Serum TNF-Alpha Levels in Acute and Chronic Pancreatitis

Kiyici, Aysel; İbi̇ş, Mehmet; Akbulut, Seval; Köklü, Seyfettin; Uçar, Engin; Ünlü, Ali

doi:10.29333/ejgm/82649

Cited by 9 publications

(5 citation statements)

References 22 publications

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“…Serum levels of TNF-α have not been considered to be a good indicator of disease severity because the liver is able to rapidly clear TNF-α before it reaches the general circulation; therefore, it is often difficult to detect TNF-α in the serum of acute pancreatitis patients[ 59 ]. One study indicates that TNF-α levels were higher in acute pancreatitis as compared to the chronic form of the disease, but its concentration did not correlate with the severity of disease[ 60 ]. In contrast to this, a recent study has shown levels of TNF-α are also increased in patients with chronic pancreatitis and the concentration of TNF-α coordinately increases in advanced chronic pancreatitis[ 61 ].…”

Section: Tnf-αmentioning

confidence: 99%

Pathogenic mechanisms of pancreatitis

Manohar¹,

Verma²,

Venkateshaiah³

et al. 2017

WJGPT

207

152

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Pancreatitis is inflammation of pancreas and caused by a number of factors including pancreatic duct obstruction, alcoholism, and mutation in the cationic trypsinogen gene. Pancreatitis is represented as acute pancreatitis with acute inflammatory responses and; chronic pancreatitis characterized by marked stroma formation with a high number of infiltrating granulocytes (such as neutrophils, eosinophils), monocytes, macrophages and pancreatic stellate cells (PSCs). These inflammatory cells are known to play a central role in initiating and promoting inflammation including pancreatic fibrosis, i.e., a major risk factor for pancreatic cancer. A number of inflammatory cytokines are known to involve in promoting pancreatic pathogenesis that lead pancreatic fibrosis. Pancreatic fibrosis is a dynamic phenomenon that requires an intricate network of several autocrine and paracrine signaling pathways. In this review, we have provided the details of various cytokines and molecular mechanistic pathways (i.e., Transforming growth factor-β/SMAD, mitogen-activated protein kinases, Rho kinase, Janus kinase/signal transducers and activators, and phosphatidylinositol 3 kinase) that have a critical role in the activation of PSCs to promote chronic pancreatitis and trigger the phenomenon of pancreatic fibrogenesis. In this review of literature, we discuss the involvement of several pro-inflammatory and anti-inflammatory cytokines, such as in interleukin (IL)-1, IL-1β, IL-6, IL-8 IL-10, IL-18, IL-33 and tumor necrosis factor-α, in the pathogenesis of disease. Our review also highlights the significance of several experimental animal models that have an important role in dissecting the mechanistic pathways operating in the development of chronic pancreatitis, including pancreatic fibrosis. Additionally, we provided several intermediary molecules that are involved in major signaling pathways that might provide target molecules for future therapeutic treatment strategies for pancreatic pathogenesis.

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Section: Tnf-αmentioning

confidence: 99%

Pathogenic mechanisms of pancreatitis

Manohar¹,

Verma²,

Venkateshaiah³

et al. 2017

WJGPT

207

152

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“…Thus, it makes the measurement of TNFα serum level time dependant. 17 Kiyici et al 19 indicates that both acute and chronic pancreatitis show an increase in serum TNFα. A study from Japan also showed that the use of anti-TNFα therapy in AP showed promising results.…”

Section: Discussionmentioning

confidence: 98%

Role of glycodeoxycholic acid to induce acute pancreatitis in Macaca nemestrina

Fauzi

Suwarto

Simadibrata

et al. 2022

J of Medical Primatology

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Background Acute pancreatitis exhibits a rapid clinical progression which makes it difficult to observe in human; hence, an experimental animal model is needed. This preliminary study performed an induction of acute pancreatitis using glycodeoxycholic acid (GDOC) in an experimental macaque model. Methods GDOC injections (initial dose of 11.20 mg/kg) were administered in an escalating manner at specific time points. The injection was given along the bilio‐pancreatic duct, followed by measurement of vital signs, serum amylase‐lipase, TNF‐α, procalcitonin, oxidative stress parameters, and microscopic and macroscopic findings. Results The results indicated that acute pancreatitis occurred following induction with low‐dose GDOC. Serum amylase and lipase levels increased with subsequent GDOC injections. Blood pressure and heart rate were elevated, indicating abdominal pain. Changes in TNF‐α, procalcitonin, and oxidative stress values showed active inflammation. We observed histologic features of pancreatitis and as the dose increased, vasodilation of the splanchnic vasculatures was observed. Conclusions Small dose GDOC injection in the bilio‐pancreatic duct may have a role to induce acute pancreatitis in Macaca nemestrina.

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“…However, both the studies signify that the patients with ACP had less severe disease and a lower mortality rate compared to patients with AP without CP [ 18 ]. The AP episodes with underlying CP have reduced levels of cytokines like tumor necrosis factor α leading into less systemic inflammation and organ failure in comparison to AP without underlying CP [ 19 ]. This discrepancy in the severity of attack between ACP and AP without CP can be also explained by the presence of increased fibrosis surrounding the intra-pancreatic fat in CP patients reducing lipolytic flux between acinar cells and adipocytes and also confines the spread of FN and PFAN [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Acute-on-Chronic Pancreatitis: Analysis of Clinical Profile and Outcome

Sharma¹,

Mallick²,

Samanta³

et al. 2021

Cureus

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Objective: Overall, a handful of studies are available on the outcomes of acute-on-chronic pancreatitis (ACP). We aimed to provide a more complete and updated picture of ACP. Methods: We evaluated consecutive patients of acute exacerbation of chronic pancreatitis (CP) in a tertiary care center located in north India and studied their epidemiological profiles, etiological factors as well as outcomes. Results: Forty-five patients of ACP with a mean age of 37±13 years were evaluated. The majority of the patients were male (75%) and alcohol was the most common detectable etiology while no etiology could be identified in 35% of patients after extensive laboratory investigations and imaging. Moderately severe pancreatitis was noted in 73% of patients and 49% of patients had necrotizing pancreatitis out of which the majority (33%) had both pancreatic as well as extra-pancreatic necrosis (EPN). Five patients (11%) were subjected to percutaneous catheter drainage. Persistent organ failure was noted in 9% of patients and two (4.5%) patients had died from organ failure. Conclusion: To conclude, this study has demonstrated that ACP has a milder disease course and low morbidity and mortality. Early elimination of the etiological factor is essential for optimal outcome.

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Serum TNF-Alpha Levels in Acute and Chronic Pancreatitis

Cited by 9 publications

References 22 publications

Pathogenic mechanisms of pancreatitis

Pathogenic mechanisms of pancreatitis

Role of glycodeoxycholic acid to induce acute pancreatitis in Macaca nemestrina

Acute-on-Chronic Pancreatitis: Analysis of Clinical Profile and Outcome

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