Screening of antigliadin and antitissue transglutaminase antibodies in patients with chronic plaque psoriasis: a case-control study

Abstract

Background/aim In this study, we aimed to investigate different types of celiac antibodies in psoriasis patients and to see if the presence of the antibodies was associated with other variables. Materials and methods We included patients with plaque psoriasis who were followed up in our dermatology clinic between February 2019 and February 2021 and added a healthy control group for comparison. The antibodies studied were serum antitissue transglutaminase (tTG)-IgA, tTG-IgG, antigliadin antibody (AGA)-IgA, and AGA-IgG. The patients’ records were used to note age, sex, the pattern of psoriasis involvement, psoriasis area and severity index (PASI), presence of hypertension, presence of type 2 diabetes mellitus, use of methotrexate, and use of biologic agents. Results Sixty-five psoriasis patients (31 F, 34 M, mean age: 38.9 ± 15.2) and 65 controls (42 F, 23 M, mean age: 40.7 ± 13.2) were included in the study. There was no significant difference in antibody levels between the groups: tTG-IgA (2.4 U/mL vs 3.2 U/mL, p = 0.11), tTG-IgG (2.2 U/mL vs 3.2 U/mL, p = 0.74), AGA-IgA (2.4 U/mL vs 3.5 U/mL, p = 0.068), and AGA-IgG (3.2 U/mL vs 4.2 U/mL, p = 0.15). One patient from the psoriasis group only had borderline positive antibody levels whereas the rest of the psoriasis and control group had negative levels. Hypertensive psoriasis patients had significantly higher AGA-IgA titers compared to normotensive psoriasis patients (4.2 U/mL vs 2.3 U/mL, p = 0.005). Conclusion There was no increase in the AGA-IgA/IgG and tTG-IgA/IgG levels in psoriasis patients compared to the healthy population. However, hypertensive psoriasis patients had higher AGA-IgA levels compared to normotensive ones.

Noval advance of histone modification in inflammatory skin diseases and related treatment methods

“…Histone modification has been shown to interact with the immune microenvironment and promote the occurrence and development of inflammatory skin diseases. A study reported that the α-KG–H3K9me3–BBOX1 axis is critical in the metabolic reprogramming of cluster of differentiation (CD)147, which is pivotal in glycolysis reprogramming during the pathogenesis of psoriasis ( 25 ). One of the histone deacetylases, SIRT1, potentially inhibits the apoptosis of keratinocytes induced by UVB in cutaneous lupus erythematosus ( 26 ).…”