Unsuccessful treatment of recalcitrant cutaneous discoid lupus erythematosus with photodynamic therapy

Abstract

Discoid lupus erythematosus (DLE) can be a therapeutic challenge. Antimalarials and topic steroids are the first-line standard therapies, while systemic steroids, immunomodulators (as azathioprine, methotrexate, cyclosporine), retinoids (acitretin), thalidomide, auranofin and dapsone are used as second-line therapies. We report two patients with recalcitrant DLE who were treated with three and two sessions of 5-aminolevulinic photodynamic therapy without an improvement and with a bad tolerance to the therapy.

Current Insights in Cutaneous Lupus Erythematosus Immunopathogenesis

“…However, filgotinib (JAK1) did not reach its primary endpoint in a phase II double blind study, underscoring the need for a better understanding of which JAKs and STATs drive CLE (172)(173)(174). Similarly, the roles of IL-12 and IL-23 need to be revisited, as ustekinumab has been reported to both treat (175)(176)(177)(178) and cause CLE (179).…”

<p>Current Insights Into The Management Of Discoid Lupus Erythematosus</p>

“…They performed three and two sessions (one per month) of 5-ALA-PDT (20% 5-aminolevulinic acid), respectively. Maybe the use of ALA instead of MAL played its part in the final result 78…”

The pathogenesis of cutaneous lupus erythematosus: The aberrant distribution and function of different cell types in skin lesions

“…UV, ultraviolet; pDCs, plasmacytoid dendritic cells; IFN, interferon; NETs, neutrophil extracellular traps manifestation. [132][133][134][135] Spleen tyrosine kinase (SYK) is a protein kinase involved in cell proliferation and regulation of inflammatory pathways, and significant expression of phosphorylated SYK (pSYK) is observed in keratinocytes of CLE skin. 136 GSK143, a SYK inhibitor, is utilized in keratinocytes with synthetic immunostimulatory nucleic acid poly(I:C) and poly(dA:dT) stimulation, and GSK143 significantly inhibits keratinocytes to produce pro-inflammatory cytokines that are induced by type I IFNs, 136 indicating that pSYK may be a promising drug target for CLE treatment.…”

“…In a trial, an anti–IL‐10 monoclonal antibody decreased cutaneous lesions, joint symptoms and SLEDAI scores of SLE subjects 131 . Ustekinumab is a monoantibody for IL‐12 and IL‐23, 132 and several cases report ustekinumab is effective in treating cutaneous manifestation 132‐135 . Spleen tyrosine kinase (SYK) is a protein kinase involved in cell proliferation and regulation of inflammatory pathways, and significant expression of phosphorylated SYK (pSYK) is observed in keratinocytes of CLE skin 136 .…”