ABSTRACT
BACKGROUND: Lupus enteritis (LE), a main cause of acute abdominal pain in systemic lupus erythematosus (SLE) patients, is a serious and potentially fatal complication. This study aimed to identify clinical serological indicators to establish a nomogram to assess LE in SLE patients with gastrointestinal manifestations. METHODS: The clinical and laboratory data of SLE patients with gastrointestinal manifestations that were hospitalized in the West China Hospital from January 2010 to January 2020 were retrospectively analyzed. The least absolute shrinkage and selection operator logistic regression model was used to select potentially relevant features. Subsequently, a nomogram was developed using multivariable logistic analysis. The performance of the nomogram was evaluated using a receiver operating characteristic curve, a calibration curve, and decision curve analysis (DCA). FINDINGS: We included a total of 8,505 SLE patients, of which 251 had experienced gastrointestinal manifestations. The patients were randomly divided into training (n = 176) and validation (n = 75) groups. The LRA (LE Risk Assessment) model consisted of 11 significantly associated variables, which included complement 4, antineutrophil cytoplasmic antibody, albumin, anion gap, age, d-dimer, platelet, serum chlorine, anti-Sjögren's-syndrome-related antigen A, anti-ribosomal P protein, and anti-ribonucleoprotein. In the training and validation cohorts, the areas under the curve were 0.919 (95% confidence interval [CI]: 0.876-0.962) and 0.870 (95% CI: 0.775-0.964), respectively. The nomogram demonstrated excellent performance in the calibration curve and DCA. INTERPRETATION: The LRA model exhibits good predictive ability in assessing LE risk in SLE patients with gastrointestinal manifestations.
ABSTRACT
C-X-C motif chemokine ligand 8 (CXCL8) is involved in tumor proliferation, migration, and invasion. However, the function of CXCL8 in colorectal cancer (CRC) is controversial. Here, we analyzed RNA-sequencing (RNA-seq) data to identify differentially expressed genes and pathways according to gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with CRC. The levels of the mRNA encoding CXCL8 were significantly increased in early and advanced stages of CRC, as well as in metastases and nonmetastasis cases using RNA-seq analysis (n = 91). These findings were consistent with immunohistochemical analysis of CXCL8 expression (n = 87). Protein-protein interaction (PPI) prediction combined with transcriptional profiling data revealed that CXCL8 levels positively correlated with cAMP responsive element binding protein 1 (CREB1)/ribosomal protein S6 kinase B1 (RPS6KB1) expression, which promotes cell proliferation and differentiation in high expression, while inversely correlated with the expression of Bcl2 associated agonist of cell death (BAD) protein to inhibit apoptosis during the progression of CRC. These findings provide compelling clinical and molecular evidence to support the conclusion that CXCL8 contributes to the genesis and progression of CRC.
