The Clinical Significance of Serum Interleukin-36α Levels in Patients with Gout.

BACKGROUND: Gout is a chronic inflammatory diseases caused by monosodium urate crystal deposition. However, the role of interleukin (IL)-36 in gout has not dbeen elucidated. METHODS: We enrolled 75 subjects, including 20 healthy controls (HC), 30 patients with acute gout attack and 25 patients in remission. Baseline data were obtained through clinical interrogation and laboratory data were obtained through tests of blood samples. Serum levels of IL-36α were detected using enzyme-linked immunosorbent assay. Spearman correlation analysis was used to investigate the correlation of IL-36α with other parameters. The diagnostic value of IL-36α was demonstrated using a receiver operating characteristic curve. RESULTS: The serum IL-36α level of gout patients in acute attack and remission stage was significantly higher than that of HC. Serum IL-36α was positively correlated with alanine transaminase (ALT) and aspartate transaminase (AST). Serum amyloid A (SAA) levels positively correlated with C-reactive protein levels and erythrocyte sedimentation rates. Glutamyl transpeptidase levels positively correlated with AST and ALT levels. CONCLUSION: In conclusion, serum IL-36α levels were elevated in patients with gout and correlated with the clinical markers of inflammation. Our findings suggest that IL-36α may be a novel inflammatory indicator for gout.

Elevated serum IL-36γ levels in patients with ankylosing spondylitis and its association with disease activity.

Ankylosing spondylitis (AS) is a chronic autoimmune disease. The purpose of this study was to investigate the levels of serum IL-36γ in AS patients and their association with AS. The study enrolled 131 subjects, including 45 with active AS, 46 with inactive AS, and 40 healthy controls (HCs). The basic clinical information of each participant was obtained through physical examination and relevant clinical medical records. Serum IL-36γ levels were detected through an enzyme-linked immunosorbent assay. Serum IL-36γ levels in the active AS group were significantly higher than those in the HC group (94.72 vs. 65.76 pg/mL, P = 0.0087). The serum IL-36γ concentration in the inactive AS group was increased as compared to that in the HC group (100.90 vs. 65.76 pg/mL, P = 0.0138). Correlation analysis indicated that serum IL-36γ was positively correlated with glutamyl transferase in the active AS group (P = 0.0172), while serum IL-36γ was positively correlated with uric acid in the inactive AS group (P = 0.0151). The area under the curve (AUC) for IL-36γ was 0.6824 (P = 0.0009), and the AUC for IL-36γ combined with the erythrocyte sedimentation rate and C-reactive protein levels was 0.8102 (P < 0.0001), according to receiver operating characteristic curve analysis. This study found that serum IL-36γ levels were elevated in AS patients and correlated with disease activity. Our results suggest that IL-36γ may be involved in the progression of AS disease and is a potential biomarker for AS.

Potential clinical value of serum interleukin-41 levels in patients with acute gout.

BACKGROUND: Gout is a common metabolic rheumatic disease, and there have been no reports on the serum levels of interleukin (IL)-41 in gout patients. The purpose of this study was to therefore determine the expression of IL-41 in the serum of gout patients. METHODS: Eighty-one participants were enrolled in this study, including 34 patients with acute gout, 27 gout patients in remission, and 20 healthy controls (HCs). Baseline data were obtained through interviews and laboratory parameters were acquired via blood sample testing. We measured serum IL-41 concentrations with an enzyme-linked immunosorbent assay, and executed Spearman's correlation analysis to investigate the correlation between IL-41 and other parameters, and the diagnostic value for IL-41 was demonstrated using a receiver operating characteristic curve. Multivariate analysis was conducted by adopting logistic regression. RESULTS: Serum IL-41 concentrations in acute-gout patients were higher than those in HCs and there was no significant difference in serum IL-41 levels between remission gout patients and HCs. In addition, IL-41 was positively correlated with white blood cell count, erythrocyte sedimentation rate, and C-reactive protein and serum amyloid A concentrations, while it was negatively correlated with triglyceride levels. IL-41 showed good diagnostic value for gout, and the combination of IL-41 and uric acid produced a superior diagnostic value. We also noted that IL-41 was an independent risk factor for acute gout. CONCLUSIONS: This study revealed that serum IL-41 was elevated in patients with acute gout, and suggests that IL-41 may constitute a novel diagnostic marker for acute gout.

Clinical significance of elevated serum IL-36γ levels in patients with early-stage Hashimoto's thyroiditis.

OBJECTIVES: Hashimoto's thyroiditis (HT) is the predominant cause of primary hypothyroidism. Interleukin (IL)-36γ is a member of the IL-36 family. Recently, IL-36γ was shown to possess proinflammatory properties in autoimmune diseases. However, the role of IL-36γ in HT is insufficiently understood. The purpose of the present study was to investigate the potential relationship between IL-36γ and HT. DESIGN & METHODS: We included 100 subjects, among whom, 52 had early-stage HT and 48 were healthy controls (HC). The subjects' basic clinical information was obtained through physical examination and clinical histories of signs and symptoms. Thyroid function and measurements of thyroid-stimulating hormone (TSH), free triiodothyronine 3, free triiodothyronine 4 (FT4), thyroid peroxidase antibody (TPO-Ab), and thyroid globulin antibody were measured using a fully automated chemiluminescent immunoassay analyzer. The expression levels of serum IL-36γ were determined using an enzyme-linked immunosorbent assay. RESULTS: The serum IL-36γ level in the HT group was significantly higher compared with that of the HC group [91.91 (67.52, 130.90) pg/mL vs 62.50 (44.61, 91.53) pg/mL, P < 0.0001]. Correlation analysis showed a negative correlation between serum IL-36γ and TPO-Ab titers in the HT group (r = -0.3507, P = 0.0054). According to receiver operating characteristic curve analysis, the area under the curve (AUC) for IL-36γ was 0.7278 (P < 0.0001), and the AUC for IL-36γ combined with TSH and FT4 was 0.8109 (P < 0.0001). CONCLUSIONS: The present study indicates that serum IL-36γ expression is increased in patients with HT and negatively correlates with TPO-Ab. Our findings suggest that IL-36γ may be involved in the development of HT and may therefore serve as a potential new diagnostic biomarker for HT.

Increased serum IL-41 is associated with disease activity in rheumatoid arthritis.

BACKGROUND: Interleukin (IL)-41 is upregulated in the synovial tissue of rheumatoid arthritis (RA) patients, but its serum level has not been reported. The present study aimed to determine IL-41 expression in serum from RA patients and to clarify the relationships between IL-41 and disease-related parameters in RA patients. METHODS: The study included 46 RA patients and 32 healthy controls (HC). Baseline data were obtained by routine physical examinations and immune-related parameters were measured by an automated chemiluminescent immunoassay analyzer. The correlations between IL-41 and disease activity score in 28 joints (DAS28) and serum clinical data were analyzed using the Pearson correlation test. RESULTS: Serum IL-41 concentrations were higher in RA patients than in HC. Serum IL-41 was positively correlated with DAS28 based on C-reactive protein (DAS28-CRP), CRP, erythrocyte sedimentation rate (ESR), mean platelet volume (MPV), and CRP-to-albumin ratio (CAR) and negatively correlated with platelet count, while rheumatoid factor was significantly correlated with ESR, CRP, and CAR. Receiver operating characteristic curve analysis showed that IL-41 had diagnostic value for RA, especially when combined with MPV. CONCLUSIONS: The present findings suggest that IL-41 is increased in the serum of RA patients and may be a potential new diagnostic biomarker for RA.