Patients With Pancreatitis-Related Gene Variants Showed Higher Incidence of Hyperpancreatic Enzymemia After Endoscopic Retrograde Cholangiopancreatography.
Patients with pancreatitis-related gene variants showed a significantly higher incidence of post-ERCP hyperpancreatic enzymemia, but not post-ERCP pancreatitis.
Where it sits
this study against the rest of the teriparatide (pth 1-34) corpusSummary and findings
This study investigated the association between pancreatitis-related gene variants and post-endoscopic retrograde cholangiopancreatography (ERCP) outcomes in 94 patients. The incidence of post-ERCP hyperpancreatic enzymemia (PEH) was significantly higher in patients with gene variants. The study found that 4% of patients experienced post-ERCP pancreatitis (PEP).
Abstract
<h4>Background</h4>Post-endoscopic retrograde cholangiopancreatography (post-ERCP) pancreatitis (PEP) is the most severe adverse event associated with ERCP. Although numerous studies have identified risk factors for PEP, the role of genetic background in its development remains unexplored. The present study investigated the association between pancreatitis-related gene variants (PRG-variants) and PEP.<h4>Methods</h4>This prospective, single-center study included 94 patients with naïve papilla who underwent ERCP between October 2021 and August 2023. Targeted sequencing was performed to analyze variants in four PRGs: <i>PRSS1</i>, <i>SPINK1</i>, <i>CTRC</i>, and <i>CPA1</i>. Patients were classified into two groups based on the presence or absence of PRG-variants, and the incidences of PEP and of post-ERCP hyperpancreatic enzymemia (PEH) were compared.<h4>Results</h4>PRG-variants, regardless of their pathogenicity, were identified in 16 (17%) patients. Among all cases, PEP occurred in four (4%) patients, and PEH occurred in 27 (29%) patients. The incidence of PEP did not differ significantly with and without PRG-variants (<i>p</i> = 0.532). However, the group with PRG-variants had a significantly higher incidence of PEH, as demonstrated by both univariate (<i>p</i> = 0.013) and multivariate analyses (odds ratio, 6.291; 95% confidence interval, 1.133-34.934).<h4>Conclusions</h4>The present pilot study suggests that patients with PRG-variants, regardless of their pathogenicity, demonstrated a significantly higher incidence of PEH but not PEP. PEH may reflect pancreatic parenchyma injury and may progress to PEP when additional factors are present. Thus, PRG-variants may contribute to biochemical pancreatic injury after ERCP. Further large-scale studies and comprehensive genomic profiling of patients with PEH/PEP are warranted.<h4>Trial registration</h4>The central ethics committee approved the study protocol (M21-0066).
Background
This paper addresses the role of genetic background in the development of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis, a severe adverse event. While risk factors for post-ERCP pancreatitis (PEP) have been identified in previous studies, the impact of pancreatitis-related gene variants (PRG-variants) had not been explored. Understanding these associations may provide insights into the mechanisms underlying pancreatic injury following ERCP.
Methods
This was a prospective, single-center study involving 94 patients with naïve papilla who underwent ERCP from October 2021 to August 2023. Targeted sequencing analyzed variants in four pancreatitis-related genes: PRSS1, SPINK1, CTRC, and CPA1. Patients were divided into two groups based on the presence or absence of PRG-variants, and the incidences of PEP and post-ERCP hyperpancreatic enzymemia (PEH) were compared.
Results
Among the 94 patients, PRG-variants were identified in 16 (17%) patients. PEP occurred in four (4%) patients, while PEH occurred in 27 (29%) patients. The incidence of PEP did not differ significantly between the groups with and without PRG-variants (p = 0.532). However, the group with PRG-variants demonstrated a significantly higher incidence of PEH (p = 0.013), with an odds ratio of 6.291 (95% CI, 1.133-34.934).
Interpretation
The findings suggest that while PRG-variants do not significantly increase the risk of PEP, they are associated with a higher incidence of PEH, indicating potential biochemical pancreatic injury. This contrasts with prior literature that may not have considered genetic factors in post-ERCP outcomes. The small effect size and limited sample size raise questions about the clinical significance and applicability of these results, emphasizing the need for larger studies to confirm these associations.
Key findings
- PRG-variants identified in 16 (17%) patients.
- PEP occurred in four (4%) patients.
- PEH occurred in 27 (29%) patients.
- Incidence of PEP did not differ significantly with and without PRG-variants (p = 0.532).
- Group with PRG-variants had a significantly higher incidence of PEH (p = 0.013).
- Odds ratio for PEH in patients with PRG-variants was 6.291 (95% CI, 1.133-34.934).
Limitations
- small sample size of 94 patients
- single-center design limits generalizability
- pilot study nature suggests preliminary findings