It was close to 2 decades ago, but it is still as clear as if it had been yesterday. I sat in the intensive care unit, fresh from my residency, tears streaming down my face, which was firmly nestled between my hands as I tried to hide my pain from every soul around me – doctors, nurses, patients’ family members – anyone and everyone.

I had just lost a very dear patient and emotions were running high. I only hoped no one at the nurses’ station would notice me, at least until I had a chance to regain my composure. After all, who would expect to see, or even respect, a doctor found sobbing like a child over a patient who died? Isn’t that all part of the job? Don’t we anticipate the death of some of our most critically ill patients?

Almost paralyzed with grief, I had a hard decision to make.

Option one: I could sit firmly planted in my seat and deal with my personal loss, the loss of my patient with chart number 0001 – yes, my very first patient in private practice. Over time, she and I had developed a very warm, loving relationship, almost like that of a mother and daughter as she was several decades my elder. I had a right to grieve my loss just as anyone else would grieve after losing someone they cared for, didn’t I?

Option two: I could bury my personal feelings and deal with them later in the comfort of my home, safe from the incessant pages from nurses calling about other patients’ urgent needs, hidden from accusing, sometimes condescending glances from other medical professionals who could never understand why I would react so strongly to the death of a patient – especially in a place surrounded by the watchful eyes of others who hold physicians to such a high standard.

Not so much to save face, but for the sake of other critically ill patients who needed a calm, clear-thinking physician to make prudent decisions regarding their care, I chose option two.

As hospitalists, our work is exciting and extremely rewarding, yet with all the suffering and death we see, we must be very careful to guard our hearts and minds, lest we fall into a state of perpetual inner turmoil and stress, and find ourselves seeking counseling or even prescription medication to cope. Compassion satisfaction and compassion fatigue are two ends of a spectrum that caregivers, including medical professionals, often experience. As the names suggest, the former refers to the positive feelings of helping others in need, while the latter refers to a potentially pathologic psychological adaptation to the suffering we experience.

Dr. Charles Figley, director of the Tulane Traumatology Institute in New Orleans, describes compassion fatigue as “a state experienced by those helping people or animals in distress; it is an extreme state of tension and preoccupation with the suffering of those being helped to the degree that it can create a secondary traumatic stress for the helper.”

We all have different coping mechanisms. Some hospitalists are so focused on the art of healing the sick that they have learned to dissociate themselves from the suffering of the individuals they serve, while still delivering excellent care to each and every patient. Not everyone has reached that level.

“Striking the right work-life balance helps me,” said Dr. Marianne Cunanan-Bush, medical director of the inpatient team at Baltimore Washington Medical Center in Glen Burnie, Md. “The first part of my day is spent in personal quiet time, [so] I can just relax and let my mind go free. And my family life is vital. My husband and I play tennis with our children and do other fun things as a family and that helps keep me grounded.”

Dr. Jiayan Chen, a hospitalist at Baltimore Washington Medical Center, finds it almost impossible to completely avoid compassion fatigue. “As hospitalists, I think we can only try to minimize it,” she said. “Try to be sympathetic to patient and family but remain neutral to avoid too high compassion fatigue. Talk to colleagues a couple of times a day, give yourself a few small breaks, including lunch time, drink a cup of water, anything to help break the tension of care during the day.”

Whatever your personal style or inner make-up, be true to yourself. It’s okay to be stoic and to cry sometimes, but if you need help dealing with the trauma and stress this profession sometimes brings, don’t be ashamed to seek the counsel of friends, family members, or even professionals. Two useful resources for help in dealing with, and preventing, compassion fatigue are the Compassion Fatigue Awareness Project and ProQOL.org.

Those of you with small children will appreciate this more than others: As the words of a popular song sung by little girls from coast to coast say, “Let it go, let it go. Don’t hold it back anymore!”

Dr. Hester is a hospitalist at Baltimore Washington Medical Center in Glen Burnie, Md. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at [email protected].

It was close to 2 decades ago, but it is still as clear as if it had been yesterday. I sat in the intensive care unit, fresh from my residency, tears streaming down my face, which was firmly nestled between my hands as I tried to hide my pain from every soul around me – doctors, nurses, patients’ family members – anyone and everyone.

I had just lost a very dear patient and emotions were running high. I only hoped no one at the nurses’ station would notice me, at least until I had a chance to regain my composure. After all, who would expect to see, or even respect, a doctor found sobbing like a child over a patient who died? Isn’t that all part of the job? Don’t we anticipate the death of some of our most critically ill patients?

Almost paralyzed with grief, I had a hard decision to make.

Option one: I could sit firmly planted in my seat and deal with my personal loss, the loss of my patient with chart number 0001 – yes, my very first patient in private practice. Over time, she and I had developed a very warm, loving relationship, almost like that of a mother and daughter as she was several decades my elder. I had a right to grieve my loss just as anyone else would grieve after losing someone they cared for, didn’t I?

Option two: I could bury my personal feelings and deal with them later in the comfort of my home, safe from the incessant pages from nurses calling about other patients’ urgent needs, hidden from accusing, sometimes condescending glances from other medical professionals who could never understand why I would react so strongly to the death of a patient – especially in a place surrounded by the watchful eyes of others who hold physicians to such a high standard.

Not so much to save face, but for the sake of other critically ill patients who needed a calm, clear-thinking physician to make prudent decisions regarding their care, I chose option two.

As hospitalists, our work is exciting and extremely rewarding, yet with all the suffering and death we see, we must be very careful to guard our hearts and minds, lest we fall into a state of perpetual inner turmoil and stress, and find ourselves seeking counseling or even prescription medication to cope. Compassion satisfaction and compassion fatigue are two ends of a spectrum that caregivers, including medical professionals, often experience. As the names suggest, the former refers to the positive feelings of helping others in need, while the latter refers to a potentially pathologic psychological adaptation to the suffering we experience.

Dr. Charles Figley, director of the Tulane Traumatology Institute in New Orleans, describes compassion fatigue as “a state experienced by those helping people or animals in distress; it is an extreme state of tension and preoccupation with the suffering of those being helped to the degree that it can create a secondary traumatic stress for the helper.”

We all have different coping mechanisms. Some hospitalists are so focused on the art of healing the sick that they have learned to dissociate themselves from the suffering of the individuals they serve, while still delivering excellent care to each and every patient. Not everyone has reached that level.

“Striking the right work-life balance helps me,” said Dr. Marianne Cunanan-Bush, medical director of the inpatient team at Baltimore Washington Medical Center in Glen Burnie, Md. “The first part of my day is spent in personal quiet time, [so] I can just relax and let my mind go free. And my family life is vital. My husband and I play tennis with our children and do other fun things as a family and that helps keep me grounded.”

Dr. Jiayan Chen, a hospitalist at Baltimore Washington Medical Center, finds it almost impossible to completely avoid compassion fatigue. “As hospitalists, I think we can only try to minimize it,” she said. “Try to be sympathetic to patient and family but remain neutral to avoid too high compassion fatigue. Talk to colleagues a couple of times a day, give yourself a few small breaks, including lunch time, drink a cup of water, anything to help break the tension of care during the day.”

Whatever your personal style or inner make-up, be true to yourself. It’s okay to be stoic and to cry sometimes, but if you need help dealing with the trauma and stress this profession sometimes brings, don’t be ashamed to seek the counsel of friends, family members, or even professionals. Two useful resources for help in dealing with, and preventing, compassion fatigue are the Compassion Fatigue Awareness Project and ProQOL.org.

Those of you with small children will appreciate this more than others: As the words of a popular song sung by little girls from coast to coast say, “Let it go, let it go. Don’t hold it back anymore!”

Dr. Hester is a hospitalist at Baltimore Washington Medical Center in Glen Burnie, Md. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at [email protected].

It was close to 2 decades ago, but it is still as clear as if it had been yesterday. I sat in the intensive care unit, fresh from my residency, tears streaming down my face, which was firmly nestled between my hands as I tried to hide my pain from every soul around me – doctors, nurses, patients’ family members – anyone and everyone.

I had just lost a very dear patient and emotions were running high. I only hoped no one at the nurses’ station would notice me, at least until I had a chance to regain my composure. After all, who would expect to see, or even respect, a doctor found sobbing like a child over a patient who died? Isn’t that all part of the job? Don’t we anticipate the death of some of our most critically ill patients?

Almost paralyzed with grief, I had a hard decision to make.

Option one: I could sit firmly planted in my seat and deal with my personal loss, the loss of my patient with chart number 0001 – yes, my very first patient in private practice. Over time, she and I had developed a very warm, loving relationship, almost like that of a mother and daughter as she was several decades my elder. I had a right to grieve my loss just as anyone else would grieve after losing someone they cared for, didn’t I?

Option two: I could bury my personal feelings and deal with them later in the comfort of my home, safe from the incessant pages from nurses calling about other patients’ urgent needs, hidden from accusing, sometimes condescending glances from other medical professionals who could never understand why I would react so strongly to the death of a patient – especially in a place surrounded by the watchful eyes of others who hold physicians to such a high standard.

Not so much to save face, but for the sake of other critically ill patients who needed a calm, clear-thinking physician to make prudent decisions regarding their care, I chose option two.

As hospitalists, our work is exciting and extremely rewarding, yet with all the suffering and death we see, we must be very careful to guard our hearts and minds, lest we fall into a state of perpetual inner turmoil and stress, and find ourselves seeking counseling or even prescription medication to cope. Compassion satisfaction and compassion fatigue are two ends of a spectrum that caregivers, including medical professionals, often experience. As the names suggest, the former refers to the positive feelings of helping others in need, while the latter refers to a potentially pathologic psychological adaptation to the suffering we experience.

Dr. Charles Figley, director of the Tulane Traumatology Institute in New Orleans, describes compassion fatigue as “a state experienced by those helping people or animals in distress; it is an extreme state of tension and preoccupation with the suffering of those being helped to the degree that it can create a secondary traumatic stress for the helper.”

We all have different coping mechanisms. Some hospitalists are so focused on the art of healing the sick that they have learned to dissociate themselves from the suffering of the individuals they serve, while still delivering excellent care to each and every patient. Not everyone has reached that level.

“Striking the right work-life balance helps me,” said Dr. Marianne Cunanan-Bush, medical director of the inpatient team at Baltimore Washington Medical Center in Glen Burnie, Md. “The first part of my day is spent in personal quiet time, [so] I can just relax and let my mind go free. And my family life is vital. My husband and I play tennis with our children and do other fun things as a family and that helps keep me grounded.”

Dr. Jiayan Chen, a hospitalist at Baltimore Washington Medical Center, finds it almost impossible to completely avoid compassion fatigue. “As hospitalists, I think we can only try to minimize it,” she said. “Try to be sympathetic to patient and family but remain neutral to avoid too high compassion fatigue. Talk to colleagues a couple of times a day, give yourself a few small breaks, including lunch time, drink a cup of water, anything to help break the tension of care during the day.”

Whatever your personal style or inner make-up, be true to yourself. It’s okay to be stoic and to cry sometimes, but if you need help dealing with the trauma and stress this profession sometimes brings, don’t be ashamed to seek the counsel of friends, family members, or even professionals. Two useful resources for help in dealing with, and preventing, compassion fatigue are the Compassion Fatigue Awareness Project and ProQOL.org.

Those of you with small children will appreciate this more than others: As the words of a popular song sung by little girls from coast to coast say, “Let it go, let it go. Don’t hold it back anymore!”

Dr. Hester is a hospitalist at Baltimore Washington Medical Center in Glen Burnie, Md. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at [email protected].

Vitiligo is a common, asymptomatic, acquired depigmentation disorder that is caused by an unknown etiology. Lesions appear as sharply demarcated, depigmented macules and patches that are scattered symmetrically or unsymmetrically over the body. The presentation can be delineated based on the segmental or nonsegmental nature of the disease. According to the revised classification/nomenclature of vitiligo,¹ the disorder can be classified as nonsegmental, segmental, mixed, or unclassified. The pathogenesis of the vitiligo disease process is due to multiple modalities that contribute to melanocyte loss. Theories for melanocyte destruction include but are not limited to autoimmunity, biochemicals, epidermal cytokines, increased hydrogen peroxide and free radicals, and humoral and cellular immune alteration.^2,3

Despite its long history, the most frustrating aspect of the vitiligo disease process remains its treatment due to limited efficacy, frequent application of topicals, and the need for high-potency steroids. Medical therapies usually are the first line of treatment and are most effective with few side effects for bilateral nonsegmental or evolving vitiligo.² Some of the primary therapies with the highest efficacies appear to be calcipotriene and psoralen plus UVA, psoralen plus UVA as monotherapy, excimer laser, narrowband UVB, oral steroids, 8-methoxypsoralen, tacrolimus, and topical steroids.⁴ The theory is that these treatments would be successful if the patient had active melanocytes in the external root sheath that would be able to repigment a patch of vitiligo.⁵ Hence, it would be more difficult to treat areas such as the dorsal aspect of the fingers and toes because they lack hair-bearing areas with melanocytes.⁶ The alternative approach to treating vitiligo patches would be surgical intervention techniques, as they provide melanocytic cells to a previously depigmented area.^3,5 The focus of this article is to evaluate the efficacy and appropriate use of some of the surgical procedures that can be used in the treatment of vitiligo patients.

Candidate Selection

First, vitiligo patients for whom first-line treatment with medical therapies has failed are candidates for surgical techniques. The second vital component is to clinically confirm the diagnosis of vitiligo as opposed to other genetic, infectious, or autoimmune causes of pigment loss. Lastly, the vitiligo patch should be stable. A stable vitiligo patch does not continue to progress and is no longer responsive to topical medications that are meant to repigment for a discernible period of time.⁷

Classification of Disease Stage

To classify the stage of vitiligo prior to surgical intervention, Gauthier⁸ created a basic grading system: grade I, with partial depletion of epidermal melanocytes in a vitiligo patch that responds to repigmentation in a follicular pattern evenly such as on the face and neck; grade II, with complete depletion of epidermal melanocytes with a usual follicular pattern of repigmentation; and grade III, indicating complete depletion of follicular melanocytes with no hope of response to medical therapy. According to Rusfianti and Wirohadidjodjo,² the surgical techniques that have developed over the years for treatment of grade III vitiligo patients include split-thickness skin grafting, suction blister grafting, miniature punch grafting, and cultured melanocyte transplantation.

Surgical Techniques

Split-thickness skin grafting is an older procedure that entails the use of a harvesting graft site with no pigment loss and dermabrasion of the recipient area to allow interaction with the wound bed.⁹ With proper care and minimal movement or wrinkling of the graft site, patients can have repigmentation without skip areas.

Suction blister grafting is another tried and tested surgical intervention. Hasegawa et al¹⁰ conducted a study of 15 patients (13 males, 2 females; age range, 16–38 years) diagnosed with segmental vitiligo who were treated using the suction blister grafting technique with CO₂ laser resurfacing. Patients were recruited 1 month prior to initiating therapy and no other treatments were used during the month or in conjunction with the surgical intervention. Suction blisters were harvested from the left thigh and transferred in saline to the recipient site, which was abraded with 1 pass of the short-pulse CO₂ laser system. The recipient sites were then closed with 7-0 nylon sutures and covered tightly with tie-over dressings for at least 1 week. Within 6 months of the procedure, a treatment response of 100% was seen in 15 patients, making it an effective method for treatment-resistant vitiligo patients.¹⁰

Miniature punch grafting is another possible treatment option for resistant cases of vitiligo. Mapar et al¹¹ conducted a study in 25 patients (21 women, 4 men; age range, 20–47 years) who had been diagnosed with stable vitiligo (ie, no progression in the last 2 years) and were treated with single hair follicle transplant versus miniature punch grafting. The theory behind the study was to use the melanocytic reservoir noted in the normal hair follicle to repigment the vitiligo patch. With follow-up of both methods of treatment, there was no statistical difference in treatment results.¹¹ A similar study was conducted by Malakar and Lahiri¹² in patients with lip leukoderma (a variant of vitiligo). One hundred eight patients (41 males, 67 females; age range, 14–62 years) who had been diagnosed with stable lip leukoderma (ie, stable vitiligo for at least 6 months) underwent treatment via autologous miniature punch grafting. Punch biopsies were performed in donor sites of the buttocks and upper thighs with 72% of patients noting complete repigmentation. Complications noted were herpes labialis–induced lip leukoderma, which ultimately led to rejection of the graft site.¹² Overall, however, miniature punch grafting is a viable surgical option in stable vitiligo patients.

Cultured melanocyte transplantation, or a noncultured epidermal suspension, was first initiated in 1992.¹³ Silpa-Archa et al¹⁴ conducted an open, split-comparison study of 6 vitiligo patients (5 women, 1 man; age range, 20–65 years) with stable lesions. Fifty percent of patients received autologous pigmented skin cellular suspension, which was applied to vitiligo-affected skin that was treated with a fractionated CO₂ laser, and 50% received dermabrasion. Composite dressing was placed overlying the site with dressing removal in 1 week. The degree of repigmentation was based on a modified vitiligo area scoring index scale of poor (0%–25%), fair (26%–50%), good (51%–75%), very good (76%–90%), or excellent (91%–100%). Overall repigmentation was very good to excellent in all 6 patients.¹⁴ Potentially, this method can far improve the surgical treatment options for future vitiligo patients.

Final Thoughts

Overall, when evaluating surgical interventions for the treatment of vitiligo, careful consideration of the patient’s disease progression, failed therapies, outcome expectations, and repigmentation is warranted prior to initiating any procedure. For appropriate candidates, a range of surgical methodologies has proven to be effective in treatment of stable vitiligo patients.

Vitiligo is a common, asymptomatic, acquired depigmentation disorder that is caused by an unknown etiology. Lesions appear as sharply demarcated, depigmented macules and patches that are scattered symmetrically or unsymmetrically over the body. The presentation can be delineated based on the segmental or nonsegmental nature of the disease. According to the revised classification/nomenclature of vitiligo,¹ the disorder can be classified as nonsegmental, segmental, mixed, or unclassified. The pathogenesis of the vitiligo disease process is due to multiple modalities that contribute to melanocyte loss. Theories for melanocyte destruction include but are not limited to autoimmunity, biochemicals, epidermal cytokines, increased hydrogen peroxide and free radicals, and humoral and cellular immune alteration.^2,3

Despite its long history, the most frustrating aspect of the vitiligo disease process remains its treatment due to limited efficacy, frequent application of topicals, and the need for high-potency steroids. Medical therapies usually are the first line of treatment and are most effective with few side effects for bilateral nonsegmental or evolving vitiligo.² Some of the primary therapies with the highest efficacies appear to be calcipotriene and psoralen plus UVA, psoralen plus UVA as monotherapy, excimer laser, narrowband UVB, oral steroids, 8-methoxypsoralen, tacrolimus, and topical steroids.⁴ The theory is that these treatments would be successful if the patient had active melanocytes in the external root sheath that would be able to repigment a patch of vitiligo.⁵ Hence, it would be more difficult to treat areas such as the dorsal aspect of the fingers and toes because they lack hair-bearing areas with melanocytes.⁶ The alternative approach to treating vitiligo patches would be surgical intervention techniques, as they provide melanocytic cells to a previously depigmented area.^3,5 The focus of this article is to evaluate the efficacy and appropriate use of some of the surgical procedures that can be used in the treatment of vitiligo patients.

Candidate Selection

First, vitiligo patients for whom first-line treatment with medical therapies has failed are candidates for surgical techniques. The second vital component is to clinically confirm the diagnosis of vitiligo as opposed to other genetic, infectious, or autoimmune causes of pigment loss. Lastly, the vitiligo patch should be stable. A stable vitiligo patch does not continue to progress and is no longer responsive to topical medications that are meant to repigment for a discernible period of time.⁷

Classification of Disease Stage

To classify the stage of vitiligo prior to surgical intervention, Gauthier⁸ created a basic grading system: grade I, with partial depletion of epidermal melanocytes in a vitiligo patch that responds to repigmentation in a follicular pattern evenly such as on the face and neck; grade II, with complete depletion of epidermal melanocytes with a usual follicular pattern of repigmentation; and grade III, indicating complete depletion of follicular melanocytes with no hope of response to medical therapy. According to Rusfianti and Wirohadidjodjo,² the surgical techniques that have developed over the years for treatment of grade III vitiligo patients include split-thickness skin grafting, suction blister grafting, miniature punch grafting, and cultured melanocyte transplantation.

Surgical Techniques

Split-thickness skin grafting is an older procedure that entails the use of a harvesting graft site with no pigment loss and dermabrasion of the recipient area to allow interaction with the wound bed.⁹ With proper care and minimal movement or wrinkling of the graft site, patients can have repigmentation without skip areas.

Suction blister grafting is another tried and tested surgical intervention. Hasegawa et al¹⁰ conducted a study of 15 patients (13 males, 2 females; age range, 16–38 years) diagnosed with segmental vitiligo who were treated using the suction blister grafting technique with CO₂ laser resurfacing. Patients were recruited 1 month prior to initiating therapy and no other treatments were used during the month or in conjunction with the surgical intervention. Suction blisters were harvested from the left thigh and transferred in saline to the recipient site, which was abraded with 1 pass of the short-pulse CO₂ laser system. The recipient sites were then closed with 7-0 nylon sutures and covered tightly with tie-over dressings for at least 1 week. Within 6 months of the procedure, a treatment response of 100% was seen in 15 patients, making it an effective method for treatment-resistant vitiligo patients.¹⁰

Miniature punch grafting is another possible treatment option for resistant cases of vitiligo. Mapar et al¹¹ conducted a study in 25 patients (21 women, 4 men; age range, 20–47 years) who had been diagnosed with stable vitiligo (ie, no progression in the last 2 years) and were treated with single hair follicle transplant versus miniature punch grafting. The theory behind the study was to use the melanocytic reservoir noted in the normal hair follicle to repigment the vitiligo patch. With follow-up of both methods of treatment, there was no statistical difference in treatment results.¹¹ A similar study was conducted by Malakar and Lahiri¹² in patients with lip leukoderma (a variant of vitiligo). One hundred eight patients (41 males, 67 females; age range, 14–62 years) who had been diagnosed with stable lip leukoderma (ie, stable vitiligo for at least 6 months) underwent treatment via autologous miniature punch grafting. Punch biopsies were performed in donor sites of the buttocks and upper thighs with 72% of patients noting complete repigmentation. Complications noted were herpes labialis–induced lip leukoderma, which ultimately led to rejection of the graft site.¹² Overall, however, miniature punch grafting is a viable surgical option in stable vitiligo patients.

Cultured melanocyte transplantation, or a noncultured epidermal suspension, was first initiated in 1992.¹³ Silpa-Archa et al¹⁴ conducted an open, split-comparison study of 6 vitiligo patients (5 women, 1 man; age range, 20–65 years) with stable lesions. Fifty percent of patients received autologous pigmented skin cellular suspension, which was applied to vitiligo-affected skin that was treated with a fractionated CO₂ laser, and 50% received dermabrasion. Composite dressing was placed overlying the site with dressing removal in 1 week. The degree of repigmentation was based on a modified vitiligo area scoring index scale of poor (0%–25%), fair (26%–50%), good (51%–75%), very good (76%–90%), or excellent (91%–100%). Overall repigmentation was very good to excellent in all 6 patients.¹⁴ Potentially, this method can far improve the surgical treatment options for future vitiligo patients.

Final Thoughts

Overall, when evaluating surgical interventions for the treatment of vitiligo, careful consideration of the patient’s disease progression, failed therapies, outcome expectations, and repigmentation is warranted prior to initiating any procedure. For appropriate candidates, a range of surgical methodologies has proven to be effective in treatment of stable vitiligo patients.

Vitiligo is a common, asymptomatic, acquired depigmentation disorder that is caused by an unknown etiology. Lesions appear as sharply demarcated, depigmented macules and patches that are scattered symmetrically or unsymmetrically over the body. The presentation can be delineated based on the segmental or nonsegmental nature of the disease. According to the revised classification/nomenclature of vitiligo,¹ the disorder can be classified as nonsegmental, segmental, mixed, or unclassified. The pathogenesis of the vitiligo disease process is due to multiple modalities that contribute to melanocyte loss. Theories for melanocyte destruction include but are not limited to autoimmunity, biochemicals, epidermal cytokines, increased hydrogen peroxide and free radicals, and humoral and cellular immune alteration.^2,3

Despite its long history, the most frustrating aspect of the vitiligo disease process remains its treatment due to limited efficacy, frequent application of topicals, and the need for high-potency steroids. Medical therapies usually are the first line of treatment and are most effective with few side effects for bilateral nonsegmental or evolving vitiligo.² Some of the primary therapies with the highest efficacies appear to be calcipotriene and psoralen plus UVA, psoralen plus UVA as monotherapy, excimer laser, narrowband UVB, oral steroids, 8-methoxypsoralen, tacrolimus, and topical steroids.⁴ The theory is that these treatments would be successful if the patient had active melanocytes in the external root sheath that would be able to repigment a patch of vitiligo.⁵ Hence, it would be more difficult to treat areas such as the dorsal aspect of the fingers and toes because they lack hair-bearing areas with melanocytes.⁶ The alternative approach to treating vitiligo patches would be surgical intervention techniques, as they provide melanocytic cells to a previously depigmented area.^3,5 The focus of this article is to evaluate the efficacy and appropriate use of some of the surgical procedures that can be used in the treatment of vitiligo patients.

Candidate Selection

First, vitiligo patients for whom first-line treatment with medical therapies has failed are candidates for surgical techniques. The second vital component is to clinically confirm the diagnosis of vitiligo as opposed to other genetic, infectious, or autoimmune causes of pigment loss. Lastly, the vitiligo patch should be stable. A stable vitiligo patch does not continue to progress and is no longer responsive to topical medications that are meant to repigment for a discernible period of time.⁷

Classification of Disease Stage

To classify the stage of vitiligo prior to surgical intervention, Gauthier⁸ created a basic grading system: grade I, with partial depletion of epidermal melanocytes in a vitiligo patch that responds to repigmentation in a follicular pattern evenly such as on the face and neck; grade II, with complete depletion of epidermal melanocytes with a usual follicular pattern of repigmentation; and grade III, indicating complete depletion of follicular melanocytes with no hope of response to medical therapy. According to Rusfianti and Wirohadidjodjo,² the surgical techniques that have developed over the years for treatment of grade III vitiligo patients include split-thickness skin grafting, suction blister grafting, miniature punch grafting, and cultured melanocyte transplantation.

Surgical Techniques

Split-thickness skin grafting is an older procedure that entails the use of a harvesting graft site with no pigment loss and dermabrasion of the recipient area to allow interaction with the wound bed.⁹ With proper care and minimal movement or wrinkling of the graft site, patients can have repigmentation without skip areas.

Suction blister grafting is another tried and tested surgical intervention. Hasegawa et al¹⁰ conducted a study of 15 patients (13 males, 2 females; age range, 16–38 years) diagnosed with segmental vitiligo who were treated using the suction blister grafting technique with CO₂ laser resurfacing. Patients were recruited 1 month prior to initiating therapy and no other treatments were used during the month or in conjunction with the surgical intervention. Suction blisters were harvested from the left thigh and transferred in saline to the recipient site, which was abraded with 1 pass of the short-pulse CO₂ laser system. The recipient sites were then closed with 7-0 nylon sutures and covered tightly with tie-over dressings for at least 1 week. Within 6 months of the procedure, a treatment response of 100% was seen in 15 patients, making it an effective method for treatment-resistant vitiligo patients.¹⁰

Miniature punch grafting is another possible treatment option for resistant cases of vitiligo. Mapar et al¹¹ conducted a study in 25 patients (21 women, 4 men; age range, 20–47 years) who had been diagnosed with stable vitiligo (ie, no progression in the last 2 years) and were treated with single hair follicle transplant versus miniature punch grafting. The theory behind the study was to use the melanocytic reservoir noted in the normal hair follicle to repigment the vitiligo patch. With follow-up of both methods of treatment, there was no statistical difference in treatment results.¹¹ A similar study was conducted by Malakar and Lahiri¹² in patients with lip leukoderma (a variant of vitiligo). One hundred eight patients (41 males, 67 females; age range, 14–62 years) who had been diagnosed with stable lip leukoderma (ie, stable vitiligo for at least 6 months) underwent treatment via autologous miniature punch grafting. Punch biopsies were performed in donor sites of the buttocks and upper thighs with 72% of patients noting complete repigmentation. Complications noted were herpes labialis–induced lip leukoderma, which ultimately led to rejection of the graft site.¹² Overall, however, miniature punch grafting is a viable surgical option in stable vitiligo patients.

Cultured melanocyte transplantation, or a noncultured epidermal suspension, was first initiated in 1992.¹³ Silpa-Archa et al¹⁴ conducted an open, split-comparison study of 6 vitiligo patients (5 women, 1 man; age range, 20–65 years) with stable lesions. Fifty percent of patients received autologous pigmented skin cellular suspension, which was applied to vitiligo-affected skin that was treated with a fractionated CO₂ laser, and 50% received dermabrasion. Composite dressing was placed overlying the site with dressing removal in 1 week. The degree of repigmentation was based on a modified vitiligo area scoring index scale of poor (0%–25%), fair (26%–50%), good (51%–75%), very good (76%–90%), or excellent (91%–100%). Overall repigmentation was very good to excellent in all 6 patients.¹⁴ Potentially, this method can far improve the surgical treatment options for future vitiligo patients.

Final Thoughts

Overall, when evaluating surgical interventions for the treatment of vitiligo, careful consideration of the patient’s disease progression, failed therapies, outcome expectations, and repigmentation is warranted prior to initiating any procedure. For appropriate candidates, a range of surgical methodologies has proven to be effective in treatment of stable vitiligo patients.

BALTIMORE – Children with systemic juvenile idiopathic arthritis have the best odds for responding to initial treatment with a nonsteroidal anti-inflammatory drug if they are no older than 6 years old, have five or fewer involved joints, and have a serum level of C-reactive protein that is at or below 13 mg/dL, based on a review of 57 children with systemic juvenile idiopathic arthritis treated with these drugs at a single U.S. center during 2000-2014.

“We recommend a trial of NSAID [nonsteroidal anti-inflammatory drug] monotherapy for these patients with systemic juvenile idiopathic arthritis [JIA],” Dr. Anjali S. Sura said at the annual meeting of the Pediatric Academic Societies. A reasonable trial of NSAID monotherapy would last 6 weeks; if patients failed to adequately respond at the end of 6 weeks, it would be reasonable to switch to another of the first-line drugs recommended for children starting treatment for JIA, either a glucocorticoid or the biological agent anakinra (Kineret), said Dr. Sura, a pediatrician at the University of Michigan in Ann Arbor.

Initial treatment with a NSAID is preferred, even though it will probably work in only about a quarter of patients, because it generally has the best safety profile among these three options, Dr. Sura said in an interview. “If we can risk-stratify children with systemic JIA for NSAID therapy” using these three criteria, “then NSAID monotherapy may be more effective,” she explained.

The NSAIDs most commonly used to treat systemic JIA are naproxen or indomethacin, at anti-inflammatory dosages, which for naproxen is 15-20 mg/kg per day, and for indomethacin 3-4 mg/kg per day, she said.

But Dr. Sura also cautioned that the analysis she presented focused on a relatively small and selected group of children with systemic JIA who received initial NSAID monotherapy. The series she and her associates reviewed included 99 patients, of whom 57 received NSAID monotherapy; 35 of these patients were 6 years old or younger.

The researchers compared the 15 NSAID responders (26%), defined as patients who had clinically inactive disease, with the 42 nonresponders and identified the three clinical and demographic characteristics that occurred much more often among responders. The ideal candidates for initial NSAID monotherapy should fulfill all three criteria: age, number of affected joints, and serum level of C-reactive protein, Dr. Sura said in her report.

Dr. Sura noted that a panel of the American College of Rheumatology said that NSAIDs, glucocorticoids, and anakinra were equally good options for initial treatment of JIA in their 2013 update of JIA recommendations (Arthritis Rheum. 2013 Oct;65[10]:2499-512). This 2013 update excepted patients with no actively affected joints, whom the panel said should specifically receive an NSAID, and excepted patients with a high global severity score as rated by their physicians, whom the panel said should receive either a glucocorticoid or anakinra but not NSAID monotherapy. The European League Against Rheumatism has not issued recommendations for managing systemic JIA.

Dr. Sura had no disclosures.

[email protected]

On Twitter @mitchelzoler

BALTIMORE – Children with systemic juvenile idiopathic arthritis have the best odds for responding to initial treatment with a nonsteroidal anti-inflammatory drug if they are no older than 6 years old, have five or fewer involved joints, and have a serum level of C-reactive protein that is at or below 13 mg/dL, based on a review of 57 children with systemic juvenile idiopathic arthritis treated with these drugs at a single U.S. center during 2000-2014.

“We recommend a trial of NSAID [nonsteroidal anti-inflammatory drug] monotherapy for these patients with systemic juvenile idiopathic arthritis [JIA],” Dr. Anjali S. Sura said at the annual meeting of the Pediatric Academic Societies. A reasonable trial of NSAID monotherapy would last 6 weeks; if patients failed to adequately respond at the end of 6 weeks, it would be reasonable to switch to another of the first-line drugs recommended for children starting treatment for JIA, either a glucocorticoid or the biological agent anakinra (Kineret), said Dr. Sura, a pediatrician at the University of Michigan in Ann Arbor.

Initial treatment with a NSAID is preferred, even though it will probably work in only about a quarter of patients, because it generally has the best safety profile among these three options, Dr. Sura said in an interview. “If we can risk-stratify children with systemic JIA for NSAID therapy” using these three criteria, “then NSAID monotherapy may be more effective,” she explained.

The NSAIDs most commonly used to treat systemic JIA are naproxen or indomethacin, at anti-inflammatory dosages, which for naproxen is 15-20 mg/kg per day, and for indomethacin 3-4 mg/kg per day, she said.

But Dr. Sura also cautioned that the analysis she presented focused on a relatively small and selected group of children with systemic JIA who received initial NSAID monotherapy. The series she and her associates reviewed included 99 patients, of whom 57 received NSAID monotherapy; 35 of these patients were 6 years old or younger.

The researchers compared the 15 NSAID responders (26%), defined as patients who had clinically inactive disease, with the 42 nonresponders and identified the three clinical and demographic characteristics that occurred much more often among responders. The ideal candidates for initial NSAID monotherapy should fulfill all three criteria: age, number of affected joints, and serum level of C-reactive protein, Dr. Sura said in her report.

Dr. Sura noted that a panel of the American College of Rheumatology said that NSAIDs, glucocorticoids, and anakinra were equally good options for initial treatment of JIA in their 2013 update of JIA recommendations (Arthritis Rheum. 2013 Oct;65[10]:2499-512). This 2013 update excepted patients with no actively affected joints, whom the panel said should specifically receive an NSAID, and excepted patients with a high global severity score as rated by their physicians, whom the panel said should receive either a glucocorticoid or anakinra but not NSAID monotherapy. The European League Against Rheumatism has not issued recommendations for managing systemic JIA.

Dr. Sura had no disclosures.

[email protected]

On Twitter @mitchelzoler

BALTIMORE – Children with systemic juvenile idiopathic arthritis have the best odds for responding to initial treatment with a nonsteroidal anti-inflammatory drug if they are no older than 6 years old, have five or fewer involved joints, and have a serum level of C-reactive protein that is at or below 13 mg/dL, based on a review of 57 children with systemic juvenile idiopathic arthritis treated with these drugs at a single U.S. center during 2000-2014.

“We recommend a trial of NSAID [nonsteroidal anti-inflammatory drug] monotherapy for these patients with systemic juvenile idiopathic arthritis [JIA],” Dr. Anjali S. Sura said at the annual meeting of the Pediatric Academic Societies. A reasonable trial of NSAID monotherapy would last 6 weeks; if patients failed to adequately respond at the end of 6 weeks, it would be reasonable to switch to another of the first-line drugs recommended for children starting treatment for JIA, either a glucocorticoid or the biological agent anakinra (Kineret), said Dr. Sura, a pediatrician at the University of Michigan in Ann Arbor.

Initial treatment with a NSAID is preferred, even though it will probably work in only about a quarter of patients, because it generally has the best safety profile among these three options, Dr. Sura said in an interview. “If we can risk-stratify children with systemic JIA for NSAID therapy” using these three criteria, “then NSAID monotherapy may be more effective,” she explained.

The NSAIDs most commonly used to treat systemic JIA are naproxen or indomethacin, at anti-inflammatory dosages, which for naproxen is 15-20 mg/kg per day, and for indomethacin 3-4 mg/kg per day, she said.

But Dr. Sura also cautioned that the analysis she presented focused on a relatively small and selected group of children with systemic JIA who received initial NSAID monotherapy. The series she and her associates reviewed included 99 patients, of whom 57 received NSAID monotherapy; 35 of these patients were 6 years old or younger.

The researchers compared the 15 NSAID responders (26%), defined as patients who had clinically inactive disease, with the 42 nonresponders and identified the three clinical and demographic characteristics that occurred much more often among responders. The ideal candidates for initial NSAID monotherapy should fulfill all three criteria: age, number of affected joints, and serum level of C-reactive protein, Dr. Sura said in her report.

Dr. Sura noted that a panel of the American College of Rheumatology said that NSAIDs, glucocorticoids, and anakinra were equally good options for initial treatment of JIA in their 2013 update of JIA recommendations (Arthritis Rheum. 2013 Oct;65[10]:2499-512). This 2013 update excepted patients with no actively affected joints, whom the panel said should specifically receive an NSAID, and excepted patients with a high global severity score as rated by their physicians, whom the panel said should receive either a glucocorticoid or anakinra but not NSAID monotherapy. The European League Against Rheumatism has not issued recommendations for managing systemic JIA.

Dr. Sura had no disclosures.

[email protected]

On Twitter @mitchelzoler

My newest iteration of a VIP, or very ill patient, is a lovely middle-aged gentleman who has been sick for a year with a multisystem disorder. It started with severely swollen hands and feet along with significant anemia and fatigue. One year, many imaging studies, a couple of biopsies, and a latent tuberculosis infection later, he is still very sick. Throughout his ordeal he has often said to me: “You are the quarterback.” I’ve taken that to heart.

I don’t know why this surprises me, but insurance companies are being increasingly difficult. They’re passing more of the cost of health care to patients, and they’re less willing to cover medications and procedures. I have patients who can’t get physical therapy because they can’t afford the $45 copay for each visit. One patient stopped her hydroxychloroquine because it went from $4/month to $90/month. A couple of patients have opted not to take risedronate because the copay per month is $200 – that’s $200 for one generic pill.

At a recent morbidity and mortality conference, the attendees, nonrheumatologists all, were incredulous that cyclophosphamide, which has been around for ages and should be generic, is not covered by Medicare. Our patient with granulomatosis with polyangiitis and alveolar hemorrhage was on the hook for several hundred dollars per month, which he couldn’t afford.

Insurers also have been giving me more pushback for medications. For example, I recently tried to start one of my patients on etanercept for rheumatoid arthritis. His insurance company wrote to say etanercept was not their “preferred” first-line biologic. I explained that their preferred anti-TNF agents all carried the potential for developing anti-drug antibodies when used without methotrexate, which was contraindicated in my patient. They were unmoved.

I had a similar experience with my VIP. He was denied tocilizumab because he had not yet tried and failed two anti-TNF agents. I appealed the decision because I thought etanercept had caused a side effect that might be a class effect. To my surprise, rather than getting an approval, I received instead a request for medical literature to support my theory. Who knew that the decision-bots were so sophisticated?

Ultimately, I got the drug approved, but of course this process was an inconvenience to me, adding unnecessarily to the work of doctoring. More importantly, it was time wasted for my patient who was suffering tremendously.

My point is this: The idea of me as quarterback is quaint. Ultimately, it is the insurance company that dictates testing, treatment, physician, and facility.

There is an expectation that physicians are perfect, and we have internalized that expectation to some degree, holding ourselves to exacting standards, guided by what’s in the patient’s best interest. I want to know what sort of standards insurance companies hold themselves to, because I think they – out of all of us involved in health care – they who have the greatest resources should be absolutely unimpeachable.

Dr. Chan practices rheumatology in Pawtucket, R.I.

My newest iteration of a VIP, or very ill patient, is a lovely middle-aged gentleman who has been sick for a year with a multisystem disorder. It started with severely swollen hands and feet along with significant anemia and fatigue. One year, many imaging studies, a couple of biopsies, and a latent tuberculosis infection later, he is still very sick. Throughout his ordeal he has often said to me: “You are the quarterback.” I’ve taken that to heart.

I don’t know why this surprises me, but insurance companies are being increasingly difficult. They’re passing more of the cost of health care to patients, and they’re less willing to cover medications and procedures. I have patients who can’t get physical therapy because they can’t afford the $45 copay for each visit. One patient stopped her hydroxychloroquine because it went from $4/month to $90/month. A couple of patients have opted not to take risedronate because the copay per month is $200 – that’s $200 for one generic pill.

At a recent morbidity and mortality conference, the attendees, nonrheumatologists all, were incredulous that cyclophosphamide, which has been around for ages and should be generic, is not covered by Medicare. Our patient with granulomatosis with polyangiitis and alveolar hemorrhage was on the hook for several hundred dollars per month, which he couldn’t afford.

Insurers also have been giving me more pushback for medications. For example, I recently tried to start one of my patients on etanercept for rheumatoid arthritis. His insurance company wrote to say etanercept was not their “preferred” first-line biologic. I explained that their preferred anti-TNF agents all carried the potential for developing anti-drug antibodies when used without methotrexate, which was contraindicated in my patient. They were unmoved.

I had a similar experience with my VIP. He was denied tocilizumab because he had not yet tried and failed two anti-TNF agents. I appealed the decision because I thought etanercept had caused a side effect that might be a class effect. To my surprise, rather than getting an approval, I received instead a request for medical literature to support my theory. Who knew that the decision-bots were so sophisticated?

Ultimately, I got the drug approved, but of course this process was an inconvenience to me, adding unnecessarily to the work of doctoring. More importantly, it was time wasted for my patient who was suffering tremendously.

My point is this: The idea of me as quarterback is quaint. Ultimately, it is the insurance company that dictates testing, treatment, physician, and facility.

There is an expectation that physicians are perfect, and we have internalized that expectation to some degree, holding ourselves to exacting standards, guided by what’s in the patient’s best interest. I want to know what sort of standards insurance companies hold themselves to, because I think they – out of all of us involved in health care – they who have the greatest resources should be absolutely unimpeachable.

Dr. Chan practices rheumatology in Pawtucket, R.I.

My newest iteration of a VIP, or very ill patient, is a lovely middle-aged gentleman who has been sick for a year with a multisystem disorder. It started with severely swollen hands and feet along with significant anemia and fatigue. One year, many imaging studies, a couple of biopsies, and a latent tuberculosis infection later, he is still very sick. Throughout his ordeal he has often said to me: “You are the quarterback.” I’ve taken that to heart.

I don’t know why this surprises me, but insurance companies are being increasingly difficult. They’re passing more of the cost of health care to patients, and they’re less willing to cover medications and procedures. I have patients who can’t get physical therapy because they can’t afford the $45 copay for each visit. One patient stopped her hydroxychloroquine because it went from $4/month to $90/month. A couple of patients have opted not to take risedronate because the copay per month is $200 – that’s $200 for one generic pill.

At a recent morbidity and mortality conference, the attendees, nonrheumatologists all, were incredulous that cyclophosphamide, which has been around for ages and should be generic, is not covered by Medicare. Our patient with granulomatosis with polyangiitis and alveolar hemorrhage was on the hook for several hundred dollars per month, which he couldn’t afford.

Insurers also have been giving me more pushback for medications. For example, I recently tried to start one of my patients on etanercept for rheumatoid arthritis. His insurance company wrote to say etanercept was not their “preferred” first-line biologic. I explained that their preferred anti-TNF agents all carried the potential for developing anti-drug antibodies when used without methotrexate, which was contraindicated in my patient. They were unmoved.

I had a similar experience with my VIP. He was denied tocilizumab because he had not yet tried and failed two anti-TNF agents. I appealed the decision because I thought etanercept had caused a side effect that might be a class effect. To my surprise, rather than getting an approval, I received instead a request for medical literature to support my theory. Who knew that the decision-bots were so sophisticated?

Ultimately, I got the drug approved, but of course this process was an inconvenience to me, adding unnecessarily to the work of doctoring. More importantly, it was time wasted for my patient who was suffering tremendously.

My point is this: The idea of me as quarterback is quaint. Ultimately, it is the insurance company that dictates testing, treatment, physician, and facility.

There is an expectation that physicians are perfect, and we have internalized that expectation to some degree, holding ourselves to exacting standards, guided by what’s in the patient’s best interest. I want to know what sort of standards insurance companies hold themselves to, because I think they – out of all of us involved in health care – they who have the greatest resources should be absolutely unimpeachable.

Dr. Chan practices rheumatology in Pawtucket, R.I.

San Francisco – Routine ganglionic plexus ablation increases risk and offers no clinical benefit in patients undergoing thoracoscopic surgery for advanced atrial fibrillation, according to a randomized Dutch trial.

“Most surgeons who do epicardial ablation do GP [ganglionic plexus] ablation because of the assumption that they are doing something good; that assumption is wrong. GP ablation should not be performed in patients with advanced AF [atrial fibrillation],” said lead investigator Dr. Joris de Groot, a cardiologist at the University of Amsterdam.

Following pulmonary vein isolation (PVI), 117 patients were randomized to GP ablation, and 123 to no GP ablation. GP ablation eliminated 100% of evoked vagal responses; vagal responses remained intact in nearly all of the control subjects.

At 1 year, 70.9% in the GP group compared with 68.4% in control arm were free of recurrence (P = .7); there were no statistically significant differences when the analysis was limited to the 59% of patients who went into the trial with persistent AF or limited to the rest of the patients with paroxysmal AF. Recurrences constituted significantly more atrial tachycardia in the GP group than in the control group. Even after the researchers controlled for a wide variety of demographic, anatomical, and clinical variables, “GP ablation made no difference in atrial fibrillation recurrence at 1 year,” Dr. de Groot said at the annual scientific sessions of the Hearth Rhythm Society.

Meanwhile, major perioperative bleeding occurred in nine patients, all in the GP group, and one required a sternotomy for hemostatic control. Clinically relevant sinus node dysfunction occurred in 12 of the GP group, but only four control patients; six GP patients – but no one in the control arm – required subsequent pacemakers, three while in the hospital after surgery and three during follow-up. Almost 30 patients in each arm required cardioversion during the 3-month blanking period, and about 20 in each arm afterwards.

“The largest randomized study in thoracoscopic surgery for advanced AF to date demonstrates that GP ablation is associated with significantly more periprocedural major bleeding, sinus node dysfunction, and pacemaker implantation, but not with improved rhythm outcome,” the investigators concluded.

Procedure time was 185 +/– 54 minutes in the GP arm, and 168 +/– 54 minutes in the control arm (P = .015). In the GP group, four major GPs and the ligament of Marshall were ablated.

Patients were 60 years old, on average, and three-quarters were men. AF duration was a median of 4 years. Four patients had died at 1 year, all in the GP arm, but none related to the procedure. All antiarrhythmic drugs were stopped after the blanking period; any atrial arrhythmia lasting 30 seconds or longer thereafter was considered a recurrence.

Dr. de Groot disclosed payments for services from AtriCure, Daiichi, and St. Jude Medical and research funding from AtriCure and St. Jude.

[email protected]

San Francisco – Routine ganglionic plexus ablation increases risk and offers no clinical benefit in patients undergoing thoracoscopic surgery for advanced atrial fibrillation, according to a randomized Dutch trial.

“Most surgeons who do epicardial ablation do GP [ganglionic plexus] ablation because of the assumption that they are doing something good; that assumption is wrong. GP ablation should not be performed in patients with advanced AF [atrial fibrillation],” said lead investigator Dr. Joris de Groot, a cardiologist at the University of Amsterdam.

Following pulmonary vein isolation (PVI), 117 patients were randomized to GP ablation, and 123 to no GP ablation. GP ablation eliminated 100% of evoked vagal responses; vagal responses remained intact in nearly all of the control subjects.

At 1 year, 70.9% in the GP group compared with 68.4% in control arm were free of recurrence (P = .7); there were no statistically significant differences when the analysis was limited to the 59% of patients who went into the trial with persistent AF or limited to the rest of the patients with paroxysmal AF. Recurrences constituted significantly more atrial tachycardia in the GP group than in the control group. Even after the researchers controlled for a wide variety of demographic, anatomical, and clinical variables, “GP ablation made no difference in atrial fibrillation recurrence at 1 year,” Dr. de Groot said at the annual scientific sessions of the Hearth Rhythm Society.

Meanwhile, major perioperative bleeding occurred in nine patients, all in the GP group, and one required a sternotomy for hemostatic control. Clinically relevant sinus node dysfunction occurred in 12 of the GP group, but only four control patients; six GP patients – but no one in the control arm – required subsequent pacemakers, three while in the hospital after surgery and three during follow-up. Almost 30 patients in each arm required cardioversion during the 3-month blanking period, and about 20 in each arm afterwards.

“The largest randomized study in thoracoscopic surgery for advanced AF to date demonstrates that GP ablation is associated with significantly more periprocedural major bleeding, sinus node dysfunction, and pacemaker implantation, but not with improved rhythm outcome,” the investigators concluded.

Procedure time was 185 +/– 54 minutes in the GP arm, and 168 +/– 54 minutes in the control arm (P = .015). In the GP group, four major GPs and the ligament of Marshall were ablated.

Patients were 60 years old, on average, and three-quarters were men. AF duration was a median of 4 years. Four patients had died at 1 year, all in the GP arm, but none related to the procedure. All antiarrhythmic drugs were stopped after the blanking period; any atrial arrhythmia lasting 30 seconds or longer thereafter was considered a recurrence.

Dr. de Groot disclosed payments for services from AtriCure, Daiichi, and St. Jude Medical and research funding from AtriCure and St. Jude.

[email protected]

San Francisco – Routine ganglionic plexus ablation increases risk and offers no clinical benefit in patients undergoing thoracoscopic surgery for advanced atrial fibrillation, according to a randomized Dutch trial.

“Most surgeons who do epicardial ablation do GP [ganglionic plexus] ablation because of the assumption that they are doing something good; that assumption is wrong. GP ablation should not be performed in patients with advanced AF [atrial fibrillation],” said lead investigator Dr. Joris de Groot, a cardiologist at the University of Amsterdam.

Following pulmonary vein isolation (PVI), 117 patients were randomized to GP ablation, and 123 to no GP ablation. GP ablation eliminated 100% of evoked vagal responses; vagal responses remained intact in nearly all of the control subjects.

At 1 year, 70.9% in the GP group compared with 68.4% in control arm were free of recurrence (P = .7); there were no statistically significant differences when the analysis was limited to the 59% of patients who went into the trial with persistent AF or limited to the rest of the patients with paroxysmal AF. Recurrences constituted significantly more atrial tachycardia in the GP group than in the control group. Even after the researchers controlled for a wide variety of demographic, anatomical, and clinical variables, “GP ablation made no difference in atrial fibrillation recurrence at 1 year,” Dr. de Groot said at the annual scientific sessions of the Hearth Rhythm Society.

Meanwhile, major perioperative bleeding occurred in nine patients, all in the GP group, and one required a sternotomy for hemostatic control. Clinically relevant sinus node dysfunction occurred in 12 of the GP group, but only four control patients; six GP patients – but no one in the control arm – required subsequent pacemakers, three while in the hospital after surgery and three during follow-up. Almost 30 patients in each arm required cardioversion during the 3-month blanking period, and about 20 in each arm afterwards.

“The largest randomized study in thoracoscopic surgery for advanced AF to date demonstrates that GP ablation is associated with significantly more periprocedural major bleeding, sinus node dysfunction, and pacemaker implantation, but not with improved rhythm outcome,” the investigators concluded.

Procedure time was 185 +/– 54 minutes in the GP arm, and 168 +/– 54 minutes in the control arm (P = .015). In the GP group, four major GPs and the ligament of Marshall were ablated.

Patients were 60 years old, on average, and three-quarters were men. AF duration was a median of 4 years. Four patients had died at 1 year, all in the GP arm, but none related to the procedure. All antiarrhythmic drugs were stopped after the blanking period; any atrial arrhythmia lasting 30 seconds or longer thereafter was considered a recurrence.

Dr. de Groot disclosed payments for services from AtriCure, Daiichi, and St. Jude Medical and research funding from AtriCure and St. Jude.

[email protected]

The U.S. Food and Drug Administration has issued revised draft guidance intended to foster the development of direct-acting antiviral drugs to treat chronic hepatitis C virus infection.

The guidance, developed by the FDA’s Center for Drug Evaluation and Research, delineates the drug development process from the preinvestigational new drug application through the new drug application and postmarketing stages.

Courtesy US. Dept of Veterans Affairs

According to the FDA, the draft guidance, when finalized, will represent the current thinking of the agency on development of direct-acting antivirals and clinical trial designs, but is not binding on the FDA or the public. It explicitly states that industry may use an alternative approach to drug development if it “satisfies the requirements of the applicable statutes and regulations.” For the purposes of drug development, the FDA defines direct-acting HCV antivirals as drugs that “interfere with specific steps in the HCV replication cycle through a direct interaction with the HCV genome, polyprotein, or its polyprotein cleavage products.”

The guidance does not address the development of drugs that target host functions necessary for viral replication or immune-based drugs for the treatment of HCV infection, including new interferon drugs or therapeutics “without antiviral mechanisms intended to mitigate or reverse clinical or pathophysiological outcomes” of chronic HCV infection, such as prevention of hepatocellular carcinoma or reversal of fibrosis.

Once the draft guidance has been published in the Federal Register, the FDA will accept comments and suggestions at www.regulations.gov for 60 days.

[email protected]

On Twitter @richpizzi

The U.S. Food and Drug Administration has issued revised draft guidance intended to foster the development of direct-acting antiviral drugs to treat chronic hepatitis C virus infection.

The guidance, developed by the FDA’s Center for Drug Evaluation and Research, delineates the drug development process from the preinvestigational new drug application through the new drug application and postmarketing stages.

Courtesy US. Dept of Veterans Affairs

According to the FDA, the draft guidance, when finalized, will represent the current thinking of the agency on development of direct-acting antivirals and clinical trial designs, but is not binding on the FDA or the public. It explicitly states that industry may use an alternative approach to drug development if it “satisfies the requirements of the applicable statutes and regulations.” For the purposes of drug development, the FDA defines direct-acting HCV antivirals as drugs that “interfere with specific steps in the HCV replication cycle through a direct interaction with the HCV genome, polyprotein, or its polyprotein cleavage products.”

The guidance does not address the development of drugs that target host functions necessary for viral replication or immune-based drugs for the treatment of HCV infection, including new interferon drugs or therapeutics “without antiviral mechanisms intended to mitigate or reverse clinical or pathophysiological outcomes” of chronic HCV infection, such as prevention of hepatocellular carcinoma or reversal of fibrosis.

Once the draft guidance has been published in the Federal Register, the FDA will accept comments and suggestions at www.regulations.gov for 60 days.

[email protected]

On Twitter @richpizzi

The U.S. Food and Drug Administration has issued revised draft guidance intended to foster the development of direct-acting antiviral drugs to treat chronic hepatitis C virus infection.

The guidance, developed by the FDA’s Center for Drug Evaluation and Research, delineates the drug development process from the preinvestigational new drug application through the new drug application and postmarketing stages.

Courtesy US. Dept of Veterans Affairs

According to the FDA, the draft guidance, when finalized, will represent the current thinking of the agency on development of direct-acting antivirals and clinical trial designs, but is not binding on the FDA or the public. It explicitly states that industry may use an alternative approach to drug development if it “satisfies the requirements of the applicable statutes and regulations.” For the purposes of drug development, the FDA defines direct-acting HCV antivirals as drugs that “interfere with specific steps in the HCV replication cycle through a direct interaction with the HCV genome, polyprotein, or its polyprotein cleavage products.”

The guidance does not address the development of drugs that target host functions necessary for viral replication or immune-based drugs for the treatment of HCV infection, including new interferon drugs or therapeutics “without antiviral mechanisms intended to mitigate or reverse clinical or pathophysiological outcomes” of chronic HCV infection, such as prevention of hepatocellular carcinoma or reversal of fibrosis.

Once the draft guidance has been published in the Federal Register, the FDA will accept comments and suggestions at www.regulations.gov for 60 days.

[email protected]

On Twitter @richpizzi

In Japan, sentinel disease surveillance systems may underestimate the actual number of patients with methicillin-resistant Staphylococcus aureus (MRSA) infection because they do not include information about patients who visit nonsentinel medical facilities, according to a study published in Epidemiology and Infection.

Dr. Shinichi Tanihara of the department of public health and preventive medicine in the School of Medicine at Fukuoka University and Dr. Satowa Suzuki of the department of bacteriology II at the National Institute of Infectious Diseases in Tokyo assessed and compared the incidences of MRSA patients based on health insurance claims data and data reported to the Japan Nosocomial Infections Surveillance system (Epidemiol Infect. 2016 April 8. doi: 10.1017/S0950268816000674).

The study results suggested that health insurance claims data for MRSA cases were more useful for determining the incidence of MRSA cases in Japan from 2011 to 2012. For example, of the 2,052 eligible hospitals with 200 or more beds in 2011, roughly one-quarter (495, 23.8%) participated in the Japan Nosocomial Infections Surveillance system. Data from this relatively low percentage of eligible facilities most likely underestimated the true number of MRSA patients in Japan, the authors said.

©Photo Researchers/NHGRI

Based on their findings, the investigators noted three major advantages of using health insurance claims data for infection surveillance. Firstly, information from health insurance claims data is not affected by health care providers’ notifications to surveillance systems. Secondly, data on patients with MRSA can be collected at low cost because of Japan’s uniform and computerized health insurance system, and the data are easy to access. Lastly, health insurance claims data prevent the duplication of patient information, as insurers can determine if a patient was treated at multiple medical facilities for the same disease.

The only noted drawback involving the use of health insurance claims data for infection surveillance pertained to its timeliness, the researchers wrote. This issue arises because these data are submitted monthly rather than immediately, which may limit their use in surveillance systems.

According to Dr. Tanihara and Dr. Suzuki, strengths of the study include its evaluation of sentinel surveillance quality through the use of data that were not based on physician reports, as well as the calculation of MRSA incidence by use of a standardized definition in a specific population. Reported limitations included the assessment of anti-MRSA medicine use and patients’ age only, and the lack of information on the degree of drug resistance from health insurance claims data.

Funding was provided by the Ministry of Health, Labour, and Welfare of Japan, and by the Research Programme on Emerging and Re-emerging Infectious Diseases from the Japan Agency for Medical Research and Development. Neither author reported any conflicts of interest.

In Japan, sentinel disease surveillance systems may underestimate the actual number of patients with methicillin-resistant Staphylococcus aureus (MRSA) infection because they do not include information about patients who visit nonsentinel medical facilities, according to a study published in Epidemiology and Infection.

Dr. Shinichi Tanihara of the department of public health and preventive medicine in the School of Medicine at Fukuoka University and Dr. Satowa Suzuki of the department of bacteriology II at the National Institute of Infectious Diseases in Tokyo assessed and compared the incidences of MRSA patients based on health insurance claims data and data reported to the Japan Nosocomial Infections Surveillance system (Epidemiol Infect. 2016 April 8. doi: 10.1017/S0950268816000674).

The study results suggested that health insurance claims data for MRSA cases were more useful for determining the incidence of MRSA cases in Japan from 2011 to 2012. For example, of the 2,052 eligible hospitals with 200 or more beds in 2011, roughly one-quarter (495, 23.8%) participated in the Japan Nosocomial Infections Surveillance system. Data from this relatively low percentage of eligible facilities most likely underestimated the true number of MRSA patients in Japan, the authors said.

©Photo Researchers/NHGRI

Based on their findings, the investigators noted three major advantages of using health insurance claims data for infection surveillance. Firstly, information from health insurance claims data is not affected by health care providers’ notifications to surveillance systems. Secondly, data on patients with MRSA can be collected at low cost because of Japan’s uniform and computerized health insurance system, and the data are easy to access. Lastly, health insurance claims data prevent the duplication of patient information, as insurers can determine if a patient was treated at multiple medical facilities for the same disease.

The only noted drawback involving the use of health insurance claims data for infection surveillance pertained to its timeliness, the researchers wrote. This issue arises because these data are submitted monthly rather than immediately, which may limit their use in surveillance systems.

According to Dr. Tanihara and Dr. Suzuki, strengths of the study include its evaluation of sentinel surveillance quality through the use of data that were not based on physician reports, as well as the calculation of MRSA incidence by use of a standardized definition in a specific population. Reported limitations included the assessment of anti-MRSA medicine use and patients’ age only, and the lack of information on the degree of drug resistance from health insurance claims data.

Funding was provided by the Ministry of Health, Labour, and Welfare of Japan, and by the Research Programme on Emerging and Re-emerging Infectious Diseases from the Japan Agency for Medical Research and Development. Neither author reported any conflicts of interest.

In Japan, sentinel disease surveillance systems may underestimate the actual number of patients with methicillin-resistant Staphylococcus aureus (MRSA) infection because they do not include information about patients who visit nonsentinel medical facilities, according to a study published in Epidemiology and Infection.

Dr. Shinichi Tanihara of the department of public health and preventive medicine in the School of Medicine at Fukuoka University and Dr. Satowa Suzuki of the department of bacteriology II at the National Institute of Infectious Diseases in Tokyo assessed and compared the incidences of MRSA patients based on health insurance claims data and data reported to the Japan Nosocomial Infections Surveillance system (Epidemiol Infect. 2016 April 8. doi: 10.1017/S0950268816000674).

The study results suggested that health insurance claims data for MRSA cases were more useful for determining the incidence of MRSA cases in Japan from 2011 to 2012. For example, of the 2,052 eligible hospitals with 200 or more beds in 2011, roughly one-quarter (495, 23.8%) participated in the Japan Nosocomial Infections Surveillance system. Data from this relatively low percentage of eligible facilities most likely underestimated the true number of MRSA patients in Japan, the authors said.

©Photo Researchers/NHGRI

Based on their findings, the investigators noted three major advantages of using health insurance claims data for infection surveillance. Firstly, information from health insurance claims data is not affected by health care providers’ notifications to surveillance systems. Secondly, data on patients with MRSA can be collected at low cost because of Japan’s uniform and computerized health insurance system, and the data are easy to access. Lastly, health insurance claims data prevent the duplication of patient information, as insurers can determine if a patient was treated at multiple medical facilities for the same disease.

The only noted drawback involving the use of health insurance claims data for infection surveillance pertained to its timeliness, the researchers wrote. This issue arises because these data are submitted monthly rather than immediately, which may limit their use in surveillance systems.

According to Dr. Tanihara and Dr. Suzuki, strengths of the study include its evaluation of sentinel surveillance quality through the use of data that were not based on physician reports, as well as the calculation of MRSA incidence by use of a standardized definition in a specific population. Reported limitations included the assessment of anti-MRSA medicine use and patients’ age only, and the lack of information on the degree of drug resistance from health insurance claims data.

Funding was provided by the Ministry of Health, Labour, and Welfare of Japan, and by the Research Programme on Emerging and Re-emerging Infectious Diseases from the Japan Agency for Medical Research and Development. Neither author reported any conflicts of interest.

Global climate appears to be changing at an unprecedented rate. Climate change can be caused by many factors, including variations in solar radiation received by the earth, oceanic circulation, plate tectonics, as well as human-induced alterations of the natural world. Many human activities, such as the use of fossil fuel and the consequent accumulation of greenhouse gases in the atmosphere, land consumption, deforestation, industrial processes, as well as some agriculture practices, are contributing to global climate change. Many have reported on the current trend toward global warming (average surface temperature has augmented by 0.6°C over the past 100 years), decreased precipitation, atmospheric humidity changes, and the rise in global extreme climatic events. The magnitude and cause of these changes and their impact on human activity have become important matters of debate worldwide, representing climate change as one of the greatest challenges of the modern age.

Although many articles have been written based on observations and various predictive models of how climate change could affect social, economic, and health systems, only a few studies exist about the effects of this change on skin and skin disease. However, the skin is the most highly exposed organ to the environment; therefore, cutaneous conditions are inclined to respond to changes in climate.

Skin cancer

The World Health Organization predicts that the depletion of the ozone layer could lead to further increased rates of melanoma and nonmelanoma skin cancer. In humans, it has been speculated that a long-term rise of temperature by 2°C could increase the carcinogenic effectiveness of solar UV by 10%.

Strictly speaking, stratospheric ozone depletion is not part of “global climate change,” which occurs in the troposphere. There are, however, several recently described interactions between ozone depletion and greenhouse gas–induced warming. Stratospheric ozone absorbs much of the incoming solar ultraviolet radiation, especially the biologically more damaging, shorter-wavelength UVB wavelengths. We now know that various industrial halogenated chemicals such as the chlorofluorocarbons or CFCs (used in refrigeration, insulation, and spray-can propellants) and methyl bromide, while inert at ambient Earth-surface temperatures, react with ozone in the extremely cold polar stratosphere. This destruction of ozone occurs especially in late winter and early spring.

During the 1980s and 1990s at northern midlatitudes (such as Europe), the average year-round ozone concentration declined by around 4% per decade; over the southern regions of Australia, New Zealand, Argentina, and South Africa, the figure approximated 6%-7%. UV exposures at northern midlatitudes are likely to peak around 2020, with an estimated 10% increase in effective ultraviolet radiation relative to 1980s levels.

The modeling of future ozone levels and UV radiation (UVR) exposures has estimated that, in consequence, a ‘European’ population living at around 45 degrees North will experience, by 2050, an approximate 5% excess of total skin cancer incidence (assuming, conservatively, no change in age distribution). The equivalent estimation for the U.S. population is for a 10% increase in skin cancer incidence by around 2050.

In the mid-1980s, governments recognized the emerging hazard from ozone depletion. The Montreal Protocol of 1987 was adopted, and the phasing out of major ozone-destroying gases began. Some anticipate a slow but near-complete recovery of stratospheric ozone by the middle of the twenty-first century; the Environmental Protection Agency (EPA) estimates recovery by 2065 with strict adherence to protection protocols.

Increased exposure to UVR also leads to increased rates of lens opacification, cataracts, and whole-body immunosuppression. UVR-induced immunosuppression could influence patterns of infectious disease. It may also influence the occurrence and progression of various autoimmune diseases and, less certainly, vaccine efficacy.

Extreme weather events

The International Society of Dermatology Task Force on Climate Change reports that weather phenomena such as El Niño also result in changes to dermatologic conditions. The El Niño Southern Oscillation (ENSO) is a complex climate phenomenon occurring in the Pacific Ocean at intervals of 2-7 years. The term refers to fluctuations in ocean temperatures in the tropical eastern Pacific Ocean (El Niño, the warm phase of ENSO, and La Niña, the cool phase of ENSO) and in atmospheric pressure across the Pacific basin (Southern Oscillation). This weather pattern is attributed with causing climate change in certain parts of the world and is associated with disease outbreaks.

El Niño has been associated with increases in the occurrence of actinic keratosis, tinea, pityriasis versicolor, miliaria, folliculitis, rosacea, dermatitis caused by Paederus irritans and Paederus sabaeus, and certain vector-borne and waterborne diseases (such as dengue fever, leishmaniasis, Chagas disease, Barmah Forest virus, and leptospirosis), and with decreases in the occurrence of dermatitis, scabies, psoriasis, and papular urticaria. La Niña has been associated with increases in the occurrence of varicella; hand, foot, and mouth disease; and Ross River virus (in certain areas), and decreases in viral warts and leishmaniasis.

Separately, global warming is expected to affect the start, duration, and intensity of the pollen season, and secondarily the rate of asthma exacerbations due to air pollution, respiratory infections, and/or cold air inhalation, with probable increases in eczema and other atopy-related conditions as well.

Vector-borne diseases

In the past year, the largest Ebola virus outbreak in West Africa has resulted in importation of the virus to other countries and secondary local transmission. Autochthonous transmission of Chikungunya virus has occurred in nonendemic areas, including Europe, the Caribbean, and the Americas. Zika virus has re-emerged in the Pacific with local transmission from imported cases. Climate change, deforestation, and changes in precipitation have been linked to variations in the geographical distribution of vectors of some infectious diseases (leishmaniasis, Lyme disease, and now Zika virus) by changing their spread. A warm and humid environment from global warming can also encourage the colonization of the skin by bacteria and fungi.

Finally, there is a wider, ecological dimension to consider. UV radiation impairs the molecular chemistry of photosynthesis both on land (terrestrial plants) and at sea (phytoplankton). This could affect world food production, at least marginally, and thus contribute to nutritional and health problems in food-insecure populations.

Another reason of many, but from a dermatologist’s point of view, to be mindful of taking care of the planet and our environment.

References

1. World Health Organization (WHO).

2. Photochem Photobiol Sci. 2002 May;1(5):324-6.

3. G Ital Dermatol Venereol. 2013 Feb;148(1):135-46.

4. Int J Dermatol. 2012 Jun;51(6):656-61.

5. Int J Dermatol. 2015 Dec;54(12):1343-51.

6. Curr Opin Infect Dis. 2015 Apr;28(2):139-50.

Dr. Wesley and Dr. Talakoub are co-contributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Wesley. Write to them at [email protected].

Global climate appears to be changing at an unprecedented rate. Climate change can be caused by many factors, including variations in solar radiation received by the earth, oceanic circulation, plate tectonics, as well as human-induced alterations of the natural world. Many human activities, such as the use of fossil fuel and the consequent accumulation of greenhouse gases in the atmosphere, land consumption, deforestation, industrial processes, as well as some agriculture practices, are contributing to global climate change. Many have reported on the current trend toward global warming (average surface temperature has augmented by 0.6°C over the past 100 years), decreased precipitation, atmospheric humidity changes, and the rise in global extreme climatic events. The magnitude and cause of these changes and their impact on human activity have become important matters of debate worldwide, representing climate change as one of the greatest challenges of the modern age.

Although many articles have been written based on observations and various predictive models of how climate change could affect social, economic, and health systems, only a few studies exist about the effects of this change on skin and skin disease. However, the skin is the most highly exposed organ to the environment; therefore, cutaneous conditions are inclined to respond to changes in climate.

Skin cancer

The World Health Organization predicts that the depletion of the ozone layer could lead to further increased rates of melanoma and nonmelanoma skin cancer. In humans, it has been speculated that a long-term rise of temperature by 2°C could increase the carcinogenic effectiveness of solar UV by 10%.

Strictly speaking, stratospheric ozone depletion is not part of “global climate change,” which occurs in the troposphere. There are, however, several recently described interactions between ozone depletion and greenhouse gas–induced warming. Stratospheric ozone absorbs much of the incoming solar ultraviolet radiation, especially the biologically more damaging, shorter-wavelength UVB wavelengths. We now know that various industrial halogenated chemicals such as the chlorofluorocarbons or CFCs (used in refrigeration, insulation, and spray-can propellants) and methyl bromide, while inert at ambient Earth-surface temperatures, react with ozone in the extremely cold polar stratosphere. This destruction of ozone occurs especially in late winter and early spring.

During the 1980s and 1990s at northern midlatitudes (such as Europe), the average year-round ozone concentration declined by around 4% per decade; over the southern regions of Australia, New Zealand, Argentina, and South Africa, the figure approximated 6%-7%. UV exposures at northern midlatitudes are likely to peak around 2020, with an estimated 10% increase in effective ultraviolet radiation relative to 1980s levels.

The modeling of future ozone levels and UV radiation (UVR) exposures has estimated that, in consequence, a ‘European’ population living at around 45 degrees North will experience, by 2050, an approximate 5% excess of total skin cancer incidence (assuming, conservatively, no change in age distribution). The equivalent estimation for the U.S. population is for a 10% increase in skin cancer incidence by around 2050.

In the mid-1980s, governments recognized the emerging hazard from ozone depletion. The Montreal Protocol of 1987 was adopted, and the phasing out of major ozone-destroying gases began. Some anticipate a slow but near-complete recovery of stratospheric ozone by the middle of the twenty-first century; the Environmental Protection Agency (EPA) estimates recovery by 2065 with strict adherence to protection protocols.

Increased exposure to UVR also leads to increased rates of lens opacification, cataracts, and whole-body immunosuppression. UVR-induced immunosuppression could influence patterns of infectious disease. It may also influence the occurrence and progression of various autoimmune diseases and, less certainly, vaccine efficacy.

Extreme weather events

The International Society of Dermatology Task Force on Climate Change reports that weather phenomena such as El Niño also result in changes to dermatologic conditions. The El Niño Southern Oscillation (ENSO) is a complex climate phenomenon occurring in the Pacific Ocean at intervals of 2-7 years. The term refers to fluctuations in ocean temperatures in the tropical eastern Pacific Ocean (El Niño, the warm phase of ENSO, and La Niña, the cool phase of ENSO) and in atmospheric pressure across the Pacific basin (Southern Oscillation). This weather pattern is attributed with causing climate change in certain parts of the world and is associated with disease outbreaks.

El Niño has been associated with increases in the occurrence of actinic keratosis, tinea, pityriasis versicolor, miliaria, folliculitis, rosacea, dermatitis caused by Paederus irritans and Paederus sabaeus, and certain vector-borne and waterborne diseases (such as dengue fever, leishmaniasis, Chagas disease, Barmah Forest virus, and leptospirosis), and with decreases in the occurrence of dermatitis, scabies, psoriasis, and papular urticaria. La Niña has been associated with increases in the occurrence of varicella; hand, foot, and mouth disease; and Ross River virus (in certain areas), and decreases in viral warts and leishmaniasis.

Separately, global warming is expected to affect the start, duration, and intensity of the pollen season, and secondarily the rate of asthma exacerbations due to air pollution, respiratory infections, and/or cold air inhalation, with probable increases in eczema and other atopy-related conditions as well.

Vector-borne diseases

In the past year, the largest Ebola virus outbreak in West Africa has resulted in importation of the virus to other countries and secondary local transmission. Autochthonous transmission of Chikungunya virus has occurred in nonendemic areas, including Europe, the Caribbean, and the Americas. Zika virus has re-emerged in the Pacific with local transmission from imported cases. Climate change, deforestation, and changes in precipitation have been linked to variations in the geographical distribution of vectors of some infectious diseases (leishmaniasis, Lyme disease, and now Zika virus) by changing their spread. A warm and humid environment from global warming can also encourage the colonization of the skin by bacteria and fungi.

Finally, there is a wider, ecological dimension to consider. UV radiation impairs the molecular chemistry of photosynthesis both on land (terrestrial plants) and at sea (phytoplankton). This could affect world food production, at least marginally, and thus contribute to nutritional and health problems in food-insecure populations.

Another reason of many, but from a dermatologist’s point of view, to be mindful of taking care of the planet and our environment.

References

1. World Health Organization (WHO).

2. Photochem Photobiol Sci. 2002 May;1(5):324-6.

3. G Ital Dermatol Venereol. 2013 Feb;148(1):135-46.

4. Int J Dermatol. 2012 Jun;51(6):656-61.

5. Int J Dermatol. 2015 Dec;54(12):1343-51.

6. Curr Opin Infect Dis. 2015 Apr;28(2):139-50.

Dr. Wesley and Dr. Talakoub are co-contributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Wesley. Write to them at [email protected].

Global climate appears to be changing at an unprecedented rate. Climate change can be caused by many factors, including variations in solar radiation received by the earth, oceanic circulation, plate tectonics, as well as human-induced alterations of the natural world. Many human activities, such as the use of fossil fuel and the consequent accumulation of greenhouse gases in the atmosphere, land consumption, deforestation, industrial processes, as well as some agriculture practices, are contributing to global climate change. Many have reported on the current trend toward global warming (average surface temperature has augmented by 0.6°C over the past 100 years), decreased precipitation, atmospheric humidity changes, and the rise in global extreme climatic events. The magnitude and cause of these changes and their impact on human activity have become important matters of debate worldwide, representing climate change as one of the greatest challenges of the modern age.

Although many articles have been written based on observations and various predictive models of how climate change could affect social, economic, and health systems, only a few studies exist about the effects of this change on skin and skin disease. However, the skin is the most highly exposed organ to the environment; therefore, cutaneous conditions are inclined to respond to changes in climate.

Skin cancer

The World Health Organization predicts that the depletion of the ozone layer could lead to further increased rates of melanoma and nonmelanoma skin cancer. In humans, it has been speculated that a long-term rise of temperature by 2°C could increase the carcinogenic effectiveness of solar UV by 10%.

Strictly speaking, stratospheric ozone depletion is not part of “global climate change,” which occurs in the troposphere. There are, however, several recently described interactions between ozone depletion and greenhouse gas–induced warming. Stratospheric ozone absorbs much of the incoming solar ultraviolet radiation, especially the biologically more damaging, shorter-wavelength UVB wavelengths. We now know that various industrial halogenated chemicals such as the chlorofluorocarbons or CFCs (used in refrigeration, insulation, and spray-can propellants) and methyl bromide, while inert at ambient Earth-surface temperatures, react with ozone in the extremely cold polar stratosphere. This destruction of ozone occurs especially in late winter and early spring.

During the 1980s and 1990s at northern midlatitudes (such as Europe), the average year-round ozone concentration declined by around 4% per decade; over the southern regions of Australia, New Zealand, Argentina, and South Africa, the figure approximated 6%-7%. UV exposures at northern midlatitudes are likely to peak around 2020, with an estimated 10% increase in effective ultraviolet radiation relative to 1980s levels.

The modeling of future ozone levels and UV radiation (UVR) exposures has estimated that, in consequence, a ‘European’ population living at around 45 degrees North will experience, by 2050, an approximate 5% excess of total skin cancer incidence (assuming, conservatively, no change in age distribution). The equivalent estimation for the U.S. population is for a 10% increase in skin cancer incidence by around 2050.

In the mid-1980s, governments recognized the emerging hazard from ozone depletion. The Montreal Protocol of 1987 was adopted, and the phasing out of major ozone-destroying gases began. Some anticipate a slow but near-complete recovery of stratospheric ozone by the middle of the twenty-first century; the Environmental Protection Agency (EPA) estimates recovery by 2065 with strict adherence to protection protocols.

Increased exposure to UVR also leads to increased rates of lens opacification, cataracts, and whole-body immunosuppression. UVR-induced immunosuppression could influence patterns of infectious disease. It may also influence the occurrence and progression of various autoimmune diseases and, less certainly, vaccine efficacy.

Extreme weather events

The International Society of Dermatology Task Force on Climate Change reports that weather phenomena such as El Niño also result in changes to dermatologic conditions. The El Niño Southern Oscillation (ENSO) is a complex climate phenomenon occurring in the Pacific Ocean at intervals of 2-7 years. The term refers to fluctuations in ocean temperatures in the tropical eastern Pacific Ocean (El Niño, the warm phase of ENSO, and La Niña, the cool phase of ENSO) and in atmospheric pressure across the Pacific basin (Southern Oscillation). This weather pattern is attributed with causing climate change in certain parts of the world and is associated with disease outbreaks.

El Niño has been associated with increases in the occurrence of actinic keratosis, tinea, pityriasis versicolor, miliaria, folliculitis, rosacea, dermatitis caused by Paederus irritans and Paederus sabaeus, and certain vector-borne and waterborne diseases (such as dengue fever, leishmaniasis, Chagas disease, Barmah Forest virus, and leptospirosis), and with decreases in the occurrence of dermatitis, scabies, psoriasis, and papular urticaria. La Niña has been associated with increases in the occurrence of varicella; hand, foot, and mouth disease; and Ross River virus (in certain areas), and decreases in viral warts and leishmaniasis.

Separately, global warming is expected to affect the start, duration, and intensity of the pollen season, and secondarily the rate of asthma exacerbations due to air pollution, respiratory infections, and/or cold air inhalation, with probable increases in eczema and other atopy-related conditions as well.

Vector-borne diseases

In the past year, the largest Ebola virus outbreak in West Africa has resulted in importation of the virus to other countries and secondary local transmission. Autochthonous transmission of Chikungunya virus has occurred in nonendemic areas, including Europe, the Caribbean, and the Americas. Zika virus has re-emerged in the Pacific with local transmission from imported cases. Climate change, deforestation, and changes in precipitation have been linked to variations in the geographical distribution of vectors of some infectious diseases (leishmaniasis, Lyme disease, and now Zika virus) by changing their spread. A warm and humid environment from global warming can also encourage the colonization of the skin by bacteria and fungi.

Finally, there is a wider, ecological dimension to consider. UV radiation impairs the molecular chemistry of photosynthesis both on land (terrestrial plants) and at sea (phytoplankton). This could affect world food production, at least marginally, and thus contribute to nutritional and health problems in food-insecure populations.

Another reason of many, but from a dermatologist’s point of view, to be mindful of taking care of the planet and our environment.

References

1. World Health Organization (WHO).

2. Photochem Photobiol Sci. 2002 May;1(5):324-6.

3. G Ital Dermatol Venereol. 2013 Feb;148(1):135-46.

4. Int J Dermatol. 2012 Jun;51(6):656-61.

5. Int J Dermatol. 2015 Dec;54(12):1343-51.

6. Curr Opin Infect Dis. 2015 Apr;28(2):139-50.

Dr. Wesley and Dr. Talakoub are co-contributors to this column. Dr. Talakoub is in private practice in McLean, Va. Dr. Wesley practices dermatology in Beverly Hills, Calif. This month’s column is by Dr. Wesley. Write to them at [email protected].

In my last column, I mentioned RSS news feeds as a useful, versatile online tool. As my editor later reminded me, however, it has been over a decade since I’ve discussed RSS feeds – so an update is certainly in order.

The sheer volume of information on the web makes quick and efficient searching an indispensable skill, but once you become quick and efficient at finding the information you need, a new problem arises: The information changes! All the good medical, news, and other information-based websites change and update their content on a regular but unpredictable basis. And checking each one for new information can be very tedious, if you can remember to do it at all.

Many sites offer an email service to notify you of new content, but multiple email subscriptions clutter your inbox and often can’t select out the information you’re really interested in. RSS feeds are a more efficient and increasingly popular method of staying current on all the subjects that interest you – medical and otherwise. RSS (which stands for Rich Site Summary or Really Simple Syndication, depending on whom you ask) is a file format that websites use (or a similar one called Atom) to produce a summary file, or “feed,” of new content, along with links to full versions of that content. When you subscribe to a given website’s feed, you’ll receive a summary of new content each time the website is updated.

Thousands of websites now offer RSS feeds, including most of the large medical information services, all the major news organizations, and many web logs.

To subscribe to feeds, you must download a program called a feed reader, which is basically just a browser specializing in RSS and Atom files. Dozens of readers (also known as aggregators) are available. Some can be accessed through browsers, others are integrated into email programs, and still others run as standalone applications. With the rise of cloud computing, some cloud-based services offer feed aggregation as part of their service.

Many readers are free, but those with the most advanced features usually come with a fee of some sort. (As always, I have no financial interest in any enterprise discussed in this column.) A comprehensive list of available readers can be found in the Wikipedia article “Comparison of Feed Aggregators.”

It’s not always easy to find out whether a particular website offers a feed, because there is no universally recognized method of indicating its existence. Look for a link to “RSS” or “Syndicate This,” or an orange rectangle with the letters “RSS” or “XML” (don’t ask). These links are not always on the home page. You may need to consult the site map to find a link to a page explaining available feeds and how to find them.

Some of the major sites have multiple feeds to choose from. For example, you can generate a feed of current stories related to the page that you are following on Google News by clicking the RSS link on any Google News page.

Once you know the URL of the RSS feed you want, you provide it to your reader program, which will monitor the feed for you. (Many RSS aggregators come preconfigured with a list of feed URLs for popular news websites.)

In addition to notifying you of important news headlines, changes to your favorite websites, and new developments in any medical (or other) field of interest to you, RSS feeds have many other uses. Some will notify you of new products in a store or catalog, new newsletter issues (including email newsletters), weather and other changing-condition alerts, and the addition of new items to a database – or new members to a group.

It can work the other way as well: If you want readers of your website, blog, or podcast to receive the latest news about your practice, such as new treatments and procedures you’re offering – or if you want to know immediately anytime your name pops up in news or gossip sites – you can create your own RSS feed. In my next column, I’ll explain exactly how to do that.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

In my last column, I mentioned RSS news feeds as a useful, versatile online tool. As my editor later reminded me, however, it has been over a decade since I’ve discussed RSS feeds – so an update is certainly in order.

The sheer volume of information on the web makes quick and efficient searching an indispensable skill, but once you become quick and efficient at finding the information you need, a new problem arises: The information changes! All the good medical, news, and other information-based websites change and update their content on a regular but unpredictable basis. And checking each one for new information can be very tedious, if you can remember to do it at all.

Many sites offer an email service to notify you of new content, but multiple email subscriptions clutter your inbox and often can’t select out the information you’re really interested in. RSS feeds are a more efficient and increasingly popular method of staying current on all the subjects that interest you – medical and otherwise. RSS (which stands for Rich Site Summary or Really Simple Syndication, depending on whom you ask) is a file format that websites use (or a similar one called Atom) to produce a summary file, or “feed,” of new content, along with links to full versions of that content. When you subscribe to a given website’s feed, you’ll receive a summary of new content each time the website is updated.

Thousands of websites now offer RSS feeds, including most of the large medical information services, all the major news organizations, and many web logs.

To subscribe to feeds, you must download a program called a feed reader, which is basically just a browser specializing in RSS and Atom files. Dozens of readers (also known as aggregators) are available. Some can be accessed through browsers, others are integrated into email programs, and still others run as standalone applications. With the rise of cloud computing, some cloud-based services offer feed aggregation as part of their service.

Many readers are free, but those with the most advanced features usually come with a fee of some sort. (As always, I have no financial interest in any enterprise discussed in this column.) A comprehensive list of available readers can be found in the Wikipedia article “Comparison of Feed Aggregators.”

It’s not always easy to find out whether a particular website offers a feed, because there is no universally recognized method of indicating its existence. Look for a link to “RSS” or “Syndicate This,” or an orange rectangle with the letters “RSS” or “XML” (don’t ask). These links are not always on the home page. You may need to consult the site map to find a link to a page explaining available feeds and how to find them.

Some of the major sites have multiple feeds to choose from. For example, you can generate a feed of current stories related to the page that you are following on Google News by clicking the RSS link on any Google News page.

Once you know the URL of the RSS feed you want, you provide it to your reader program, which will monitor the feed for you. (Many RSS aggregators come preconfigured with a list of feed URLs for popular news websites.)

In addition to notifying you of important news headlines, changes to your favorite websites, and new developments in any medical (or other) field of interest to you, RSS feeds have many other uses. Some will notify you of new products in a store or catalog, new newsletter issues (including email newsletters), weather and other changing-condition alerts, and the addition of new items to a database – or new members to a group.

It can work the other way as well: If you want readers of your website, blog, or podcast to receive the latest news about your practice, such as new treatments and procedures you’re offering – or if you want to know immediately anytime your name pops up in news or gossip sites – you can create your own RSS feed. In my next column, I’ll explain exactly how to do that.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

In my last column, I mentioned RSS news feeds as a useful, versatile online tool. As my editor later reminded me, however, it has been over a decade since I’ve discussed RSS feeds – so an update is certainly in order.

The sheer volume of information on the web makes quick and efficient searching an indispensable skill, but once you become quick and efficient at finding the information you need, a new problem arises: The information changes! All the good medical, news, and other information-based websites change and update their content on a regular but unpredictable basis. And checking each one for new information can be very tedious, if you can remember to do it at all.

Many sites offer an email service to notify you of new content, but multiple email subscriptions clutter your inbox and often can’t select out the information you’re really interested in. RSS feeds are a more efficient and increasingly popular method of staying current on all the subjects that interest you – medical and otherwise. RSS (which stands for Rich Site Summary or Really Simple Syndication, depending on whom you ask) is a file format that websites use (or a similar one called Atom) to produce a summary file, or “feed,” of new content, along with links to full versions of that content. When you subscribe to a given website’s feed, you’ll receive a summary of new content each time the website is updated.

Thousands of websites now offer RSS feeds, including most of the large medical information services, all the major news organizations, and many web logs.

To subscribe to feeds, you must download a program called a feed reader, which is basically just a browser specializing in RSS and Atom files. Dozens of readers (also known as aggregators) are available. Some can be accessed through browsers, others are integrated into email programs, and still others run as standalone applications. With the rise of cloud computing, some cloud-based services offer feed aggregation as part of their service.

Many readers are free, but those with the most advanced features usually come with a fee of some sort. (As always, I have no financial interest in any enterprise discussed in this column.) A comprehensive list of available readers can be found in the Wikipedia article “Comparison of Feed Aggregators.”

It’s not always easy to find out whether a particular website offers a feed, because there is no universally recognized method of indicating its existence. Look for a link to “RSS” or “Syndicate This,” or an orange rectangle with the letters “RSS” or “XML” (don’t ask). These links are not always on the home page. You may need to consult the site map to find a link to a page explaining available feeds and how to find them.

Some of the major sites have multiple feeds to choose from. For example, you can generate a feed of current stories related to the page that you are following on Google News by clicking the RSS link on any Google News page.

Once you know the URL of the RSS feed you want, you provide it to your reader program, which will monitor the feed for you. (Many RSS aggregators come preconfigured with a list of feed URLs for popular news websites.)

In addition to notifying you of important news headlines, changes to your favorite websites, and new developments in any medical (or other) field of interest to you, RSS feeds have many other uses. Some will notify you of new products in a store or catalog, new newsletter issues (including email newsletters), weather and other changing-condition alerts, and the addition of new items to a database – or new members to a group.

It can work the other way as well: If you want readers of your website, blog, or podcast to receive the latest news about your practice, such as new treatments and procedures you’re offering – or if you want to know immediately anytime your name pops up in news or gossip sites – you can create your own RSS feed. In my next column, I’ll explain exactly how to do that.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at [email protected].

BALTIMORE – A cardioplegic solution developed by a noted cardiac surgeon has been deemed a “simple and safe” cardio protective strategy in a study presented at the annual meeting of the American Association for Thoracic Surgery.

In an interview at the event, Pedro J. del Nido, MD, chief of cardiac surgery at Boston Children’s Hospital, and inventor of the long-acting Del Nido solution, explained how and why he and his colleagues developed the new cardioplegic solution. He praised the study as uniquely important, given that there have been few prospective, randomized, and controlled comparative studies of cardioplegia targeted at pediatric patients.

“Baby hearts have a slightly different metabolism than adult hearts,” Dr. del Nido said. “Typically in pediatric procedures we not only cool the heart but we lower the whole body temperature... In the adult world we don’t drop the temperature so much.” He also said the method and flow rate of cardioplegia delivery was unique for pediatric patients, given the fragility of the endothelial cells lining their blood vessels.

The study compared the Del Nido solution with the St. Thomas cardioplegia solution. The investigators praised the Del Nido solution’s performance for “better cardiac index profile, lesser troponin-I release, and decreased morbidity.”

Dr. del Nido developed the Del Nido cardioplegic solution, but reported no other relevant financial disclosures.

[email protected]

On Twitter @richpizzi

BALTIMORE – A cardioplegic solution developed by a noted cardiac surgeon has been deemed a “simple and safe” cardio protective strategy in a study presented at the annual meeting of the American Association for Thoracic Surgery.

In an interview at the event, Pedro J. del Nido, MD, chief of cardiac surgery at Boston Children’s Hospital, and inventor of the long-acting Del Nido solution, explained how and why he and his colleagues developed the new cardioplegic solution. He praised the study as uniquely important, given that there have been few prospective, randomized, and controlled comparative studies of cardioplegia targeted at pediatric patients.

“Baby hearts have a slightly different metabolism than adult hearts,” Dr. del Nido said. “Typically in pediatric procedures we not only cool the heart but we lower the whole body temperature... In the adult world we don’t drop the temperature so much.” He also said the method and flow rate of cardioplegia delivery was unique for pediatric patients, given the fragility of the endothelial cells lining their blood vessels.

The study compared the Del Nido solution with the St. Thomas cardioplegia solution. The investigators praised the Del Nido solution’s performance for “better cardiac index profile, lesser troponin-I release, and decreased morbidity.”

Dr. del Nido developed the Del Nido cardioplegic solution, but reported no other relevant financial disclosures.

[email protected]

On Twitter @richpizzi

BALTIMORE – A cardioplegic solution developed by a noted cardiac surgeon has been deemed a “simple and safe” cardio protective strategy in a study presented at the annual meeting of the American Association for Thoracic Surgery.

In an interview at the event, Pedro J. del Nido, MD, chief of cardiac surgery at Boston Children’s Hospital, and inventor of the long-acting Del Nido solution, explained how and why he and his colleagues developed the new cardioplegic solution. He praised the study as uniquely important, given that there have been few prospective, randomized, and controlled comparative studies of cardioplegia targeted at pediatric patients.

“Baby hearts have a slightly different metabolism than adult hearts,” Dr. del Nido said. “Typically in pediatric procedures we not only cool the heart but we lower the whole body temperature... In the adult world we don’t drop the temperature so much.” He also said the method and flow rate of cardioplegia delivery was unique for pediatric patients, given the fragility of the endothelial cells lining their blood vessels.

The study compared the Del Nido solution with the St. Thomas cardioplegia solution. The investigators praised the Del Nido solution’s performance for “better cardiac index profile, lesser troponin-I release, and decreased morbidity.”

Dr. del Nido developed the Del Nido cardioplegic solution, but reported no other relevant financial disclosures.

[email protected]

On Twitter @richpizzi