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Moderate-to-severe atopic dermatitis patients show increases in serum C-reactive protein levels, correlating with skin disease activity.

ABSTRACT: Background: Atopic dermatitis (AD), the most common chronic inflammatory skin disease, is evolving as a systemic disease, and associated systemic inflammation is possibly linked to increases in cardiovascular disease. Methods: We assessed levels of the inflammatory marker CRP in 59 patients with moderate-to-severe AD compared to matched healthy controls, and to determine correlation with skin disease severity. Clinical severity was measured using SCORing of Atopic Dermatitis (SCORAD) and body surface area (BSA). Control subjects (n=118), matched by age, gender, smoking status and ethnicity, were obtained from the National Health and Nutrition Survey (NHANES). Results: AD patients had significantly increased serum CRP levels compared to controls (0.7±1.0 vs. 0.4±0.7mg/dl; p=0.001), and 52.5% of them showed CRP levels >0.3mg/dl, predicting high cardiovascular risk. CRP levels were significantly correlated with both SCORAD (r=0.427, p=0.0008) and BSA (r=0.407, p=0.0015). IgE levels in AD were highly elevated (median 2903U/ml, IQR [234,10655]), but only weakly correlated with SCORAD (r=0.282, p=0.0427) and BSA (r=0.382, p=0.0052), but not with CRP levels. AD patients also showed increased LDH levels, but without significant correlations with disease severity (SCORAD, BSA) or CRP. Conclusions: Our study strongly supports CRP as a marker for disease severity in moderate-to-severe AD patients, further demonstrating its chronic systemic nature.

SUBMITTER: Vekaria AS

PROVIDER: S-EPMC5698919 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundAtopic dermatitis (AD) is a skin barrier dysfunction characterized by tissue eosinophilia.ObjectiveIn patients with AD, we evaluated the effect of eosinophil depletion with benralizumab on markers of inflammation in skin after intradermal allergen challenge.MethodsA total of 20 patients with moderate-to-severe AD completed a randomized, double-blind, placebo-controlled parallel-group study comparing 3 doses of benralizumab (30 mg each) administered subcutaneously every 4 weeks (n = 9) with placebo (n = 11). Allergen and saline control intradermal challenges were conducted before and after treatment, with skin biopsy samples collected 24 hours after challenge. Early and late cutaneous responses were measured by skin wheal size. Levels of eosinophils and IL-5 receptor-α-bearing cells, including eosinophil progenitor (EoP) cells, basophils, and mast cells, in papillary dermis were measured by immunofluorescence microscopy, and levels of EoP cells, hematopoietic progenitor cells, and type 2 innate lymphoid cells in the blood were measured by flow cytometry. Outcomes were compared between the placebo and benralizumab treatment groups by using the Mann-Whitney U test.ResultsBenralizumab reduced eosinophil counts in the blood (P < .0001) and allergen-challenged skin, as measured by hematoxylin and eosin staining and eosinophil cationic protein antibody concentration (P < .05). Benralizumab lowered the levels of EoP cells, mast cells, and basophils in the skin, as well as the levels of EoP cells, hematopoietic progenitor cells, and type 2 innate lymphoid cells in the blood (all P < .05). There was a trend toward improvement in the early cutaneous response (P = .095) but no effect on the late cutaneous response.ConclusionIn patients with moderate-to-severe AD, benralizumab treatment significantly inhibited accumulation of eosinophils and other IL-5 receptor-α-expressing cells in the papillary dermis after intradermal allergen challenge. Targeting IL-5 receptor-α-positive cells did not modulate the size of the allergen-induced skin wheal (ClincialTrials.gov identifier NCT03563066).

Project description:ImportanceCendakimab selectively targets interleukin (IL)-13, a type 2 cytokine implicated in atopic dermatitis (AD) pathogenesis, by inhibiting binding to its receptors (IL13R-α1 and IL13R-α2). Proof-of-concept work in AD supports using cendakimab for type 2 inflammatory diseases.ObjectiveTo evaluate the efficacy and safety of cendakimab compared with placebo in patients with moderate to severe AD.Design, setting, and participantsThis phase 2, randomized, double-blind, placebo-controlled, parallel-group, dose-ranging clinical trial was conducted from May 2021 to November 2022. Adult patients with moderate to severe AD and inadequate response to topical medications were enrolled at 69 sites in 5 countries (US [n = 26], Japan [n = 17], Canada [n = 9], Poland [n = 9], and Czech Republic [n = 8]). Data were analyzed between April 25, 2023, and October 16, 2023.InterventionsPatients were randomized (1:1:1:1) to receive subcutaneous cendakimab, 360 mg, every 2 weeks; 720 mg, every 2 weeks; 720 mg, once weekly; or placebo.Main outcome and measureMean percentage change in Eczema Area and Severity Index scores from baseline to week 16. Hierarchical testing with multiplicity adjustment was performed for 720 mg, once weekly vs placebo, then 720 mg, every 2 weeks vs placebo, and then 360 mg, every 2 weeks vs placebo.ResultsOverall, 221 patients were randomized, and 220 received study drug (95 women [43%]; mean [SD] age, 37.7 [13.9] years; 720 mg, once weekly [54 (24%)]; 720 mg, every 2 weeks [55 (25%)]; 360 mg, every 2 weeks [55 (25%)]; placebo [56 (26%)]). The primary efficacy end point was met for cendakimab, 720 mg, once weekly vs placebo (-84.4 vs -62.7; P = .003) but missed statistical significance for 720 mg, every 2 weeks (-76.0 vs -62.7; P = .06). The treatment effect for 360 mg, every 2 weeks (-16.3; nominal P = .03 vs placebo) was comparable with 720 mg, once weekly (-21.8); however, significance was not claimed because the hierarchical testing sequence was interrupted. Of patients with treatment-emergent adverse events leading to discontinuation, 4 (7.4%) received 720 mg, once weekly; 2 (3.6%) 720 mg, every 2 weeks; 1 (1.8%) 360 mg, every 2 weeks; and 2 (3.6%) placebo.Conclusions and relevanceThe results of this randomized clinical trial indicated that cendakimab was effective, generally safe, and well-tolerated in patients with moderate to severe AD. The primary end point was met with a significant reduction in Eczema Area and Severity Index scores with 720 mg, once weekly at week 16. Cendakimab demonstrated progressive AD improvement at all doses during 16 weeks of treatment.Trial registrationClinicalTrials.gov Identifier: NCT04800315.

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Moderate-to-severe atopic dermatitis patients show increases in serum C-reactive protein levels, correlating with skin disease activity.

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