Actinic Keratosis

WAILEA, HAWAII – Oral capecitabine shows considerable early promise for the secondary prevention of nonmelanoma skin cancers in solid organ transplant recipients and other immunosuppressed individuals, according to Dr. Paul Nghiem.

Organ transplant recipients are at sharply increased risk of nonmelanoma skin cancer (NMSC). Many transplant recipients develop dozens of squamous cell carcinomas and/or basal cell carcinomas per year, and these tumors often behave very aggressively.

Dermatologists are sorely in need of additional tools to protect organ transplant recipients from NMSC – and capecitabine could fill the bill, he said at the SDEF Hawaii Dermatology Seminar.

Capecitabine (Xeloda) is a 5-fluorouracil (5-FU) precursor widely used for the treatment of colorectal cancer and metastatic breast cancer. Dr. Nghiem, a dermatologist at the University of Washington and the Fred Hutchinson Cancer Center in Seattle, credits University of Minnesota dermatologists with doing the pioneering work in developing capecitabine as a novel means of secondary prevention of NMSCs in the transplant population.

In a recent observational study, the Minnesota group reported on 15 solid organ transplant recipients, mean age 57 years, with recurrent NMSCs who were placed on low-dose capecitabine for the off-label purpose of preventing further NMSCs. The regimen was 1 g/m² daily on days 1-14 of a 21-day cycle.

Comparing cumulative incidence rates for NMSC during the first year on capecitabine to those the year before, the investigators found the mean number of squamous cell carcinomas per month declined by 0.33, the mean number of actinic keratoses fell by 2.45 per month, and the mean number of basal cell carcinomas dropped by 0.04 per month. All these reductions were statistically significant.

Toxicities were deemed manageable. Grade 3/4 toxicities consisted of fatigue in 40% of patients, hand-foot syndrome in 20%, and diarrhea in 20%. One-third of subjects discontinued capecitabine by 1 year (Clin. Transplant. 2010 Nov. 2 [doi:10.1111/j.1399-0012.2010.01348.x]).

There are no definitive data yet, but Dr. Ngheim predicted there will not be a major rebound in NMSCs upon discontinuation of capecitabine, as occurs when systemic retinoids given for the treatment of multiple NMSCs are stopped. That’s because capecitabine is actually killing cancer cells.

"After all, we don’t see a rebound after we treat squamous cell carcinomas with topical 5-FU. I would suspect there is going to be a longer-lasting benefit than with retinoids, and that capecitabine really might be a boon to these folks," he said.

While studies of capecitabine for the secondary prevention of NMSCs continue, physicians can use several other means to protect transplant and other immunosuppressed patients. Dermatologic examinations at intervals of every 3 months or less are important to detect these cutaneous tumors before they metastasize. In addition, regular use of a broad-spectrum sunscreen has been shown to prevent the development of actinic keratoses and invasive squamous cell carcinomas in a randomized trial involving 120 immunocompromised organ transplant recipients (Br. J. Dermatol. 2009;161[suppl. 3]:78-84).

Also, Dr. Nghiem said, it has become clear in the last several years that the calcineurin inhibitors prescribed by transplant physicians to improve graft survival have a highly unwelcome ancillary effect: "They act directly on keratinocytes as a second-level fertilizer to make squamous cell carcinomas grow and become more aggressive."

Unlike the calcineurin inhibitors, sirolimus does not have a direct carcinogenic effect on keratinocytes. In animal studies, substituting sirolimus for calcineurin inhibitors in order to prevent graft rejection results in a striking reduction in NMSCs. Whether the same holds true in humans is now under formal study.

Systemic retinoids can be used in the treatment of multiple NMSCs. However, this is a therapy fraught with significant side effects, including an adverse effect on bone health, as well as a major rebound in squamous cell carcinomas after treatment cessation.

"I pretty much never use this," Dr. Nghiem said.

He said he had no relevant financial disclosures. SDEF and this news organization are owned by Elsevier.

WAILEA, HAWAII – Oral capecitabine shows considerable early promise for the secondary prevention of nonmelanoma skin cancers in solid organ transplant recipients and other immunosuppressed individuals, according to Dr. Paul Nghiem.

Organ transplant recipients are at sharply increased risk of nonmelanoma skin cancer (NMSC). Many transplant recipients develop dozens of squamous cell carcinomas and/or basal cell carcinomas per year, and these tumors often behave very aggressively.

Dermatologists are sorely in need of additional tools to protect organ transplant recipients from NMSC – and capecitabine could fill the bill, he said at the SDEF Hawaii Dermatology Seminar.

Capecitabine (Xeloda) is a 5-fluorouracil (5-FU) precursor widely used for the treatment of colorectal cancer and metastatic breast cancer. Dr. Nghiem, a dermatologist at the University of Washington and the Fred Hutchinson Cancer Center in Seattle, credits University of Minnesota dermatologists with doing the pioneering work in developing capecitabine as a novel means of secondary prevention of NMSCs in the transplant population.

In a recent observational study, the Minnesota group reported on 15 solid organ transplant recipients, mean age 57 years, with recurrent NMSCs who were placed on low-dose capecitabine for the off-label purpose of preventing further NMSCs. The regimen was 1 g/m² daily on days 1-14 of a 21-day cycle.

Comparing cumulative incidence rates for NMSC during the first year on capecitabine to those the year before, the investigators found the mean number of squamous cell carcinomas per month declined by 0.33, the mean number of actinic keratoses fell by 2.45 per month, and the mean number of basal cell carcinomas dropped by 0.04 per month. All these reductions were statistically significant.

Toxicities were deemed manageable. Grade 3/4 toxicities consisted of fatigue in 40% of patients, hand-foot syndrome in 20%, and diarrhea in 20%. One-third of subjects discontinued capecitabine by 1 year (Clin. Transplant. 2010 Nov. 2 [doi:10.1111/j.1399-0012.2010.01348.x]).

There are no definitive data yet, but Dr. Ngheim predicted there will not be a major rebound in NMSCs upon discontinuation of capecitabine, as occurs when systemic retinoids given for the treatment of multiple NMSCs are stopped. That’s because capecitabine is actually killing cancer cells.

"After all, we don’t see a rebound after we treat squamous cell carcinomas with topical 5-FU. I would suspect there is going to be a longer-lasting benefit than with retinoids, and that capecitabine really might be a boon to these folks," he said.

While studies of capecitabine for the secondary prevention of NMSCs continue, physicians can use several other means to protect transplant and other immunosuppressed patients. Dermatologic examinations at intervals of every 3 months or less are important to detect these cutaneous tumors before they metastasize. In addition, regular use of a broad-spectrum sunscreen has been shown to prevent the development of actinic keratoses and invasive squamous cell carcinomas in a randomized trial involving 120 immunocompromised organ transplant recipients (Br. J. Dermatol. 2009;161[suppl. 3]:78-84).

Also, Dr. Nghiem said, it has become clear in the last several years that the calcineurin inhibitors prescribed by transplant physicians to improve graft survival have a highly unwelcome ancillary effect: "They act directly on keratinocytes as a second-level fertilizer to make squamous cell carcinomas grow and become more aggressive."

Unlike the calcineurin inhibitors, sirolimus does not have a direct carcinogenic effect on keratinocytes. In animal studies, substituting sirolimus for calcineurin inhibitors in order to prevent graft rejection results in a striking reduction in NMSCs. Whether the same holds true in humans is now under formal study.

Systemic retinoids can be used in the treatment of multiple NMSCs. However, this is a therapy fraught with significant side effects, including an adverse effect on bone health, as well as a major rebound in squamous cell carcinomas after treatment cessation.

"I pretty much never use this," Dr. Nghiem said.

He said he had no relevant financial disclosures. SDEF and this news organization are owned by Elsevier.

WAILEA, HAWAII – Oral capecitabine shows considerable early promise for the secondary prevention of nonmelanoma skin cancers in solid organ transplant recipients and other immunosuppressed individuals, according to Dr. Paul Nghiem.

Organ transplant recipients are at sharply increased risk of nonmelanoma skin cancer (NMSC). Many transplant recipients develop dozens of squamous cell carcinomas and/or basal cell carcinomas per year, and these tumors often behave very aggressively.

Dermatologists are sorely in need of additional tools to protect organ transplant recipients from NMSC – and capecitabine could fill the bill, he said at the SDEF Hawaii Dermatology Seminar.

Capecitabine (Xeloda) is a 5-fluorouracil (5-FU) precursor widely used for the treatment of colorectal cancer and metastatic breast cancer. Dr. Nghiem, a dermatologist at the University of Washington and the Fred Hutchinson Cancer Center in Seattle, credits University of Minnesota dermatologists with doing the pioneering work in developing capecitabine as a novel means of secondary prevention of NMSCs in the transplant population.

In a recent observational study, the Minnesota group reported on 15 solid organ transplant recipients, mean age 57 years, with recurrent NMSCs who were placed on low-dose capecitabine for the off-label purpose of preventing further NMSCs. The regimen was 1 g/m² daily on days 1-14 of a 21-day cycle.

Comparing cumulative incidence rates for NMSC during the first year on capecitabine to those the year before, the investigators found the mean number of squamous cell carcinomas per month declined by 0.33, the mean number of actinic keratoses fell by 2.45 per month, and the mean number of basal cell carcinomas dropped by 0.04 per month. All these reductions were statistically significant.

Toxicities were deemed manageable. Grade 3/4 toxicities consisted of fatigue in 40% of patients, hand-foot syndrome in 20%, and diarrhea in 20%. One-third of subjects discontinued capecitabine by 1 year (Clin. Transplant. 2010 Nov. 2 [doi:10.1111/j.1399-0012.2010.01348.x]).

There are no definitive data yet, but Dr. Ngheim predicted there will not be a major rebound in NMSCs upon discontinuation of capecitabine, as occurs when systemic retinoids given for the treatment of multiple NMSCs are stopped. That’s because capecitabine is actually killing cancer cells.

"After all, we don’t see a rebound after we treat squamous cell carcinomas with topical 5-FU. I would suspect there is going to be a longer-lasting benefit than with retinoids, and that capecitabine really might be a boon to these folks," he said.

While studies of capecitabine for the secondary prevention of NMSCs continue, physicians can use several other means to protect transplant and other immunosuppressed patients. Dermatologic examinations at intervals of every 3 months or less are important to detect these cutaneous tumors before they metastasize. In addition, regular use of a broad-spectrum sunscreen has been shown to prevent the development of actinic keratoses and invasive squamous cell carcinomas in a randomized trial involving 120 immunocompromised organ transplant recipients (Br. J. Dermatol. 2009;161[suppl. 3]:78-84).

Also, Dr. Nghiem said, it has become clear in the last several years that the calcineurin inhibitors prescribed by transplant physicians to improve graft survival have a highly unwelcome ancillary effect: "They act directly on keratinocytes as a second-level fertilizer to make squamous cell carcinomas grow and become more aggressive."

Unlike the calcineurin inhibitors, sirolimus does not have a direct carcinogenic effect on keratinocytes. In animal studies, substituting sirolimus for calcineurin inhibitors in order to prevent graft rejection results in a striking reduction in NMSCs. Whether the same holds true in humans is now under formal study.

Systemic retinoids can be used in the treatment of multiple NMSCs. However, this is a therapy fraught with significant side effects, including an adverse effect on bone health, as well as a major rebound in squamous cell carcinomas after treatment cessation.

"I pretty much never use this," Dr. Nghiem said.

He said he had no relevant financial disclosures. SDEF and this news organization are owned by Elsevier.

ORLANDO - Limiting treatment of actinic keratoses to cryosurgery is a disservice to patients, according to Dr. Neil A. Fenske.

Every patient with AKs deserves consideration for field therapy, he said at the Orlando Dermatology Aesthetic and Clinical Conference. Mutated cells occur not only within the visible AKs, but also in the surrounding, normal-looking skin.

"Most patients don't have one AK," said Dr. Fenske of the Moffitt Cancer Center at the University of South Florida in Tampa. Data based on mathematical models suggest that 6%-10% of typical patients with an average of eight AKs will develop at least one squamous cell carcinoma over a 10-year period.

For more complete treatment, following cryosurgery with field therapy a week later. Field therapy using methyl aminolevulinate (MAL) plus a red light–emitting diode (LED) is an up-and-coming option.

MAL has a higher relative porphyrin enrichment in AKs than in normal skin, and is able to penetrate deeply compared with 5-aminolevulinic acid, Dr. Fenske explained. In addition, the red LED at 630 nm requires a lower light dose than other light options, so there is less heating of the skin.

Dr. Fenske cited a study of MAL-PDT plus red LED at 630 nm in which 14 patients with a total of 223 AKs on the scalp and face underwent two treatments. The total number of AKs decreased by 55% after the first treatment and by 62% after the second treatment. Although global photodamage scores improved, pain was an issue (J. Dermatolog. Treat. 2010;21:252-7).

Dr. Fenske said he often uses aminolevulinic acid plus blue light, but to treat and kill bacteria deep in the sebaceous glands, "I would use red light and [MAL]," he said.

Dr. Fenske disclosed serving as a consultant and speaker for Graceway Pharmaceuticals, and serving as a speaker for Sanofi-Aventis.

ORLANDO - Limiting treatment of actinic keratoses to cryosurgery is a disservice to patients, according to Dr. Neil A. Fenske.

Every patient with AKs deserves consideration for field therapy, he said at the Orlando Dermatology Aesthetic and Clinical Conference. Mutated cells occur not only within the visible AKs, but also in the surrounding, normal-looking skin.

"Most patients don't have one AK," said Dr. Fenske of the Moffitt Cancer Center at the University of South Florida in Tampa. Data based on mathematical models suggest that 6%-10% of typical patients with an average of eight AKs will develop at least one squamous cell carcinoma over a 10-year period.

For more complete treatment, following cryosurgery with field therapy a week later. Field therapy using methyl aminolevulinate (MAL) plus a red light–emitting diode (LED) is an up-and-coming option.

MAL has a higher relative porphyrin enrichment in AKs than in normal skin, and is able to penetrate deeply compared with 5-aminolevulinic acid, Dr. Fenske explained. In addition, the red LED at 630 nm requires a lower light dose than other light options, so there is less heating of the skin.

Dr. Fenske cited a study of MAL-PDT plus red LED at 630 nm in which 14 patients with a total of 223 AKs on the scalp and face underwent two treatments. The total number of AKs decreased by 55% after the first treatment and by 62% after the second treatment. Although global photodamage scores improved, pain was an issue (J. Dermatolog. Treat. 2010;21:252-7).

Dr. Fenske said he often uses aminolevulinic acid plus blue light, but to treat and kill bacteria deep in the sebaceous glands, "I would use red light and [MAL]," he said.

Dr. Fenske disclosed serving as a consultant and speaker for Graceway Pharmaceuticals, and serving as a speaker for Sanofi-Aventis.

ORLANDO - Limiting treatment of actinic keratoses to cryosurgery is a disservice to patients, according to Dr. Neil A. Fenske.

Every patient with AKs deserves consideration for field therapy, he said at the Orlando Dermatology Aesthetic and Clinical Conference. Mutated cells occur not only within the visible AKs, but also in the surrounding, normal-looking skin.

"Most patients don't have one AK," said Dr. Fenske of the Moffitt Cancer Center at the University of South Florida in Tampa. Data based on mathematical models suggest that 6%-10% of typical patients with an average of eight AKs will develop at least one squamous cell carcinoma over a 10-year period.

For more complete treatment, following cryosurgery with field therapy a week later. Field therapy using methyl aminolevulinate (MAL) plus a red light–emitting diode (LED) is an up-and-coming option.

MAL has a higher relative porphyrin enrichment in AKs than in normal skin, and is able to penetrate deeply compared with 5-aminolevulinic acid, Dr. Fenske explained. In addition, the red LED at 630 nm requires a lower light dose than other light options, so there is less heating of the skin.

Dr. Fenske cited a study of MAL-PDT plus red LED at 630 nm in which 14 patients with a total of 223 AKs on the scalp and face underwent two treatments. The total number of AKs decreased by 55% after the first treatment and by 62% after the second treatment. Although global photodamage scores improved, pain was an issue (J. Dermatolog. Treat. 2010;21:252-7).

Dr. Fenske said he often uses aminolevulinic acid plus blue light, but to treat and kill bacteria deep in the sebaceous glands, "I would use red light and [MAL]," he said.

Dr. Fenske disclosed serving as a consultant and speaker for Graceway Pharmaceuticals, and serving as a speaker for Sanofi-Aventis.

ORLANDO – The photodynamic therapy protocol that works best on the face is not necessarily the best protocol for the scalp, according to Dr. Amy Forman Taub of Northwestern University in Chicago.

The main indications for PDT are actinic keratoses, acne, and photorejuvenation, but other indications include psoriasis, vulvar neoplasia, methicillin-resistant Staphylococcus aureus, and onychomycosis.

"For long-term cosmesis, nothing stands up like PDT," said Dr. Taub at the Orlando Dermatology Aesthetic and Clinical Conference. She explained her protocols for using PDT for actinic keratoses on different parts of the body.

• Scalp. To treat actinic keratoses on the scalp, Dr. Taub recommended incubation for 60-90 minutes with 5-aminolevulinic acid (5-ALA), followed by exposure to blue light at 2-4 inches for 20 minutes. Next, prescribe emollients for morning use and fluticasone for nighttime use. Check the scalp at 4 weeks. Repeat the PDT protocol after 8 weeks. Check the patient again in 12-16 weeks and biopsy any residual lesions, Dr. Taub said.

• Face. For severe actinic keratoses on the face, Dr. Taub recommended incubation with 5-ALA for 1 hour, followed by exposure to blue light for 16 minutes. Next, instruct the patient to apply zinc oxide sunscreen on top of topical emollients in the morning, and to use topical emollients at night. If 20% or fewer lesions remain at a 4-week follow-up visit, use an alternate therapy. But if more than 20% of the lesions remain, repeat the PDT with 90 minutes of incubation and 1 minute of blue light, Dr. Taub advised.

• Arms and hands. Be sure to elevate the arms so they are 2-4 inches from the light source, Dr. Taub said. She recommended using the push-up handles sold at sporting goods stores to elevate a patient’s arms for more effective PDT. Her preferred protocol for treatment of the arms and hands is to incubate with 5-ALA for 2 hours using Saran Wrap and gloves for occlusion, followed by exposure to blue light for 20 minutes. Repeat the procedure in 4-8 weeks, then examine the patient 12 weeks later and biopsy any residual lesions.

• Legs and feet. When planning PDT for the legs, remove or biopsy any lesions 4 weeks before PDT, said Dr. Taub. She recommended dividing the legs into four quadrants that each take one stick of ALA: upper, lower, anterior, and posterior. Perform the PDT on each quadrant separately, she said. Incubate the area for 2-3 hours, ideally after 1 week of 5-fluorouracil treatment. Next, expose the quadrant to blue light for 20 minutes. Repeat the protocol 8 weeks later, and re-evaluate the patient 12 weeks after the second treatment, she said.

Tricky areas such as the arms, legs, and chest can respond especially well to intense pulsed light (IPL)-PDT, Dr. Taub noted. The cost to the patient is higher, but she has seen dramatic improvements. Another option is to do one IPL-PDT treatment and follow with a blue light treatment if necessary, she said.

Dr. Taub disclosed serving as a consultant and speaker for, and receiving research funding from, DUSA Pharmaceuticals and Syneron.

ORLANDO – The photodynamic therapy protocol that works best on the face is not necessarily the best protocol for the scalp, according to Dr. Amy Forman Taub of Northwestern University in Chicago.

The main indications for PDT are actinic keratoses, acne, and photorejuvenation, but other indications include psoriasis, vulvar neoplasia, methicillin-resistant Staphylococcus aureus, and onychomycosis.

"For long-term cosmesis, nothing stands up like PDT," said Dr. Taub at the Orlando Dermatology Aesthetic and Clinical Conference. She explained her protocols for using PDT for actinic keratoses on different parts of the body.

• Scalp. To treat actinic keratoses on the scalp, Dr. Taub recommended incubation for 60-90 minutes with 5-aminolevulinic acid (5-ALA), followed by exposure to blue light at 2-4 inches for 20 minutes. Next, prescribe emollients for morning use and fluticasone for nighttime use. Check the scalp at 4 weeks. Repeat the PDT protocol after 8 weeks. Check the patient again in 12-16 weeks and biopsy any residual lesions, Dr. Taub said.

• Face. For severe actinic keratoses on the face, Dr. Taub recommended incubation with 5-ALA for 1 hour, followed by exposure to blue light for 16 minutes. Next, instruct the patient to apply zinc oxide sunscreen on top of topical emollients in the morning, and to use topical emollients at night. If 20% or fewer lesions remain at a 4-week follow-up visit, use an alternate therapy. But if more than 20% of the lesions remain, repeat the PDT with 90 minutes of incubation and 1 minute of blue light, Dr. Taub advised.

• Arms and hands. Be sure to elevate the arms so they are 2-4 inches from the light source, Dr. Taub said. She recommended using the push-up handles sold at sporting goods stores to elevate a patient’s arms for more effective PDT. Her preferred protocol for treatment of the arms and hands is to incubate with 5-ALA for 2 hours using Saran Wrap and gloves for occlusion, followed by exposure to blue light for 20 minutes. Repeat the procedure in 4-8 weeks, then examine the patient 12 weeks later and biopsy any residual lesions.

• Legs and feet. When planning PDT for the legs, remove or biopsy any lesions 4 weeks before PDT, said Dr. Taub. She recommended dividing the legs into four quadrants that each take one stick of ALA: upper, lower, anterior, and posterior. Perform the PDT on each quadrant separately, she said. Incubate the area for 2-3 hours, ideally after 1 week of 5-fluorouracil treatment. Next, expose the quadrant to blue light for 20 minutes. Repeat the protocol 8 weeks later, and re-evaluate the patient 12 weeks after the second treatment, she said.

Tricky areas such as the arms, legs, and chest can respond especially well to intense pulsed light (IPL)-PDT, Dr. Taub noted. The cost to the patient is higher, but she has seen dramatic improvements. Another option is to do one IPL-PDT treatment and follow with a blue light treatment if necessary, she said.

Dr. Taub disclosed serving as a consultant and speaker for, and receiving research funding from, DUSA Pharmaceuticals and Syneron.

ORLANDO – The photodynamic therapy protocol that works best on the face is not necessarily the best protocol for the scalp, according to Dr. Amy Forman Taub of Northwestern University in Chicago.

The main indications for PDT are actinic keratoses, acne, and photorejuvenation, but other indications include psoriasis, vulvar neoplasia, methicillin-resistant Staphylococcus aureus, and onychomycosis.

"For long-term cosmesis, nothing stands up like PDT," said Dr. Taub at the Orlando Dermatology Aesthetic and Clinical Conference. She explained her protocols for using PDT for actinic keratoses on different parts of the body.

• Scalp. To treat actinic keratoses on the scalp, Dr. Taub recommended incubation for 60-90 minutes with 5-aminolevulinic acid (5-ALA), followed by exposure to blue light at 2-4 inches for 20 minutes. Next, prescribe emollients for morning use and fluticasone for nighttime use. Check the scalp at 4 weeks. Repeat the PDT protocol after 8 weeks. Check the patient again in 12-16 weeks and biopsy any residual lesions, Dr. Taub said.

• Face. For severe actinic keratoses on the face, Dr. Taub recommended incubation with 5-ALA for 1 hour, followed by exposure to blue light for 16 minutes. Next, instruct the patient to apply zinc oxide sunscreen on top of topical emollients in the morning, and to use topical emollients at night. If 20% or fewer lesions remain at a 4-week follow-up visit, use an alternate therapy. But if more than 20% of the lesions remain, repeat the PDT with 90 minutes of incubation and 1 minute of blue light, Dr. Taub advised.

• Arms and hands. Be sure to elevate the arms so they are 2-4 inches from the light source, Dr. Taub said. She recommended using the push-up handles sold at sporting goods stores to elevate a patient’s arms for more effective PDT. Her preferred protocol for treatment of the arms and hands is to incubate with 5-ALA for 2 hours using Saran Wrap and gloves for occlusion, followed by exposure to blue light for 20 minutes. Repeat the procedure in 4-8 weeks, then examine the patient 12 weeks later and biopsy any residual lesions.

• Legs and feet. When planning PDT for the legs, remove or biopsy any lesions 4 weeks before PDT, said Dr. Taub. She recommended dividing the legs into four quadrants that each take one stick of ALA: upper, lower, anterior, and posterior. Perform the PDT on each quadrant separately, she said. Incubate the area for 2-3 hours, ideally after 1 week of 5-fluorouracil treatment. Next, expose the quadrant to blue light for 20 minutes. Repeat the protocol 8 weeks later, and re-evaluate the patient 12 weeks after the second treatment, she said.

Tricky areas such as the arms, legs, and chest can respond especially well to intense pulsed light (IPL)-PDT, Dr. Taub noted. The cost to the patient is higher, but she has seen dramatic improvements. Another option is to do one IPL-PDT treatment and follow with a blue light treatment if necessary, she said.

Dr. Taub disclosed serving as a consultant and speaker for, and receiving research funding from, DUSA Pharmaceuticals and Syneron.

NEW ORLEANS - Serial screening of patients at high risk for melanoma is effective for detecting lesions, and appears to have prevented the development of aggressive advanced nodular melanoma.

For the past 19 years, Dr. Ronald N. Shore has been conducting serial screening on patients at high risk for melanoma, as many as 1,100 patients per year. He reported finding no metastases, recurrences, or deaths during this time period.

In addition, only one of his patients developed nodular melanoma, a phenomenon that Dr. Shore, who is in private practice in Rockville, Md., attributes to serial screening. The one patient who developed nodular melanoma failed to return for screening for 27 months.

Dr. Shore said that he believes the total absence of nodular melanoma for the first 17 years of his program is best explained by the program's detection of previously unrecognized early melanomas that he suspects have the potential to become nodular lesions.

He presented his most recent findings at the annual meeting of the American Academy of Dermatology.

He described finding what he termed "papular erythematous melanomas," which are distinct, amelanotic, red or pink, symmetrical lesions that closely resemble some of the recently described early nodular melanomas. The lesions were distinguished by their smaller size, lack of rapid growth, and radial growth phase histopathology.

The absence of classic ABCDE features may be another reason why the lesions had not been recognized, he said.

These findings raise the possibility that these lesions are recognizable precursors of nodular melanoma, he said. If the theory proves correct, "it reveals a way we can prevent development of nodular melanoma and by doing so, save lives," he added.

Dr. Shore noted that two prior studies have also reported 100% survival of screened patients at increased risk for melanoma: one led by Dr. Darrell S. Rigel, a professor of dermatology and dermatologic surgery at New York University Medical Center (Cancer 1989;63:386-9), and another more recent study led by Dr. Stephen Wang of the Memorial Sloan-Kettering Cancer Center in New York (J. Am. Acad. Dermatol. 2004;50:15-20). Dr. Shore pointed out that the studies share two common features: the use of serial screening, and performance of thorough examinations by dermatologists.

Analysis of 5 years of study data showed that 10 new cases of melanoma were detected in serially screened patients. The greatest Breslow depth was 0.15 mm; the lesions were all in radial growth phase; 70% were in men aged older than 50 years; and only 10% of the lesions were detected by patients.

The latter finding is one that Dr. Shore emphasized.

"Neither random screenings nor patient self-examinations can provide anywhere near the efficacy provided by serial professional examinations in the office setting," Dr. Shore said.

"Patients are very symptom oriented," he said, but early melanomas are mostly asymptomatic. In addition, "our records clearly show that some patients – especially men over 50 – are very poor at self-examination."

The study classified high-risk patients as those with significant past sun exposure and damage, especially multiple or severe sunburns; numerous or dysplastic nevi; actinic keratoses; any skin cancer; and family history of melanoma, especially in multiple blood relatives.

His practice has implemented a recall system, in which high-risk patients get reminders for their 6-month visit and continued follow-up reminders if they do not schedule an appointment.

Dr. Shore's findings are scheduled to appear in an upcoming issue of the Journal of Drugs in Dermatology.

He said that he had no financial interests relevant to his study.

NEW ORLEANS - Serial screening of patients at high risk for melanoma is effective for detecting lesions, and appears to have prevented the development of aggressive advanced nodular melanoma.

For the past 19 years, Dr. Ronald N. Shore has been conducting serial screening on patients at high risk for melanoma, as many as 1,100 patients per year. He reported finding no metastases, recurrences, or deaths during this time period.

In addition, only one of his patients developed nodular melanoma, a phenomenon that Dr. Shore, who is in private practice in Rockville, Md., attributes to serial screening. The one patient who developed nodular melanoma failed to return for screening for 27 months.

Dr. Shore said that he believes the total absence of nodular melanoma for the first 17 years of his program is best explained by the program's detection of previously unrecognized early melanomas that he suspects have the potential to become nodular lesions.

He presented his most recent findings at the annual meeting of the American Academy of Dermatology.

He described finding what he termed "papular erythematous melanomas," which are distinct, amelanotic, red or pink, symmetrical lesions that closely resemble some of the recently described early nodular melanomas. The lesions were distinguished by their smaller size, lack of rapid growth, and radial growth phase histopathology.

The absence of classic ABCDE features may be another reason why the lesions had not been recognized, he said.

These findings raise the possibility that these lesions are recognizable precursors of nodular melanoma, he said. If the theory proves correct, "it reveals a way we can prevent development of nodular melanoma and by doing so, save lives," he added.

Dr. Shore noted that two prior studies have also reported 100% survival of screened patients at increased risk for melanoma: one led by Dr. Darrell S. Rigel, a professor of dermatology and dermatologic surgery at New York University Medical Center (Cancer 1989;63:386-9), and another more recent study led by Dr. Stephen Wang of the Memorial Sloan-Kettering Cancer Center in New York (J. Am. Acad. Dermatol. 2004;50:15-20). Dr. Shore pointed out that the studies share two common features: the use of serial screening, and performance of thorough examinations by dermatologists.

Analysis of 5 years of study data showed that 10 new cases of melanoma were detected in serially screened patients. The greatest Breslow depth was 0.15 mm; the lesions were all in radial growth phase; 70% were in men aged older than 50 years; and only 10% of the lesions were detected by patients.

The latter finding is one that Dr. Shore emphasized.

"Neither random screenings nor patient self-examinations can provide anywhere near the efficacy provided by serial professional examinations in the office setting," Dr. Shore said.

"Patients are very symptom oriented," he said, but early melanomas are mostly asymptomatic. In addition, "our records clearly show that some patients – especially men over 50 – are very poor at self-examination."

The study classified high-risk patients as those with significant past sun exposure and damage, especially multiple or severe sunburns; numerous or dysplastic nevi; actinic keratoses; any skin cancer; and family history of melanoma, especially in multiple blood relatives.

His practice has implemented a recall system, in which high-risk patients get reminders for their 6-month visit and continued follow-up reminders if they do not schedule an appointment.

Dr. Shore's findings are scheduled to appear in an upcoming issue of the Journal of Drugs in Dermatology.

He said that he had no financial interests relevant to his study.

NEW ORLEANS - Serial screening of patients at high risk for melanoma is effective for detecting lesions, and appears to have prevented the development of aggressive advanced nodular melanoma.

For the past 19 years, Dr. Ronald N. Shore has been conducting serial screening on patients at high risk for melanoma, as many as 1,100 patients per year. He reported finding no metastases, recurrences, or deaths during this time period.

In addition, only one of his patients developed nodular melanoma, a phenomenon that Dr. Shore, who is in private practice in Rockville, Md., attributes to serial screening. The one patient who developed nodular melanoma failed to return for screening for 27 months.

Dr. Shore said that he believes the total absence of nodular melanoma for the first 17 years of his program is best explained by the program's detection of previously unrecognized early melanomas that he suspects have the potential to become nodular lesions.

He presented his most recent findings at the annual meeting of the American Academy of Dermatology.

He described finding what he termed "papular erythematous melanomas," which are distinct, amelanotic, red or pink, symmetrical lesions that closely resemble some of the recently described early nodular melanomas. The lesions were distinguished by their smaller size, lack of rapid growth, and radial growth phase histopathology.

The absence of classic ABCDE features may be another reason why the lesions had not been recognized, he said.

These findings raise the possibility that these lesions are recognizable precursors of nodular melanoma, he said. If the theory proves correct, "it reveals a way we can prevent development of nodular melanoma and by doing so, save lives," he added.

Dr. Shore noted that two prior studies have also reported 100% survival of screened patients at increased risk for melanoma: one led by Dr. Darrell S. Rigel, a professor of dermatology and dermatologic surgery at New York University Medical Center (Cancer 1989;63:386-9), and another more recent study led by Dr. Stephen Wang of the Memorial Sloan-Kettering Cancer Center in New York (J. Am. Acad. Dermatol. 2004;50:15-20). Dr. Shore pointed out that the studies share two common features: the use of serial screening, and performance of thorough examinations by dermatologists.

Analysis of 5 years of study data showed that 10 new cases of melanoma were detected in serially screened patients. The greatest Breslow depth was 0.15 mm; the lesions were all in radial growth phase; 70% were in men aged older than 50 years; and only 10% of the lesions were detected by patients.

The latter finding is one that Dr. Shore emphasized.

"Neither random screenings nor patient self-examinations can provide anywhere near the efficacy provided by serial professional examinations in the office setting," Dr. Shore said.

"Patients are very symptom oriented," he said, but early melanomas are mostly asymptomatic. In addition, "our records clearly show that some patients – especially men over 50 – are very poor at self-examination."

The study classified high-risk patients as those with significant past sun exposure and damage, especially multiple or severe sunburns; numerous or dysplastic nevi; actinic keratoses; any skin cancer; and family history of melanoma, especially in multiple blood relatives.

His practice has implemented a recall system, in which high-risk patients get reminders for their 6-month visit and continued follow-up reminders if they do not schedule an appointment.

Dr. Shore's findings are scheduled to appear in an upcoming issue of the Journal of Drugs in Dermatology.

He said that he had no financial interests relevant to his study.