Perspectives

We have already come a long way from thinking that psoriasis is merely a cutaneous disease caused by a defect in cellular replication; we now recognize that psoriasis is a systemic inflammatory process that has broad health implications. This association is manifested by comorbidities such as the occurrence of the metabolic syndrome and an increased risk for myocardial infarction. An increased incidence of chronic obstructive pulmonary disease also has been demonstrated in patients with psoriasis, especially those who smoke. Unfortunately, recent publications have highlighted investigative work that expands the scope of psoriatic comorbidity into new realms.

Li and colleagues (Ann Rheum Dis. 2013;72:1200-1205) performed a retrospective analysis of 174,476 women enrolled in several large national health studies. They found an increased risk for incident Crohn disease (relative risk [RR], 4.00; 95% confidence interval [CI], 1.72-9.27) among women with psoriasis. This increased risk rose (RR, 6.43; 95% CI, 2.04-20.32) if both psoriasis and psoriatic arthritis were present. Although the risk for those who already have Crohn disease to develop psoriasis has been previously noted, this study provides the first convincing clinical evidence that the converse association also is true, which is is not totally surprising when one considers common genetic and aberrant cytokine profiles between Crohn disease and psoriasis to suggest an overlap in pathogenic mechanisms.

Perhaps more ominous was the recently published work of Wan and associates (BMJ. 2013;347:f5961). In this massive retrospective analysis utilizing detailed British electronic medical records, 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were matched to 689,702 unaffected patients. The investigators found a clear increased risk for chronic renal disease (RR, 1.93; 95% CI, 1.79-2.08) among those with severe psoriasis. The risk was higher in younger patients; for example, among those aged 30 years, the RR rose to 3.82 (95% CI, 3.15-4.64). The risk for developing renal disease was independent of well-known predisposing factors, such as diabetes mellitus and hypertension. The association between severe psoriasis and renal disease also appeared to be independent of medications administered for psoriasis (eg, cyclosporine).

Also alarming was a recently published systematic review and meta-analysis of 1080 publications concerning the potential association between psoriasis and cancer (J Eur Acad Dermatol Venereol. 2013;27[suppl 3]:36-46). Pouplard et al found that there may be an increased risk for the following solid cancers in psoriasis patients: respiratory tract cancer (RR, 1.52; 95% CI, 1.35-1.71), upper aerodigestive tract cancer (RR, 3.05; 95% CI, 1.74-5.32), urinary tract cancer (RR, 1.31; 95% CI, 1.11-1.55), and liver cancer (RR, 1.90; 95% CI, 1.48-2.44). To the authors, the association seemed particularly strong with these neoplasms, which are associated with excessive alcohol ingestion and smoking.

What’s the issue?

Why might these comorbidities occur? Perhaps chronic inflammation due to abnormal cytokine production and/or deviant immune defenses may promote these new (or better documented) psoriatic comorbidities. Why are they of importance to dermatologists? Because we are the primary source of care for patients with psoriasis, especially those with severe disease. We cannot stop our historical reviews and physical examination with the skin and joints; rather, we must consider the whole patient. We probably should at least perform a comprehensive history at each visit, being carefully attune to any new concerns that suggest gastrointestinal, pulmonary, and renal disease or internal neoplasia, which places an extra (and perhaps unwanted) burden of care on the dermatologist. However, the way I see it is that our role in early detection of an ever-expanding list of serious psoriatic comorbidities may be crucial to the ultimate long-term health of our patients. Are you ready to accept that intensified and enhanced medical responsibility?

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

We have already come a long way from thinking that psoriasis is merely a cutaneous disease caused by a defect in cellular replication; we now recognize that psoriasis is a systemic inflammatory process that has broad health implications. This association is manifested by comorbidities such as the occurrence of the metabolic syndrome and an increased risk for myocardial infarction. An increased incidence of chronic obstructive pulmonary disease also has been demonstrated in patients with psoriasis, especially those who smoke. Unfortunately, recent publications have highlighted investigative work that expands the scope of psoriatic comorbidity into new realms.

Li and colleagues (Ann Rheum Dis. 2013;72:1200-1205) performed a retrospective analysis of 174,476 women enrolled in several large national health studies. They found an increased risk for incident Crohn disease (relative risk [RR], 4.00; 95% confidence interval [CI], 1.72-9.27) among women with psoriasis. This increased risk rose (RR, 6.43; 95% CI, 2.04-20.32) if both psoriasis and psoriatic arthritis were present. Although the risk for those who already have Crohn disease to develop psoriasis has been previously noted, this study provides the first convincing clinical evidence that the converse association also is true, which is is not totally surprising when one considers common genetic and aberrant cytokine profiles between Crohn disease and psoriasis to suggest an overlap in pathogenic mechanisms.

Perhaps more ominous was the recently published work of Wan and associates (BMJ. 2013;347:f5961). In this massive retrospective analysis utilizing detailed British electronic medical records, 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were matched to 689,702 unaffected patients. The investigators found a clear increased risk for chronic renal disease (RR, 1.93; 95% CI, 1.79-2.08) among those with severe psoriasis. The risk was higher in younger patients; for example, among those aged 30 years, the RR rose to 3.82 (95% CI, 3.15-4.64). The risk for developing renal disease was independent of well-known predisposing factors, such as diabetes mellitus and hypertension. The association between severe psoriasis and renal disease also appeared to be independent of medications administered for psoriasis (eg, cyclosporine).

Also alarming was a recently published systematic review and meta-analysis of 1080 publications concerning the potential association between psoriasis and cancer (J Eur Acad Dermatol Venereol. 2013;27[suppl 3]:36-46). Pouplard et al found that there may be an increased risk for the following solid cancers in psoriasis patients: respiratory tract cancer (RR, 1.52; 95% CI, 1.35-1.71), upper aerodigestive tract cancer (RR, 3.05; 95% CI, 1.74-5.32), urinary tract cancer (RR, 1.31; 95% CI, 1.11-1.55), and liver cancer (RR, 1.90; 95% CI, 1.48-2.44). To the authors, the association seemed particularly strong with these neoplasms, which are associated with excessive alcohol ingestion and smoking.

What’s the issue?

Why might these comorbidities occur? Perhaps chronic inflammation due to abnormal cytokine production and/or deviant immune defenses may promote these new (or better documented) psoriatic comorbidities. Why are they of importance to dermatologists? Because we are the primary source of care for patients with psoriasis, especially those with severe disease. We cannot stop our historical reviews and physical examination with the skin and joints; rather, we must consider the whole patient. We probably should at least perform a comprehensive history at each visit, being carefully attune to any new concerns that suggest gastrointestinal, pulmonary, and renal disease or internal neoplasia, which places an extra (and perhaps unwanted) burden of care on the dermatologist. However, the way I see it is that our role in early detection of an ever-expanding list of serious psoriatic comorbidities may be crucial to the ultimate long-term health of our patients. Are you ready to accept that intensified and enhanced medical responsibility?

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

We have already come a long way from thinking that psoriasis is merely a cutaneous disease caused by a defect in cellular replication; we now recognize that psoriasis is a systemic inflammatory process that has broad health implications. This association is manifested by comorbidities such as the occurrence of the metabolic syndrome and an increased risk for myocardial infarction. An increased incidence of chronic obstructive pulmonary disease also has been demonstrated in patients with psoriasis, especially those who smoke. Unfortunately, recent publications have highlighted investigative work that expands the scope of psoriatic comorbidity into new realms.

Li and colleagues (Ann Rheum Dis. 2013;72:1200-1205) performed a retrospective analysis of 174,476 women enrolled in several large national health studies. They found an increased risk for incident Crohn disease (relative risk [RR], 4.00; 95% confidence interval [CI], 1.72-9.27) among women with psoriasis. This increased risk rose (RR, 6.43; 95% CI, 2.04-20.32) if both psoriasis and psoriatic arthritis were present. Although the risk for those who already have Crohn disease to develop psoriasis has been previously noted, this study provides the first convincing clinical evidence that the converse association also is true, which is is not totally surprising when one considers common genetic and aberrant cytokine profiles between Crohn disease and psoriasis to suggest an overlap in pathogenic mechanisms.

Perhaps more ominous was the recently published work of Wan and associates (BMJ. 2013;347:f5961). In this massive retrospective analysis utilizing detailed British electronic medical records, 136,529 patients with mild psoriasis and 7354 patients with severe psoriasis based on treatment patterns were matched to 689,702 unaffected patients. The investigators found a clear increased risk for chronic renal disease (RR, 1.93; 95% CI, 1.79-2.08) among those with severe psoriasis. The risk was higher in younger patients; for example, among those aged 30 years, the RR rose to 3.82 (95% CI, 3.15-4.64). The risk for developing renal disease was independent of well-known predisposing factors, such as diabetes mellitus and hypertension. The association between severe psoriasis and renal disease also appeared to be independent of medications administered for psoriasis (eg, cyclosporine).

Also alarming was a recently published systematic review and meta-analysis of 1080 publications concerning the potential association between psoriasis and cancer (J Eur Acad Dermatol Venereol. 2013;27[suppl 3]:36-46). Pouplard et al found that there may be an increased risk for the following solid cancers in psoriasis patients: respiratory tract cancer (RR, 1.52; 95% CI, 1.35-1.71), upper aerodigestive tract cancer (RR, 3.05; 95% CI, 1.74-5.32), urinary tract cancer (RR, 1.31; 95% CI, 1.11-1.55), and liver cancer (RR, 1.90; 95% CI, 1.48-2.44). To the authors, the association seemed particularly strong with these neoplasms, which are associated with excessive alcohol ingestion and smoking.

What’s the issue?

Why might these comorbidities occur? Perhaps chronic inflammation due to abnormal cytokine production and/or deviant immune defenses may promote these new (or better documented) psoriatic comorbidities. Why are they of importance to dermatologists? Because we are the primary source of care for patients with psoriasis, especially those with severe disease. We cannot stop our historical reviews and physical examination with the skin and joints; rather, we must consider the whole patient. We probably should at least perform a comprehensive history at each visit, being carefully attune to any new concerns that suggest gastrointestinal, pulmonary, and renal disease or internal neoplasia, which places an extra (and perhaps unwanted) burden of care on the dermatologist. However, the way I see it is that our role in early detection of an ever-expanding list of serious psoriatic comorbidities may be crucial to the ultimate long-term health of our patients. Are you ready to accept that intensified and enhanced medical responsibility?

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

Without reading too much into CVS’s decision to stop selling cigarettes by October 1st (they may lose a small percentage of their profits, but have already gained exponentially in publicity), I will say that it echoes a message that health care providers have been proclaiming loudly for a long time: It makes no sense for a health-related business to sell tobacco-related products.

In time, I think we’ll come to see this announcement as a watershed event in the fight against Big Tobacco, setting off what I hope will be a trend in that direction on the part of all other drug stores, then grocery stores and other tobacco outlets. No, this won’t stop smokers from getting their fix, but it makes it a bit more difficult—and perhaps more importantly, it makes smoking just a bit less socially acceptable. We’ve known for years that this is what we need: for smoking to be out of fashion, to be seen for exactly what it is—a useless, dangerous, nasty addiction with absolutely no upside.

I never thought I’d live long enough to see this happen. But in 2000, a major college stadium where I was attending a football game (along with 85,000 others), had just been declared a no-smoking zone by the university. One man, who apparently hadn’t gotten the news, lit up during the game. Immediately, the security people were there to make him put out his cigarette. The other fans—myself included—actually applauded. I knew right then that as a society, we had turned a corner.

Now, most hospitals are smoke-free zones. I was part of that effort and, believe me, as obvious as that concept is, it was a struggle to achieve. Most businesses and other public gathering places are nonsmoking now, too. This movement is picking up steam, and it’s high time it does. But to fully appreciate where we are, you have to know where we’ve been.

I go back to a time when everybody smoked everywhere. Almost 60% of American adults smoked. Clinic waiting rooms had ashtrays by every chair. The receptionists and nurses smoked, and when the doctor came in the exam room to examine you, chances are, he would smoke during the exam! He would smoke (as could nurses and patients) in the hospital as well. It was just an accepted part of society.

But think about that for a minute: Suppose there was no such thing as smoking. Imagine that someone came along with that as a new idea.

“Let’s see: I want to take this cured vegetable leaf that I’ve chopped up into tiny slivers, and wrap it with thin paper. Then I want to set fire to the end of it, place the other end in my mouth, suck the smoke out of it, and breathe it into my lungs, where it will burn and most likely make me cough. The chemicals in the smoke will make my heart race initially, but then it will have the effect of a depressant. The first 100 or so times I do this, I will become nauseated, and may even throw up. But then those effects lessen, and before you know it, I feel very uncomfortable if I don’t smoke.”

“In fact, I begin to crave it so strongly that the next thing I know, I’m smoking 20 cigarettes a day. When I try to stop, I go crazy, so I keep smoking despite the fact that I’m paying $50 to $60 per carton—taking money away from my family, stinking up my whole house, my own body, and my breath, ruining my own health as well as my teeth, putting my family at risk as well, and getting nothing positive in return.”

Such a product would never get off the ground, legal or not. No one would be dumb enough to do it. Yet here we are in the 21st century, where smoking is, by far, the biggest preventable health problem in this country. It kills almost 450,000 Americans a year and cripples far more than that. And we finally have one major chain of drugstores announcing they will no longer sell cigarettes. It’s just another brick in the wall.

Have a comment? Email CRnewseditor@frontlinemedcom.com 

Without reading too much into CVS’s decision to stop selling cigarettes by October 1st (they may lose a small percentage of their profits, but have already gained exponentially in publicity), I will say that it echoes a message that health care providers have been proclaiming loudly for a long time: It makes no sense for a health-related business to sell tobacco-related products.

In time, I think we’ll come to see this announcement as a watershed event in the fight against Big Tobacco, setting off what I hope will be a trend in that direction on the part of all other drug stores, then grocery stores and other tobacco outlets. No, this won’t stop smokers from getting their fix, but it makes it a bit more difficult—and perhaps more importantly, it makes smoking just a bit less socially acceptable. We’ve known for years that this is what we need: for smoking to be out of fashion, to be seen for exactly what it is—a useless, dangerous, nasty addiction with absolutely no upside.

I never thought I’d live long enough to see this happen. But in 2000, a major college stadium where I was attending a football game (along with 85,000 others), had just been declared a no-smoking zone by the university. One man, who apparently hadn’t gotten the news, lit up during the game. Immediately, the security people were there to make him put out his cigarette. The other fans—myself included—actually applauded. I knew right then that as a society, we had turned a corner.

Now, most hospitals are smoke-free zones. I was part of that effort and, believe me, as obvious as that concept is, it was a struggle to achieve. Most businesses and other public gathering places are nonsmoking now, too. This movement is picking up steam, and it’s high time it does. But to fully appreciate where we are, you have to know where we’ve been.

I go back to a time when everybody smoked everywhere. Almost 60% of American adults smoked. Clinic waiting rooms had ashtrays by every chair. The receptionists and nurses smoked, and when the doctor came in the exam room to examine you, chances are, he would smoke during the exam! He would smoke (as could nurses and patients) in the hospital as well. It was just an accepted part of society.

But think about that for a minute: Suppose there was no such thing as smoking. Imagine that someone came along with that as a new idea.

“Let’s see: I want to take this cured vegetable leaf that I’ve chopped up into tiny slivers, and wrap it with thin paper. Then I want to set fire to the end of it, place the other end in my mouth, suck the smoke out of it, and breathe it into my lungs, where it will burn and most likely make me cough. The chemicals in the smoke will make my heart race initially, but then it will have the effect of a depressant. The first 100 or so times I do this, I will become nauseated, and may even throw up. But then those effects lessen, and before you know it, I feel very uncomfortable if I don’t smoke.”

“In fact, I begin to crave it so strongly that the next thing I know, I’m smoking 20 cigarettes a day. When I try to stop, I go crazy, so I keep smoking despite the fact that I’m paying $50 to $60 per carton—taking money away from my family, stinking up my whole house, my own body, and my breath, ruining my own health as well as my teeth, putting my family at risk as well, and getting nothing positive in return.”

Such a product would never get off the ground, legal or not. No one would be dumb enough to do it. Yet here we are in the 21st century, where smoking is, by far, the biggest preventable health problem in this country. It kills almost 450,000 Americans a year and cripples far more than that. And we finally have one major chain of drugstores announcing they will no longer sell cigarettes. It’s just another brick in the wall.

Have a comment? Email CRnewseditor@frontlinemedcom.com 

Without reading too much into CVS’s decision to stop selling cigarettes by October 1st (they may lose a small percentage of their profits, but have already gained exponentially in publicity), I will say that it echoes a message that health care providers have been proclaiming loudly for a long time: It makes no sense for a health-related business to sell tobacco-related products.

In time, I think we’ll come to see this announcement as a watershed event in the fight against Big Tobacco, setting off what I hope will be a trend in that direction on the part of all other drug stores, then grocery stores and other tobacco outlets. No, this won’t stop smokers from getting their fix, but it makes it a bit more difficult—and perhaps more importantly, it makes smoking just a bit less socially acceptable. We’ve known for years that this is what we need: for smoking to be out of fashion, to be seen for exactly what it is—a useless, dangerous, nasty addiction with absolutely no upside.

I never thought I’d live long enough to see this happen. But in 2000, a major college stadium where I was attending a football game (along with 85,000 others), had just been declared a no-smoking zone by the university. One man, who apparently hadn’t gotten the news, lit up during the game. Immediately, the security people were there to make him put out his cigarette. The other fans—myself included—actually applauded. I knew right then that as a society, we had turned a corner.

Now, most hospitals are smoke-free zones. I was part of that effort and, believe me, as obvious as that concept is, it was a struggle to achieve. Most businesses and other public gathering places are nonsmoking now, too. This movement is picking up steam, and it’s high time it does. But to fully appreciate where we are, you have to know where we’ve been.

I go back to a time when everybody smoked everywhere. Almost 60% of American adults smoked. Clinic waiting rooms had ashtrays by every chair. The receptionists and nurses smoked, and when the doctor came in the exam room to examine you, chances are, he would smoke during the exam! He would smoke (as could nurses and patients) in the hospital as well. It was just an accepted part of society.

But think about that for a minute: Suppose there was no such thing as smoking. Imagine that someone came along with that as a new idea.

“Let’s see: I want to take this cured vegetable leaf that I’ve chopped up into tiny slivers, and wrap it with thin paper. Then I want to set fire to the end of it, place the other end in my mouth, suck the smoke out of it, and breathe it into my lungs, where it will burn and most likely make me cough. The chemicals in the smoke will make my heart race initially, but then it will have the effect of a depressant. The first 100 or so times I do this, I will become nauseated, and may even throw up. But then those effects lessen, and before you know it, I feel very uncomfortable if I don’t smoke.”

“In fact, I begin to crave it so strongly that the next thing I know, I’m smoking 20 cigarettes a day. When I try to stop, I go crazy, so I keep smoking despite the fact that I’m paying $50 to $60 per carton—taking money away from my family, stinking up my whole house, my own body, and my breath, ruining my own health as well as my teeth, putting my family at risk as well, and getting nothing positive in return.”

Such a product would never get off the ground, legal or not. No one would be dumb enough to do it. Yet here we are in the 21st century, where smoking is, by far, the biggest preventable health problem in this country. It kills almost 450,000 Americans a year and cripples far more than that. And we finally have one major chain of drugstores announcing they will no longer sell cigarettes. It’s just another brick in the wall.

Have a comment? Email CRnewseditor@frontlinemedcom.com 

In the January 2014 issue of Aesthetic Surgery Journal (2014;34:118-132), van Rozelaar et al studied the quality-of-life (QOL) effects and magnetic resonance imaging (MRI) changes seen in patients who are human immunodeficiency virus (HIV) positive and are treated with semipermanent fillers, poly-L-lactic acid (PLLA) and calcium hydroxylapatite (CaHA). They followed an 82-patient cohort for 1 year; all patients had facial lipoatrophy (FLA) of grades 2 to 4. Forty-one patients had PLLA injected (mean volume, 58.2 mL; range, 12–105 mL) and 41 patients had CaHA injected (mean volume, 9.1 mL; range, 3–23 mL) done in multiple sessions. The MRI examinations were performed prior to treatment and again 12 months after. The severity of FLA as well as QOL was measured using self-reported questionnaires based on the 36-Item Short Form Health Survey, Medical Outcomes Study HIV Health Survey, and Center for Epidemiologic Studies Depression Scale formats.

Of the patients enrolled, 49 patients completed the 1-year follow-up posttreatment MRI: 26 treated with PLLA and 23 treated with CaHA. Eleven CaHA patients (47.8%) were treated in the buccal region only, while 6 patients (23.1%) in the PLLA group were injected in the buccal region only. No significant change in total subcutaneous thickness (TST) was observed at the level of the mandibular head. Injection of PLLA and CaHA showed an increase in TST buccally (P=.69) and temporally (P=.26). Temporal TST increase was more pronounced in PLLA patients compared with CaHA-treated patients. Of note, collagen formation also was observed in 25 PLLA patients (96.2%) and 19 CaHA patients (82.6%) and was defined as well-demarcated hypointense subcutaneous tissue on MRI. Adipose tissue also was shown to increase significantly in both groups (19 PLLA patients [73.1%] and 15 CaHA patients [65.2%]). The MRI examinations revealed only 1 nodule in a PLLA patient.

Quality of life improved significantly on all subscales tested (P<.01), including role functioning (physical and emotional), social functioning, and mental health. Depressive symptoms also were reported to decrease significantly over time (P<.001). Interestingly, the percentage of patients receiving sickness benefits because of lipoatrophy decreased significantly over time (P<.001). Patients treated with CaHA had more favorable scores than patients treated with PLLA regarding self-rated severity of lipoatrophy.

What’s the issue?

It is well known that FLA is a cutaneous side effect of both HIV itself and medication usage, which has notable QOL effects. This prospective study showed that the use of semipermanent fillers had a remarkable impact on self-reported QOL parameters. The authors also reported that it was the first study using MRI as a measurement tool. Although this cohort study did have a notable number of patients who did not complete the MRI evaluation, it did show that there were lasting results 1 year after treatment. The treatment of FLA with PLLA and CaHA injections increased TST in both buccal and temporal regions, which was associated with QOL improvement in all subscales after start of treatment. The CaHA cohort obtained higher scores in the QOL assessment, which was postulated to be the result of CaHA’s immediate results. With the wide use of fillers, it is important to understand the QOL effects for all populations. Do you think all populations have similar increases in QOL?

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

In the January 2014 issue of Aesthetic Surgery Journal (2014;34:118-132), van Rozelaar et al studied the quality-of-life (QOL) effects and magnetic resonance imaging (MRI) changes seen in patients who are human immunodeficiency virus (HIV) positive and are treated with semipermanent fillers, poly-L-lactic acid (PLLA) and calcium hydroxylapatite (CaHA). They followed an 82-patient cohort for 1 year; all patients had facial lipoatrophy (FLA) of grades 2 to 4. Forty-one patients had PLLA injected (mean volume, 58.2 mL; range, 12–105 mL) and 41 patients had CaHA injected (mean volume, 9.1 mL; range, 3–23 mL) done in multiple sessions. The MRI examinations were performed prior to treatment and again 12 months after. The severity of FLA as well as QOL was measured using self-reported questionnaires based on the 36-Item Short Form Health Survey, Medical Outcomes Study HIV Health Survey, and Center for Epidemiologic Studies Depression Scale formats.

Of the patients enrolled, 49 patients completed the 1-year follow-up posttreatment MRI: 26 treated with PLLA and 23 treated with CaHA. Eleven CaHA patients (47.8%) were treated in the buccal region only, while 6 patients (23.1%) in the PLLA group were injected in the buccal region only. No significant change in total subcutaneous thickness (TST) was observed at the level of the mandibular head. Injection of PLLA and CaHA showed an increase in TST buccally (P=.69) and temporally (P=.26). Temporal TST increase was more pronounced in PLLA patients compared with CaHA-treated patients. Of note, collagen formation also was observed in 25 PLLA patients (96.2%) and 19 CaHA patients (82.6%) and was defined as well-demarcated hypointense subcutaneous tissue on MRI. Adipose tissue also was shown to increase significantly in both groups (19 PLLA patients [73.1%] and 15 CaHA patients [65.2%]). The MRI examinations revealed only 1 nodule in a PLLA patient.

Quality of life improved significantly on all subscales tested (P<.01), including role functioning (physical and emotional), social functioning, and mental health. Depressive symptoms also were reported to decrease significantly over time (P<.001). Interestingly, the percentage of patients receiving sickness benefits because of lipoatrophy decreased significantly over time (P<.001). Patients treated with CaHA had more favorable scores than patients treated with PLLA regarding self-rated severity of lipoatrophy.

What’s the issue?

It is well known that FLA is a cutaneous side effect of both HIV itself and medication usage, which has notable QOL effects. This prospective study showed that the use of semipermanent fillers had a remarkable impact on self-reported QOL parameters. The authors also reported that it was the first study using MRI as a measurement tool. Although this cohort study did have a notable number of patients who did not complete the MRI evaluation, it did show that there were lasting results 1 year after treatment. The treatment of FLA with PLLA and CaHA injections increased TST in both buccal and temporal regions, which was associated with QOL improvement in all subscales after start of treatment. The CaHA cohort obtained higher scores in the QOL assessment, which was postulated to be the result of CaHA’s immediate results. With the wide use of fillers, it is important to understand the QOL effects for all populations. Do you think all populations have similar increases in QOL?

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

In the January 2014 issue of Aesthetic Surgery Journal (2014;34:118-132), van Rozelaar et al studied the quality-of-life (QOL) effects and magnetic resonance imaging (MRI) changes seen in patients who are human immunodeficiency virus (HIV) positive and are treated with semipermanent fillers, poly-L-lactic acid (PLLA) and calcium hydroxylapatite (CaHA). They followed an 82-patient cohort for 1 year; all patients had facial lipoatrophy (FLA) of grades 2 to 4. Forty-one patients had PLLA injected (mean volume, 58.2 mL; range, 12–105 mL) and 41 patients had CaHA injected (mean volume, 9.1 mL; range, 3–23 mL) done in multiple sessions. The MRI examinations were performed prior to treatment and again 12 months after. The severity of FLA as well as QOL was measured using self-reported questionnaires based on the 36-Item Short Form Health Survey, Medical Outcomes Study HIV Health Survey, and Center for Epidemiologic Studies Depression Scale formats.

Of the patients enrolled, 49 patients completed the 1-year follow-up posttreatment MRI: 26 treated with PLLA and 23 treated with CaHA. Eleven CaHA patients (47.8%) were treated in the buccal region only, while 6 patients (23.1%) in the PLLA group were injected in the buccal region only. No significant change in total subcutaneous thickness (TST) was observed at the level of the mandibular head. Injection of PLLA and CaHA showed an increase in TST buccally (P=.69) and temporally (P=.26). Temporal TST increase was more pronounced in PLLA patients compared with CaHA-treated patients. Of note, collagen formation also was observed in 25 PLLA patients (96.2%) and 19 CaHA patients (82.6%) and was defined as well-demarcated hypointense subcutaneous tissue on MRI. Adipose tissue also was shown to increase significantly in both groups (19 PLLA patients [73.1%] and 15 CaHA patients [65.2%]). The MRI examinations revealed only 1 nodule in a PLLA patient.

Quality of life improved significantly on all subscales tested (P<.01), including role functioning (physical and emotional), social functioning, and mental health. Depressive symptoms also were reported to decrease significantly over time (P<.001). Interestingly, the percentage of patients receiving sickness benefits because of lipoatrophy decreased significantly over time (P<.001). Patients treated with CaHA had more favorable scores than patients treated with PLLA regarding self-rated severity of lipoatrophy.

What’s the issue?

It is well known that FLA is a cutaneous side effect of both HIV itself and medication usage, which has notable QOL effects. This prospective study showed that the use of semipermanent fillers had a remarkable impact on self-reported QOL parameters. The authors also reported that it was the first study using MRI as a measurement tool. Although this cohort study did have a notable number of patients who did not complete the MRI evaluation, it did show that there were lasting results 1 year after treatment. The treatment of FLA with PLLA and CaHA injections increased TST in both buccal and temporal regions, which was associated with QOL improvement in all subscales after start of treatment. The CaHA cohort obtained higher scores in the QOL assessment, which was postulated to be the result of CaHA’s immediate results. With the wide use of fillers, it is important to understand the QOL effects for all populations. Do you think all populations have similar increases in QOL?

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

The passage of the Biologics Price Competition and Innovation Act of 2009 (BPCI Act) allowed for the creation of a regulatory pathway for new, safe, and effective biosimilar agents. Although the medical community always needs new and affordable treatments, patients and physicians are aware of and concerned about the risks associated with biologics and the lack of long-term safety data for new treatments.

In contrast to generic drugs, which are chemically identical to their branded counterparts, biosimilar agents are not chemically identical to their branded biologic counterparts because as large complex molecules derived from living cells using recombinant DNA technology, biologics can never be exactly replicated due to their inherent variability.

Because of these substantial differences, the National Psoriasis Foundation released a policy in July 2013 to ensure patient safety.

The National Psoriasis Foundation recommends that the patient-provider relationship remain at the center of all treatment planning and supports a prohibition on biosimilar substitution unless all of the following minimal thresholds are met:

1. the biosimilar has been designated by the Food and Drug Administration as interchangeable with the prescribed biologic for the specified indicated use;
2. the biosimilar has a unique nonproprietary name to eliminate confusion, to allow providers to accurately track the therapeutic agent in a patient's permanent record, and to allow for the collection of adverse event information;
3. the biosimilar product follows the same route of administration and dosage form as the reference product;
4. the pharmacist notifies the prescriber in writing or electronic communication of the intention to substitute at least 24 hours prior to the substitution;
5. if explicit permission from prescribing physician and patient is not obtained within 24 hours, then the original prescription must be filled;
6. the patient (or patient's authorized representative) must be informed and educated about a biosimilar substitution at the point of sale; and
7. upon notification of a substitution, the pharmacy and the prescribing physician are to retain a permanent record in the patient's medical record of the biosimilar substitution.

What’s the issue?

The tension between lowering costs and using trusted therapeutic options will be at the center of the debate over biosimilar agents. The National Psoriasis Foundation policy protects physicians and patients and helps maintain their autonomy. As these drugs are developed and studied, we will have more information to inform our decisions. How will you and your patients respond to the availability of biosimilar agents?

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

The passage of the Biologics Price Competition and Innovation Act of 2009 (BPCI Act) allowed for the creation of a regulatory pathway for new, safe, and effective biosimilar agents. Although the medical community always needs new and affordable treatments, patients and physicians are aware of and concerned about the risks associated with biologics and the lack of long-term safety data for new treatments.

In contrast to generic drugs, which are chemically identical to their branded counterparts, biosimilar agents are not chemically identical to their branded biologic counterparts because as large complex molecules derived from living cells using recombinant DNA technology, biologics can never be exactly replicated due to their inherent variability.

Because of these substantial differences, the National Psoriasis Foundation released a policy in July 2013 to ensure patient safety.

The National Psoriasis Foundation recommends that the patient-provider relationship remain at the center of all treatment planning and supports a prohibition on biosimilar substitution unless all of the following minimal thresholds are met:

1. the biosimilar has been designated by the Food and Drug Administration as interchangeable with the prescribed biologic for the specified indicated use;
2. the biosimilar has a unique nonproprietary name to eliminate confusion, to allow providers to accurately track the therapeutic agent in a patient's permanent record, and to allow for the collection of adverse event information;
3. the biosimilar product follows the same route of administration and dosage form as the reference product;
4. the pharmacist notifies the prescriber in writing or electronic communication of the intention to substitute at least 24 hours prior to the substitution;
5. if explicit permission from prescribing physician and patient is not obtained within 24 hours, then the original prescription must be filled;
6. the patient (or patient's authorized representative) must be informed and educated about a biosimilar substitution at the point of sale; and
7. upon notification of a substitution, the pharmacy and the prescribing physician are to retain a permanent record in the patient's medical record of the biosimilar substitution.

What’s the issue?

The tension between lowering costs and using trusted therapeutic options will be at the center of the debate over biosimilar agents. The National Psoriasis Foundation policy protects physicians and patients and helps maintain their autonomy. As these drugs are developed and studied, we will have more information to inform our decisions. How will you and your patients respond to the availability of biosimilar agents?

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

The passage of the Biologics Price Competition and Innovation Act of 2009 (BPCI Act) allowed for the creation of a regulatory pathway for new, safe, and effective biosimilar agents. Although the medical community always needs new and affordable treatments, patients and physicians are aware of and concerned about the risks associated with biologics and the lack of long-term safety data for new treatments.

In contrast to generic drugs, which are chemically identical to their branded counterparts, biosimilar agents are not chemically identical to their branded biologic counterparts because as large complex molecules derived from living cells using recombinant DNA technology, biologics can never be exactly replicated due to their inherent variability.

Because of these substantial differences, the National Psoriasis Foundation released a policy in July 2013 to ensure patient safety.

The National Psoriasis Foundation recommends that the patient-provider relationship remain at the center of all treatment planning and supports a prohibition on biosimilar substitution unless all of the following minimal thresholds are met:

1. the biosimilar has been designated by the Food and Drug Administration as interchangeable with the prescribed biologic for the specified indicated use;
2. the biosimilar has a unique nonproprietary name to eliminate confusion, to allow providers to accurately track the therapeutic agent in a patient's permanent record, and to allow for the collection of adverse event information;
3. the biosimilar product follows the same route of administration and dosage form as the reference product;
4. the pharmacist notifies the prescriber in writing or electronic communication of the intention to substitute at least 24 hours prior to the substitution;
5. if explicit permission from prescribing physician and patient is not obtained within 24 hours, then the original prescription must be filled;
6. the patient (or patient's authorized representative) must be informed and educated about a biosimilar substitution at the point of sale; and
7. upon notification of a substitution, the pharmacy and the prescribing physician are to retain a permanent record in the patient's medical record of the biosimilar substitution.

What’s the issue?

The tension between lowering costs and using trusted therapeutic options will be at the center of the debate over biosimilar agents. The National Psoriasis Foundation policy protects physicians and patients and helps maintain their autonomy. As these drugs are developed and studied, we will have more information to inform our decisions. How will you and your patients respond to the availability of biosimilar agents?

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

In December 2013, the Annals of Internal Medicine amassed 2 original research articles, 1 review, and 1 editorial analyzing and supporting the hypothesis that vitamin and mineral supplementation may not be beneficial for many facets of total health. One study assessed daily multivitamin efficacy in older adults for prevention of cognitive decline (Ann Intern Med. 2013;159:806-814); one evaluated high-dosage daily multivitamin in myocardial infarction patients for prevention of repeated cardiovascular events (Ann Intern Med. 2013;159:797-805); and the systematic review reported all-cause mortality, cardiovascular disease, and cancer in multivitamin users (Ann Intern Med. 2013;159:824-834). All 3 concluded that there was no significant benefit, and the editorial asked that we close the book on this question (Ann Intern Med. 2013;159:850-851).

What’s the issue?

In dermatology, patients often inquire about supplements, dietary changes, and natural methods for aiding in their recovery and for preventing disease. This set of publications attempts to steer us to summarily discourage widespread multivitamin and supplement use. However, there are certainly instances in which dogma from medical school training, smaller patient cohorts, and anecdotal cases compel us to continue them. The first things to come to mind in dermatology (and beyond) are biotin for hair and nail growth, folic acid for preconception and pregnancy prevention of fetal neural defects, and vitamin D for bone health.

Should everyone be on a multivitamin? For which diagnoses do you routinely recommend vitamin or mineral supplementation? In fact, in which instances do you take supplementation yourself? Do you feel comfortable with the evidence that supports it? Which references do you trust in this facet?

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

In December 2013, the Annals of Internal Medicine amassed 2 original research articles, 1 review, and 1 editorial analyzing and supporting the hypothesis that vitamin and mineral supplementation may not be beneficial for many facets of total health. One study assessed daily multivitamin efficacy in older adults for prevention of cognitive decline (Ann Intern Med. 2013;159:806-814); one evaluated high-dosage daily multivitamin in myocardial infarction patients for prevention of repeated cardiovascular events (Ann Intern Med. 2013;159:797-805); and the systematic review reported all-cause mortality, cardiovascular disease, and cancer in multivitamin users (Ann Intern Med. 2013;159:824-834). All 3 concluded that there was no significant benefit, and the editorial asked that we close the book on this question (Ann Intern Med. 2013;159:850-851).

What’s the issue?

In dermatology, patients often inquire about supplements, dietary changes, and natural methods for aiding in their recovery and for preventing disease. This set of publications attempts to steer us to summarily discourage widespread multivitamin and supplement use. However, there are certainly instances in which dogma from medical school training, smaller patient cohorts, and anecdotal cases compel us to continue them. The first things to come to mind in dermatology (and beyond) are biotin for hair and nail growth, folic acid for preconception and pregnancy prevention of fetal neural defects, and vitamin D for bone health.

Should everyone be on a multivitamin? For which diagnoses do you routinely recommend vitamin or mineral supplementation? In fact, in which instances do you take supplementation yourself? Do you feel comfortable with the evidence that supports it? Which references do you trust in this facet?

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

In December 2013, the Annals of Internal Medicine amassed 2 original research articles, 1 review, and 1 editorial analyzing and supporting the hypothesis that vitamin and mineral supplementation may not be beneficial for many facets of total health. One study assessed daily multivitamin efficacy in older adults for prevention of cognitive decline (Ann Intern Med. 2013;159:806-814); one evaluated high-dosage daily multivitamin in myocardial infarction patients for prevention of repeated cardiovascular events (Ann Intern Med. 2013;159:797-805); and the systematic review reported all-cause mortality, cardiovascular disease, and cancer in multivitamin users (Ann Intern Med. 2013;159:824-834). All 3 concluded that there was no significant benefit, and the editorial asked that we close the book on this question (Ann Intern Med. 2013;159:850-851).

What’s the issue?

In dermatology, patients often inquire about supplements, dietary changes, and natural methods for aiding in their recovery and for preventing disease. This set of publications attempts to steer us to summarily discourage widespread multivitamin and supplement use. However, there are certainly instances in which dogma from medical school training, smaller patient cohorts, and anecdotal cases compel us to continue them. The first things to come to mind in dermatology (and beyond) are biotin for hair and nail growth, folic acid for preconception and pregnancy prevention of fetal neural defects, and vitamin D for bone health.

Should everyone be on a multivitamin? For which diagnoses do you routinely recommend vitamin or mineral supplementation? In fact, in which instances do you take supplementation yourself? Do you feel comfortable with the evidence that supports it? Which references do you trust in this facet?

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

In an article published online in Maclean’s magazine on October 15, 2013, the concept of developing artificial body parts is discussed. The technology now exists for scientists to grow tissue organs, such as ears, noses, and fingers. Several groups of investigators, including Anthony Atala, MD (Wake Forest Institute for Regenerative Medicine, Winston-Salem, North Carolina) and Alexander Seifalian, PhD (University College London, England), are busy making ears by creating a biodegradable scaffold onto which cells—either stem cells from the patient or cells that have been harvested from the patient’s original organ—are layered and permitted to multiply. The cell-layered scaffold is then placed in a bioreactor for a couple of weeks. Once ready, the new ear is transplanted onto the patient; subsequently, the scaffold melts away.

Dr. Atala’s laboratory also is busy growing fingers. Meanwhile, Dr. Seifalian grew a nose (inside the patient’s own arm) in only 3 months after the patient lost his nose to skin cancer. He made a mold based on the patient’s original nose, created a scaffold composed of nanocomposite material, added the patient’s stem cells to the scaffold, and put the nose in a bioreactor to mature. Meanwhile, he placed a tissue expander in the patient’s arm and subsequently inserted the nose into the arm so that it could become vascularized and covered by skin. The nose was transplanted to the patient’s face; additional surgery is planned to open the nostrils, followed by seeding them with stem cells to return his sense of smell.

Marc Jeschke, MD, PhD (Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Toronto, Ontario) is developing a bioprinter to create skin. The bioprinter dispenses different types of cells (grown from the patient’s own cells) into a hydrogel matrix in 3 dimensions. Currently, Dr. Jeschke is working with mice; however, in a few years, he anticipates treating human patients. Other investigators, such as Michael C. McAlpine (Princeton University, New Jersey), recently used a commercial 3-dimensional printer to make an ear; the “inks” included calf cells and a silver nanoparticle paste that formed a coiled antenna inside the cartilage that was capable of receiving electromagnetic signals and transmitting them to the brain.

What’s the issue?

The ability to grow tissue organs is going to revolutionize the surgical management of patients who need solid organ replacement; kidneys, lungs, pancreases, spleens, and tracheas have already been successfully grown. Indeed several investigators are making ears and noses. How long will it be before flaps and grafts to repair wound defects following extensive and deforming skin cancer surgery are replaced by ears and noses that are grown from the patient’s own tissue cells or stem cells? Although it seems like science fiction today, how soon will it be before a cutaneous 3-dimensional printer becomes a standard piece of equipment in the dermatologist and dermatologic surgeon’s office for use to create skin to cover postoperative sites that cannot be closed by directly bringing the wound edges together?

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

In an article published online in Maclean’s magazine on October 15, 2013, the concept of developing artificial body parts is discussed. The technology now exists for scientists to grow tissue organs, such as ears, noses, and fingers. Several groups of investigators, including Anthony Atala, MD (Wake Forest Institute for Regenerative Medicine, Winston-Salem, North Carolina) and Alexander Seifalian, PhD (University College London, England), are busy making ears by creating a biodegradable scaffold onto which cells—either stem cells from the patient or cells that have been harvested from the patient’s original organ—are layered and permitted to multiply. The cell-layered scaffold is then placed in a bioreactor for a couple of weeks. Once ready, the new ear is transplanted onto the patient; subsequently, the scaffold melts away.

Dr. Atala’s laboratory also is busy growing fingers. Meanwhile, Dr. Seifalian grew a nose (inside the patient’s own arm) in only 3 months after the patient lost his nose to skin cancer. He made a mold based on the patient’s original nose, created a scaffold composed of nanocomposite material, added the patient’s stem cells to the scaffold, and put the nose in a bioreactor to mature. Meanwhile, he placed a tissue expander in the patient’s arm and subsequently inserted the nose into the arm so that it could become vascularized and covered by skin. The nose was transplanted to the patient’s face; additional surgery is planned to open the nostrils, followed by seeding them with stem cells to return his sense of smell.

Marc Jeschke, MD, PhD (Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Toronto, Ontario) is developing a bioprinter to create skin. The bioprinter dispenses different types of cells (grown from the patient’s own cells) into a hydrogel matrix in 3 dimensions. Currently, Dr. Jeschke is working with mice; however, in a few years, he anticipates treating human patients. Other investigators, such as Michael C. McAlpine (Princeton University, New Jersey), recently used a commercial 3-dimensional printer to make an ear; the “inks” included calf cells and a silver nanoparticle paste that formed a coiled antenna inside the cartilage that was capable of receiving electromagnetic signals and transmitting them to the brain.

What’s the issue?

The ability to grow tissue organs is going to revolutionize the surgical management of patients who need solid organ replacement; kidneys, lungs, pancreases, spleens, and tracheas have already been successfully grown. Indeed several investigators are making ears and noses. How long will it be before flaps and grafts to repair wound defects following extensive and deforming skin cancer surgery are replaced by ears and noses that are grown from the patient’s own tissue cells or stem cells? Although it seems like science fiction today, how soon will it be before a cutaneous 3-dimensional printer becomes a standard piece of equipment in the dermatologist and dermatologic surgeon’s office for use to create skin to cover postoperative sites that cannot be closed by directly bringing the wound edges together?

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

In an article published online in Maclean’s magazine on October 15, 2013, the concept of developing artificial body parts is discussed. The technology now exists for scientists to grow tissue organs, such as ears, noses, and fingers. Several groups of investigators, including Anthony Atala, MD (Wake Forest Institute for Regenerative Medicine, Winston-Salem, North Carolina) and Alexander Seifalian, PhD (University College London, England), are busy making ears by creating a biodegradable scaffold onto which cells—either stem cells from the patient or cells that have been harvested from the patient’s original organ—are layered and permitted to multiply. The cell-layered scaffold is then placed in a bioreactor for a couple of weeks. Once ready, the new ear is transplanted onto the patient; subsequently, the scaffold melts away.

Dr. Atala’s laboratory also is busy growing fingers. Meanwhile, Dr. Seifalian grew a nose (inside the patient’s own arm) in only 3 months after the patient lost his nose to skin cancer. He made a mold based on the patient’s original nose, created a scaffold composed of nanocomposite material, added the patient’s stem cells to the scaffold, and put the nose in a bioreactor to mature. Meanwhile, he placed a tissue expander in the patient’s arm and subsequently inserted the nose into the arm so that it could become vascularized and covered by skin. The nose was transplanted to the patient’s face; additional surgery is planned to open the nostrils, followed by seeding them with stem cells to return his sense of smell.

Marc Jeschke, MD, PhD (Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Toronto, Ontario) is developing a bioprinter to create skin. The bioprinter dispenses different types of cells (grown from the patient’s own cells) into a hydrogel matrix in 3 dimensions. Currently, Dr. Jeschke is working with mice; however, in a few years, he anticipates treating human patients. Other investigators, such as Michael C. McAlpine (Princeton University, New Jersey), recently used a commercial 3-dimensional printer to make an ear; the “inks” included calf cells and a silver nanoparticle paste that formed a coiled antenna inside the cartilage that was capable of receiving electromagnetic signals and transmitting them to the brain.

What’s the issue?

The ability to grow tissue organs is going to revolutionize the surgical management of patients who need solid organ replacement; kidneys, lungs, pancreases, spleens, and tracheas have already been successfully grown. Indeed several investigators are making ears and noses. How long will it be before flaps and grafts to repair wound defects following extensive and deforming skin cancer surgery are replaced by ears and noses that are grown from the patient’s own tissue cells or stem cells? Although it seems like science fiction today, how soon will it be before a cutaneous 3-dimensional printer becomes a standard piece of equipment in the dermatologist and dermatologic surgeon’s office for use to create skin to cover postoperative sites that cannot be closed by directly bringing the wound edges together?

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

The US Food and Drug Administration recently approved a new use for Botox Cosmetic (onabotulinumtoxinA)(Allergan, Inc): temporary improvement in the appearance of moderate to severe crow’s-feet (lateral canthal lines). As reported in the prescribing information, 2 placebo-controlled clinical studies evaluated 833 adult participants with moderate to severe lateral canthal lines. Each participant received 4 U of onabotulinumtoxinA or placebo into 3 sites per side for a total of 24 U in the lateral orbicularis oculi muscle. The first injection was placed approximately 1.5 to 2.0 cm temporal to the lateral canthus and just temporal to the orbital rim. The second and third injection was either above and below, respectively, the first injection or both below the first injection depending on the appearance of wrinkles. Results showed that participants treated with onabotulinumtoxinA had greater improvement compared to placebo in the appearance of crow’s-feet. The most common side effect was lid edema, which occurred in 1% of participants.

What’s the issue?

Although dermatologists and cosmetic surgeons have been using onabotulinumtoxinA and other neurotoxins for treatment of crow’s-feet for a long time (off label), it is now approved for this indication. The volume used on label also is important because it gives guidance as to how much product can be used. Of course each patient is different and many clinicians may decide to use more or less product to achieve a desired correction. The fact that onabotulinumtoxinA is now deemed safe to be used in the crow’s-feet area also is important because it gives the physician some medical/legal protection. Will this approval really change anything that you currently do or don’t do?

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

The US Food and Drug Administration recently approved a new use for Botox Cosmetic (onabotulinumtoxinA)(Allergan, Inc): temporary improvement in the appearance of moderate to severe crow’s-feet (lateral canthal lines). As reported in the prescribing information, 2 placebo-controlled clinical studies evaluated 833 adult participants with moderate to severe lateral canthal lines. Each participant received 4 U of onabotulinumtoxinA or placebo into 3 sites per side for a total of 24 U in the lateral orbicularis oculi muscle. The first injection was placed approximately 1.5 to 2.0 cm temporal to the lateral canthus and just temporal to the orbital rim. The second and third injection was either above and below, respectively, the first injection or both below the first injection depending on the appearance of wrinkles. Results showed that participants treated with onabotulinumtoxinA had greater improvement compared to placebo in the appearance of crow’s-feet. The most common side effect was lid edema, which occurred in 1% of participants.

What’s the issue?

Although dermatologists and cosmetic surgeons have been using onabotulinumtoxinA and other neurotoxins for treatment of crow’s-feet for a long time (off label), it is now approved for this indication. The volume used on label also is important because it gives guidance as to how much product can be used. Of course each patient is different and many clinicians may decide to use more or less product to achieve a desired correction. The fact that onabotulinumtoxinA is now deemed safe to be used in the crow’s-feet area also is important because it gives the physician some medical/legal protection. Will this approval really change anything that you currently do or don’t do?

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

The US Food and Drug Administration recently approved a new use for Botox Cosmetic (onabotulinumtoxinA)(Allergan, Inc): temporary improvement in the appearance of moderate to severe crow’s-feet (lateral canthal lines). As reported in the prescribing information, 2 placebo-controlled clinical studies evaluated 833 adult participants with moderate to severe lateral canthal lines. Each participant received 4 U of onabotulinumtoxinA or placebo into 3 sites per side for a total of 24 U in the lateral orbicularis oculi muscle. The first injection was placed approximately 1.5 to 2.0 cm temporal to the lateral canthus and just temporal to the orbital rim. The second and third injection was either above and below, respectively, the first injection or both below the first injection depending on the appearance of wrinkles. Results showed that participants treated with onabotulinumtoxinA had greater improvement compared to placebo in the appearance of crow’s-feet. The most common side effect was lid edema, which occurred in 1% of participants.

What’s the issue?

Although dermatologists and cosmetic surgeons have been using onabotulinumtoxinA and other neurotoxins for treatment of crow’s-feet for a long time (off label), it is now approved for this indication. The volume used on label also is important because it gives guidance as to how much product can be used. Of course each patient is different and many clinicians may decide to use more or less product to achieve a desired correction. The fact that onabotulinumtoxinA is now deemed safe to be used in the crow’s-feet area also is important because it gives the physician some medical/legal protection. Will this approval really change anything that you currently do or don’t do?

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

Along with 80 other medical societies, the American Academy of Dermatology (AAD) recently published a list of unnecessary medical tests and procedures as part of a stewardship effort called Choosing Wisely, orchestrated by the American Board of Internal Medicine (ABIM) Foundation to conserve health care resources. For dermatologists, the list includes:

1. Don’t prescribe oral antifungal therapy for suspected nail fungus without confirmation of fungal infection.
2. Don’t perform sentinel lymph node biopsy or other diagnostic tests for the evaluation of early, thin melanoma because they do not improve survival.
3. Don’t treat uncomplicated, nonmelanoma skin cancer less than 1 centimeter in size on the trunk and extremities with Mohs micrographic surgery.
4. Don’t use oral antibiotics for treatment of atopic dermatitis unless there is clinical evidence of infection.
5. Don’t routinely use topical antibiotics on a surgical wound.

What’s the issue?

Read the list. Assess your current clinical practices. Note where health care waste exists. A November 2013 ABC News investigation noted that hospital charges are the largest source of medical inflation, and I thought to myself, “Yes, think of all the emergency department and inpatients who are reflexively on expensive broad-spectrum antibiotics, or think of the number of patients admitted for stable conditions.” However, from a different standpoint, some might say that dermatology costs are extravagant based on the items on this list, particularly the surgical inconsistencies. Therefore, we should try not to cast the first stone unless our own specialty’s waste is managed. What are examples of regional sources of excess that you can identify?

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

Along with 80 other medical societies, the American Academy of Dermatology (AAD) recently published a list of unnecessary medical tests and procedures as part of a stewardship effort called Choosing Wisely, orchestrated by the American Board of Internal Medicine (ABIM) Foundation to conserve health care resources. For dermatologists, the list includes:

1. Don’t prescribe oral antifungal therapy for suspected nail fungus without confirmation of fungal infection.
2. Don’t perform sentinel lymph node biopsy or other diagnostic tests for the evaluation of early, thin melanoma because they do not improve survival.
3. Don’t treat uncomplicated, nonmelanoma skin cancer less than 1 centimeter in size on the trunk and extremities with Mohs micrographic surgery.
4. Don’t use oral antibiotics for treatment of atopic dermatitis unless there is clinical evidence of infection.
5. Don’t routinely use topical antibiotics on a surgical wound.

What’s the issue?

Read the list. Assess your current clinical practices. Note where health care waste exists. A November 2013 ABC News investigation noted that hospital charges are the largest source of medical inflation, and I thought to myself, “Yes, think of all the emergency department and inpatients who are reflexively on expensive broad-spectrum antibiotics, or think of the number of patients admitted for stable conditions.” However, from a different standpoint, some might say that dermatology costs are extravagant based on the items on this list, particularly the surgical inconsistencies. Therefore, we should try not to cast the first stone unless our own specialty’s waste is managed. What are examples of regional sources of excess that you can identify?

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

Along with 80 other medical societies, the American Academy of Dermatology (AAD) recently published a list of unnecessary medical tests and procedures as part of a stewardship effort called Choosing Wisely, orchestrated by the American Board of Internal Medicine (ABIM) Foundation to conserve health care resources. For dermatologists, the list includes:

1. Don’t prescribe oral antifungal therapy for suspected nail fungus without confirmation of fungal infection.
2. Don’t perform sentinel lymph node biopsy or other diagnostic tests for the evaluation of early, thin melanoma because they do not improve survival.
3. Don’t treat uncomplicated, nonmelanoma skin cancer less than 1 centimeter in size on the trunk and extremities with Mohs micrographic surgery.
4. Don’t use oral antibiotics for treatment of atopic dermatitis unless there is clinical evidence of infection.
5. Don’t routinely use topical antibiotics on a surgical wound.

What’s the issue?

Read the list. Assess your current clinical practices. Note where health care waste exists. A November 2013 ABC News investigation noted that hospital charges are the largest source of medical inflation, and I thought to myself, “Yes, think of all the emergency department and inpatients who are reflexively on expensive broad-spectrum antibiotics, or think of the number of patients admitted for stable conditions.” However, from a different standpoint, some might say that dermatology costs are extravagant based on the items on this list, particularly the surgical inconsistencies. Therefore, we should try not to cast the first stone unless our own specialty’s waste is managed. What are examples of regional sources of excess that you can identify?

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

I have taken beta-blockers for nearly 30 years to combat a non–life-threatening but very disconcerting supraventricular arrhythmia. Also being fair skinned and having suffered through many a blistering sunburn in my youth, I was excited to read the most recent publication regarding the relationship between beta-blocker ingestion and survival from melanoma by De Giorgi et al (Mayo Clin Proc. 2013;88:1196-1203). The Italian investigators collected data from all melanoma patients diagnosed in the dermatology department at the University of Florence (1993-2009). After excluding patients who presented with metastatic disease, they then compared the courses of the remaining patients based on whether or not they had been prescribed beta-blockers for at least 1 year before or after their cutaneous melanoma diagnosis. Of 741 consecutive patients who fit the retrospective study criteria, 79 (11%) had been taking beta-blockers and the remaining 662 (89%) had not been taking beta-blockers.

An analysis based on the multivariate Cox model indicated that the beta-blocker group had improved overall survival after a median follow-up of 4.2 years (P=.005). Looked at in another way, significantly more patients in the untreated group (8%) than the beta-blocker group (3%) experienced disease progression or death (P<.001). The “protective” effect of beta-blockers was so striking that it could be quantified; for each year of beta-blocker use, the risk for death was reduced by 38%. More notable was the fact that the beneficial effect of beta-blocker administration was consistent, even among patients with inherently unfavorable prognostic factors, such as advanced age, thicker lesions, higher frequency of mitoses and ulceration, and nodular melanoma subtype. This large study confirms the results of a much smaller study (N=121) published by the same group in 2011 (Arch Intern Med. 2011;171:779-781).

What’s the issue?

Why might this phenomenon occur? Perhaps blocking sympathetic nervous system neurotransmitters might help avoid the suspected immunosuppression that accompanies stress. Sympathetic neurotransmitters also are known to interact with molecular pathways implicated in abnormal cellular replication, such as the p38/MAPK pathway. Thus, blunting the effects of epinephrine and norepinephrine by blocking some of their receptors might produce a salutatory benefit in the cancer (in this case, melanoma) patient.

Before we all rush out and give all our melanoma patients daily doses of metoprolol, however, De Giorgi et al noted in the most recent study that about two-thirds of the patients were already taking a beta-blocker when their melanoma was diagnosed. Although this study suggests that beta-blockers reduce the risk for recurrence and disease-specific mortality, these drugs clearly do not prevent melanoma in the first place. Furthermore, it should be noted that the number of melanoma patients receiving beta-blockers was small, and conclusions should always be tempered in a retrospective study. The authors duly admit that their investigation indicates the strong need for a truly randomized prospective clinical trial. Of course, administration of beta-blockers is not a totally benign endeavor, as serious hypotension and/or bradycardia may occur, leading to syncope or even worse problems. Finally, the evidence of beta-blocker benefit in melanoma patients is contradictory! A Dutch cohort of 709 melanoma patients recently was studied (Eur J Cancer. 2013;49:3863-3871); this set of investigators found that exposure to beta-blockers did not impact overall melanoma survival regardless of the timing, duration, or dosage of beta-blocker use. In summary, therefore, we still need to determine many things about the relationship between beta-blockers and melanoma survival. That is, if there is a relationship at all. What do you think?

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

I have taken beta-blockers for nearly 30 years to combat a non–life-threatening but very disconcerting supraventricular arrhythmia. Also being fair skinned and having suffered through many a blistering sunburn in my youth, I was excited to read the most recent publication regarding the relationship between beta-blocker ingestion and survival from melanoma by De Giorgi et al (Mayo Clin Proc. 2013;88:1196-1203). The Italian investigators collected data from all melanoma patients diagnosed in the dermatology department at the University of Florence (1993-2009). After excluding patients who presented with metastatic disease, they then compared the courses of the remaining patients based on whether or not they had been prescribed beta-blockers for at least 1 year before or after their cutaneous melanoma diagnosis. Of 741 consecutive patients who fit the retrospective study criteria, 79 (11%) had been taking beta-blockers and the remaining 662 (89%) had not been taking beta-blockers.

An analysis based on the multivariate Cox model indicated that the beta-blocker group had improved overall survival after a median follow-up of 4.2 years (P=.005). Looked at in another way, significantly more patients in the untreated group (8%) than the beta-blocker group (3%) experienced disease progression or death (P<.001). The “protective” effect of beta-blockers was so striking that it could be quantified; for each year of beta-blocker use, the risk for death was reduced by 38%. More notable was the fact that the beneficial effect of beta-blocker administration was consistent, even among patients with inherently unfavorable prognostic factors, such as advanced age, thicker lesions, higher frequency of mitoses and ulceration, and nodular melanoma subtype. This large study confirms the results of a much smaller study (N=121) published by the same group in 2011 (Arch Intern Med. 2011;171:779-781).

What’s the issue?

Why might this phenomenon occur? Perhaps blocking sympathetic nervous system neurotransmitters might help avoid the suspected immunosuppression that accompanies stress. Sympathetic neurotransmitters also are known to interact with molecular pathways implicated in abnormal cellular replication, such as the p38/MAPK pathway. Thus, blunting the effects of epinephrine and norepinephrine by blocking some of their receptors might produce a salutatory benefit in the cancer (in this case, melanoma) patient.

Before we all rush out and give all our melanoma patients daily doses of metoprolol, however, De Giorgi et al noted in the most recent study that about two-thirds of the patients were already taking a beta-blocker when their melanoma was diagnosed. Although this study suggests that beta-blockers reduce the risk for recurrence and disease-specific mortality, these drugs clearly do not prevent melanoma in the first place. Furthermore, it should be noted that the number of melanoma patients receiving beta-blockers was small, and conclusions should always be tempered in a retrospective study. The authors duly admit that their investigation indicates the strong need for a truly randomized prospective clinical trial. Of course, administration of beta-blockers is not a totally benign endeavor, as serious hypotension and/or bradycardia may occur, leading to syncope or even worse problems. Finally, the evidence of beta-blocker benefit in melanoma patients is contradictory! A Dutch cohort of 709 melanoma patients recently was studied (Eur J Cancer. 2013;49:3863-3871); this set of investigators found that exposure to beta-blockers did not impact overall melanoma survival regardless of the timing, duration, or dosage of beta-blocker use. In summary, therefore, we still need to determine many things about the relationship between beta-blockers and melanoma survival. That is, if there is a relationship at all. What do you think?

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

I have taken beta-blockers for nearly 30 years to combat a non–life-threatening but very disconcerting supraventricular arrhythmia. Also being fair skinned and having suffered through many a blistering sunburn in my youth, I was excited to read the most recent publication regarding the relationship between beta-blocker ingestion and survival from melanoma by De Giorgi et al (Mayo Clin Proc. 2013;88:1196-1203). The Italian investigators collected data from all melanoma patients diagnosed in the dermatology department at the University of Florence (1993-2009). After excluding patients who presented with metastatic disease, they then compared the courses of the remaining patients based on whether or not they had been prescribed beta-blockers for at least 1 year before or after their cutaneous melanoma diagnosis. Of 741 consecutive patients who fit the retrospective study criteria, 79 (11%) had been taking beta-blockers and the remaining 662 (89%) had not been taking beta-blockers.

An analysis based on the multivariate Cox model indicated that the beta-blocker group had improved overall survival after a median follow-up of 4.2 years (P=.005). Looked at in another way, significantly more patients in the untreated group (8%) than the beta-blocker group (3%) experienced disease progression or death (P<.001). The “protective” effect of beta-blockers was so striking that it could be quantified; for each year of beta-blocker use, the risk for death was reduced by 38%. More notable was the fact that the beneficial effect of beta-blocker administration was consistent, even among patients with inherently unfavorable prognostic factors, such as advanced age, thicker lesions, higher frequency of mitoses and ulceration, and nodular melanoma subtype. This large study confirms the results of a much smaller study (N=121) published by the same group in 2011 (Arch Intern Med. 2011;171:779-781).

What’s the issue?

Why might this phenomenon occur? Perhaps blocking sympathetic nervous system neurotransmitters might help avoid the suspected immunosuppression that accompanies stress. Sympathetic neurotransmitters also are known to interact with molecular pathways implicated in abnormal cellular replication, such as the p38/MAPK pathway. Thus, blunting the effects of epinephrine and norepinephrine by blocking some of their receptors might produce a salutatory benefit in the cancer (in this case, melanoma) patient.

Before we all rush out and give all our melanoma patients daily doses of metoprolol, however, De Giorgi et al noted in the most recent study that about two-thirds of the patients were already taking a beta-blocker when their melanoma was diagnosed. Although this study suggests that beta-blockers reduce the risk for recurrence and disease-specific mortality, these drugs clearly do not prevent melanoma in the first place. Furthermore, it should be noted that the number of melanoma patients receiving beta-blockers was small, and conclusions should always be tempered in a retrospective study. The authors duly admit that their investigation indicates the strong need for a truly randomized prospective clinical trial. Of course, administration of beta-blockers is not a totally benign endeavor, as serious hypotension and/or bradycardia may occur, leading to syncope or even worse problems. Finally, the evidence of beta-blocker benefit in melanoma patients is contradictory! A Dutch cohort of 709 melanoma patients recently was studied (Eur J Cancer. 2013;49:3863-3871); this set of investigators found that exposure to beta-blockers did not impact overall melanoma survival regardless of the timing, duration, or dosage of beta-blocker use. In summary, therefore, we still need to determine many things about the relationship between beta-blockers and melanoma survival. That is, if there is a relationship at all. What do you think?

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