IL-23 Inhibition as a Key Component in Psoriasis Treatment is Here to Stay
Prof Elke de Jong focussed her presentation on data from randomised clinical trials (RCT) and real-world evidence (RWE) from psoriasis patient registries. Such data is complementary with RCT having high internal validity but low external validity, and RWE having low internal validity but high extern...
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description | Prof Elke de Jong focussed her presentation on data from randomised clinical trials (RCT) and real-world evidence (RWE) from psoriasis patient registries. Such data is complementary with RCT having high internal validity but low external validity, and RWE having low internal validity but high external validity. She reviewed the predictors for stopping psoriasis biological treatment of high BMI and female sex and predictors for continuing treatment as concurrent psoriatic arthritis.
Current unmet needs in psoriasis that demonstrate the requirement for additional treatments include patients experiencing psoriasis for roughly 20 years before being prescribed biologics, prevention of damage (e.g., psoriatic arthritis), achieving sustained effectiveness or cure, developing better patient-reported outcome measures, and better treatment of specific psoriatic areas (scalp, face, nails, and genitalia).
Dr Andreas Pinter reviewed the role played by IL-23, IL-17A, and IL-22 in psoriasis, and new agents including ustekinumab blocking both IL-12 and IL-23; guselkumab, tildrakizumab, and risankizumab blocking IL-23; and brodalumab blocking IL-17A.
He explored VOYAGE 1 data that showed that the IL-23 inhibitor guselkumab maintained Psoriasis Area and Severity Index (PASI) 90 response through Week 156 in >80% of patients. Furthermore, VOYAGE 2 results showed PASI 90 response was maintained in >50% of patients 6 months after guselkumab withdrawal.
He demonstrated how re-treatment with guselkumab led to a high PASI 90 response in patients who lost PASI 90 response after withdrawal of treatment. Data from the VOYAGE 1 study further showed that guselkumab produced statistically significant improvements in scalp and palmar plantar scores over adalimumab, and comparable nail scores to adalimumab.
Data from the UltlMMa-1 and ULtlMMa-2 studies showed that IL-23 inhibition with risankizumab produced better quality of life scores than with ustekinumab. Additionally, the ECLIPSE trial showed that IL-23 inhibition with guselkumab produced higher PASI 90 response rates than IL-17 inhibition with secukinumab at Week 48. |
doi_str_mv | 10.33590/emjdermatol/10313052 |
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Current unmet needs in psoriasis that demonstrate the requirement for additional treatments include patients experiencing psoriasis for roughly 20 years before being prescribed biologics, prevention of damage (e.g., psoriatic arthritis), achieving sustained effectiveness or cure, developing better patient-reported outcome measures, and better treatment of specific psoriatic areas (scalp, face, nails, and genitalia).
Dr Andreas Pinter reviewed the role played by IL-23, IL-17A, and IL-22 in psoriasis, and new agents including ustekinumab blocking both IL-12 and IL-23; guselkumab, tildrakizumab, and risankizumab blocking IL-23; and brodalumab blocking IL-17A.
He explored VOYAGE 1 data that showed that the IL-23 inhibitor guselkumab maintained Psoriasis Area and Severity Index (PASI) 90 response through Week 156 in >80% of patients. Furthermore, VOYAGE 2 results showed PASI 90 response was maintained in >50% of patients 6 months after guselkumab withdrawal.
He demonstrated how re-treatment with guselkumab led to a high PASI 90 response in patients who lost PASI 90 response after withdrawal of treatment. Data from the VOYAGE 1 study further showed that guselkumab produced statistically significant improvements in scalp and palmar plantar scores over adalimumab, and comparable nail scores to adalimumab.
Data from the UltlMMa-1 and ULtlMMa-2 studies showed that IL-23 inhibition with risankizumab produced better quality of life scores than with ustekinumab. Additionally, the ECLIPSE trial showed that IL-23 inhibition with guselkumab produced higher PASI 90 response rates than IL-17 inhibition with secukinumab at Week 48.</description><identifier>ISSN: 2054-6211</identifier><identifier>EISSN: 2054-6211</identifier><identifier>DOI: 10.33590/emjdermatol/10313052</identifier><language>eng</language><ispartof>European medical journal. Dermatology, 2019-09, p.2-11</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c932-86572085c1e15b100f4ef6b4f843d1cdb319d83eaf4d7e2d949d8cbb8fb325f93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,27924,27925</link.rule.ids></links><search><creatorcontrib>Fricker, Janet</creatorcontrib><title>IL-23 Inhibition as a Key Component in Psoriasis Treatment is Here to Stay</title><title>European medical journal. Dermatology</title><description>Prof Elke de Jong focussed her presentation on data from randomised clinical trials (RCT) and real-world evidence (RWE) from psoriasis patient registries. Such data is complementary with RCT having high internal validity but low external validity, and RWE having low internal validity but high external validity. She reviewed the predictors for stopping psoriasis biological treatment of high BMI and female sex and predictors for continuing treatment as concurrent psoriatic arthritis.
Current unmet needs in psoriasis that demonstrate the requirement for additional treatments include patients experiencing psoriasis for roughly 20 years before being prescribed biologics, prevention of damage (e.g., psoriatic arthritis), achieving sustained effectiveness or cure, developing better patient-reported outcome measures, and better treatment of specific psoriatic areas (scalp, face, nails, and genitalia).
Dr Andreas Pinter reviewed the role played by IL-23, IL-17A, and IL-22 in psoriasis, and new agents including ustekinumab blocking both IL-12 and IL-23; guselkumab, tildrakizumab, and risankizumab blocking IL-23; and brodalumab blocking IL-17A.
He explored VOYAGE 1 data that showed that the IL-23 inhibitor guselkumab maintained Psoriasis Area and Severity Index (PASI) 90 response through Week 156 in >80% of patients. Furthermore, VOYAGE 2 results showed PASI 90 response was maintained in >50% of patients 6 months after guselkumab withdrawal.
He demonstrated how re-treatment with guselkumab led to a high PASI 90 response in patients who lost PASI 90 response after withdrawal of treatment. Data from the VOYAGE 1 study further showed that guselkumab produced statistically significant improvements in scalp and palmar plantar scores over adalimumab, and comparable nail scores to adalimumab.
Data from the UltlMMa-1 and ULtlMMa-2 studies showed that IL-23 inhibition with risankizumab produced better quality of life scores than with ustekinumab. Additionally, the ECLIPSE trial showed that IL-23 inhibition with guselkumab produced higher PASI 90 response rates than IL-17 inhibition with secukinumab at Week 48.</description><issn>2054-6211</issn><issn>2054-6211</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNpNkMFKxDAURYMoOIzzCUJ-oM5LXtNpl1LUqRYU7L4k7QtmmDZDkk3_XhkVZnXvPYu7OIzdC3hAVBVsaTqMFCad_HErAAWCkldsJUHlWSGFuL7ot2wT4wEAJIqiLGDFXps2k8ib-csZl5yfuY5c8zdaeO2nk59pTtzN_CP64HR0kXeBdJrOOPI9BeLJ88-klzt2Y_Ux0uYv16x7furqfda-vzT1Y5sNFcqsLNROQqkGQUIZAWBzsoXJbZnjKIbRoKjGEknbfNyRHKv8Zw7GlNagVLbCNVO_t0PwMQay_Sm4SYelF9CflfQXSvp_JfgNzKNW9A</recordid><startdate>20190911</startdate><enddate>20190911</enddate><creator>Fricker, Janet</creator><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20190911</creationdate><title>IL-23 Inhibition as a Key Component in Psoriasis Treatment is Here to Stay</title><author>Fricker, Janet</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c932-86572085c1e15b100f4ef6b4f843d1cdb319d83eaf4d7e2d949d8cbb8fb325f93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fricker, Janet</creatorcontrib><collection>CrossRef</collection><jtitle>European medical journal. Dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fricker, Janet</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-23 Inhibition as a Key Component in Psoriasis Treatment is Here to Stay</atitle><jtitle>European medical journal. Dermatology</jtitle><date>2019-09-11</date><risdate>2019</risdate><spage>2</spage><epage>11</epage><pages>2-11</pages><issn>2054-6211</issn><eissn>2054-6211</eissn><abstract>Prof Elke de Jong focussed her presentation on data from randomised clinical trials (RCT) and real-world evidence (RWE) from psoriasis patient registries. Such data is complementary with RCT having high internal validity but low external validity, and RWE having low internal validity but high external validity. She reviewed the predictors for stopping psoriasis biological treatment of high BMI and female sex and predictors for continuing treatment as concurrent psoriatic arthritis.
Current unmet needs in psoriasis that demonstrate the requirement for additional treatments include patients experiencing psoriasis for roughly 20 years before being prescribed biologics, prevention of damage (e.g., psoriatic arthritis), achieving sustained effectiveness or cure, developing better patient-reported outcome measures, and better treatment of specific psoriatic areas (scalp, face, nails, and genitalia).
Dr Andreas Pinter reviewed the role played by IL-23, IL-17A, and IL-22 in psoriasis, and new agents including ustekinumab blocking both IL-12 and IL-23; guselkumab, tildrakizumab, and risankizumab blocking IL-23; and brodalumab blocking IL-17A.
He explored VOYAGE 1 data that showed that the IL-23 inhibitor guselkumab maintained Psoriasis Area and Severity Index (PASI) 90 response through Week 156 in >80% of patients. Furthermore, VOYAGE 2 results showed PASI 90 response was maintained in >50% of patients 6 months after guselkumab withdrawal.
He demonstrated how re-treatment with guselkumab led to a high PASI 90 response in patients who lost PASI 90 response after withdrawal of treatment. Data from the VOYAGE 1 study further showed that guselkumab produced statistically significant improvements in scalp and palmar plantar scores over adalimumab, and comparable nail scores to adalimumab.
Data from the UltlMMa-1 and ULtlMMa-2 studies showed that IL-23 inhibition with risankizumab produced better quality of life scores than with ustekinumab. Additionally, the ECLIPSE trial showed that IL-23 inhibition with guselkumab produced higher PASI 90 response rates than IL-17 inhibition with secukinumab at Week 48.</abstract><doi>10.33590/emjdermatol/10313052</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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title | IL-23 Inhibition as a Key Component in Psoriasis Treatment is Here to Stay |
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