Cellular Markers of Systemic Inflammation and Immune Suppression in Patients with Organ Failure Due to Severe Acute Pancreatitis

2001 ◽  
Vol 36 (10) ◽  
pp. 1100-1107 ◽  
Author(s):  
M.-L. Kylänpää-Bäck, A. Takala, E.
Keyword(s):  
Acute Pancreatitis ◽  
Organ Failure ◽  
Severe Acute Pancreatitis ◽  
Systemic Inflammation ◽  
Immune Suppression ◽  
Cellular Markers

scholarly journals Ringer’s Lactate Prevents Early Organ Failure by Providing Extracellular Calcium

2020 ◽  
Vol 9 (1) ◽  
pp. 263 ◽  
Author(s):  
Biswajit Khatua ◽  
Jordan R. Yaron ◽  
Bara El-Kurdi ◽  
Sergiy Kostenko ◽  
Georgios I. Papachristou ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Organ Failure ◽  
Severe Acute Pancreatitis ◽  
Systemic Inflammation ◽  
Normal Saline ◽  
Meta Analysis ◽  
Extracellular Calcium ◽  
Severe Pancreatitis ◽  
Ringer’S Lactate

Objective: Ringer’s lactate may improve early systemic inflammation during critical illnesses like severe acute pancreatitis, which are associated with hypocalcemia. Ringer’s lactate is buffered and contains lactate and calcium. We, thus analyzed extracellular calcium or lactate’s effects on the mechanisms, intermediary markers, and organ failure in models mimicking human disease with nonesterified fatty acid (NEFA) elevation. Methods: Meta-analyses and experimental studies were performed. Experimentally, extracellular calcium and lactate were compared in their interaction with linoleic acid (LA; a NEFA increased in human severe pancreatitis), and its subsequent effects on mitochondrial depolarization and cytosolic calcium signaling resulting in cell injury. In vivo, the effect of LA was studied on organ failure, along with the effect of calcium or lactate (pH 7.4) on severe acute pancreatitis-associated organ failure. A meta-analysis of human randomized control trials comparing Ringer’s lactate to normal saline was done, focusing on necrosis and organ failure. Results: Calcium reacted ionically with LA and reduced lipotoxic necrosis. In vivo, LA induced organ failure and hypocalcemia. During severe pancreatitis, calcium supplementation in saline pH 7.4, unlike lactate, prevented hypocalcemia, increased NEFA saponification, reduced circulating NEFA and C-reactive protein, reduced pancreatic necrosis adjacent to fat necrosis, and normalized shock (carotid pulse distension) and blood urea nitrogen elevation on day 1. This, however, did not prevent the later increase in serum NEFA which caused delayed organ failure. Meta-analysis showed Ringer’s lactate reduced necrosis, but not organ failure, compared with normal saline. Conclusion: Hypocalcemia occurs due to excess NEFA binding calcium during a critical illness. Ringer’s lactate’s early benefits in systemic inflammation are by the calcium it provides reacting ionically with NEFA. This, however, does not prevent later organ failure from sustained NEFA generation. Future studies comparing calcium supplemented saline resuscitation to Ringer’s lactate may provide insights to this pathophysiology.

scholarly journals Assessment of Prophylactic Carbapenem Antibiotics Administration for Severe Acute Pancreatitis: An Updated Systematic Review and Meta-Analysis

Digestion ◽  
2022 ◽  
pp. 1-9
Author(s):  
Daxin Guo ◽  
Wei Dai ◽  
Jingyi Shen ◽  
Mengting Zhang ◽  
Yetan Shi ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Organ Failure ◽  
Severe Acute Pancreatitis ◽  
Pancreatic Pseudocyst ◽  
Meta Analysis ◽  
Fluid Collection ◽  
Cochrane Library ◽  
Intensive Care Unit Treatment ◽  
Significant Difference ◽  
And Control

<b><i>Background:</i></b> The effectiveness of prophylactic antibiotics in severe acute pancreatitis (SAP) remains a debatable issue. This meta-analysis aimed to determine the efficacy of prophylactic carbapenem antibiotics in SAP. <b><i>Methods:</i></b> This meta-analysis of prophylactic carbapenem antibiotics for SAP was conducted in PubMed, EMBASE, Web of Science, MEDLINE, and Cochrane Library up to February 2021. The related bibliographies were manually searched. The primary outcomes involved infected pancreatic or peripancreatic necrosis, mortality, complications, infections, and organ failure. <b><i>Results:</i></b> Seven articles comprised 5 randomized controlled trials and 2 retrospective observational studies, including 3,864 SAP participants. Prophylactic carbapenem antibiotics in SAP were associated with a statistically significant reduction in the incidence of infections (odds ratio [OR]: 0.27; <i>p</i> = 0.03) and complications (OR: 0.48; <i>p</i> = 0.009). Nevertheless, no statistically significant difference was demonstrated in the incidence of infected pancreatic or peripancreatic necrosis (OR: 0.74; <i>p</i> = 0.24), mortality (OR: 0.69; <i>p</i> = 0.17), extrapancreatic infection (OR: 0.64, <i>p</i> = 0.54), pulmonary infection (OR: 1.23; <i>p</i> = 0.69), blood infection (OR: 0.60; <i>p</i> = 0.35), urinary tract infection (OR: 0.97; <i>p</i> = 0.97), pancreatic pseudocyst (OR: 0.59; <i>p</i> = 0.28), fluid collection (OR: 0.91; <i>p</i> = 0.76), organ failure (OR: 0.63; <i>p</i> = 0.19), acute respiratory distress syndrome (OR: 0.80; <i>p</i> = 0.61), surgical intervention (OR: 0.97; <i>p</i> = 0.93), dialysis (OR: 2.34; <i>p</i> = 0.57), use of respirator or ventilator (OR: 1.90; <i>p</i> = 0.40), intensive care unit treatment (OR: 2.97; <i>p</i> = 0.18), and additional antibiotics (OR: 0.59; <i>p</i> = 0.28) between the experimental and control groups. <b><i>Conclusions:</i></b> It is not recommended to administer routine prophylactic carbapenem antibiotics in SAP.

MORTALITY IN SEVERE ACUTE PANCREATITIS WITHOUT ORGAN FAILURE IS LOW: A CASE FOR REVISING THE ATLANTA CLASSIFICATION.

Pancreas ◽  
2004 ◽  
Vol 29 (4) ◽  
pp. 332
Author(s):  
Vege Santhi Swaroop ◽  
Suresh T. Chari ◽  
Randall K. Pearson ◽  
Jonathan E. Clain ◽  
Bret T. Petersen ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Organ Failure ◽  
Severe Acute Pancreatitis

Low Mortality and High Morbidity in Severe Acute Pancreatitis Without Organ Failure

2009 ◽  
Vol 104 (3) ◽  
pp. 710-715
Author(s):  
Santhi Swaroop Vege ◽  
Timothy B. Gardner ◽  
Suresh T. Chari ◽  
Padma Munukuti ◽  
Randall K. Pearson ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Organ Failure ◽  
Severe Acute Pancreatitis ◽  
High Morbidity

Elevated intra-abdominal pressure correlates with frequency of organ failure and outcome in severe acute pancreatitis

Pancreatology ◽  
2013 ◽  
Vol 13 (3) ◽  
pp. S65-S66
Author(s):  
Mihailo Bezmarevic ◽  
Darko Mirkovic ◽  
Ivan Soldatovic ◽  
Milan Jovanovic
Keyword(s):  
Acute Pancreatitis ◽  
Organ Failure ◽  
Severe Acute Pancreatitis ◽  
Abdominal Pressure

Discrepancy Between the Extent of Pancreatic Necrosis and Multiple Organ Failure Score in Severe Acute Pancreatitis

2009 ◽  
Vol 33 (11) ◽  
pp. 2427-2432 ◽  
Author(s):  
Damian J. Mole ◽  
Katie L. McClymont ◽  
Sarah Lau ◽  
Rosamund Mills ◽  
Christopher Stamp-Vincent ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Severe Acute Pancreatitis ◽  
Pancreatic Necrosis ◽  
Multiple Organ ◽  
Organ Failure Score

scholarly journals Cytokine and chemokine levels in the heart tissue of aged rats following severe acute pancreatitis

2017 ◽  
Vol 15 (2) ◽  
pp. 102-106 ◽  
Author(s):  
Rízia Callou Amaral ◽  
Denise Frediani Barbeiro ◽  
Marcia Kiyomi Koike ◽  
Charles Mady ◽  
Marcel Cerqueira César Machado ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Pancreatitis ◽  
Growth Factors ◽  
Inflammatory Response ◽  
Severe Acute Pancreatitis ◽  
Systemic Inflammation ◽  
The Elderly ◽  
Study Groups ◽  
Interleukin 10 ◽  
The Body

Severe acute pancreatitis (AP) is a disease associated with high mortality and characterized by overwhelming systemic inflammation. Older people have a prolonged hospital stay and worst prognosis, when affected by this disease. Our group hypothesized, thus, that the systemic inflammatory response in the elderly would promote more organ damage when compared to the young. We sought to investigate the effect of systemic inflammation on the gene expression of cytokines, chemokines, and growth factors in the hearts of older and younger rats in an animal model of AP. AP was induced in all rats by injection of 0.5 mL of 2.5% taurocholate. There were two healthy age-matched control groups. An array of 79 cytokines, chemokines, and growth factors was measured in samples of cardiac tissue taken from the AP rats after 10 h, and from control rats. Older healthy rats had significantly higher levels of interleukin-10 (IL-10) and CCL1 gene expression than younger ones ( P < 0.05), but all other measurements were similar among the study groups. This study indicates the systemic inflammation may show unique features for different organs in the body, but older animals with systemic inflammation are similar to the young regarding the cardiac inflammatory response.

scholarly journals Predictors of persistent organ failure in ICU patients with severe acute pancreatitis

Critical Care ◽  
2013 ◽  
Vol 17 (S2) ◽  
Author(s):  
I Aleksandrova ◽  
M Ilynskiy ◽  
S Rei ◽  
V Kiselev ◽  
G Berdnikov ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Organ Failure ◽  
Severe Acute Pancreatitis ◽  
Icu Patients ◽  
Persistent Organ Failure

Placental Chorionic Plate-derived Mesenchymal Stem Cells Ameliorate Severe Acute Pancreatitis by Regulating Macrophages Polarization via Secreting TSG-6

2021 ◽  
Author(s):  
Qilin Huang ◽  
Xiumei Cheng ◽  
Chen Luo ◽  
Shuxu Yang ◽  
Shuai Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Acute Pancreatitis ◽  
Severe Acute Pancreatitis ◽  
Systemic Inflammation ◽  
Therapeutic Efficacy ◽  
Pancreatic Injury ◽  
Protective Mechanism ◽  
M2 Polarization ◽  
Injured Tissue ◽  
Chorionic Plate

Abstract BackgroundMesenchymal stem cells (MSCs) hold promising potential to treat systemic inflammatory diseases including severe acute pancreatitis (SAP). In our previous study, placental chorionic plate-derived MSCs (CP-MSCs) were found to possess superior immunoregulatory capability. However, the therapeutic efficacy of CP-MSCs on SAP and their underlying mechanism remain unclear.MethodsThe survival and colonization of exogenous CP-MSCs were observed by bioluminescence imaging and CM-Dil labeling in rodent animal models of SAP. The therapeutic efficacy of CP-MSCs on SAP rats was evaluated by pathology scores, the levels of pancreatitis biomarkers as well as the levels of inflammatory factors in pancreas and serum. The potential protective mechanism of CP-MSCs in SAP rats was explored by selectively depleting M1 or M2 phenotype macrophages and knocking down the expression of TSG-6.ResultsExogenous CP-MSCs could survive and colonize in the injured tissue of SAP such as lung, pancreas, intestine and liver. Meanwhile, we found that CP-MSCs alleviated pancreatic injury and systemic inflammation by inducing macrophages to polarize from M1 to M2 in SAP rats. Furthermore, our data suggested that CP-MSCs induced M2 polarization of macrophages by secreting TSG-6, and TSG-6 played a vital role in alleviating pancreatic injury and systemic inflammation in SAP rats. Notably, we found that a high inflammation environment could stimulate CP-MSCs to secrete TSG-6.ConclusionExogenous CP-MSCs tended to colonize in the injured tissue, and reduced pancreatic injury and systemic inflammation in SAP rats through inducing M2 polarization of macrophages by secreting TSG-6. Our study provides a new treatment strategy for SAP, and initially explains the potential protective mechanism of CP-MSCs on SAP rats.

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