Pancreatic Adenocarcinoma Causing Necrotizing Pancreatitis: Not as Rare as You Think?

Lewellen, Kyle A.; Maatman, Thomas K.; Heimberger, Mark A.; Ceppa, Eugene P.; House, Michael G.; Nakeeb, Attila; Schmidt, C. Max; Zyromski, Nicholas J.

doi:10.1016/j.jss.2019.12.036

Cited by 6 publications

(5 citation statements)

References 22 publications

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“…It is well established that pancreatic cancer can prompt acute pancreatitis; however, this diagnosis in NP is extremely difficult to make in the presence of parenchymal necrosis and distorted anatomy by pancreatic and peripancreatic collections. 41 The most practical message is that clinicians should be aware of this relationship, especially in middleaged or elderly patients with idiopathic etiology of NP, and have a low threshold for ordering pancreatic cancer tumor marker carbohydrate antigen 19-9 serum concentration to investigate this possibility.…”

Section: Discussionmentioning

confidence: 99%

“…These conditions occurred too infrequently to allow for subgroup analysis to identify risk factors. Infrequent complications associated with NP or its treatment included tracheal stenosis (n ¼ 19), ureteral stricture (n ¼ 7), inflammatory colon stricture (n ¼ 7), progressive renal failure (n ¼ 5), pancreatic ductal carcinoma (n ¼ 5), 41 irreversible gastrointestinal failure requiring multivisceral transplant (n ¼ 4), male impotence (n ¼ 1), metabolic peripheral polyneuropathy (n ¼ 1), deafness (n ¼ 1), and blindness (n ¼ 1).…”

Section: Uncommon Complicationsmentioning

confidence: 99%

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The continuum of complications in survivors of necrotizing pancreatitis

Maatman

Roch

Ceppa

et al. 2020

Surgery

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Background: Necrotizing pancreatitis survivors develop complications beyond infected necrosis that often require invasive intervention. Remarkably few data have cataloged these late complications after acute necrotizing pancreatitis resolution. We sought to identify the types and incidence of complications after necrotizing pancreatitis. Design: An observational study was performed evaluating 647 patients with necrotizing pancreatitis captured in a single-institution database between 2005 and 2017 at a tertiary care hospital. Retrospective review and analysis of newly diagnosed conditions attributable to necrotizing pancreatitis was performed. Exclusion criteria included the following: death before disease resolution (n ¼ 57, 9%) and patients lost to follow-up (n ¼ 12, 2%). Results: A total of 578 patients were followed for a median of 46 months (range, 8 months to 15 y) after necrotizing pancreatitis. In 489 (85%) patients 1 or more complications developed and included symptomatic disconnected pancreatic duct syndrome (285 of 578, 49%), splanchnic vein thrombosis (257 of 572, 45%), new endocrine insufficiency (195 of 549, 35%), new exocrine insufficiency (108 of 571, 19%), symptomatic chronic pancreatitis (93 of 571, 16%), incisional hernia (89 of 420, 21%), biliary stricture (90 of 576, 16%), chronic pain (44 of 575, 8%), gastrointestinal fistula (44 of 578, 8%), pancreatic duct stricture (30 of 578, 5%), and duodenal stricture (28 of 578, 5%). During the follow-up period, a total of 340 (59%) patients required an invasive intervention after necrotizing pancreatitis resolution. Invasive pancreatobiliary intervention was required in 230 (40%) patients. Conclusion: Late complications are common in necrotizing pancreatitis survivors. A broad variety of problems manifest themselves after resolution of the acute disease process and often require invasive intervention. Necrotizing pancreatitis patients should be followed lifelong by experienced clinicians.

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Section: Discussionmentioning

confidence: 99%

Section: Uncommon Complicationsmentioning

confidence: 99%

The continuum of complications in survivors of necrotizing pancreatitis

Maatman

Roch

Ceppa

et al. 2020

Surgery

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“…For successful fluorescence-guided tumor resection, it is generally important that there is prompt discrimination between the tumor and healthy surrounding tissue [ 27 ], for which the dead cell-binding in the tumor center is perhaps less relevant when dealing with solid tumors. In some cases, however, tumors may cause necrosis in the surrounding tissues [ 28 ]. In such situations, this dead cell-binding can be highly helpful in removing more diseased tissue that can increase the chance of successful surgery.…”

Section: Discussionmentioning

confidence: 99%

Necrosis binding of Ac-Lys0(IRDye800CW)-Tyr3-octreotate: a consequence from cyanine-labeling of small molecules

et al. 2021

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Background There is a growing body of nuclear contrast agents that are repurposed for fluorescence-guided surgery. New contrast agents are obtained by substituting the radioactive tag with, or adding a fluorescent cyanine to the molecular structure of antibodies or peptides. This enables intra-operative fluorescent detection of cancerous tissue, leading to more complete tumor resection. However, these fluorescent cyanines can have a remarkable influence on pharmacokinetics and tumor uptake, especially when labeled to smaller targeting vectors such as peptides. Here we demonstrate the effect of cyanine-mediated dead cell-binding of Ac-Lys0(IRDye800CW)-Tyr3-octreotate (800CW-TATE) and how this can be used as an advantage for fluorescence-guided surgery. Results Binding of 800CW-TATE could be blocked with DOTA0-Tyr3-octreotate (DOTA-TATE) on cultured SSTR2-positive U2OS cells and was absent in SSTR2 negative U2OS cells. However, strong binding was observed to dead cells, which could not be blocked with DOTA-TATE and was also present in dead SSTR2 negative cells. No SSTR2-mediated binding was observed in frozen tumor sections, possibly due to disruption of the cells in the process of sectioning the tissue before exposure to the contrast agent. DOTA-TATE blocking resulted in an incomplete reduction of 61.5 ± 5.8% fluorescence uptake by NCI-H69-tumors in mice. Near-infrared imaging and dead cell staining on paraffin sections from resected tumors revealed that fluorescence uptake persisted in necrotic regions upon blocking with DOTA-TATE. Conclusion This study shows that labeling peptides with cyanines can result in dead cell binding. This does not hamper the ultimate purpose of fluorescence-guided surgery, as necrotic tissue appears in most solid tumors. Hence, the necrosis binding can increase the overall tumor uptake. Moreover, necrotic tissue should be removed as much as possible: it cannot be salvaged, causes inflammation, and is tumorigenic. However, when performing binding experiments to cells with disrupted membrane integrity, which is routinely done with nuclear probes, this dead cell-binding can resemble non-specific binding. This study will benefit the development of fluorescent contrast agents.

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“…Other symptoms associated with PDAC such as poor appetite, diarrhea or loose stool secondary to steatorrhea, unintentional weight loss, and recent or new-onset diabetes, should raise the concern for malignancy in patients presenting with acute pancreatitis [42]. Although studies have reported that most PDAC-AP patients present with mild acute pancreatitis, based on clinical or imaging criteria for the classification of acute pancreatitis, in some patients, the presentation of PDAC-AP may be associated with severe necrotizing pancreatitis [7,43,[45][46][47][48].…”

Section: Clinical Manifestations Of Acute Pancreatitis-associated Pan...mentioning

confidence: 99%

Bidirectional relationship between acute pancreatitis and pancreatic cancer

Jeon,

Arain,

Korc

et al. 2024

Current Opinion in Gastroenterology

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Purpose of review The burdens of pancreatic ductal adenocarcinoma (PDAC) and acute pancreatitis are increasing globally. We reviewed current literature on whether acute pancreatitis is a causal factor for PDAC and examined clinical manifestations of PDAC-associated acute pancreatitis. Recent findings Recent findings detail the timing of acute pancreatitis before and after PDAC occurrence, further solidifying the evidence for PDAC-associated acute pancreatitis and for acute pancreatitis as a causal risk factor for PDAC. The risk of PDAC remains elevated above the general population in patients with distant history of acute pancreatitis. PDAC risk also increases with recurrent acute pancreatitis episodes, independent of smoking and alcohol. Mechanisms linking acute pancreatitis to PDAC include inflammation and neutrophil infiltration, which can be attenuated by suppressing inflammation and/or epigenetic modulation, thus slowing the progression of acinar-to-ductal metaplasia. Clinical presentation and management of acute pancreatitis in the context of PDAC are discussed, including challenges acute pancreatitis poses in the diagnosis and treatment of PDAC, and novel interventions for PDAC-associated acute pancreatitis. Summary PDAC risk may be reduced with improved acute pancreatitis prevention and treatment, such as antiinflammatories or epigenetic modulators. Increased acute pancreatitis and PDAC burden warrant more research on better diagnosis and management of PDAC-associated acute pancreatitis.

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Pancreatic Adenocarcinoma Causing Necrotizing Pancreatitis: Not as Rare as You Think?

Cited by 6 publications

References 22 publications

The continuum of complications in survivors of necrotizing pancreatitis

The continuum of complications in survivors of necrotizing pancreatitis

Necrosis binding of Ac-Lys0(IRDye800CW)-Tyr3-octreotate: a consequence from cyanine-labeling of small molecules

Bidirectional relationship between acute pancreatitis and pancreatic cancer

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