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2nd and 3rd infusions ( fig. 1 e and f). However, treatment with infliximab was discontinued due to an infusion-related reaction with polyarthalgia, myalgia and fever after the 3rd infusion. Although acitretin (30 mg daily) was reintroduced, some painful pustular skin lesions, erythema, fissuring and scaling started reappearing on her feet approximately 8 weeks after the 3rd infusion with infliximab. After obtaining her informed consent, treatment with the fully human anti-TNF antibody adalimumab (40 mg subcutaneous injection biweekly) was initiated. Due to partial response after 4 weeks, the dosage was increased to weekly subcutaneous injection of 40 mg adalimumab, which subsequently led to further amelioration ( fig. 1 g and h). Therapy with adalimumab (40 mg weekly) was well tolerated except for a weight gain of 5 kg within the last 3 months, which the patient attributed to therapy. In order to investigate cellular alterations and expression of TNFduring initial treatment with infliximab, punch biopsy specimens (5 mm) were obtained from lesional skin before beginning therapy and from skin adjacent to the first biopsy at week 2 (1 day after the 2nd infusion). Biopsy specimens were routinely processed for histology (HE staining) as well as for immunohistochemistry using the ABC-AP method as described previously [14] . The following primary antibodies were used: CD3 (clone: PS1, Novocastra, Newcastle-upon-Tyne, UK), CD4 (clone: 1F6, Novocastra), CD8 (clone: C8/144B, Dako Cytomation, Glostrup, Denmark), neutrophil elastase (clone: NP57, Dako Cytomation), CD1a (clone: O10, Dako Cytomation), CD68 (clone: PG-M1, Dako Cytomation) and HLA-DR (clone: CR3/43, Dako Cytomation). Immunofluorescence staining was performed with anti-TNF antibodies (clone: 28401, R&D Systems, Minneapolis, Minn., USA) as described previously [15] . Representative HE and immunohistochemical staining samples before therapy and at week 2 are shown in figure 2 a–p. In correlation with the patient’s clinical improvement, a significant decrease in different leukocyte populations including T cells (CD4+ T helper cells and CD8+ T cytotoxic cells), neutrophils, CD1a dendritic cells and CD68 macrophages was found at week 2 ( fig. 2 ). Initially, skin lesions also showed a marked expression of the activation marker HLA-DR+ particularly in the dermal infiltrate, which also decreased but still remained evident at week 2. Furthermore, strong immunofluorescence for TNFwas observed particularly in the cellular infiltrate of the skin lesion obtained before therapy ( fig. 3 a). In correlation with the reduction of the proinflammatory infiltrate, a significant decrease in TNFimmunofluorescence was observed at week 2 ( fig. 3 b).

Successful Treatment of Recalcitrant Palmoplantar Pustular Psoriasis with Sequential Use of Infliximab and Adalimumab