Patients with non–small-cell lung cancer (NSCLC) for whom adjuvant chemotherapy must be delayed for as long as 18 weeks have mortality outcomes that are no worse than those of patients who start chemotherapy soon after surgery, and those who undergo delayed chemotherapy have a significantly lower risk for death than patients who have no chemotherapy at all, investigators report.

A retrospective review of data on 12,473 patients with previously untreated NSCLC showed that there were no significant differences in 5-year overall survival (OS) estimates among patients who started multi-agent chemotherapy at 18-38 days postoperatively, from 39 to 56 days after surgery (the reference interval), or from 57 to 127 days after surgery, reported Daniel J. Boffa, MD, of Yale University, New Haven, Conn., and his colleagues.

Patients with non–small-cell lung cancer (NSCLC) for whom adjuvant chemotherapy must be delayed for as long as 18 weeks have mortality outcomes that are no worse than those of patients who start chemotherapy soon after surgery, and those who undergo delayed chemotherapy have a significantly lower risk for death than patients who have no chemotherapy at all, investigators report.

A retrospective review of data on 12,473 patients with previously untreated NSCLC showed that there were no significant differences in 5-year overall survival (OS) estimates among patients who started multi-agent chemotherapy at 18-38 days postoperatively, from 39 to 56 days after surgery (the reference interval), or from 57 to 127 days after surgery, reported Daniel J. Boffa, MD, of Yale University, New Haven, Conn., and his colleagues.

Patients with non–small-cell lung cancer (NSCLC) for whom adjuvant chemotherapy must be delayed for as long as 18 weeks have mortality outcomes that are no worse than those of patients who start chemotherapy soon after surgery, and those who undergo delayed chemotherapy have a significantly lower risk for death than patients who have no chemotherapy at all, investigators report.

A retrospective review of data on 12,473 patients with previously untreated NSCLC showed that there were no significant differences in 5-year overall survival (OS) estimates among patients who started multi-agent chemotherapy at 18-38 days postoperatively, from 39 to 56 days after surgery (the reference interval), or from 57 to 127 days after surgery, reported Daniel J. Boffa, MD, of Yale University, New Haven, Conn., and his colleagues.

One in seven women suffer with abnormal uterine bleeding during their reproductive years, according to Fraser et al. (Exp Rev Obstet Gynecol. 2009;4:179-89). Heavy menstrual bleeding (menorrhagia) is the most common pattern. Global endometrial ablation has become a very popular surgical technique for women complaining of menorrhagia, disinterested in either medical management or definitive therapy – hysterectomy – or where medical management has failed. With proper patient selection, endometrial ablation yields an 80%-90% success rate in reducing heavy menstrual flow and is associated with a 90% patient satisfaction rate (Cochrane Database Syst Rev. 2009 Oct 7;[4]:CD001501).

Dr. Miller is clinical associate professor at the University of Illinois at Chicago, and past president of the AAGL and the International Society for Gynecologic Endoscopy. He is a reproductive endocrinologist and minimally invasive gynecologic surgeon in private practice in Naperville and Schaumburg, Ill.; director of minimally invasive gynecologic surgery and the director of the AAGL/SRS fellowship in minimally invasive gynecologic surgery at Advocate Lutheran General Hospital, Park Ridge, Ill.; and the medical editor of this column, Master Class. He reported being a subinvestigator on a study sponsored by Channel Medsystems. Email him at [email protected].

Why failures occur and how to correct them

BY MORRIS WORTMAN, MD

Since the introduction almost 20 years ago of devices for nonresectoscopic – or “global” – endometrial ablation, the procedure has been widely adopted as the treatment of choice for abnormal uterine bleeding that is refractory to medical management.

Between 400,000 and 500,000 endometrial ablations are done in the United States every year in women who have completed childbearing, and it probably won’t be long before the procedure surpasses hysterectomy in prevalence for the management of abnormal bleeding.

Causes of EA failure

Untreated uterine cornua, and untreated submucous leiomyomas and endometrial polyps, are common causes of EA failure. Among the 50 women included in our retrospective review of ultrasound-guided reoperative hysteroscopy after GEA failure, 44% had intraoperative evidence of untreated cornua and nearly one-fourth had persistent or enlarging submucous leiomyomas.

Contrary to what some believe, most endometrial ablations will not adequately destroy submucous or intramural leiomyomas. Therefore, we recommend that these fibroids be entirely removed immediately before EA.

Moreover, GEA will not always provide adequate thermal destruction to the entire endometrial cavity. The cornua regions are particularly at risk; they are difficult to reach under ideal circumstances, and especially difficult to treat in patients who have a uterine septum or a T-shaped uterus (with the ostia and cornua deeply recessed). We have also seen late-onset EA failures in patients with an extended uterine transverse diameter. The limits of GEA are greatest when a device with a fixed configuration or geometry is used.

A history of abnormal hysteroscopy or other evidence of such anatomic distortions are therefore among the reported risk factors for GEA failure (J Minim Invasive Gynecol. 2015 Mar-Apr;22[3]:323-31). A history of tubal ligation also confers risk; the procedure further increases susceptibility for failure when functioning endometrial tissue remains or regrows at the cornua, because any retrograde menstrual bleeding that occurs will be constrained by the obstructed proximal portion of the fallopian tubes.

Obesity is another risk factor for GEA failure in that the condition increases the risk of endometrial cancer, making the need for reliable biopsies in the case of spotting or other signs or symptoms even more important. On the other hand, obesity may also worsen a patient’s status as a candidate for hysterectomy.

There is much to consider with these patients. For some obese patients, GEA may be less risky than hysterectomy while for others, such as those who also have polycystic ovarian syndrome (in whom the risk for developing endometrial cancer is further increased) the scale may tip in favor of hysterectomy.

Age at the time of the primary GEA may be the single most important risk factor for GEA failure and is an important predictor of success in patient selection. Numerous investigators have shown that women younger than 35 years of age at the time of their EA had a significantly increased risk for hysterectomy, compared with women who were at least 45 years old. The younger the patient, the longer the “bridge” to menopause and the greater the likelihood that bridge will fail.

While age is not necessarily a contraindication, it is worthy of serious consideration. We generally discourage GEA for patients younger than 35. We also advise ensuring that each patient undergoing initial EA is highly self-motivated to have a uterine-sparing procedure; if not, symptoms she may experience later will likely drive her toward hysterectomy anyway.

Additionally, we caution against performing GEA in patients who have chronic pelvic pain; these patients tend to have poorer outcomes with any type of hysteroscopic surgery.
 

Diagnosing failed EA

Delayed complications manifest in several ways: Renewed and increasing vaginal bleeding after a period of improvement, cyclic pelvic pain (unilateral, bilateral, or suprapubic), or both bleeding and pain. Some women – likely an underreported number of them – present with postmenopausal bleeding and proceed to have unsuccessful attempts at an endometrial biopsy due to EA-associated endometrial scarring.

The cyclic pelvic pain associated with endometrial persistence or regrowth tends to worsen over time and is often described as sharp or laborlike. In our experience, a description of “laborlike” pain and a history of EA is almost fully predictive of a finding of endometrial growth. Often a hematometra can be demonstrated on transvaginal ultrasound, but this isn’t always the case.

Pain typically precedes bleeding in patients who demonstrate both. In such cases, blood from functioning endometrial tissue or other sources becomes blocked from exiting the uterine cavity by EA-induced intrauterine scarring and contracture. Painful uterine contractions then aim to expel the pooled blood. In other cases of pain – mainly those without significant vaginal bleeding – the pain is often attributed to cornual and central hematometra.

For the majority of EA failures, the diagnosis lies in the history and current symptoms. Unfortunately, the traditional methods of assessing the endometrial cavity have little merit for women presenting with delayed-onset EA complications. A sonographically assisted pelvic examination can be useful in evaluating complications, but the interpretation of ultrasounds in women with a prior EA can be challenging and is often beyond the training of most radiologists and gynecologists.

It is not uncommon for images to be incorrectly interpreted in the emergency department or physicians’ offices as “normal” and for such readings to set off a chain of CT scans, MRIs, laparoscopies, ovarian cystectomies, and other procedures that miss the root causes of pain.

Unfortunately, there is little in the literature that describes and defines ultrasound findings after EA. We do know that sonography should be timed with episodes of pain, and that the absence of a demonstrable hematometra does not exclude a diagnosis of EA failure.
 

Correcting late-onset failures

Our office-based operating room is fitted with side-by-side monitors that enable simultaneous sonographic and hysteroscopic views for correction of GEA failures; the rest of the set-up is similar to that of other operative hysteroscopies. However, we do employ a wide variety of resectoscopes with diameters ranging from 13 to 28 Fr. The smaller-diameter scopes are particularly useful for evaluating postmenopausal bleeding in women with a prior EA.

Courtesy Dr. Morris Wortman

Courtesy Dr. Morris Wortman

Courtesy Dr. Morris Wortman

Dr. Wortman is a clinical associate professor of obstetrics and gynecology at the University of Rochester (N.Y.) and the director of the Center for Menstrual Disorders and Reproductive Choice in Rochester. He reported having no relevant financial disclosures.

One in seven women suffer with abnormal uterine bleeding during their reproductive years, according to Fraser et al. (Exp Rev Obstet Gynecol. 2009;4:179-89). Heavy menstrual bleeding (menorrhagia) is the most common pattern. Global endometrial ablation has become a very popular surgical technique for women complaining of menorrhagia, disinterested in either medical management or definitive therapy – hysterectomy – or where medical management has failed. With proper patient selection, endometrial ablation yields an 80%-90% success rate in reducing heavy menstrual flow and is associated with a 90% patient satisfaction rate (Cochrane Database Syst Rev. 2009 Oct 7;[4]:CD001501).

Dr. Miller is clinical associate professor at the University of Illinois at Chicago, and past president of the AAGL and the International Society for Gynecologic Endoscopy. He is a reproductive endocrinologist and minimally invasive gynecologic surgeon in private practice in Naperville and Schaumburg, Ill.; director of minimally invasive gynecologic surgery and the director of the AAGL/SRS fellowship in minimally invasive gynecologic surgery at Advocate Lutheran General Hospital, Park Ridge, Ill.; and the medical editor of this column, Master Class. He reported being a subinvestigator on a study sponsored by Channel Medsystems. Email him at [email protected].

Why failures occur and how to correct them

BY MORRIS WORTMAN, MD

Since the introduction almost 20 years ago of devices for nonresectoscopic – or “global” – endometrial ablation, the procedure has been widely adopted as the treatment of choice for abnormal uterine bleeding that is refractory to medical management.

Between 400,000 and 500,000 endometrial ablations are done in the United States every year in women who have completed childbearing, and it probably won’t be long before the procedure surpasses hysterectomy in prevalence for the management of abnormal bleeding.

Causes of EA failure

Untreated uterine cornua, and untreated submucous leiomyomas and endometrial polyps, are common causes of EA failure. Among the 50 women included in our retrospective review of ultrasound-guided reoperative hysteroscopy after GEA failure, 44% had intraoperative evidence of untreated cornua and nearly one-fourth had persistent or enlarging submucous leiomyomas.

Contrary to what some believe, most endometrial ablations will not adequately destroy submucous or intramural leiomyomas. Therefore, we recommend that these fibroids be entirely removed immediately before EA.

Moreover, GEA will not always provide adequate thermal destruction to the entire endometrial cavity. The cornua regions are particularly at risk; they are difficult to reach under ideal circumstances, and especially difficult to treat in patients who have a uterine septum or a T-shaped uterus (with the ostia and cornua deeply recessed). We have also seen late-onset EA failures in patients with an extended uterine transverse diameter. The limits of GEA are greatest when a device with a fixed configuration or geometry is used.

A history of abnormal hysteroscopy or other evidence of such anatomic distortions are therefore among the reported risk factors for GEA failure (J Minim Invasive Gynecol. 2015 Mar-Apr;22[3]:323-31). A history of tubal ligation also confers risk; the procedure further increases susceptibility for failure when functioning endometrial tissue remains or regrows at the cornua, because any retrograde menstrual bleeding that occurs will be constrained by the obstructed proximal portion of the fallopian tubes.

Obesity is another risk factor for GEA failure in that the condition increases the risk of endometrial cancer, making the need for reliable biopsies in the case of spotting or other signs or symptoms even more important. On the other hand, obesity may also worsen a patient’s status as a candidate for hysterectomy.

There is much to consider with these patients. For some obese patients, GEA may be less risky than hysterectomy while for others, such as those who also have polycystic ovarian syndrome (in whom the risk for developing endometrial cancer is further increased) the scale may tip in favor of hysterectomy.

Age at the time of the primary GEA may be the single most important risk factor for GEA failure and is an important predictor of success in patient selection. Numerous investigators have shown that women younger than 35 years of age at the time of their EA had a significantly increased risk for hysterectomy, compared with women who were at least 45 years old. The younger the patient, the longer the “bridge” to menopause and the greater the likelihood that bridge will fail.

While age is not necessarily a contraindication, it is worthy of serious consideration. We generally discourage GEA for patients younger than 35. We also advise ensuring that each patient undergoing initial EA is highly self-motivated to have a uterine-sparing procedure; if not, symptoms she may experience later will likely drive her toward hysterectomy anyway.

Additionally, we caution against performing GEA in patients who have chronic pelvic pain; these patients tend to have poorer outcomes with any type of hysteroscopic surgery.
 

Diagnosing failed EA

Delayed complications manifest in several ways: Renewed and increasing vaginal bleeding after a period of improvement, cyclic pelvic pain (unilateral, bilateral, or suprapubic), or both bleeding and pain. Some women – likely an underreported number of them – present with postmenopausal bleeding and proceed to have unsuccessful attempts at an endometrial biopsy due to EA-associated endometrial scarring.

The cyclic pelvic pain associated with endometrial persistence or regrowth tends to worsen over time and is often described as sharp or laborlike. In our experience, a description of “laborlike” pain and a history of EA is almost fully predictive of a finding of endometrial growth. Often a hematometra can be demonstrated on transvaginal ultrasound, but this isn’t always the case.

Pain typically precedes bleeding in patients who demonstrate both. In such cases, blood from functioning endometrial tissue or other sources becomes blocked from exiting the uterine cavity by EA-induced intrauterine scarring and contracture. Painful uterine contractions then aim to expel the pooled blood. In other cases of pain – mainly those without significant vaginal bleeding – the pain is often attributed to cornual and central hematometra.

For the majority of EA failures, the diagnosis lies in the history and current symptoms. Unfortunately, the traditional methods of assessing the endometrial cavity have little merit for women presenting with delayed-onset EA complications. A sonographically assisted pelvic examination can be useful in evaluating complications, but the interpretation of ultrasounds in women with a prior EA can be challenging and is often beyond the training of most radiologists and gynecologists.

It is not uncommon for images to be incorrectly interpreted in the emergency department or physicians’ offices as “normal” and for such readings to set off a chain of CT scans, MRIs, laparoscopies, ovarian cystectomies, and other procedures that miss the root causes of pain.

Unfortunately, there is little in the literature that describes and defines ultrasound findings after EA. We do know that sonography should be timed with episodes of pain, and that the absence of a demonstrable hematometra does not exclude a diagnosis of EA failure.
 

Correcting late-onset failures

Our office-based operating room is fitted with side-by-side monitors that enable simultaneous sonographic and hysteroscopic views for correction of GEA failures; the rest of the set-up is similar to that of other operative hysteroscopies. However, we do employ a wide variety of resectoscopes with diameters ranging from 13 to 28 Fr. The smaller-diameter scopes are particularly useful for evaluating postmenopausal bleeding in women with a prior EA.

Courtesy Dr. Morris Wortman

Courtesy Dr. Morris Wortman

Courtesy Dr. Morris Wortman

Dr. Wortman is a clinical associate professor of obstetrics and gynecology at the University of Rochester (N.Y.) and the director of the Center for Menstrual Disorders and Reproductive Choice in Rochester. He reported having no relevant financial disclosures.

One in seven women suffer with abnormal uterine bleeding during their reproductive years, according to Fraser et al. (Exp Rev Obstet Gynecol. 2009;4:179-89). Heavy menstrual bleeding (menorrhagia) is the most common pattern. Global endometrial ablation has become a very popular surgical technique for women complaining of menorrhagia, disinterested in either medical management or definitive therapy – hysterectomy – or where medical management has failed. With proper patient selection, endometrial ablation yields an 80%-90% success rate in reducing heavy menstrual flow and is associated with a 90% patient satisfaction rate (Cochrane Database Syst Rev. 2009 Oct 7;[4]:CD001501).

Dr. Miller is clinical associate professor at the University of Illinois at Chicago, and past president of the AAGL and the International Society for Gynecologic Endoscopy. He is a reproductive endocrinologist and minimally invasive gynecologic surgeon in private practice in Naperville and Schaumburg, Ill.; director of minimally invasive gynecologic surgery and the director of the AAGL/SRS fellowship in minimally invasive gynecologic surgery at Advocate Lutheran General Hospital, Park Ridge, Ill.; and the medical editor of this column, Master Class. He reported being a subinvestigator on a study sponsored by Channel Medsystems. Email him at [email protected].

Why failures occur and how to correct them

BY MORRIS WORTMAN, MD

Since the introduction almost 20 years ago of devices for nonresectoscopic – or “global” – endometrial ablation, the procedure has been widely adopted as the treatment of choice for abnormal uterine bleeding that is refractory to medical management.

Between 400,000 and 500,000 endometrial ablations are done in the United States every year in women who have completed childbearing, and it probably won’t be long before the procedure surpasses hysterectomy in prevalence for the management of abnormal bleeding.

Causes of EA failure

Untreated uterine cornua, and untreated submucous leiomyomas and endometrial polyps, are common causes of EA failure. Among the 50 women included in our retrospective review of ultrasound-guided reoperative hysteroscopy after GEA failure, 44% had intraoperative evidence of untreated cornua and nearly one-fourth had persistent or enlarging submucous leiomyomas.

Contrary to what some believe, most endometrial ablations will not adequately destroy submucous or intramural leiomyomas. Therefore, we recommend that these fibroids be entirely removed immediately before EA.

Moreover, GEA will not always provide adequate thermal destruction to the entire endometrial cavity. The cornua regions are particularly at risk; they are difficult to reach under ideal circumstances, and especially difficult to treat in patients who have a uterine septum or a T-shaped uterus (with the ostia and cornua deeply recessed). We have also seen late-onset EA failures in patients with an extended uterine transverse diameter. The limits of GEA are greatest when a device with a fixed configuration or geometry is used.

A history of abnormal hysteroscopy or other evidence of such anatomic distortions are therefore among the reported risk factors for GEA failure (J Minim Invasive Gynecol. 2015 Mar-Apr;22[3]:323-31). A history of tubal ligation also confers risk; the procedure further increases susceptibility for failure when functioning endometrial tissue remains or regrows at the cornua, because any retrograde menstrual bleeding that occurs will be constrained by the obstructed proximal portion of the fallopian tubes.

Obesity is another risk factor for GEA failure in that the condition increases the risk of endometrial cancer, making the need for reliable biopsies in the case of spotting or other signs or symptoms even more important. On the other hand, obesity may also worsen a patient’s status as a candidate for hysterectomy.

There is much to consider with these patients. For some obese patients, GEA may be less risky than hysterectomy while for others, such as those who also have polycystic ovarian syndrome (in whom the risk for developing endometrial cancer is further increased) the scale may tip in favor of hysterectomy.

Age at the time of the primary GEA may be the single most important risk factor for GEA failure and is an important predictor of success in patient selection. Numerous investigators have shown that women younger than 35 years of age at the time of their EA had a significantly increased risk for hysterectomy, compared with women who were at least 45 years old. The younger the patient, the longer the “bridge” to menopause and the greater the likelihood that bridge will fail.

While age is not necessarily a contraindication, it is worthy of serious consideration. We generally discourage GEA for patients younger than 35. We also advise ensuring that each patient undergoing initial EA is highly self-motivated to have a uterine-sparing procedure; if not, symptoms she may experience later will likely drive her toward hysterectomy anyway.

Additionally, we caution against performing GEA in patients who have chronic pelvic pain; these patients tend to have poorer outcomes with any type of hysteroscopic surgery.
 

Diagnosing failed EA

Delayed complications manifest in several ways: Renewed and increasing vaginal bleeding after a period of improvement, cyclic pelvic pain (unilateral, bilateral, or suprapubic), or both bleeding and pain. Some women – likely an underreported number of them – present with postmenopausal bleeding and proceed to have unsuccessful attempts at an endometrial biopsy due to EA-associated endometrial scarring.

The cyclic pelvic pain associated with endometrial persistence or regrowth tends to worsen over time and is often described as sharp or laborlike. In our experience, a description of “laborlike” pain and a history of EA is almost fully predictive of a finding of endometrial growth. Often a hematometra can be demonstrated on transvaginal ultrasound, but this isn’t always the case.

Pain typically precedes bleeding in patients who demonstrate both. In such cases, blood from functioning endometrial tissue or other sources becomes blocked from exiting the uterine cavity by EA-induced intrauterine scarring and contracture. Painful uterine contractions then aim to expel the pooled blood. In other cases of pain – mainly those without significant vaginal bleeding – the pain is often attributed to cornual and central hematometra.

For the majority of EA failures, the diagnosis lies in the history and current symptoms. Unfortunately, the traditional methods of assessing the endometrial cavity have little merit for women presenting with delayed-onset EA complications. A sonographically assisted pelvic examination can be useful in evaluating complications, but the interpretation of ultrasounds in women with a prior EA can be challenging and is often beyond the training of most radiologists and gynecologists.

It is not uncommon for images to be incorrectly interpreted in the emergency department or physicians’ offices as “normal” and for such readings to set off a chain of CT scans, MRIs, laparoscopies, ovarian cystectomies, and other procedures that miss the root causes of pain.

Unfortunately, there is little in the literature that describes and defines ultrasound findings after EA. We do know that sonography should be timed with episodes of pain, and that the absence of a demonstrable hematometra does not exclude a diagnosis of EA failure.
 

Correcting late-onset failures

Our office-based operating room is fitted with side-by-side monitors that enable simultaneous sonographic and hysteroscopic views for correction of GEA failures; the rest of the set-up is similar to that of other operative hysteroscopies. However, we do employ a wide variety of resectoscopes with diameters ranging from 13 to 28 Fr. The smaller-diameter scopes are particularly useful for evaluating postmenopausal bleeding in women with a prior EA.

Courtesy Dr. Morris Wortman

Courtesy Dr. Morris Wortman

Courtesy Dr. Morris Wortman

Dr. Wortman is a clinical associate professor of obstetrics and gynecology at the University of Rochester (N.Y.) and the director of the Center for Menstrual Disorders and Reproductive Choice in Rochester. He reported having no relevant financial disclosures.

Editor’s Note: This is the first 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 Inc. The series will cover key topics across the specialty, as well as general test-taking and study tips. This month’s edition of the Board Exam Corner focuses on urinary incontinence.

The literature

The American College of Obstetricians and Gynecologists and the American Urogynecologic Society recently published an updated Practice Bulletin regarding the diagnosis and management of urinary incontinence. Practice Bulletin No. 155 was also a maintenance of certification (MOC) assignment for 2016. The contents of this article are critical as urinary incontinence is a prevalent and treatable condition, and it will likely be part of this year’s board examination. This month’s Board Corner will review the key elements of the updated guidelines.

Let’s begin with a possible medical board question: An 80-year old patient has urinary leakage as a result of severe arthritis and poor vision, and is unable to reach the bathroom in time. What is the diagnosis?

A. Mixed urinary incontinence

B. Extraurethral incontinence

C. Functional incontinence

D. Postural incontinence

E. Ectopic ureter



The answer is C.

Functional incontinence occurs because of cognitive or mobility impairments in the presence of an intact lower urinary tract. The patient in the vignette has “restricted mobility” and a physical impairment that leads to urinary incontinence.

A is incorrect because mixed incontinence is an involuntary loss of urine associated with urgency and with physical exertion.

B and E are incorrect because extraurethral incontinence is urine leakage through channels other than the urethral meatus (e.g., vesicovaginal fistula or ectopic ureter).

D is incorrect because postural incontinence is the involuntary loss of urine associated with change in body positions (e.g., from sitting to standing).


The key points to remember are:

• Urinary incontinence is a prevalent condition that is treatable despite what many women believe.

• There are several types of incontinence but the main types are stress, urgency, and mixed incontinence.

• Basic office evaluation includes urinalysis and postvoid residual, but not urodynamics or cystoscopy.

• Treatment of stress incontinence includes weight loss, fluid management, pelvic floor muscle exercises (with or without assistance from a physical therapist), and suburethral sling or bulking agent injections.

• Treatment of urgency urinary incontinence includes bladder training, fluid management, decreasing caffeine, antimuscarinic and beta-3 agonists, and third-line treatments (botulinum toxin A injection, sacral neuromodulation, or tibial nerve stimulation).

• The mnemonic DIAPPERS is useful in remembering all of the reversible, nongenitourinary (i.e., functional) causes of incontinence.

Test-taking tip of the month

If you finish the test early, take the time to go back to any question for which you made an educated guess. Reread the question carefully. Don’t change your answer unless there is a very good reason for doing so because your first impression is usually the right one. Don’t change an answer just because you have a gut feeling. However, there are good reasons to change your answers when you go back. For instance, consider changing your answer if rereading the question helped you to better understand what is being asked, if you reconsidered and conceptualized a better answer, if you remembered a new piece of information, or if you learned something from a later question that will help you better answer the earlier question.

Reference

Obstet Gynecol. 2015 Nov;126(5): e66-81.
 

Dr. Sam 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.

Editor’s Note: This is the first 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 Inc. The series will cover key topics across the specialty, as well as general test-taking and study tips. This month’s edition of the Board Exam Corner focuses on urinary incontinence.

The literature

The American College of Obstetricians and Gynecologists and the American Urogynecologic Society recently published an updated Practice Bulletin regarding the diagnosis and management of urinary incontinence. Practice Bulletin No. 155 was also a maintenance of certification (MOC) assignment for 2016. The contents of this article are critical as urinary incontinence is a prevalent and treatable condition, and it will likely be part of this year’s board examination. This month’s Board Corner will review the key elements of the updated guidelines.

Let’s begin with a possible medical board question: An 80-year old patient has urinary leakage as a result of severe arthritis and poor vision, and is unable to reach the bathroom in time. What is the diagnosis?

A. Mixed urinary incontinence

B. Extraurethral incontinence

C. Functional incontinence

D. Postural incontinence

E. Ectopic ureter



The answer is C.

Functional incontinence occurs because of cognitive or mobility impairments in the presence of an intact lower urinary tract. The patient in the vignette has “restricted mobility” and a physical impairment that leads to urinary incontinence.

A is incorrect because mixed incontinence is an involuntary loss of urine associated with urgency and with physical exertion.

B and E are incorrect because extraurethral incontinence is urine leakage through channels other than the urethral meatus (e.g., vesicovaginal fistula or ectopic ureter).

D is incorrect because postural incontinence is the involuntary loss of urine associated with change in body positions (e.g., from sitting to standing).


The key points to remember are:

• Urinary incontinence is a prevalent condition that is treatable despite what many women believe.

• There are several types of incontinence but the main types are stress, urgency, and mixed incontinence.

• Basic office evaluation includes urinalysis and postvoid residual, but not urodynamics or cystoscopy.

• Treatment of stress incontinence includes weight loss, fluid management, pelvic floor muscle exercises (with or without assistance from a physical therapist), and suburethral sling or bulking agent injections.

• Treatment of urgency urinary incontinence includes bladder training, fluid management, decreasing caffeine, antimuscarinic and beta-3 agonists, and third-line treatments (botulinum toxin A injection, sacral neuromodulation, or tibial nerve stimulation).

• The mnemonic DIAPPERS is useful in remembering all of the reversible, nongenitourinary (i.e., functional) causes of incontinence.

Test-taking tip of the month

If you finish the test early, take the time to go back to any question for which you made an educated guess. Reread the question carefully. Don’t change your answer unless there is a very good reason for doing so because your first impression is usually the right one. Don’t change an answer just because you have a gut feeling. However, there are good reasons to change your answers when you go back. For instance, consider changing your answer if rereading the question helped you to better understand what is being asked, if you reconsidered and conceptualized a better answer, if you remembered a new piece of information, or if you learned something from a later question that will help you better answer the earlier question.

Reference

Obstet Gynecol. 2015 Nov;126(5): e66-81.
 

Dr. Sam 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.

Editor’s Note: This is the first 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 Inc. The series will cover key topics across the specialty, as well as general test-taking and study tips. This month’s edition of the Board Exam Corner focuses on urinary incontinence.

The literature

The American College of Obstetricians and Gynecologists and the American Urogynecologic Society recently published an updated Practice Bulletin regarding the diagnosis and management of urinary incontinence. Practice Bulletin No. 155 was also a maintenance of certification (MOC) assignment for 2016. The contents of this article are critical as urinary incontinence is a prevalent and treatable condition, and it will likely be part of this year’s board examination. This month’s Board Corner will review the key elements of the updated guidelines.

Let’s begin with a possible medical board question: An 80-year old patient has urinary leakage as a result of severe arthritis and poor vision, and is unable to reach the bathroom in time. What is the diagnosis?

A. Mixed urinary incontinence

B. Extraurethral incontinence

C. Functional incontinence

D. Postural incontinence

E. Ectopic ureter



The answer is C.

Functional incontinence occurs because of cognitive or mobility impairments in the presence of an intact lower urinary tract. The patient in the vignette has “restricted mobility” and a physical impairment that leads to urinary incontinence.

A is incorrect because mixed incontinence is an involuntary loss of urine associated with urgency and with physical exertion.

B and E are incorrect because extraurethral incontinence is urine leakage through channels other than the urethral meatus (e.g., vesicovaginal fistula or ectopic ureter).

D is incorrect because postural incontinence is the involuntary loss of urine associated with change in body positions (e.g., from sitting to standing).


The key points to remember are:

• Urinary incontinence is a prevalent condition that is treatable despite what many women believe.

• There are several types of incontinence but the main types are stress, urgency, and mixed incontinence.

• Basic office evaluation includes urinalysis and postvoid residual, but not urodynamics or cystoscopy.

• Treatment of stress incontinence includes weight loss, fluid management, pelvic floor muscle exercises (with or without assistance from a physical therapist), and suburethral sling or bulking agent injections.

• Treatment of urgency urinary incontinence includes bladder training, fluid management, decreasing caffeine, antimuscarinic and beta-3 agonists, and third-line treatments (botulinum toxin A injection, sacral neuromodulation, or tibial nerve stimulation).

• The mnemonic DIAPPERS is useful in remembering all of the reversible, nongenitourinary (i.e., functional) causes of incontinence.

Test-taking tip of the month

If you finish the test early, take the time to go back to any question for which you made an educated guess. Reread the question carefully. Don’t change your answer unless there is a very good reason for doing so because your first impression is usually the right one. Don’t change an answer just because you have a gut feeling. However, there are good reasons to change your answers when you go back. For instance, consider changing your answer if rereading the question helped you to better understand what is being asked, if you reconsidered and conceptualized a better answer, if you remembered a new piece of information, or if you learned something from a later question that will help you better answer the earlier question.

Reference

Obstet Gynecol. 2015 Nov;126(5): e66-81.
 

Dr. Sam 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.

NEW ORLEANS – A new antisense inhibitor to angiopoietinlike protein 3 (ANGPTL3) reduces lipids in healthy adults with elevated triglyceride levels, according to results of a phase I/IIa ascending-dose trial reported at the American Heart Association scientific sessions.

ANGPTL3 regulates lipid and possibly general metabolism through actions in the liver, gut, muscle, and adipose tissue, explained presenting author Sotirios Tsimikas, MD, an investigator with Ionis Pharmaceuticals, Carlsbad, Calif., and a professor of medicine and director of vascular medicine at the University of California, San Diego. Individuals having loss-of-function mutations in the gene encoding this protein have very low plasma levels of cholesterol and triglycerides.

In the trial, sponsored by Ionis Pharmaceuticals, 32 healthy volunteers with elevated triglyceride levels were treated with various doses of the antisense inhibitor, called IONIS-ANGPTL3-L_Rx, or a placebo, given by weekly subcutaneous injections for 6 weeks.

Results showed that participants treated at the higher-dose levels had a reduction from baseline of 66% in triglycerides, 68% in apoliprotein C-III (ApoC-III), 35% in LDL cholesterol, 36% in total cholesterol, and 40% in non-HDL cholesterol, as well as 25% in HDL cholesterol, Dr. Tsimikas reported. They also had reductions in apolipoprotein B (ApoB).

“All these lipid parameters are really going in the right direction in terms of postulating potential clinical benefit,” he commented.

Safety and tolerability results showed that only a single participant experienced a local injection site adverse event related to the inhibitor (erythema and pruritus). None experienced flulike symptoms, platelet reductions, or serious adverse events, and none left the study because of adverse events.

“Among all known therapies that lower triglycerides, this [IONIS-ANGPTL3-L_Rx] is also associated with a reduction not only in LDL cholesterol levels, but also in ApoB as well, which portends well for future outcomes trials,” noted Dr. Tsimikas.

“We think this is going to be a promising candidate for patients who have uncontrolled LDL cholesterol, elevated triglycerides, and possibly patients who have hepatic steatosis and NASH [nonalcoholic steatohepatitis],” he concluded.

Dr. Tsimikas, who is an employee of and shareholder in the trial’s sponsor, Ionis Pharmaceuticals, discussed his findings in a video interview.

NEW ORLEANS – A new antisense inhibitor to angiopoietinlike protein 3 (ANGPTL3) reduces lipids in healthy adults with elevated triglyceride levels, according to results of a phase I/IIa ascending-dose trial reported at the American Heart Association scientific sessions.

ANGPTL3 regulates lipid and possibly general metabolism through actions in the liver, gut, muscle, and adipose tissue, explained presenting author Sotirios Tsimikas, MD, an investigator with Ionis Pharmaceuticals, Carlsbad, Calif., and a professor of medicine and director of vascular medicine at the University of California, San Diego. Individuals having loss-of-function mutations in the gene encoding this protein have very low plasma levels of cholesterol and triglycerides.

In the trial, sponsored by Ionis Pharmaceuticals, 32 healthy volunteers with elevated triglyceride levels were treated with various doses of the antisense inhibitor, called IONIS-ANGPTL3-L_Rx, or a placebo, given by weekly subcutaneous injections for 6 weeks.

Results showed that participants treated at the higher-dose levels had a reduction from baseline of 66% in triglycerides, 68% in apoliprotein C-III (ApoC-III), 35% in LDL cholesterol, 36% in total cholesterol, and 40% in non-HDL cholesterol, as well as 25% in HDL cholesterol, Dr. Tsimikas reported. They also had reductions in apolipoprotein B (ApoB).

“All these lipid parameters are really going in the right direction in terms of postulating potential clinical benefit,” he commented.

Safety and tolerability results showed that only a single participant experienced a local injection site adverse event related to the inhibitor (erythema and pruritus). None experienced flulike symptoms, platelet reductions, or serious adverse events, and none left the study because of adverse events.

“Among all known therapies that lower triglycerides, this [IONIS-ANGPTL3-L_Rx] is also associated with a reduction not only in LDL cholesterol levels, but also in ApoB as well, which portends well for future outcomes trials,” noted Dr. Tsimikas.

“We think this is going to be a promising candidate for patients who have uncontrolled LDL cholesterol, elevated triglycerides, and possibly patients who have hepatic steatosis and NASH [nonalcoholic steatohepatitis],” he concluded.

Dr. Tsimikas, who is an employee of and shareholder in the trial’s sponsor, Ionis Pharmaceuticals, discussed his findings in a video interview.

NEW ORLEANS – A new antisense inhibitor to angiopoietinlike protein 3 (ANGPTL3) reduces lipids in healthy adults with elevated triglyceride levels, according to results of a phase I/IIa ascending-dose trial reported at the American Heart Association scientific sessions.

ANGPTL3 regulates lipid and possibly general metabolism through actions in the liver, gut, muscle, and adipose tissue, explained presenting author Sotirios Tsimikas, MD, an investigator with Ionis Pharmaceuticals, Carlsbad, Calif., and a professor of medicine and director of vascular medicine at the University of California, San Diego. Individuals having loss-of-function mutations in the gene encoding this protein have very low plasma levels of cholesterol and triglycerides.

In the trial, sponsored by Ionis Pharmaceuticals, 32 healthy volunteers with elevated triglyceride levels were treated with various doses of the antisense inhibitor, called IONIS-ANGPTL3-L_Rx, or a placebo, given by weekly subcutaneous injections for 6 weeks.

Results showed that participants treated at the higher-dose levels had a reduction from baseline of 66% in triglycerides, 68% in apoliprotein C-III (ApoC-III), 35% in LDL cholesterol, 36% in total cholesterol, and 40% in non-HDL cholesterol, as well as 25% in HDL cholesterol, Dr. Tsimikas reported. They also had reductions in apolipoprotein B (ApoB).

“All these lipid parameters are really going in the right direction in terms of postulating potential clinical benefit,” he commented.

Safety and tolerability results showed that only a single participant experienced a local injection site adverse event related to the inhibitor (erythema and pruritus). None experienced flulike symptoms, platelet reductions, or serious adverse events, and none left the study because of adverse events.

“Among all known therapies that lower triglycerides, this [IONIS-ANGPTL3-L_Rx] is also associated with a reduction not only in LDL cholesterol levels, but also in ApoB as well, which portends well for future outcomes trials,” noted Dr. Tsimikas.

“We think this is going to be a promising candidate for patients who have uncontrolled LDL cholesterol, elevated triglycerides, and possibly patients who have hepatic steatosis and NASH [nonalcoholic steatohepatitis],” he concluded.

Dr. Tsimikas, who is an employee of and shareholder in the trial’s sponsor, Ionis Pharmaceuticals, discussed his findings in a video interview.

Why start this new column on mental health with an article that focuses on sexual health? Surely that is the domain of family practice, urology, gynecology, endocrinology, or some other discipline. While it is true that all these disciplines and many others are central to the diagnosis and treatment of sexual health, mental health providers need to be an integral part of the conversations.

I have a problem with arbitrarily separating mental health and behavioral health from physical health. Mental health is directly affected by physical health and vice versa. If a woman has a urinary tract infection, she is not feeling mentally or sexually healthy. If a man has erectile dysfunction (ED), he seldom is at the top of his game emotionally. For our war-wounded who lack limbs or who have genitourinary injuries, optimal sexual functioning can be a challenge.

I am probably preaching to the choir here, so I will not belabor the point. However, I will develop this point by using lessons learned from combat-injured service members, the psychiatric adverse effects (AEs) of commonly used psychiatric medications, and most important, asking about sexual health as part of taking a mental health history.

The War-Wounded

Since 9/11, 2.7 million U.S. service members have served in wars. Much discussion has been focused on posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI), the invisible wounds of war. Probably about 25% of service members who have been deployed have PTSD, and about 300,000 service members have TBI.¹ About 50,000 have other physical injuries. These injuries directly affect intimate relationships.

The signature weapon of the wars in Iraq and Afghanistan was the bomb, or improvised explosive device. Motor vehicle accidents and gunshot wounds also have added to the myriad of injuries. Physical war wounds involve sexual functioning. These include, but are not limited to, lower extremity amputations, genitourinary injuries, and facial disfigurement or burns. All of these may involve multiple surgeries, pain, and disability and can significantly impact self-esteem.

One of the many lessons I have learned in putting together my most recent book, Intimacy Post Injury: Combat Trauma and Sexual Health, is that there is a void in the recent general medical and popular literature about optimizing sexual health in those with injuries or diseases.² The majority of wounded warriors are men, but injuries happen to women service members as well. Of course, sexual assault causes severe harm to intimate relationships as well.

At this time, most injured personnel are still in the Military Health System (MHS) or have transitioned to the VHA. However, many service members also will be treated in the civilian health system.

Psychiatric Medications and Sexual Adverse Effects

The treatment of PTSD, depression, and other psychiatric conditions often involves medications that have sexual AEs. Sexual AEs usually refer to problems with erectile function (impotence), difficulties with ejaculation, lack of orgasm or desire, or lack of lubrication for women. Selective serotonin reuptake inhibitors (SSRIs) have a very high incidence of sexual AEs, ranging from 30% to 70%.³ When I speak with clinicians about their anecdotal experience, the percentage always is high, usually more than 50%. Other psychiatric medications, such as antipsychotics, older antidepressants, and stimulants also have sexual AEs, and narcotics are notorious for their sexual AEs.

Fortunately, many solutions exist. For SSRIs, the solutions include lowering the dose of the offending agent, switching to another agent, drug holidays, or adding other medications, such as bupropion or cyproheptadine. Family practice and other physicians are very familiar with phosphodiesterase inhibitors, such as sildenafil, tadalafil, and vardenafil. Although these medications have AEs and are very expensive, they work well for impotence.

Other solutions are nonpharmacologic: Setting aside time for intimacy can be crucial. Gels and creams can help with lubrication. Communication with providers and between partners and families is the most important ingredient.

Asking About Sexual Health

I encourage all medical personnel who treat active-duty service members or veterans to (1) discuss sexual health with their patients; (2) learn the basics of how to evaluate, treat, or refer ED, including SSRI AEs; and (3) understand how to discuss the effects of physical injury, pain, and disability on sexual functioning.

The conversation should touch on sexual activity, satisfaction with intimacy, exposure to sexually transmitted diseases, and if appropriate, previous sexual abuse. The appropriate time and place for a conversation about sexual health depends on the setting. In the outpatient setting, I bring up the subject after I ask about sleep and appetite and before I ask about suicidal and homicidal thoughts; others may choose elsewhere in the patient history. However, asking about sexual issues may or may not be appropriate in an emergency department situation.

Providers often are uncomfortable with asking about sexual issues, perhaps more so if they are young and female and the patient is older and male. Therefore, I encourage expanded training in medical school and throughout residency.

Sexual Difficulties and Suicide

In the military, the suicide rate has been rising from about 10 per 100,000 per year in 2004 to about 20 per 20,000 in this decade.^4,5 According to the VA Office of Suicide Prevention, about 20 veterans die by suicide daily.⁶ One question that has received little attention is the relationship between sexual difficulties and suicide. Although there has been an important focus on causes of suicide in the military and veterans, little is known about the important issue of how many service members die by suicide because of impotence.

We do know a lot about the big picture as to why service members die by suicide. In about two-thirds of the completed suicides, there were relationship issues. In addition, there are often legal, occupational, and financial difficulties. About two-thirds of service members die by suicide using firearms. Jumping and strangulation are other common methods.^4,5

But there is much we do not know. What percentage of relationship difficulties are related to sexual dysfunction? Is ED the straw that breaks the camel’s back and leads to the shot to the chest? Other subjects outside the scope of this column (but included in Intimacy Post Injury) include sexual therapy, fertility, adaptations for those with disabilities, reproductive AEs of toxin exposure, and surgeries that include penile transplantation.

My hypothesis is that sexual problems, specifically ED or impotence, contribute to feelings of failure and inadequacy and thus to suicidal or homicidal thoughts.

Conclusion

Health care providers do not always talk to patients about their sexual health and may barely mention the sexual AEs of psychiatric or other medications. In whatever setting you practice, you should not neglect asking questions about sexual health, as it is a critical issue for many of our patients and should be for us.

Why start this new column on mental health with an article that focuses on sexual health? Surely that is the domain of family practice, urology, gynecology, endocrinology, or some other discipline. While it is true that all these disciplines and many others are central to the diagnosis and treatment of sexual health, mental health providers need to be an integral part of the conversations.

I have a problem with arbitrarily separating mental health and behavioral health from physical health. Mental health is directly affected by physical health and vice versa. If a woman has a urinary tract infection, she is not feeling mentally or sexually healthy. If a man has erectile dysfunction (ED), he seldom is at the top of his game emotionally. For our war-wounded who lack limbs or who have genitourinary injuries, optimal sexual functioning can be a challenge.

I am probably preaching to the choir here, so I will not belabor the point. However, I will develop this point by using lessons learned from combat-injured service members, the psychiatric adverse effects (AEs) of commonly used psychiatric medications, and most important, asking about sexual health as part of taking a mental health history.

The War-Wounded

Since 9/11, 2.7 million U.S. service members have served in wars. Much discussion has been focused on posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI), the invisible wounds of war. Probably about 25% of service members who have been deployed have PTSD, and about 300,000 service members have TBI.¹ About 50,000 have other physical injuries. These injuries directly affect intimate relationships.

The signature weapon of the wars in Iraq and Afghanistan was the bomb, or improvised explosive device. Motor vehicle accidents and gunshot wounds also have added to the myriad of injuries. Physical war wounds involve sexual functioning. These include, but are not limited to, lower extremity amputations, genitourinary injuries, and facial disfigurement or burns. All of these may involve multiple surgeries, pain, and disability and can significantly impact self-esteem.

One of the many lessons I have learned in putting together my most recent book, Intimacy Post Injury: Combat Trauma and Sexual Health, is that there is a void in the recent general medical and popular literature about optimizing sexual health in those with injuries or diseases.² The majority of wounded warriors are men, but injuries happen to women service members as well. Of course, sexual assault causes severe harm to intimate relationships as well.

At this time, most injured personnel are still in the Military Health System (MHS) or have transitioned to the VHA. However, many service members also will be treated in the civilian health system.

Psychiatric Medications and Sexual Adverse Effects

The treatment of PTSD, depression, and other psychiatric conditions often involves medications that have sexual AEs. Sexual AEs usually refer to problems with erectile function (impotence), difficulties with ejaculation, lack of orgasm or desire, or lack of lubrication for women. Selective serotonin reuptake inhibitors (SSRIs) have a very high incidence of sexual AEs, ranging from 30% to 70%.³ When I speak with clinicians about their anecdotal experience, the percentage always is high, usually more than 50%. Other psychiatric medications, such as antipsychotics, older antidepressants, and stimulants also have sexual AEs, and narcotics are notorious for their sexual AEs.

Fortunately, many solutions exist. For SSRIs, the solutions include lowering the dose of the offending agent, switching to another agent, drug holidays, or adding other medications, such as bupropion or cyproheptadine. Family practice and other physicians are very familiar with phosphodiesterase inhibitors, such as sildenafil, tadalafil, and vardenafil. Although these medications have AEs and are very expensive, they work well for impotence.

Other solutions are nonpharmacologic: Setting aside time for intimacy can be crucial. Gels and creams can help with lubrication. Communication with providers and between partners and families is the most important ingredient.

Asking About Sexual Health

I encourage all medical personnel who treat active-duty service members or veterans to (1) discuss sexual health with their patients; (2) learn the basics of how to evaluate, treat, or refer ED, including SSRI AEs; and (3) understand how to discuss the effects of physical injury, pain, and disability on sexual functioning.

The conversation should touch on sexual activity, satisfaction with intimacy, exposure to sexually transmitted diseases, and if appropriate, previous sexual abuse. The appropriate time and place for a conversation about sexual health depends on the setting. In the outpatient setting, I bring up the subject after I ask about sleep and appetite and before I ask about suicidal and homicidal thoughts; others may choose elsewhere in the patient history. However, asking about sexual issues may or may not be appropriate in an emergency department situation.

Providers often are uncomfortable with asking about sexual issues, perhaps more so if they are young and female and the patient is older and male. Therefore, I encourage expanded training in medical school and throughout residency.

Sexual Difficulties and Suicide

In the military, the suicide rate has been rising from about 10 per 100,000 per year in 2004 to about 20 per 20,000 in this decade.^4,5 According to the VA Office of Suicide Prevention, about 20 veterans die by suicide daily.⁶ One question that has received little attention is the relationship between sexual difficulties and suicide. Although there has been an important focus on causes of suicide in the military and veterans, little is known about the important issue of how many service members die by suicide because of impotence.

We do know a lot about the big picture as to why service members die by suicide. In about two-thirds of the completed suicides, there were relationship issues. In addition, there are often legal, occupational, and financial difficulties. About two-thirds of service members die by suicide using firearms. Jumping and strangulation are other common methods.^4,5

But there is much we do not know. What percentage of relationship difficulties are related to sexual dysfunction? Is ED the straw that breaks the camel’s back and leads to the shot to the chest? Other subjects outside the scope of this column (but included in Intimacy Post Injury) include sexual therapy, fertility, adaptations for those with disabilities, reproductive AEs of toxin exposure, and surgeries that include penile transplantation.

My hypothesis is that sexual problems, specifically ED or impotence, contribute to feelings of failure and inadequacy and thus to suicidal or homicidal thoughts.

Conclusion

Health care providers do not always talk to patients about their sexual health and may barely mention the sexual AEs of psychiatric or other medications. In whatever setting you practice, you should not neglect asking questions about sexual health, as it is a critical issue for many of our patients and should be for us.

Why start this new column on mental health with an article that focuses on sexual health? Surely that is the domain of family practice, urology, gynecology, endocrinology, or some other discipline. While it is true that all these disciplines and many others are central to the diagnosis and treatment of sexual health, mental health providers need to be an integral part of the conversations.

I have a problem with arbitrarily separating mental health and behavioral health from physical health. Mental health is directly affected by physical health and vice versa. If a woman has a urinary tract infection, she is not feeling mentally or sexually healthy. If a man has erectile dysfunction (ED), he seldom is at the top of his game emotionally. For our war-wounded who lack limbs or who have genitourinary injuries, optimal sexual functioning can be a challenge.

I am probably preaching to the choir here, so I will not belabor the point. However, I will develop this point by using lessons learned from combat-injured service members, the psychiatric adverse effects (AEs) of commonly used psychiatric medications, and most important, asking about sexual health as part of taking a mental health history.

The War-Wounded

Since 9/11, 2.7 million U.S. service members have served in wars. Much discussion has been focused on posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI), the invisible wounds of war. Probably about 25% of service members who have been deployed have PTSD, and about 300,000 service members have TBI.¹ About 50,000 have other physical injuries. These injuries directly affect intimate relationships.

The signature weapon of the wars in Iraq and Afghanistan was the bomb, or improvised explosive device. Motor vehicle accidents and gunshot wounds also have added to the myriad of injuries. Physical war wounds involve sexual functioning. These include, but are not limited to, lower extremity amputations, genitourinary injuries, and facial disfigurement or burns. All of these may involve multiple surgeries, pain, and disability and can significantly impact self-esteem.

One of the many lessons I have learned in putting together my most recent book, Intimacy Post Injury: Combat Trauma and Sexual Health, is that there is a void in the recent general medical and popular literature about optimizing sexual health in those with injuries or diseases.² The majority of wounded warriors are men, but injuries happen to women service members as well. Of course, sexual assault causes severe harm to intimate relationships as well.

At this time, most injured personnel are still in the Military Health System (MHS) or have transitioned to the VHA. However, many service members also will be treated in the civilian health system.

Psychiatric Medications and Sexual Adverse Effects

The treatment of PTSD, depression, and other psychiatric conditions often involves medications that have sexual AEs. Sexual AEs usually refer to problems with erectile function (impotence), difficulties with ejaculation, lack of orgasm or desire, or lack of lubrication for women. Selective serotonin reuptake inhibitors (SSRIs) have a very high incidence of sexual AEs, ranging from 30% to 70%.³ When I speak with clinicians about their anecdotal experience, the percentage always is high, usually more than 50%. Other psychiatric medications, such as antipsychotics, older antidepressants, and stimulants also have sexual AEs, and narcotics are notorious for their sexual AEs.

Fortunately, many solutions exist. For SSRIs, the solutions include lowering the dose of the offending agent, switching to another agent, drug holidays, or adding other medications, such as bupropion or cyproheptadine. Family practice and other physicians are very familiar with phosphodiesterase inhibitors, such as sildenafil, tadalafil, and vardenafil. Although these medications have AEs and are very expensive, they work well for impotence.

Other solutions are nonpharmacologic: Setting aside time for intimacy can be crucial. Gels and creams can help with lubrication. Communication with providers and between partners and families is the most important ingredient.

Asking About Sexual Health

I encourage all medical personnel who treat active-duty service members or veterans to (1) discuss sexual health with their patients; (2) learn the basics of how to evaluate, treat, or refer ED, including SSRI AEs; and (3) understand how to discuss the effects of physical injury, pain, and disability on sexual functioning.

The conversation should touch on sexual activity, satisfaction with intimacy, exposure to sexually transmitted diseases, and if appropriate, previous sexual abuse. The appropriate time and place for a conversation about sexual health depends on the setting. In the outpatient setting, I bring up the subject after I ask about sleep and appetite and before I ask about suicidal and homicidal thoughts; others may choose elsewhere in the patient history. However, asking about sexual issues may or may not be appropriate in an emergency department situation.

Providers often are uncomfortable with asking about sexual issues, perhaps more so if they are young and female and the patient is older and male. Therefore, I encourage expanded training in medical school and throughout residency.

Sexual Difficulties and Suicide

In the military, the suicide rate has been rising from about 10 per 100,000 per year in 2004 to about 20 per 20,000 in this decade.^4,5 According to the VA Office of Suicide Prevention, about 20 veterans die by suicide daily.⁶ One question that has received little attention is the relationship between sexual difficulties and suicide. Although there has been an important focus on causes of suicide in the military and veterans, little is known about the important issue of how many service members die by suicide because of impotence.

We do know a lot about the big picture as to why service members die by suicide. In about two-thirds of the completed suicides, there were relationship issues. In addition, there are often legal, occupational, and financial difficulties. About two-thirds of service members die by suicide using firearms. Jumping and strangulation are other common methods.^4,5

But there is much we do not know. What percentage of relationship difficulties are related to sexual dysfunction? Is ED the straw that breaks the camel’s back and leads to the shot to the chest? Other subjects outside the scope of this column (but included in Intimacy Post Injury) include sexual therapy, fertility, adaptations for those with disabilities, reproductive AEs of toxin exposure, and surgeries that include penile transplantation.

My hypothesis is that sexual problems, specifically ED or impotence, contribute to feelings of failure and inadequacy and thus to suicidal or homicidal thoughts.

Conclusion

Health care providers do not always talk to patients about their sexual health and may barely mention the sexual AEs of psychiatric or other medications. In whatever setting you practice, you should not neglect asking questions about sexual health, as it is a critical issue for many of our patients and should be for us.

Child with cancer
Photo by Bill Branson

A yoga program for children with cancer can be carried out during cancer treatment and has quality of life (QOL) benefits for the children as well as their caregivers, according to research published in Rehabilitation Oncology.

However, the program was not feasible for all patients. More than half of those initially enrolled could not complete the study due to treatment toxicity or scheduling conflicts.

Andrea Orsey, MD, of Connecticut Children’s Medical Center in Hartford, and her colleagues conducted this research to evaluate the feasibility and effectiveness of a yoga intervention for children with cancer and their families.

The team began by conducting a survey of 20 children and adolescents with cancer and their parents/guardians.

Survey respondents expressed interest in a yoga program. But they also perceived several barriers to such a program, including concerns about side effects, pain/discomfort, and physical limitations.

With these barriers in mind, Dr Orsey and her colleagues developed a yoga intervention for pediatric cancer patients, delivered by certified yoga instructors.

The program was designed to be performed in a variety of settings and tailored to the children’s physical condition or mobility issues.

A pilot evaluation included 10 children with cancer and their caregivers. Twenty-two patient/caregiver pairs were actually enrolled, but 6 pairs withdrew because of treatment toxicity, and 6 had the study window lapse due to scheduling conflicts.

Although limited by its small size, the study suggested that yoga improved health-related QOL for both caregivers and children.

The children had significant improvements in both social and emotional QOL. They had an overall improvement in fatigue, but this was not statistically significant.

Caregivers had a significant improvement in mental health but not physical health or caregiver burden.

Both caregivers and children said they were satisfied with the yoga program and would recommend it to others.

Dr Orsey and her colleagues hope this pilot study will help guide future efforts to provide yoga to children with cancer and their families.

The researchers noted that a key issue will be coordinating yoga sessions with the medical demands of chemotherapy.

Child with cancer
Photo by Bill Branson

A yoga program for children with cancer can be carried out during cancer treatment and has quality of life (QOL) benefits for the children as well as their caregivers, according to research published in Rehabilitation Oncology.

However, the program was not feasible for all patients. More than half of those initially enrolled could not complete the study due to treatment toxicity or scheduling conflicts.

Andrea Orsey, MD, of Connecticut Children’s Medical Center in Hartford, and her colleagues conducted this research to evaluate the feasibility and effectiveness of a yoga intervention for children with cancer and their families.

The team began by conducting a survey of 20 children and adolescents with cancer and their parents/guardians.

Survey respondents expressed interest in a yoga program. But they also perceived several barriers to such a program, including concerns about side effects, pain/discomfort, and physical limitations.

With these barriers in mind, Dr Orsey and her colleagues developed a yoga intervention for pediatric cancer patients, delivered by certified yoga instructors.

The program was designed to be performed in a variety of settings and tailored to the children’s physical condition or mobility issues.

A pilot evaluation included 10 children with cancer and their caregivers. Twenty-two patient/caregiver pairs were actually enrolled, but 6 pairs withdrew because of treatment toxicity, and 6 had the study window lapse due to scheduling conflicts.

Although limited by its small size, the study suggested that yoga improved health-related QOL for both caregivers and children.

The children had significant improvements in both social and emotional QOL. They had an overall improvement in fatigue, but this was not statistically significant.

Caregivers had a significant improvement in mental health but not physical health or caregiver burden.

Both caregivers and children said they were satisfied with the yoga program and would recommend it to others.

Dr Orsey and her colleagues hope this pilot study will help guide future efforts to provide yoga to children with cancer and their families.

The researchers noted that a key issue will be coordinating yoga sessions with the medical demands of chemotherapy.

Child with cancer
Photo by Bill Branson

A yoga program for children with cancer can be carried out during cancer treatment and has quality of life (QOL) benefits for the children as well as their caregivers, according to research published in Rehabilitation Oncology.

However, the program was not feasible for all patients. More than half of those initially enrolled could not complete the study due to treatment toxicity or scheduling conflicts.

Andrea Orsey, MD, of Connecticut Children’s Medical Center in Hartford, and her colleagues conducted this research to evaluate the feasibility and effectiveness of a yoga intervention for children with cancer and their families.

The team began by conducting a survey of 20 children and adolescents with cancer and their parents/guardians.

Survey respondents expressed interest in a yoga program. But they also perceived several barriers to such a program, including concerns about side effects, pain/discomfort, and physical limitations.

With these barriers in mind, Dr Orsey and her colleagues developed a yoga intervention for pediatric cancer patients, delivered by certified yoga instructors.

The program was designed to be performed in a variety of settings and tailored to the children’s physical condition or mobility issues.

A pilot evaluation included 10 children with cancer and their caregivers. Twenty-two patient/caregiver pairs were actually enrolled, but 6 pairs withdrew because of treatment toxicity, and 6 had the study window lapse due to scheduling conflicts.

Although limited by its small size, the study suggested that yoga improved health-related QOL for both caregivers and children.

The children had significant improvements in both social and emotional QOL. They had an overall improvement in fatigue, but this was not statistically significant.

Caregivers had a significant improvement in mental health but not physical health or caregiver burden.

Both caregivers and children said they were satisfied with the yoga program and would recommend it to others.

Dr Orsey and her colleagues hope this pilot study will help guide future efforts to provide yoga to children with cancer and their families.

The researchers noted that a key issue will be coordinating yoga sessions with the medical demands of chemotherapy.

Doctor consults with cancer
patient and her father
Photo by Rhoda Baer

The US may see nearly 1.7 million new cancer cases in 2017 and more than 600,000 cancer-related deaths, according to a report from the American Cancer Society (ACS).

In addition to estimates for 2017, the report, “Cancer Statistics 2017,” includes the most recent data on cancer incidence, mortality, and survival in the US.

The report was published in CA: A Cancer Journal for Clinicians.

The report projects there will be 1,688,780 new cancer cases and 600,920 cancer deaths in the US this year.

This includes:

• 80,500 new cases of lymphoma and 21,210 lymphoma deaths
• 62,130 new cases of leukemia and 24,500 leukemia deaths
• 30,280 new cases of myeloma and 12,590 myeloma deaths.

The report also shows that, from 2004 to 2013, the overall cancer incidence rate was stable in women and declined by about 2% per year in men. From 2005 to 2014, the cancer death rate declined by about 1.5% annually in both men and women.

Overall, the cancer death rate dropped 25% from its peak of 215.1 (per 100,000 population) in 1991 to 161.2 (per 100,000 population) in 2014, the latest year for which data was available. This translates to about 2,143,200 fewer cancer deaths.

“The continuing drops in the cancer death rate are a powerful sign of the potential we have to reduce cancer’s deadly toll,” said Otis W. Brawley, MD, chief medical officer of the ACS.

He said the decrease in cancer death rates is the result of steady reductions in smoking and advances in early detection and treatment. The decrease is driven by decreasing death rates for the 4 major cancer sites—lung, breast, colorectal, and prostate.

The report also shows that racial disparities in cancer death rates continue to decline. The excess risk of cancer death in black men has dropped from 47% in 1990 to 21% in 2014. The black/white disparity declined similarly in women, from a peak of 20% in 1998 to 13% in 2014.

On the other hand, significant gender disparities persist for both cancer incidence and death in the US. For all cancer sites combined, the incidence rate is 20% higher in men than in women, and the cancer death rate is 40% higher in men.

Dr Brawley said the gender gap in cancer mortality largely reflects variation in the distribution of cancers that occur in men and women, much of which is due to differences in the prevalence of cancer risk factors.

The yearly “Cancer Statistics” reports have been published by ACS researchers since 1967 to inform and guide clinicians, investigators, and others in public health in prioritizing efforts to reduce the burden of cancer.

Cancer incidence data for the current report were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics.

Doctor consults with cancer
patient and her father
Photo by Rhoda Baer

The US may see nearly 1.7 million new cancer cases in 2017 and more than 600,000 cancer-related deaths, according to a report from the American Cancer Society (ACS).

In addition to estimates for 2017, the report, “Cancer Statistics 2017,” includes the most recent data on cancer incidence, mortality, and survival in the US.

The report was published in CA: A Cancer Journal for Clinicians.

The report projects there will be 1,688,780 new cancer cases and 600,920 cancer deaths in the US this year.

This includes:

• 80,500 new cases of lymphoma and 21,210 lymphoma deaths
• 62,130 new cases of leukemia and 24,500 leukemia deaths
• 30,280 new cases of myeloma and 12,590 myeloma deaths.

The report also shows that, from 2004 to 2013, the overall cancer incidence rate was stable in women and declined by about 2% per year in men. From 2005 to 2014, the cancer death rate declined by about 1.5% annually in both men and women.

Overall, the cancer death rate dropped 25% from its peak of 215.1 (per 100,000 population) in 1991 to 161.2 (per 100,000 population) in 2014, the latest year for which data was available. This translates to about 2,143,200 fewer cancer deaths.

“The continuing drops in the cancer death rate are a powerful sign of the potential we have to reduce cancer’s deadly toll,” said Otis W. Brawley, MD, chief medical officer of the ACS.

He said the decrease in cancer death rates is the result of steady reductions in smoking and advances in early detection and treatment. The decrease is driven by decreasing death rates for the 4 major cancer sites—lung, breast, colorectal, and prostate.

The report also shows that racial disparities in cancer death rates continue to decline. The excess risk of cancer death in black men has dropped from 47% in 1990 to 21% in 2014. The black/white disparity declined similarly in women, from a peak of 20% in 1998 to 13% in 2014.

On the other hand, significant gender disparities persist for both cancer incidence and death in the US. For all cancer sites combined, the incidence rate is 20% higher in men than in women, and the cancer death rate is 40% higher in men.

Dr Brawley said the gender gap in cancer mortality largely reflects variation in the distribution of cancers that occur in men and women, much of which is due to differences in the prevalence of cancer risk factors.

The yearly “Cancer Statistics” reports have been published by ACS researchers since 1967 to inform and guide clinicians, investigators, and others in public health in prioritizing efforts to reduce the burden of cancer.

Cancer incidence data for the current report were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics.

Doctor consults with cancer
patient and her father
Photo by Rhoda Baer

The US may see nearly 1.7 million new cancer cases in 2017 and more than 600,000 cancer-related deaths, according to a report from the American Cancer Society (ACS).

In addition to estimates for 2017, the report, “Cancer Statistics 2017,” includes the most recent data on cancer incidence, mortality, and survival in the US.

The report was published in CA: A Cancer Journal for Clinicians.

The report projects there will be 1,688,780 new cancer cases and 600,920 cancer deaths in the US this year.

This includes:

• 80,500 new cases of lymphoma and 21,210 lymphoma deaths
• 62,130 new cases of leukemia and 24,500 leukemia deaths
• 30,280 new cases of myeloma and 12,590 myeloma deaths.

The report also shows that, from 2004 to 2013, the overall cancer incidence rate was stable in women and declined by about 2% per year in men. From 2005 to 2014, the cancer death rate declined by about 1.5% annually in both men and women.

Overall, the cancer death rate dropped 25% from its peak of 215.1 (per 100,000 population) in 1991 to 161.2 (per 100,000 population) in 2014, the latest year for which data was available. This translates to about 2,143,200 fewer cancer deaths.

“The continuing drops in the cancer death rate are a powerful sign of the potential we have to reduce cancer’s deadly toll,” said Otis W. Brawley, MD, chief medical officer of the ACS.

He said the decrease in cancer death rates is the result of steady reductions in smoking and advances in early detection and treatment. The decrease is driven by decreasing death rates for the 4 major cancer sites—lung, breast, colorectal, and prostate.

The report also shows that racial disparities in cancer death rates continue to decline. The excess risk of cancer death in black men has dropped from 47% in 1990 to 21% in 2014. The black/white disparity declined similarly in women, from a peak of 20% in 1998 to 13% in 2014.

On the other hand, significant gender disparities persist for both cancer incidence and death in the US. For all cancer sites combined, the incidence rate is 20% higher in men than in women, and the cancer death rate is 40% higher in men.

Dr Brawley said the gender gap in cancer mortality largely reflects variation in the distribution of cancers that occur in men and women, much of which is due to differences in the prevalence of cancer risk factors.

The yearly “Cancer Statistics” reports have been published by ACS researchers since 1967 to inform and guide clinicians, investigators, and others in public health in prioritizing efforts to reduce the burden of cancer.

Cancer incidence data for the current report were collected by the Surveillance, Epidemiology, and End Results Program; the National Program of Cancer Registries; and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics.

Genome testing
Photo courtesy of the
National Institute of
General Medical Sciences

The American Association for Cancer Research (AACR) has announced the first public release of cancer genomic data aggregated through the AACR Project Genomics Evidence Neoplasia Information Exchange (GENIE).

The data set includes nearly 19,000 de-identified genomic records collected from patients who were treated at 8 international institutions, making it one of the largest public cancer genomic data sets released to date.

The release includes data for 59 major cancer types, including leukemias, lymphomas, and multiple myeloma.

The genomic data and a limited amount of linked clinical data for each patient can be accessed via the AACR Project GENIE cBioPortal or from Sage Bionetworks. (Users must create an account for either site to access the data.)

“We are excited to make publicly available this very large set of clinical-grade, next-generation sequencing data obtained during routine patient care,” said Charles L. Sawyers, MD, AACR Project GENIE Steering Committee chairperson.

“These data were generated as part of routine patient care and, without AACR Project GENIE, they would likely never have been shared with the global cancer research community.”

AACR Project GENIE is a multi-phase, international data-sharing project aimed at catalyzing precision oncology through the development of a registry that aggregates and links clinical-grade cancer genomic data with clinical outcomes from tens of thousands of cancer patients treated at multiple institutions.

The newly released data are fully de-identified in compliance with the Health Insurance Portability and Accountability Act (HIPAA).

The data are derived from patients whose tumors were genetically sequenced as part of their care at any of the 8 institutions that participated in the first phase of AACR Project GENIE.

The goal of releasing these data to the cancer research community is to aid new research that will accelerate the pace of progress against cancer.

According to AACR, the data can be used to validate gene signatures of drug response or prognosis, identify new patient populations for drugs that are currently available, and uncover new drug targets and biomarkers.

“I am extremely proud that the American Association for Cancer Research, as the coordinating center for AACR Project GENIE, is delivering on its promise to make these important data publicly available just over a year after unveiling the initiative,” said Margaret Foti, PhD, MD, chief executive officer of the AACR.

To expand the AACR Project GENIE registry, the consortium is accepting applications for new participating centers. Any nonprofit institution that meets certain criteria can submit an application to become a project participant.

For more information on AACR Project GENIE, visit the project website or send an email to [email protected].

Genome testing
Photo courtesy of the
National Institute of
General Medical Sciences

The American Association for Cancer Research (AACR) has announced the first public release of cancer genomic data aggregated through the AACR Project Genomics Evidence Neoplasia Information Exchange (GENIE).

The data set includes nearly 19,000 de-identified genomic records collected from patients who were treated at 8 international institutions, making it one of the largest public cancer genomic data sets released to date.

The release includes data for 59 major cancer types, including leukemias, lymphomas, and multiple myeloma.

The genomic data and a limited amount of linked clinical data for each patient can be accessed via the AACR Project GENIE cBioPortal or from Sage Bionetworks. (Users must create an account for either site to access the data.)

“We are excited to make publicly available this very large set of clinical-grade, next-generation sequencing data obtained during routine patient care,” said Charles L. Sawyers, MD, AACR Project GENIE Steering Committee chairperson.

“These data were generated as part of routine patient care and, without AACR Project GENIE, they would likely never have been shared with the global cancer research community.”

AACR Project GENIE is a multi-phase, international data-sharing project aimed at catalyzing precision oncology through the development of a registry that aggregates and links clinical-grade cancer genomic data with clinical outcomes from tens of thousands of cancer patients treated at multiple institutions.

The newly released data are fully de-identified in compliance with the Health Insurance Portability and Accountability Act (HIPAA).

The data are derived from patients whose tumors were genetically sequenced as part of their care at any of the 8 institutions that participated in the first phase of AACR Project GENIE.

The goal of releasing these data to the cancer research community is to aid new research that will accelerate the pace of progress against cancer.

According to AACR, the data can be used to validate gene signatures of drug response or prognosis, identify new patient populations for drugs that are currently available, and uncover new drug targets and biomarkers.

“I am extremely proud that the American Association for Cancer Research, as the coordinating center for AACR Project GENIE, is delivering on its promise to make these important data publicly available just over a year after unveiling the initiative,” said Margaret Foti, PhD, MD, chief executive officer of the AACR.

To expand the AACR Project GENIE registry, the consortium is accepting applications for new participating centers. Any nonprofit institution that meets certain criteria can submit an application to become a project participant.

For more information on AACR Project GENIE, visit the project website or send an email to [email protected].

Genome testing
Photo courtesy of the
National Institute of
General Medical Sciences

The American Association for Cancer Research (AACR) has announced the first public release of cancer genomic data aggregated through the AACR Project Genomics Evidence Neoplasia Information Exchange (GENIE).

The data set includes nearly 19,000 de-identified genomic records collected from patients who were treated at 8 international institutions, making it one of the largest public cancer genomic data sets released to date.

The release includes data for 59 major cancer types, including leukemias, lymphomas, and multiple myeloma.

The genomic data and a limited amount of linked clinical data for each patient can be accessed via the AACR Project GENIE cBioPortal or from Sage Bionetworks. (Users must create an account for either site to access the data.)

“We are excited to make publicly available this very large set of clinical-grade, next-generation sequencing data obtained during routine patient care,” said Charles L. Sawyers, MD, AACR Project GENIE Steering Committee chairperson.

“These data were generated as part of routine patient care and, without AACR Project GENIE, they would likely never have been shared with the global cancer research community.”

AACR Project GENIE is a multi-phase, international data-sharing project aimed at catalyzing precision oncology through the development of a registry that aggregates and links clinical-grade cancer genomic data with clinical outcomes from tens of thousands of cancer patients treated at multiple institutions.

The newly released data are fully de-identified in compliance with the Health Insurance Portability and Accountability Act (HIPAA).

The data are derived from patients whose tumors were genetically sequenced as part of their care at any of the 8 institutions that participated in the first phase of AACR Project GENIE.

The goal of releasing these data to the cancer research community is to aid new research that will accelerate the pace of progress against cancer.

According to AACR, the data can be used to validate gene signatures of drug response or prognosis, identify new patient populations for drugs that are currently available, and uncover new drug targets and biomarkers.

“I am extremely proud that the American Association for Cancer Research, as the coordinating center for AACR Project GENIE, is delivering on its promise to make these important data publicly available just over a year after unveiling the initiative,” said Margaret Foti, PhD, MD, chief executive officer of the AACR.

To expand the AACR Project GENIE registry, the consortium is accepting applications for new participating centers. Any nonprofit institution that meets certain criteria can submit an application to become a project participant.

For more information on AACR Project GENIE, visit the project website or send an email to [email protected].

Micrograph showing MF

The US Food and Drug Administration (FDA) has lifted the full clinical hold placed on all clinical trials conducted under the investigational new drug application for pacritinib, an oral kinase inhibitor being developed as a treatment for myelofibrosis (MF).

The FDA placed the hold on pacritinib trials in February 2016 after results from 2 phase 3 trials, PERSIST-1 and PERSIST-2, showed excess mortality in patients who received pacritinib.

Both trials suggested pacritinib can be more effective than the best available therapy for MF.

However, interim overall survival results from PERSIST-2 indicated that pacritinib had a detrimental effect on survival, which was consistent with the results from PERSIST-1.

Due to the full clinical hold, CTI BioPharma withdrew the new drug application for pacritinib while reviewing data from PERSIST-2.

When the FDA enacted the hold, the agency recommended that CTI BioPharma conduct dose-exploration studies for pacritinib, submit final study reports and data sets for PERSIST-1 and PERSIST-2, make certain modifications to protocols and study-related documents, and request a meeting with the FDA prior to submitting a response to the full clinical hold.

CTI BioPharma followed the FDA’s recommendations and submitted a response to the hold that included final clinical study reports for PERSIST-1 and PERSIST-2 and a protocol for a dose-exploration trial. 

The trial, PAC203, should enroll up to approximately 105 patients with primary MF who have failed prior ruxolitinib therapy. The goal is to evaluate the safety and the dose-response relationship for efficacy (spleen volume reduction at 24 weeks) of pacritinib at 3 doses: 100 mg once daily, 100 mg twice daily (BID), and 200 mg BID. The 200 mg BID dose regimen was used in PERSIST-2.

CTI BioPharma said it expects to start the trial in the second quarter of 2017.

“We are pleased to resolve the full clinical hold through working diligently with the FDA to provide a comprehensive response to their requests,” said Richard Love, interim president and chief executive officer of CTI BioPharma.

“We look forward to discussing with the FDA the future development of pacritinib. We believe pacritinib can ultimately address the unmet need of patients with myelofibrosis who are ineligible to receive or are not benefitting from the approved JAK1/JAK2 inhibitor, ruxolitinib, as these patients have limited treatment options.”

Micrograph showing MF

The US Food and Drug Administration (FDA) has lifted the full clinical hold placed on all clinical trials conducted under the investigational new drug application for pacritinib, an oral kinase inhibitor being developed as a treatment for myelofibrosis (MF).

The FDA placed the hold on pacritinib trials in February 2016 after results from 2 phase 3 trials, PERSIST-1 and PERSIST-2, showed excess mortality in patients who received pacritinib.

Both trials suggested pacritinib can be more effective than the best available therapy for MF.

However, interim overall survival results from PERSIST-2 indicated that pacritinib had a detrimental effect on survival, which was consistent with the results from PERSIST-1.

Due to the full clinical hold, CTI BioPharma withdrew the new drug application for pacritinib while reviewing data from PERSIST-2.

When the FDA enacted the hold, the agency recommended that CTI BioPharma conduct dose-exploration studies for pacritinib, submit final study reports and data sets for PERSIST-1 and PERSIST-2, make certain modifications to protocols and study-related documents, and request a meeting with the FDA prior to submitting a response to the full clinical hold.

CTI BioPharma followed the FDA’s recommendations and submitted a response to the hold that included final clinical study reports for PERSIST-1 and PERSIST-2 and a protocol for a dose-exploration trial. 

The trial, PAC203, should enroll up to approximately 105 patients with primary MF who have failed prior ruxolitinib therapy. The goal is to evaluate the safety and the dose-response relationship for efficacy (spleen volume reduction at 24 weeks) of pacritinib at 3 doses: 100 mg once daily, 100 mg twice daily (BID), and 200 mg BID. The 200 mg BID dose regimen was used in PERSIST-2.

CTI BioPharma said it expects to start the trial in the second quarter of 2017.

“We are pleased to resolve the full clinical hold through working diligently with the FDA to provide a comprehensive response to their requests,” said Richard Love, interim president and chief executive officer of CTI BioPharma.

“We look forward to discussing with the FDA the future development of pacritinib. We believe pacritinib can ultimately address the unmet need of patients with myelofibrosis who are ineligible to receive or are not benefitting from the approved JAK1/JAK2 inhibitor, ruxolitinib, as these patients have limited treatment options.”

Micrograph showing MF

The US Food and Drug Administration (FDA) has lifted the full clinical hold placed on all clinical trials conducted under the investigational new drug application for pacritinib, an oral kinase inhibitor being developed as a treatment for myelofibrosis (MF).

The FDA placed the hold on pacritinib trials in February 2016 after results from 2 phase 3 trials, PERSIST-1 and PERSIST-2, showed excess mortality in patients who received pacritinib.

Both trials suggested pacritinib can be more effective than the best available therapy for MF.

However, interim overall survival results from PERSIST-2 indicated that pacritinib had a detrimental effect on survival, which was consistent with the results from PERSIST-1.

Due to the full clinical hold, CTI BioPharma withdrew the new drug application for pacritinib while reviewing data from PERSIST-2.

When the FDA enacted the hold, the agency recommended that CTI BioPharma conduct dose-exploration studies for pacritinib, submit final study reports and data sets for PERSIST-1 and PERSIST-2, make certain modifications to protocols and study-related documents, and request a meeting with the FDA prior to submitting a response to the full clinical hold.

CTI BioPharma followed the FDA’s recommendations and submitted a response to the hold that included final clinical study reports for PERSIST-1 and PERSIST-2 and a protocol for a dose-exploration trial. 

The trial, PAC203, should enroll up to approximately 105 patients with primary MF who have failed prior ruxolitinib therapy. The goal is to evaluate the safety and the dose-response relationship for efficacy (spleen volume reduction at 24 weeks) of pacritinib at 3 doses: 100 mg once daily, 100 mg twice daily (BID), and 200 mg BID. The 200 mg BID dose regimen was used in PERSIST-2.

CTI BioPharma said it expects to start the trial in the second quarter of 2017.

“We are pleased to resolve the full clinical hold through working diligently with the FDA to provide a comprehensive response to their requests,” said Richard Love, interim president and chief executive officer of CTI BioPharma.

“We look forward to discussing with the FDA the future development of pacritinib. We believe pacritinib can ultimately address the unmet need of patients with myelofibrosis who are ineligible to receive or are not benefitting from the approved JAK1/JAK2 inhibitor, ruxolitinib, as these patients have limited treatment options.”

A major change in coding for bronchoscopy occurred on January 1, 2017, as moderate (conscious) sedation is now separately identified from the work relative value units (wRVUs) for the bronchoscopy codes. While traditionally the bronchoscopist provided moderate sedation, in recent clinical practice, other individuals often provide the sedation. CMS mandated refinement of separate Current Procedural Terminology (CPT®) codes to account for the work of moderate procedural sedation. In the final rule published in November 2016, CMS removed 0.25 wRVUs from many of the bronchoscopy codes to account for the work of moderate sedation. To be reimbursed appropriately, include a moderate sedation CPT code with all bronchoscopy procedures.

Use codes 99151 and 99155 for patients younger than 5 years. For a patient 5 years or older, when the bronchoscopist provides moderate sedation, report code 99152 for the initial 15 minutes and 99153 for subsequent time in 15-minute increments. For a patient 5 years or older, when a provider other than the bronchoscopist provides moderate sedation, use code 99156 for the initial 15 minutes and 99157 for subsequent time in 15-minute increments. Utilize codes 99156 and 99157 only when a second provider (other than the bronchoscopist) performs moderate sedation in the facility setting (eg, hospital, outpatient hospital/ambulatory surgery center, skilled nursing facility). When the second provider performs these services in the nonfacility setting (eg, physician office, freestanding imaging center), do not report codes 99155, 99156, or 99157. Moderate sedation does not include minimal sedation (anxiolysis), deep sedation, or monitored anesthesia care (00100-01999).

Do not use a moderate sedation code (99151-2 or 99155-6) if providing less than 10 minutes of moderate sedation. As with other time-based codes, use the subsequent codes 99153 and 99157 when moderate sedation lasts 8 minutes or longer than the initial 15 minutes. The time for moderate sedation begins with the administration of the sedating agent and concludes when the continuous face-to-face presence of the bronchoscopist ends after completion of the procedure. Intermittent, re-evaluation of the patient afterward is postservice work and is not included in the time for moderate sedation. For example, if the bronchoscopist provides moderate sedation for 25 minutes in a 65-year-old man, report 99152 (for the initial 15 minutes) and 99153 (for the subsequent 10 minutes). If an individual other than the bronchoscopist provides moderate sedation for 41 minutes in a 57-year-old woman, use 99156 (for the initial 15 minutes) and two units of 99157 (for the subsequent 26 minutes). If a bronchoscopist provides moderate sedation and reports the appropriate codes after January 1, the 0.25 wRVU change will have no financial impact compared with 2016. If a second provider performs the moderate sedation, expect an approximately $8.72 drop in reimbursement per procedure.

A major change in coding for bronchoscopy occurred on January 1, 2017, as moderate (conscious) sedation is now separately identified from the work relative value units (wRVUs) for the bronchoscopy codes. While traditionally the bronchoscopist provided moderate sedation, in recent clinical practice, other individuals often provide the sedation. CMS mandated refinement of separate Current Procedural Terminology (CPT®) codes to account for the work of moderate procedural sedation. In the final rule published in November 2016, CMS removed 0.25 wRVUs from many of the bronchoscopy codes to account for the work of moderate sedation. To be reimbursed appropriately, include a moderate sedation CPT code with all bronchoscopy procedures.

Use codes 99151 and 99155 for patients younger than 5 years. For a patient 5 years or older, when the bronchoscopist provides moderate sedation, report code 99152 for the initial 15 minutes and 99153 for subsequent time in 15-minute increments. For a patient 5 years or older, when a provider other than the bronchoscopist provides moderate sedation, use code 99156 for the initial 15 minutes and 99157 for subsequent time in 15-minute increments. Utilize codes 99156 and 99157 only when a second provider (other than the bronchoscopist) performs moderate sedation in the facility setting (eg, hospital, outpatient hospital/ambulatory surgery center, skilled nursing facility). When the second provider performs these services in the nonfacility setting (eg, physician office, freestanding imaging center), do not report codes 99155, 99156, or 99157. Moderate sedation does not include minimal sedation (anxiolysis), deep sedation, or monitored anesthesia care (00100-01999).

Do not use a moderate sedation code (99151-2 or 99155-6) if providing less than 10 minutes of moderate sedation. As with other time-based codes, use the subsequent codes 99153 and 99157 when moderate sedation lasts 8 minutes or longer than the initial 15 minutes. The time for moderate sedation begins with the administration of the sedating agent and concludes when the continuous face-to-face presence of the bronchoscopist ends after completion of the procedure. Intermittent, re-evaluation of the patient afterward is postservice work and is not included in the time for moderate sedation. For example, if the bronchoscopist provides moderate sedation for 25 minutes in a 65-year-old man, report 99152 (for the initial 15 minutes) and 99153 (for the subsequent 10 minutes). If an individual other than the bronchoscopist provides moderate sedation for 41 minutes in a 57-year-old woman, use 99156 (for the initial 15 minutes) and two units of 99157 (for the subsequent 26 minutes). If a bronchoscopist provides moderate sedation and reports the appropriate codes after January 1, the 0.25 wRVU change will have no financial impact compared with 2016. If a second provider performs the moderate sedation, expect an approximately $8.72 drop in reimbursement per procedure.

A major change in coding for bronchoscopy occurred on January 1, 2017, as moderate (conscious) sedation is now separately identified from the work relative value units (wRVUs) for the bronchoscopy codes. While traditionally the bronchoscopist provided moderate sedation, in recent clinical practice, other individuals often provide the sedation. CMS mandated refinement of separate Current Procedural Terminology (CPT®) codes to account for the work of moderate procedural sedation. In the final rule published in November 2016, CMS removed 0.25 wRVUs from many of the bronchoscopy codes to account for the work of moderate sedation. To be reimbursed appropriately, include a moderate sedation CPT code with all bronchoscopy procedures.

Use codes 99151 and 99155 for patients younger than 5 years. For a patient 5 years or older, when the bronchoscopist provides moderate sedation, report code 99152 for the initial 15 minutes and 99153 for subsequent time in 15-minute increments. For a patient 5 years or older, when a provider other than the bronchoscopist provides moderate sedation, use code 99156 for the initial 15 minutes and 99157 for subsequent time in 15-minute increments. Utilize codes 99156 and 99157 only when a second provider (other than the bronchoscopist) performs moderate sedation in the facility setting (eg, hospital, outpatient hospital/ambulatory surgery center, skilled nursing facility). When the second provider performs these services in the nonfacility setting (eg, physician office, freestanding imaging center), do not report codes 99155, 99156, or 99157. Moderate sedation does not include minimal sedation (anxiolysis), deep sedation, or monitored anesthesia care (00100-01999).

Do not use a moderate sedation code (99151-2 or 99155-6) if providing less than 10 minutes of moderate sedation. As with other time-based codes, use the subsequent codes 99153 and 99157 when moderate sedation lasts 8 minutes or longer than the initial 15 minutes. The time for moderate sedation begins with the administration of the sedating agent and concludes when the continuous face-to-face presence of the bronchoscopist ends after completion of the procedure. Intermittent, re-evaluation of the patient afterward is postservice work and is not included in the time for moderate sedation. For example, if the bronchoscopist provides moderate sedation for 25 minutes in a 65-year-old man, report 99152 (for the initial 15 minutes) and 99153 (for the subsequent 10 minutes). If an individual other than the bronchoscopist provides moderate sedation for 41 minutes in a 57-year-old woman, use 99156 (for the initial 15 minutes) and two units of 99157 (for the subsequent 26 minutes). If a bronchoscopist provides moderate sedation and reports the appropriate codes after January 1, the 0.25 wRVU change will have no financial impact compared with 2016. If a second provider performs the moderate sedation, expect an approximately $8.72 drop in reimbursement per procedure.