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Treat actinic keratoses initially with field therapy and follow with lesional therapy

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SONOMA, CALIF. – Combining lesional and field therapy may be the most effective way to treat actinic keratoses, Dr. David Pariser said at the annual Coastal Dermatology Symposium.

Because there’s no way to tell which actinic keratoses will progress to invasive squamous cell carcinoma, it’s reasonable to treat all lesions, said Dr. Pariser of Eastern Virginia Medical School, Norfolk, Va.

Studies comparing field versus lesional therapy to treat grade 1 and 2 lesions that were minimally or moderately thick found better long-term efficacy rates and better sustained clearance with field therapy, he said.

Dr. Pariser said he tends to treat actinic keratoses first with field therapy using photodynamic therapy or a topical agent, “then clean up what’s left with cryotherapy.”

Dr. David M. Pariser
Dr. David M. Pariser

Field therapy options include topical agents, laser ablation, or photodynamic therapy. Lesion-targeted therapies include cryosurgery, curettage, electrosurgery, or photodynamic therapy. Cryotherapy was the third most effective treatment in a review of the literature, he noted, after photodynamic therapies.

“None of these” other treatments “are going to put us out of the cryotherapy business,” Dr. Pariser said, “The best reimbursement is for cryotherapy, but the best way today is to do both” targeted and field therapy, he said at the symposium, jointly presented by the University of Louisville, Ky. and the Global Academy for Medical Education. This news organization and the Global Academy for Medical Education are owned by the same parent company.

He summarized the efficacy of various treatments for actinic keratoses from data in trials comparing cryotherapy versus photodynamic therapy or imiquimod and for other therapies from data in randomized controlled trials or prescribing information.

Photodynamic therapy after application of the photosensitizing agent aminolevulinic acid (ALA-PDT) cured 89% of actinic keratoses, compared with 12% using vehicle only. Photodynamic therapy after application of the photosensitizing agent methylaminolevulinate (MAL-PDT) cured 82% of lesions, compared with 37% in the vehicle group. Cryotherapy cured 72% in the studies he reviewed.

“I like photodynamic therapy. The evidence is as strong as any other treatment,” and it causes less scarring than destructive modalities, but reimbursement issues have been an impediment to widespread acceptance of photodynamic therapy in the United States, Dr. Pariser said.

He tells patients that they’ll need two photodynamic therapy treatments, 4 weeks apart. Some patients have such a good response to the first treatment that they don’t need another treatment when they come for the second visit.

For actinic keratoses on the upper extremities, occluding the area during the incubation period following application of topical ALA significantly increased clearance rates in studies. “Just wrap it with (plastic wrap),” he suggested. Occlusion may increase efficacy by raising skin temperature, he speculated.

In a separate study, the results seen with incubating for 1 hour was as good as 2 or 3 hours. “Now, I incubate for 1 hour. In good conscience, I can tell patients it will work just as well,” he said. The study also found similar clearance rates using spot therapy or broad-area application, “which was surprising to me,” he added, but lesions that cleared after broad-area treatment were more likely to remain clear from week 12 to week 24, compared with lesions that received spot treatment.

Among topical agents, 5-fluorouracil or ingenol cleared 58% of actinic keratoses, compared with 2% or 4% of lesions treated by vehicle, respectively, in the studies Dr. Pariser reviewed. Diclofenac cleared 47%, compared with 19% in the vehicle groups, and imiquimod cleared 46%, compared with 3% in the vehicle groups.

Most patients treated with 5-fluorouracil will develop mild to moderate skin irritation. Lesion site reactions also are an issue with ingenol mebutate, “the newest kid on the block for actinic keratoses,” he said. “Tell patients it’s going to happen. Show them photos.”

Dr. Pariser reported having no financial disclosures.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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SONOMA, CALIF. – Combining lesional and field therapy may be the most effective way to treat actinic keratoses, Dr. David Pariser said at the annual Coastal Dermatology Symposium.

Because there’s no way to tell which actinic keratoses will progress to invasive squamous cell carcinoma, it’s reasonable to treat all lesions, said Dr. Pariser of Eastern Virginia Medical School, Norfolk, Va.

Studies comparing field versus lesional therapy to treat grade 1 and 2 lesions that were minimally or moderately thick found better long-term efficacy rates and better sustained clearance with field therapy, he said.

Dr. Pariser said he tends to treat actinic keratoses first with field therapy using photodynamic therapy or a topical agent, “then clean up what’s left with cryotherapy.”

Dr. David M. Pariser
Dr. David M. Pariser

Field therapy options include topical agents, laser ablation, or photodynamic therapy. Lesion-targeted therapies include cryosurgery, curettage, electrosurgery, or photodynamic therapy. Cryotherapy was the third most effective treatment in a review of the literature, he noted, after photodynamic therapies.

“None of these” other treatments “are going to put us out of the cryotherapy business,” Dr. Pariser said, “The best reimbursement is for cryotherapy, but the best way today is to do both” targeted and field therapy, he said at the symposium, jointly presented by the University of Louisville, Ky. and the Global Academy for Medical Education. This news organization and the Global Academy for Medical Education are owned by the same parent company.

He summarized the efficacy of various treatments for actinic keratoses from data in trials comparing cryotherapy versus photodynamic therapy or imiquimod and for other therapies from data in randomized controlled trials or prescribing information.

Photodynamic therapy after application of the photosensitizing agent aminolevulinic acid (ALA-PDT) cured 89% of actinic keratoses, compared with 12% using vehicle only. Photodynamic therapy after application of the photosensitizing agent methylaminolevulinate (MAL-PDT) cured 82% of lesions, compared with 37% in the vehicle group. Cryotherapy cured 72% in the studies he reviewed.

“I like photodynamic therapy. The evidence is as strong as any other treatment,” and it causes less scarring than destructive modalities, but reimbursement issues have been an impediment to widespread acceptance of photodynamic therapy in the United States, Dr. Pariser said.

He tells patients that they’ll need two photodynamic therapy treatments, 4 weeks apart. Some patients have such a good response to the first treatment that they don’t need another treatment when they come for the second visit.

For actinic keratoses on the upper extremities, occluding the area during the incubation period following application of topical ALA significantly increased clearance rates in studies. “Just wrap it with (plastic wrap),” he suggested. Occlusion may increase efficacy by raising skin temperature, he speculated.

In a separate study, the results seen with incubating for 1 hour was as good as 2 or 3 hours. “Now, I incubate for 1 hour. In good conscience, I can tell patients it will work just as well,” he said. The study also found similar clearance rates using spot therapy or broad-area application, “which was surprising to me,” he added, but lesions that cleared after broad-area treatment were more likely to remain clear from week 12 to week 24, compared with lesions that received spot treatment.

Among topical agents, 5-fluorouracil or ingenol cleared 58% of actinic keratoses, compared with 2% or 4% of lesions treated by vehicle, respectively, in the studies Dr. Pariser reviewed. Diclofenac cleared 47%, compared with 19% in the vehicle groups, and imiquimod cleared 46%, compared with 3% in the vehicle groups.

Most patients treated with 5-fluorouracil will develop mild to moderate skin irritation. Lesion site reactions also are an issue with ingenol mebutate, “the newest kid on the block for actinic keratoses,” he said. “Tell patients it’s going to happen. Show them photos.”

Dr. Pariser reported having no financial disclosures.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SONOMA, CALIF. – Combining lesional and field therapy may be the most effective way to treat actinic keratoses, Dr. David Pariser said at the annual Coastal Dermatology Symposium.

Because there’s no way to tell which actinic keratoses will progress to invasive squamous cell carcinoma, it’s reasonable to treat all lesions, said Dr. Pariser of Eastern Virginia Medical School, Norfolk, Va.

Studies comparing field versus lesional therapy to treat grade 1 and 2 lesions that were minimally or moderately thick found better long-term efficacy rates and better sustained clearance with field therapy, he said.

Dr. Pariser said he tends to treat actinic keratoses first with field therapy using photodynamic therapy or a topical agent, “then clean up what’s left with cryotherapy.”

Dr. David M. Pariser
Dr. David M. Pariser

Field therapy options include topical agents, laser ablation, or photodynamic therapy. Lesion-targeted therapies include cryosurgery, curettage, electrosurgery, or photodynamic therapy. Cryotherapy was the third most effective treatment in a review of the literature, he noted, after photodynamic therapies.

“None of these” other treatments “are going to put us out of the cryotherapy business,” Dr. Pariser said, “The best reimbursement is for cryotherapy, but the best way today is to do both” targeted and field therapy, he said at the symposium, jointly presented by the University of Louisville, Ky. and the Global Academy for Medical Education. This news organization and the Global Academy for Medical Education are owned by the same parent company.

He summarized the efficacy of various treatments for actinic keratoses from data in trials comparing cryotherapy versus photodynamic therapy or imiquimod and for other therapies from data in randomized controlled trials or prescribing information.

Photodynamic therapy after application of the photosensitizing agent aminolevulinic acid (ALA-PDT) cured 89% of actinic keratoses, compared with 12% using vehicle only. Photodynamic therapy after application of the photosensitizing agent methylaminolevulinate (MAL-PDT) cured 82% of lesions, compared with 37% in the vehicle group. Cryotherapy cured 72% in the studies he reviewed.

“I like photodynamic therapy. The evidence is as strong as any other treatment,” and it causes less scarring than destructive modalities, but reimbursement issues have been an impediment to widespread acceptance of photodynamic therapy in the United States, Dr. Pariser said.

He tells patients that they’ll need two photodynamic therapy treatments, 4 weeks apart. Some patients have such a good response to the first treatment that they don’t need another treatment when they come for the second visit.

For actinic keratoses on the upper extremities, occluding the area during the incubation period following application of topical ALA significantly increased clearance rates in studies. “Just wrap it with (plastic wrap),” he suggested. Occlusion may increase efficacy by raising skin temperature, he speculated.

In a separate study, the results seen with incubating for 1 hour was as good as 2 or 3 hours. “Now, I incubate for 1 hour. In good conscience, I can tell patients it will work just as well,” he said. The study also found similar clearance rates using spot therapy or broad-area application, “which was surprising to me,” he added, but lesions that cleared after broad-area treatment were more likely to remain clear from week 12 to week 24, compared with lesions that received spot treatment.

Among topical agents, 5-fluorouracil or ingenol cleared 58% of actinic keratoses, compared with 2% or 4% of lesions treated by vehicle, respectively, in the studies Dr. Pariser reviewed. Diclofenac cleared 47%, compared with 19% in the vehicle groups, and imiquimod cleared 46%, compared with 3% in the vehicle groups.

Most patients treated with 5-fluorouracil will develop mild to moderate skin irritation. Lesion site reactions also are an issue with ingenol mebutate, “the newest kid on the block for actinic keratoses,” he said. “Tell patients it’s going to happen. Show them photos.”

Dr. Pariser reported having no financial disclosures.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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Select biologics for dose escalation in psoriasis

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SONOMA, CALIF.– Data support dosage escalation or intensification for patients who don’t respond to biologic therapy for psoriasis, but only for three of the four biologic agents available in the United States, Dr. April W. Armstrong said at the annual Coastal Dermatology Symposium.

It may make sense to increase the dose or shorten the intervals between doses in some patients with psoriasis who don’t respond to etanercept, adalimumab, or ustekinumab, she suggested.

Dr. April W. Armstrong
Dr. April W. Armstrong

For infliximab, however, increasing the standard 5-mg/kg dose to 10 mg/kg in nonresponders did not significantly improve efficacy in one randomized study of patients with moderate to severe psoriasis. Consider combination therapy instead of dose escalation in those patients, said Dr. Armstrong, director of the psoriasis program at the University of Colorado, Denver.

Most clinical trials of dose escalation for psoriasis target patients in whom conventional doses produce only a partial response, defined as a Psoriasis Area and Severity Index (PASI) score of 50-75, or no response, defined as a PASI score below 50, she said.

A conventional dosage of etanercept for psoriasis uses 50 mg twice weekly for 12 weeks, followed by 50 mg once weekly for maintenance, Dr. Armstrong said. In an open-label extension of a study of 912 patients with moderate to severe psoriasis who received 12 weeks of etanercept therapy, nonresponders who escalated the maintenance dosage to 50 mg twice weekly boosted the likelihood of achieving a PASI 75 from 33% at 12 weeks to 44% at 48 weeks and 43% at 72 weeks (J. Drugs Dermatol. 2010;9:928-37).

Safety profiles were similar between standard dosing and escalated or intensified dosing in studies of all four biologic therapies, Dr. Armstrong said at the symposium, jointly presented by the University of Louisville (Ky.) and the Global Academy for Medical Education.

In the etanercept study, rates of serious infections were 0.9 events per 100 patient-years on standard maintenance therapy and 1.9 events per 100 patient-years on the escalated dosage. Myocardial infarctions occurred in none of 321 patients on standard maintenance therapy and in 2 of 591 patients on the twice-weekly dosage.

The conventional dosage of adalimumab for psoriasis is 80 mg at the start of therapy, followed by 40 mg every other week starting at week 1. In an open-label extension of a study of 147 patients, those who did not achieve a PASI 50 by week 25 were allowed to escalate the maintenance therapy dosage to 40 mg weekly. By week 60, 64% of patients in the dose-escalation group achieved a PASI 75, compared with 56% of patients who had been on the standard regimen and 45% of patients who had started with placebo for 12 weeks and then went on the standard dosage (J. Am. Acad. Dermatol. 2006;55:598-606). The mean PASI score improved by 27% after 8 weeks on the escalated dose, Dr. Armstrong said.

Three malignancies and two cardiovascular events (one leading to death) developed in the escalated-dosage group, compared with two malignancies and a serious case of coccidiomycosis in the standard-therapy group, she noted.

The conventional dosage for ustekinumab is 45 mg in patients weighing up to 100 kg or 90 mg in heavier patients, administered in subcutaneous injections at weeks 0 and 4, then every 12 weeks thereafter. In the only head-to-head study comparing biologic therapies for psoriasis, ustekinumab was more effective than etanercept in the first 3 months, Dr. Armstrong noted. The 12-week Active Comparator (CNTO1275/Enbrel) Psoriasis Trial (ACCEPT) found that 74% of 347 patients on 90 mg of ustekinumab and 68% of 209 patients on 45 mg of ustekinumab achieved a PASI 75, compared with 57% of 347 patients on etanercept (N. Engl. J. Med. 2010;362:118-28).

In a separate study of 158 patients with psoriasis who only partially responded to standard ustekinumab therapy after 24 weeks, maintenance dose escalation to every 8 weeks instead of 12 significantly improved response rates in patients on 90 mg but not in those on 45 mg. By week 52, 69% of patients receiving 90 mg ustekinumab every 8 weeks achieved a PASI 75, compared with 33% of patients on ustekinumab 90 mg every 12 weeks (Lancet 2008;371:1675-84). In the patients on 45 mg ustekinumab, the proportions achieving PASI 75 by week 52 did not differ significantly between those receiving the drug every 8 or 12 weeks.

One cutaneous malignancy, one noncutaneous malignancy, and two other serious adverse events occurred in the intensified-therapy groups, compared with one serious infection and two other serious adverse events in the standard-therapy groups.

The conventional dosage of infliximab for psoriasis is 5 mg/kg at weeks 0, 2, and 6, then every 8 weeks. A study that randomized 33 patients with moderate to severe psoriasis to 10 weeks of therapy with placebo or 5 mg/kg or 10 mg/kg of infliximab at weeks 0, 2, and 6 found that 91% of patients on the escalated dose and 82% on the standard dose of infliximab achieved a Physician Global Assessment score of good, excellent, or clear, compared with 18% of patients on placebo (Lancet 2001;357:1842-7).

 

 

The proportions of patients achieving a PASI 75 were not significantly different between the standard-dosage group and the escalated-dosage group (82% vs. 73%, respectively), although both were significantly higher than in the placebo group (18%). “So, there’s not much difference if you give 5 or 10 mg/kg” of infliximab, Dr. Armstrong said.

One of 11 patients on 5 mg/kg infliximab developed a dental abscess, and 1 of 11 patients on 10 mg/kg infliximab developed pneumonia.

Dr. Armstrong reported financial associations with AbbVie, Amgen, Celgene, Lilly, Novartis, Merck, Pfizer, UCB, Modernizing Medicine, and Janssen. This publication and the Global Academy for Medical Education are owned by the same parent company.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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SONOMA, CALIF.– Data support dosage escalation or intensification for patients who don’t respond to biologic therapy for psoriasis, but only for three of the four biologic agents available in the United States, Dr. April W. Armstrong said at the annual Coastal Dermatology Symposium.

It may make sense to increase the dose or shorten the intervals between doses in some patients with psoriasis who don’t respond to etanercept, adalimumab, or ustekinumab, she suggested.

Dr. April W. Armstrong
Dr. April W. Armstrong

For infliximab, however, increasing the standard 5-mg/kg dose to 10 mg/kg in nonresponders did not significantly improve efficacy in one randomized study of patients with moderate to severe psoriasis. Consider combination therapy instead of dose escalation in those patients, said Dr. Armstrong, director of the psoriasis program at the University of Colorado, Denver.

Most clinical trials of dose escalation for psoriasis target patients in whom conventional doses produce only a partial response, defined as a Psoriasis Area and Severity Index (PASI) score of 50-75, or no response, defined as a PASI score below 50, she said.

A conventional dosage of etanercept for psoriasis uses 50 mg twice weekly for 12 weeks, followed by 50 mg once weekly for maintenance, Dr. Armstrong said. In an open-label extension of a study of 912 patients with moderate to severe psoriasis who received 12 weeks of etanercept therapy, nonresponders who escalated the maintenance dosage to 50 mg twice weekly boosted the likelihood of achieving a PASI 75 from 33% at 12 weeks to 44% at 48 weeks and 43% at 72 weeks (J. Drugs Dermatol. 2010;9:928-37).

Safety profiles were similar between standard dosing and escalated or intensified dosing in studies of all four biologic therapies, Dr. Armstrong said at the symposium, jointly presented by the University of Louisville (Ky.) and the Global Academy for Medical Education.

In the etanercept study, rates of serious infections were 0.9 events per 100 patient-years on standard maintenance therapy and 1.9 events per 100 patient-years on the escalated dosage. Myocardial infarctions occurred in none of 321 patients on standard maintenance therapy and in 2 of 591 patients on the twice-weekly dosage.

The conventional dosage of adalimumab for psoriasis is 80 mg at the start of therapy, followed by 40 mg every other week starting at week 1. In an open-label extension of a study of 147 patients, those who did not achieve a PASI 50 by week 25 were allowed to escalate the maintenance therapy dosage to 40 mg weekly. By week 60, 64% of patients in the dose-escalation group achieved a PASI 75, compared with 56% of patients who had been on the standard regimen and 45% of patients who had started with placebo for 12 weeks and then went on the standard dosage (J. Am. Acad. Dermatol. 2006;55:598-606). The mean PASI score improved by 27% after 8 weeks on the escalated dose, Dr. Armstrong said.

Three malignancies and two cardiovascular events (one leading to death) developed in the escalated-dosage group, compared with two malignancies and a serious case of coccidiomycosis in the standard-therapy group, she noted.

The conventional dosage for ustekinumab is 45 mg in patients weighing up to 100 kg or 90 mg in heavier patients, administered in subcutaneous injections at weeks 0 and 4, then every 12 weeks thereafter. In the only head-to-head study comparing biologic therapies for psoriasis, ustekinumab was more effective than etanercept in the first 3 months, Dr. Armstrong noted. The 12-week Active Comparator (CNTO1275/Enbrel) Psoriasis Trial (ACCEPT) found that 74% of 347 patients on 90 mg of ustekinumab and 68% of 209 patients on 45 mg of ustekinumab achieved a PASI 75, compared with 57% of 347 patients on etanercept (N. Engl. J. Med. 2010;362:118-28).

In a separate study of 158 patients with psoriasis who only partially responded to standard ustekinumab therapy after 24 weeks, maintenance dose escalation to every 8 weeks instead of 12 significantly improved response rates in patients on 90 mg but not in those on 45 mg. By week 52, 69% of patients receiving 90 mg ustekinumab every 8 weeks achieved a PASI 75, compared with 33% of patients on ustekinumab 90 mg every 12 weeks (Lancet 2008;371:1675-84). In the patients on 45 mg ustekinumab, the proportions achieving PASI 75 by week 52 did not differ significantly between those receiving the drug every 8 or 12 weeks.

One cutaneous malignancy, one noncutaneous malignancy, and two other serious adverse events occurred in the intensified-therapy groups, compared with one serious infection and two other serious adverse events in the standard-therapy groups.

The conventional dosage of infliximab for psoriasis is 5 mg/kg at weeks 0, 2, and 6, then every 8 weeks. A study that randomized 33 patients with moderate to severe psoriasis to 10 weeks of therapy with placebo or 5 mg/kg or 10 mg/kg of infliximab at weeks 0, 2, and 6 found that 91% of patients on the escalated dose and 82% on the standard dose of infliximab achieved a Physician Global Assessment score of good, excellent, or clear, compared with 18% of patients on placebo (Lancet 2001;357:1842-7).

 

 

The proportions of patients achieving a PASI 75 were not significantly different between the standard-dosage group and the escalated-dosage group (82% vs. 73%, respectively), although both were significantly higher than in the placebo group (18%). “So, there’s not much difference if you give 5 or 10 mg/kg” of infliximab, Dr. Armstrong said.

One of 11 patients on 5 mg/kg infliximab developed a dental abscess, and 1 of 11 patients on 10 mg/kg infliximab developed pneumonia.

Dr. Armstrong reported financial associations with AbbVie, Amgen, Celgene, Lilly, Novartis, Merck, Pfizer, UCB, Modernizing Medicine, and Janssen. This publication and the Global Academy for Medical Education are owned by the same parent company.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SONOMA, CALIF.– Data support dosage escalation or intensification for patients who don’t respond to biologic therapy for psoriasis, but only for three of the four biologic agents available in the United States, Dr. April W. Armstrong said at the annual Coastal Dermatology Symposium.

It may make sense to increase the dose or shorten the intervals between doses in some patients with psoriasis who don’t respond to etanercept, adalimumab, or ustekinumab, she suggested.

Dr. April W. Armstrong
Dr. April W. Armstrong

For infliximab, however, increasing the standard 5-mg/kg dose to 10 mg/kg in nonresponders did not significantly improve efficacy in one randomized study of patients with moderate to severe psoriasis. Consider combination therapy instead of dose escalation in those patients, said Dr. Armstrong, director of the psoriasis program at the University of Colorado, Denver.

Most clinical trials of dose escalation for psoriasis target patients in whom conventional doses produce only a partial response, defined as a Psoriasis Area and Severity Index (PASI) score of 50-75, or no response, defined as a PASI score below 50, she said.

A conventional dosage of etanercept for psoriasis uses 50 mg twice weekly for 12 weeks, followed by 50 mg once weekly for maintenance, Dr. Armstrong said. In an open-label extension of a study of 912 patients with moderate to severe psoriasis who received 12 weeks of etanercept therapy, nonresponders who escalated the maintenance dosage to 50 mg twice weekly boosted the likelihood of achieving a PASI 75 from 33% at 12 weeks to 44% at 48 weeks and 43% at 72 weeks (J. Drugs Dermatol. 2010;9:928-37).

Safety profiles were similar between standard dosing and escalated or intensified dosing in studies of all four biologic therapies, Dr. Armstrong said at the symposium, jointly presented by the University of Louisville (Ky.) and the Global Academy for Medical Education.

In the etanercept study, rates of serious infections were 0.9 events per 100 patient-years on standard maintenance therapy and 1.9 events per 100 patient-years on the escalated dosage. Myocardial infarctions occurred in none of 321 patients on standard maintenance therapy and in 2 of 591 patients on the twice-weekly dosage.

The conventional dosage of adalimumab for psoriasis is 80 mg at the start of therapy, followed by 40 mg every other week starting at week 1. In an open-label extension of a study of 147 patients, those who did not achieve a PASI 50 by week 25 were allowed to escalate the maintenance therapy dosage to 40 mg weekly. By week 60, 64% of patients in the dose-escalation group achieved a PASI 75, compared with 56% of patients who had been on the standard regimen and 45% of patients who had started with placebo for 12 weeks and then went on the standard dosage (J. Am. Acad. Dermatol. 2006;55:598-606). The mean PASI score improved by 27% after 8 weeks on the escalated dose, Dr. Armstrong said.

Three malignancies and two cardiovascular events (one leading to death) developed in the escalated-dosage group, compared with two malignancies and a serious case of coccidiomycosis in the standard-therapy group, she noted.

The conventional dosage for ustekinumab is 45 mg in patients weighing up to 100 kg or 90 mg in heavier patients, administered in subcutaneous injections at weeks 0 and 4, then every 12 weeks thereafter. In the only head-to-head study comparing biologic therapies for psoriasis, ustekinumab was more effective than etanercept in the first 3 months, Dr. Armstrong noted. The 12-week Active Comparator (CNTO1275/Enbrel) Psoriasis Trial (ACCEPT) found that 74% of 347 patients on 90 mg of ustekinumab and 68% of 209 patients on 45 mg of ustekinumab achieved a PASI 75, compared with 57% of 347 patients on etanercept (N. Engl. J. Med. 2010;362:118-28).

In a separate study of 158 patients with psoriasis who only partially responded to standard ustekinumab therapy after 24 weeks, maintenance dose escalation to every 8 weeks instead of 12 significantly improved response rates in patients on 90 mg but not in those on 45 mg. By week 52, 69% of patients receiving 90 mg ustekinumab every 8 weeks achieved a PASI 75, compared with 33% of patients on ustekinumab 90 mg every 12 weeks (Lancet 2008;371:1675-84). In the patients on 45 mg ustekinumab, the proportions achieving PASI 75 by week 52 did not differ significantly between those receiving the drug every 8 or 12 weeks.

One cutaneous malignancy, one noncutaneous malignancy, and two other serious adverse events occurred in the intensified-therapy groups, compared with one serious infection and two other serious adverse events in the standard-therapy groups.

The conventional dosage of infliximab for psoriasis is 5 mg/kg at weeks 0, 2, and 6, then every 8 weeks. A study that randomized 33 patients with moderate to severe psoriasis to 10 weeks of therapy with placebo or 5 mg/kg or 10 mg/kg of infliximab at weeks 0, 2, and 6 found that 91% of patients on the escalated dose and 82% on the standard dose of infliximab achieved a Physician Global Assessment score of good, excellent, or clear, compared with 18% of patients on placebo (Lancet 2001;357:1842-7).

 

 

The proportions of patients achieving a PASI 75 were not significantly different between the standard-dosage group and the escalated-dosage group (82% vs. 73%, respectively), although both were significantly higher than in the placebo group (18%). “So, there’s not much difference if you give 5 or 10 mg/kg” of infliximab, Dr. Armstrong said.

One of 11 patients on 5 mg/kg infliximab developed a dental abscess, and 1 of 11 patients on 10 mg/kg infliximab developed pneumonia.

Dr. Armstrong reported financial associations with AbbVie, Amgen, Celgene, Lilly, Novartis, Merck, Pfizer, UCB, Modernizing Medicine, and Janssen. This publication and the Global Academy for Medical Education are owned by the same parent company.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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VIDEO: Scabies epidemic plagues nursing homes

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SONOMA, CALIF. – Dr. Miriam S. Bettencourt is seeing what she considers an epidemic of scabies among elderly patients in nursing homes.

The problem is a lack of detection, she said in an interview at the annual Coastal Dermatology Symposium.

Dermatologists who see elderly patients should look for scabies in unusual bodily locations and remember that scabies in the elderly can produce atypical lesions, said Dr. Bettencourt of the University of Nevada, Las Vegas.

Permethrin cream alone probably won’t be enough to treat these patients, she said at the symposium, jointly presented by the University of Louisville, Kentucky, and the Global Academy for Medical Education. This publication and the Global Academy for Medical Education are owned by the same parent company.

How would you treat scabies in an elderly patient? Dr. Bettencourt discussed several effective options.

Dr. Bettencourt reported having no financial disclosures.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

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SONOMA, CALIF. – Dr. Miriam S. Bettencourt is seeing what she considers an epidemic of scabies among elderly patients in nursing homes.

The problem is a lack of detection, she said in an interview at the annual Coastal Dermatology Symposium.

Dermatologists who see elderly patients should look for scabies in unusual bodily locations and remember that scabies in the elderly can produce atypical lesions, said Dr. Bettencourt of the University of Nevada, Las Vegas.

Permethrin cream alone probably won’t be enough to treat these patients, she said at the symposium, jointly presented by the University of Louisville, Kentucky, and the Global Academy for Medical Education. This publication and the Global Academy for Medical Education are owned by the same parent company.

How would you treat scabies in an elderly patient? Dr. Bettencourt discussed several effective options.

Dr. Bettencourt reported having no financial disclosures.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SONOMA, CALIF. – Dr. Miriam S. Bettencourt is seeing what she considers an epidemic of scabies among elderly patients in nursing homes.

The problem is a lack of detection, she said in an interview at the annual Coastal Dermatology Symposium.

Dermatologists who see elderly patients should look for scabies in unusual bodily locations and remember that scabies in the elderly can produce atypical lesions, said Dr. Bettencourt of the University of Nevada, Las Vegas.

Permethrin cream alone probably won’t be enough to treat these patients, she said at the symposium, jointly presented by the University of Louisville, Kentucky, and the Global Academy for Medical Education. This publication and the Global Academy for Medical Education are owned by the same parent company.

How would you treat scabies in an elderly patient? Dr. Bettencourt discussed several effective options.

Dr. Bettencourt reported having no financial disclosures.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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VIDEO: Don’t fear fungal infections in psoriasis patients on biologics

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SONOMA, CALIF. – Concerns about the risk of developing deep fungal infections in patients on biologic therapies for psoriasis are real, but not as significant as some may think, Dr. Miriam S. Bettencourt said at the annual Coastal Dermatology Symposium.

Data suggest that 98% of all patients who developed deep fungal infection while taking a biologic drug also were taking another immunosuppressant, usually prednisone, said Dr. Bettencourt of the University of Nevada, Las Vegas.

Among a subgroup of patients taking a biologic drug for psoriasis or psoriatic arthritis, the risk of developing a deep fungal infection is significantly lower than among all patients on biologics, she said at the symposium, jointly presented by the University of Louisville (Ky.) and Global Academy for Medical Education. This publication and Global Academy for Medical Education are owned by the same parent company.

Dr. Bettencourt reported having no financial disclosures.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

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SONOMA, CALIF. – Concerns about the risk of developing deep fungal infections in patients on biologic therapies for psoriasis are real, but not as significant as some may think, Dr. Miriam S. Bettencourt said at the annual Coastal Dermatology Symposium.

Data suggest that 98% of all patients who developed deep fungal infection while taking a biologic drug also were taking another immunosuppressant, usually prednisone, said Dr. Bettencourt of the University of Nevada, Las Vegas.

Among a subgroup of patients taking a biologic drug for psoriasis or psoriatic arthritis, the risk of developing a deep fungal infection is significantly lower than among all patients on biologics, she said at the symposium, jointly presented by the University of Louisville (Ky.) and Global Academy for Medical Education. This publication and Global Academy for Medical Education are owned by the same parent company.

Dr. Bettencourt reported having no financial disclosures.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SONOMA, CALIF. – Concerns about the risk of developing deep fungal infections in patients on biologic therapies for psoriasis are real, but not as significant as some may think, Dr. Miriam S. Bettencourt said at the annual Coastal Dermatology Symposium.

Data suggest that 98% of all patients who developed deep fungal infection while taking a biologic drug also were taking another immunosuppressant, usually prednisone, said Dr. Bettencourt of the University of Nevada, Las Vegas.

Among a subgroup of patients taking a biologic drug for psoriasis or psoriatic arthritis, the risk of developing a deep fungal infection is significantly lower than among all patients on biologics, she said at the symposium, jointly presented by the University of Louisville (Ky.) and Global Academy for Medical Education. This publication and Global Academy for Medical Education are owned by the same parent company.

Dr. Bettencourt reported having no financial disclosures.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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VIDEO: Don’t miss reactions to these up and coming allergens

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SONOMA, CALIF. – Skin reactions to components of baby wipes, cosmetics, leather, and even artificial hips or knees top an informal list of dermatoses caused by newer allergens for dermatologists to consider, Dr. Joseph F. Fowler Jr. said at the annual Coastal Dermatology Symposium.

He described some of these new allergens in a video interview at the symposium, jointly presented by the University of Louisville, Kentucky, and the Global Academy for Medical Education.

A relatively new preservative found in baby wipes and hair and skin products is one of the main culprits – methylisothiazolinone, said Dr. Fowler of the university. Bee glue (also called propolis) is another problematic material, found in some lip moisturizers and other personal-care products.

Shellac (the same shellac that’s often used as a furniture coating) in mascara and nail products can cause skin reactions, too.

Leather can cause dermatoses because of the chromium used in leather processing, but recent reports also point to cobalt, another product used in leather processing, as an allergen source, Dr. Fowler said.

Also, in rare cases, components of orthopedic implants are causing allergic reactions that sometimes necessitate removal of the implant, he added.

Dr. Fowler reported financial associations with Bayer, Valeant, Amgen, AbbVie, Allergan, Celgene, Galderma, Novartis, and Lilly. This publication and the Global Academy for Medical Education are owned by the same parent company.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

sboschert@frontlinemedcom.com

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SONOMA, CALIF. – Skin reactions to components of baby wipes, cosmetics, leather, and even artificial hips or knees top an informal list of dermatoses caused by newer allergens for dermatologists to consider, Dr. Joseph F. Fowler Jr. said at the annual Coastal Dermatology Symposium.

He described some of these new allergens in a video interview at the symposium, jointly presented by the University of Louisville, Kentucky, and the Global Academy for Medical Education.

A relatively new preservative found in baby wipes and hair and skin products is one of the main culprits – methylisothiazolinone, said Dr. Fowler of the university. Bee glue (also called propolis) is another problematic material, found in some lip moisturizers and other personal-care products.

Shellac (the same shellac that’s often used as a furniture coating) in mascara and nail products can cause skin reactions, too.

Leather can cause dermatoses because of the chromium used in leather processing, but recent reports also point to cobalt, another product used in leather processing, as an allergen source, Dr. Fowler said.

Also, in rare cases, components of orthopedic implants are causing allergic reactions that sometimes necessitate removal of the implant, he added.

Dr. Fowler reported financial associations with Bayer, Valeant, Amgen, AbbVie, Allergan, Celgene, Galderma, Novartis, and Lilly. This publication and the Global Academy for Medical Education are owned by the same parent company.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SONOMA, CALIF. – Skin reactions to components of baby wipes, cosmetics, leather, and even artificial hips or knees top an informal list of dermatoses caused by newer allergens for dermatologists to consider, Dr. Joseph F. Fowler Jr. said at the annual Coastal Dermatology Symposium.

He described some of these new allergens in a video interview at the symposium, jointly presented by the University of Louisville, Kentucky, and the Global Academy for Medical Education.

A relatively new preservative found in baby wipes and hair and skin products is one of the main culprits – methylisothiazolinone, said Dr. Fowler of the university. Bee glue (also called propolis) is another problematic material, found in some lip moisturizers and other personal-care products.

Shellac (the same shellac that’s often used as a furniture coating) in mascara and nail products can cause skin reactions, too.

Leather can cause dermatoses because of the chromium used in leather processing, but recent reports also point to cobalt, another product used in leather processing, as an allergen source, Dr. Fowler said.

Also, in rare cases, components of orthopedic implants are causing allergic reactions that sometimes necessitate removal of the implant, he added.

Dr. Fowler reported financial associations with Bayer, Valeant, Amgen, AbbVie, Allergan, Celgene, Galderma, Novartis, and Lilly. This publication and the Global Academy for Medical Education are owned by the same parent company.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

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