Commentary

“THE FDA’S REVIEW OF THE DATA ON OPEN POWER MORCELLATION WAS INADEQUATE”
WILLIAM H. PARKER, MD (AUDIO; NOVEMBER 2014)

Why is traditional open myomectomy acceptable if power morcellation isn’t?
The actions taken by the US Food and Drug Administration (FDA) and medical device companies to limit use of power morcellation have effectively led to a halt in the use of minimally invasive surgery for removal of large uterine fibroids. This would seem to leave open laparotomy as the only viable choice for the conservative removal of these benign tumors in women who choose to retain their uterus for personal, cultural, or childbearing reasons. Or does it?

Any open myomectomy of an intramural or subserosal myoma involves an incision into the uterine serosa and muscularis, thus exposing the surface of the tumor to the peritoneal environment. The mass is then grasped with penetrating instruments and manipulated free of its myometrial attachments with other instruments such as forceps, scissors, and electrocautery devices. Suction instruments are freely employed over the operative field. The gloved digits of the surgeon are frequently used to bluntly dissect the tumor from the surrounding myometrial bed.

Because of the desire to maximize future fertility potential by minimizing adhesions, frequent irrigation is considered by most reproductive surgeons to be a necessary part of good surgical technique. Irrigation hydrates the tissues and carries away blood, but it can be counted on to disperse countless cells from the exposed surface of the tumor. After resection, the tumor is removed from the operative field and handed off, usually to the gloved hand of an assistant who will be handling all of the tools that are used from that point forward. If an abscess is a “dirty case” from the standpoint of the spread of infection, then any myomectomy is a potentially “dirty case” from the standpoint of the spread of neoplasia. Given the fundamental nature of this procedure, there seems to be no way to do a “clean” myomectomy. 

Since any form of myomectomy involves at least as much manipulation of the tumor mass as morcellation, it should be at least as likely as morcellation to spread aberrant cells. An inadvertent exposure of the unprotected surface of a leiomyosarcoma at the time of a traditional open myomectomy is not different in any essential way from the exposure of the surface of the same tumor at the time of a myomectomy followed by any type of morcellation. 

It is logical then that if morcellation can be proscribed by regulation and litigation, myomectomy itself will be proscribed on the exact same lines of reasoning.

Despite the widespread use of either abdominal or minimally invasive myomectomy over the last 75 years, disseminated uterine leiomyosarcoma is now and always has been a rare disease. This fact has always been accounted for in our risk assessments of leiomyoma surgeries. In addition, there is no scientific evidence that power morcellation, nonpowered morcellation, or abdominal myomectomy without morcellation has ever been causative in the spread of even one patient’s leiomyosarcoma. Leiomyosarcoma is by definition capable of disseminating by itself.

No medical authority would recommend total hysterectomy for every patient with any myoma, based on the possibility that any individual patient might be harboring a uterine cancer that can spread. This is, however, the exact evolutionary endpoint of the reasoning of the FDA and our legal system. The device companies are to be the deep pockets of the morcellation lawsuits and physicians will be the deep pockets of future myomectomy lawsuits. Gynecologists have always considered risk/reward factors in decisions regarding myomectomy and morcellation. We have an obligation to defend the reproductive rights of our patients. Lawyers, regulators, and even the corporations that dominate the medical device market are motivated by other concerns.

The practice of modern medicine aggressively challenges clinical decision-making based solely on anecdotal evidence. It has done so for well over a century now. It is one of the few standards that still unites good doctors under the battered and tattered umbrella of our professionalism. Our challenge as modern physicians is to stand fast against our new regulatory masters (as well as their former and future law partners) with their grave misunderstandings of the very character of gynecologic decision-making.
Michael C. Doody, MD, PhD
Knoxville, Tennessee
 

“THE EXTRACORPOREAL C-INCISION TISSUE EXTRACTION (EXCITE) TECHNIQUE”
MIREILLE D. TRUONG, MD, AND ARNOLD P. ADVINCULA, MD (VIDEO; NOVEMBER 2014)

Awesome video!
I tried this technique as outlined in the video—totally awesome! It worked really well! Thanks to the surgeons who came up with it!
Ravindhra Mamilla, MD
Thief River Falls, Minnesota
 

“HOW USEFUL IS RANDOM BIOPSY WHEN NO COLPOSCOPIC LESIONS ARE SEEN?”
ANDREW M. KAUNITZ, MD (EXAMINING THE EVIDENCE; OCTOBER 2014)

Additional clarification would be appreciated
According to Dr. Kaunitz’s summary of the findings of Huh and colleagues,¹ the population group included women with low-grade squamous intraepithelial lesions (LSIL) or high-grade squamous intraepithelial lesions (HSIL) (ie, anything above atypical cells of undetermined significance [ASCUS]), along with women who tested positive for human papillomavirus (HPV) 16/18, regardless of cytology.

It would have been useful to have the LSIL and HSIL populations (independent or dependent of HPV status) broken down into subgroups.

The expert commentary does not indicate whether the 2.7% of biopsy-proven cervical ­intraepithelial neoplasia (CIN) 2 and CIN 3 were predominantly confined to women with HSIL or equally prevalent in the LSIL population.

Without this information, I am not convinced that LSIL requires a random biopsy when colposcopy is adequate and normal, regardless of HPV status.
Jonathan Kew
Maitland, New South Wales, Australia

Reference
1. Huh WK, Sideri M, Stoler M, Zhang G, Feldman R, Behrens CM. Relevance of random biopsy at the transformation zone when colposcopy is negative. Obstet Gynecol. 2014;124(4):670–678.

Are we reverting to past practices?
For someone who has done colposcopy for about 35 years, I find the conclusions of Huh and colleagues nonsensical. If the squamocolumnar junction is visible and an endocervical curettage is done, this is adequate. Performing random biopsies takes us back to the days before we had the colposcope. I was there, and I’m not proud of how we handled abnormal Pap results.

Another issue: If you find severe dysplasia on random biopsy in a 40-year-old woman, how and what do you treat? Is this a case of treating the lab and not the patient? Or is this a case of inadequately trained gynecologists and/or pathologists?
Anton Strocel, MD
Grand Blanc, Michigan
 

Dr. Kaunitz responds
I thank Dr. Kew and Dr. Strocel for their interest in this commentary on the value of random biopsies during colposcopy when lesions are not visualized. Dr. Kew is correct that the authors did not separate findings in women with low-grade versus high-grade intraepithelial cytology. Dr. Strocel refers to the value of ­clinical experience when performing colposcopy. Both the current article by Huh and colleagues,¹ as well an earlier high-quality report by Gage and colleagues,² point out that, even in skilled hands, colposcopy is not as sensitive in detecting CIN as we have believed in the past. These reports present convincing evidence that, regardless of clinical experience, when no lesion is seen at the time of colposcopy, performing one or two random biopsies substantially increases diagnostic yield of clinically actionable (CIN 2 or worse) disease. 

References
1. Huh WK, Sideri M, Stoler M, Zhang G, Feldman R, Behrens CM. Relevance of random biopsy at the transformation zone when colposcopy is negative. Obstet Gynecol. 2014;124(4):670–678.

2. Gage JC, Hanson VW, Abbey K, et al. Number of cervical biopsies and sensitivity of colposcopy. Obstet Gynecol. 2006;108(2):264–272.
 

“CONJUGATED ESTROGEN PLUS BAZEDOXIFENE—A NEW APPROACH TO ESTROGEN THERAPY”
ANNE A. MOORE, DNP, APN (CASES IN MENOPAUSE; OCTOBER 2014)

Why not encourage soy intake?
Thanks for an interesting discussion on conjugated estrogen/bazedoxifene (CE/BZA; Duavee). I note that:

• CE/BZA is manufactured by Pfizer
• Dr. JoAnn Pinkerton, who is interviewed by Anne Moore, DNP, APN, is affiliated with Pfizer, and
• CE/BZA costs $120 per month.

Since menopausal symptoms are caused by the decreased production of ovarian estradiol, why not prescribe estradiol 0.5–1 mg, which costs only $4 monthly?

Another point to consider: Over several decades of providing care to ethnically diverse women, my observation is that Japanese/Korean and Latina women report far fewer hot flushes than their white sisters.

I believe that it is because of their soy and yam intake. I personally eat about 0.25 lb of tofu per week. It can be diced for salad or soup or served with soy sauce, ginger, and bonito (fish) flakes. It can also be crushed and mixed with lean ground beef, pork, chicken, or turkey to make lean, healthy meatloaf.

Tofu is rich in phytoestrogens, lowers cholesterol, and promotes local soy farmers—a win-win situation.
Yasuo Ishida, MD
St. Louis, Missouri
 

‡‡Dr. Barbieri responds
Dr. Ishida raises an important issue of managing conflicts of interest in medical publications. Dr. Ishida notes that, in the past, Dr. Pinkerton was supported by Pfizer, the company that manufactures (CE/BZA, Duavee). Dr. Ishida also points out that, in a recent OBG Management article, Dr. Pinkerton provided her clinical perspective on the use of CE/BZA in practice.

Often, with a new medication, the physicians with the most expertise in using it have helped with key clinical trials. The results of these trials provide the basis for FDA approval of the medication. Prior to FDA approval of a drug, only experts involved in the clinical trial have first-hand experience with the new treatment.

Dr. Pinkerton is an internationally respected expert in the field and provided a balanced overview of CE/BZA and how it might be used in practice. Dr. Pinkerton disclosed that she personally receives no current support from Pfizer, but that she was supported by Pfizer years ago.

This potential conflict of interest was reported in the article.

Dr. Pinkerton responds
I am proud to serve as a key researcher, consultant, and writer for publications exploring the newest hormonal option for menopausal women—CE/BZA. All of my contracting and fees for my research and consulting with Pfizer have been paid through the University of Virginia, not to me personally. This allows me to be involved in innovative women’s health research and disseminate results without the same conflicts as those who receive reimbursements directly from Pfizer. My relationship to any pharmaceutical company with which I am involved is always through my university and disclosed on every paper, presentation, and talk that I give.

The best way to learn about the pros and cons of a product is to be involved in the sentinel research, to have access to all data, including adverse effects, and to be able to evaluate who might be the best candidates for a new product in women’s health.

Although oral estradiol is inexpensive, women with a uterus also need a progestogen to protect against uterine cancer. It appears that the combination of estrogen and synthetic progestins carry a greater risk of breast cancer than estrogen alone. Estradiol is also available as a patch, gel, lotion, and ring but, again, needs to be paired with a progestogen if a woman has a uterus.

This new drug is well established in published randomized clinical trial data as an effective alternative to traditional estrogen-progestogen therapy (EPT) in symptomatic postmenopausal women with a uterus. Results from Selective Estrogens, Menopause, and Response to Therapy (SMART)¹ randomized controlled trials (RCTs) have shown improvements in symptoms similar to those seen with EPT. These include a reduction in hot flash frequency and severity; a reduction in night sweats, with fewer sleep disruptions; and bone loss prevention. The effects on total cholesterol (an increase in triglycerides) and the drug’s mild effect on vulvovaginal atrophy (VVA) also are similar to those observed with EPT. The drug has a neutral effect on breast tenderness, breast density, and the risk of breast cancer.^1,2 It also protects against endometrial hyperplasia and cancer and increases amenorrhea rates. VTE and stroke risks are expected to be similar to traditional oral hormone therapy (HT). The major benefit of CE/BZA, compared with traditional EPT, is the lack of significant breast tenderness and changes in breast density or vaginal bleeding often seen with traditional EPT.³ 

As for the benefits of soy for menopausal women, clinical data imply that phytoestrogens and soy foods may be of benefit for postmenopausal women. According to a recent review article by Messina⁴ (an international authority on phytoestrogens), isoflavone supplements relieve menopausal hot flashes if they have enough of the isoflavone genistein. Soy has shown benefits with regard to ischemic heart disease—by lowering low-density lipoprotein (LDL) levels and providing a source of omega fatty acids. However, no clear effect has been seen with soy for the prevention of bone loss. The effect on breast cancer risk is unclear. Soy binds to estrogen receptors, which could be harmful. However, soy may bind preferentially to estrogen-receptor beta, thus acting more SERM-like or protective, particularly if given during childhood or adolescence.

For any woman, the decision about using a food source, such as tofu, or isoflavone-rich supplements, such as one containing equol, should be based on a discussion with her clinician regarding her individual needs and the risks and benefits of all options.

In our Midlife Clinic at University of Virginia, we discuss over-the-counter products, lifestyle and dietary changes, and nonhormonal and hormonal options with our patients to help them identify the best choices.

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

“THE FDA’S REVIEW OF THE DATA ON OPEN POWER MORCELLATION WAS INADEQUATE”
WILLIAM H. PARKER, MD (AUDIO; NOVEMBER 2014)

Why is traditional open myomectomy acceptable if power morcellation isn’t?
The actions taken by the US Food and Drug Administration (FDA) and medical device companies to limit use of power morcellation have effectively led to a halt in the use of minimally invasive surgery for removal of large uterine fibroids. This would seem to leave open laparotomy as the only viable choice for the conservative removal of these benign tumors in women who choose to retain their uterus for personal, cultural, or childbearing reasons. Or does it?

Any open myomectomy of an intramural or subserosal myoma involves an incision into the uterine serosa and muscularis, thus exposing the surface of the tumor to the peritoneal environment. The mass is then grasped with penetrating instruments and manipulated free of its myometrial attachments with other instruments such as forceps, scissors, and electrocautery devices. Suction instruments are freely employed over the operative field. The gloved digits of the surgeon are frequently used to bluntly dissect the tumor from the surrounding myometrial bed.

Because of the desire to maximize future fertility potential by minimizing adhesions, frequent irrigation is considered by most reproductive surgeons to be a necessary part of good surgical technique. Irrigation hydrates the tissues and carries away blood, but it can be counted on to disperse countless cells from the exposed surface of the tumor. After resection, the tumor is removed from the operative field and handed off, usually to the gloved hand of an assistant who will be handling all of the tools that are used from that point forward. If an abscess is a “dirty case” from the standpoint of the spread of infection, then any myomectomy is a potentially “dirty case” from the standpoint of the spread of neoplasia. Given the fundamental nature of this procedure, there seems to be no way to do a “clean” myomectomy. 

Since any form of myomectomy involves at least as much manipulation of the tumor mass as morcellation, it should be at least as likely as morcellation to spread aberrant cells. An inadvertent exposure of the unprotected surface of a leiomyosarcoma at the time of a traditional open myomectomy is not different in any essential way from the exposure of the surface of the same tumor at the time of a myomectomy followed by any type of morcellation. 

It is logical then that if morcellation can be proscribed by regulation and litigation, myomectomy itself will be proscribed on the exact same lines of reasoning.

Despite the widespread use of either abdominal or minimally invasive myomectomy over the last 75 years, disseminated uterine leiomyosarcoma is now and always has been a rare disease. This fact has always been accounted for in our risk assessments of leiomyoma surgeries. In addition, there is no scientific evidence that power morcellation, nonpowered morcellation, or abdominal myomectomy without morcellation has ever been causative in the spread of even one patient’s leiomyosarcoma. Leiomyosarcoma is by definition capable of disseminating by itself.

No medical authority would recommend total hysterectomy for every patient with any myoma, based on the possibility that any individual patient might be harboring a uterine cancer that can spread. This is, however, the exact evolutionary endpoint of the reasoning of the FDA and our legal system. The device companies are to be the deep pockets of the morcellation lawsuits and physicians will be the deep pockets of future myomectomy lawsuits. Gynecologists have always considered risk/reward factors in decisions regarding myomectomy and morcellation. We have an obligation to defend the reproductive rights of our patients. Lawyers, regulators, and even the corporations that dominate the medical device market are motivated by other concerns.

The practice of modern medicine aggressively challenges clinical decision-making based solely on anecdotal evidence. It has done so for well over a century now. It is one of the few standards that still unites good doctors under the battered and tattered umbrella of our professionalism. Our challenge as modern physicians is to stand fast against our new regulatory masters (as well as their former and future law partners) with their grave misunderstandings of the very character of gynecologic decision-making.
Michael C. Doody, MD, PhD
Knoxville, Tennessee
 

“THE EXTRACORPOREAL C-INCISION TISSUE EXTRACTION (EXCITE) TECHNIQUE”
MIREILLE D. TRUONG, MD, AND ARNOLD P. ADVINCULA, MD (VIDEO; NOVEMBER 2014)

Awesome video!
I tried this technique as outlined in the video—totally awesome! It worked really well! Thanks to the surgeons who came up with it!
Ravindhra Mamilla, MD
Thief River Falls, Minnesota
 

“HOW USEFUL IS RANDOM BIOPSY WHEN NO COLPOSCOPIC LESIONS ARE SEEN?”
ANDREW M. KAUNITZ, MD (EXAMINING THE EVIDENCE; OCTOBER 2014)

Additional clarification would be appreciated
According to Dr. Kaunitz’s summary of the findings of Huh and colleagues,¹ the population group included women with low-grade squamous intraepithelial lesions (LSIL) or high-grade squamous intraepithelial lesions (HSIL) (ie, anything above atypical cells of undetermined significance [ASCUS]), along with women who tested positive for human papillomavirus (HPV) 16/18, regardless of cytology.

It would have been useful to have the LSIL and HSIL populations (independent or dependent of HPV status) broken down into subgroups.

The expert commentary does not indicate whether the 2.7% of biopsy-proven cervical ­intraepithelial neoplasia (CIN) 2 and CIN 3 were predominantly confined to women with HSIL or equally prevalent in the LSIL population.

Without this information, I am not convinced that LSIL requires a random biopsy when colposcopy is adequate and normal, regardless of HPV status.
Jonathan Kew
Maitland, New South Wales, Australia

Reference
1. Huh WK, Sideri M, Stoler M, Zhang G, Feldman R, Behrens CM. Relevance of random biopsy at the transformation zone when colposcopy is negative. Obstet Gynecol. 2014;124(4):670–678.

Are we reverting to past practices?
For someone who has done colposcopy for about 35 years, I find the conclusions of Huh and colleagues nonsensical. If the squamocolumnar junction is visible and an endocervical curettage is done, this is adequate. Performing random biopsies takes us back to the days before we had the colposcope. I was there, and I’m not proud of how we handled abnormal Pap results.

Another issue: If you find severe dysplasia on random biopsy in a 40-year-old woman, how and what do you treat? Is this a case of treating the lab and not the patient? Or is this a case of inadequately trained gynecologists and/or pathologists?
Anton Strocel, MD
Grand Blanc, Michigan
 

Dr. Kaunitz responds
I thank Dr. Kew and Dr. Strocel for their interest in this commentary on the value of random biopsies during colposcopy when lesions are not visualized. Dr. Kew is correct that the authors did not separate findings in women with low-grade versus high-grade intraepithelial cytology. Dr. Strocel refers to the value of ­clinical experience when performing colposcopy. Both the current article by Huh and colleagues,¹ as well an earlier high-quality report by Gage and colleagues,² point out that, even in skilled hands, colposcopy is not as sensitive in detecting CIN as we have believed in the past. These reports present convincing evidence that, regardless of clinical experience, when no lesion is seen at the time of colposcopy, performing one or two random biopsies substantially increases diagnostic yield of clinically actionable (CIN 2 or worse) disease. 

References
1. Huh WK, Sideri M, Stoler M, Zhang G, Feldman R, Behrens CM. Relevance of random biopsy at the transformation zone when colposcopy is negative. Obstet Gynecol. 2014;124(4):670–678.

2. Gage JC, Hanson VW, Abbey K, et al. Number of cervical biopsies and sensitivity of colposcopy. Obstet Gynecol. 2006;108(2):264–272.
 

“CONJUGATED ESTROGEN PLUS BAZEDOXIFENE—A NEW APPROACH TO ESTROGEN THERAPY”
ANNE A. MOORE, DNP, APN (CASES IN MENOPAUSE; OCTOBER 2014)

Why not encourage soy intake?
Thanks for an interesting discussion on conjugated estrogen/bazedoxifene (CE/BZA; Duavee). I note that:

• CE/BZA is manufactured by Pfizer
• Dr. JoAnn Pinkerton, who is interviewed by Anne Moore, DNP, APN, is affiliated with Pfizer, and
• CE/BZA costs $120 per month.

Since menopausal symptoms are caused by the decreased production of ovarian estradiol, why not prescribe estradiol 0.5–1 mg, which costs only $4 monthly?

Another point to consider: Over several decades of providing care to ethnically diverse women, my observation is that Japanese/Korean and Latina women report far fewer hot flushes than their white sisters.

I believe that it is because of their soy and yam intake. I personally eat about 0.25 lb of tofu per week. It can be diced for salad or soup or served with soy sauce, ginger, and bonito (fish) flakes. It can also be crushed and mixed with lean ground beef, pork, chicken, or turkey to make lean, healthy meatloaf.

Tofu is rich in phytoestrogens, lowers cholesterol, and promotes local soy farmers—a win-win situation.
Yasuo Ishida, MD
St. Louis, Missouri
 

‡‡Dr. Barbieri responds
Dr. Ishida raises an important issue of managing conflicts of interest in medical publications. Dr. Ishida notes that, in the past, Dr. Pinkerton was supported by Pfizer, the company that manufactures (CE/BZA, Duavee). Dr. Ishida also points out that, in a recent OBG Management article, Dr. Pinkerton provided her clinical perspective on the use of CE/BZA in practice.

Often, with a new medication, the physicians with the most expertise in using it have helped with key clinical trials. The results of these trials provide the basis for FDA approval of the medication. Prior to FDA approval of a drug, only experts involved in the clinical trial have first-hand experience with the new treatment.

Dr. Pinkerton is an internationally respected expert in the field and provided a balanced overview of CE/BZA and how it might be used in practice. Dr. Pinkerton disclosed that she personally receives no current support from Pfizer, but that she was supported by Pfizer years ago.

This potential conflict of interest was reported in the article.

Dr. Pinkerton responds
I am proud to serve as a key researcher, consultant, and writer for publications exploring the newest hormonal option for menopausal women—CE/BZA. All of my contracting and fees for my research and consulting with Pfizer have been paid through the University of Virginia, not to me personally. This allows me to be involved in innovative women’s health research and disseminate results without the same conflicts as those who receive reimbursements directly from Pfizer. My relationship to any pharmaceutical company with which I am involved is always through my university and disclosed on every paper, presentation, and talk that I give.

The best way to learn about the pros and cons of a product is to be involved in the sentinel research, to have access to all data, including adverse effects, and to be able to evaluate who might be the best candidates for a new product in women’s health.

Although oral estradiol is inexpensive, women with a uterus also need a progestogen to protect against uterine cancer. It appears that the combination of estrogen and synthetic progestins carry a greater risk of breast cancer than estrogen alone. Estradiol is also available as a patch, gel, lotion, and ring but, again, needs to be paired with a progestogen if a woman has a uterus.

This new drug is well established in published randomized clinical trial data as an effective alternative to traditional estrogen-progestogen therapy (EPT) in symptomatic postmenopausal women with a uterus. Results from Selective Estrogens, Menopause, and Response to Therapy (SMART)¹ randomized controlled trials (RCTs) have shown improvements in symptoms similar to those seen with EPT. These include a reduction in hot flash frequency and severity; a reduction in night sweats, with fewer sleep disruptions; and bone loss prevention. The effects on total cholesterol (an increase in triglycerides) and the drug’s mild effect on vulvovaginal atrophy (VVA) also are similar to those observed with EPT. The drug has a neutral effect on breast tenderness, breast density, and the risk of breast cancer.^1,2 It also protects against endometrial hyperplasia and cancer and increases amenorrhea rates. VTE and stroke risks are expected to be similar to traditional oral hormone therapy (HT). The major benefit of CE/BZA, compared with traditional EPT, is the lack of significant breast tenderness and changes in breast density or vaginal bleeding often seen with traditional EPT.³ 

As for the benefits of soy for menopausal women, clinical data imply that phytoestrogens and soy foods may be of benefit for postmenopausal women. According to a recent review article by Messina⁴ (an international authority on phytoestrogens), isoflavone supplements relieve menopausal hot flashes if they have enough of the isoflavone genistein. Soy has shown benefits with regard to ischemic heart disease—by lowering low-density lipoprotein (LDL) levels and providing a source of omega fatty acids. However, no clear effect has been seen with soy for the prevention of bone loss. The effect on breast cancer risk is unclear. Soy binds to estrogen receptors, which could be harmful. However, soy may bind preferentially to estrogen-receptor beta, thus acting more SERM-like or protective, particularly if given during childhood or adolescence.

For any woman, the decision about using a food source, such as tofu, or isoflavone-rich supplements, such as one containing equol, should be based on a discussion with her clinician regarding her individual needs and the risks and benefits of all options.

In our Midlife Clinic at University of Virginia, we discuss over-the-counter products, lifestyle and dietary changes, and nonhormonal and hormonal options with our patients to help them identify the best choices.

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

“THE FDA’S REVIEW OF THE DATA ON OPEN POWER MORCELLATION WAS INADEQUATE”
WILLIAM H. PARKER, MD (AUDIO; NOVEMBER 2014)

Why is traditional open myomectomy acceptable if power morcellation isn’t?
The actions taken by the US Food and Drug Administration (FDA) and medical device companies to limit use of power morcellation have effectively led to a halt in the use of minimally invasive surgery for removal of large uterine fibroids. This would seem to leave open laparotomy as the only viable choice for the conservative removal of these benign tumors in women who choose to retain their uterus for personal, cultural, or childbearing reasons. Or does it?

Any open myomectomy of an intramural or subserosal myoma involves an incision into the uterine serosa and muscularis, thus exposing the surface of the tumor to the peritoneal environment. The mass is then grasped with penetrating instruments and manipulated free of its myometrial attachments with other instruments such as forceps, scissors, and electrocautery devices. Suction instruments are freely employed over the operative field. The gloved digits of the surgeon are frequently used to bluntly dissect the tumor from the surrounding myometrial bed.

Because of the desire to maximize future fertility potential by minimizing adhesions, frequent irrigation is considered by most reproductive surgeons to be a necessary part of good surgical technique. Irrigation hydrates the tissues and carries away blood, but it can be counted on to disperse countless cells from the exposed surface of the tumor. After resection, the tumor is removed from the operative field and handed off, usually to the gloved hand of an assistant who will be handling all of the tools that are used from that point forward. If an abscess is a “dirty case” from the standpoint of the spread of infection, then any myomectomy is a potentially “dirty case” from the standpoint of the spread of neoplasia. Given the fundamental nature of this procedure, there seems to be no way to do a “clean” myomectomy. 

Since any form of myomectomy involves at least as much manipulation of the tumor mass as morcellation, it should be at least as likely as morcellation to spread aberrant cells. An inadvertent exposure of the unprotected surface of a leiomyosarcoma at the time of a traditional open myomectomy is not different in any essential way from the exposure of the surface of the same tumor at the time of a myomectomy followed by any type of morcellation. 

It is logical then that if morcellation can be proscribed by regulation and litigation, myomectomy itself will be proscribed on the exact same lines of reasoning.

Despite the widespread use of either abdominal or minimally invasive myomectomy over the last 75 years, disseminated uterine leiomyosarcoma is now and always has been a rare disease. This fact has always been accounted for in our risk assessments of leiomyoma surgeries. In addition, there is no scientific evidence that power morcellation, nonpowered morcellation, or abdominal myomectomy without morcellation has ever been causative in the spread of even one patient’s leiomyosarcoma. Leiomyosarcoma is by definition capable of disseminating by itself.

No medical authority would recommend total hysterectomy for every patient with any myoma, based on the possibility that any individual patient might be harboring a uterine cancer that can spread. This is, however, the exact evolutionary endpoint of the reasoning of the FDA and our legal system. The device companies are to be the deep pockets of the morcellation lawsuits and physicians will be the deep pockets of future myomectomy lawsuits. Gynecologists have always considered risk/reward factors in decisions regarding myomectomy and morcellation. We have an obligation to defend the reproductive rights of our patients. Lawyers, regulators, and even the corporations that dominate the medical device market are motivated by other concerns.

The practice of modern medicine aggressively challenges clinical decision-making based solely on anecdotal evidence. It has done so for well over a century now. It is one of the few standards that still unites good doctors under the battered and tattered umbrella of our professionalism. Our challenge as modern physicians is to stand fast against our new regulatory masters (as well as their former and future law partners) with their grave misunderstandings of the very character of gynecologic decision-making.
Michael C. Doody, MD, PhD
Knoxville, Tennessee
 

“THE EXTRACORPOREAL C-INCISION TISSUE EXTRACTION (EXCITE) TECHNIQUE”
MIREILLE D. TRUONG, MD, AND ARNOLD P. ADVINCULA, MD (VIDEO; NOVEMBER 2014)

Awesome video!
I tried this technique as outlined in the video—totally awesome! It worked really well! Thanks to the surgeons who came up with it!
Ravindhra Mamilla, MD
Thief River Falls, Minnesota
 

“HOW USEFUL IS RANDOM BIOPSY WHEN NO COLPOSCOPIC LESIONS ARE SEEN?”
ANDREW M. KAUNITZ, MD (EXAMINING THE EVIDENCE; OCTOBER 2014)

Additional clarification would be appreciated
According to Dr. Kaunitz’s summary of the findings of Huh and colleagues,¹ the population group included women with low-grade squamous intraepithelial lesions (LSIL) or high-grade squamous intraepithelial lesions (HSIL) (ie, anything above atypical cells of undetermined significance [ASCUS]), along with women who tested positive for human papillomavirus (HPV) 16/18, regardless of cytology.

It would have been useful to have the LSIL and HSIL populations (independent or dependent of HPV status) broken down into subgroups.

The expert commentary does not indicate whether the 2.7% of biopsy-proven cervical ­intraepithelial neoplasia (CIN) 2 and CIN 3 were predominantly confined to women with HSIL or equally prevalent in the LSIL population.

Without this information, I am not convinced that LSIL requires a random biopsy when colposcopy is adequate and normal, regardless of HPV status.
Jonathan Kew
Maitland, New South Wales, Australia

Reference
1. Huh WK, Sideri M, Stoler M, Zhang G, Feldman R, Behrens CM. Relevance of random biopsy at the transformation zone when colposcopy is negative. Obstet Gynecol. 2014;124(4):670–678.

Are we reverting to past practices?
For someone who has done colposcopy for about 35 years, I find the conclusions of Huh and colleagues nonsensical. If the squamocolumnar junction is visible and an endocervical curettage is done, this is adequate. Performing random biopsies takes us back to the days before we had the colposcope. I was there, and I’m not proud of how we handled abnormal Pap results.

Another issue: If you find severe dysplasia on random biopsy in a 40-year-old woman, how and what do you treat? Is this a case of treating the lab and not the patient? Or is this a case of inadequately trained gynecologists and/or pathologists?
Anton Strocel, MD
Grand Blanc, Michigan
 

Dr. Kaunitz responds
I thank Dr. Kew and Dr. Strocel for their interest in this commentary on the value of random biopsies during colposcopy when lesions are not visualized. Dr. Kew is correct that the authors did not separate findings in women with low-grade versus high-grade intraepithelial cytology. Dr. Strocel refers to the value of ­clinical experience when performing colposcopy. Both the current article by Huh and colleagues,¹ as well an earlier high-quality report by Gage and colleagues,² point out that, even in skilled hands, colposcopy is not as sensitive in detecting CIN as we have believed in the past. These reports present convincing evidence that, regardless of clinical experience, when no lesion is seen at the time of colposcopy, performing one or two random biopsies substantially increases diagnostic yield of clinically actionable (CIN 2 or worse) disease. 

References
1. Huh WK, Sideri M, Stoler M, Zhang G, Feldman R, Behrens CM. Relevance of random biopsy at the transformation zone when colposcopy is negative. Obstet Gynecol. 2014;124(4):670–678.

2. Gage JC, Hanson VW, Abbey K, et al. Number of cervical biopsies and sensitivity of colposcopy. Obstet Gynecol. 2006;108(2):264–272.
 

“CONJUGATED ESTROGEN PLUS BAZEDOXIFENE—A NEW APPROACH TO ESTROGEN THERAPY”
ANNE A. MOORE, DNP, APN (CASES IN MENOPAUSE; OCTOBER 2014)

Why not encourage soy intake?
Thanks for an interesting discussion on conjugated estrogen/bazedoxifene (CE/BZA; Duavee). I note that:

• CE/BZA is manufactured by Pfizer
• Dr. JoAnn Pinkerton, who is interviewed by Anne Moore, DNP, APN, is affiliated with Pfizer, and
• CE/BZA costs $120 per month.

Since menopausal symptoms are caused by the decreased production of ovarian estradiol, why not prescribe estradiol 0.5–1 mg, which costs only $4 monthly?

Another point to consider: Over several decades of providing care to ethnically diverse women, my observation is that Japanese/Korean and Latina women report far fewer hot flushes than their white sisters.

I believe that it is because of their soy and yam intake. I personally eat about 0.25 lb of tofu per week. It can be diced for salad or soup or served with soy sauce, ginger, and bonito (fish) flakes. It can also be crushed and mixed with lean ground beef, pork, chicken, or turkey to make lean, healthy meatloaf.

Tofu is rich in phytoestrogens, lowers cholesterol, and promotes local soy farmers—a win-win situation.
Yasuo Ishida, MD
St. Louis, Missouri
 

‡‡Dr. Barbieri responds
Dr. Ishida raises an important issue of managing conflicts of interest in medical publications. Dr. Ishida notes that, in the past, Dr. Pinkerton was supported by Pfizer, the company that manufactures (CE/BZA, Duavee). Dr. Ishida also points out that, in a recent OBG Management article, Dr. Pinkerton provided her clinical perspective on the use of CE/BZA in practice.

Often, with a new medication, the physicians with the most expertise in using it have helped with key clinical trials. The results of these trials provide the basis for FDA approval of the medication. Prior to FDA approval of a drug, only experts involved in the clinical trial have first-hand experience with the new treatment.

Dr. Pinkerton is an internationally respected expert in the field and provided a balanced overview of CE/BZA and how it might be used in practice. Dr. Pinkerton disclosed that she personally receives no current support from Pfizer, but that she was supported by Pfizer years ago.

This potential conflict of interest was reported in the article.

Dr. Pinkerton responds
I am proud to serve as a key researcher, consultant, and writer for publications exploring the newest hormonal option for menopausal women—CE/BZA. All of my contracting and fees for my research and consulting with Pfizer have been paid through the University of Virginia, not to me personally. This allows me to be involved in innovative women’s health research and disseminate results without the same conflicts as those who receive reimbursements directly from Pfizer. My relationship to any pharmaceutical company with which I am involved is always through my university and disclosed on every paper, presentation, and talk that I give.

The best way to learn about the pros and cons of a product is to be involved in the sentinel research, to have access to all data, including adverse effects, and to be able to evaluate who might be the best candidates for a new product in women’s health.

Although oral estradiol is inexpensive, women with a uterus also need a progestogen to protect against uterine cancer. It appears that the combination of estrogen and synthetic progestins carry a greater risk of breast cancer than estrogen alone. Estradiol is also available as a patch, gel, lotion, and ring but, again, needs to be paired with a progestogen if a woman has a uterus.

This new drug is well established in published randomized clinical trial data as an effective alternative to traditional estrogen-progestogen therapy (EPT) in symptomatic postmenopausal women with a uterus. Results from Selective Estrogens, Menopause, and Response to Therapy (SMART)¹ randomized controlled trials (RCTs) have shown improvements in symptoms similar to those seen with EPT. These include a reduction in hot flash frequency and severity; a reduction in night sweats, with fewer sleep disruptions; and bone loss prevention. The effects on total cholesterol (an increase in triglycerides) and the drug’s mild effect on vulvovaginal atrophy (VVA) also are similar to those observed with EPT. The drug has a neutral effect on breast tenderness, breast density, and the risk of breast cancer.^1,2 It also protects against endometrial hyperplasia and cancer and increases amenorrhea rates. VTE and stroke risks are expected to be similar to traditional oral hormone therapy (HT). The major benefit of CE/BZA, compared with traditional EPT, is the lack of significant breast tenderness and changes in breast density or vaginal bleeding often seen with traditional EPT.³ 

As for the benefits of soy for menopausal women, clinical data imply that phytoestrogens and soy foods may be of benefit for postmenopausal women. According to a recent review article by Messina⁴ (an international authority on phytoestrogens), isoflavone supplements relieve menopausal hot flashes if they have enough of the isoflavone genistein. Soy has shown benefits with regard to ischemic heart disease—by lowering low-density lipoprotein (LDL) levels and providing a source of omega fatty acids. However, no clear effect has been seen with soy for the prevention of bone loss. The effect on breast cancer risk is unclear. Soy binds to estrogen receptors, which could be harmful. However, soy may bind preferentially to estrogen-receptor beta, thus acting more SERM-like or protective, particularly if given during childhood or adolescence.

For any woman, the decision about using a food source, such as tofu, or isoflavone-rich supplements, such as one containing equol, should be based on a discussion with her clinician regarding her individual needs and the risks and benefits of all options.

In our Midlife Clinic at University of Virginia, we discuss over-the-counter products, lifestyle and dietary changes, and nonhormonal and hormonal options with our patients to help them identify the best choices.

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

Dr. Wilkoff gives all the good reasons for NOT allowing one’s son to play football in his Letters From Maine column entitled “Your son and football” in the December 2014 issue of Pediatric News, and then rationalizes the opposite. As society evolves from gladiators killing their defeated opponents to abolishing boxing as a college sport, so too should we encourage our children to engage in safer sports. Soccer without head-butting and hockey without fighting and body checking would be a good start. There’s no way to make football safe. It just gets more dangerous, as 350-pound gorillas run smack-dab into each other. But humans evolve slowly. We have not been down very long from the trees in evolutionary terms, when the “accepted” way to get a female mate was to club her senseless and carry her off (as the chroniclers of primitive societies have repeatedly shown). Nor do we tolerate dueling, or drawing and quartering or torture any longer. Watching the development of MMA (mixed marital arts) and female boxing just goes to show how primitive and inconsistent we can still be. So, just like Dr. Wilkoff, I confess to being inconsistent, and addicted to watching the genius play of the Aaron Rodgers and Peyton Mannings of football. Maybe we just need a few more centuries to evolve into a civilized society, a bit of help from female leadership to encourage alternative sports to develop. This retired pediatrician, who also was a team football physician, and who also was nonchalant about concussions, now comes down solidly against allowing any of our sons to play football in light of the new scientific evidence. Guess I’m not too old to learn.

Michael L. McCann, M.D.

Duluth, Minn.

Dr. Wilkoff responds: Thanks for your great e-mail. Obviously, we are both conflicted in our own ways. I guess I should have ended my column with the unrealistic wish that football could remain as a sport for young kids so they could play rough and still be protected by their equipment. Then, eliminate it as a division one and professional activity. Obviously, it’s not going to happen because otherwise what would all those folks on their couches do on Saturday and Sunday afternoons?

A benefit of football

Dr. Wilkoff, thank you for being a sane man in a sea of fear and ill thought out conclusions. As a pediatrician for over 40 years and as a postcollegiate football player, I do appreciate the sincere fear of major injuries to any child. However, eliminating a sport because it has some inherent potential for serious damage is not the right answer. All these years I have been preaching both to my patients and to younger physicians the balance of risk versus benefit in all decision making. Now you may or may not agree with me, but the benefits of football experience are tremendous, whether it stops at the high school or the collegiate level. I noticed that you listed many of these benefits of football in your article, but the major one I did not see is the understanding that one’s input into a project, whether football competition or treating a complicated patient, often determines the outcome of the project. Call it “cause and effect” if you like. Certainly one begins learning these lessons in a home in which personal responsibility is stressed, but I wholeheartedly believe that this specific lesson was reinforced time and again during my football upbringing, and I tend to credit a successful career in pediatrics with that education. Just to be as direct as possible, I too played other high school sports, but football was a unique experience in my mind, and I have encouraged my son and grandsons to participate, mainly because the sport and most of the men that gathered around our youth in this area are teachers. They teach hard work, they teach desire for success, and they teach personal responsibility for actions. Yes, we have all viewed those screaming poor sports who occasionally don a coach’s uniform, but they are far less frequent that the good guys who give their time to our children. Thanks again for a well thought out article. Your articles are consistently written well and thoughtful.

Stuart J. Yoffe, M.D.

Brenham, Texas

Dr Wilkoff responds: Thanks for your kind and thoughtful comments. It is hard to get many people to understand the kind of formative experiences that you and I shared playing football. My wife still doesn’t get it.

Each week’s game was a project that involved planning, preparation, cooperation, and commitment to execute.

No to football

Would I let my son play football? No.

A few years ago I had a patient who won a full ride football scholarship to a division 3 college. He wasn’t National Football League material and knew it. He was a brilliant student who majored in engineering and wanted a free education. After a big time concussion in practice his freshman year, he’s had to drop out of college. He can’t do the work anymore.

I’ve been at pediatrics for 35 years and when I ask kids (in front of their parents) why they want to change from soccer to American football, they say it’s because they like the 49ers or Raiders (I practice in the periphery of the San Francisco Bay Area). When I ask them alone, the answer is different –“because I want to hit someone.”

I have a couple of Dads who are coaches and both suggested the answer is to eliminate helmets and protective padding. They think it would make the kids more careful. I worry more about steroids. When you were playing, how many 300 plus pounds opponents did you face? I think the high schools need to do random drug testing.

Some of the local Pop Warner leagues are having trouble getting liability insurance. I suspect that’ll spread to the schools soon as well. In a state such as California, I suspect that schools will drop football as well for insurance reasons soon.

It’s too bad; I’ve enjoyed watching football. But then, when younger, I used to watch and root for Mohammad Ali. Look what’s happened to him. I don’t believe it’s all Parkinson’s disease.

Steve Jacobs M.D.

Modesto, Calif.

Dr. Wilkoff responds: There weren’t any 300 pounders when I played because they couldn’t make the team. There are some pretty hefty guys on our high school team here in Brunswick, but they are more like Pillsbury Doughboys and aren’t going to do much harm. I agree that eliminating helmets and pads makes a lot of sense. Which would make it rugby, a much more interesting game that requires more conditioning.

The bulk of the e-mails I have received about the column have supported football. As I think more about, I think a solution – but not one that will fly – is to eliminate football beyond high school or maybe even middle school when it begins to get ugly and dangerous. Young boys do like to hit, tussle, and knock each other around, and seldom do much harm, with or without equipment.

No to football – again

Nearly everyone in our University of California, Los Angeles, pediatric faculty won’t allow their child to play Pop Warner football. It is just too dangerous.

I fortunately was too thin to play football, but agree completely that athletics were a good influence growing up in a fatherless home in Madison, Wisc. I played tennis and basketball instead.

The American Academy of Pediatrics should take a stand. No kids should play football.

As someone said, everyone in 1936 knew who the heavy weight boxing champion was – now no one knows. My alma mater, the University of Wisconsin, gave up boxing after someone died after a blow to the head.

How many cord transections, concussions, and sudden deaths can we tolerate?

Richard Stiehm, M.D.

Distinguished Research Professor of Pediatrics Emeritus

University of California, Los Angeles

Dr. Wilkoff responds: I agree that very few people know the names of professional fighters today, but many people (none of them with whom you and I are likely on a first name basis) know the names of successful mixed-martial arts/cage fighters. Now that is a brutal sport. The fact that it is popular should remind us that the desire to watch and participate in those activities runs pretty deep in us – which of course doesn’t make it right.

In response to your question of how many cord transections, concussions, and sudden deaths will we tolerate, I would be interested in your response. If the number is zero, then we have to broaden the discussion to a consideration of what activities we should allow children (particularly boys) to pursue to be physically active and receive the enjoyment that (for lack of a better term) rough housing provides. Zero tolerance can be a double-edged sword.

[Dr. Stiehm responds: Yes to soccer, basketball, and lacrosse, where the object is not to hurt the opponent – unlike boxing and tackle football.

Dr. Wilkoff replies: My perspective is colored by being here in Maine, where football is small time and even smaller in our community. One solution, but of course one that wouldn’t fly, is to make football a sport that ends at or just after middle school. It would allow young children to rough house in the context of a fun game protected by equipment before the g-forces that come with puberty create the serious dangers. Well coached and refereed football needn’t be a sport where one of the goals is to injure.]

An honest column

I want to thank you for your column entitled “Your son and football.” I am a pediatric primary care sports physician who runs a sports medicine clinic and a concussion clinic through Children’s Hospital of Wisconsin and the Medical College of Wisconsin. I am happy that you wrote about pro football and youth sports honestly – the perceived lack of moral character of many professional athletes and the craziness / win at all costs attitude of some youth coaches (and parents). And the fact that most kids will not become professional athletes. I believe treating kids just like a “collegiate or pro athlete” is a disservice to the child, as they are not at that level of emotional or physical maturity. I like the benefits of football and other contact sports – when taught and coached well, played well, and done under the realistic vision that this is for fun, and you learn life’s lessons and how to compete, win, and lose – not just done to win and earn a scholarship.

Kevin D. Walter, M.D.

Medical College of Wisconsin

Milwaukee

Sports role models

It is too bad Maine, where Dr. Wilkoff lives, does not have a professional sports team; Peyton Manning, the quarterback for the Denver Broncos, is one of the most “admirable role models in the ranks of high-profile athletes.” He is well respected and loved both here and still in the Indianapolis area and in Tennessee, where he played college football. Missy Franklin, a high profile athlete, just finished a day visiting patients at Children’s Hospital of Colorado. It was on the news last night. She is beloved here in Colorado for her smile, enthusiasm, professionalism, kindness, and overall just for being a wonderful person and amazing athlete. Although the high-profile headlines dominate, the acts of kindness and compassion by many athletes at many levels are not covered to the same degree.

It has been shown that high school and college athletes do better than their counterparts in school. My daughter was a swimmer in high school and thus avoided the drug crowd for which her class was known locally. I hope Dr. Wilkoff’s son learns the same lessons so many athletes learn in competition: teamwork, hard work, meeting and exceeding goals, and learning to deal with disappointment and victory – lessons that are hard to learn in the classroom. He will be a better person for that.

Stephen Fries, M.D.

Boulder, Colo.

Dr. Wilkoff responds: I agree there are still some shining stars in pro sports, but it seems to me that they are badly overshadowed by the bad apples. That may simply be a function of media exposure, but that’s what the kids see. My son was and still is at age 39 a hockey player and a fine young man in some part because of his athletic past.

Dr. Wilkoff gives all the good reasons for NOT allowing one’s son to play football in his Letters From Maine column entitled “Your son and football” in the December 2014 issue of Pediatric News, and then rationalizes the opposite. As society evolves from gladiators killing their defeated opponents to abolishing boxing as a college sport, so too should we encourage our children to engage in safer sports. Soccer without head-butting and hockey without fighting and body checking would be a good start. There’s no way to make football safe. It just gets more dangerous, as 350-pound gorillas run smack-dab into each other. But humans evolve slowly. We have not been down very long from the trees in evolutionary terms, when the “accepted” way to get a female mate was to club her senseless and carry her off (as the chroniclers of primitive societies have repeatedly shown). Nor do we tolerate dueling, or drawing and quartering or torture any longer. Watching the development of MMA (mixed marital arts) and female boxing just goes to show how primitive and inconsistent we can still be. So, just like Dr. Wilkoff, I confess to being inconsistent, and addicted to watching the genius play of the Aaron Rodgers and Peyton Mannings of football. Maybe we just need a few more centuries to evolve into a civilized society, a bit of help from female leadership to encourage alternative sports to develop. This retired pediatrician, who also was a team football physician, and who also was nonchalant about concussions, now comes down solidly against allowing any of our sons to play football in light of the new scientific evidence. Guess I’m not too old to learn.

Michael L. McCann, M.D.

Duluth, Minn.

Dr. Wilkoff responds: Thanks for your great e-mail. Obviously, we are both conflicted in our own ways. I guess I should have ended my column with the unrealistic wish that football could remain as a sport for young kids so they could play rough and still be protected by their equipment. Then, eliminate it as a division one and professional activity. Obviously, it’s not going to happen because otherwise what would all those folks on their couches do on Saturday and Sunday afternoons?

A benefit of football

Dr. Wilkoff, thank you for being a sane man in a sea of fear and ill thought out conclusions. As a pediatrician for over 40 years and as a postcollegiate football player, I do appreciate the sincere fear of major injuries to any child. However, eliminating a sport because it has some inherent potential for serious damage is not the right answer. All these years I have been preaching both to my patients and to younger physicians the balance of risk versus benefit in all decision making. Now you may or may not agree with me, but the benefits of football experience are tremendous, whether it stops at the high school or the collegiate level. I noticed that you listed many of these benefits of football in your article, but the major one I did not see is the understanding that one’s input into a project, whether football competition or treating a complicated patient, often determines the outcome of the project. Call it “cause and effect” if you like. Certainly one begins learning these lessons in a home in which personal responsibility is stressed, but I wholeheartedly believe that this specific lesson was reinforced time and again during my football upbringing, and I tend to credit a successful career in pediatrics with that education. Just to be as direct as possible, I too played other high school sports, but football was a unique experience in my mind, and I have encouraged my son and grandsons to participate, mainly because the sport and most of the men that gathered around our youth in this area are teachers. They teach hard work, they teach desire for success, and they teach personal responsibility for actions. Yes, we have all viewed those screaming poor sports who occasionally don a coach’s uniform, but they are far less frequent that the good guys who give their time to our children. Thanks again for a well thought out article. Your articles are consistently written well and thoughtful.

Stuart J. Yoffe, M.D.

Brenham, Texas

Dr Wilkoff responds: Thanks for your kind and thoughtful comments. It is hard to get many people to understand the kind of formative experiences that you and I shared playing football. My wife still doesn’t get it.

Each week’s game was a project that involved planning, preparation, cooperation, and commitment to execute.

No to football

Would I let my son play football? No.

A few years ago I had a patient who won a full ride football scholarship to a division 3 college. He wasn’t National Football League material and knew it. He was a brilliant student who majored in engineering and wanted a free education. After a big time concussion in practice his freshman year, he’s had to drop out of college. He can’t do the work anymore.

I’ve been at pediatrics for 35 years and when I ask kids (in front of their parents) why they want to change from soccer to American football, they say it’s because they like the 49ers or Raiders (I practice in the periphery of the San Francisco Bay Area). When I ask them alone, the answer is different –“because I want to hit someone.”

I have a couple of Dads who are coaches and both suggested the answer is to eliminate helmets and protective padding. They think it would make the kids more careful. I worry more about steroids. When you were playing, how many 300 plus pounds opponents did you face? I think the high schools need to do random drug testing.

Some of the local Pop Warner leagues are having trouble getting liability insurance. I suspect that’ll spread to the schools soon as well. In a state such as California, I suspect that schools will drop football as well for insurance reasons soon.

It’s too bad; I’ve enjoyed watching football. But then, when younger, I used to watch and root for Mohammad Ali. Look what’s happened to him. I don’t believe it’s all Parkinson’s disease.

Steve Jacobs M.D.

Modesto, Calif.

Dr. Wilkoff responds: There weren’t any 300 pounders when I played because they couldn’t make the team. There are some pretty hefty guys on our high school team here in Brunswick, but they are more like Pillsbury Doughboys and aren’t going to do much harm. I agree that eliminating helmets and pads makes a lot of sense. Which would make it rugby, a much more interesting game that requires more conditioning.

The bulk of the e-mails I have received about the column have supported football. As I think more about, I think a solution – but not one that will fly – is to eliminate football beyond high school or maybe even middle school when it begins to get ugly and dangerous. Young boys do like to hit, tussle, and knock each other around, and seldom do much harm, with or without equipment.

No to football – again

Nearly everyone in our University of California, Los Angeles, pediatric faculty won’t allow their child to play Pop Warner football. It is just too dangerous.

I fortunately was too thin to play football, but agree completely that athletics were a good influence growing up in a fatherless home in Madison, Wisc. I played tennis and basketball instead.

The American Academy of Pediatrics should take a stand. No kids should play football.

As someone said, everyone in 1936 knew who the heavy weight boxing champion was – now no one knows. My alma mater, the University of Wisconsin, gave up boxing after someone died after a blow to the head.

How many cord transections, concussions, and sudden deaths can we tolerate?

Richard Stiehm, M.D.

Distinguished Research Professor of Pediatrics Emeritus

University of California, Los Angeles

Dr. Wilkoff responds: I agree that very few people know the names of professional fighters today, but many people (none of them with whom you and I are likely on a first name basis) know the names of successful mixed-martial arts/cage fighters. Now that is a brutal sport. The fact that it is popular should remind us that the desire to watch and participate in those activities runs pretty deep in us – which of course doesn’t make it right.

In response to your question of how many cord transections, concussions, and sudden deaths will we tolerate, I would be interested in your response. If the number is zero, then we have to broaden the discussion to a consideration of what activities we should allow children (particularly boys) to pursue to be physically active and receive the enjoyment that (for lack of a better term) rough housing provides. Zero tolerance can be a double-edged sword.

[Dr. Stiehm responds: Yes to soccer, basketball, and lacrosse, where the object is not to hurt the opponent – unlike boxing and tackle football.

Dr. Wilkoff replies: My perspective is colored by being here in Maine, where football is small time and even smaller in our community. One solution, but of course one that wouldn’t fly, is to make football a sport that ends at or just after middle school. It would allow young children to rough house in the context of a fun game protected by equipment before the g-forces that come with puberty create the serious dangers. Well coached and refereed football needn’t be a sport where one of the goals is to injure.]

An honest column

I want to thank you for your column entitled “Your son and football.” I am a pediatric primary care sports physician who runs a sports medicine clinic and a concussion clinic through Children’s Hospital of Wisconsin and the Medical College of Wisconsin. I am happy that you wrote about pro football and youth sports honestly – the perceived lack of moral character of many professional athletes and the craziness / win at all costs attitude of some youth coaches (and parents). And the fact that most kids will not become professional athletes. I believe treating kids just like a “collegiate or pro athlete” is a disservice to the child, as they are not at that level of emotional or physical maturity. I like the benefits of football and other contact sports – when taught and coached well, played well, and done under the realistic vision that this is for fun, and you learn life’s lessons and how to compete, win, and lose – not just done to win and earn a scholarship.

Kevin D. Walter, M.D.

Medical College of Wisconsin

Milwaukee

Sports role models

It is too bad Maine, where Dr. Wilkoff lives, does not have a professional sports team; Peyton Manning, the quarterback for the Denver Broncos, is one of the most “admirable role models in the ranks of high-profile athletes.” He is well respected and loved both here and still in the Indianapolis area and in Tennessee, where he played college football. Missy Franklin, a high profile athlete, just finished a day visiting patients at Children’s Hospital of Colorado. It was on the news last night. She is beloved here in Colorado for her smile, enthusiasm, professionalism, kindness, and overall just for being a wonderful person and amazing athlete. Although the high-profile headlines dominate, the acts of kindness and compassion by many athletes at many levels are not covered to the same degree.

It has been shown that high school and college athletes do better than their counterparts in school. My daughter was a swimmer in high school and thus avoided the drug crowd for which her class was known locally. I hope Dr. Wilkoff’s son learns the same lessons so many athletes learn in competition: teamwork, hard work, meeting and exceeding goals, and learning to deal with disappointment and victory – lessons that are hard to learn in the classroom. He will be a better person for that.

Stephen Fries, M.D.

Boulder, Colo.

Dr. Wilkoff responds: I agree there are still some shining stars in pro sports, but it seems to me that they are badly overshadowed by the bad apples. That may simply be a function of media exposure, but that’s what the kids see. My son was and still is at age 39 a hockey player and a fine young man in some part because of his athletic past.

Dr. Wilkoff gives all the good reasons for NOT allowing one’s son to play football in his Letters From Maine column entitled “Your son and football” in the December 2014 issue of Pediatric News, and then rationalizes the opposite. As society evolves from gladiators killing their defeated opponents to abolishing boxing as a college sport, so too should we encourage our children to engage in safer sports. Soccer without head-butting and hockey without fighting and body checking would be a good start. There’s no way to make football safe. It just gets more dangerous, as 350-pound gorillas run smack-dab into each other. But humans evolve slowly. We have not been down very long from the trees in evolutionary terms, when the “accepted” way to get a female mate was to club her senseless and carry her off (as the chroniclers of primitive societies have repeatedly shown). Nor do we tolerate dueling, or drawing and quartering or torture any longer. Watching the development of MMA (mixed marital arts) and female boxing just goes to show how primitive and inconsistent we can still be. So, just like Dr. Wilkoff, I confess to being inconsistent, and addicted to watching the genius play of the Aaron Rodgers and Peyton Mannings of football. Maybe we just need a few more centuries to evolve into a civilized society, a bit of help from female leadership to encourage alternative sports to develop. This retired pediatrician, who also was a team football physician, and who also was nonchalant about concussions, now comes down solidly against allowing any of our sons to play football in light of the new scientific evidence. Guess I’m not too old to learn.

Michael L. McCann, M.D.

Duluth, Minn.

Dr. Wilkoff responds: Thanks for your great e-mail. Obviously, we are both conflicted in our own ways. I guess I should have ended my column with the unrealistic wish that football could remain as a sport for young kids so they could play rough and still be protected by their equipment. Then, eliminate it as a division one and professional activity. Obviously, it’s not going to happen because otherwise what would all those folks on their couches do on Saturday and Sunday afternoons?

A benefit of football

Dr. Wilkoff, thank you for being a sane man in a sea of fear and ill thought out conclusions. As a pediatrician for over 40 years and as a postcollegiate football player, I do appreciate the sincere fear of major injuries to any child. However, eliminating a sport because it has some inherent potential for serious damage is not the right answer. All these years I have been preaching both to my patients and to younger physicians the balance of risk versus benefit in all decision making. Now you may or may not agree with me, but the benefits of football experience are tremendous, whether it stops at the high school or the collegiate level. I noticed that you listed many of these benefits of football in your article, but the major one I did not see is the understanding that one’s input into a project, whether football competition or treating a complicated patient, often determines the outcome of the project. Call it “cause and effect” if you like. Certainly one begins learning these lessons in a home in which personal responsibility is stressed, but I wholeheartedly believe that this specific lesson was reinforced time and again during my football upbringing, and I tend to credit a successful career in pediatrics with that education. Just to be as direct as possible, I too played other high school sports, but football was a unique experience in my mind, and I have encouraged my son and grandsons to participate, mainly because the sport and most of the men that gathered around our youth in this area are teachers. They teach hard work, they teach desire for success, and they teach personal responsibility for actions. Yes, we have all viewed those screaming poor sports who occasionally don a coach’s uniform, but they are far less frequent that the good guys who give their time to our children. Thanks again for a well thought out article. Your articles are consistently written well and thoughtful.

Stuart J. Yoffe, M.D.

Brenham, Texas

Dr Wilkoff responds: Thanks for your kind and thoughtful comments. It is hard to get many people to understand the kind of formative experiences that you and I shared playing football. My wife still doesn’t get it.

Each week’s game was a project that involved planning, preparation, cooperation, and commitment to execute.

No to football

Would I let my son play football? No.

A few years ago I had a patient who won a full ride football scholarship to a division 3 college. He wasn’t National Football League material and knew it. He was a brilliant student who majored in engineering and wanted a free education. After a big time concussion in practice his freshman year, he’s had to drop out of college. He can’t do the work anymore.

I’ve been at pediatrics for 35 years and when I ask kids (in front of their parents) why they want to change from soccer to American football, they say it’s because they like the 49ers or Raiders (I practice in the periphery of the San Francisco Bay Area). When I ask them alone, the answer is different –“because I want to hit someone.”

I have a couple of Dads who are coaches and both suggested the answer is to eliminate helmets and protective padding. They think it would make the kids more careful. I worry more about steroids. When you were playing, how many 300 plus pounds opponents did you face? I think the high schools need to do random drug testing.

Some of the local Pop Warner leagues are having trouble getting liability insurance. I suspect that’ll spread to the schools soon as well. In a state such as California, I suspect that schools will drop football as well for insurance reasons soon.

It’s too bad; I’ve enjoyed watching football. But then, when younger, I used to watch and root for Mohammad Ali. Look what’s happened to him. I don’t believe it’s all Parkinson’s disease.

Steve Jacobs M.D.

Modesto, Calif.

Dr. Wilkoff responds: There weren’t any 300 pounders when I played because they couldn’t make the team. There are some pretty hefty guys on our high school team here in Brunswick, but they are more like Pillsbury Doughboys and aren’t going to do much harm. I agree that eliminating helmets and pads makes a lot of sense. Which would make it rugby, a much more interesting game that requires more conditioning.

The bulk of the e-mails I have received about the column have supported football. As I think more about, I think a solution – but not one that will fly – is to eliminate football beyond high school or maybe even middle school when it begins to get ugly and dangerous. Young boys do like to hit, tussle, and knock each other around, and seldom do much harm, with or without equipment.

No to football – again

Nearly everyone in our University of California, Los Angeles, pediatric faculty won’t allow their child to play Pop Warner football. It is just too dangerous.

I fortunately was too thin to play football, but agree completely that athletics were a good influence growing up in a fatherless home in Madison, Wisc. I played tennis and basketball instead.

The American Academy of Pediatrics should take a stand. No kids should play football.

As someone said, everyone in 1936 knew who the heavy weight boxing champion was – now no one knows. My alma mater, the University of Wisconsin, gave up boxing after someone died after a blow to the head.

How many cord transections, concussions, and sudden deaths can we tolerate?

Richard Stiehm, M.D.

Distinguished Research Professor of Pediatrics Emeritus

University of California, Los Angeles

Dr. Wilkoff responds: I agree that very few people know the names of professional fighters today, but many people (none of them with whom you and I are likely on a first name basis) know the names of successful mixed-martial arts/cage fighters. Now that is a brutal sport. The fact that it is popular should remind us that the desire to watch and participate in those activities runs pretty deep in us – which of course doesn’t make it right.

In response to your question of how many cord transections, concussions, and sudden deaths will we tolerate, I would be interested in your response. If the number is zero, then we have to broaden the discussion to a consideration of what activities we should allow children (particularly boys) to pursue to be physically active and receive the enjoyment that (for lack of a better term) rough housing provides. Zero tolerance can be a double-edged sword.

[Dr. Stiehm responds: Yes to soccer, basketball, and lacrosse, where the object is not to hurt the opponent – unlike boxing and tackle football.

Dr. Wilkoff replies: My perspective is colored by being here in Maine, where football is small time and even smaller in our community. One solution, but of course one that wouldn’t fly, is to make football a sport that ends at or just after middle school. It would allow young children to rough house in the context of a fun game protected by equipment before the g-forces that come with puberty create the serious dangers. Well coached and refereed football needn’t be a sport where one of the goals is to injure.]

An honest column

I want to thank you for your column entitled “Your son and football.” I am a pediatric primary care sports physician who runs a sports medicine clinic and a concussion clinic through Children’s Hospital of Wisconsin and the Medical College of Wisconsin. I am happy that you wrote about pro football and youth sports honestly – the perceived lack of moral character of many professional athletes and the craziness / win at all costs attitude of some youth coaches (and parents). And the fact that most kids will not become professional athletes. I believe treating kids just like a “collegiate or pro athlete” is a disservice to the child, as they are not at that level of emotional or physical maturity. I like the benefits of football and other contact sports – when taught and coached well, played well, and done under the realistic vision that this is for fun, and you learn life’s lessons and how to compete, win, and lose – not just done to win and earn a scholarship.

Kevin D. Walter, M.D.

Medical College of Wisconsin

Milwaukee

Sports role models

It is too bad Maine, where Dr. Wilkoff lives, does not have a professional sports team; Peyton Manning, the quarterback for the Denver Broncos, is one of the most “admirable role models in the ranks of high-profile athletes.” He is well respected and loved both here and still in the Indianapolis area and in Tennessee, where he played college football. Missy Franklin, a high profile athlete, just finished a day visiting patients at Children’s Hospital of Colorado. It was on the news last night. She is beloved here in Colorado for her smile, enthusiasm, professionalism, kindness, and overall just for being a wonderful person and amazing athlete. Although the high-profile headlines dominate, the acts of kindness and compassion by many athletes at many levels are not covered to the same degree.

It has been shown that high school and college athletes do better than their counterparts in school. My daughter was a swimmer in high school and thus avoided the drug crowd for which her class was known locally. I hope Dr. Wilkoff’s son learns the same lessons so many athletes learn in competition: teamwork, hard work, meeting and exceeding goals, and learning to deal with disappointment and victory – lessons that are hard to learn in the classroom. He will be a better person for that.

Stephen Fries, M.D.

Boulder, Colo.

Dr. Wilkoff responds: I agree there are still some shining stars in pro sports, but it seems to me that they are badly overshadowed by the bad apples. That may simply be a function of media exposure, but that’s what the kids see. My son was and still is at age 39 a hockey player and a fine young man in some part because of his athletic past.

Dr. Henry A. Nasrallah is correct that wild salmon is a good choice for pregnant women who want to boost intake of omega-3 fatty acids (Current Psychiatry, Comments & Controversies, December 2014; pg 33 [http://bit.ly/1wQoXdP]). The main concern about fish intake during preg­nancy is exposure to methylmercury, and much of this concern is derived from the tragic results of epic mercury poisonings of food sources in the past.

The FDA advises that pregnant women and children avoid eat­ing shark, tilefish, king mackerel, and swordfish because these fish have a relatively high level of mer­cury.¹ Fish that are low in methyl-mercury include salmon and canned light tuna. (More information is avail­able at http://www.fda.gov/Food/ResourcesForYou/HealthEducators/ucm083324.htm.)

Although wild fish tend to be higher in omega-3 fatty acids than farm-raised fish, farmed fish can be an excellent source of omega-3 fatty acids. This is analogous to eating farm-produced livestock vs free-range, grass-fed live­stock: Animals in their natural envi­ronment eat healthier and have more omega-3 fatty acids, whereas farmed livestock generally eat cheap and less healthy feed. Because wild fish can be pricey, it’s important that women understand that farm-raised fish are a good source of protein and other nutri­ents such as omega-3 fatty acids.

Research has been inconclusive regarding the antidepressant benefits of omega-3 fatty acids, with some, but not all, studies demonstrating an add-on benefit of omega-3 fatty acid supple­ments for mood disorders. However, several epidemiological studies have reported that the low quality of dietary intake of omega-3 fatty acids is associ­ated with psychiatric illness, and fish and seafood are sources of essential fatty acids and other nutrients.²

Dr. Henry A. Nasrallah is correct that wild salmon is a good choice for pregnant women who want to boost intake of omega-3 fatty acids (Current Psychiatry, Comments & Controversies, December 2014; pg 33 [http://bit.ly/1wQoXdP]). The main concern about fish intake during preg­nancy is exposure to methylmercury, and much of this concern is derived from the tragic results of epic mercury poisonings of food sources in the past.

The FDA advises that pregnant women and children avoid eat­ing shark, tilefish, king mackerel, and swordfish because these fish have a relatively high level of mer­cury.¹ Fish that are low in methyl-mercury include salmon and canned light tuna. (More information is avail­able at http://www.fda.gov/Food/ResourcesForYou/HealthEducators/ucm083324.htm.)

Although wild fish tend to be higher in omega-3 fatty acids than farm-raised fish, farmed fish can be an excellent source of omega-3 fatty acids. This is analogous to eating farm-produced livestock vs free-range, grass-fed live­stock: Animals in their natural envi­ronment eat healthier and have more omega-3 fatty acids, whereas farmed livestock generally eat cheap and less healthy feed. Because wild fish can be pricey, it’s important that women understand that farm-raised fish are a good source of protein and other nutri­ents such as omega-3 fatty acids.

Research has been inconclusive regarding the antidepressant benefits of omega-3 fatty acids, with some, but not all, studies demonstrating an add-on benefit of omega-3 fatty acid supple­ments for mood disorders. However, several epidemiological studies have reported that the low quality of dietary intake of omega-3 fatty acids is associ­ated with psychiatric illness, and fish and seafood are sources of essential fatty acids and other nutrients.²

Dr. Henry A. Nasrallah is correct that wild salmon is a good choice for pregnant women who want to boost intake of omega-3 fatty acids (Current Psychiatry, Comments & Controversies, December 2014; pg 33 [http://bit.ly/1wQoXdP]). The main concern about fish intake during preg­nancy is exposure to methylmercury, and much of this concern is derived from the tragic results of epic mercury poisonings of food sources in the past.

The FDA advises that pregnant women and children avoid eat­ing shark, tilefish, king mackerel, and swordfish because these fish have a relatively high level of mer­cury.¹ Fish that are low in methyl-mercury include salmon and canned light tuna. (More information is avail­able at http://www.fda.gov/Food/ResourcesForYou/HealthEducators/ucm083324.htm.)

Although wild fish tend to be higher in omega-3 fatty acids than farm-raised fish, farmed fish can be an excellent source of omega-3 fatty acids. This is analogous to eating farm-produced livestock vs free-range, grass-fed live­stock: Animals in their natural envi­ronment eat healthier and have more omega-3 fatty acids, whereas farmed livestock generally eat cheap and less healthy feed. Because wild fish can be pricey, it’s important that women understand that farm-raised fish are a good source of protein and other nutri­ents such as omega-3 fatty acids.

Research has been inconclusive regarding the antidepressant benefits of omega-3 fatty acids, with some, but not all, studies demonstrating an add-on benefit of omega-3 fatty acid supple­ments for mood disorders. However, several epidemiological studies have reported that the low quality of dietary intake of omega-3 fatty acids is associ­ated with psychiatric illness, and fish and seafood are sources of essential fatty acids and other nutrients.²

A 29-year-old woman presents for evaluation. She reports that she has had frequent headaches over the past 12 months that include pressure pain on her forehead, under her eyes, and over her cheeks. She usually has nasal congestion as well. She has not had any fevers or purulent nasal discharge. What is the most likely diagnosis?

A. Cluster headaches.

B. Migraine headaches.

C. Sinus headaches.

D. Tension headaches.

Myth: Recurrent sinus headaches are common.

Most physicians and patients would diagnose this case as sinus headache, but it is actually a common variant of migraine headache. Sinus headaches are rare, and when they do occur, they are almost always in the setting of acute sinusitis. Recurring headaches are rarely due to sinus problems.

In regard to sinus headache, the International Headache Society (IHS) classification states that chronic sinusitis is not a cause of headache and facial pain unless it relapses into an acute sinusitis (Expert Rev. Neurother. 2009;9:439-44). The recurrent nature of the headaches in this patient suggests a primary headache disorder, with migraine being the most likely.

In a study of 2,991 patients with self-diagnosed or physician-diagnosed “sinus headaches,” 88% of the patients met IHS criteria for migraine (Arch. Intern. Med. 2004;164:1769-72). In this study, most of the patients had symptoms suggesting sinus problems, with the most common symptoms being sinus pressure (84%), sinus pain (82%), and nasal congestion (63%).

The likely cause for these symptoms in migraine patients is vasodilation of the nasal mucosa that can be part of the migraine event (Expert Rev. Neurother. 2009;9:439-44).

In the Sinus, Allergy and Migraine Study, 100 patients who believed they had sinus headaches were recruited. All of the patients received a detailed history and physical exam, and all received a headache diagnosis based on IHS criteria (Headache 2007;47:213-24).

Final diagnoses were as follows: Migraine with or without aura, 52%; probable migraine, 23%; chronic migraine with medication overuse headache, 11%; nonclassifiable headache, 9%. A total of 76% of migraine patients reported pain in the distribution of the second division of the trigeminal nerve, and 62% experienced bilateral forehead and maxillary pain with their headaches.

It is interesting that both these studies showed the same thing: More than 85% of patients who think they have sinus headache actually meet criteria for migraine headache.

Two other articles also give strong evidence that patients with recurrent “sinus” headaches have causes other than sinus disease as the cause.

Dr. Mustafa Kaymakci and his colleagues studied 98 patients who had headaches diagnosed as “sinus” headaches (J. Int. Med. Res. 2013;41:218-23). All patients received a detailed history and physical, nasal endoscopy, and sinus CT scans. All patients who did not have findings that could be considered the cause of the headaches were diagnosed according to IHS criteria.

A total of 61 (62%) were diagnosed with migraine headache, 26 (27%) diagnosed with tension-type headache, and 11 (11%) had cluster headache. Seventy-seven percent of these patients had previously received at least one treatment for sinusitis.

Another study, by Dr. Mohsen Foroughipour and his colleagues, gave similar results (Eur. Arch. Otorhinolaryngol. 2011;268:1593-6). In this study, 58 patients with “sinus” headache were evaluated, with final diagnosis of migraine in 40 patients (69%), tension-type headache in 16 patients (27%), and chronic sinusitis with recurrent acute episodes in 2 patients (3%). Recurrent antibiotic therapy was given to 73% of the tension-type headache patients and 66% of the migraine patients.

In a study by Dr. Elina Kari and her colleagues, patients who had a history of “sinus headaches” were treated as though all these headaches were migraines (Laryngoscope 2008;118:2235-9). Fifty-four patients were enrolled, and 38 patients completed the study. All patients had nasal endoscopy and sinus CT scans that were negative. They were then given migraine-directed treatment to use for their headaches.

The majority of the patients who dropped out of the study did so because they did not believe their headaches could be due to migraines, and they did not want to take the migraine medications.

Of the 38 patient who completed the study, 31 patients (82%) had a significant reduction of headache pain with triptan use, and 35 patients (92%) had a significant response to migraine-directed therapy.

These studies show us that recurrent “sinus headaches” are unlikely to be due to sinus disease. More likely, they represent migraine headache or, less likely, tension headache or cluster headache. Evaluation should include categorizing the headache by clinical features (IHS criteria) to make a diagnosis, followed by a trial of appropriate treatment for headache type. In patients who don’t meet criteria for a specific headache type, a trial of migraine-directed therapy is reasonable.

Dr. Paauw is a professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington Medical School. He is the Rathmann Family Foundation Chair in Patient-Centered Clinical Education. Contact Dr. Paauw at [email protected].

A 29-year-old woman presents for evaluation. She reports that she has had frequent headaches over the past 12 months that include pressure pain on her forehead, under her eyes, and over her cheeks. She usually has nasal congestion as well. She has not had any fevers or purulent nasal discharge. What is the most likely diagnosis?

A. Cluster headaches.

B. Migraine headaches.

C. Sinus headaches.

D. Tension headaches.

Myth: Recurrent sinus headaches are common.

Most physicians and patients would diagnose this case as sinus headache, but it is actually a common variant of migraine headache. Sinus headaches are rare, and when they do occur, they are almost always in the setting of acute sinusitis. Recurring headaches are rarely due to sinus problems.

In regard to sinus headache, the International Headache Society (IHS) classification states that chronic sinusitis is not a cause of headache and facial pain unless it relapses into an acute sinusitis (Expert Rev. Neurother. 2009;9:439-44). The recurrent nature of the headaches in this patient suggests a primary headache disorder, with migraine being the most likely.

In a study of 2,991 patients with self-diagnosed or physician-diagnosed “sinus headaches,” 88% of the patients met IHS criteria for migraine (Arch. Intern. Med. 2004;164:1769-72). In this study, most of the patients had symptoms suggesting sinus problems, with the most common symptoms being sinus pressure (84%), sinus pain (82%), and nasal congestion (63%).

The likely cause for these symptoms in migraine patients is vasodilation of the nasal mucosa that can be part of the migraine event (Expert Rev. Neurother. 2009;9:439-44).

In the Sinus, Allergy and Migraine Study, 100 patients who believed they had sinus headaches were recruited. All of the patients received a detailed history and physical exam, and all received a headache diagnosis based on IHS criteria (Headache 2007;47:213-24).

Final diagnoses were as follows: Migraine with or without aura, 52%; probable migraine, 23%; chronic migraine with medication overuse headache, 11%; nonclassifiable headache, 9%. A total of 76% of migraine patients reported pain in the distribution of the second division of the trigeminal nerve, and 62% experienced bilateral forehead and maxillary pain with their headaches.

It is interesting that both these studies showed the same thing: More than 85% of patients who think they have sinus headache actually meet criteria for migraine headache.

Two other articles also give strong evidence that patients with recurrent “sinus” headaches have causes other than sinus disease as the cause.

Dr. Mustafa Kaymakci and his colleagues studied 98 patients who had headaches diagnosed as “sinus” headaches (J. Int. Med. Res. 2013;41:218-23). All patients received a detailed history and physical, nasal endoscopy, and sinus CT scans. All patients who did not have findings that could be considered the cause of the headaches were diagnosed according to IHS criteria.

A total of 61 (62%) were diagnosed with migraine headache, 26 (27%) diagnosed with tension-type headache, and 11 (11%) had cluster headache. Seventy-seven percent of these patients had previously received at least one treatment for sinusitis.

Another study, by Dr. Mohsen Foroughipour and his colleagues, gave similar results (Eur. Arch. Otorhinolaryngol. 2011;268:1593-6). In this study, 58 patients with “sinus” headache were evaluated, with final diagnosis of migraine in 40 patients (69%), tension-type headache in 16 patients (27%), and chronic sinusitis with recurrent acute episodes in 2 patients (3%). Recurrent antibiotic therapy was given to 73% of the tension-type headache patients and 66% of the migraine patients.

In a study by Dr. Elina Kari and her colleagues, patients who had a history of “sinus headaches” were treated as though all these headaches were migraines (Laryngoscope 2008;118:2235-9). Fifty-four patients were enrolled, and 38 patients completed the study. All patients had nasal endoscopy and sinus CT scans that were negative. They were then given migraine-directed treatment to use for their headaches.

The majority of the patients who dropped out of the study did so because they did not believe their headaches could be due to migraines, and they did not want to take the migraine medications.

Of the 38 patient who completed the study, 31 patients (82%) had a significant reduction of headache pain with triptan use, and 35 patients (92%) had a significant response to migraine-directed therapy.

These studies show us that recurrent “sinus headaches” are unlikely to be due to sinus disease. More likely, they represent migraine headache or, less likely, tension headache or cluster headache. Evaluation should include categorizing the headache by clinical features (IHS criteria) to make a diagnosis, followed by a trial of appropriate treatment for headache type. In patients who don’t meet criteria for a specific headache type, a trial of migraine-directed therapy is reasonable.

Dr. Paauw is a professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington Medical School. He is the Rathmann Family Foundation Chair in Patient-Centered Clinical Education. Contact Dr. Paauw at [email protected].

A 29-year-old woman presents for evaluation. She reports that she has had frequent headaches over the past 12 months that include pressure pain on her forehead, under her eyes, and over her cheeks. She usually has nasal congestion as well. She has not had any fevers or purulent nasal discharge. What is the most likely diagnosis?

A. Cluster headaches.

B. Migraine headaches.

C. Sinus headaches.

D. Tension headaches.

Myth: Recurrent sinus headaches are common.

Most physicians and patients would diagnose this case as sinus headache, but it is actually a common variant of migraine headache. Sinus headaches are rare, and when they do occur, they are almost always in the setting of acute sinusitis. Recurring headaches are rarely due to sinus problems.

In regard to sinus headache, the International Headache Society (IHS) classification states that chronic sinusitis is not a cause of headache and facial pain unless it relapses into an acute sinusitis (Expert Rev. Neurother. 2009;9:439-44). The recurrent nature of the headaches in this patient suggests a primary headache disorder, with migraine being the most likely.

In a study of 2,991 patients with self-diagnosed or physician-diagnosed “sinus headaches,” 88% of the patients met IHS criteria for migraine (Arch. Intern. Med. 2004;164:1769-72). In this study, most of the patients had symptoms suggesting sinus problems, with the most common symptoms being sinus pressure (84%), sinus pain (82%), and nasal congestion (63%).

The likely cause for these symptoms in migraine patients is vasodilation of the nasal mucosa that can be part of the migraine event (Expert Rev. Neurother. 2009;9:439-44).

In the Sinus, Allergy and Migraine Study, 100 patients who believed they had sinus headaches were recruited. All of the patients received a detailed history and physical exam, and all received a headache diagnosis based on IHS criteria (Headache 2007;47:213-24).

Final diagnoses were as follows: Migraine with or without aura, 52%; probable migraine, 23%; chronic migraine with medication overuse headache, 11%; nonclassifiable headache, 9%. A total of 76% of migraine patients reported pain in the distribution of the second division of the trigeminal nerve, and 62% experienced bilateral forehead and maxillary pain with their headaches.

It is interesting that both these studies showed the same thing: More than 85% of patients who think they have sinus headache actually meet criteria for migraine headache.

Two other articles also give strong evidence that patients with recurrent “sinus” headaches have causes other than sinus disease as the cause.

Dr. Mustafa Kaymakci and his colleagues studied 98 patients who had headaches diagnosed as “sinus” headaches (J. Int. Med. Res. 2013;41:218-23). All patients received a detailed history and physical, nasal endoscopy, and sinus CT scans. All patients who did not have findings that could be considered the cause of the headaches were diagnosed according to IHS criteria.

A total of 61 (62%) were diagnosed with migraine headache, 26 (27%) diagnosed with tension-type headache, and 11 (11%) had cluster headache. Seventy-seven percent of these patients had previously received at least one treatment for sinusitis.

Another study, by Dr. Mohsen Foroughipour and his colleagues, gave similar results (Eur. Arch. Otorhinolaryngol. 2011;268:1593-6). In this study, 58 patients with “sinus” headache were evaluated, with final diagnosis of migraine in 40 patients (69%), tension-type headache in 16 patients (27%), and chronic sinusitis with recurrent acute episodes in 2 patients (3%). Recurrent antibiotic therapy was given to 73% of the tension-type headache patients and 66% of the migraine patients.

In a study by Dr. Elina Kari and her colleagues, patients who had a history of “sinus headaches” were treated as though all these headaches were migraines (Laryngoscope 2008;118:2235-9). Fifty-four patients were enrolled, and 38 patients completed the study. All patients had nasal endoscopy and sinus CT scans that were negative. They were then given migraine-directed treatment to use for their headaches.

The majority of the patients who dropped out of the study did so because they did not believe their headaches could be due to migraines, and they did not want to take the migraine medications.

Of the 38 patient who completed the study, 31 patients (82%) had a significant reduction of headache pain with triptan use, and 35 patients (92%) had a significant response to migraine-directed therapy.

These studies show us that recurrent “sinus headaches” are unlikely to be due to sinus disease. More likely, they represent migraine headache or, less likely, tension headache or cluster headache. Evaluation should include categorizing the headache by clinical features (IHS criteria) to make a diagnosis, followed by a trial of appropriate treatment for headache type. In patients who don’t meet criteria for a specific headache type, a trial of migraine-directed therapy is reasonable.

Dr. Paauw is a professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington Medical School. He is the Rathmann Family Foundation Chair in Patient-Centered Clinical Education. Contact Dr. Paauw at [email protected].

Fetal alcohol spectrum disorders are a vibrant area of development and research. Awareness about this preventable group of conditions appears to be growing.

In fact, the Centers for Disease Control and Prevention has released an app that emphasizes how to recognize, prevent, and treat fetal alcohol spectrum disorders. Earlier rates of fetal alcohol syndrome were estimated at 1/1,000, but FASD is estimated to occur at rates of 1/100. However, as I will illustrate below, the rates of FASD are even higher – much higher among some populations than previously thought.

The DSM-5 included in its appendix the diagnostic category of neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE), which theoretically should help psychiatrists identify FASD. Of course, the DSM-5 also includes an official diagnosis of disruptive mood dysregulation disorder (DMDD), and for the life of me, I have a difficult time differentiating between the two clinically except that children and adults with ND-PAE, in contrast to patients with DMDD who are described as persistently irritable or angry most of the day, can be very amicable, naive, and overly friendly between outbursts. The other difference is that ND-PAE needs a history of the mother’s having more than minimal exposure to alcohol during gestation, including prior to pregnancy recognition, and DMDD does not have this criteria, although it may be present. And, lastly DMDD is official and ND-PAE not.

Last year, Philip A. May, Ph.D., and his associates published an important paper, “Prevalence and Characteristics of Fetal Alcohol Spectrum Disorders” (Pediatrics 2014 [doi.10.1542/peds.2013-3319]). The authors looked at a representative Midwestern U.S. community with a population base of 160,000, 87% of which were white. The per-capita income of the population was $28,000, the median household income was $51,800, and 11% were below the poverty line.

Dr. May and his associates examined 70.5% (1,433 of 2,033) of all first-graders. Using one method of prevalence estimation, they found that 28.6/1,000 had FASD. Using a second method of prevalence estimation calculated from cases of FASD, they found an FASD rate of 82/1,000. The take-home message is, regardless of the academic fine points of how prevalence is estimated, these prevalence rates are much higher than previously reported.

In a second paper by Dr. Ira J. Chasnoff and his associates – “Misdiagnosis and Missed Diagnosis in Foster Care and Adopted Children with Prenatal Alcohol Exposure” – also published in Pediatrics, the rates of FASD in foster care and adopted youth were estimated to be even higher.

This study looked at 547 youth (50.6% African American, 1.3% Asian, 32.2% white, 0.7% Native American, 12.2% biracial, and 3% other/unknown) referred for severe behavioral disorders. The researchers found that 28.5% of these youth had FASD, 86.5% of the youth had never been diagnosed or were misdiagnosed, and 26.4% of these youth were misdiagnosed as having ADHD (Pediatrics 2014 [doi:10.1542/peds.2014-2171]).

Radhika L. Chimata and I published the third paper of significance online in Psychiatric Services. This paper, which is also slated for publication in print, focused on our work in a family medicine clinic on Chicago’s South Side, serving a population of 143,000. We looked at 611 patients (96% African American with a median household income of $33,809 – only 21 were youth, the rest were adults) and found that 297 (49%) of the adults and youth had neurodevelopmental disorders with 237 (39%) having clinical profiles consistent with neurobehavioral disorders associated with prenatal alcohol exposure. Thus, this clinic population has a rate of 388/1,000.

Considering emerging research that suggests that this acquired biological disorder is being driven by the social determinants of health, for example, some low-income African Americans are living not only in food deserts but food swamps (where the liquid is alcohol; consider the plethora of liquor stores in low-income African American communities), we must recognize that FASD can be prevented prenatally and possibly improved postnatally by increasing the amount of choline in the diet. This is a potential prevention intervention issue that we cannot afford to overlook if psychiatry is going to maintain its relevance in the 21st century.

Dr. Bell is a retired professor of psychiatry and public health at the University of Illinois at Chicago and staff psychiatrist at Jackson Park Hospital’s Outpatient Family Practice Clinic in Chicago. Dr. Bell is the former president and CEO of the Community Mental Health Council and former director of the Institute for Juvenile Research (birthplace of child psychiatry) at the university.

Fetal alcohol spectrum disorders are a vibrant area of development and research. Awareness about this preventable group of conditions appears to be growing.

In fact, the Centers for Disease Control and Prevention has released an app that emphasizes how to recognize, prevent, and treat fetal alcohol spectrum disorders. Earlier rates of fetal alcohol syndrome were estimated at 1/1,000, but FASD is estimated to occur at rates of 1/100. However, as I will illustrate below, the rates of FASD are even higher – much higher among some populations than previously thought.

The DSM-5 included in its appendix the diagnostic category of neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE), which theoretically should help psychiatrists identify FASD. Of course, the DSM-5 also includes an official diagnosis of disruptive mood dysregulation disorder (DMDD), and for the life of me, I have a difficult time differentiating between the two clinically except that children and adults with ND-PAE, in contrast to patients with DMDD who are described as persistently irritable or angry most of the day, can be very amicable, naive, and overly friendly between outbursts. The other difference is that ND-PAE needs a history of the mother’s having more than minimal exposure to alcohol during gestation, including prior to pregnancy recognition, and DMDD does not have this criteria, although it may be present. And, lastly DMDD is official and ND-PAE not.

Last year, Philip A. May, Ph.D., and his associates published an important paper, “Prevalence and Characteristics of Fetal Alcohol Spectrum Disorders” (Pediatrics 2014 [doi.10.1542/peds.2013-3319]). The authors looked at a representative Midwestern U.S. community with a population base of 160,000, 87% of which were white. The per-capita income of the population was $28,000, the median household income was $51,800, and 11% were below the poverty line.

Dr. May and his associates examined 70.5% (1,433 of 2,033) of all first-graders. Using one method of prevalence estimation, they found that 28.6/1,000 had FASD. Using a second method of prevalence estimation calculated from cases of FASD, they found an FASD rate of 82/1,000. The take-home message is, regardless of the academic fine points of how prevalence is estimated, these prevalence rates are much higher than previously reported.

In a second paper by Dr. Ira J. Chasnoff and his associates – “Misdiagnosis and Missed Diagnosis in Foster Care and Adopted Children with Prenatal Alcohol Exposure” – also published in Pediatrics, the rates of FASD in foster care and adopted youth were estimated to be even higher.

This study looked at 547 youth (50.6% African American, 1.3% Asian, 32.2% white, 0.7% Native American, 12.2% biracial, and 3% other/unknown) referred for severe behavioral disorders. The researchers found that 28.5% of these youth had FASD, 86.5% of the youth had never been diagnosed or were misdiagnosed, and 26.4% of these youth were misdiagnosed as having ADHD (Pediatrics 2014 [doi:10.1542/peds.2014-2171]).

Radhika L. Chimata and I published the third paper of significance online in Psychiatric Services. This paper, which is also slated for publication in print, focused on our work in a family medicine clinic on Chicago’s South Side, serving a population of 143,000. We looked at 611 patients (96% African American with a median household income of $33,809 – only 21 were youth, the rest were adults) and found that 297 (49%) of the adults and youth had neurodevelopmental disorders with 237 (39%) having clinical profiles consistent with neurobehavioral disorders associated with prenatal alcohol exposure. Thus, this clinic population has a rate of 388/1,000.

Considering emerging research that suggests that this acquired biological disorder is being driven by the social determinants of health, for example, some low-income African Americans are living not only in food deserts but food swamps (where the liquid is alcohol; consider the plethora of liquor stores in low-income African American communities), we must recognize that FASD can be prevented prenatally and possibly improved postnatally by increasing the amount of choline in the diet. This is a potential prevention intervention issue that we cannot afford to overlook if psychiatry is going to maintain its relevance in the 21st century.

Dr. Bell is a retired professor of psychiatry and public health at the University of Illinois at Chicago and staff psychiatrist at Jackson Park Hospital’s Outpatient Family Practice Clinic in Chicago. Dr. Bell is the former president and CEO of the Community Mental Health Council and former director of the Institute for Juvenile Research (birthplace of child psychiatry) at the university.

Fetal alcohol spectrum disorders are a vibrant area of development and research. Awareness about this preventable group of conditions appears to be growing.

In fact, the Centers for Disease Control and Prevention has released an app that emphasizes how to recognize, prevent, and treat fetal alcohol spectrum disorders. Earlier rates of fetal alcohol syndrome were estimated at 1/1,000, but FASD is estimated to occur at rates of 1/100. However, as I will illustrate below, the rates of FASD are even higher – much higher among some populations than previously thought.

The DSM-5 included in its appendix the diagnostic category of neurobehavioral disorder associated with prenatal alcohol exposure (ND-PAE), which theoretically should help psychiatrists identify FASD. Of course, the DSM-5 also includes an official diagnosis of disruptive mood dysregulation disorder (DMDD), and for the life of me, I have a difficult time differentiating between the two clinically except that children and adults with ND-PAE, in contrast to patients with DMDD who are described as persistently irritable or angry most of the day, can be very amicable, naive, and overly friendly between outbursts. The other difference is that ND-PAE needs a history of the mother’s having more than minimal exposure to alcohol during gestation, including prior to pregnancy recognition, and DMDD does not have this criteria, although it may be present. And, lastly DMDD is official and ND-PAE not.

Last year, Philip A. May, Ph.D., and his associates published an important paper, “Prevalence and Characteristics of Fetal Alcohol Spectrum Disorders” (Pediatrics 2014 [doi.10.1542/peds.2013-3319]). The authors looked at a representative Midwestern U.S. community with a population base of 160,000, 87% of which were white. The per-capita income of the population was $28,000, the median household income was $51,800, and 11% were below the poverty line.

Dr. May and his associates examined 70.5% (1,433 of 2,033) of all first-graders. Using one method of prevalence estimation, they found that 28.6/1,000 had FASD. Using a second method of prevalence estimation calculated from cases of FASD, they found an FASD rate of 82/1,000. The take-home message is, regardless of the academic fine points of how prevalence is estimated, these prevalence rates are much higher than previously reported.

In a second paper by Dr. Ira J. Chasnoff and his associates – “Misdiagnosis and Missed Diagnosis in Foster Care and Adopted Children with Prenatal Alcohol Exposure” – also published in Pediatrics, the rates of FASD in foster care and adopted youth were estimated to be even higher.

This study looked at 547 youth (50.6% African American, 1.3% Asian, 32.2% white, 0.7% Native American, 12.2% biracial, and 3% other/unknown) referred for severe behavioral disorders. The researchers found that 28.5% of these youth had FASD, 86.5% of the youth had never been diagnosed or were misdiagnosed, and 26.4% of these youth were misdiagnosed as having ADHD (Pediatrics 2014 [doi:10.1542/peds.2014-2171]).

Radhika L. Chimata and I published the third paper of significance online in Psychiatric Services. This paper, which is also slated for publication in print, focused on our work in a family medicine clinic on Chicago’s South Side, serving a population of 143,000. We looked at 611 patients (96% African American with a median household income of $33,809 – only 21 were youth, the rest were adults) and found that 297 (49%) of the adults and youth had neurodevelopmental disorders with 237 (39%) having clinical profiles consistent with neurobehavioral disorders associated with prenatal alcohol exposure. Thus, this clinic population has a rate of 388/1,000.

Considering emerging research that suggests that this acquired biological disorder is being driven by the social determinants of health, for example, some low-income African Americans are living not only in food deserts but food swamps (where the liquid is alcohol; consider the plethora of liquor stores in low-income African American communities), we must recognize that FASD can be prevented prenatally and possibly improved postnatally by increasing the amount of choline in the diet. This is a potential prevention intervention issue that we cannot afford to overlook if psychiatry is going to maintain its relevance in the 21st century.

Dr. Bell is a retired professor of psychiatry and public health at the University of Illinois at Chicago and staff psychiatrist at Jackson Park Hospital’s Outpatient Family Practice Clinic in Chicago. Dr. Bell is the former president and CEO of the Community Mental Health Council and former director of the Institute for Juvenile Research (birthplace of child psychiatry) at the university.