Med. 1978;298(10):531-4.

4. Lyras, D et al. Toxin B is essential for virulence of Clostridium difficile. Nature. 2009;458:1176-9.

5. Reineke, J et al. Autocatalytic cleavage of Clostridium difficile toxin B. Nature. 2007;446:415-9.

6. Leav, BA et al. Serum anti-toxin B antibody correlates with protection from recurrent Clostridium difficile infection (CDI). Vaccine. 2010;28:965-9.

7. Orth, P et al. Mechanism of action and epitopes of Clostridium difficile toxin B-neutralizing antibody bezlotoxumab revealed by X-ray crystallography. J Biol Chem. 2014;289:18008-21.

8. Wilcox, MH et al. Bezlotoxumab for prevention of recurrent Clostridium difficile infection. N Engl J Med. 2017;376:305-17.

9. Louie, TJ et al. Fidaxomicin preserves the intestinal microbiome during and after treatment of Clostridium difficile infection (CDI) and reduces both toxin reexpression and recurrence of CDI. Clin Infect Dis. 2012;5(Suppl 2):S132-42.

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Infections resulting from Clostridium difficile are a major clinical challenge. In hematology and oncology, the widespread use of broad-spectrum antibiotics is essential for patients with profound neutropenia and infectious complications, which are a high-risk factor for C. difficile enteritis.

C. difficile enteritis occurs in 5%-20% of cancer patients.1 With standard of care antibiotics, oral metronidazole or oral vancomycin, high C. difficile cure rates are possible, but up to 25% of these infections recur. Recently, oral fidaxomicin was approved for treatment of C. difficile enteritis and was associated with high cure rates and, more importantly, with significantly lower recurrence rates.2

Dr. Thomas Fischer
About 40 years ago, the pathogenesis of C. difficile enteritis was described when toxin A (enterotoxin) and toxin B (cytotoxin) were identified.3 There is good evidence that, among both toxins, toxin B plays the essential role in virulence of C. difficile.4C. difficile toxin B uses eukaryotic signals for induced autoproteolysis to deliver its toxic products into the cytosol of target cells. Toxin B binds to the surface of intestinal epithelial cells, where it is internalized and catalyzes the glucosylation of cytoplasmic-rho proteins, leading to disaggregation of the cytoskeleton and cell death.5 Toxin B must be neutralized to protect against recurrent infection.6

Bezlotoxumab, a fully humanized monoclonal antibody against C. difficile toxin B, has been shown by x-ray crystallography to neutralize toxin B by blocking its ability to bind to host cells.7 Most recently, this new therapeutic approach was investigated in humans.8

Wilcox et al. used pooled data of 2655 adults treated in two double-blind, randomized, placebo-controlled phase III clinical trials (MODIFY I and MODIFY II) for primary or recurrent C. difficile enteritis. This industry-sponsored trial was conducted at 322 sites in 30 countries.

In one treatment group, patients received a single infusion of bezlotoxumab (781 patients) or placebo (773 patients) and one of the three oral standard-of-care C. difficile antibiotics. Importantly, the primary end point of this trial was recurrent infection within 12 weeks. About 28% of the patients in both the bezlotoxumab group and the placebo group previously had at least one episode of C. difficile enteritis. About 20% of the patients in both groups were immunocompromised.

Pooled data showed that recurrent infection was significantly lower (P less than 0.001) in the bezlotoxumab group (17%), compared with the placebo group (27%). The difference in recurrence rate (25% vs. 41%) was even more pronounced in patients with one or more episodes of recurrent C. difficile enteritis in the past 6 months. Furthermore, a benefit for bezlotoxumab was seen in immunocompromised patients, whose recurrence rates were 15% with bezlotoxumab, vs. 28% with placebo. After the 12 weeks of follow-up, the absolute difference in the Kaplan-Meier rates of recurrent infection was 13% (absolute rate, 21% in bezlotoxumab group vs. 34% in placebo group; P less than 0.001).

The results indicate that bezlotoxumab, which was approved in 2016 by the U.S. Food and Drug Administration, might improve the outcome of patients with C. difficile enteritis. However, bezlotoxumab is not a “magic bullet.” The number needed to treat to prevent one episode of C. difficile enteritis is 10.

It is conceivable that bezlotoxumab may find its role in high-risk patients – those older than 65 years or patients with recurrent C. difficile enteritis – since the number needed to treat is only 6 in these subgroups.8

This new agent could be an important treatment option for our high-risk patients in hematology. However, more studies concerning costs and real-life efficacy are needed.

The new approach of passive immunization for prevention of recurrent C. difficile enteritis shows the importance and the role of toxin B – not only the bacterium per se – in pathogenesis and virulence of C. difficile. This could mean that we have to renew our view on the role of antibiotics against C. difficile. However, in contrast, bezlotoxumab does not affect the efficacy of standard of care antibiotics since the initial cure rates were 80% for both the antibody and the placebo groups.8 Toxin B levels are not detectable in stool samples between days 4 and 10 of standard of care antibiotic treatment. Afterward, however, they increase again.9 Most of the patients had received bezlotoxumab 3 or more days after they began standard-of-care antibiotic treatment – in the time period when toxin B is undetectable in stool – which underlines the importance of toxin B in the pathogenesis of recurrent C. difficile enteritis.8

In summary, the introduction of bezlotoxumab in clinical care gives new and important insights and solutions not only for treatment options but also for our understanding of C. difficile pathogenesis.
 

 

Dr. Schalk is consultant of internal medicine at the department of hematology and oncology, Magdeburg University Hospital, Germany, with clinical and research focus on infectious diseases in hematology and oncology.

Dr. Fischer is professor of internal medicine, hematology and oncology, at the Otto-von-Guericke University Hospital Magdeburg, Germany. He is head of the department of hematology and oncology and a clinical/molecular researcher in myeloid neoplasms. He is a member of the editorial advisory board of Hematology News.

Contact Dr. Schalk at enrico.schalk@med.ovgu.de.

References

1. Vehreschild, MJ et al. Diagnosis and management of gastrointestinal complications in adult cancer patients: Wvidence-based guidelines of the Infectious Diseases Working Party (AGIHO) of the German Society of Hematology and Oncology (DGHO). Ann Oncol. 2013;24:1189-202

2. Cornely, OA. Current and emerging management options for Clostridium difficile infection: What is the role of fidaxomicin? Clin Microbiol Infect. 2012;18(Suppl 6):28-35.

3. Bartlett, JG et al. Antibiotic-associated pseudomembranous colitis due to toxin-producing clostridia. N Engl J Med. 1978;298(10):531-4.

4. Lyras, D et al. Toxin B is essential for virulence of Clostridium difficile. Nature. 2009;458:1176-9.

5. Reineke, J et al. Autocatalytic cleavage of Clostridium difficile toxin B. Nature. 2007;446:415-9.

6. Leav, BA et al. Serum anti-toxin B antibody correlates with protection from recurrent Clostridium difficile infection (CDI). Vaccine. 2010;28:965-9.

7. Orth, P et al. Mechanism of action and epitopes of Clostridium difficile toxin B-neutralizing antibody bezlotoxumab revealed by X-ray crystallography. J Biol Chem. 2014;289:18008-21.

8. Wilcox, MH et al. Bezlotoxumab for prevention of recurrent Clostridium difficile infection. N Engl J Med. 2017;376:305-17.

9. Louie, TJ et al. Fidaxomicin preserves the intestinal microbiome during and after treatment of Clostridium difficile infection (CDI) and reduces both toxin reexpression and recurrence of CDI. Clin Infect Dis. 2012;5(Suppl 2):S132-42.

 

Infections resulting from Clostridium difficile are a major clinical challenge. In hematology and oncology, the widespread use of broad-spectrum antibiotics is essential for patients with profound neutropenia and infectious complications, which are a high-risk factor for C. difficile enteritis.

C. difficile enteritis occurs in 5%-20% of cancer patients.1 With standard of care antibiotics, oral metronidazole or oral vancomycin, high C. difficile cure rates are possible, but up to 25% of these infections recur. Recently, oral fidaxomicin was approved for treatment of C. difficile enteritis and was associated with high cure rates and, more importantly, with significantly lower recurrence rates.2

Dr. Thomas Fischer
About 40 years ago, the pathogenesis of C. difficile enteritis was described when toxin A (enterotoxin) and toxin B (cytotoxin) were identified.3 There is good evidence that, among both toxins, toxin B plays the essential role in virulence of C. difficile.4C. difficile toxin B uses eukaryotic signals for induced autoproteolysis to deliver its toxic products into the cytosol of target cells. Toxin B binds to the surface of intestinal epithelial cells, where it is internalized and catalyzes the glucosylation of cytoplasmic-rho proteins, leading to disaggregation of the cytoskeleton and cell death.5 Toxin B must be neutralized to protect against recurrent infection.6

Bezlotoxumab, a fully humanized monoclonal antibody against C. difficile toxin B, has been shown by x-ray crystallography to neutralize toxin B by blocking its ability to bind to host cells.7 Most recently, this new therapeutic approach was investigated in humans.8

Wilcox et al. used pooled data of 2655 adults treated in two double-blind, randomized, placebo-controlled phase III clinical trials (MODIFY I and MODIFY II) for primary or recurrent C. difficile enteritis. This industry-sponsored trial was conducted at 322 sites in 30 countries.

In one treatment group, patients received a single infusion of bezlotoxumab (781 patients) or placebo (773 patients) and one of the three oral standard-of-care C. difficile antibiotics. Importantly, the primary end point of this trial was recurrent infection within 12 weeks. About 28% of the patients in both the bezlotoxumab group and the placebo group previously had at least one episode of C. difficile enteritis. About 20% of the patients in both groups were immunocompromised.

Pooled data showed that recurrent infection was significantly lower (P less than 0.001) in the bezlotoxumab group (17%), compared with the placebo group (27%). The difference in recurrence rate (25% vs. 41%) was even more pronounced in patients with one or more episodes of recurrent C. difficile enteritis in the past 6 months. Furthermore, a benefit for bezlotoxumab was seen in immunocompromised patients, whose recurrence rates were 15% with bezlotoxumab, vs. 28% with placebo. After the 12 weeks of follow-up, the absolute difference in the Kaplan-Meier rates of recurrent infection was 13% (absolute rate, 21% in bezlotoxumab group vs. 34% in placebo group; P less than 0.001).

The results indicate that bezlotoxumab, which was approved in 2016 by the U.S. Food and Drug Administration, might improve the outcome of patients with C. difficile enteritis. However, bezlotoxumab is not a “magic bullet.” The number needed to treat to prevent one episode of C. difficile enteritis is 10.

It is conceivable that bezlotoxumab may find its role in high-risk patients – those older than 65 years or patients with recurrent C. difficile enteritis – since the number needed to treat is only 6 in these subgroups.8

This new agent could be an important treatment option for our high-risk patients in hematology. However, more studies concerning costs and real-life efficacy are needed.

The new approach of passive immunization for prevention of recurrent C. difficile enteritis shows the importance and the role of toxin B – not only the bacterium per se – in pathogenesis and virulence of C. difficile. This could mean that we have to renew our view on the role of antibiotics against C. difficile. However, in contrast, bezlotoxumab does not affect the efficacy of standard of care antibiotics since the initial cure rates were 80% for both the antibody and the placebo groups.8 Toxin B levels are not detectable in stool samples between days 4 and 10 of standard of care antibiotic treatment. Afterward, however, they increase again.9 Most of the patients had received bezlotoxumab 3 or more days after they began standard-of-care antibiotic treatment – in the time period when toxin B is undetectable in stool – which underlines the importance of toxin B in the pathogenesis of recurrent C. difficile enteritis.8

In summary, the introduction of bezlotoxumab in clinical care gives new and important insights and solutions not only for treatment options but also for our understanding of C. difficile pathogenesis.
 

 

Dr. Schalk is consultant of internal medicine at the department of hematology and oncology, Magdeburg University Hospital, Germany, with clinical and research focus on infectious diseases in hematology and oncology.

Dr. Fischer is professor of internal medicine, hematology and oncology, at the Otto-von-Guericke University Hospital Magdeburg, Germany. He is head of the department of hematology and oncology and a clinical/molecular researcher in myeloid neoplasms. He is a member of the editorial advisory board of Hematology News.

Contact Dr. Schalk at enrico.schalk@med.ovgu.de.

References

1. Vehreschild, MJ et al. Diagnosis and management of gastrointestinal complications in adult cancer patients: Wvidence-based guidelines of the Infectious Diseases Working Party (AGIHO) of the German Society of Hematology and Oncology (DGHO). Ann Oncol. 2013;24:1189-202

2. Cornely, OA. Current and emerging management options for Clostridium difficile infection: What is the role of fidaxomicin? Clin Microbiol Infect. 2012;18(Suppl 6):28-35.

3. Bartlett, JG et al. Antibiotic-associated pseudomembranous colitis due to toxin-producing clostridia. N Engl J Med. 1978;298(10):531-4.

4. Lyras, D et al. Toxin B is essential for virulence of Clostridium difficile. Nature. 2009;458:1176-9.

5. Reineke, J et al. Autocatalytic cleavage of Clostridium difficile toxin B. Nature. 2007;446:415-9.

6. Leav, BA et al. Serum anti-toxin B antibody correlates with protection from recurrent Clostridium difficile infection (CDI). Vaccine. 2010;28:965-9.

7. Orth, P et al. Mechanism of action and epitopes of Clostridium difficile toxin B-neutralizing antibody bezlotoxumab revealed by X-ray crystallography. J Biol Chem. 2014;289:18008-21.

8. Wilcox, MH et al. Bezlotoxumab for prevention of recurrent Clostridium difficile infection. N Engl J Med. 2017;376:305-17.

9. Louie, TJ et al. Fidaxomicin preserves the intestinal microbiome during and after treatment of Clostridium difficile infection (CDI) and reduces both toxin reexpression and recurrence of CDI. Clin Infect Dis. 2012;5(Suppl 2):S132-42.

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Foodborne illnesses of foreign, domestic origin: On the rise?

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Are foodborne illness outbreaks more common now, or are we simply better at detection? Have the foods and sources associated with foodborne illness changed? Two recent Centers for Disease Control & Prevention reports provide insight.1,2 In 2016, the Foodborne Diseases Active Surveillance Network (FoodNet) detected 24,029 infections, 5,212 hospitalizations, and 98 fatalities.1 FoodNet has 10 sites serving 49 million people (15% of the U.S. population). These 2016 numbers changed only modestly from the 3 prior years.

The big two

The most frequent 2016 foodborne pathogens were Campylobacter and Salmonella, at approximately 8,000 illnesses each, detected by traditional cultures or culture-independent diagnostic tests (CIDTs). (See table.) CIDTs are relatively new molecular-based, mostly multiplex assays that test for more than a dozen pathogens in one assay.

Dr. Christopher J. Harrison
Campylobacter-contaminated domestic food in 2016 was mostly raw/undercooked poultry or unpasteurized milk/fruit drinks. Campylobacter can be detected in up to 88% of chicken carcasses at processing plants and approximately 50% of raw chicken at grocery stores. However, Campylobacter from imported food most often came from fresh produce.2

Overall, Salmonella originated from diverse sources (eggs, poultry, meat, unpasteurized milk/juice/cheese, or raw fruits/vegetables/spices/nuts). But, in 2016, U.S. Salmonella outbreaks were from eggs, alfalfa sprouts, poultry, pistachios, and organic shake/meal products.

The runners-up

Most of the remainder of the 2016 foodborne illnesses were caused by Shigella, with nearly 3,000 cases; shigatoxin-producing Escherichia coli (STEC), with nearly 2,000 cases; and Cryptosporidium, also with nearly 2,000 cases. (See table.)

Hemolytic uremic syndrome (HUS)

HUS rates, mostly resulting from E. coli 0157 H7 in meat, did not vary from 2013 to 2016, with a total 62 pediatric HUS cases in FoodNet (0.56 /100,000 population). Slightly over half (56%) occurred in children under 5 years old at 1.18 per 100,000 population.

Does CIDT increase detection rates?

Detection of the “big two” did not change from 2013 to 2016 or over the past 2 decades. That said, Campylobacter detection was actually down 11% if considering only culture-confirmed cases. That is, if we do not count detections made exclusively by CIDT.

This is important because CIDT – now supplanting culture in many laboratories – identifies pathogens not likely detected by standard culture because culture is generally selective and CIDT is more sensitive. CIDT can increase detection rates (solo and multiple pathogens), even if illnesses do not really increase. The CDC suggested that this contributed to increased STEC and Yersinia detection in 2016. Some would not have been detected if only culture had been utilized.

Viable bacterial/viral isolates are not available from CIDT. A replicating pathogen is needed to characterize shifting/emerging pathogen strains (for example, analysis for mutations or new pathogens via sequencing or antimicrobial susceptibility testing).

To compensate, some CIDT-using laboratories perform “reflex cultures.” CIDT positive specimens also are cultured to provide viable isolates. However, this adds cost to an already costly CIDT test.

The role of imported food

Surveillance systems, such as the Foodborne Disease Outbreak Surveillance System, also track imported foodborne illness. Despite an approximately 50% decrease in overall U.S. foodborne outbreaks since 2000, imported food-related outbreaks increased to 195 during 2006-2014 from 54 during 1996-2004, with 10,685 illnesses, 1,017 hospitalizations, and 19 deaths since 2009. Also, imported food-related outbreaks rose from a mean 3 per year pre-2000 to a mean 18 per year during 2009-2014. Most imported food outbreaks (86% of total) had three causes: scombroid toxin (42% of total), Salmonella (33%), and hepatitis A virus (11%).

A foreign origin for approximately 19% of U.S.-consumed food makes it unsurprising that imported foods increasingly cause foodborne outbreaks. Much imported food is “outbreak prone.” Perhaps surprising is that a staggering 97% of fish/shellfish, 50% of fresh fruits, and 20% of fresh vegetables are imported, according to 2016 estimates by the U.S. Department of Agriculture.

Most imported food illnesses were from Salmonella (4,421 from 52 outbreaks), Cyclospora (2,533 from 33 outbreaks), hepatitis A virus (1,150 from 11 outbreaks), and Shigella (625 from 6 outbreaks). While eggs, ice cream, and poultry are notorious origins for Salmonella in domestic food, most imported Salmonella were from produce: fruits (26%), seeded vegetables (20%), sprouts (11%), nuts/seeds (10%), spices (7%), and herbs (2%).

Seafood/fish caused 55% of outbreaks but few illnesses per outbreak (median 3 illnesses/outbreak), so only 11% of total illnesses were caused by seafood/fish. In contrast, fresh produce caused only 33% of outbreaks but 84% of illnesses (median 40 illnesses/outbreak).

Geographic source, outbreak locations

The origin was known in 91% of outbreaks. Latin America and the Caribbean were most common, followed by Asia.3 Main contributing countries were Mexico (42 outbreaks), Indonesia (17) and Canada (11).

 

 

Contaminated fish/shellfish originated from all regions except Europe, most commonly from Asia (the majority of fish/shellfish outbreaks were from Indonesia, Vietnam, China, Philippines, Taiwan, and Thailand) with smaller contributions from the Bahamas and Ecuador.

Contaminated produce originated from all regions, mostly (64%) from Mexico and the Americas (Chile, Guatemala, and Honduras). All but one dairy outbreak originated in Latin America/the Caribbean.3 Outbreaks occurred in 31 states, most commonly California (30), Florida (25), and New York (16). Additionally, 43 (22%) were multistate outbreaks.

Conclusions

Outbreaks from domestic foods decreased, but those from imported foods increased. This makes sense given recent increases in outbreak-prone food imports, such as seafood/fish and produce.

To reduce overall foodborne illness outbreaks, governmental agencies need to:

  • Develop/enforce regulations that promote proper growing, handling, and processing of foods.
  • Strengthen surveillance networks and share standard culture and molecular detection/characterization protocols to identify outbreaks as close to real time as possible.
  • Ensure rapid traceability not only to country of origin but to an exact farm or seafood/fish harvesting entity.
  • Provide rapid public knowledge of outbreaks and origins, plus outbreak-specific recommendations to control/minimize resultant illnesses.

Individuals can help protect themselves by avoiding inadequately washed or incompletely cooked foods or foods of uncertain origin.

Dr. Harrison is professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics, Kansas City, Mo. He said he had no relevant financial disclosures. Email him at pdnews@frontlinemedcom.com.

References

1. MMWR. 2017 Apr 21;66(15):397-403.

2. Emerg Infect Dis. 2017 Mar;23(3):525-8.

3. Technical appendix in Emerg Infect Dis. 2017 Mar;23(3):525-8.

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Are foodborne illness outbreaks more common now, or are we simply better at detection? Have the foods and sources associated with foodborne illness changed? Two recent Centers for Disease Control & Prevention reports provide insight.1,2 In 2016, the Foodborne Diseases Active Surveillance Network (FoodNet) detected 24,029 infections, 5,212 hospitalizations, and 98 fatalities.1 FoodNet has 10 sites serving 49 million people (15% of the U.S. population). These 2016 numbers changed only modestly from the 3 prior years.

The big two

The most frequent 2016 foodborne pathogens were Campylobacter and Salmonella, at approximately 8,000 illnesses each, detected by traditional cultures or culture-independent diagnostic tests (CIDTs). (See table.) CIDTs are relatively new molecular-based, mostly multiplex assays that test for more than a dozen pathogens in one assay.

Dr. Christopher J. Harrison
Campylobacter-contaminated domestic food in 2016 was mostly raw/undercooked poultry or unpasteurized milk/fruit drinks. Campylobacter can be detected in up to 88% of chicken carcasses at processing plants and approximately 50% of raw chicken at grocery stores. However, Campylobacter from imported food most often came from fresh produce.2

Overall, Salmonella originated from diverse sources (eggs, poultry, meat, unpasteurized milk/juice/cheese, or raw fruits/vegetables/spices/nuts). But, in 2016, U.S. Salmonella outbreaks were from eggs, alfalfa sprouts, poultry, pistachios, and organic shake/meal products.

The runners-up

Most of the remainder of the 2016 foodborne illnesses were caused by Shigella, with nearly 3,000 cases; shigatoxin-producing Escherichia coli (STEC), with nearly 2,000 cases; and Cryptosporidium, also with nearly 2,000 cases. (See table.)

Hemolytic uremic syndrome (HUS)

HUS rates, mostly resulting from E. coli 0157 H7 in meat, did not vary from 2013 to 2016, with a total 62 pediatric HUS cases in FoodNet (0.56 /100,000 population). Slightly over half (56%) occurred in children under 5 years old at 1.18 per 100,000 population.

Does CIDT increase detection rates?

Detection of the “big two” did not change from 2013 to 2016 or over the past 2 decades. That said, Campylobacter detection was actually down 11% if considering only culture-confirmed cases. That is, if we do not count detections made exclusively by CIDT.

This is important because CIDT – now supplanting culture in many laboratories – identifies pathogens not likely detected by standard culture because culture is generally selective and CIDT is more sensitive. CIDT can increase detection rates (solo and multiple pathogens), even if illnesses do not really increase. The CDC suggested that this contributed to increased STEC and Yersinia detection in 2016. Some would not have been detected if only culture had been utilized.

Viable bacterial/viral isolates are not available from CIDT. A replicating pathogen is needed to characterize shifting/emerging pathogen strains (for example, analysis for mutations or new pathogens via sequencing or antimicrobial susceptibility testing).

To compensate, some CIDT-using laboratories perform “reflex cultures.” CIDT positive specimens also are cultured to provide viable isolates. However, this adds cost to an already costly CIDT test.

The role of imported food

Surveillance systems, such as the Foodborne Disease Outbreak Surveillance System, also track imported foodborne illness. Despite an approximately 50% decrease in overall U.S. foodborne outbreaks since 2000, imported food-related outbreaks increased to 195 during 2006-2014 from 54 during 1996-2004, with 10,685 illnesses, 1,017 hospitalizations, and 19 deaths since 2009. Also, imported food-related outbreaks rose from a mean 3 per year pre-2000 to a mean 18 per year during 2009-2014. Most imported food outbreaks (86% of total) had three causes: scombroid toxin (42% of total), Salmonella (33%), and hepatitis A virus (11%).

A foreign origin for approximately 19% of U.S.-consumed food makes it unsurprising that imported foods increasingly cause foodborne outbreaks. Much imported food is “outbreak prone.” Perhaps surprising is that a staggering 97% of fish/shellfish, 50% of fresh fruits, and 20% of fresh vegetables are imported, according to 2016 estimates by the U.S. Department of Agriculture.

Most imported food illnesses were from Salmonella (4,421 from 52 outbreaks), Cyclospora (2,533 from 33 outbreaks), hepatitis A virus (1,150 from 11 outbreaks), and Shigella (625 from 6 outbreaks). While eggs, ice cream, and poultry are notorious origins for Salmonella in domestic food, most imported Salmonella were from produce: fruits (26%), seeded vegetables (20%), sprouts (11%), nuts/seeds (10%), spices (7%), and herbs (2%).

Seafood/fish caused 55% of outbreaks but few illnesses per outbreak (median 3 illnesses/outbreak), so only 11% of total illnesses were caused by seafood/fish. In contrast, fresh produce caused only 33% of outbreaks but 84% of illnesses (median 40 illnesses/outbreak).

Geographic source, outbreak locations

The origin was known in 91% of outbreaks. Latin America and the Caribbean were most common, followed by Asia.3 Main contributing countries were Mexico (42 outbreaks), Indonesia (17) and Canada (11).

 

 

Contaminated fish/shellfish originated from all regions except Europe, most commonly from Asia (the majority of fish/shellfish outbreaks were from Indonesia, Vietnam, China, Philippines, Taiwan, and Thailand) with smaller contributions from the Bahamas and Ecuador.

Contaminated produce originated from all regions, mostly (64%) from Mexico and the Americas (Chile, Guatemala, and Honduras). All but one dairy outbreak originated in Latin America/the Caribbean.3 Outbreaks occurred in 31 states, most commonly California (30), Florida (25), and New York (16). Additionally, 43 (22%) were multistate outbreaks.

Conclusions

Outbreaks from domestic foods decreased, but those from imported foods increased. This makes sense given recent increases in outbreak-prone food imports, such as seafood/fish and produce.

To reduce overall foodborne illness outbreaks, governmental agencies need to:

  • Develop/enforce regulations that promote proper growing, handling, and processing of foods.
  • Strengthen surveillance networks and share standard culture and molecular detection/characterization protocols to identify outbreaks as close to real time as possible.
  • Ensure rapid traceability not only to country of origin but to an exact farm or seafood/fish harvesting entity.
  • Provide rapid public knowledge of outbreaks and origins, plus outbreak-specific recommendations to control/minimize resultant illnesses.

Individuals can help protect themselves by avoiding inadequately washed or incompletely cooked foods or foods of uncertain origin.

Dr. Harrison is professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics, Kansas City, Mo. He said he had no relevant financial disclosures. Email him at pdnews@frontlinemedcom.com.

References

1. MMWR. 2017 Apr 21;66(15):397-403.

2. Emerg Infect Dis. 2017 Mar;23(3):525-8.

3. Technical appendix in Emerg Infect Dis. 2017 Mar;23(3):525-8.

 

Are foodborne illness outbreaks more common now, or are we simply better at detection? Have the foods and sources associated with foodborne illness changed? Two recent Centers for Disease Control & Prevention reports provide insight.1,2 In 2016, the Foodborne Diseases Active Surveillance Network (FoodNet) detected 24,029 infections, 5,212 hospitalizations, and 98 fatalities.1 FoodNet has 10 sites serving 49 million people (15% of the U.S. population). These 2016 numbers changed only modestly from the 3 prior years.

The big two

The most frequent 2016 foodborne pathogens were Campylobacter and Salmonella, at approximately 8,000 illnesses each, detected by traditional cultures or culture-independent diagnostic tests (CIDTs). (See table.) CIDTs are relatively new molecular-based, mostly multiplex assays that test for more than a dozen pathogens in one assay.

Dr. Christopher J. Harrison
Campylobacter-contaminated domestic food in 2016 was mostly raw/undercooked poultry or unpasteurized milk/fruit drinks. Campylobacter can be detected in up to 88% of chicken carcasses at processing plants and approximately 50% of raw chicken at grocery stores. However, Campylobacter from imported food most often came from fresh produce.2

Overall, Salmonella originated from diverse sources (eggs, poultry, meat, unpasteurized milk/juice/cheese, or raw fruits/vegetables/spices/nuts). But, in 2016, U.S. Salmonella outbreaks were from eggs, alfalfa sprouts, poultry, pistachios, and organic shake/meal products.

The runners-up

Most of the remainder of the 2016 foodborne illnesses were caused by Shigella, with nearly 3,000 cases; shigatoxin-producing Escherichia coli (STEC), with nearly 2,000 cases; and Cryptosporidium, also with nearly 2,000 cases. (See table.)

Hemolytic uremic syndrome (HUS)

HUS rates, mostly resulting from E. coli 0157 H7 in meat, did not vary from 2013 to 2016, with a total 62 pediatric HUS cases in FoodNet (0.56 /100,000 population). Slightly over half (56%) occurred in children under 5 years old at 1.18 per 100,000 population.

Does CIDT increase detection rates?

Detection of the “big two” did not change from 2013 to 2016 or over the past 2 decades. That said, Campylobacter detection was actually down 11% if considering only culture-confirmed cases. That is, if we do not count detections made exclusively by CIDT.

This is important because CIDT – now supplanting culture in many laboratories – identifies pathogens not likely detected by standard culture because culture is generally selective and CIDT is more sensitive. CIDT can increase detection rates (solo and multiple pathogens), even if illnesses do not really increase. The CDC suggested that this contributed to increased STEC and Yersinia detection in 2016. Some would not have been detected if only culture had been utilized.

Viable bacterial/viral isolates are not available from CIDT. A replicating pathogen is needed to characterize shifting/emerging pathogen strains (for example, analysis for mutations or new pathogens via sequencing or antimicrobial susceptibility testing).

To compensate, some CIDT-using laboratories perform “reflex cultures.” CIDT positive specimens also are cultured to provide viable isolates. However, this adds cost to an already costly CIDT test.

The role of imported food

Surveillance systems, such as the Foodborne Disease Outbreak Surveillance System, also track imported foodborne illness. Despite an approximately 50% decrease in overall U.S. foodborne outbreaks since 2000, imported food-related outbreaks increased to 195 during 2006-2014 from 54 during 1996-2004, with 10,685 illnesses, 1,017 hospitalizations, and 19 deaths since 2009. Also, imported food-related outbreaks rose from a mean 3 per year pre-2000 to a mean 18 per year during 2009-2014. Most imported food outbreaks (86% of total) had three causes: scombroid toxin (42% of total), Salmonella (33%), and hepatitis A virus (11%).

A foreign origin for approximately 19% of U.S.-consumed food makes it unsurprising that imported foods increasingly cause foodborne outbreaks. Much imported food is “outbreak prone.” Perhaps surprising is that a staggering 97% of fish/shellfish, 50% of fresh fruits, and 20% of fresh vegetables are imported, according to 2016 estimates by the U.S. Department of Agriculture.

Most imported food illnesses were from Salmonella (4,421 from 52 outbreaks), Cyclospora (2,533 from 33 outbreaks), hepatitis A virus (1,150 from 11 outbreaks), and Shigella (625 from 6 outbreaks). While eggs, ice cream, and poultry are notorious origins for Salmonella in domestic food, most imported Salmonella were from produce: fruits (26%), seeded vegetables (20%), sprouts (11%), nuts/seeds (10%), spices (7%), and herbs (2%).

Seafood/fish caused 55% of outbreaks but few illnesses per outbreak (median 3 illnesses/outbreak), so only 11% of total illnesses were caused by seafood/fish. In contrast, fresh produce caused only 33% of outbreaks but 84% of illnesses (median 40 illnesses/outbreak).

Geographic source, outbreak locations

The origin was known in 91% of outbreaks. Latin America and the Caribbean were most common, followed by Asia.3 Main contributing countries were Mexico (42 outbreaks), Indonesia (17) and Canada (11).

 

 

Contaminated fish/shellfish originated from all regions except Europe, most commonly from Asia (the majority of fish/shellfish outbreaks were from Indonesia, Vietnam, China, Philippines, Taiwan, and Thailand) with smaller contributions from the Bahamas and Ecuador.

Contaminated produce originated from all regions, mostly (64%) from Mexico and the Americas (Chile, Guatemala, and Honduras). All but one dairy outbreak originated in Latin America/the Caribbean.3 Outbreaks occurred in 31 states, most commonly California (30), Florida (25), and New York (16). Additionally, 43 (22%) were multistate outbreaks.

Conclusions

Outbreaks from domestic foods decreased, but those from imported foods increased. This makes sense given recent increases in outbreak-prone food imports, such as seafood/fish and produce.

To reduce overall foodborne illness outbreaks, governmental agencies need to:

  • Develop/enforce regulations that promote proper growing, handling, and processing of foods.
  • Strengthen surveillance networks and share standard culture and molecular detection/characterization protocols to identify outbreaks as close to real time as possible.
  • Ensure rapid traceability not only to country of origin but to an exact farm or seafood/fish harvesting entity.
  • Provide rapid public knowledge of outbreaks and origins, plus outbreak-specific recommendations to control/minimize resultant illnesses.

Individuals can help protect themselves by avoiding inadequately washed or incompletely cooked foods or foods of uncertain origin.

Dr. Harrison is professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics, Kansas City, Mo. He said he had no relevant financial disclosures. Email him at pdnews@frontlinemedcom.com.

References

1. MMWR. 2017 Apr 21;66(15):397-403.

2. Emerg Infect Dis. 2017 Mar;23(3):525-8.

3. Technical appendix in Emerg Infect Dis. 2017 Mar;23(3):525-8.

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