WCD 2015

VANCOUVER – Here’s a key message to bear in mind in the current era of methicillin-resistant Staphylococcus aureus: “Don’t forget streptococci,” Dr. Dirk M. Elston urged at the World Congress of Dermatology.

“Cellulitis is usually not staphylococcal, it’s streptococcal. Erysipelas, of course, is also streptococcal. And almost all impetigo probably begins as a streptococcal infection, even though the staphylococci outnumber the streptococci over time,” said Dr. Elston, managing director of the Ackerman Academy of Dermatopathology in New York.

The reason this message is important is because sulfa drugs are unreliable for the treatment of streptococcal infections.

Bruce Jancin/Frontline Medical News

“There is no indication for the treatment of active streptococcal disease with sulfa drugs,” the dermatologist said.

He cited a retrospective case-control study of 2,096 children with undrained, noncultured skin and soft tissue infections treated empirically on an outpatient basis with beta-lactams, clindamycin, or trimethoprim-sulfamethoxazole as monotherapy. The treatment failure rate was significantly higher in patients receiving trimethoprim-sulfamethoxazole. Clindamycin and beta-lactams were equally effective as first-line empiric therapy (Pediatrics 2009;123:e959-66).

Clindamycin has the added advantage of providing a two for one benefit: It’s effective against both MRSA and strep, Dr. Elston noted.

Necrotizing fasciitis is increasing in prevalence, and in a recent case series from Belfast, the most commonly isolated causative organism obtained from debrided tissue cultures was group A Streptococcus. The investigators found the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) scoring system lacked diagnostic sensitivity; however, an elevated serum lactate at presentation had 90% diagnostic sensitivity and provided added value as a prognostic indicator (J. Plast. Reconstr. Aesthet. Surg. 2015;68:304-11).

“Necrotizing fasciitis often begins as a minor skin infection. Any patient with pain out of proportion to the clinical appearance or just the opposite – they look horrible and yet it’s relatively nontender – those are both potentially true medical emergencies,” Dr. Elston said.

It’s important to understand that streptococcal virulence is not a static phenomenon, he added.

“We’ve seen changes in strep virulence periodically. You’ll have waves of much more toxic strep. There was a wave a number of years ago in Missouri where there was a very high death rate among 19- and 20-year-olds. Right now Australia is seeing an epidemic of severe streptococcal disease, with sepsis and toxic shock,” according to the dermatologist.

Many of these Northern Australian cases begin with pyoderma, and many of those pyodermas occurred secondary to scabies (Trop. Med. Int. Health 2015;20:40-7).

Dr. Elston reported receiving research support from more than a dozen pharmaceutical companies and serving as a consultant to half a dozen.

[email protected]

VANCOUVER – Here’s a key message to bear in mind in the current era of methicillin-resistant Staphylococcus aureus: “Don’t forget streptococci,” Dr. Dirk M. Elston urged at the World Congress of Dermatology.

“Cellulitis is usually not staphylococcal, it’s streptococcal. Erysipelas, of course, is also streptococcal. And almost all impetigo probably begins as a streptococcal infection, even though the staphylococci outnumber the streptococci over time,” said Dr. Elston, managing director of the Ackerman Academy of Dermatopathology in New York.

The reason this message is important is because sulfa drugs are unreliable for the treatment of streptococcal infections.

Bruce Jancin/Frontline Medical News

“There is no indication for the treatment of active streptococcal disease with sulfa drugs,” the dermatologist said.

He cited a retrospective case-control study of 2,096 children with undrained, noncultured skin and soft tissue infections treated empirically on an outpatient basis with beta-lactams, clindamycin, or trimethoprim-sulfamethoxazole as monotherapy. The treatment failure rate was significantly higher in patients receiving trimethoprim-sulfamethoxazole. Clindamycin and beta-lactams were equally effective as first-line empiric therapy (Pediatrics 2009;123:e959-66).

Clindamycin has the added advantage of providing a two for one benefit: It’s effective against both MRSA and strep, Dr. Elston noted.

Necrotizing fasciitis is increasing in prevalence, and in a recent case series from Belfast, the most commonly isolated causative organism obtained from debrided tissue cultures was group A Streptococcus. The investigators found the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) scoring system lacked diagnostic sensitivity; however, an elevated serum lactate at presentation had 90% diagnostic sensitivity and provided added value as a prognostic indicator (J. Plast. Reconstr. Aesthet. Surg. 2015;68:304-11).

“Necrotizing fasciitis often begins as a minor skin infection. Any patient with pain out of proportion to the clinical appearance or just the opposite – they look horrible and yet it’s relatively nontender – those are both potentially true medical emergencies,” Dr. Elston said.

It’s important to understand that streptococcal virulence is not a static phenomenon, he added.

“We’ve seen changes in strep virulence periodically. You’ll have waves of much more toxic strep. There was a wave a number of years ago in Missouri where there was a very high death rate among 19- and 20-year-olds. Right now Australia is seeing an epidemic of severe streptococcal disease, with sepsis and toxic shock,” according to the dermatologist.

Many of these Northern Australian cases begin with pyoderma, and many of those pyodermas occurred secondary to scabies (Trop. Med. Int. Health 2015;20:40-7).

Dr. Elston reported receiving research support from more than a dozen pharmaceutical companies and serving as a consultant to half a dozen.

[email protected]

VANCOUVER – Here’s a key message to bear in mind in the current era of methicillin-resistant Staphylococcus aureus: “Don’t forget streptococci,” Dr. Dirk M. Elston urged at the World Congress of Dermatology.

“Cellulitis is usually not staphylococcal, it’s streptococcal. Erysipelas, of course, is also streptococcal. And almost all impetigo probably begins as a streptococcal infection, even though the staphylococci outnumber the streptococci over time,” said Dr. Elston, managing director of the Ackerman Academy of Dermatopathology in New York.

The reason this message is important is because sulfa drugs are unreliable for the treatment of streptococcal infections.

Bruce Jancin/Frontline Medical News

“There is no indication for the treatment of active streptococcal disease with sulfa drugs,” the dermatologist said.

He cited a retrospective case-control study of 2,096 children with undrained, noncultured skin and soft tissue infections treated empirically on an outpatient basis with beta-lactams, clindamycin, or trimethoprim-sulfamethoxazole as monotherapy. The treatment failure rate was significantly higher in patients receiving trimethoprim-sulfamethoxazole. Clindamycin and beta-lactams were equally effective as first-line empiric therapy (Pediatrics 2009;123:e959-66).

Clindamycin has the added advantage of providing a two for one benefit: It’s effective against both MRSA and strep, Dr. Elston noted.

Necrotizing fasciitis is increasing in prevalence, and in a recent case series from Belfast, the most commonly isolated causative organism obtained from debrided tissue cultures was group A Streptococcus. The investigators found the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) scoring system lacked diagnostic sensitivity; however, an elevated serum lactate at presentation had 90% diagnostic sensitivity and provided added value as a prognostic indicator (J. Plast. Reconstr. Aesthet. Surg. 2015;68:304-11).

“Necrotizing fasciitis often begins as a minor skin infection. Any patient with pain out of proportion to the clinical appearance or just the opposite – they look horrible and yet it’s relatively nontender – those are both potentially true medical emergencies,” Dr. Elston said.

It’s important to understand that streptococcal virulence is not a static phenomenon, he added.

“We’ve seen changes in strep virulence periodically. You’ll have waves of much more toxic strep. There was a wave a number of years ago in Missouri where there was a very high death rate among 19- and 20-year-olds. Right now Australia is seeing an epidemic of severe streptococcal disease, with sepsis and toxic shock,” according to the dermatologist.

Many of these Northern Australian cases begin with pyoderma, and many of those pyodermas occurred secondary to scabies (Trop. Med. Int. Health 2015;20:40-7).

Dr. Elston reported receiving research support from more than a dozen pharmaceutical companies and serving as a consultant to half a dozen.

[email protected]

VANCOUVER, B.C. – So far, monoclonal antibodies that specifically target IL-23p19 are showing promise for treating chronic plaque psoriasis and are usually well tolerated, Dr. Elisabeth Riedl said at the World Congress of Dermatology.

The agents target the interleukin (IL)-23 cytokine, which is important in the induction of T-helper-17 cells in psoriasis and several other inflammatory disorders, said Dr. Riedl of the department of dermatology at Mount Sinai Hospital in New York. IL-23 has two subunits – p40, which it shares with IL-12, and p19, which is specific for IL-23, she said. Based on earlier research, the effectiveness of psoriasis treatments that target the p40 subunit seems to depend mostly on their ability to neutralize IL-23, not IL-12, she noted.

That observation helped spur several psoriasis trials of monoclonal antibodies that target IL-23p19, according to Dr. Riedl. Among the most promising of the monoclonal antibodies is BI 655066, which significantly outperformed placebo in a randomized, double-blind phase I trial reported earlier in 2015. At week 12, 87% of patients who received intravenous or oral BI65506 achieved a PASI (Psoriasis Area and Severity Index) 75 score, while 58% achieved a PASI 90 score and 16% achieved PASI 100, compared with none of the placebo group.

Another IL-23p19 inhibitor, guselkumab (CNTO 1959), beat placebo in a small randomized, double-blind phase I trial, Dr. Riedl noted. All patients who received a single subcutaneous injection of 300 mg of guselkumab achieved a PASI 75 score, and about 80% achieved PASI 90, compared with none of the placebo group, she noted.

The third IL-23p19 inhibitor, tildrakizumab (MK-3222), also beat placebo at all doses tested in a three-part, randomized, placebo-controlled phase I trial, Dr. Riedl said. Furthermore, the histopathology of a subgroup of patients revealed significant decreases in lesions, compared with baseline, and a significant correlation between histopathologic and clinical scores, she noted. “In phase II, there was a significant response for all dosing cohorts, with a durable response to 52 weeks,” she added.

The primary safety concern for IL-23 inhibitors appears to be increased infection risk, although patients with genetic diseases connected to the IL-23/Th17 pathway already are at increased risk for infections such as candidiasis, mycobacteriosis, salmonellosis, and staphylococcal and Klebsiella infections, Dr. Riedl noted. “Ustekinumab targets IL-12/IL-23 and so far has shown a favorable safety profile,” she said, pointing to a 5-year follow-up study of the antibody that found no increase over time in adverse events and similar rates of adverse events among dosing groups.

Infections and headaches were the most commonly reported adverse events in phase I and II trials of targeted anti–IL-23p19 antibodies, Dr. Riedl said. In the phase I trial of BI 655066, rates of adverse events were similar for treatment and placebo except for nasopharyngitis, which affected 13% of the BI 655066 group and none of the placebo group, she noted. Guselkumab also was associated with similar rates of overall adverse events, compared with placebo, in its phase I trial, although 6 of 20 patients who received guselkumab developed infections, including two upper respiratory tract infections and one event each of bronchitis, folliculitis, viral gastroenteritis, herpes simplex infection, lower respiratory tract infection, vaginal infection, and nasopharyngitis, she said. Tildrakizumab was generally well tolerated in its phase IIb trial, she added. Serious adverse events that might have been related to treatment were rare but included bacterial arthritis, lymphedema, melanoma, stroke, epiglottitis, and knee infection.

Taken together, the data for IL-23p19 inhibitors are encouraging, according to Dr. Riedl. “The results suggest that selective inhibition of IL-23p19 is a promising target for novel therapies,” she said.

Dr. Riedl reported receiving grant support or serving as a consultant, advisory board member, or speakers bureau member for Abbvie, Celgen, Merck, Pfizer, and Janssen.

[email protected]

VANCOUVER, B.C. – So far, monoclonal antibodies that specifically target IL-23p19 are showing promise for treating chronic plaque psoriasis and are usually well tolerated, Dr. Elisabeth Riedl said at the World Congress of Dermatology.

The agents target the interleukin (IL)-23 cytokine, which is important in the induction of T-helper-17 cells in psoriasis and several other inflammatory disorders, said Dr. Riedl of the department of dermatology at Mount Sinai Hospital in New York. IL-23 has two subunits – p40, which it shares with IL-12, and p19, which is specific for IL-23, she said. Based on earlier research, the effectiveness of psoriasis treatments that target the p40 subunit seems to depend mostly on their ability to neutralize IL-23, not IL-12, she noted.

That observation helped spur several psoriasis trials of monoclonal antibodies that target IL-23p19, according to Dr. Riedl. Among the most promising of the monoclonal antibodies is BI 655066, which significantly outperformed placebo in a randomized, double-blind phase I trial reported earlier in 2015. At week 12, 87% of patients who received intravenous or oral BI65506 achieved a PASI (Psoriasis Area and Severity Index) 75 score, while 58% achieved a PASI 90 score and 16% achieved PASI 100, compared with none of the placebo group.

Another IL-23p19 inhibitor, guselkumab (CNTO 1959), beat placebo in a small randomized, double-blind phase I trial, Dr. Riedl noted. All patients who received a single subcutaneous injection of 300 mg of guselkumab achieved a PASI 75 score, and about 80% achieved PASI 90, compared with none of the placebo group, she noted.

The third IL-23p19 inhibitor, tildrakizumab (MK-3222), also beat placebo at all doses tested in a three-part, randomized, placebo-controlled phase I trial, Dr. Riedl said. Furthermore, the histopathology of a subgroup of patients revealed significant decreases in lesions, compared with baseline, and a significant correlation between histopathologic and clinical scores, she noted. “In phase II, there was a significant response for all dosing cohorts, with a durable response to 52 weeks,” she added.

The primary safety concern for IL-23 inhibitors appears to be increased infection risk, although patients with genetic diseases connected to the IL-23/Th17 pathway already are at increased risk for infections such as candidiasis, mycobacteriosis, salmonellosis, and staphylococcal and Klebsiella infections, Dr. Riedl noted. “Ustekinumab targets IL-12/IL-23 and so far has shown a favorable safety profile,” she said, pointing to a 5-year follow-up study of the antibody that found no increase over time in adverse events and similar rates of adverse events among dosing groups.

Infections and headaches were the most commonly reported adverse events in phase I and II trials of targeted anti–IL-23p19 antibodies, Dr. Riedl said. In the phase I trial of BI 655066, rates of adverse events were similar for treatment and placebo except for nasopharyngitis, which affected 13% of the BI 655066 group and none of the placebo group, she noted. Guselkumab also was associated with similar rates of overall adverse events, compared with placebo, in its phase I trial, although 6 of 20 patients who received guselkumab developed infections, including two upper respiratory tract infections and one event each of bronchitis, folliculitis, viral gastroenteritis, herpes simplex infection, lower respiratory tract infection, vaginal infection, and nasopharyngitis, she said. Tildrakizumab was generally well tolerated in its phase IIb trial, she added. Serious adverse events that might have been related to treatment were rare but included bacterial arthritis, lymphedema, melanoma, stroke, epiglottitis, and knee infection.

Taken together, the data for IL-23p19 inhibitors are encouraging, according to Dr. Riedl. “The results suggest that selective inhibition of IL-23p19 is a promising target for novel therapies,” she said.

Dr. Riedl reported receiving grant support or serving as a consultant, advisory board member, or speakers bureau member for Abbvie, Celgen, Merck, Pfizer, and Janssen.

[email protected]

VANCOUVER, B.C. – So far, monoclonal antibodies that specifically target IL-23p19 are showing promise for treating chronic plaque psoriasis and are usually well tolerated, Dr. Elisabeth Riedl said at the World Congress of Dermatology.

The agents target the interleukin (IL)-23 cytokine, which is important in the induction of T-helper-17 cells in psoriasis and several other inflammatory disorders, said Dr. Riedl of the department of dermatology at Mount Sinai Hospital in New York. IL-23 has two subunits – p40, which it shares with IL-12, and p19, which is specific for IL-23, she said. Based on earlier research, the effectiveness of psoriasis treatments that target the p40 subunit seems to depend mostly on their ability to neutralize IL-23, not IL-12, she noted.

That observation helped spur several psoriasis trials of monoclonal antibodies that target IL-23p19, according to Dr. Riedl. Among the most promising of the monoclonal antibodies is BI 655066, which significantly outperformed placebo in a randomized, double-blind phase I trial reported earlier in 2015. At week 12, 87% of patients who received intravenous or oral BI65506 achieved a PASI (Psoriasis Area and Severity Index) 75 score, while 58% achieved a PASI 90 score and 16% achieved PASI 100, compared with none of the placebo group.

Another IL-23p19 inhibitor, guselkumab (CNTO 1959), beat placebo in a small randomized, double-blind phase I trial, Dr. Riedl noted. All patients who received a single subcutaneous injection of 300 mg of guselkumab achieved a PASI 75 score, and about 80% achieved PASI 90, compared with none of the placebo group, she noted.

The third IL-23p19 inhibitor, tildrakizumab (MK-3222), also beat placebo at all doses tested in a three-part, randomized, placebo-controlled phase I trial, Dr. Riedl said. Furthermore, the histopathology of a subgroup of patients revealed significant decreases in lesions, compared with baseline, and a significant correlation between histopathologic and clinical scores, she noted. “In phase II, there was a significant response for all dosing cohorts, with a durable response to 52 weeks,” she added.

The primary safety concern for IL-23 inhibitors appears to be increased infection risk, although patients with genetic diseases connected to the IL-23/Th17 pathway already are at increased risk for infections such as candidiasis, mycobacteriosis, salmonellosis, and staphylococcal and Klebsiella infections, Dr. Riedl noted. “Ustekinumab targets IL-12/IL-23 and so far has shown a favorable safety profile,” she said, pointing to a 5-year follow-up study of the antibody that found no increase over time in adverse events and similar rates of adverse events among dosing groups.

Infections and headaches were the most commonly reported adverse events in phase I and II trials of targeted anti–IL-23p19 antibodies, Dr. Riedl said. In the phase I trial of BI 655066, rates of adverse events were similar for treatment and placebo except for nasopharyngitis, which affected 13% of the BI 655066 group and none of the placebo group, she noted. Guselkumab also was associated with similar rates of overall adverse events, compared with placebo, in its phase I trial, although 6 of 20 patients who received guselkumab developed infections, including two upper respiratory tract infections and one event each of bronchitis, folliculitis, viral gastroenteritis, herpes simplex infection, lower respiratory tract infection, vaginal infection, and nasopharyngitis, she said. Tildrakizumab was generally well tolerated in its phase IIb trial, she added. Serious adverse events that might have been related to treatment were rare but included bacterial arthritis, lymphedema, melanoma, stroke, epiglottitis, and knee infection.

Taken together, the data for IL-23p19 inhibitors are encouraging, according to Dr. Riedl. “The results suggest that selective inhibition of IL-23p19 is a promising target for novel therapies,” she said.

Dr. Riedl reported receiving grant support or serving as a consultant, advisory board member, or speakers bureau member for Abbvie, Celgen, Merck, Pfizer, and Janssen.

[email protected]

VANCOUVER, B.C. – A simple mnemonic – Talk, Time, Training, and Tools – can help dermatologists optimize outcomes when facing “bad” scars after skin surgery, Dr. Evans Bailey said at the World Congress of Dermatology.

Cosmetically challenging wounds can occur because the patient is on anticoagulants or for other reasons that the clinician cannot control, noted Dr. Bailey, a dermatologist with the Surgical Dermatology Group in Birmingham, Ala. Managing these situations begins during the informed consent process, when dermatologists should educate patients about the procedure and set reasonable expectations for cosmetic outcomes, he said.

“When it comes to scars, the battle is won or lost before you do surgery,” he said. “If you tell patients beforehand, it’s an explanation. If you tell them afterward, it’s an excuse.”

When obtaining informed consent, Dr. Bailey uses a digital tablet to take presurgical photos and draw options for surgical repair, he said. “I let them hold the tablet and show them the possibilities, because sometimes the smallest spots turn out to be the biggest tumors.”

When a patient returns after surgery with a “bad” scar, “never show surprise!” Dr. Bailey emphasized. “Don’t give up. Don’t show surprise, but be compassionate and pull hard for your patient.” Continuing to talk with patients at this point is key, he said. He shows patients the preoperative photographs and explains why he chose the surgical approach. Then he verbally commits to sticking with the patient during the entire process of wound healing and repair. “Say, ‘don’t worry; this is all under control; this will take longer than we thought. But I will make sure everything heals well.’ ”

Besides talking extensively with patients, dermatologists it is important to allow time for the scar to fully mature and involute before they intervene, said Dr. Bailey. “Allow scars to repair themselves,” he said. “Do not jump in too quickly. The body is really quite dynamic and capable – often more capable than we are.”

It’s equally important to stick to the fundamental principles of skin surgery, no matter how formidable the wound, Dr. Bailey noted. “Remember your training,” he said. “Protect the free margin and redefine the cosmetic subunits.” Tacking or suspension sutures can be used to redefine the cosmetic subunit and eliminate or minimize tension across the tissue flap, leading to better cosmetic outcomes.

For scars that still need improvement, tools such as wire brush dermabrasion can be used for raised scars, and TCA CROSS (trichloroacetic acid chemical reconstruction of skin scars) for depressed scars, Dr. Bailey noted. Both techniques can dramatically improve the final appearance of the scar, he noted.

“But the enemy of good is better,” he said. “So at some point I say, ‘you’re done.’ ”

Dr. Bailey reported having no relevant conflicts of interest.

VANCOUVER, B.C. – A simple mnemonic – Talk, Time, Training, and Tools – can help dermatologists optimize outcomes when facing “bad” scars after skin surgery, Dr. Evans Bailey said at the World Congress of Dermatology.

Cosmetically challenging wounds can occur because the patient is on anticoagulants or for other reasons that the clinician cannot control, noted Dr. Bailey, a dermatologist with the Surgical Dermatology Group in Birmingham, Ala. Managing these situations begins during the informed consent process, when dermatologists should educate patients about the procedure and set reasonable expectations for cosmetic outcomes, he said.

“When it comes to scars, the battle is won or lost before you do surgery,” he said. “If you tell patients beforehand, it’s an explanation. If you tell them afterward, it’s an excuse.”

When obtaining informed consent, Dr. Bailey uses a digital tablet to take presurgical photos and draw options for surgical repair, he said. “I let them hold the tablet and show them the possibilities, because sometimes the smallest spots turn out to be the biggest tumors.”

When a patient returns after surgery with a “bad” scar, “never show surprise!” Dr. Bailey emphasized. “Don’t give up. Don’t show surprise, but be compassionate and pull hard for your patient.” Continuing to talk with patients at this point is key, he said. He shows patients the preoperative photographs and explains why he chose the surgical approach. Then he verbally commits to sticking with the patient during the entire process of wound healing and repair. “Say, ‘don’t worry; this is all under control; this will take longer than we thought. But I will make sure everything heals well.’ ”

Besides talking extensively with patients, dermatologists it is important to allow time for the scar to fully mature and involute before they intervene, said Dr. Bailey. “Allow scars to repair themselves,” he said. “Do not jump in too quickly. The body is really quite dynamic and capable – often more capable than we are.”

It’s equally important to stick to the fundamental principles of skin surgery, no matter how formidable the wound, Dr. Bailey noted. “Remember your training,” he said. “Protect the free margin and redefine the cosmetic subunits.” Tacking or suspension sutures can be used to redefine the cosmetic subunit and eliminate or minimize tension across the tissue flap, leading to better cosmetic outcomes.

For scars that still need improvement, tools such as wire brush dermabrasion can be used for raised scars, and TCA CROSS (trichloroacetic acid chemical reconstruction of skin scars) for depressed scars, Dr. Bailey noted. Both techniques can dramatically improve the final appearance of the scar, he noted.

“But the enemy of good is better,” he said. “So at some point I say, ‘you’re done.’ ”

Dr. Bailey reported having no relevant conflicts of interest.

VANCOUVER, B.C. – A simple mnemonic – Talk, Time, Training, and Tools – can help dermatologists optimize outcomes when facing “bad” scars after skin surgery, Dr. Evans Bailey said at the World Congress of Dermatology.

Cosmetically challenging wounds can occur because the patient is on anticoagulants or for other reasons that the clinician cannot control, noted Dr. Bailey, a dermatologist with the Surgical Dermatology Group in Birmingham, Ala. Managing these situations begins during the informed consent process, when dermatologists should educate patients about the procedure and set reasonable expectations for cosmetic outcomes, he said.

“When it comes to scars, the battle is won or lost before you do surgery,” he said. “If you tell patients beforehand, it’s an explanation. If you tell them afterward, it’s an excuse.”

When obtaining informed consent, Dr. Bailey uses a digital tablet to take presurgical photos and draw options for surgical repair, he said. “I let them hold the tablet and show them the possibilities, because sometimes the smallest spots turn out to be the biggest tumors.”

When a patient returns after surgery with a “bad” scar, “never show surprise!” Dr. Bailey emphasized. “Don’t give up. Don’t show surprise, but be compassionate and pull hard for your patient.” Continuing to talk with patients at this point is key, he said. He shows patients the preoperative photographs and explains why he chose the surgical approach. Then he verbally commits to sticking with the patient during the entire process of wound healing and repair. “Say, ‘don’t worry; this is all under control; this will take longer than we thought. But I will make sure everything heals well.’ ”

Besides talking extensively with patients, dermatologists it is important to allow time for the scar to fully mature and involute before they intervene, said Dr. Bailey. “Allow scars to repair themselves,” he said. “Do not jump in too quickly. The body is really quite dynamic and capable – often more capable than we are.”

It’s equally important to stick to the fundamental principles of skin surgery, no matter how formidable the wound, Dr. Bailey noted. “Remember your training,” he said. “Protect the free margin and redefine the cosmetic subunits.” Tacking or suspension sutures can be used to redefine the cosmetic subunit and eliminate or minimize tension across the tissue flap, leading to better cosmetic outcomes.

For scars that still need improvement, tools such as wire brush dermabrasion can be used for raised scars, and TCA CROSS (trichloroacetic acid chemical reconstruction of skin scars) for depressed scars, Dr. Bailey noted. Both techniques can dramatically improve the final appearance of the scar, he noted.

“But the enemy of good is better,” he said. “So at some point I say, ‘you’re done.’ ”

Dr. Bailey reported having no relevant conflicts of interest.

VANCOUVER, B.C. – Laser treatment can markedly improve the appearance of lentigines and nevi of Ota, although response is variable for most other benign pigmented lesions of the epidermis and dermis, Dr. Jason Rivers said at the World Congress of Dermatology.

“The best approach is to choose the device based on the location of pigment within the skin,” said Dr. Rivers, a dermatologist with Pacific Dermaesthetics in Vancouver. “Melanin has a fairly wide absorption spectrum, from the 400s down into the infrared spectrum. As we go further down into the infrared spectrum, we need to use higher fluencies, because we need to penetrate deeper into the skin.”

Q-switched 532-nm Nd:YAG laser is a good choice for facial lentigines, according to Dr. Rivers. “You can see marked improvement after one treatment, but you can be quite effective with various modalities,” he said. Intense pulsed light (IPL) therapy also can be effective for lentigines, including for patients with darker skin, although there is a risk of postinflammatory hyperpigmentation, he cautioned. Another option is 1,927 nm fractionated thulium fiber laser, he said. “Mopping up a lot of things at one time can be extremely effective, especially for lentigines on the face.”

For patients seeking removal of freckles, intense pulse light can clear a wide area of dyschromia in one session, Dr. Rivers continued. For mucosal melanosis, Q-switched lasers such as 532-nm frequency-doubled Nd:YAG, 694-nm ruby, or 755-nm alexandrite can be effective and are associated with minimal or no scarring, he added.

Café au lait patches typically respond well to combined treatment with 532-nm and 1,064-nm lasers, according to Dr. Rivers. A total of 10 treatment sessions spaced over 2-3 years has given him a durable response and without skin changes as a result of laser treatment, he said. However, some data indicate that café au lait patches might respond even better to Q-switched 755-nm alexandrite laser instead of conventional Q-switched lasers, he noted.

Becker’s nevus presents a much greater challenge. “Studies have looked at many kinds of lasers, and in all cases results may be suboptimal,” Dr. Rivers said. “For one of my patients with Becker’s nevus, I’ve basically thrown the kitchen sink at her, and we’re pretty much back to square one.” Q-switched 755-nm alexandrite laser can provide substantial clearing after 3 treatments in 4 weeks, but results might not be durable, he added. Laser therapy of nevus spilus also is “hit or miss,” although some studies suggest that Q-switched ruby laser is more effective than alexandrite for these lesions, he added.

Among the benign pigmented lesions of the dermis, nevus of Ota usually responds best to laser treatment, particularly with Q-switched 694-nm ruby or Q-switched 1,064-nm Nd:YAG, Dr. Rivers said. Data indicate that children younger than 10 years might have more superficially placed pigment cells that can be treated with lower fluence, such as 2.2 instead of 2.8 J, he noted.

Both congenital and acquired melanocytic nevi respond variably to laser therapy, Dr. Rivers said. For acquired lesions, options include Q-switched 532-nm, fully ablative carbon dioxide resurfacing, and continuous wave laser, he said. Long-pulsed alexandrite laser therapy can partiallyly clear congenital lesions after just one treatment session, and patients can then be given the option of fully ablative carbon dioxide resurfacing, he said.

Dermatologic laser therapy can, of course, cause adverse effects. The best treatment for laser-induced chrysiasis is prevention, but lesions can clear with Q-switched 1,064-nm laser treatment, Dr. Rivers said. Pigmentation might occur at the lesion margin, but fades with time, he noted.

Melanoma also has been reported as a consequence of dermatologic laser therapy. While sublethal laser damage can increase DNA damage in vitro, Q-switched ruby laser does not seem to induce genetic changes, Dr. Rivers said. In addition, some lesions were probably melanoma to begin with, he said, noting that failure to diagnose malignant melanoma is among the most common allegations in medical liability claims against dermatologists.

Dr. Rivers disclosed no relevant conflicts of interest.

VANCOUVER, B.C. – Laser treatment can markedly improve the appearance of lentigines and nevi of Ota, although response is variable for most other benign pigmented lesions of the epidermis and dermis, Dr. Jason Rivers said at the World Congress of Dermatology.

“The best approach is to choose the device based on the location of pigment within the skin,” said Dr. Rivers, a dermatologist with Pacific Dermaesthetics in Vancouver. “Melanin has a fairly wide absorption spectrum, from the 400s down into the infrared spectrum. As we go further down into the infrared spectrum, we need to use higher fluencies, because we need to penetrate deeper into the skin.”

Q-switched 532-nm Nd:YAG laser is a good choice for facial lentigines, according to Dr. Rivers. “You can see marked improvement after one treatment, but you can be quite effective with various modalities,” he said. Intense pulsed light (IPL) therapy also can be effective for lentigines, including for patients with darker skin, although there is a risk of postinflammatory hyperpigmentation, he cautioned. Another option is 1,927 nm fractionated thulium fiber laser, he said. “Mopping up a lot of things at one time can be extremely effective, especially for lentigines on the face.”

For patients seeking removal of freckles, intense pulse light can clear a wide area of dyschromia in one session, Dr. Rivers continued. For mucosal melanosis, Q-switched lasers such as 532-nm frequency-doubled Nd:YAG, 694-nm ruby, or 755-nm alexandrite can be effective and are associated with minimal or no scarring, he added.

Café au lait patches typically respond well to combined treatment with 532-nm and 1,064-nm lasers, according to Dr. Rivers. A total of 10 treatment sessions spaced over 2-3 years has given him a durable response and without skin changes as a result of laser treatment, he said. However, some data indicate that café au lait patches might respond even better to Q-switched 755-nm alexandrite laser instead of conventional Q-switched lasers, he noted.

Becker’s nevus presents a much greater challenge. “Studies have looked at many kinds of lasers, and in all cases results may be suboptimal,” Dr. Rivers said. “For one of my patients with Becker’s nevus, I’ve basically thrown the kitchen sink at her, and we’re pretty much back to square one.” Q-switched 755-nm alexandrite laser can provide substantial clearing after 3 treatments in 4 weeks, but results might not be durable, he added. Laser therapy of nevus spilus also is “hit or miss,” although some studies suggest that Q-switched ruby laser is more effective than alexandrite for these lesions, he added.

Among the benign pigmented lesions of the dermis, nevus of Ota usually responds best to laser treatment, particularly with Q-switched 694-nm ruby or Q-switched 1,064-nm Nd:YAG, Dr. Rivers said. Data indicate that children younger than 10 years might have more superficially placed pigment cells that can be treated with lower fluence, such as 2.2 instead of 2.8 J, he noted.

Both congenital and acquired melanocytic nevi respond variably to laser therapy, Dr. Rivers said. For acquired lesions, options include Q-switched 532-nm, fully ablative carbon dioxide resurfacing, and continuous wave laser, he said. Long-pulsed alexandrite laser therapy can partiallyly clear congenital lesions after just one treatment session, and patients can then be given the option of fully ablative carbon dioxide resurfacing, he said.

Dermatologic laser therapy can, of course, cause adverse effects. The best treatment for laser-induced chrysiasis is prevention, but lesions can clear with Q-switched 1,064-nm laser treatment, Dr. Rivers said. Pigmentation might occur at the lesion margin, but fades with time, he noted.

Melanoma also has been reported as a consequence of dermatologic laser therapy. While sublethal laser damage can increase DNA damage in vitro, Q-switched ruby laser does not seem to induce genetic changes, Dr. Rivers said. In addition, some lesions were probably melanoma to begin with, he said, noting that failure to diagnose malignant melanoma is among the most common allegations in medical liability claims against dermatologists.

Dr. Rivers disclosed no relevant conflicts of interest.

VANCOUVER, B.C. – Laser treatment can markedly improve the appearance of lentigines and nevi of Ota, although response is variable for most other benign pigmented lesions of the epidermis and dermis, Dr. Jason Rivers said at the World Congress of Dermatology.

“The best approach is to choose the device based on the location of pigment within the skin,” said Dr. Rivers, a dermatologist with Pacific Dermaesthetics in Vancouver. “Melanin has a fairly wide absorption spectrum, from the 400s down into the infrared spectrum. As we go further down into the infrared spectrum, we need to use higher fluencies, because we need to penetrate deeper into the skin.”

Q-switched 532-nm Nd:YAG laser is a good choice for facial lentigines, according to Dr. Rivers. “You can see marked improvement after one treatment, but you can be quite effective with various modalities,” he said. Intense pulsed light (IPL) therapy also can be effective for lentigines, including for patients with darker skin, although there is a risk of postinflammatory hyperpigmentation, he cautioned. Another option is 1,927 nm fractionated thulium fiber laser, he said. “Mopping up a lot of things at one time can be extremely effective, especially for lentigines on the face.”

For patients seeking removal of freckles, intense pulse light can clear a wide area of dyschromia in one session, Dr. Rivers continued. For mucosal melanosis, Q-switched lasers such as 532-nm frequency-doubled Nd:YAG, 694-nm ruby, or 755-nm alexandrite can be effective and are associated with minimal or no scarring, he added.

Café au lait patches typically respond well to combined treatment with 532-nm and 1,064-nm lasers, according to Dr. Rivers. A total of 10 treatment sessions spaced over 2-3 years has given him a durable response and without skin changes as a result of laser treatment, he said. However, some data indicate that café au lait patches might respond even better to Q-switched 755-nm alexandrite laser instead of conventional Q-switched lasers, he noted.

Becker’s nevus presents a much greater challenge. “Studies have looked at many kinds of lasers, and in all cases results may be suboptimal,” Dr. Rivers said. “For one of my patients with Becker’s nevus, I’ve basically thrown the kitchen sink at her, and we’re pretty much back to square one.” Q-switched 755-nm alexandrite laser can provide substantial clearing after 3 treatments in 4 weeks, but results might not be durable, he added. Laser therapy of nevus spilus also is “hit or miss,” although some studies suggest that Q-switched ruby laser is more effective than alexandrite for these lesions, he added.

Among the benign pigmented lesions of the dermis, nevus of Ota usually responds best to laser treatment, particularly with Q-switched 694-nm ruby or Q-switched 1,064-nm Nd:YAG, Dr. Rivers said. Data indicate that children younger than 10 years might have more superficially placed pigment cells that can be treated with lower fluence, such as 2.2 instead of 2.8 J, he noted.

Both congenital and acquired melanocytic nevi respond variably to laser therapy, Dr. Rivers said. For acquired lesions, options include Q-switched 532-nm, fully ablative carbon dioxide resurfacing, and continuous wave laser, he said. Long-pulsed alexandrite laser therapy can partiallyly clear congenital lesions after just one treatment session, and patients can then be given the option of fully ablative carbon dioxide resurfacing, he said.

Dermatologic laser therapy can, of course, cause adverse effects. The best treatment for laser-induced chrysiasis is prevention, but lesions can clear with Q-switched 1,064-nm laser treatment, Dr. Rivers said. Pigmentation might occur at the lesion margin, but fades with time, he noted.

Melanoma also has been reported as a consequence of dermatologic laser therapy. While sublethal laser damage can increase DNA damage in vitro, Q-switched ruby laser does not seem to induce genetic changes, Dr. Rivers said. In addition, some lesions were probably melanoma to begin with, he said, noting that failure to diagnose malignant melanoma is among the most common allegations in medical liability claims against dermatologists.

Dr. Rivers disclosed no relevant conflicts of interest.

VANCOUVER, B.C. – Ixekizumab-treated patients with plaque psoriasis reported markedly faster and larger improvements in itch severity than those on high-dose etanercept or placebo in a large head-to-head phase III randomized trial.

Ixekizumab is an investigational humanized IgG4 monoclonal antibody directed against the proinflammatory cytokines interleukin-17A. In the 1,224-patient phase III UNCOVER-2 trial, itch severity was rapidly reduced in ixekizumab-treated patients as early as week 1, when the first assessment occurred, Dr. Gil Yosipovitch reported at the World Congress of Dermatology.

Moreover, a clinically meaningful itch response – defined by Dr. Yosipovitch and coinvestigators as at least a 4-point drop from baseline on a 0-10 Itch Numeric Rating Scale based upon 24-hour recall – occurred in the ixekizumab-treated patients by week 4. Patients randomized to etanercept (Enbrel) at 50 mg twice per week never reached that bar during the 12-week study. Neither did the placebo-treated controls, noted Dr. Yosipovitch, professor and chairman of the department of dermatology at Temple University in Philadelphia.

The average baseline itch severity score in UNCOVER-2 was 6.6 points. The mean 12-week reduction in itch score was 0.4 points, or 14%, with placebo; 3.6 points, or 51%, with etanercept; 4.9 points, or 75%, with ixekizumab at 80 mg every 4 weeks; and 5.2 points, or 76%, with ixekizumab 80 mg every 2 weeks.

“The most important part of my presentation today is the rapid response to ixekizumab. There’s a significant reduction in itch in the first week and a 75% reduction at 12 weeks. I have to tell you, as someone who’s been in the itch field for a very long time, those are very impressive results,” the dermatologist declared. “Fast improvement is the issue, really. It we want a drug that claims to have an antipruritic effect, it has to work fast, because that’s what really bothers the patient.”

Another impressive statistic: 41% of ixekizumab-treated patients reported “no itching” at 12 weeks, compared with 17% on high-dose etanercept and 2% with placebo, he continued.

A recurring theme at WCD 2015, bolstered by an impressively large survey of North American and European dermatologists, rheumatologists, and patients, is that psoriasis patients feel itch hasn’t gotten the attention it deserves from physicians. Itch is the most common symptom of psoriasis, and more psoriasis patients rate itch as the most bothersome aspect of their chronic inflammatory skin disease than they do any other symptom, Dr. Yosipovitch noted.

Aside from this UNCOVER-2 analysis, very few data exist regarding the antipruritic effects of various biologic agents, he observed.

“I am very excited about this type of approach. Hopefully other companies wil now put more focus on itch. I think this is what the patients want, and if we can achieve fast responses, we are doing our job well,” the dermatologist said.

One audience member asked why the itch score is based upon recall over the previous 24 hours. Why not a week?

Dr. Yosipovitch replied that from other studies he’s done, he has found itch recall beyond 24 hours to be highly problematic.

“I actually recommend doing it twice a day, because itch is not constant throughout the day. It fluctuates. It is worst at nighttime, and that affects quality of life. In trials, I try to have patients keep a diary capturing itch evening and morning,” Dr. Yosipovitch said.

Another audience member asked whether a rapid response to itch might be a biomarker predictive of a later favorable response in terms of lesion size. If so, he continued, perhaps failure to experience a reduction in itch within the first week or so on an agent such a ixekizumab might be a signal to switch to another drug, rather than waiting for 4-8 weeks.

Dr. Yosipovitch replied that it’s an excellent thought and worthy of study, but the answer simply isn’t known yet.

The primary outcomes of UNCOVER-2 have previously been presented (Lancet 2015 June 10 [doi: 10.1016/S0140-6736(15)60125-8]). Briefly, the Psoriasis Area Severity Index (PASI) 75 response rate was 2% with placebo, 42% with etanercept, 78% with ixekizumab every 4 weeks, and 90% with ixekizumab every 2 weeks. When the bar was set higher – a PASI 100 – the response rate was 1% with placebo, 5% with etanercept, and 31% and 41% with ixekizumab every 4 and 2 weeks.

The UNCOVER-2 trial was sponsored by Eli Lilly. Dr. Yosipovitch is a recipient of research grants from and/or a consultant to Eli Lilly and roughly a dozen other pharmaceutical companies.

[email protected]

VANCOUVER, B.C. – Ixekizumab-treated patients with plaque psoriasis reported markedly faster and larger improvements in itch severity than those on high-dose etanercept or placebo in a large head-to-head phase III randomized trial.

Ixekizumab is an investigational humanized IgG4 monoclonal antibody directed against the proinflammatory cytokines interleukin-17A. In the 1,224-patient phase III UNCOVER-2 trial, itch severity was rapidly reduced in ixekizumab-treated patients as early as week 1, when the first assessment occurred, Dr. Gil Yosipovitch reported at the World Congress of Dermatology.

Moreover, a clinically meaningful itch response – defined by Dr. Yosipovitch and coinvestigators as at least a 4-point drop from baseline on a 0-10 Itch Numeric Rating Scale based upon 24-hour recall – occurred in the ixekizumab-treated patients by week 4. Patients randomized to etanercept (Enbrel) at 50 mg twice per week never reached that bar during the 12-week study. Neither did the placebo-treated controls, noted Dr. Yosipovitch, professor and chairman of the department of dermatology at Temple University in Philadelphia.

The average baseline itch severity score in UNCOVER-2 was 6.6 points. The mean 12-week reduction in itch score was 0.4 points, or 14%, with placebo; 3.6 points, or 51%, with etanercept; 4.9 points, or 75%, with ixekizumab at 80 mg every 4 weeks; and 5.2 points, or 76%, with ixekizumab 80 mg every 2 weeks.

“The most important part of my presentation today is the rapid response to ixekizumab. There’s a significant reduction in itch in the first week and a 75% reduction at 12 weeks. I have to tell you, as someone who’s been in the itch field for a very long time, those are very impressive results,” the dermatologist declared. “Fast improvement is the issue, really. It we want a drug that claims to have an antipruritic effect, it has to work fast, because that’s what really bothers the patient.”

Another impressive statistic: 41% of ixekizumab-treated patients reported “no itching” at 12 weeks, compared with 17% on high-dose etanercept and 2% with placebo, he continued.

A recurring theme at WCD 2015, bolstered by an impressively large survey of North American and European dermatologists, rheumatologists, and patients, is that psoriasis patients feel itch hasn’t gotten the attention it deserves from physicians. Itch is the most common symptom of psoriasis, and more psoriasis patients rate itch as the most bothersome aspect of their chronic inflammatory skin disease than they do any other symptom, Dr. Yosipovitch noted.

Aside from this UNCOVER-2 analysis, very few data exist regarding the antipruritic effects of various biologic agents, he observed.

“I am very excited about this type of approach. Hopefully other companies wil now put more focus on itch. I think this is what the patients want, and if we can achieve fast responses, we are doing our job well,” the dermatologist said.

One audience member asked why the itch score is based upon recall over the previous 24 hours. Why not a week?

Dr. Yosipovitch replied that from other studies he’s done, he has found itch recall beyond 24 hours to be highly problematic.

“I actually recommend doing it twice a day, because itch is not constant throughout the day. It fluctuates. It is worst at nighttime, and that affects quality of life. In trials, I try to have patients keep a diary capturing itch evening and morning,” Dr. Yosipovitch said.

Another audience member asked whether a rapid response to itch might be a biomarker predictive of a later favorable response in terms of lesion size. If so, he continued, perhaps failure to experience a reduction in itch within the first week or so on an agent such a ixekizumab might be a signal to switch to another drug, rather than waiting for 4-8 weeks.

Dr. Yosipovitch replied that it’s an excellent thought and worthy of study, but the answer simply isn’t known yet.

The primary outcomes of UNCOVER-2 have previously been presented (Lancet 2015 June 10 [doi: 10.1016/S0140-6736(15)60125-8]). Briefly, the Psoriasis Area Severity Index (PASI) 75 response rate was 2% with placebo, 42% with etanercept, 78% with ixekizumab every 4 weeks, and 90% with ixekizumab every 2 weeks. When the bar was set higher – a PASI 100 – the response rate was 1% with placebo, 5% with etanercept, and 31% and 41% with ixekizumab every 4 and 2 weeks.

The UNCOVER-2 trial was sponsored by Eli Lilly. Dr. Yosipovitch is a recipient of research grants from and/or a consultant to Eli Lilly and roughly a dozen other pharmaceutical companies.

[email protected]

VANCOUVER, B.C. – Ixekizumab-treated patients with plaque psoriasis reported markedly faster and larger improvements in itch severity than those on high-dose etanercept or placebo in a large head-to-head phase III randomized trial.

Ixekizumab is an investigational humanized IgG4 monoclonal antibody directed against the proinflammatory cytokines interleukin-17A. In the 1,224-patient phase III UNCOVER-2 trial, itch severity was rapidly reduced in ixekizumab-treated patients as early as week 1, when the first assessment occurred, Dr. Gil Yosipovitch reported at the World Congress of Dermatology.

Moreover, a clinically meaningful itch response – defined by Dr. Yosipovitch and coinvestigators as at least a 4-point drop from baseline on a 0-10 Itch Numeric Rating Scale based upon 24-hour recall – occurred in the ixekizumab-treated patients by week 4. Patients randomized to etanercept (Enbrel) at 50 mg twice per week never reached that bar during the 12-week study. Neither did the placebo-treated controls, noted Dr. Yosipovitch, professor and chairman of the department of dermatology at Temple University in Philadelphia.

The average baseline itch severity score in UNCOVER-2 was 6.6 points. The mean 12-week reduction in itch score was 0.4 points, or 14%, with placebo; 3.6 points, or 51%, with etanercept; 4.9 points, or 75%, with ixekizumab at 80 mg every 4 weeks; and 5.2 points, or 76%, with ixekizumab 80 mg every 2 weeks.

“The most important part of my presentation today is the rapid response to ixekizumab. There’s a significant reduction in itch in the first week and a 75% reduction at 12 weeks. I have to tell you, as someone who’s been in the itch field for a very long time, those are very impressive results,” the dermatologist declared. “Fast improvement is the issue, really. It we want a drug that claims to have an antipruritic effect, it has to work fast, because that’s what really bothers the patient.”

Another impressive statistic: 41% of ixekizumab-treated patients reported “no itching” at 12 weeks, compared with 17% on high-dose etanercept and 2% with placebo, he continued.

A recurring theme at WCD 2015, bolstered by an impressively large survey of North American and European dermatologists, rheumatologists, and patients, is that psoriasis patients feel itch hasn’t gotten the attention it deserves from physicians. Itch is the most common symptom of psoriasis, and more psoriasis patients rate itch as the most bothersome aspect of their chronic inflammatory skin disease than they do any other symptom, Dr. Yosipovitch noted.

Aside from this UNCOVER-2 analysis, very few data exist regarding the antipruritic effects of various biologic agents, he observed.

“I am very excited about this type of approach. Hopefully other companies wil now put more focus on itch. I think this is what the patients want, and if we can achieve fast responses, we are doing our job well,” the dermatologist said.

One audience member asked why the itch score is based upon recall over the previous 24 hours. Why not a week?

Dr. Yosipovitch replied that from other studies he’s done, he has found itch recall beyond 24 hours to be highly problematic.

“I actually recommend doing it twice a day, because itch is not constant throughout the day. It fluctuates. It is worst at nighttime, and that affects quality of life. In trials, I try to have patients keep a diary capturing itch evening and morning,” Dr. Yosipovitch said.

Another audience member asked whether a rapid response to itch might be a biomarker predictive of a later favorable response in terms of lesion size. If so, he continued, perhaps failure to experience a reduction in itch within the first week or so on an agent such a ixekizumab might be a signal to switch to another drug, rather than waiting for 4-8 weeks.

Dr. Yosipovitch replied that it’s an excellent thought and worthy of study, but the answer simply isn’t known yet.

The primary outcomes of UNCOVER-2 have previously been presented (Lancet 2015 June 10 [doi: 10.1016/S0140-6736(15)60125-8]). Briefly, the Psoriasis Area Severity Index (PASI) 75 response rate was 2% with placebo, 42% with etanercept, 78% with ixekizumab every 4 weeks, and 90% with ixekizumab every 2 weeks. When the bar was set higher – a PASI 100 – the response rate was 1% with placebo, 5% with etanercept, and 31% and 41% with ixekizumab every 4 and 2 weeks.

The UNCOVER-2 trial was sponsored by Eli Lilly. Dr. Yosipovitch is a recipient of research grants from and/or a consultant to Eli Lilly and roughly a dozen other pharmaceutical companies.

[email protected]

VANCOUVER, B.C. – In the first head-to-head trial in atopic dermatitis, cyclosporine was about five times more effective in terms of SCORAD 50 but was associated with more adverse events, Dr. Catherine Goujon-Henry reported at the World Congress of Dermatology.

Based on the findings, dermatologists should consider treating AD patients with a relatively high dose of methotrexate, such as 15 mg weekly, or first stabilize flaring patients with cyclosporine and then switch them to methotrexate for long-term disease control, said Dr. Goujon-Henry, who is with the Clinical Research Unit in Immunology at Lyon-Sud Hospital in Lyon, France.

Methotrexate is recommended in atopic dermatitis but has never been directly compared with cyclosporine, Dr. Goujon-Henry noted. For the study, she and her colleagues randomized 97 adults with moderate to severe AD to 8 weeks of treatment with either methotrexate at 15 mg per week or cyclosporine at 2.5 mg per kg per day. Patients only were allowed to use topical glucocorticoids or tacrolimus during the first month of the trial.

Only 8% of the methotrexate group achieved SCORAD 50 by week 8, compared with 42% of cyclosporine patients, Dr. Goujon-Henry reported. Furthermore, only 35% of the methotrexate group achieved EASI 50 compared with 68% of the cyclosporine group, she said. In addition, Dermatology Life Quality Index (DLQI) scores were 5 or less for only 37% of methotrexate patients, compared with 56% of cyclosporine patients, she reported.

The protocol called for increasing the methotrexate dose to 25 mg per week and the cyclosporine dose to 5 mg per kg per day for patients who did not achieve SCORAD 50 by week 8. Dose increases were performed for 74% of the methotrexate group and for 58% of the cyclosporine group, Dr. Goujon-Henry said. At week 12, 15 of the 50 methotrexate patients were considered non-responders and went off study, as did three cyclosporine patients. At this point, 43% of the methotrexate patients who remained on study had achieved SCORAD 50, as had 62% of cyclosporine patients.

Also at week 16, two-thirds of methotrexate patients and 79% of cyclosporine patients had achieved EASI 50, and 61% of methotrexate patients and 77% of cyclosporine patients scored 5 or less on the DLQI, Dr. Goujon-Henry reported. However, about 53% of cyclosporine patients experienced drug-related adverse events, compared with 40% of the methotrexate group, she said. Serious adverse events that led to treatment discontinuation included arterial hypertension and hypertrichosis for the cyclosporine group, and lymphopenia and hepatitis for the methotrexate group, she reported.

Taken together, the findings support using methotrexate as first-line therapy for moderate to severe atopic dermatitis, but patients need to expect a slower treatment response in exchange for the better safety profile, Dr. Goujon-Henry said.

She disclosed no relevant conflicts of interest.

VANCOUVER, B.C. – In the first head-to-head trial in atopic dermatitis, cyclosporine was about five times more effective in terms of SCORAD 50 but was associated with more adverse events, Dr. Catherine Goujon-Henry reported at the World Congress of Dermatology.

Based on the findings, dermatologists should consider treating AD patients with a relatively high dose of methotrexate, such as 15 mg weekly, or first stabilize flaring patients with cyclosporine and then switch them to methotrexate for long-term disease control, said Dr. Goujon-Henry, who is with the Clinical Research Unit in Immunology at Lyon-Sud Hospital in Lyon, France.

Methotrexate is recommended in atopic dermatitis but has never been directly compared with cyclosporine, Dr. Goujon-Henry noted. For the study, she and her colleagues randomized 97 adults with moderate to severe AD to 8 weeks of treatment with either methotrexate at 15 mg per week or cyclosporine at 2.5 mg per kg per day. Patients only were allowed to use topical glucocorticoids or tacrolimus during the first month of the trial.

Only 8% of the methotrexate group achieved SCORAD 50 by week 8, compared with 42% of cyclosporine patients, Dr. Goujon-Henry reported. Furthermore, only 35% of the methotrexate group achieved EASI 50 compared with 68% of the cyclosporine group, she said. In addition, Dermatology Life Quality Index (DLQI) scores were 5 or less for only 37% of methotrexate patients, compared with 56% of cyclosporine patients, she reported.

The protocol called for increasing the methotrexate dose to 25 mg per week and the cyclosporine dose to 5 mg per kg per day for patients who did not achieve SCORAD 50 by week 8. Dose increases were performed for 74% of the methotrexate group and for 58% of the cyclosporine group, Dr. Goujon-Henry said. At week 12, 15 of the 50 methotrexate patients were considered non-responders and went off study, as did three cyclosporine patients. At this point, 43% of the methotrexate patients who remained on study had achieved SCORAD 50, as had 62% of cyclosporine patients.

Also at week 16, two-thirds of methotrexate patients and 79% of cyclosporine patients had achieved EASI 50, and 61% of methotrexate patients and 77% of cyclosporine patients scored 5 or less on the DLQI, Dr. Goujon-Henry reported. However, about 53% of cyclosporine patients experienced drug-related adverse events, compared with 40% of the methotrexate group, she said. Serious adverse events that led to treatment discontinuation included arterial hypertension and hypertrichosis for the cyclosporine group, and lymphopenia and hepatitis for the methotrexate group, she reported.

Taken together, the findings support using methotrexate as first-line therapy for moderate to severe atopic dermatitis, but patients need to expect a slower treatment response in exchange for the better safety profile, Dr. Goujon-Henry said.

She disclosed no relevant conflicts of interest.

VANCOUVER, B.C. – In the first head-to-head trial in atopic dermatitis, cyclosporine was about five times more effective in terms of SCORAD 50 but was associated with more adverse events, Dr. Catherine Goujon-Henry reported at the World Congress of Dermatology.

Based on the findings, dermatologists should consider treating AD patients with a relatively high dose of methotrexate, such as 15 mg weekly, or first stabilize flaring patients with cyclosporine and then switch them to methotrexate for long-term disease control, said Dr. Goujon-Henry, who is with the Clinical Research Unit in Immunology at Lyon-Sud Hospital in Lyon, France.

Methotrexate is recommended in atopic dermatitis but has never been directly compared with cyclosporine, Dr. Goujon-Henry noted. For the study, she and her colleagues randomized 97 adults with moderate to severe AD to 8 weeks of treatment with either methotrexate at 15 mg per week or cyclosporine at 2.5 mg per kg per day. Patients only were allowed to use topical glucocorticoids or tacrolimus during the first month of the trial.

Only 8% of the methotrexate group achieved SCORAD 50 by week 8, compared with 42% of cyclosporine patients, Dr. Goujon-Henry reported. Furthermore, only 35% of the methotrexate group achieved EASI 50 compared with 68% of the cyclosporine group, she said. In addition, Dermatology Life Quality Index (DLQI) scores were 5 or less for only 37% of methotrexate patients, compared with 56% of cyclosporine patients, she reported.

The protocol called for increasing the methotrexate dose to 25 mg per week and the cyclosporine dose to 5 mg per kg per day for patients who did not achieve SCORAD 50 by week 8. Dose increases were performed for 74% of the methotrexate group and for 58% of the cyclosporine group, Dr. Goujon-Henry said. At week 12, 15 of the 50 methotrexate patients were considered non-responders and went off study, as did three cyclosporine patients. At this point, 43% of the methotrexate patients who remained on study had achieved SCORAD 50, as had 62% of cyclosporine patients.

Also at week 16, two-thirds of methotrexate patients and 79% of cyclosporine patients had achieved EASI 50, and 61% of methotrexate patients and 77% of cyclosporine patients scored 5 or less on the DLQI, Dr. Goujon-Henry reported. However, about 53% of cyclosporine patients experienced drug-related adverse events, compared with 40% of the methotrexate group, she said. Serious adverse events that led to treatment discontinuation included arterial hypertension and hypertrichosis for the cyclosporine group, and lymphopenia and hepatitis for the methotrexate group, she reported.

Taken together, the findings support using methotrexate as first-line therapy for moderate to severe atopic dermatitis, but patients need to expect a slower treatment response in exchange for the better safety profile, Dr. Goujon-Henry said.

She disclosed no relevant conflicts of interest.

VANCOUVER, B.C. – Amgen’s recent announcement that it is pulling the plug on further development of the investigational interleukin-17 receptor A inhibitor brodalumab was the red hot topic among psoriasis experts at the World Congress of Dermatology.

The biologic agent had seemingly been breezing through phase III clinical trials, racking up head-turning efficacy and reasonable safety numbers in a series of very large randomized studies conducted in patients with moderate-to-severe chronic plaque psoriasis. Then came the surprise announcement a scant couple of weeks before WCD 2015.

Brodalumab was also in codevelopment by Amgen and AstraZeneca for psoriatic arthritis and axial spondyloarthritis. Amgen is halting all participation in those research projects as well.

The company’s decision was based upon preliminary indications from the Food and Drug Administration that, as a condition for marketing approval, there would likely need to be restrictive labeling calling for physician monitoring for suicidality, something few dermatologists or rheumatologists are comfortable with.

“During our preparation process for regulatory submissions, we came to believe that labeling requirements likely would limit the appropriate patient population for brodalumab,” Dr. Sean E. Harper, executive vice president of research and development at Amgen, said in the company’s announcement.

AstraZeneca officials said in a separate statement that they will review all the brodalumab data in detail and make a decision as soon as possible regarding whether to pursue unilateral development of the biologic agent.

Dr. Richard G. Langley, who at WCD 2015 presented the results of the AMAGINE-3 trial – 1,881 psoriasis patients randomized to ustekinumab (Stelara) at the approved dosing, placebo, or brodalumab at either 140 mg or 210 mg subcutaneously – noted that rates of depression and suicidal ideation were similarly low in the ustekinumab and brodalumab groups during the 52-week study, and there were no suicide attempts.

The problem for Amgen was a single-digit numeric imbalance in these adverse events in some of the earlier, considerably smaller studies of brodalumab, according to Dr. Langley, professor of dermatology at Dalhousie University in Halifax, Nova Scotia.

“We have to remember that we can sometimes make spurious assumptions about rare events and perhaps cast a shadow on a pathway or molecule before we have full information,” he said diplomatically. “The Amgen decision is particularly unfortunate for patients because with brodalumab the only patients I’ve had who were depressed were the ones I’ve told are now no longer going to get the medication.”

Session chair Dr. Yves Poulin of Laval University in Quebec City, Quebec, said his experience has been similar: Patients love the unprecedented effectiveness of brodalumab and are crestfallen at learning they have to go off it.

Indeed, in AMAGINE-3, the 12-week PASI 75 rate among patients on brodalumab at 210 mg every 2 weeks – the more effective dose of the IL-17A inhibitor – was 85.1%, compared with 69.2% for ustekinumab, which is one of the most widely prescribed biologics. The PASI 100 rate was 36.7% for brodalumab, twice the 18.5% rate with ustekinumab. And the Investigator’s Global Assessment rating of 0 or 1 – clear or almost clear – was 79.6% with brodalumab, compared with 59% for ustekinumab, Dr. Langley reported.

“A consistent finding with brodalumab and the other IL-17 inhibitors is the remarkably fast improvement: within the first 2-4 weeks there’s a robust response,” he added.

Elsewhere at WCD 2015, Dr. Alan Menter presented the findings of the AMAGINE-2 trial, an 1,831-patient study identical in design to AMAGINE-3. The efficacy and safety results were virtually the same as in AMAGINE-3 as well, both in the 12-week induction phase and out to 52 weeks.

“We have a major issue that I think people haven’t understood well over the years relating to depression and psoriasis. Suicidal ideation has always been an issue. If you’re a 25-year-old and you’re trying to make your way in life and you’ve got significant psoriasis, you’re going to get depressed. But the suicidal ideation is twice as high in young people with psoriasis at baseline than in all the other autoimmune diseases put together,” said Dr. Menter, chair of dermatology at Baylor University Medical Center, Dallas, and the founding president of the International Psoriasis Council.

There has been no suicidality signal with secukinumab (Cosentyx), which in January became the first and, to date, only IL-17 inhibitor approved for marketing, nor with ixekizumab, which is in phase III clinical trials. There are distinct differences between the IL-17 inhibitor molecules – for example, brodalumab is IgG2, secukinumab is IgG1, and ixekizumab is IgG4. And brodalumab is a receptor antibody that not only inhibits the activity of IL-17A, but of IL-17F and -E as well, whereas secukinumab and ixekizumab work by other mechanisms. Investigators are now taking a close look at these differences to see if they have effects in terms of clinical outcomes and side effect profiles, he said.

Dr. Langley and Dr. Menter reported having financial relationships with Amgen and numerous other pharmaceutical companies.

[email protected]

VANCOUVER, B.C. – Amgen’s recent announcement that it is pulling the plug on further development of the investigational interleukin-17 receptor A inhibitor brodalumab was the red hot topic among psoriasis experts at the World Congress of Dermatology.

The biologic agent had seemingly been breezing through phase III clinical trials, racking up head-turning efficacy and reasonable safety numbers in a series of very large randomized studies conducted in patients with moderate-to-severe chronic plaque psoriasis. Then came the surprise announcement a scant couple of weeks before WCD 2015.

Brodalumab was also in codevelopment by Amgen and AstraZeneca for psoriatic arthritis and axial spondyloarthritis. Amgen is halting all participation in those research projects as well.

The company’s decision was based upon preliminary indications from the Food and Drug Administration that, as a condition for marketing approval, there would likely need to be restrictive labeling calling for physician monitoring for suicidality, something few dermatologists or rheumatologists are comfortable with.

“During our preparation process for regulatory submissions, we came to believe that labeling requirements likely would limit the appropriate patient population for brodalumab,” Dr. Sean E. Harper, executive vice president of research and development at Amgen, said in the company’s announcement.

AstraZeneca officials said in a separate statement that they will review all the brodalumab data in detail and make a decision as soon as possible regarding whether to pursue unilateral development of the biologic agent.

Dr. Richard G. Langley, who at WCD 2015 presented the results of the AMAGINE-3 trial – 1,881 psoriasis patients randomized to ustekinumab (Stelara) at the approved dosing, placebo, or brodalumab at either 140 mg or 210 mg subcutaneously – noted that rates of depression and suicidal ideation were similarly low in the ustekinumab and brodalumab groups during the 52-week study, and there were no suicide attempts.

The problem for Amgen was a single-digit numeric imbalance in these adverse events in some of the earlier, considerably smaller studies of brodalumab, according to Dr. Langley, professor of dermatology at Dalhousie University in Halifax, Nova Scotia.

“We have to remember that we can sometimes make spurious assumptions about rare events and perhaps cast a shadow on a pathway or molecule before we have full information,” he said diplomatically. “The Amgen decision is particularly unfortunate for patients because with brodalumab the only patients I’ve had who were depressed were the ones I’ve told are now no longer going to get the medication.”

Session chair Dr. Yves Poulin of Laval University in Quebec City, Quebec, said his experience has been similar: Patients love the unprecedented effectiveness of brodalumab and are crestfallen at learning they have to go off it.

Indeed, in AMAGINE-3, the 12-week PASI 75 rate among patients on brodalumab at 210 mg every 2 weeks – the more effective dose of the IL-17A inhibitor – was 85.1%, compared with 69.2% for ustekinumab, which is one of the most widely prescribed biologics. The PASI 100 rate was 36.7% for brodalumab, twice the 18.5% rate with ustekinumab. And the Investigator’s Global Assessment rating of 0 or 1 – clear or almost clear – was 79.6% with brodalumab, compared with 59% for ustekinumab, Dr. Langley reported.

“A consistent finding with brodalumab and the other IL-17 inhibitors is the remarkably fast improvement: within the first 2-4 weeks there’s a robust response,” he added.

Elsewhere at WCD 2015, Dr. Alan Menter presented the findings of the AMAGINE-2 trial, an 1,831-patient study identical in design to AMAGINE-3. The efficacy and safety results were virtually the same as in AMAGINE-3 as well, both in the 12-week induction phase and out to 52 weeks.

“We have a major issue that I think people haven’t understood well over the years relating to depression and psoriasis. Suicidal ideation has always been an issue. If you’re a 25-year-old and you’re trying to make your way in life and you’ve got significant psoriasis, you’re going to get depressed. But the suicidal ideation is twice as high in young people with psoriasis at baseline than in all the other autoimmune diseases put together,” said Dr. Menter, chair of dermatology at Baylor University Medical Center, Dallas, and the founding president of the International Psoriasis Council.

There has been no suicidality signal with secukinumab (Cosentyx), which in January became the first and, to date, only IL-17 inhibitor approved for marketing, nor with ixekizumab, which is in phase III clinical trials. There are distinct differences between the IL-17 inhibitor molecules – for example, brodalumab is IgG2, secukinumab is IgG1, and ixekizumab is IgG4. And brodalumab is a receptor antibody that not only inhibits the activity of IL-17A, but of IL-17F and -E as well, whereas secukinumab and ixekizumab work by other mechanisms. Investigators are now taking a close look at these differences to see if they have effects in terms of clinical outcomes and side effect profiles, he said.

Dr. Langley and Dr. Menter reported having financial relationships with Amgen and numerous other pharmaceutical companies.

[email protected]

VANCOUVER, B.C. – Amgen’s recent announcement that it is pulling the plug on further development of the investigational interleukin-17 receptor A inhibitor brodalumab was the red hot topic among psoriasis experts at the World Congress of Dermatology.

The biologic agent had seemingly been breezing through phase III clinical trials, racking up head-turning efficacy and reasonable safety numbers in a series of very large randomized studies conducted in patients with moderate-to-severe chronic plaque psoriasis. Then came the surprise announcement a scant couple of weeks before WCD 2015.

Brodalumab was also in codevelopment by Amgen and AstraZeneca for psoriatic arthritis and axial spondyloarthritis. Amgen is halting all participation in those research projects as well.

The company’s decision was based upon preliminary indications from the Food and Drug Administration that, as a condition for marketing approval, there would likely need to be restrictive labeling calling for physician monitoring for suicidality, something few dermatologists or rheumatologists are comfortable with.

“During our preparation process for regulatory submissions, we came to believe that labeling requirements likely would limit the appropriate patient population for brodalumab,” Dr. Sean E. Harper, executive vice president of research and development at Amgen, said in the company’s announcement.

AstraZeneca officials said in a separate statement that they will review all the brodalumab data in detail and make a decision as soon as possible regarding whether to pursue unilateral development of the biologic agent.

Dr. Richard G. Langley, who at WCD 2015 presented the results of the AMAGINE-3 trial – 1,881 psoriasis patients randomized to ustekinumab (Stelara) at the approved dosing, placebo, or brodalumab at either 140 mg or 210 mg subcutaneously – noted that rates of depression and suicidal ideation were similarly low in the ustekinumab and brodalumab groups during the 52-week study, and there were no suicide attempts.

The problem for Amgen was a single-digit numeric imbalance in these adverse events in some of the earlier, considerably smaller studies of brodalumab, according to Dr. Langley, professor of dermatology at Dalhousie University in Halifax, Nova Scotia.

“We have to remember that we can sometimes make spurious assumptions about rare events and perhaps cast a shadow on a pathway or molecule before we have full information,” he said diplomatically. “The Amgen decision is particularly unfortunate for patients because with brodalumab the only patients I’ve had who were depressed were the ones I’ve told are now no longer going to get the medication.”

Session chair Dr. Yves Poulin of Laval University in Quebec City, Quebec, said his experience has been similar: Patients love the unprecedented effectiveness of brodalumab and are crestfallen at learning they have to go off it.

Indeed, in AMAGINE-3, the 12-week PASI 75 rate among patients on brodalumab at 210 mg every 2 weeks – the more effective dose of the IL-17A inhibitor – was 85.1%, compared with 69.2% for ustekinumab, which is one of the most widely prescribed biologics. The PASI 100 rate was 36.7% for brodalumab, twice the 18.5% rate with ustekinumab. And the Investigator’s Global Assessment rating of 0 or 1 – clear or almost clear – was 79.6% with brodalumab, compared with 59% for ustekinumab, Dr. Langley reported.

“A consistent finding with brodalumab and the other IL-17 inhibitors is the remarkably fast improvement: within the first 2-4 weeks there’s a robust response,” he added.

Elsewhere at WCD 2015, Dr. Alan Menter presented the findings of the AMAGINE-2 trial, an 1,831-patient study identical in design to AMAGINE-3. The efficacy and safety results were virtually the same as in AMAGINE-3 as well, both in the 12-week induction phase and out to 52 weeks.

“We have a major issue that I think people haven’t understood well over the years relating to depression and psoriasis. Suicidal ideation has always been an issue. If you’re a 25-year-old and you’re trying to make your way in life and you’ve got significant psoriasis, you’re going to get depressed. But the suicidal ideation is twice as high in young people with psoriasis at baseline than in all the other autoimmune diseases put together,” said Dr. Menter, chair of dermatology at Baylor University Medical Center, Dallas, and the founding president of the International Psoriasis Council.

There has been no suicidality signal with secukinumab (Cosentyx), which in January became the first and, to date, only IL-17 inhibitor approved for marketing, nor with ixekizumab, which is in phase III clinical trials. There are distinct differences between the IL-17 inhibitor molecules – for example, brodalumab is IgG2, secukinumab is IgG1, and ixekizumab is IgG4. And brodalumab is a receptor antibody that not only inhibits the activity of IL-17A, but of IL-17F and -E as well, whereas secukinumab and ixekizumab work by other mechanisms. Investigators are now taking a close look at these differences to see if they have effects in terms of clinical outcomes and side effect profiles, he said.

Dr. Langley and Dr. Menter reported having financial relationships with Amgen and numerous other pharmaceutical companies.

[email protected]