Background Acute pancreatitis (AP) is a common acute abdominal disease. Rapid evaluation of the severity is important for AP prognosis and treatment. Free triiodothyronine (fT3) level is associated with the prognosis of AP patients. This study aimed to investigate the fT3 level in patients with acute pancreatitis; early warning signs of inflammation, including interleukin-6 (IL-6) and interleukin-10 (IL-10); and the correlation of fT3 level with illness severity. Material/Methods Enrolled AP patients (N=312) were divided into an SAP group (N=92) and a non-SAP group (N=220) according to the Revision of Atlanta classification. Blood or tissue samples and baseline clinical characteristics were recorded. The t test and chi-square test were used to evaluate differences between the 2 groups. Multivariate logistic regression analysis and receiver operating characteristic (ROC) curves were used to investigate protective factors. One-way repeated measures analysis of variance was used to evaluate the prognosis of SAP patients. Results In our study, compared with APACHII score (AUC 0.829 [95% CIs 0.769–0.889]) and Ranson score (AUC 0.629 [95% CIs 0.542–0.715]), our predictive model (AUC 0.918 [95% CIs 0.875–0.961]) showed better prognostic performance in predicting poor patient outcomes. In the SAP group, changes in fT3 level were significantly associated with prognosis ( P <0.05). Conclusions The predictive model can improve the diagnostic accuracy and prediction of the severity of disease. FT3 level could be used as an independent risk factor to predict the mortality of SAP patients.

No abstract

Objective To analyze genotypes and phenotypes of a child with Developmental Dysplasia of Hip (DDH), developmental delays, recurrent fever, hypothyroidism and cleft palate. Methods G-banding karyotypeing analysis and Next-generation Sequencing(NGS) were performed on the child. The parents of the child were verified by copy number variations (CNV) and Sanger sequencing to determine the source of variations. Results The karyotype of the child was 46, XX. A 10.44Mb deletion(chr18:67562936-78005270del) at 18q22.2q23 was found by NGS, as well as HSPG2 variation (chr1: 22206699, c.2244c > A, exon 17, p.h748q; chr1: 22157321–22157321, c.11671 + 154insA, Intron) originated from father and mother, respectively. Conclusion This is the first 18q deletion syndrome case which accompanied by DDH. Most phenotypes of the child ,such as developmental delays, cleft palate, may be related to 18q22 2q23 deletion, while no variant genes related to DDH were found in this deletion region. DDH may be related to mutation of HSPG2.

No abstract