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H D De Koning - One of the best experts on this subject based on the ideXlab platform.

  • mast cell interleukin 1β neutrophil interleukin 17 and epidermal antimicrobial proteins in the neutrophilic Urticarial dermatosis in schnitzler s syndrome
    British Journal of Dermatology, 2015
    Co-Authors: H D De Koning, I M J J Van Vlijmenwillems, Diana Rodijkolthuis, J W M Van Der Meer, Patrick L J M Zeeuwen, Anna Simon, J Schalkwijk
    Abstract:

    BACKGROUND: Schnitzler's syndrome (SchS) is an autoinflammatory disease characterized by a chronic Urticarial rash, a monoclonal component and signs of systemic inflammation. Interleukin (IL)-1beta is pivotal in the pathophysiology. OBJECTIVES: Here we investigated the cellular source of proinflammatory mediators in the skin of patients with SchS. METHODS: Skin biopsies of lesional and nonlesional skin from eight patients with SchS and healthy controls, and patients with cryopyrin-associated periodic syndrome (CAPS), delayed-Pressure Urticaria (DPU) and cold-contact Urticaria (CCU) were studied. We studied in vivoIL-1beta, IL-17 and antimicrobial protein (AMP) expression in resident skin cells and infiltrating cells. In addition we investigated the in vitro effect of IL-1beta, IL-17 and polyinosinic-polycytidylic acid (poly:IC) stimulation on cultured epidermal keratinocytes. RESULTS: Remarkably, we found IL-1beta-positive dermal mast cells in both lesional and nonlesional skin of patients with SchS, but not in healthy control skin and CCU, and fewer in CAPS. IL-17-positive neutrophils were observed only in lesional SchS and DPU skin. In lesional SchS epidermis, mRNA and protein expression levels of AMPs were strongly increased compared with nonlesional skin and that of healthy controls. When exposed to IL-1beta, poly:IC or IL-17, patient and control primary human keratinocytes produced AMPs in similar amounts. CONCLUSIONS: Dermal mast cells of patients with SchS produce IL-1beta. This presumably leads to activation of keratinocytes and neutrophil influx, and further amplification of inflammation by IL-17 (from neutrophils and mast cells) and epidermal AMP production leading to chronic histamine-independent neutrophilic Urticarial dermatosis.

  • Mast-cell interleukin-1beta, neutrophil interleukin-17 and epidermal antimicrobial proteins in the neutrophilic Urticarial dermatosis in Schnitzler's syndrome
    'Wiley', 2015
    Co-Authors: H D De Koning, Vlijmen-willems, I.m.j.j. Van, Rodijk-olthuis D., Meer, J.w.m. Van Der, Zeeuwen P.l.j.m., Simon A., Schalkwijk J.
    Abstract:

    Item does not contain fulltextBACKGROUND: Schnitzler's syndrome (SchS) is an autoinflammatory disease characterized by a chronic Urticarial rash, a monoclonal component and signs of systemic inflammation. Interleukin (IL)-1beta is pivotal in the pathophysiology. OBJECTIVES: Here we investigated the cellular source of proinflammatory mediators in the skin of patients with SchS. METHODS: Skin biopsies of lesional and nonlesional skin from eight patients with SchS and healthy controls, and patients with cryopyrin-associated periodic syndrome (CAPS), delayed-Pressure Urticaria (DPU) and cold-contact Urticaria (CCU) were studied. We studied in vivoIL-1beta, IL-17 and antimicrobial protein (AMP) expression in resident skin cells and infiltrating cells. In addition we investigated the in vitro effect of IL-1beta, IL-17 and polyinosinic-polycytidylic acid (poly:IC) stimulation on cultured epidermal keratinocytes. RESULTS: Remarkably, we found IL-1beta-positive dermal mast cells in both lesional and nonlesional skin of patients with SchS, but not in healthy control skin and CCU, and fewer in CAPS. IL-17-positive neutrophils were observed only in lesional SchS and DPU skin. In lesional SchS epidermis, mRNA and protein expression levels of AMPs were strongly increased compared with nonlesional skin and that of healthy controls. When exposed to IL-1beta, poly:IC or IL-17, patient and control primary human keratinocytes produced AMPs in similar amounts. CONCLUSIONS: Dermal mast cells of patients with SchS produce IL-1beta. This presumably leads to activation of keratinocytes and neutrophil influx, and further amplification of inflammation by IL-17 (from neutrophils and mast cells) and epidermal AMP production leading to chronic histamine-independent neutrophilic Urticarial dermatosis

  • Mast-cell interleukin-1beta, neutrophil interleukin-17 and epidermal antimicrobial proteins in the neutrophilic Urticarial dermatosis in Schnitzler's syndrome
    'Wiley', 2015
    Co-Authors: H D De Koning, Vlijmen-willems, I.m.j.j. Van, Rodijk-olthuis D., Meer, J.w.m. Van Der, Zeeuwen P.l.j.m., Simon A., Schalkwijk J.
    Abstract:

    BACKGROUND: Schnitzler's syndrome (SchS) is an autoinflammatory disease characterized by a chronic Urticarial rash, a monoclonal component and signs of systemic inflammation. Interleukin (IL)-1beta is pivotal in the pathophysiology. OBJECTIVES: Here we investigated the cellular source of proinflammatory mediators in the skin of patients with SchS. METHODS: Skin biopsies of lesional and nonlesional skin from eight patients with SchS and healthy controls, and patients with cryopyrin-associated periodic syndrome (CAPS), delayed-Pressure Urticaria (DPU) and cold-contact Urticaria (CCU) were studied. We studied in vivoIL-1beta, IL-17 and antimicrobial protein (AMP) expression in resident skin cells and infiltrating cells. In addition we investigated the in vitro effect of IL-1beta, IL-17 and polyinosinic-polycytidylic acid (poly:IC) stimulation on cultured epidermal keratinocytes. RESULTS: Remarkably, we found IL-1beta-positive dermal mast cells in both lesional and nonlesional skin of patients with SchS, but not in healthy control skin and CCU, and fewer in CAPS. IL-17-positive neutrophils were observed only in lesional SchS and DPU skin. In lesional SchS epidermis, mRNA and protein expression levels of AMPs were strongly increased compared with nonlesional skin and that of healthy controls. When exposed to IL-1beta, poly:IC or IL-17, patient and control primary human keratinocytes produced AMPs in similar amounts. CONCLUSIONS: Dermal mast cells of patients with SchS produce IL-1beta. This presumably leads to activation of keratinocytes and neutrophil influx, and further amplification of inflammation by IL-17 (from neutrophils and mast cells) and epidermal AMP production leading to chronic histamine-independent neutrophilic Urticarial dermatosis

J Schalkwijk - One of the best experts on this subject based on the ideXlab platform.

  • mast cell interleukin 1β neutrophil interleukin 17 and epidermal antimicrobial proteins in the neutrophilic Urticarial dermatosis in schnitzler s syndrome
    British Journal of Dermatology, 2015
    Co-Authors: H D De Koning, I M J J Van Vlijmenwillems, Diana Rodijkolthuis, J W M Van Der Meer, Patrick L J M Zeeuwen, Anna Simon, J Schalkwijk
    Abstract:

    BACKGROUND: Schnitzler's syndrome (SchS) is an autoinflammatory disease characterized by a chronic Urticarial rash, a monoclonal component and signs of systemic inflammation. Interleukin (IL)-1beta is pivotal in the pathophysiology. OBJECTIVES: Here we investigated the cellular source of proinflammatory mediators in the skin of patients with SchS. METHODS: Skin biopsies of lesional and nonlesional skin from eight patients with SchS and healthy controls, and patients with cryopyrin-associated periodic syndrome (CAPS), delayed-Pressure Urticaria (DPU) and cold-contact Urticaria (CCU) were studied. We studied in vivoIL-1beta, IL-17 and antimicrobial protein (AMP) expression in resident skin cells and infiltrating cells. In addition we investigated the in vitro effect of IL-1beta, IL-17 and polyinosinic-polycytidylic acid (poly:IC) stimulation on cultured epidermal keratinocytes. RESULTS: Remarkably, we found IL-1beta-positive dermal mast cells in both lesional and nonlesional skin of patients with SchS, but not in healthy control skin and CCU, and fewer in CAPS. IL-17-positive neutrophils were observed only in lesional SchS and DPU skin. In lesional SchS epidermis, mRNA and protein expression levels of AMPs were strongly increased compared with nonlesional skin and that of healthy controls. When exposed to IL-1beta, poly:IC or IL-17, patient and control primary human keratinocytes produced AMPs in similar amounts. CONCLUSIONS: Dermal mast cells of patients with SchS produce IL-1beta. This presumably leads to activation of keratinocytes and neutrophil influx, and further amplification of inflammation by IL-17 (from neutrophils and mast cells) and epidermal AMP production leading to chronic histamine-independent neutrophilic Urticarial dermatosis.

Massimo Milani - One of the best experts on this subject based on the ideXlab platform.

  • clobetasol propionate 0 05 in a novel foam formulation is safe and effective in the short term treatment of patients with delayed Pressure Urticaria a randomized double blind placebo controlled trial
    British Journal of Dermatology, 2006
    Co-Authors: G A Vena, Nicoletta Cassano, V Dargento, Massimo Milani
    Abstract:

    Summary Background  Delayed Pressure Urticaria (DPU) is characterized by the appearance of typical painful skin lesions (weals) after Pressure stimulus. Oral corticosteroids are effective treatments but long-term therapy is problematic. A new topical formulation of clobetasol propionate 0·05% in thermophobic foam (CF) (Olux®) has recently become available. The foam is easy to apply, with low skin residues. Objectives  To evaluate in a double-blind placebo-controlled trial the efficacy, tolerability and safety of CF in the topical treatment of DPU. Methods  Twenty-six subjects with a positive history of DPU (13 men, mean age 44 years) were enrolled in a 4-week trial. CF or the corresponding placebo were applied twice daily. Drug application was performed in the most affected areas and in a target area where a standardized Pressure challenge test was performed at baseline and at week 4. Efficacy was evaluated by scoring skin lesions regarding erythema, oedema and itching (0, no sign; 4, severe signs) and by calculating the area of the Pressure challenge-induced lesion. Safety was evaluated by measuring plasma levels of adrenocorticotropic hormone (ACTH) and cortisol. Results  CF significantly (P = 0·0001) reduced lesion area by 84% in comparison with baseline values and by 97% in comparison with the placebo group values. Lesion area in the CF group was reduced from 144 cm2 to 21 cm2 at the end of the study. No significant differences in lesion area and clinical lesion scores were observed in the placebo group (lesion area 201 cm2 at baseline; 216 cm2 after 4 weeks). A significant clinical improvement was observed in all treated skin areas in the CF group. Mean ± SD erythema score was reduced by CF from 1·8 ± 0·6 at baseline to 0·6 ± 0·5 at the end of the treatment (P = 0·001). Similar modifications were observed also for oedema (from 1·6 ± 0·6 to 0·2 ± 0·5) and itching score. Nonsignificant modifications of plasma levels of ACTH, cortisol and glucose were observed in both study groups, in comparison with baseline values. No adverse events were recorded during the trial in either treatment group. Conclusions  CF is effective, safe, convenient and well tolerated in the short-term treatment of DPU.

Angelo Vacca - One of the best experts on this subject based on the ideXlab platform.

  • desloratadine in combination with montelukast suppresses the dermographometer challenge test papule and is effective in the treatment of delayed Pressure Urticaria a randomized double blind placebo controlled study
    British Journal of Dermatology, 2006
    Co-Authors: Eustachio Nettis, Anna Lucia Soccio, M. C. Colanardi, Antonio Ferrannini, Angelo Vacca
    Abstract:

    Summary Background  Delayed Pressure Urticaria (DPU) comes under the heading of physical Urticaria. Characteristically itchy, tender or painful weals occur at sites of local Pressure including the waistband, soles of the feet and palms of the hands. Lesion onset is typically 3–12 h after the application of Pressure, and lesions may persist for more than 24 h. The treatment of DPU is often unsatisfactory. Objectives  To determine the efficacy of desloratadine and montelukast in the treatment of DPU. Methods  The study was conducted in 36 subjects affected by DPU. A challenge test with a dermographometer was administered to confirm the diagnosis. After diagnosis, patients were randomized to receive the following treatment once daily for 2 weeks: (i) oral desloratadine 5 mg plus oral placebo; (ii) oral desloratadine 5 mg plus montelukast 10 mg; and (iii) oral placebo alone. Results  At rechallenge, patients from the treatment groups (desloratadine plus montelukast group and desloratadine alone group) demonstrated a significant reduction in mean diameter of papules after 70 s of Pressure compared with the placebo group (P < 0·05). Moreover, patients treated with desloratadine plus montelukast showed a significant reduction in mean diameter of papules at 70 s of Pressure compared with those treated with desloratadine alone (P < 0·05). In addition, the combination was effective in improving clinical parameters (erythema, oedema and pruritus, and number of separate Urticarial episodes). Conclusions  This study has demonstrated that both desloratadine alone and desloratadine plus montelukast administered once daily yield improvements with respect to the baseline assessment, regarding the suppression of the dermographometer challenge test papule and clinical improvement of Urticaria. However, the combination of desloratadine and montelukast was shown to be more efficacious and may therefore be proposed in patients with DPU, in order to avoid corticosteroid therapy.

Schalkwijk J. - One of the best experts on this subject based on the ideXlab platform.

  • Mast-cell interleukin-1beta, neutrophil interleukin-17 and epidermal antimicrobial proteins in the neutrophilic Urticarial dermatosis in Schnitzler's syndrome
    'Wiley', 2015
    Co-Authors: H D De Koning, Vlijmen-willems, I.m.j.j. Van, Rodijk-olthuis D., Meer, J.w.m. Van Der, Zeeuwen P.l.j.m., Simon A., Schalkwijk J.
    Abstract:

    Item does not contain fulltextBACKGROUND: Schnitzler's syndrome (SchS) is an autoinflammatory disease characterized by a chronic Urticarial rash, a monoclonal component and signs of systemic inflammation. Interleukin (IL)-1beta is pivotal in the pathophysiology. OBJECTIVES: Here we investigated the cellular source of proinflammatory mediators in the skin of patients with SchS. METHODS: Skin biopsies of lesional and nonlesional skin from eight patients with SchS and healthy controls, and patients with cryopyrin-associated periodic syndrome (CAPS), delayed-Pressure Urticaria (DPU) and cold-contact Urticaria (CCU) were studied. We studied in vivoIL-1beta, IL-17 and antimicrobial protein (AMP) expression in resident skin cells and infiltrating cells. In addition we investigated the in vitro effect of IL-1beta, IL-17 and polyinosinic-polycytidylic acid (poly:IC) stimulation on cultured epidermal keratinocytes. RESULTS: Remarkably, we found IL-1beta-positive dermal mast cells in both lesional and nonlesional skin of patients with SchS, but not in healthy control skin and CCU, and fewer in CAPS. IL-17-positive neutrophils were observed only in lesional SchS and DPU skin. In lesional SchS epidermis, mRNA and protein expression levels of AMPs were strongly increased compared with nonlesional skin and that of healthy controls. When exposed to IL-1beta, poly:IC or IL-17, patient and control primary human keratinocytes produced AMPs in similar amounts. CONCLUSIONS: Dermal mast cells of patients with SchS produce IL-1beta. This presumably leads to activation of keratinocytes and neutrophil influx, and further amplification of inflammation by IL-17 (from neutrophils and mast cells) and epidermal AMP production leading to chronic histamine-independent neutrophilic Urticarial dermatosis

  • Mast-cell interleukin-1beta, neutrophil interleukin-17 and epidermal antimicrobial proteins in the neutrophilic Urticarial dermatosis in Schnitzler's syndrome
    'Wiley', 2015
    Co-Authors: H D De Koning, Vlijmen-willems, I.m.j.j. Van, Rodijk-olthuis D., Meer, J.w.m. Van Der, Zeeuwen P.l.j.m., Simon A., Schalkwijk J.
    Abstract:

    BACKGROUND: Schnitzler's syndrome (SchS) is an autoinflammatory disease characterized by a chronic Urticarial rash, a monoclonal component and signs of systemic inflammation. Interleukin (IL)-1beta is pivotal in the pathophysiology. OBJECTIVES: Here we investigated the cellular source of proinflammatory mediators in the skin of patients with SchS. METHODS: Skin biopsies of lesional and nonlesional skin from eight patients with SchS and healthy controls, and patients with cryopyrin-associated periodic syndrome (CAPS), delayed-Pressure Urticaria (DPU) and cold-contact Urticaria (CCU) were studied. We studied in vivoIL-1beta, IL-17 and antimicrobial protein (AMP) expression in resident skin cells and infiltrating cells. In addition we investigated the in vitro effect of IL-1beta, IL-17 and polyinosinic-polycytidylic acid (poly:IC) stimulation on cultured epidermal keratinocytes. RESULTS: Remarkably, we found IL-1beta-positive dermal mast cells in both lesional and nonlesional skin of patients with SchS, but not in healthy control skin and CCU, and fewer in CAPS. IL-17-positive neutrophils were observed only in lesional SchS and DPU skin. In lesional SchS epidermis, mRNA and protein expression levels of AMPs were strongly increased compared with nonlesional skin and that of healthy controls. When exposed to IL-1beta, poly:IC or IL-17, patient and control primary human keratinocytes produced AMPs in similar amounts. CONCLUSIONS: Dermal mast cells of patients with SchS produce IL-1beta. This presumably leads to activation of keratinocytes and neutrophil influx, and further amplification of inflammation by IL-17 (from neutrophils and mast cells) and epidermal AMP production leading to chronic histamine-independent neutrophilic Urticarial dermatosis