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.
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.
The study's objective was to assess the association between the PRSS1R122H and N29I and the SPINK1 N34S mutations and acute pancreatitis (AP) and recurrent pancreatitis in Mexican pediatric patients.
Overall, no significant association was found between TNF-α gene -308A/G polymorphism and AP risk when all studies were pooled into the meta-analysis (for A/A+A/G versus G/G: OR = 1.03, 95% CI = 0.83-1.28, P = 0.79; for A/A versus A/G+G/G: OR = 0.97, 95% CI = 0.65-1.45, P = 0.87; for A/A versus G/G: OR = 1.23, 95% CI = 0.79-1.91, P = 0.37; for A allele versus G allele: OR = 0.99, 95% CI = 0.83-1.18, P = 0.90).
In conclusion, we suggest that IL-10-1082A/G gene polymorphisms contribute to the development of acute pancreatitis in codominant, dominant and recessive models.
The moderately severe group of 27 patients (according to Atlanta 2012) had significantly better outcomes when compared to those 47 patients classified as severe form of AP (according to Atlanta 1992) with lower incidence of necrosis and sepsis, lower APACHE II (<i>P</i> = 0.002) and MODS (<i>P</i> = 0.001) scores, shorter ICU stay, decreased need for interventional and surgical treatment.
Early-onset disease was associated with mutations in cationic trypsinogen (PRSS1) (P < .01), chymotrypsin C (CTRC) (P = .01), family history of acute pancreatitis (P = .02), family history of CP (P < .01), biliary cysts (P = .04), or chronic renal failure (P = .02).
We found that the IL-8 -251T/A polymorphism is associated with an increased risk of acute pancreatitis, and no significant association between IL-1βand IL-10 gene polymorphisms and risk of acute pancreatitis was detected.
Eligible records provided data from consecutive AP cases and used CTSI or modified CTSI (mCTSI) alone or in combination with other prognostic scores [Ranson, bedside index of severity in acute pancreatitis (BISAP), Acute Physiology, and Chronic Health Examination II (APACHE II), C-reactive protein (CRP)] for the evaluation of severity or mortality of AP.
The SPINK1 variant p.N34S is overrepresented in patients with acute pancreatitis, but more studies distinguishing between first-time and recurrent acute pancreatitis have to be done to determine whether this is only true for patients with recurrent acute pancreatitis.
Plasma levels of amylase and lipase, pancreatic myeloperoxidase (MPO), histology, visceral hypernociception and motor coordination were evaluated 11 and 24 h after acute pancreatitis (AP) induction.
However, we found no significant association between IL-1β +3954 C/T, IL-1β -511 C/T, IL-6 -174 G/C, IL-6-174 G/C, IL-6 -634 C/G, IL-10 -1082A/G, or IL-10 -819C/T polymorphisms and risk of acute pancreatitis.
Attacks of acute pancreatitis in HP subjects appear to be independent of the relative expression of the mutant PRSS1 H122 allele or SPINK1 gene expression.
However, there were no significant associations between IL-1β (IL-1β +3954 C/T (rs1143634) and IL-1β -511 C/T (rs16944)), IL-6 (IL-6 -174 G/C (rs1800795) and IL-6 -634 C/G (rs1800796)) and IL-10 (IL-10-1082 A/G (rs1800896), IL-10-819 C/T (rs1800871) and IL-10-592 C/A (rs1800872)) gene polymorphisms and AP risk.
We suggest that both SNPs of TNFalpha are not genetic risk factor for AP susceptibility (OR = 1.63; 95% CI: 1.13-4.01 for TNFalpha(-308) and OR = 0.86; 95% CI: 0.75-1.77 for TNFalpha(-238)).