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Will FDA Deliver a Knock-Out Punch to Indoor Tanning?
The Food and Drug Administration (FDA) has announced that it will finally be taking a closer look at the health effects of indoor tanning, starting with an advisory committee meeting on March 25.
Considering that the agency has taken a decade (and counting) to release regulations guiding the manufacture, composition and advertising of sunscreens, the FDA is acting relatively quickly on indoor tanning.
Dermatologists, cancer advocates, and pediatricians, among others, have been seeking some kind of stricter regulations on indoor tanning, or, more hopefully, an outright ban. Many states and localities have begun to restrict the use of indoor tanning by minors. But, despite a wealth of evidence that excessive exposure to ultraviolet radiation, even when delivered indoors, leads to skin cancer, the federal government has not moved to more strictly police tanning salons.
Congress has been prodding the FDA for years. In 2007, the Tanning Accountability and Notification Act was included in the Food and Drug Administration Amendments Act of 2007. The TAN Act (see page 36 here) directed the FDA to study tanning bed warning labels that had been in place since 1985, with an eye towards making them more prominent and comprehensible by consumers. The FDA was then to report back to Congress.
In December 2008, the agency told lawmakers in its required report that it was considering updating the warning labels. A series of focus groups led it to believe that maybe the almost-quarter-century-old labels might have reached their expiration date.
A year later, the FDA created a web page warning consumers about the dangers of tanning indoors.
And now, the advisory panel. According to the announcement, "There continues to be a growing body of literature showing association of skin cancer with use of tanning lamps and the committee will discuss this information and other information related to the association of UV and skin cancer (both melanoma and non-melanoma). The committee will be asked to recommend whether changes to current classification or current regulatory controls of UV emitting devices (lamps) used for tanning are needed."
Expect a lively discussion at the meeting, with likely appearances by tanning salon owners and the Indoor Tanning Association. Those groups are already unhappy about a 10% tax on tanning users that's being proposed as part of health reform.
The agency usually takes its' advisory committees' advice to heart. We'll be keeping an eye on this panel's proceedings.
Alicia Ault (on Twitter @aliciaault)
Image courtesy Flickr user cogdogblog (cc)
Read more at:
The Food and Drug Administration (FDA) has announced that it will finally be taking a closer look at the health effects of indoor tanning, starting with an advisory committee meeting on March 25.
Considering that the agency has taken a decade (and counting) to release regulations guiding the manufacture, composition and advertising of sunscreens, the FDA is acting relatively quickly on indoor tanning.
Dermatologists, cancer advocates, and pediatricians, among others, have been seeking some kind of stricter regulations on indoor tanning, or, more hopefully, an outright ban. Many states and localities have begun to restrict the use of indoor tanning by minors. But, despite a wealth of evidence that excessive exposure to ultraviolet radiation, even when delivered indoors, leads to skin cancer, the federal government has not moved to more strictly police tanning salons.
Congress has been prodding the FDA for years. In 2007, the Tanning Accountability and Notification Act was included in the Food and Drug Administration Amendments Act of 2007. The TAN Act (see page 36 here) directed the FDA to study tanning bed warning labels that had been in place since 1985, with an eye towards making them more prominent and comprehensible by consumers. The FDA was then to report back to Congress.
In December 2008, the agency told lawmakers in its required report that it was considering updating the warning labels. A series of focus groups led it to believe that maybe the almost-quarter-century-old labels might have reached their expiration date.
A year later, the FDA created a web page warning consumers about the dangers of tanning indoors.
And now, the advisory panel. According to the announcement, "There continues to be a growing body of literature showing association of skin cancer with use of tanning lamps and the committee will discuss this information and other information related to the association of UV and skin cancer (both melanoma and non-melanoma). The committee will be asked to recommend whether changes to current classification or current regulatory controls of UV emitting devices (lamps) used for tanning are needed."
Expect a lively discussion at the meeting, with likely appearances by tanning salon owners and the Indoor Tanning Association. Those groups are already unhappy about a 10% tax on tanning users that's being proposed as part of health reform.
The agency usually takes its' advisory committees' advice to heart. We'll be keeping an eye on this panel's proceedings.
Alicia Ault (on Twitter @aliciaault)
Image courtesy Flickr user cogdogblog (cc)
Read more at:
The Food and Drug Administration (FDA) has announced that it will finally be taking a closer look at the health effects of indoor tanning, starting with an advisory committee meeting on March 25.
Considering that the agency has taken a decade (and counting) to release regulations guiding the manufacture, composition and advertising of sunscreens, the FDA is acting relatively quickly on indoor tanning.
Dermatologists, cancer advocates, and pediatricians, among others, have been seeking some kind of stricter regulations on indoor tanning, or, more hopefully, an outright ban. Many states and localities have begun to restrict the use of indoor tanning by minors. But, despite a wealth of evidence that excessive exposure to ultraviolet radiation, even when delivered indoors, leads to skin cancer, the federal government has not moved to more strictly police tanning salons.
Congress has been prodding the FDA for years. In 2007, the Tanning Accountability and Notification Act was included in the Food and Drug Administration Amendments Act of 2007. The TAN Act (see page 36 here) directed the FDA to study tanning bed warning labels that had been in place since 1985, with an eye towards making them more prominent and comprehensible by consumers. The FDA was then to report back to Congress.
In December 2008, the agency told lawmakers in its required report that it was considering updating the warning labels. A series of focus groups led it to believe that maybe the almost-quarter-century-old labels might have reached their expiration date.
A year later, the FDA created a web page warning consumers about the dangers of tanning indoors.
And now, the advisory panel. According to the announcement, "There continues to be a growing body of literature showing association of skin cancer with use of tanning lamps and the committee will discuss this information and other information related to the association of UV and skin cancer (both melanoma and non-melanoma). The committee will be asked to recommend whether changes to current classification or current regulatory controls of UV emitting devices (lamps) used for tanning are needed."
Expect a lively discussion at the meeting, with likely appearances by tanning salon owners and the Indoor Tanning Association. Those groups are already unhappy about a 10% tax on tanning users that's being proposed as part of health reform.
The agency usually takes its' advisory committees' advice to heart. We'll be keeping an eye on this panel's proceedings.
Alicia Ault (on Twitter @aliciaault)
Image courtesy Flickr user cogdogblog (cc)
Read more at:
Incidence of Melanoma Expected to Rise Again This Year
SAN DIEGO — Data on the estimated incidence of melanoma in the United States in 2010 from the National Cancer Institute's Surveillance, Epidemiology and End Results program will not be available until later this year, but Dr. Darrell S. Rigel does not expect the news to be good.
"Melanoma rates are rising significantly in the United States and in other parts of the world," he said at a melanoma update sponsored by the Scripps Clinic.
"Whatever criteria you use, it's clear that we're seeing more melanomas than we've seen in the past, and we'll probably continue to do so in the next 5-10 years."
According to the most recent SEER data, in 2009 there were 68,720 newly diagnosed cases of invasive melanoma and 53,120 cases of in situ melanoma. Dr. Rigel and his associates at the New York University Interdisciplinary Melanoma Cooperative Group estimate that the projected lifetime risk of invasive melanoma was 1:58 in 2009, up from 1:65 in 2004.
"Should that rate of increase continue, the risk will be about 1:50 by the year 2015," said Dr. Rigel, who is a professor of dermatology and dermatologic surgery at New York University Medical Center. "We've been pretty close on these projections over the last few years. One in 50 is a lot. That's 2% of the population."
Factor in the incidence of in situ melanoma, and the risk of any American getting any kind of melanoma jumps to 1:30, which would be 121,840 total cases in 2009.
"It's a significant problem," he said.
Nine years ago, researchers who analyzed the melanoma incidence rates in the United States from 1960-1997 forecasted a subsequent growing incidence of melanoma. They concluded that the increase in melanoma incidence is real - "not due to improved diagnosis," Dr. Rigel said - and predicted that the incidence would continue to rise for the next decade or more (J. Natl. Cancer Inst. 2001;93:67-83).
Results from studies published in the past decade suggest that the incidence of melanoma is also rising in other parts of the world. In Finland, for example, the incidence of melanoma increased from 1.5 cases to 12.8 cases per 100,000 men between 1953 and 2003, and from 1.8 cases to 10.4 cases per 100,000 women during the same time period (Int. J. Cancer 2006;119:380-4).
In central Greece, the incidence increased from 1.4 cases to 5.2 cases per 100,000 people between 1988 and 1998 (Int. J. Tissue React. 2005;27:173-9). Melanomas were most frequently located on the head and neck, extremities, and trunk.
In Columbia, the incidence of melanoma increased from 2.7 cases to 13 cases per 100,000 people between 2003 and 2005 (Rev. Salud Pública 2007;9:595-601).
Dr. Rigel emphasized that results from the best available studies in the medical literature suggest that the rising incidence of melanoma cannot be explained by increased surveillance, awareness, or by changing histologic criteria. However, while the number of melanoma deaths continues to rise, 5-year survival rates are improving - from 86% between 1985 and 1989 to 92% between 1995 and 2002 (Cancer J. Clin. 2007;57:43-66).
"That seems incongruous," Dr. Rigel said. "The only way that can be happening mathematically is that the incidence has to be rising even faster. That's a compelling reason to explain why the rising incidence is real. According to the World Health Organization, melanoma is rising faster than any other cancer worldwide, on a percentage basis."
He went on to note that the current incidence of melanoma is probably underreported because data from SEER are collected primarily from hospitals.
"The biopsy may be done in an outpatient setting," he explained. "It may go to an outpatient lab; it may be re-excised, and then it may go back to the same lab. It may never hit a hospital. That's why melanoma probably is significantly undercounted."
According to the American Cancer Society, melanoma kills one American citizen per hour. "Some people pooh-pooh skin cancer," Dr. Rigel said. "It's the most common cancer in women aged 25-29, and it's the number one cancer killer in women aged 30-35. There are some subsets of the population that are particularly hurt by this disease."
Dr. Rigel disclosed that he receives grants and advising and consulting fees from a number of pharmaceutical companies, including Neutrogena, Johnson & Johnson, Procter & Gamble, and Beiersdorf.
SAN DIEGO — Data on the estimated incidence of melanoma in the United States in 2010 from the National Cancer Institute's Surveillance, Epidemiology and End Results program will not be available until later this year, but Dr. Darrell S. Rigel does not expect the news to be good.
"Melanoma rates are rising significantly in the United States and in other parts of the world," he said at a melanoma update sponsored by the Scripps Clinic.
"Whatever criteria you use, it's clear that we're seeing more melanomas than we've seen in the past, and we'll probably continue to do so in the next 5-10 years."
According to the most recent SEER data, in 2009 there were 68,720 newly diagnosed cases of invasive melanoma and 53,120 cases of in situ melanoma. Dr. Rigel and his associates at the New York University Interdisciplinary Melanoma Cooperative Group estimate that the projected lifetime risk of invasive melanoma was 1:58 in 2009, up from 1:65 in 2004.
"Should that rate of increase continue, the risk will be about 1:50 by the year 2015," said Dr. Rigel, who is a professor of dermatology and dermatologic surgery at New York University Medical Center. "We've been pretty close on these projections over the last few years. One in 50 is a lot. That's 2% of the population."
Factor in the incidence of in situ melanoma, and the risk of any American getting any kind of melanoma jumps to 1:30, which would be 121,840 total cases in 2009.
"It's a significant problem," he said.
Nine years ago, researchers who analyzed the melanoma incidence rates in the United States from 1960-1997 forecasted a subsequent growing incidence of melanoma. They concluded that the increase in melanoma incidence is real - "not due to improved diagnosis," Dr. Rigel said - and predicted that the incidence would continue to rise for the next decade or more (J. Natl. Cancer Inst. 2001;93:67-83).
Results from studies published in the past decade suggest that the incidence of melanoma is also rising in other parts of the world. In Finland, for example, the incidence of melanoma increased from 1.5 cases to 12.8 cases per 100,000 men between 1953 and 2003, and from 1.8 cases to 10.4 cases per 100,000 women during the same time period (Int. J. Cancer 2006;119:380-4).
In central Greece, the incidence increased from 1.4 cases to 5.2 cases per 100,000 people between 1988 and 1998 (Int. J. Tissue React. 2005;27:173-9). Melanomas were most frequently located on the head and neck, extremities, and trunk.
In Columbia, the incidence of melanoma increased from 2.7 cases to 13 cases per 100,000 people between 2003 and 2005 (Rev. Salud Pública 2007;9:595-601).
Dr. Rigel emphasized that results from the best available studies in the medical literature suggest that the rising incidence of melanoma cannot be explained by increased surveillance, awareness, or by changing histologic criteria. However, while the number of melanoma deaths continues to rise, 5-year survival rates are improving - from 86% between 1985 and 1989 to 92% between 1995 and 2002 (Cancer J. Clin. 2007;57:43-66).
"That seems incongruous," Dr. Rigel said. "The only way that can be happening mathematically is that the incidence has to be rising even faster. That's a compelling reason to explain why the rising incidence is real. According to the World Health Organization, melanoma is rising faster than any other cancer worldwide, on a percentage basis."
He went on to note that the current incidence of melanoma is probably underreported because data from SEER are collected primarily from hospitals.
"The biopsy may be done in an outpatient setting," he explained. "It may go to an outpatient lab; it may be re-excised, and then it may go back to the same lab. It may never hit a hospital. That's why melanoma probably is significantly undercounted."
According to the American Cancer Society, melanoma kills one American citizen per hour. "Some people pooh-pooh skin cancer," Dr. Rigel said. "It's the most common cancer in women aged 25-29, and it's the number one cancer killer in women aged 30-35. There are some subsets of the population that are particularly hurt by this disease."
Dr. Rigel disclosed that he receives grants and advising and consulting fees from a number of pharmaceutical companies, including Neutrogena, Johnson & Johnson, Procter & Gamble, and Beiersdorf.
SAN DIEGO — Data on the estimated incidence of melanoma in the United States in 2010 from the National Cancer Institute's Surveillance, Epidemiology and End Results program will not be available until later this year, but Dr. Darrell S. Rigel does not expect the news to be good.
"Melanoma rates are rising significantly in the United States and in other parts of the world," he said at a melanoma update sponsored by the Scripps Clinic.
"Whatever criteria you use, it's clear that we're seeing more melanomas than we've seen in the past, and we'll probably continue to do so in the next 5-10 years."
According to the most recent SEER data, in 2009 there were 68,720 newly diagnosed cases of invasive melanoma and 53,120 cases of in situ melanoma. Dr. Rigel and his associates at the New York University Interdisciplinary Melanoma Cooperative Group estimate that the projected lifetime risk of invasive melanoma was 1:58 in 2009, up from 1:65 in 2004.
"Should that rate of increase continue, the risk will be about 1:50 by the year 2015," said Dr. Rigel, who is a professor of dermatology and dermatologic surgery at New York University Medical Center. "We've been pretty close on these projections over the last few years. One in 50 is a lot. That's 2% of the population."
Factor in the incidence of in situ melanoma, and the risk of any American getting any kind of melanoma jumps to 1:30, which would be 121,840 total cases in 2009.
"It's a significant problem," he said.
Nine years ago, researchers who analyzed the melanoma incidence rates in the United States from 1960-1997 forecasted a subsequent growing incidence of melanoma. They concluded that the increase in melanoma incidence is real - "not due to improved diagnosis," Dr. Rigel said - and predicted that the incidence would continue to rise for the next decade or more (J. Natl. Cancer Inst. 2001;93:67-83).
Results from studies published in the past decade suggest that the incidence of melanoma is also rising in other parts of the world. In Finland, for example, the incidence of melanoma increased from 1.5 cases to 12.8 cases per 100,000 men between 1953 and 2003, and from 1.8 cases to 10.4 cases per 100,000 women during the same time period (Int. J. Cancer 2006;119:380-4).
In central Greece, the incidence increased from 1.4 cases to 5.2 cases per 100,000 people between 1988 and 1998 (Int. J. Tissue React. 2005;27:173-9). Melanomas were most frequently located on the head and neck, extremities, and trunk.
In Columbia, the incidence of melanoma increased from 2.7 cases to 13 cases per 100,000 people between 2003 and 2005 (Rev. Salud Pública 2007;9:595-601).
Dr. Rigel emphasized that results from the best available studies in the medical literature suggest that the rising incidence of melanoma cannot be explained by increased surveillance, awareness, or by changing histologic criteria. However, while the number of melanoma deaths continues to rise, 5-year survival rates are improving - from 86% between 1985 and 1989 to 92% between 1995 and 2002 (Cancer J. Clin. 2007;57:43-66).
"That seems incongruous," Dr. Rigel said. "The only way that can be happening mathematically is that the incidence has to be rising even faster. That's a compelling reason to explain why the rising incidence is real. According to the World Health Organization, melanoma is rising faster than any other cancer worldwide, on a percentage basis."
He went on to note that the current incidence of melanoma is probably underreported because data from SEER are collected primarily from hospitals.
"The biopsy may be done in an outpatient setting," he explained. "It may go to an outpatient lab; it may be re-excised, and then it may go back to the same lab. It may never hit a hospital. That's why melanoma probably is significantly undercounted."
According to the American Cancer Society, melanoma kills one American citizen per hour. "Some people pooh-pooh skin cancer," Dr. Rigel said. "It's the most common cancer in women aged 25-29, and it's the number one cancer killer in women aged 30-35. There are some subsets of the population that are particularly hurt by this disease."
Dr. Rigel disclosed that he receives grants and advising and consulting fees from a number of pharmaceutical companies, including Neutrogena, Johnson & Johnson, Procter & Gamble, and Beiersdorf.
It Was 20 Years Ago Today …
This past weekend in San Diego, the duo marked the 20th anniversary of the annual cutaneous malignancy update.
"As the course grew in popularity, and word got out about the content of the course, we were able to invite more faculty from across the country and get specific experts in their fields to bring us up to date on the new developments in melanoma," Dr. Barrett, professor of pathology and dermatology at the University of Texas, Southwestern School of Medicine in Dallas, recalled in an interview. "The course has evolved as the knowledge base has evolved."
Dr. Greenway, who chairs the division of Mohs and cutaneous surgery at Scripps Clinic, La Jolla, Calif., said that one important development over the 20-year life of the course has been sentinel node biopsy, which is used primarily as a diagnostic tool. "That has been a tremendous advance," said Dr. Greenway, who was fellowship trained by Dr. Frederic E. Mohs. "It’s brought forth the concept that melanoma requires a team [treatment approach]."
Even though the incidence of melanoma is likely to continue to rise over the next few years, Dr. Barrett noted that clinicians "have a much better understanding, statistics, and data on which to base prognosis and guide treatment."
As for the future, researchers studying the human genome and how it relates to the development of melanoma are "on the beginning of understanding," said Dr. Barrett, who is also director of ProPath Dermatopathology in Dallas. "In the next decade, I think we’re going to see an explosion of knowledge as it relates to molecular pathology and genetic understanding of the disease."
VIDEO:
Doug Brunk (on Twitter @dougbrunk)
San Diego Bureau
This past weekend in San Diego, the duo marked the 20th anniversary of the annual cutaneous malignancy update.
"As the course grew in popularity, and word got out about the content of the course, we were able to invite more faculty from across the country and get specific experts in their fields to bring us up to date on the new developments in melanoma," Dr. Barrett, professor of pathology and dermatology at the University of Texas, Southwestern School of Medicine in Dallas, recalled in an interview. "The course has evolved as the knowledge base has evolved."
Dr. Greenway, who chairs the division of Mohs and cutaneous surgery at Scripps Clinic, La Jolla, Calif., said that one important development over the 20-year life of the course has been sentinel node biopsy, which is used primarily as a diagnostic tool. "That has been a tremendous advance," said Dr. Greenway, who was fellowship trained by Dr. Frederic E. Mohs. "It’s brought forth the concept that melanoma requires a team [treatment approach]."
Even though the incidence of melanoma is likely to continue to rise over the next few years, Dr. Barrett noted that clinicians "have a much better understanding, statistics, and data on which to base prognosis and guide treatment."
As for the future, researchers studying the human genome and how it relates to the development of melanoma are "on the beginning of understanding," said Dr. Barrett, who is also director of ProPath Dermatopathology in Dallas. "In the next decade, I think we’re going to see an explosion of knowledge as it relates to molecular pathology and genetic understanding of the disease."
VIDEO:
Doug Brunk (on Twitter @dougbrunk)
San Diego Bureau
This past weekend in San Diego, the duo marked the 20th anniversary of the annual cutaneous malignancy update.
"As the course grew in popularity, and word got out about the content of the course, we were able to invite more faculty from across the country and get specific experts in their fields to bring us up to date on the new developments in melanoma," Dr. Barrett, professor of pathology and dermatology at the University of Texas, Southwestern School of Medicine in Dallas, recalled in an interview. "The course has evolved as the knowledge base has evolved."
Dr. Greenway, who chairs the division of Mohs and cutaneous surgery at Scripps Clinic, La Jolla, Calif., said that one important development over the 20-year life of the course has been sentinel node biopsy, which is used primarily as a diagnostic tool. "That has been a tremendous advance," said Dr. Greenway, who was fellowship trained by Dr. Frederic E. Mohs. "It’s brought forth the concept that melanoma requires a team [treatment approach]."
Even though the incidence of melanoma is likely to continue to rise over the next few years, Dr. Barrett noted that clinicians "have a much better understanding, statistics, and data on which to base prognosis and guide treatment."
As for the future, researchers studying the human genome and how it relates to the development of melanoma are "on the beginning of understanding," said Dr. Barrett, who is also director of ProPath Dermatopathology in Dallas. "In the next decade, I think we’re going to see an explosion of knowledge as it relates to molecular pathology and genetic understanding of the disease."
VIDEO:
Doug Brunk (on Twitter @dougbrunk)
San Diego Bureau
Long-Term Voriconazole Tied to Melanoma in Situ
Voriconazole, approved for use against serious fungal infections in 2002, has been linked to five more cases of melanoma in situ in two patients, according to a report published online Jan. 18 in the Archives of Dermatology.
Both patients, aged 20 and 39 years, first exhibited photosensitivity followed by extensive photodamage before the lesions were identified in affected areas.
These cases, even added to the four already reported in the literature, are not enough to establish that the drug plays “a definitive causal role” in skin malignancy. However, “we believe that the presence of accelerated photodamage in [two relatively young] patients, coupled with the recent reports supporting an association between voriconazole use and [aggressive] squamous cell carcinoma, warrant further exploration of the role of the drug in skin cancer formation,” said Dr. Daniel D. Miller of the University of California, San Francisco, and his associates (Arch Dermatol. 2010 [doi:10.1001/archdermatol.2009.362]).
“Until such studies further define the skin cancer risk associated with voriconazole, we recommend surveillance for skin cancer formation in all patients who require long-term voriconazole treatment, particularly those who manifest signs or symptoms of photosensitivity or chronic photodamage,” the investigators noted.
They described the two most recent patients in case reports.
The first patient was a 39-year-old woman who was first referred for severe photosensitivity and extensive lentigines on the photoexposed surfaces of the face, upper trunk, and extensor extremities. There was no personal or family history of photosensitivity or skin cancer.
The woman lived in an area endemic for coccidioidomycosis and had been receiving oral voriconazole for 3 years to treat coccidioidomycosis meningitis. Severe erythema with eruptive pigmented macules had developed 1 year after starting treatment.
Histopathology of a specimen taken from an erythematous macule on the right helix showed melanoma in situ.
Five months later, Dr. Miller and his colleagues discovered another ill-defined lesion on the patient —“a brownish blue patch within a field of solar lentigines on severely sun-damaged skin on the mid-upper chest”— that proved to be another melanoma in situ.
One year later, two additional in situ melanomas were identified on the right forearm and the dorsal surface of the left hand. Voriconazole therapy was discontinued, and the patient continues to be monitored for suspicious skin lesions every 3-6 months.
In the second case, an adolescent male with chronic granulomatous disease had been taking long-term voriconazole to treat pulmonary Aspergillus infection. After 2 years of the therapy, he had begun to develop lentigines on sun-exposed areas of his body, including the face, forearms, and dorsal surfaces of his hands.
At age 20 years, after 55 months of treatment, an irregular, darkly pigmented macule on his left forearm was found to be melanoma in situ. His therapy was switched from voriconazole to posaconazole. No subsequent lesions have been identified, and the patient reports fading of his extensive lentigines since discontinuing voriconazole.
The courses of these two patients are clinically similar to what happens in patients who undergo long-term PUVA therapy and in those with xeroderma pigmentosum. However, in the two case reports, "the rapid onset of extensive lentigines, as well as the short interval of voriconazole therapy before melanoma developed (relative to that seen due to PUVA), suggest perhaps an even more accelerated process of carcinogenesis," Dr. Miller and his colleagues said.
“Future comparisons between xeroderma pigmentosum-associated melanomas and those occurring in the setting of voriconazole-associated phototoxic effects may provide valuable insight into the contribution of UV light to melanoma genesis,” they added.
Dr. Miller reported no relevant conflicts of interest.
Voriconazole, approved for use against serious fungal infections in 2002, has been linked to five more cases of melanoma in situ in two patients, according to a report published online Jan. 18 in the Archives of Dermatology.
Both patients, aged 20 and 39 years, first exhibited photosensitivity followed by extensive photodamage before the lesions were identified in affected areas.
These cases, even added to the four already reported in the literature, are not enough to establish that the drug plays “a definitive causal role” in skin malignancy. However, “we believe that the presence of accelerated photodamage in [two relatively young] patients, coupled with the recent reports supporting an association between voriconazole use and [aggressive] squamous cell carcinoma, warrant further exploration of the role of the drug in skin cancer formation,” said Dr. Daniel D. Miller of the University of California, San Francisco, and his associates (Arch Dermatol. 2010 [doi:10.1001/archdermatol.2009.362]).
“Until such studies further define the skin cancer risk associated with voriconazole, we recommend surveillance for skin cancer formation in all patients who require long-term voriconazole treatment, particularly those who manifest signs or symptoms of photosensitivity or chronic photodamage,” the investigators noted.
They described the two most recent patients in case reports.
The first patient was a 39-year-old woman who was first referred for severe photosensitivity and extensive lentigines on the photoexposed surfaces of the face, upper trunk, and extensor extremities. There was no personal or family history of photosensitivity or skin cancer.
The woman lived in an area endemic for coccidioidomycosis and had been receiving oral voriconazole for 3 years to treat coccidioidomycosis meningitis. Severe erythema with eruptive pigmented macules had developed 1 year after starting treatment.
Histopathology of a specimen taken from an erythematous macule on the right helix showed melanoma in situ.
Five months later, Dr. Miller and his colleagues discovered another ill-defined lesion on the patient —“a brownish blue patch within a field of solar lentigines on severely sun-damaged skin on the mid-upper chest”— that proved to be another melanoma in situ.
One year later, two additional in situ melanomas were identified on the right forearm and the dorsal surface of the left hand. Voriconazole therapy was discontinued, and the patient continues to be monitored for suspicious skin lesions every 3-6 months.
In the second case, an adolescent male with chronic granulomatous disease had been taking long-term voriconazole to treat pulmonary Aspergillus infection. After 2 years of the therapy, he had begun to develop lentigines on sun-exposed areas of his body, including the face, forearms, and dorsal surfaces of his hands.
At age 20 years, after 55 months of treatment, an irregular, darkly pigmented macule on his left forearm was found to be melanoma in situ. His therapy was switched from voriconazole to posaconazole. No subsequent lesions have been identified, and the patient reports fading of his extensive lentigines since discontinuing voriconazole.
The courses of these two patients are clinically similar to what happens in patients who undergo long-term PUVA therapy and in those with xeroderma pigmentosum. However, in the two case reports, "the rapid onset of extensive lentigines, as well as the short interval of voriconazole therapy before melanoma developed (relative to that seen due to PUVA), suggest perhaps an even more accelerated process of carcinogenesis," Dr. Miller and his colleagues said.
“Future comparisons between xeroderma pigmentosum-associated melanomas and those occurring in the setting of voriconazole-associated phototoxic effects may provide valuable insight into the contribution of UV light to melanoma genesis,” they added.
Dr. Miller reported no relevant conflicts of interest.
Voriconazole, approved for use against serious fungal infections in 2002, has been linked to five more cases of melanoma in situ in two patients, according to a report published online Jan. 18 in the Archives of Dermatology.
Both patients, aged 20 and 39 years, first exhibited photosensitivity followed by extensive photodamage before the lesions were identified in affected areas.
These cases, even added to the four already reported in the literature, are not enough to establish that the drug plays “a definitive causal role” in skin malignancy. However, “we believe that the presence of accelerated photodamage in [two relatively young] patients, coupled with the recent reports supporting an association between voriconazole use and [aggressive] squamous cell carcinoma, warrant further exploration of the role of the drug in skin cancer formation,” said Dr. Daniel D. Miller of the University of California, San Francisco, and his associates (Arch Dermatol. 2010 [doi:10.1001/archdermatol.2009.362]).
“Until such studies further define the skin cancer risk associated with voriconazole, we recommend surveillance for skin cancer formation in all patients who require long-term voriconazole treatment, particularly those who manifest signs or symptoms of photosensitivity or chronic photodamage,” the investigators noted.
They described the two most recent patients in case reports.
The first patient was a 39-year-old woman who was first referred for severe photosensitivity and extensive lentigines on the photoexposed surfaces of the face, upper trunk, and extensor extremities. There was no personal or family history of photosensitivity or skin cancer.
The woman lived in an area endemic for coccidioidomycosis and had been receiving oral voriconazole for 3 years to treat coccidioidomycosis meningitis. Severe erythema with eruptive pigmented macules had developed 1 year after starting treatment.
Histopathology of a specimen taken from an erythematous macule on the right helix showed melanoma in situ.
Five months later, Dr. Miller and his colleagues discovered another ill-defined lesion on the patient —“a brownish blue patch within a field of solar lentigines on severely sun-damaged skin on the mid-upper chest”— that proved to be another melanoma in situ.
One year later, two additional in situ melanomas were identified on the right forearm and the dorsal surface of the left hand. Voriconazole therapy was discontinued, and the patient continues to be monitored for suspicious skin lesions every 3-6 months.
In the second case, an adolescent male with chronic granulomatous disease had been taking long-term voriconazole to treat pulmonary Aspergillus infection. After 2 years of the therapy, he had begun to develop lentigines on sun-exposed areas of his body, including the face, forearms, and dorsal surfaces of his hands.
At age 20 years, after 55 months of treatment, an irregular, darkly pigmented macule on his left forearm was found to be melanoma in situ. His therapy was switched from voriconazole to posaconazole. No subsequent lesions have been identified, and the patient reports fading of his extensive lentigines since discontinuing voriconazole.
The courses of these two patients are clinically similar to what happens in patients who undergo long-term PUVA therapy and in those with xeroderma pigmentosum. However, in the two case reports, "the rapid onset of extensive lentigines, as well as the short interval of voriconazole therapy before melanoma developed (relative to that seen due to PUVA), suggest perhaps an even more accelerated process of carcinogenesis," Dr. Miller and his colleagues said.
“Future comparisons between xeroderma pigmentosum-associated melanomas and those occurring in the setting of voriconazole-associated phototoxic effects may provide valuable insight into the contribution of UV light to melanoma genesis,” they added.
Dr. Miller reported no relevant conflicts of interest.
Study Implicates COX Enzyme in Development of Basal Cell Carcinoma
Oral celecoxib inhibited basal cell carcinoma carcinogenesis in mice and had a chemopreventive effect on basal cell carcinoma in humans with less severe disease, results from a novel investigation demonstrated.
The findings, published in Cancer Prevention Research, help to explain what causes basal cell carcinoma tumors, lead study author Jean Y. Tang said in an interview.
"We always used to think that BCC was caused only by mutations in the hedgehog pathway," said Dr. Tang of Stanford (Calif.) University. "Now we know that the [cyclooxygenase] enzyme is also important for BCC development. That means we can find drugs that target COX. That should prevent or treat BCCs."
She and her associates conducted two trials: one in mice and one in humans.
For the mouse trial, the investigators compared the relative anti-BCC effects of genetic deletion and nonsteroidal anti-inflammatory pharmacologic inhibition of cyclooxygenase enzymes in the skin of Ptch+/- mice (Cancer Prev. Res. 2010; 3[1]:25-34).
For the phase II human trial, which began in May of 2001 at four clinical sites, 60 patients with basal cell nevus syndrome were randomized to placebo or to 200 mg celecoxib twice daily for 24 months. Patients with this syndrome are genetically predisposed to developing multiple basal cell carcinomas.
Participants returned to the study sites every 3 months for physical examinations, which included the measurement and counting of BCCs.
Patients discontinued taking study medications in December 2004 after news of potential cardiovascular adverse events in persons treated with celecoxib (N. Engl. J. Med. 2005;352:1071-80).
In the mouse trial, genetic deletion of COX1 or COX2 decreased microscopic tumor burden by 75% while pharmacologic inhibition with celecoxib reduced microscopic BCCs by 35%. "That tells us that the [COX] enzyme is important for BCC tumor development," Dr. Tang said.
In the human trial, patients in the placebo group had a 37% increase of BCCs per year, compared with a 26% increase among patients in the celecoxib group, a difference that was not statistically significant. However, when the researchers stratified patients by the number of BCC tumors at baseline (fewer than 15 vs. 15 or more), celecoxib reduced the change in the number of BCCs in patients with fewer than 15 BCCs at baseline (48% vs. 22% in the placebo group) but did not have an effect in patients with 15 or more BCCs at baseline.
"That's the surprising part," Dr. Tang commented. "We were hoping that this drug would have more of an impact on the patients with really severe disease."
The researchers also found that patients in the placebo group who had fewer than 15 BCCs at baseline had a 50% increase in BCC burden per year, while patients in the celecoxib group had a 20% increase, a difference that was statistically significant.
Dr. Tang said that the findings "open the field for people to explore other drugs that inhibit the COX enzymes for BCC treatment or prevention. There are safer drugs that don't have as much cardiovascular toxicity [as celecoxib]. For example, aspirin, ibuprofen, and other COX1 and COX2 inhibitors may work."
She acknowledged certain limitations of the study, including the fact that the human trial was limited to 60 patients with basal cell nevus syndrome, which is also known as Gorlin's syndrome. "Most patients with sporadic BCCs don't have the Gorlin's syndrome," she explained. "So we don't know if celecoxib would work against sporadic BCCs in non-Gorlin's patients."
In an accompanying editorial, Dr. Charles M. Rudin of the department of oncology at Johns Hopkins University, Baltimore, called the findings "encouraging" but emphasized that they should be interpreted with caution (Cancer Prev. Res. 2010; 3[1]:1-3).
"In each of their several murine experiments, the effect of genetic or pharmacologic COX inhibition on tumor burden was predominantly attributable to a decrease in tumor size, with a lesser, if any, effect in reducing tumor number," he noted. "This result suggests that the primary effect of COX inhibition may be on proliferation rate rather than on malignant transformation per se. In this scenario, the reported minor decreases in tumor number could reflect maintenance of a small number of tumors at a size below clinical detection. These observations may be reminiscent of the differentiating effects of retinoids, which may suppress tumorigenesis, but in a transient and thus questionable manner."
The researchers had no conflicts of interest to disclose.
The study was funded by grants from the National Institutes of Health, the Mike Rainen Family Foundation, and the National Center for Research Resources (University of California, San Francisco).
Oral celecoxib inhibited basal cell carcinoma carcinogenesis in mice and had a chemopreventive effect on basal cell carcinoma in humans with less severe disease, results from a novel investigation demonstrated.
The findings, published in Cancer Prevention Research, help to explain what causes basal cell carcinoma tumors, lead study author Jean Y. Tang said in an interview.
"We always used to think that BCC was caused only by mutations in the hedgehog pathway," said Dr. Tang of Stanford (Calif.) University. "Now we know that the [cyclooxygenase] enzyme is also important for BCC development. That means we can find drugs that target COX. That should prevent or treat BCCs."
She and her associates conducted two trials: one in mice and one in humans.
For the mouse trial, the investigators compared the relative anti-BCC effects of genetic deletion and nonsteroidal anti-inflammatory pharmacologic inhibition of cyclooxygenase enzymes in the skin of Ptch+/- mice (Cancer Prev. Res. 2010; 3[1]:25-34).
For the phase II human trial, which began in May of 2001 at four clinical sites, 60 patients with basal cell nevus syndrome were randomized to placebo or to 200 mg celecoxib twice daily for 24 months. Patients with this syndrome are genetically predisposed to developing multiple basal cell carcinomas.
Participants returned to the study sites every 3 months for physical examinations, which included the measurement and counting of BCCs.
Patients discontinued taking study medications in December 2004 after news of potential cardiovascular adverse events in persons treated with celecoxib (N. Engl. J. Med. 2005;352:1071-80).
In the mouse trial, genetic deletion of COX1 or COX2 decreased microscopic tumor burden by 75% while pharmacologic inhibition with celecoxib reduced microscopic BCCs by 35%. "That tells us that the [COX] enzyme is important for BCC tumor development," Dr. Tang said.
In the human trial, patients in the placebo group had a 37% increase of BCCs per year, compared with a 26% increase among patients in the celecoxib group, a difference that was not statistically significant. However, when the researchers stratified patients by the number of BCC tumors at baseline (fewer than 15 vs. 15 or more), celecoxib reduced the change in the number of BCCs in patients with fewer than 15 BCCs at baseline (48% vs. 22% in the placebo group) but did not have an effect in patients with 15 or more BCCs at baseline.
"That's the surprising part," Dr. Tang commented. "We were hoping that this drug would have more of an impact on the patients with really severe disease."
The researchers also found that patients in the placebo group who had fewer than 15 BCCs at baseline had a 50% increase in BCC burden per year, while patients in the celecoxib group had a 20% increase, a difference that was statistically significant.
Dr. Tang said that the findings "open the field for people to explore other drugs that inhibit the COX enzymes for BCC treatment or prevention. There are safer drugs that don't have as much cardiovascular toxicity [as celecoxib]. For example, aspirin, ibuprofen, and other COX1 and COX2 inhibitors may work."
She acknowledged certain limitations of the study, including the fact that the human trial was limited to 60 patients with basal cell nevus syndrome, which is also known as Gorlin's syndrome. "Most patients with sporadic BCCs don't have the Gorlin's syndrome," she explained. "So we don't know if celecoxib would work against sporadic BCCs in non-Gorlin's patients."
In an accompanying editorial, Dr. Charles M. Rudin of the department of oncology at Johns Hopkins University, Baltimore, called the findings "encouraging" but emphasized that they should be interpreted with caution (Cancer Prev. Res. 2010; 3[1]:1-3).
"In each of their several murine experiments, the effect of genetic or pharmacologic COX inhibition on tumor burden was predominantly attributable to a decrease in tumor size, with a lesser, if any, effect in reducing tumor number," he noted. "This result suggests that the primary effect of COX inhibition may be on proliferation rate rather than on malignant transformation per se. In this scenario, the reported minor decreases in tumor number could reflect maintenance of a small number of tumors at a size below clinical detection. These observations may be reminiscent of the differentiating effects of retinoids, which may suppress tumorigenesis, but in a transient and thus questionable manner."
The researchers had no conflicts of interest to disclose.
The study was funded by grants from the National Institutes of Health, the Mike Rainen Family Foundation, and the National Center for Research Resources (University of California, San Francisco).
Oral celecoxib inhibited basal cell carcinoma carcinogenesis in mice and had a chemopreventive effect on basal cell carcinoma in humans with less severe disease, results from a novel investigation demonstrated.
The findings, published in Cancer Prevention Research, help to explain what causes basal cell carcinoma tumors, lead study author Jean Y. Tang said in an interview.
"We always used to think that BCC was caused only by mutations in the hedgehog pathway," said Dr. Tang of Stanford (Calif.) University. "Now we know that the [cyclooxygenase] enzyme is also important for BCC development. That means we can find drugs that target COX. That should prevent or treat BCCs."
She and her associates conducted two trials: one in mice and one in humans.
For the mouse trial, the investigators compared the relative anti-BCC effects of genetic deletion and nonsteroidal anti-inflammatory pharmacologic inhibition of cyclooxygenase enzymes in the skin of Ptch+/- mice (Cancer Prev. Res. 2010; 3[1]:25-34).
For the phase II human trial, which began in May of 2001 at four clinical sites, 60 patients with basal cell nevus syndrome were randomized to placebo or to 200 mg celecoxib twice daily for 24 months. Patients with this syndrome are genetically predisposed to developing multiple basal cell carcinomas.
Participants returned to the study sites every 3 months for physical examinations, which included the measurement and counting of BCCs.
Patients discontinued taking study medications in December 2004 after news of potential cardiovascular adverse events in persons treated with celecoxib (N. Engl. J. Med. 2005;352:1071-80).
In the mouse trial, genetic deletion of COX1 or COX2 decreased microscopic tumor burden by 75% while pharmacologic inhibition with celecoxib reduced microscopic BCCs by 35%. "That tells us that the [COX] enzyme is important for BCC tumor development," Dr. Tang said.
In the human trial, patients in the placebo group had a 37% increase of BCCs per year, compared with a 26% increase among patients in the celecoxib group, a difference that was not statistically significant. However, when the researchers stratified patients by the number of BCC tumors at baseline (fewer than 15 vs. 15 or more), celecoxib reduced the change in the number of BCCs in patients with fewer than 15 BCCs at baseline (48% vs. 22% in the placebo group) but did not have an effect in patients with 15 or more BCCs at baseline.
"That's the surprising part," Dr. Tang commented. "We were hoping that this drug would have more of an impact on the patients with really severe disease."
The researchers also found that patients in the placebo group who had fewer than 15 BCCs at baseline had a 50% increase in BCC burden per year, while patients in the celecoxib group had a 20% increase, a difference that was statistically significant.
Dr. Tang said that the findings "open the field for people to explore other drugs that inhibit the COX enzymes for BCC treatment or prevention. There are safer drugs that don't have as much cardiovascular toxicity [as celecoxib]. For example, aspirin, ibuprofen, and other COX1 and COX2 inhibitors may work."
She acknowledged certain limitations of the study, including the fact that the human trial was limited to 60 patients with basal cell nevus syndrome, which is also known as Gorlin's syndrome. "Most patients with sporadic BCCs don't have the Gorlin's syndrome," she explained. "So we don't know if celecoxib would work against sporadic BCCs in non-Gorlin's patients."
In an accompanying editorial, Dr. Charles M. Rudin of the department of oncology at Johns Hopkins University, Baltimore, called the findings "encouraging" but emphasized that they should be interpreted with caution (Cancer Prev. Res. 2010; 3[1]:1-3).
"In each of their several murine experiments, the effect of genetic or pharmacologic COX inhibition on tumor burden was predominantly attributable to a decrease in tumor size, with a lesser, if any, effect in reducing tumor number," he noted. "This result suggests that the primary effect of COX inhibition may be on proliferation rate rather than on malignant transformation per se. In this scenario, the reported minor decreases in tumor number could reflect maintenance of a small number of tumors at a size below clinical detection. These observations may be reminiscent of the differentiating effects of retinoids, which may suppress tumorigenesis, but in a transient and thus questionable manner."
The researchers had no conflicts of interest to disclose.
The study was funded by grants from the National Institutes of Health, the Mike Rainen Family Foundation, and the National Center for Research Resources (University of California, San Francisco).
Sunscreen with EGCG
DermaDoctor Body Guard SPF-30 sunscreen works to avert sun damage on the face and body. The formulation contains the antioxidant epigallocatechin gallate (EGCG), the active ingredient in green tea, to counter UV damage to the skin. It also contains sebum-sequestering microparticles, which reduce excess surface oils that are already present on the skin, as well as botanicals for soothing and sodium hyaluronate for moisturizing. The product is noncomedogenic and leaves a matte finish. A tube of the sunscreen retails for about $25.
DermaDoctor Inc.
DermaDoctor Body Guard SPF-30 sunscreen works to avert sun damage on the face and body. The formulation contains the antioxidant epigallocatechin gallate (EGCG), the active ingredient in green tea, to counter UV damage to the skin. It also contains sebum-sequestering microparticles, which reduce excess surface oils that are already present on the skin, as well as botanicals for soothing and sodium hyaluronate for moisturizing. The product is noncomedogenic and leaves a matte finish. A tube of the sunscreen retails for about $25.
DermaDoctor Inc.
DermaDoctor Body Guard SPF-30 sunscreen works to avert sun damage on the face and body. The formulation contains the antioxidant epigallocatechin gallate (EGCG), the active ingredient in green tea, to counter UV damage to the skin. It also contains sebum-sequestering microparticles, which reduce excess surface oils that are already present on the skin, as well as botanicals for soothing and sodium hyaluronate for moisturizing. The product is noncomedogenic and leaves a matte finish. A tube of the sunscreen retails for about $25.
DermaDoctor Inc.
Leukemia Cutis in a Patient With Acute Myelogenous Leukemia: A Case Report and Review of the Literature
AAD Phasing Out 'Seal of Recognition' Program
The American Academy of Dermatology is phasing out its “Seal of Recognition” program, partly because a low participation rate meant that it was not meeting the AAD's goals, according to AAD President David Pariser.
In fact, “the program costs exceeded revenue,” Dr. Pariser said in an interview, which was not mentioned in the initial AAD statement announcing the phase-out.
The academy said it was ending the program because it expected the Food and Drug Administration to soon issue sunscreen labeling criteria that would “likely be aligned with the stringent criteria of the AAD Seal of Recognition program.” The FDA sunscreen rules have been in the works for almost a decade.
Dr. Pariser said that when the AAD Board first discussed ending the sunscreen program, public statements made by the FDA suggested that the rules would be issued by the end of 2009. The FDA has since announced that it may not release the guidelines until spring.
Even so, once the FDA acts, the rules are “likely to diminish the need” for the AAD program, he said.
More importantly, the program did not generate money to fund skin cancer awareness programs, as had been planned. Manufacturers paid a $5,000 application fee, followed by a $10,000 annual licensing fee upon approval.
As of September 2009, six sunscreens carried the Seal of Recognition: AminoGenesis Anti-Aging Day Cream with SPF 18, AminoGenesis Derma Scyne Wrinkle Arrest with SPF 18, Coolibar Sun Protection Clothing UPF 50+, Aveeno Continuous Protection Sunblock SPF 55, Aveeno Baby Continuous Protection Sunblock SPF 55, and Mederma Cream plus SPF 30.
The AAD will not accept any new applications. Products that currently carry the AAD's imprimatur will continue to have that label until the end of each product's 2-year recognition period.
Despite losing a potentially dedicated source of funding for skin cancer awareness, the AAD will not stop its public education efforts. It will continue to fund education and awareness through its general operating fund, Dr. Pariser said.
The AAD began the Seal of Recognition program in 2007 and envisioned that it would eventually be applied to cosmetics, moisturizers, clothing, hats, laundry additives, shade structures, and window films and tints meeting evidence-based criteria for reducing sun exposure to consumers.
The organization noted it started the program because a survey found that 86% of AAD members thought the Seal of Recognition would help consumers make better-informed choices.
The program, though, was met with disapproval from many dermatologists. Those who opposed the seal said that it gave the appearance of a conflict of interest since the AAD often promotes sunscreens to consumers.
Dr. Pariser said that the AAD had not received any complaints about the program in the past year.
Once the FDA issues sunscreen labeling criteria, the rules are 'likely to diminish the need' for the AAD program.
Source DR. PARISER
The American Academy of Dermatology is phasing out its “Seal of Recognition” program, partly because a low participation rate meant that it was not meeting the AAD's goals, according to AAD President David Pariser.
In fact, “the program costs exceeded revenue,” Dr. Pariser said in an interview, which was not mentioned in the initial AAD statement announcing the phase-out.
The academy said it was ending the program because it expected the Food and Drug Administration to soon issue sunscreen labeling criteria that would “likely be aligned with the stringent criteria of the AAD Seal of Recognition program.” The FDA sunscreen rules have been in the works for almost a decade.
Dr. Pariser said that when the AAD Board first discussed ending the sunscreen program, public statements made by the FDA suggested that the rules would be issued by the end of 2009. The FDA has since announced that it may not release the guidelines until spring.
Even so, once the FDA acts, the rules are “likely to diminish the need” for the AAD program, he said.
More importantly, the program did not generate money to fund skin cancer awareness programs, as had been planned. Manufacturers paid a $5,000 application fee, followed by a $10,000 annual licensing fee upon approval.
As of September 2009, six sunscreens carried the Seal of Recognition: AminoGenesis Anti-Aging Day Cream with SPF 18, AminoGenesis Derma Scyne Wrinkle Arrest with SPF 18, Coolibar Sun Protection Clothing UPF 50+, Aveeno Continuous Protection Sunblock SPF 55, Aveeno Baby Continuous Protection Sunblock SPF 55, and Mederma Cream plus SPF 30.
The AAD will not accept any new applications. Products that currently carry the AAD's imprimatur will continue to have that label until the end of each product's 2-year recognition period.
Despite losing a potentially dedicated source of funding for skin cancer awareness, the AAD will not stop its public education efforts. It will continue to fund education and awareness through its general operating fund, Dr. Pariser said.
The AAD began the Seal of Recognition program in 2007 and envisioned that it would eventually be applied to cosmetics, moisturizers, clothing, hats, laundry additives, shade structures, and window films and tints meeting evidence-based criteria for reducing sun exposure to consumers.
The organization noted it started the program because a survey found that 86% of AAD members thought the Seal of Recognition would help consumers make better-informed choices.
The program, though, was met with disapproval from many dermatologists. Those who opposed the seal said that it gave the appearance of a conflict of interest since the AAD often promotes sunscreens to consumers.
Dr. Pariser said that the AAD had not received any complaints about the program in the past year.
Once the FDA issues sunscreen labeling criteria, the rules are 'likely to diminish the need' for the AAD program.
Source DR. PARISER
The American Academy of Dermatology is phasing out its “Seal of Recognition” program, partly because a low participation rate meant that it was not meeting the AAD's goals, according to AAD President David Pariser.
In fact, “the program costs exceeded revenue,” Dr. Pariser said in an interview, which was not mentioned in the initial AAD statement announcing the phase-out.
The academy said it was ending the program because it expected the Food and Drug Administration to soon issue sunscreen labeling criteria that would “likely be aligned with the stringent criteria of the AAD Seal of Recognition program.” The FDA sunscreen rules have been in the works for almost a decade.
Dr. Pariser said that when the AAD Board first discussed ending the sunscreen program, public statements made by the FDA suggested that the rules would be issued by the end of 2009. The FDA has since announced that it may not release the guidelines until spring.
Even so, once the FDA acts, the rules are “likely to diminish the need” for the AAD program, he said.
More importantly, the program did not generate money to fund skin cancer awareness programs, as had been planned. Manufacturers paid a $5,000 application fee, followed by a $10,000 annual licensing fee upon approval.
As of September 2009, six sunscreens carried the Seal of Recognition: AminoGenesis Anti-Aging Day Cream with SPF 18, AminoGenesis Derma Scyne Wrinkle Arrest with SPF 18, Coolibar Sun Protection Clothing UPF 50+, Aveeno Continuous Protection Sunblock SPF 55, Aveeno Baby Continuous Protection Sunblock SPF 55, and Mederma Cream plus SPF 30.
The AAD will not accept any new applications. Products that currently carry the AAD's imprimatur will continue to have that label until the end of each product's 2-year recognition period.
Despite losing a potentially dedicated source of funding for skin cancer awareness, the AAD will not stop its public education efforts. It will continue to fund education and awareness through its general operating fund, Dr. Pariser said.
The AAD began the Seal of Recognition program in 2007 and envisioned that it would eventually be applied to cosmetics, moisturizers, clothing, hats, laundry additives, shade structures, and window films and tints meeting evidence-based criteria for reducing sun exposure to consumers.
The organization noted it started the program because a survey found that 86% of AAD members thought the Seal of Recognition would help consumers make better-informed choices.
The program, though, was met with disapproval from many dermatologists. Those who opposed the seal said that it gave the appearance of a conflict of interest since the AAD often promotes sunscreens to consumers.
Dr. Pariser said that the AAD had not received any complaints about the program in the past year.
Once the FDA issues sunscreen labeling criteria, the rules are 'likely to diminish the need' for the AAD program.
Source DR. PARISER
Study Backs Radiation After Lymphadenectomy
CHICAGO — Radiation therapy significantly reduced the risk of recurrence in melanoma patients at high risk of relapse after lymphadenectomy, according to a phase III intergroup trial.
Among 217 fully evaluable patients, 68% of patients treated with external beam radiation after surgery had lymph node field recurrence at 2 years, compared with 80% of those observed after surgery. In an intent-to-treat analysis in 248 patients, recurrence rates were 65% vs. 82%, respectively. Median follow-up was 39 months.
Early radiotherapy toxicity appears minimal, Dr. Bryan Burmeister reported on behalf of the Trans Tasman Radiation Oncology Group 02.01/Australia and New Zealand Melanoma Trial Group 01.02 at the annual meeting of the American Society for Radiation Oncology (ASTRO).
“I believe this is the only real advance in the management of melanoma to happen in the last 15 years, since the interferon data came out,” Dr. Burmeister said in a press briefing. He urged physicians to discuss radiation therapy as an option with their melanoma patients.
Dr. Matthew Ballo, who was invited to discuss the results during the plenary presentation, said that the value of adjuvant radiotherapy in melanoma has been debated for years, and that as recently as 2004 it was viewed as a management approach of undetermined potential that should not be considered in routine practice.
“We now have high-level evidence supporting radiation therapy in selected patients with lymph node disease from malignant melanoma,” he said.
He cautioned that the lack of overall survival benefit observed in the trial may impede rapid acceptance of the data. Median survival times were 31 months with radiotherapy and 34 months with observation (P= .14). There were 120 deaths, 2 of which were not melanoma related.
Dr. Ballo suggested that radiologists in the clinical arena stress the importance of regional control, and remind colleagues in the academic arena that improvements in outcome occur in small steps. Relapse rates in patients with high-risk features, such as those in the study, are 30%–50%, he noted.
Patients were eligible if they had involvement of at least one parotid, at least two cervical or axillary, or at least three groin nodes; or extranodal spread; or a minimum metastatic node diameter of 3 cm in the neck or axilla or 4 cm in the groin. Patients randomized to radiation received 48 Gy in 20 fractions. Radiotherapy compliance was 79%.
Grade 3 toxicities 2 weeks post radiation included 18 cases of dermatitis and 2 of pain. At 6 weeks, there were five cases of dermatitis, two of pain, and one of fatigue, said Dr. Burmeister, director of radiation oncology at Princess Alexandra Hospital in Brisbane, Australia. No grade 4 early toxicities were reported.
Longer-term results are needed to assess fibrosis, lymphedema, and brachial plexopathy, as well as recurrence-related morbidity in the control arm, said Dr. Ballo, head of radiation oncology at the M.D. Anderson Clinical Care Center in Nassau Bay, Tex.
'I believe this is the only real advance in the management of melanoma to happen in the last 15 years.'
Source DR. BURMEISTER
Vitals
Major Finding: Radiation therapy after lymphadenectomy reduces melanoma recurrence in patients at high risk.
Source of Data: Phase III intergroup trial of 217 fully evaluable patients.
Disclosures: The study was supported by the Australia and New Zealand Melanoma Trial Group, National Health and Medical Research Council of Australia, and Cancer Council Victoria. Dr. Burmeister and Dr. Ballo reported no conflicts of interest.
CHICAGO — Radiation therapy significantly reduced the risk of recurrence in melanoma patients at high risk of relapse after lymphadenectomy, according to a phase III intergroup trial.
Among 217 fully evaluable patients, 68% of patients treated with external beam radiation after surgery had lymph node field recurrence at 2 years, compared with 80% of those observed after surgery. In an intent-to-treat analysis in 248 patients, recurrence rates were 65% vs. 82%, respectively. Median follow-up was 39 months.
Early radiotherapy toxicity appears minimal, Dr. Bryan Burmeister reported on behalf of the Trans Tasman Radiation Oncology Group 02.01/Australia and New Zealand Melanoma Trial Group 01.02 at the annual meeting of the American Society for Radiation Oncology (ASTRO).
“I believe this is the only real advance in the management of melanoma to happen in the last 15 years, since the interferon data came out,” Dr. Burmeister said in a press briefing. He urged physicians to discuss radiation therapy as an option with their melanoma patients.
Dr. Matthew Ballo, who was invited to discuss the results during the plenary presentation, said that the value of adjuvant radiotherapy in melanoma has been debated for years, and that as recently as 2004 it was viewed as a management approach of undetermined potential that should not be considered in routine practice.
“We now have high-level evidence supporting radiation therapy in selected patients with lymph node disease from malignant melanoma,” he said.
He cautioned that the lack of overall survival benefit observed in the trial may impede rapid acceptance of the data. Median survival times were 31 months with radiotherapy and 34 months with observation (P= .14). There were 120 deaths, 2 of which were not melanoma related.
Dr. Ballo suggested that radiologists in the clinical arena stress the importance of regional control, and remind colleagues in the academic arena that improvements in outcome occur in small steps. Relapse rates in patients with high-risk features, such as those in the study, are 30%–50%, he noted.
Patients were eligible if they had involvement of at least one parotid, at least two cervical or axillary, or at least three groin nodes; or extranodal spread; or a minimum metastatic node diameter of 3 cm in the neck or axilla or 4 cm in the groin. Patients randomized to radiation received 48 Gy in 20 fractions. Radiotherapy compliance was 79%.
Grade 3 toxicities 2 weeks post radiation included 18 cases of dermatitis and 2 of pain. At 6 weeks, there were five cases of dermatitis, two of pain, and one of fatigue, said Dr. Burmeister, director of radiation oncology at Princess Alexandra Hospital in Brisbane, Australia. No grade 4 early toxicities were reported.
Longer-term results are needed to assess fibrosis, lymphedema, and brachial plexopathy, as well as recurrence-related morbidity in the control arm, said Dr. Ballo, head of radiation oncology at the M.D. Anderson Clinical Care Center in Nassau Bay, Tex.
'I believe this is the only real advance in the management of melanoma to happen in the last 15 years.'
Source DR. BURMEISTER
Vitals
Major Finding: Radiation therapy after lymphadenectomy reduces melanoma recurrence in patients at high risk.
Source of Data: Phase III intergroup trial of 217 fully evaluable patients.
Disclosures: The study was supported by the Australia and New Zealand Melanoma Trial Group, National Health and Medical Research Council of Australia, and Cancer Council Victoria. Dr. Burmeister and Dr. Ballo reported no conflicts of interest.
CHICAGO — Radiation therapy significantly reduced the risk of recurrence in melanoma patients at high risk of relapse after lymphadenectomy, according to a phase III intergroup trial.
Among 217 fully evaluable patients, 68% of patients treated with external beam radiation after surgery had lymph node field recurrence at 2 years, compared with 80% of those observed after surgery. In an intent-to-treat analysis in 248 patients, recurrence rates were 65% vs. 82%, respectively. Median follow-up was 39 months.
Early radiotherapy toxicity appears minimal, Dr. Bryan Burmeister reported on behalf of the Trans Tasman Radiation Oncology Group 02.01/Australia and New Zealand Melanoma Trial Group 01.02 at the annual meeting of the American Society for Radiation Oncology (ASTRO).
“I believe this is the only real advance in the management of melanoma to happen in the last 15 years, since the interferon data came out,” Dr. Burmeister said in a press briefing. He urged physicians to discuss radiation therapy as an option with their melanoma patients.
Dr. Matthew Ballo, who was invited to discuss the results during the plenary presentation, said that the value of adjuvant radiotherapy in melanoma has been debated for years, and that as recently as 2004 it was viewed as a management approach of undetermined potential that should not be considered in routine practice.
“We now have high-level evidence supporting radiation therapy in selected patients with lymph node disease from malignant melanoma,” he said.
He cautioned that the lack of overall survival benefit observed in the trial may impede rapid acceptance of the data. Median survival times were 31 months with radiotherapy and 34 months with observation (P= .14). There were 120 deaths, 2 of which were not melanoma related.
Dr. Ballo suggested that radiologists in the clinical arena stress the importance of regional control, and remind colleagues in the academic arena that improvements in outcome occur in small steps. Relapse rates in patients with high-risk features, such as those in the study, are 30%–50%, he noted.
Patients were eligible if they had involvement of at least one parotid, at least two cervical or axillary, or at least three groin nodes; or extranodal spread; or a minimum metastatic node diameter of 3 cm in the neck or axilla or 4 cm in the groin. Patients randomized to radiation received 48 Gy in 20 fractions. Radiotherapy compliance was 79%.
Grade 3 toxicities 2 weeks post radiation included 18 cases of dermatitis and 2 of pain. At 6 weeks, there were five cases of dermatitis, two of pain, and one of fatigue, said Dr. Burmeister, director of radiation oncology at Princess Alexandra Hospital in Brisbane, Australia. No grade 4 early toxicities were reported.
Longer-term results are needed to assess fibrosis, lymphedema, and brachial plexopathy, as well as recurrence-related morbidity in the control arm, said Dr. Ballo, head of radiation oncology at the M.D. Anderson Clinical Care Center in Nassau Bay, Tex.
'I believe this is the only real advance in the management of melanoma to happen in the last 15 years.'
Source DR. BURMEISTER
Vitals
Major Finding: Radiation therapy after lymphadenectomy reduces melanoma recurrence in patients at high risk.
Source of Data: Phase III intergroup trial of 217 fully evaluable patients.
Disclosures: The study was supported by the Australia and New Zealand Melanoma Trial Group, National Health and Medical Research Council of Australia, and Cancer Council Victoria. Dr. Burmeister and Dr. Ballo reported no conflicts of interest.
Assess Future Risk Before Mohs Defect Repair
SEATTLE — Successful reconstruction of facial defects created by Mohs surgery requires knowledge not only of appropriate operative techniques, but also of patients and their cancers.
Assessing a patient's skin cancer risk factors is key before repairing any Mohs defect, according to Dr. Michael L. Bentz, professor and chairman of the division of plastic and reconstructive surgery at the University of Wisconsin, Madison' “It's important to know who is more likely to come back with other skin cancers because it may change the way you stage and think about the reconstruction,” he said.
A prerequisite for successful reconstruction is ensuring that the cancer has been adequately treated, Dr. Bentz said at the annual meeting of the American Society of Plastic Surgeons.
“The first thing you are going to throw at these patients reconstructively is your best option, so you want to make sure that you have not compromised that by inadequate primary tumor treatment.” He recommended a good working relationship between the Mohs and reconstructing surgeon (if applicable), a careful review of pathology reports, and, if necessary, a reassessment of margins.
“Knowing your tumor is important,” he said. It is prudent to avoid initial definitive reconstruction of defects from dermatofibrosarcoma protuberans because of its high recurrence rate. “My goal with these is to get them grafted, let them sit a year or two, and then come back and do the definitive reconstruction,” he explained.
Maximizing the likelihood of a successful and uneventful reconstruction also requires a thorough preoperative assessment of the patient, given that most patients with skin cancer are older, with comorbidities, and that many take medications, particularly anticoagulants, that may need to be tapered.
Dr. Bentz and Dr. Frederick J. Menick, a plastic surgeon in private practice in Tucson, Ariz., went on to discuss the best way to repair defects and the best flaps to use.
▸ Pericranial flaps. These flaps are often a good option for repairing Mohs defects of the forehead, especially if bone is exposed, noted Dr. Bentz. “For patients who particularly are at risk of other skin cancers, you want to use big flaps because if you use small flaps, you will have difficulty using them again,” he said.
▸ Cheek flaps. If they are elevated to reconstruct lateral forehead defects, cheek flaps should be suspended from bone. “They weigh a fair amount and there is some tension on them,” he said. “So taking a permanent suture and suspending them to the appropriate tension point in bone, with or without drilling holes, helps avoid postoperative complications.”
Reconstructing Mohs cheek defects poses several challenges, including the limited number of lines available for hiding donor sites and the potential for distorting the eyelid. “You want to be thoughtful about how you reallocate cheek tissue, trying to hide your donor site and yet minimize the associated complications,” he said.
▸ Lip defects. Principles of cleft lip repair are often helpful in reconstructing larger Mohs defects of the lip, according to Dr. Bentz. “Don't be afraid to take the whole lip down to full-thickness fashion and put it back together,” he advised.
▸ Ear defects. Small defects can be reconstructed with full-thickness grafts, ideally taken from somewhere other than the ipsilateral retroauricular area, given the possibility of subsequent cancers of that ear requiring a retroauricular flap. Large ear defects can be reconstructed with a variety of techniques, but they all require attention to avoid constricting or accentuating the ear.
▸ Nose defects. When reconstructing small, superficial Mohs defects of the nose, Dr. Menick said that he mainly uses secondary healing, small composite grafts (for minor rim defects), and one-stage nasolabial flaps (for alar sidewall defects), along with a lot of full-thickness forehead skin grafts.
When reconstructing Mohs defects of the nose that are large (over 1.5 cm in diameter), deep, or adversely located (affecting the tip or columella), he recommended a forehead flap over the two-stage nasolabial flap. The forehead flap does not distort the nasolabial fold, is less obvious during the maturation phase, and never dies or contracts excessively.
▸ Forehead grafts. The secret to getting good results with a forehead skin graft is to not apply it right after the Mohs excision or if a Bovie has been used in the area, noted Dr. Menick. “I send the patient home, have them put Vaseline on the defect, wash it with soap and water, [and] wait about 14 days till it starts to granulate and all that burn injury is spit out,” he explained.
As to the type of forehead flap, he expressed a preference for the vertical flap, which, compared with the oblique flap, is much less likely to distort the eyebrow and leaves more options if patients need a second flap. “The vertical forehead flap is reliable, efficient, more vascular, and more widely applicable—it works like a charm,” he said.
Dr. Menick also endorsed the three-stage forehead flap over the two-stage because the added intermediate operation provides the ability to sculpt and contour the nose. Other relative merits include its provision of a thin, supple cover; a maximal blood supply; and an ideal framework. Adding an intermediate operation lengthens reconstruction from a 1-month procedure to a 2-month procedure, he acknowledged, but patients generally tolerate it, especially given the aesthetic outcome.
Disclosures: Dr. Bentz and Dr. Menick had no relevant conflicts of interest.
This patient's defect from Mohs surgery was repaired with a modified folding line technique developed by Dr. Frederick J. Menick as part of his three-stage forehead flap approach.
Source Photos courtesy Dr. Frederick J. Menick
SEATTLE — Successful reconstruction of facial defects created by Mohs surgery requires knowledge not only of appropriate operative techniques, but also of patients and their cancers.
Assessing a patient's skin cancer risk factors is key before repairing any Mohs defect, according to Dr. Michael L. Bentz, professor and chairman of the division of plastic and reconstructive surgery at the University of Wisconsin, Madison' “It's important to know who is more likely to come back with other skin cancers because it may change the way you stage and think about the reconstruction,” he said.
A prerequisite for successful reconstruction is ensuring that the cancer has been adequately treated, Dr. Bentz said at the annual meeting of the American Society of Plastic Surgeons.
“The first thing you are going to throw at these patients reconstructively is your best option, so you want to make sure that you have not compromised that by inadequate primary tumor treatment.” He recommended a good working relationship between the Mohs and reconstructing surgeon (if applicable), a careful review of pathology reports, and, if necessary, a reassessment of margins.
“Knowing your tumor is important,” he said. It is prudent to avoid initial definitive reconstruction of defects from dermatofibrosarcoma protuberans because of its high recurrence rate. “My goal with these is to get them grafted, let them sit a year or two, and then come back and do the definitive reconstruction,” he explained.
Maximizing the likelihood of a successful and uneventful reconstruction also requires a thorough preoperative assessment of the patient, given that most patients with skin cancer are older, with comorbidities, and that many take medications, particularly anticoagulants, that may need to be tapered.
Dr. Bentz and Dr. Frederick J. Menick, a plastic surgeon in private practice in Tucson, Ariz., went on to discuss the best way to repair defects and the best flaps to use.
▸ Pericranial flaps. These flaps are often a good option for repairing Mohs defects of the forehead, especially if bone is exposed, noted Dr. Bentz. “For patients who particularly are at risk of other skin cancers, you want to use big flaps because if you use small flaps, you will have difficulty using them again,” he said.
▸ Cheek flaps. If they are elevated to reconstruct lateral forehead defects, cheek flaps should be suspended from bone. “They weigh a fair amount and there is some tension on them,” he said. “So taking a permanent suture and suspending them to the appropriate tension point in bone, with or without drilling holes, helps avoid postoperative complications.”
Reconstructing Mohs cheek defects poses several challenges, including the limited number of lines available for hiding donor sites and the potential for distorting the eyelid. “You want to be thoughtful about how you reallocate cheek tissue, trying to hide your donor site and yet minimize the associated complications,” he said.
▸ Lip defects. Principles of cleft lip repair are often helpful in reconstructing larger Mohs defects of the lip, according to Dr. Bentz. “Don't be afraid to take the whole lip down to full-thickness fashion and put it back together,” he advised.
▸ Ear defects. Small defects can be reconstructed with full-thickness grafts, ideally taken from somewhere other than the ipsilateral retroauricular area, given the possibility of subsequent cancers of that ear requiring a retroauricular flap. Large ear defects can be reconstructed with a variety of techniques, but they all require attention to avoid constricting or accentuating the ear.
▸ Nose defects. When reconstructing small, superficial Mohs defects of the nose, Dr. Menick said that he mainly uses secondary healing, small composite grafts (for minor rim defects), and one-stage nasolabial flaps (for alar sidewall defects), along with a lot of full-thickness forehead skin grafts.
When reconstructing Mohs defects of the nose that are large (over 1.5 cm in diameter), deep, or adversely located (affecting the tip or columella), he recommended a forehead flap over the two-stage nasolabial flap. The forehead flap does not distort the nasolabial fold, is less obvious during the maturation phase, and never dies or contracts excessively.
▸ Forehead grafts. The secret to getting good results with a forehead skin graft is to not apply it right after the Mohs excision or if a Bovie has been used in the area, noted Dr. Menick. “I send the patient home, have them put Vaseline on the defect, wash it with soap and water, [and] wait about 14 days till it starts to granulate and all that burn injury is spit out,” he explained.
As to the type of forehead flap, he expressed a preference for the vertical flap, which, compared with the oblique flap, is much less likely to distort the eyebrow and leaves more options if patients need a second flap. “The vertical forehead flap is reliable, efficient, more vascular, and more widely applicable—it works like a charm,” he said.
Dr. Menick also endorsed the three-stage forehead flap over the two-stage because the added intermediate operation provides the ability to sculpt and contour the nose. Other relative merits include its provision of a thin, supple cover; a maximal blood supply; and an ideal framework. Adding an intermediate operation lengthens reconstruction from a 1-month procedure to a 2-month procedure, he acknowledged, but patients generally tolerate it, especially given the aesthetic outcome.
Disclosures: Dr. Bentz and Dr. Menick had no relevant conflicts of interest.
This patient's defect from Mohs surgery was repaired with a modified folding line technique developed by Dr. Frederick J. Menick as part of his three-stage forehead flap approach.
Source Photos courtesy Dr. Frederick J. Menick
SEATTLE — Successful reconstruction of facial defects created by Mohs surgery requires knowledge not only of appropriate operative techniques, but also of patients and their cancers.
Assessing a patient's skin cancer risk factors is key before repairing any Mohs defect, according to Dr. Michael L. Bentz, professor and chairman of the division of plastic and reconstructive surgery at the University of Wisconsin, Madison' “It's important to know who is more likely to come back with other skin cancers because it may change the way you stage and think about the reconstruction,” he said.
A prerequisite for successful reconstruction is ensuring that the cancer has been adequately treated, Dr. Bentz said at the annual meeting of the American Society of Plastic Surgeons.
“The first thing you are going to throw at these patients reconstructively is your best option, so you want to make sure that you have not compromised that by inadequate primary tumor treatment.” He recommended a good working relationship between the Mohs and reconstructing surgeon (if applicable), a careful review of pathology reports, and, if necessary, a reassessment of margins.
“Knowing your tumor is important,” he said. It is prudent to avoid initial definitive reconstruction of defects from dermatofibrosarcoma protuberans because of its high recurrence rate. “My goal with these is to get them grafted, let them sit a year or two, and then come back and do the definitive reconstruction,” he explained.
Maximizing the likelihood of a successful and uneventful reconstruction also requires a thorough preoperative assessment of the patient, given that most patients with skin cancer are older, with comorbidities, and that many take medications, particularly anticoagulants, that may need to be tapered.
Dr. Bentz and Dr. Frederick J. Menick, a plastic surgeon in private practice in Tucson, Ariz., went on to discuss the best way to repair defects and the best flaps to use.
▸ Pericranial flaps. These flaps are often a good option for repairing Mohs defects of the forehead, especially if bone is exposed, noted Dr. Bentz. “For patients who particularly are at risk of other skin cancers, you want to use big flaps because if you use small flaps, you will have difficulty using them again,” he said.
▸ Cheek flaps. If they are elevated to reconstruct lateral forehead defects, cheek flaps should be suspended from bone. “They weigh a fair amount and there is some tension on them,” he said. “So taking a permanent suture and suspending them to the appropriate tension point in bone, with or without drilling holes, helps avoid postoperative complications.”
Reconstructing Mohs cheek defects poses several challenges, including the limited number of lines available for hiding donor sites and the potential for distorting the eyelid. “You want to be thoughtful about how you reallocate cheek tissue, trying to hide your donor site and yet minimize the associated complications,” he said.
▸ Lip defects. Principles of cleft lip repair are often helpful in reconstructing larger Mohs defects of the lip, according to Dr. Bentz. “Don't be afraid to take the whole lip down to full-thickness fashion and put it back together,” he advised.
▸ Ear defects. Small defects can be reconstructed with full-thickness grafts, ideally taken from somewhere other than the ipsilateral retroauricular area, given the possibility of subsequent cancers of that ear requiring a retroauricular flap. Large ear defects can be reconstructed with a variety of techniques, but they all require attention to avoid constricting or accentuating the ear.
▸ Nose defects. When reconstructing small, superficial Mohs defects of the nose, Dr. Menick said that he mainly uses secondary healing, small composite grafts (for minor rim defects), and one-stage nasolabial flaps (for alar sidewall defects), along with a lot of full-thickness forehead skin grafts.
When reconstructing Mohs defects of the nose that are large (over 1.5 cm in diameter), deep, or adversely located (affecting the tip or columella), he recommended a forehead flap over the two-stage nasolabial flap. The forehead flap does not distort the nasolabial fold, is less obvious during the maturation phase, and never dies or contracts excessively.
▸ Forehead grafts. The secret to getting good results with a forehead skin graft is to not apply it right after the Mohs excision or if a Bovie has been used in the area, noted Dr. Menick. “I send the patient home, have them put Vaseline on the defect, wash it with soap and water, [and] wait about 14 days till it starts to granulate and all that burn injury is spit out,” he explained.
As to the type of forehead flap, he expressed a preference for the vertical flap, which, compared with the oblique flap, is much less likely to distort the eyebrow and leaves more options if patients need a second flap. “The vertical forehead flap is reliable, efficient, more vascular, and more widely applicable—it works like a charm,” he said.
Dr. Menick also endorsed the three-stage forehead flap over the two-stage because the added intermediate operation provides the ability to sculpt and contour the nose. Other relative merits include its provision of a thin, supple cover; a maximal blood supply; and an ideal framework. Adding an intermediate operation lengthens reconstruction from a 1-month procedure to a 2-month procedure, he acknowledged, but patients generally tolerate it, especially given the aesthetic outcome.
Disclosures: Dr. Bentz and Dr. Menick had no relevant conflicts of interest.
This patient's defect from Mohs surgery was repaired with a modified folding line technique developed by Dr. Frederick J. Menick as part of his three-stage forehead flap approach.
Source Photos courtesy Dr. Frederick J. Menick