Marco Galluzzo1, Simone D'Adamio2, Elena Campione2, Luca Bianchi2, Marina Talamonti2. 1. Dermatology, Department of "Medicina dei Sistemi", University of Rome "Tor Vergata", Viale Oxford, 81, 00133, Rome, Italy. marco.galluzzo83@gmail.com. 2. Dermatology, Department of "Medicina dei Sistemi", University of Rome "Tor Vergata", Viale Oxford, 81, 00133, Rome, Italy.
Abstract
BACKGROUND: Nowadays, even though several biologic therapies are available to treat psoriasis, multidrug-resistant disease continues to be a therapeutic challenge. Combination therapy has therefore become increasingly important. In this context, apremilast, according to its safety profile, could easily be combined with biologics in patients with comorbidities and/or recalcitrant multidrug-resistant psoriasis. OBJECTIVE: Our goal is to share experience from our institution in the observation of a patient with severe chronic plaque psoriasis that was unresponsive to all anti-tumor necrosis factor-α treatment and to an anti-interleukin (IL)-17A drug and only partially responsive to ustekinumab, even in combination with apremilast. The patient carried a rare allele infrequently found in Caucasian people: human leukocyte antigen (HLA)-C*18:01. This allele has been found to be positively associated with psoriasis in Brazilian patients. METHODS: The patient was typed for the HLA-C locus at high resolution via polymerase chain reaction sequence-specific oligonucleotide probes (PCR-SSOP) using a commercial kit (LAB®Type, One Lambda Inc., Canoga Park, CA, USA). RESULTS: Our patient, previously described as having multidrug-resistant psoriasis, commenced ustekinumab and apremilast combination therapy. After 12 weeks, the Psoriasis Area Severity Index score had worsened, and we suspended combination therapy because the patient reported an absence of any benefit and was experiencing side effects from the induction therapy with apremilast. CONCLUSIONS: Expanding on the previously reported experience with this patient, we conclude that HLA-C*18:01 probably indicates a severe, recalcitrant, multidrug-resistant psoriasis phenotype for which proper therapy remains to be identified.
BACKGROUND: Nowadays, even though several biologic therapies are available to treat psoriasis, multidrug-resistant disease continues to be a therapeutic challenge. Combination therapy has therefore become increasingly important. In this context, apremilast, according to its safety profile, could easily be combined with biologics in patients with comorbidities and/or recalcitrant multidrug-resistant psoriasis. OBJECTIVE: Our goal is to share experience from our institution in the observation of a patient with severe chronic plaque psoriasis that was unresponsive to all anti-tumor necrosis factor-α treatment and to an anti-interleukin (IL)-17A drug and only partially responsive to ustekinumab, even in combination with apremilast. The patient carried a rare allele infrequently found in Caucasian people: humanleukocyte antigen (HLA)-C*18:01. This allele has been found to be positively associated with psoriasis in Brazilian patients. METHODS: The patient was typed for the HLA-C locus at high resolution via polymerase chain reaction sequence-specific oligonucleotide probes (PCR-SSOP) using a commercial kit (LAB®Type, One Lambda Inc., Canoga Park, CA, USA). RESULTS: Our patient, previously described as having multidrug-resistant psoriasis, commenced ustekinumab and apremilast combination therapy. After 12 weeks, the Psoriasis Area Severity Index score had worsened, and we suspended combination therapy because the patient reported an absence of any benefit and was experiencing side effects from the induction therapy with apremilast. CONCLUSIONS: Expanding on the previously reported experience with this patient, we conclude that HLA-C*18:01 probably indicates a severe, recalcitrant, multidrug-resistant psoriasis phenotype for which proper therapy remains to be identified.
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