Our study found that HBV infection was associated with better OS among mPC patients. We also developed a nomogram based on HBV infection status, nutritional indicators, and clinicopathological characteristics that may be useful for identifying mPC patients at higher risk of poor prognosis. This may guide the personalization of treatment and help focus medical resources as efficiently as possible.
Several studies suggest that HBV infection contributes to the occurrence and progression of pancreatic cancer. 21,22 However, whether such infection influences prognosis in pancreatic cancer remains controversial. For example, HBV infection was associated in one study with higher risk of synchronous liver metastases and therefore worse prognosis. (21) However, another study found no significant difference in short- or long-term survival between HBV-positive or -negative patients following pancreatic cancer resection. (22) This discrepancy may reflect differences in the patient samples. Future research should explore the relationship between mPC patients and OS by Further large sample and multi-center studies.
Perhaps surprisingly, we found that HBV infection appears to improve prognosis in mPC. Future research should explore the potential mechanisms behind this. At first, HBV is thought to be hepatotropic and is strongly linked to end-stage chronic liver disease. (23) HBV infection, on the other hand, is a systemic infection process that can spread through blood and be deposited in organs other than the liver.(14, 15) The pancreas and liver are next to each other, but since they share blood arteries and ducts and progenitor cells that originate from the endoderm cells of the embryonic foregut, the pancreas may also be a target organ for HBV. (24, 25) According to certain research, pancreatic cancer patients' cancer tissues had signs of HBV infection.(9, 26) Batskikh et al(27) found evidence of HBV DNA and HBV X antigen expression in the tissues of people with pancreatic cancer, showing the ability of HBV virus replication in pancreatic cancer tissues. As a result, we surmised that HBV could infect PC cells and be capable of active replication in the pancreas. Furthermore, Substantial evidence points to the ability of HBV to stimulate persistent inflammation by causing immune cells to secrete pro-inflammatory cytokines, including IL-6, IL-10, IL-12, TNF- and IFN-γ.(28–30) At the same time, HBV promotes immunosuppression through upregulation of COX2. (31, 32) Therefore, we speculate that there is a relationship between persistent inflammation and the occurrence and development of cancer. HBV may actively replicate in pancreatic cancer cells, secrete these cytokines and act on pancreatic cancer cells, modulating the pancreatic cancer tumor microenvironment, potentially influencing the prognosis of mPC patients. Finally, the patient has been receiving regular anti-HBV treatment since hospitalization, and anti-HBV drugs have been shown to have immunomodulatory effects,which can impact the effectiveness of chemotherapy and the immune system's ability to fight tumors. (33)
Several factors that our study identified as independent risk factors for poor OS in mPC have already been linked to prognosis of patients with pancreatic cancer patients following radical resection or incurable pancreatic cancer, including high CA125, HALP and NAR. (2, 18, 34) This overlap with the literature suggests that our analyses and the resulting nomogram are reliable.
At the same time, our findings should be interpreted with caution in light of our small sample; the retrospective study design, which increases the risk of selection bias; and the fact that our sample covered nearly 10 years, during which the use and efficacy of anti-viral treatments may have changed. Therefore the generalizability of our findings should be verified and extended in multi-site prospective studies, which should also be used to externally validate our nomogram.