Risk factors for the flare of systemic lupus erythematosus and its influence on prognosis: a single-center retrospective analysis.

OBJECTIVES: To explore the risk factors for systemic lupus erythematosus (SLE) flare and their impact on prognosis. METHODS: The clinical characteristics, laboratory results, and treatment plans of 121 patients with SLE flare were retrospectively analyzed. Ninety-eight SLE outpatients with sustained remission during the same period were selected as controls. Logistic multivariate regression analysis was employed to screen for risk factors for SLE flare. RESULTS: Infection, thrombocytopenia, arthritis, anti-nucleosome antibodies positive, anti-ß2-glycoprotein I (IgG) antibodies positive, and patient's self-discontinuation of medicine maintenance therapy might be risk factors for SLE flare. Patients who discontinued medicine maintenance therapy by themselves had a significantly higher rate of severe SLE flare than patients with regular medicine maintenance therapy (P = 0.033). The incidence of anemia associated with SLE (P = 0.001), serositis (P = 0.005), and pulmonary hypertension (P = 0.003) in patients who discontinued medicine maintenance therapy were significantly higher than patients with regular medicine maintenance therapy. SLE patients with regular medicine maintenance therapy for less than 3 years had a higher risk of pulmonary hypertension than those with regular medicine maintenance therapy longer than 3 years (P = 0.034). CONCLUSIONS: The accompanying thrombocytopenia, arthritis, anti-nucleosome antibodies positive and anti-ß2-glycoprotein I (IgG) antibodies positive at the onset of SLE may affect the prognosis of SLE. Patient's self-discontinuation of medicine maintenance therapy is the main cause of SLE flare, which may induce severe flare in SLE patients and lead to a significantly higher incidence of pulmonary hypertension.

Predictive Value of Active Sacroiliitis in MRI for Flare Among Chinese Patients with Axial Spondyloarthritis in Remission.

INTRODUCTION: In recent axSpAx patients with remission lasting at least 3 months and later followed-up monthly for a median of 8 months, we compared the predictive value of baseline MRI of sacroiliac joints and constructed a nomogram model for predicting flare. METHODS: This study included 251 patients with axial spondyloarthritis, according to the ASAS axSpA classification criteria, who achieved Low Disease Activity (ASDAS) and underwent MRI examination. A total of 144 patients from the First Affiliated Hospital of Xiamen University were used as the nomogram training set; 107 from the First Affiliated Hospital of Fujian Medical University were for external validation. RESULTS: The median time of relapse was 8.705 months (95% CI 8.215-9.195) and 7.781 months (95% CI 7.075-8.486) for MRI-positive patients and 9.8 months (95% CI 9.273-10.474) for MRI negative patients, respectively. Both active sacroiliitis on MRI (HR 1.792, 95% CI 1.230-2.611) and anti-TNF-α treatments (HR 0.507, 95% CI 0.349-0.736) were significantly associated with disease flares. Gender, disease duration, HLA-B27, MRI, and anti-TNF-α treatment were selected as predictors of the nomogram. The areas under the ROC curve (AUROCs) of the 1-year remission probability in the training and validation groups were 0.71 and 0.729, respectively. Nomogram prediction models present better AUROCs, C-indices, and decision curve analysis cure than the clinical experience model. CONCLUSIONS: Active sacroiliitis in MRI requires weighting in order to estimate remission and disease flares, when axSpA patients achieve low disease activity. The simple nomogram might be able to discriminate and calibrate in clinical practice. TRIAL REGISTRATION: ClinicalTrials, NCT03425812, Registered 8 February 2018, https://clinicaltrials.gov.

Risk factors for the flare of systemic lupus erythematosus and its influence on prognosis: a single-center retrospective analysis

Abstract Objectives: To explore the risk factors for systemic lupus erythematosus (SLE) flare and their impact on prognosis. Methods: The clinical characteristics, laboratory results, and treatment plans of 121 patients with SLE flare were retrospectively analyzed. Ninety-eight SLE outpatients with sustained remission during the same period were selected as controls. Logistic multivariate regression analysis was employed to screen for risk factors for SLE flare. Results: Infection, thrombocytopenia, arthritis, anti-nucleosome antibodies positive, anti-β2-glycoprotein I (IgG) antibodies positive, and patient's self-discontinuation of medicine maintenance therapy might be risk factors for SLE flare. Patients who discontinued medicine maintenance therapy by themselves had a significantly higher rate of severe SLE flare than patients with regular medicine maintenance therapy ( P = 0.033). The incidence of anemia associated with SLE ( P = 0.001), serositis ( P = 0.005), and pulmonary hypertension ( P = 0.003) in patients who discontinued medicine maintenance therapy were significantly higher than patients with regular medicine maintenance therapy. SLE patients with regular medicine maintenance therapy for less than 3years had a higher risk of pulmonary hypertension than those with regular medicine maintenance therapy longer than 3years ( P = 0.034). Conclusions: The accompanying thrombocytopenia, arthritis, anti-nucleosome antibodies positive and anti-β2-glycoprotein I (IgG) antibodies positive at the onset of SLE may affect the prognosis of SLE. Patient's self-discontinuation of medicine maintenance therapy is the main cause of SLE flare, which may induce severe flare in SLE patients and lead to a significantly higher incidence of pulmonary hypertension.

[Arresting effect of p16 and dll4 transfection on cell cycle of K562 cells].

This study was purposed to investigate the expression and role of eukaryotic expression vector containing p16, dll4 genes in leukemia K562 cells. A vector pBudCE4.1-16-dll4 containing wild type p16cDNA and dll4cDNA was designed and constructed, then this vector was transfected into leukemia K562 cells by using lipofectamine 2000. The expression of p16 and dll4 genes was detected by Western blot, the cell growth curve and cell cycle were determined by CCK-8 kit and flow cytometry respectively. The results showed that the recombinant plasmid pBudCE4.1-16-dll4 was constructed and transfected into K562 cells in vitro successfully. The expression of exogenous P16 and Dll4 proteins could be detected in K562 cells. After transfection for 48 hours, the K562 cells were arrested in G(1) phase, the cell count increased in G(0)/G(1) phase and reduced in S phase, the cell proliferation decreased as compared with control. It is concluded that the p16 and dll4 genes can simultaneously express in K562 cells transfected with recombinant plasmid pBudCE4.1-16-dll4 in vitro which results in G(0)/G(1) arrest and reduces cell proliferation.

[Inhibitory effect of p16, p53 transfection on leukemic cell lines K562 and HL-60].

This study was purposed to construct a vector containing human suppressor gene p53 and p16, and to investigate their expression and effect on K562 and HL-60 cells. pBudCE4.1-53-16 is a vector designed for simultaneous expression of human suppressor gene p53 and p16 in mammalian cell line. After transfection into K562 cells with lipofectamine(TM) 2000, the expression of p53 and p16 genes was detected by Western blot and immunocytochemical method. The growth curve, apoptosis, cell cycle were assayed by CCK-8 and flow cytometry. The results showed that the recombinant plasmid pBudCE4.1-53-16 was constructed successfully and were verified by PCR and restriction analysis. The expression of P53 and P16 protein could be detected after transfection into leukemia cells (K562 and HL-60) for 48 hours. As compared with control group, the cell proliferation in experimental group was inhibited, the cells were arrested in G0 phase and apoptotic cells increased (p<0.001). It is concluded that the recombinant plasmid pBudCE4.1-53-16 has been established. p16 and p53 in the recombinant plasmid pBudCE4.1-53-16 synchronously express in leukemic cells after transfection in vitro for 2 days and results in reduced proliferation, G0 arrest and apoptosis increase.

[Inhibition of K562 cell proliferation by wild type p16 and p53 genes co-transfection].

The tumor suppressor gene p53 and p16, both of which play an important role in inhibition of tumorigenesis, are homozygously deleted in human myeloid leukemia cell line K562. To explore the inhibition of K562 cell proliferation by wild type p16 and p53 genes, both p16 and p53 genes were co-transfected into K562 cells mediated by liposome. The expression of the two genes was measured by immunocytochemical method, the cell cycle was analysed by flow cytometry, and the number of recovered viable cells was assessed after transfection. After co-transfection, the p53 and p16 positive cells were 23% and 28%, respectively. The results showed that co-transfection of p16 and p53 genes significantly inhibits cell proliferation comparing with transfection either by p16 gene or by p53 gene (P < 0.05). Expression of p16 and p53 proteins increased the cell number in G(1) phase but decreased the cell number in S phase. It is concluded that co-transfection of p16 and p53 genes has a stronger growth-inhibitory effect on K562 cell growth than that of transfection only by p16 gene or by p53 gene, may be a pathway for gene therapy in leukemia.