{"id":686,"date":"2023-04-08T10:59:08","date_gmt":"2023-04-08T10:59:08","guid":{"rendered":"http:\/\/elmoustkbal.com\/?p=686"},"modified":"2023-04-08T10:59:08","modified_gmt":"2023-04-08T10:59:08","slug":"the-level-of-serum-dkk-1-was-correlated-with-a-swollen-joint-count-and-levels-of-complement-components-3-and-4","status":"publish","type":"post","link":"https:\/\/elmoustkbal.com\/?p=686","title":{"rendered":"\ufeffThe level of serum Dkk-1 was correlated with a swollen joint count, and levels of complement components 3 and 4"},"content":{"rendered":"<p>\ufeffThe level of serum Dkk-1 was correlated with a swollen joint count, and levels of complement components 3 and 4. 3 and 4. Elevated Dkk-1 level (odds ratio?=?4.440, 95% confidence interval: 1.246C15.817, (percentage), mean??standard deviation, or median (P25, P75). Statistical significance between groups was assessed with values? ?0.050 were considered significant. The cut-off value of Dkk-1 concentrations was decided using a receiver operating characteristic (ROC) curve. Results Characteristics of study participants The major demographic, clinical and laboratory features, and radiographic evaluations are shown in Table ?Table1.1. Among NVP-BHG712 69 patients with PsA, 56.5% were female, the mean age was 52.7??13.0 years, mean arthritis and psoriasis duration were 5.0 (1.6, 13.0) and 12.0 (5.0, 20.0) years, and 17.4% (12\/69) of them had a family history of skin psoriasis or PsA. Nail psoriasis, dactylitis, enthesitis, and uveitis were observed in 43.5%, 10.1%, 27.5%, and 2.9% of the PsA patients, respectively. <a href=\"https:\/\/www.adooq.com\/nvp-bhg712.html\">NVP-BHG712<\/a> Positive RF (8.7% values(%)12 (17.4)NANACCTender joint count, 0C46, (%)6.0 (2.0, 12.5)8.0 (5.0, 12.0)NA?1.400?0.161Swollen joint count, 0C44, (%)3.0 (0, 8.0)4.0 (2.0, 7.0)NA?1.445?0.148Nail psoriasis, (%)30 (43.5)NANACCDactylitis, (%)7 (10.1)NANACCEnthesitis, (%)19 (27.5)NANACCUveitis, (%)2 (2.9)NANACCRF-positive, (%)6 (8.7)31 (79.5)NA55.440? 0.010Anti-CCP-positive, (%)4 (5.8)38 (97.4)NA87.130? 0.010HLA-B27-positive, (%)14 (20.3)NANACCSacroiliitis, (%)32 NVP-BHG712 (46.4)NANACCBone erosion, (%)26 (37.7)19 (48.7)NA1.249?0.264 Open in a separate window Age and disease duration are respectively presented as mean??SD and median (P25, P75). ?Differences were analyzed by one-way analysis of variance (ANOVA) with Holm-Sidak multiple comparisons test for three groups, the statistics value was Anti-CCP: Anti-cyclic citrullinated peptide; HCs: Healthy controls; HLA-B27: Human leukocyte antigen-B27; NA: Not assessed; Ps: Psoriasis; PsA: Psoriatic arthritis; RA: Rheumatoid arthritis; RF: Rheumatoid factor; SD: Standard deviation. Dkk-1 level was elevated in sera of patients with PsA As shown in Figure ?Physique1,1, Dkk-1 was elevated in 68.1% (47\/69) of the patients with PsA, 46.2% (18\/39) of RA patients, and 9.5% (2\/21) of HCs. Serum Dkk-1 level in PsA patients (9.269??3.276 ng\/mL) was significantly higher than that in patients with RA (7.862??2.487 ng\/mL, valuesvalue(%)8 (17.0)4 (18.2)0?1.000Tender joint count, (%)6.0 (2.0, 13.8)6.0 (3.5, 10.8)?0.019?0.985Swollen joint count, (%)4.0 (1.0, 9.3)1.0 (0, 4.5)?2.103?0.035Nail psoriasis, (%)20 (42.6)10 (45.5)0.051?0.821Dactylitis, (%)6 (12.8)1 (4.5)0.392?0.531Enthesitis, (%)16 (34.0)3 (13.6)3.127?0.077Uveitis, (%)1 (2.1)1 (4.5)0?1.000WBC (109\/L)6.62??1.757.73??4.21?1.199?0.242Hb (g\/L)117.60??18.17121.58??15.17?0.892?0.376PLT (109\/L)250.00 (180.00, 287.30)248.00 (198.25, 329.33)?0.579?0.562ESR (mm\/h)46.00 (15.00, 74.00)40.50 (15.75, 88.00)?0.161?0.872CRP (mg\/L)16.60 (5.01, 48.70)25.50 (8.09, 92.00)?1.275?0.202IgA (g\/L)3.31 (2.14, 5.04)3.26 (2.25, 5.05)?0.262?0.793IgG (g\/L)13.59??3.7017.29??9.39?1.781?0.087IgM (g\/L)0.90 (0.71, 1.30)1.02 (0.89, 1.49)?1.265?0.206Complement C3 (g\/L)1.11??0.341.29??0.26?2.133?0.037Complement C4 (g\/L)0.25??0.090.26??0.08?0.548?0.586RF-positive, (%)3 (6.4)3 (13.6)0.290?0.590Anti-CCP-positive, (%)3 (6.4)1 (4.5)0?1.000HLA-B27-positive, (%)9 (19.1)5 (22.7)0.001?0.981Sharp score9.0 (0, 17.0)3.0 (0, 7.0)?2.067?0.039Sacroiliitis, (%)27 (57.4)5 (22.7)7.264? 0.010RAD, (%)30 (63.8)8 (36.4)4.569?0.033Bone erosion, (%)22 (46.8)4 (18.2)5.230?0.022 Open in a separate window ?Differences were analyzed by values \/thead Univariate?Age0.9950.958C1.0330.786?Dkk-1 elevated3.9601.163C13.4880.028?Duration of arthritis1.0030.965C1.0430.871?Duration of psoriasis1.0280.984C1.0740.222?Tender joint count1.0170.969C1.0670.490?Swollen joint count1.0340.955C1.1190.414?Nail psoriasis2.5450.937C6.9140.067?Dactylitis4.8810.872C27.3150.071?Enthesitis1.7470.597C5.1130.309?Uveitis1.6800.101C28.0640.718Multivariate?Dkk-1 elevated4.4401.246C15.8170.021 Open in a separate window CI: Confidence intervals; Dkk-1: Dickkopf-1; OR: Odds ratio; PsA: Psoriatic arthritis. Discussion In this study, we exhibited that serum Dkk-1 was significantly elevated in PsA patients compared with RA patients and HCs, supporting the idea that Dkk-1 might be involved in the pathogenesis of PsA. A key obtaining of our study is that increased Dkk-1 was correlated with bone erosion in PsA patients. PsA is usually a chronic autoimmune disorder that attacks enthesis and synovial joints, resulting in bone destruction. Progressive bone erosion and new bone formation are hallmarks of PsA, so finding <a href=\"http:\/\/www.ncbi.nlm.nih.gov\/sites\/entrez?Db=gene&#038;Cmd=ShowDetailView&#038;TermToSearch=23616&#038;ordinalpos=1&#038;itool=EntrezSystem2.PEntrez.Gene.Gene_ResultsPanel.Gene_RVDocSum\">SH3BP1<\/a> the main molecules involved in bone erosion is essential for determining the mechanism of PsA. Dkk-1 is usually a key inhibitor in Wnt signaling by binding to the Wnt co-receptor low density lipoprotein receptor-related protein 5\/6 (LRP5\/6).[18,19] Wnt signaling via LRP5 impacts accrual and is crucial for peak bone mass establishment.[20] The LPR5 mutation causes high bone density, by reducing the action of a normal antagonist of the Wnt-mediated pathway and thus promoting Wnt signaling.[21] These findings indicate that Dkk-1 is a potential treatment or prevention target of osteoporosis or bone erosion.[8,20C22] Dkk-1 functions directly in the differential remodeling of human joint architecture by diverse mechanisms. For example, an elevated level of Dkk-1 impairs bone formation by upregulating the expression of inflammatory cytokines including tumor necrosis factor (TNF).[23,24] Additionally, lower Dkk-1 contributes to the appearance of osteophytes.[24] PsA is a heterogeneous disease that may manifest both patterns of osteopathology, either bone loss or bone remodeling.[3,4,16] The mechanism of PsA joint remodeling is unknown.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>\ufeffThe level of serum Dkk-1 was correlated with a swollen joint count, and levels of complement components 3 and 4. 3 and 4. 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