These findings indicate that leptin and TNFα are associated with IPFD independent of abdominal fat distribution and other covariates in individuals after AP.
Taken together, exogenous leptin administration regulated inflammatory factors and the expression of OB‑Rb at the early stage of AP, which exerted protective effects by through the immunological and endocrinal pathways.
The aim of the present study was: (1) to assess plasma leptin levels in rats with caerulein-induced pancreatitis (CIP) and humans with acute pancreatitis; and (2) to determine the effects of exogenous leptin on the course of acute CIP in rats.
Serum Serine Peptidase Inhibitor Kazal-Type 1, Trypsinogens 1 to 3, and Complex of Trypsin 2 and α1-Antitrypsin in the Diagnosis of Severe Acute Pancreatitis.
This study aimed to investigate the clinical and analytical features and the APOE genotypes in patients with acute pancreatitis and severe hypertriglyceridemia.
Because apoprotein E (Apo E) genetic polymorphism has an important influence on CMR clearance, we compared frequency distribution of Apo E phenotypes in 52 patients with AP, 109 patients with gallstones, and 110 control subjects.
A binomial logistic regression was performed to evaluate Ranson's criteria and IL6, IL8, and IL10 (at admission and after 48 hours) in the course of AP.
Increased expression of PRSS1 or PRSS1<sup>R122H</sup> increased focal damage in pancreatic tissues and increased the severity of acute pancreatitis after caerulein injection.
NLRP3 Inflammasome Regulates Development of Systemic Inflammatory Response and Compensatory Anti-Inflammatory Response Syndromes in Mice With Acute Pancreatitis.
A binomial logistic regression was performed to evaluate Ranson's criteria and IL6, IL8, and IL10 (at admission and after 48 hours) in the course of AP.
Glucagon explained up to 86% of the variance in glucagon-like peptide 1, whereas cortisol explained up to 89% of the variance in interleukin 6 in hyperglycemia after AP.
The results of pooled analyses showed that CLDN2 rs7057398, MORC4 rs12688220 and PRSS1-PRSS2 rs10273639 polymorphisms were all significantly associated with susceptibility to acute pancreatitis in Caucasians.
Disruption of the locus that encodes cationic trypsinogen in mice (T7) causes loss of expression of the protein, but only partially decreases the severity of secretagogue-induced acute pancreatitis and has no effect on chronic pancreatitis.
Increase in α-smooth muscle actin and nestin-positive stellate cell numbers in acute pancreatitis was correlated to increase in numbers of CD34-positive vascular endothelium, CD68- or CD163-positive macrophages, CD138-positive plasmacytes, CD3-positive T lymphocytes, and myeloperoxidase-positive leucocytes.
Our goal was to assess PTX3 as a predictor of systemic inflammatory response syndrome (SIRS), death and disease severity in acute pancreatitis (AP) in comparison to C-reactive protein (CRP) and the APACHE II score.
Targeted deletion of β-arr1 notably upregulated expression of the pancreatic inflammatory mediators including tumor necrosis factor α and interleukin 1β as well as interleukin 6 and aggravated AP in caerulein-induced mice.
These findings indicate that leptin and TNFα are associated with IPFD independent of abdominal fat distribution and other covariates in individuals after AP.
None of the patients who remained on CFTR modulators developed an episode of AP or required hospitalization for AP related abdominal pain during follow-up.