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Introduction: Acute appendicitis (AA) is one of the most common causes of urgent admission to the hospital. Clinically applicable classification distinguishes simple and complex inflammation. Among commonly used inflammation markers of AA, bilirubin concentration is not well studied and thus is rarely applied. Aim: To examine the association between increased serum total bilirubin concentration and the severity of AA. Material and methods: This retrospective study included 169 patients with a presumptive diagnosis of AA who were operated upon between 2015 and 2017. The determined study endpoints were simple complex inflammation and a different diagnosis after surgery. The Mann-Whitney U, Kruskal-Wallis, Fisher's exact, Spearman correlation coefficient and logistic regression tests and receiver-operating characteristics (ROC) were used in analyses. The area under the curve (AUC) was presented with 95% confidence intervals (95% CIs). Statistical significance was set at 0.05. Results: In total, 84 (49.7%) patients underwent laparotomy and 85 (50.3%) laparoscopy. After surgery, 45 (26.6%) patients had a diagnosis other than AA. Furthermore, 83 (49.1%) and 41 (24.3%) patients had simple and complex AA, respectively. The median bilirubin concentration was 0.56, 0.69, and 1.08 mg/dl in patients without AA, with simple, and complex AA, respectively (p < 0.01). The optimal cut-off for serum bilirubin concentration to predict AA severity was = 0.94 mg/dl (AUC = 0.652; 95% CI: 0.543-0.761) with a 44.9% positive and 83.9% negative predictive value (p = 0.006). Conclusions: The serum bilirubin concentration should be considered as one of the possible markers of AA. Moreover, it can be used to predict the severity of AA. [ABSTRACT FROM AUTHOR]

Background: Pediatric appendicitis is a common, potentially serious condition. Determining perforation status is crucial to planning effective management.Purpose: Determine the efficacy of serum total bilirubin concentration [STBC] in distinguishing perforation status in children with appendicitis.Methods: Retrospective review of 257 cases of appendicitis who received abdominal CT scan and measurement of STBC.Results: There were 109 with perforation vs 148 without perforation. Although elevated STBC was significantly more common in those with [36%] vs without perforation [22%], the mean difference in elevated values between groups [0.1mg/dL] was clinically insignificant. Higher degrees of hyperbilirubinemia [>2mg/dL] were rarely encountered [5%]. Predictive values for elevated STBC in distinguishing perforation outcome were imprecise [sensitivity 38.5%, specificity 78.4%, PPV 56.8%, NPV 63.4%]. ROC curve analysis of multiple clinical and other laboratory factors for predicting perforation status was unenhanced by adding the STBC variable. Specific analysis of those with perforated appendicitis and percutaneously-drained intra-abdominal abscess which was culture-positive for Escherichia coli showed an identical rate of STBC elevation compared to all with perforation.Conclusions: The routine measurement of STBC does not accurately distinguish perforation status in children with appendicitis, nor discern infecting organism in those with perforation and intra-abdominal abscess. [ABSTRACT FROM AUTHOR]

Abstract: UGT1A1 enzyme defects are responsible of both Gilbert syndrome (GS) and Crigler–Najjar syndrome (CNS). GS depends on a variant TATAA element (which contains two extra TA nucleotides as compared to the wild type genotype) in the UGT1A1 gene promoter resulting in a reduced gene expression. On the contrary, CNS forms are classified in two types depending on serum total bilirubin concentrations (STBC): the more severe (CNS-I) is characterized by high levels of STBC (342–684μmol/L), due to total deficiency of the UGT1A1 enzyme, while the milder one, namely CNS-II, is characterized by partial UGT1A1 deficiency with STBC ranging from 103 to 342μmol/L. GS and CNS are caused by genetic lesions involving a complex locus encoding the UGT1A1 gene. The present report provides an update of all reported UGT1A1 gene mutations associated to GS and CNS. [Copyright &y& Elsevier]