Peripancreatic Fat Necrosis Research Articles

Combined CT and serum CA19-9 for stratifying risk for progression in patients with locally advanced pancreatic cancer receiving intraoperative radiotherapy.

The aim of this study was to evaluate the significance of baseline computed tomography (CT) imaging features and carbohydrate antigen 19-9 (CA19-9) in predicting prognosis of locally advanced pancreatic cancer (LAPC) receiving intraoperative radiotherapy (IORT) and to establish a progression risk nomogram that helps to identify the potential beneficiary of IORT. A total of 88 LAPC patients with IORT as their initial treatment were enrolled retrospectively. Clinical data and CT imaging features were analyzed. Cox regression analyses were performed to identify the independent risk factors for progression-free survival (PFS) and to establish a nomogram. A risk-score was calculated by the coefficients of the regression model to stratify the risk of progression. Multivariate analyses revealed that relative enhanced value in portal-venous phase (REV-PVP), peripancreatic fat infiltration, necrosis, and CA19-9 were significantly associated with PFS (all p < 0.05). The nomogram was constructed according to the above variables and showed a good performance in predicting the risk of progression with a concordance index (C-index) of 0.779. Our nomogram stratified patients with LAPC into low- and high-risk groups with distinct differences in progression after IORT (p < 0.001). The integrated nomogram would help clinicians to identify appropriate patients who might benefit from IORT before treatment and to adapt an individualized treatment strategy.

Accuracy of a CT density threshold enhancement to identify pancreatic parenchyma necrosis in acute pancreatitis during the first week

PurposeThe purpose of this study was to identify attenuation threshold value on computed tomography (CT) that allowed discriminating between interstitial edematous pancreatitis (IEP) and necrotizing pancreatitis (NP) in patients with acute pancreatitis during the first week of the disease and evaluate interobserver reproducibility for the diagnosis of acute pancreatitis category. Materials and methodsPatients with acute pancreatitis who underwent CT examination of the abdomen between March 2015 and December 2019 were retrospectively included. Actual diagnosis of IEP or NP was based on final clinical report, follow-up evaluation, and complications. Six regions of interest were manually placed in the pancreatic gland and peripancreatic fat, and differences in CT attenuation values before contrast injection and during the portal venous phase of enhancement were computed. Performance in the diagnosis of AP category was evaluated using receiver operating characteristic analysis. Interobserver agreement was estimated by the intraclass correlation coefficient (ICC) and Bland Altman analysis was used to estimate reproducibility between pairs of observers. ResultsSixty-six patients with NP (46 men, 20 women; mean age, 55 ± 17 [SD] years; age range: 20-89 years) and 70 patients with IEP (39 men, 31 women; mean age, 54 ± 18 [SD] years; age range: 21–87 years) were included. An enhancement value less than 30 Hounsfield units (HU) in the pancreatic gland during the portal phase compared to non-contrast phase, yielded 90.9% sensitivity (60/66; 95% CI: 81.3–96.6), 94.3% specificity (66/70; 95% CI: 86.0–98.4) and an area under curve of 0.958 (95% CI: 0.919–0.996) for the diagnosis of NP versus IEP. Interobserver reproducibility for pancreas enhancement was good using Bland Altman plot and ICC was excellent for pancreatic gland analysis (ICC 0.978; 95% CI: 0.961–0.988) but poor or moderate (ICC ≤0.634) regarding peripancreatic fat necrosis. ConclusionBy using a pancreas enhancement threshold value of 30 HU, CT is accurate and reproducible for the diagnosis of NP during the first week of the disease.

Correlation between the liver injury and the expression of interleukin-10 in severe acute pancreatitis at high altitude: a rat experimental result

To observe the indexes of liver injury and the expression of inflammation-related factor interleukin-10 (IL-10) in rats with severe acute pancreatitis (SAP), and to discuss the correlation between the expression of IL-10 and the related factors of liver injury in SAP rats at different altitudes. 280 male Wistar rats with SPF grade aged 5 to 6 months were divided into four groups according to random number table with 70 rats in each group, and the rats were placed in different altitudes such as Xi'an (at an altitude of 1 027 m), Xining (at an altitude of 2 260 m), Xinghai (at an altitude of 3 300 m) and Wenquan (at an altitude of 3 950 m). The rats in each altitude were randomly divided into sham operation group (Sham group, n = 10) and SAP 1, 6, 12, 24 hours groups (all n = 15). SAP rat model was reproduced by injecting sodium cholate into the posterior membrane of pancreas, and the rats of Sham group were only turned pancreas over several times after opening the abdomen and then closed the abdomen. The rats were sacrificed at the corresponding time points after model reproduction in SAP groups, and rats in Sham group were sacrificed at 6 hours after sham operation. At the same time, the abdominal aorta blood was harvested, and the contents of serum amylase (AMY), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined by automatic biochemical analyzer. Liver tissues were harvested, and the expression level of IL-10 was determined by immunohistochemistry. Pancreatic tissues were harvested, and hematoxylin-eosin (HE) staining was performed to observe the pathological changes under light microscopy. The correlations among the indicators were analyzed by Pearson correlation. At different altitudes, no significant abnormality was found in the pancreas of Sham group, but significant pathological changes were found in the pancreas of all SAP groups, mainly manifested as pancreatic acinar swelling, inflammatory cell infiltration, vascular congestion and hemorrhage, acinar cell degeneration and dissolution, changes in glandular lobule structure, peri-pancreatic fat necrosis, and continuous aggravation with the increasing of time and altitude. At the same altitude, the pancreatic pathology score, the serum AMY, ALT and AST levels, and the hepatic IL-10 expression were all significantly increased in all the SAP groups as compared with those in Sham group, and they were continuously increased with time. In Sham group, there was no statistically significant difference in pancreatic pathology score, AMY, ALT, AST, or IL-10 level among different altitudes. At the corresponding time point after model reproduction, the pancreatic pathology score, AMY, ALT, AST and IL-10 levels in the SAP groups were also shown a continuous rising tendency with altitude increase, and the differences in above parameters of SAP 24 hours group in Wenquan area were statistically significant as compared with those of Sham group [pathology score: 11.06±0.94 vs. 0.23±0.15, AMY (mmol/L): 2 706.6±208.3 vs. 336.5±94.3, ALT (U/L): 267.00±5.37 vs. 52.00±4.84, AST (U/L): 465.88±11.02 vs. 139.00±11.61, IL-10 (A value): 0.579±0.006 vs. 0.281±0.006, all P < 0.05]. It was shown by correlation analysis that IL-10 of SAP rats at different altitudes was positively correlated with pancreatic pathology score, AMY, ALT and AST, the correlation coefficient (r value) between IL-10 and the above indicators in the Wenquan area with the highest altitude was 0.959, 0.928, 0.977, 0.983, respectively (all P < 0.01). The severity of SAP rats was positively correlated with altitude. IL-10 was involved in the pathological expression process of SAP liver damage, and its expression level was positively correlated with altitude and the degree of SAP liver damage.

Obesity and pancreatitis.

The obesity pandemic poses a unique set of problems for acute pancreatitis - both by increasing acute pancreatitis incidence, and worsening acute pancreatitis severity. This review explores these associations, underlying mechanisms, and potential therapies. We review how the obesity associated increase in gallstones, surgical, and endoscopic interventions for obesity management, diabetes, and related medications such as incretin-based therapies and hypertriglyceridemia may increase the incidence of acute pancreatitis. The mechanism of how obesity may increase acute pancreatitis severity are discussed with a focus on cytokines, adipokines, damage-associated molecular patterns and unsaturated fatty acid-mediated lipotoxicity. The role of obesity in exacerbating pancreatic necrosis is discussed; focusing on obesity-associated pancreatic steatosis. We also discuss how peripancreatic fat necrosis worsens organ failure independent of pancreatic necrosis. Last, we discuss emerging therapies including choice of intravenous fluids and the use of lipase inhibitors which have shown promise during severe acute pancreatitis. We discuss how obesity may contribute to increasing acute pancreatitis incidence, the role of lipolytic unsaturated fatty acid release in worsening acute pancreatitis, and potential approaches, including appropriate fluid management and lipase inhibition in improving acute pancreatitis outcomes.

Últimos avances en pancreatitis aguda

The present article analyses the main presentations on acute pancreatitis at Digestive Disease Week 2015. Arterial pseudoaneurysm is an uncommon complication of acute pancreatitis (incidence 0.7%) and mortality from this cause is currently anecdotal. Diabetes mellitus has little impact on the clinical course of acute pancreatitis, unlike cirrhosis, which doubles the risk of mortality. Intake of unsaturated fat could be associated with an increased severity of acute pancreatitis and is a confounding factor in studies evaluating the relationship between obesity and morbidity and mortality. PET-CT (positron emission tomography-computed tomography) could be a non-invasive tool to detect infection of collections in acute pancreatitis. Peripancreatic fat necrosis is less frequent than pancreatic fat necrosis and is associated with a better clinical course. If the clinical course is poor, increasing the calibre of the percutaneous drains used in the treatment of infected necrosis can avoid surgery in 20% of patients. The use of low molecular-weight heparin in moderate or severe pancreatitis could be associated with a better clinical course, specifically with a lower incidence of necrosis. In acute recurrent pancreatitis, simvastatin is a promising drug for prophylaxis of new episodes of acute pancreatitis. Nutritional support through a nasogastric tube does not improve clinical course compared with oral nutrition.

Peripancreatic fat necrosis worsens acute pancreatitis independent of pancreatic necrosis via unsaturated fatty acids increased in human pancreatic necrosis collections

Background and aimsPeripancreatic fat necrosis occurs frequently in necrotising pancreatitis. Distinguishing markers from mediators of severe acute pancreatitis (SAP) is important since targeting mediators may improve outcomes. We evaluated potential...

Effect of necrosis status at the time of intervention on the outcome of severe acute pancreatitis

Effect of necrosis status at the time of intervention on the outcome of severe acute pancreatitis

Advantages of lumboscopy in surgery of peripancreatic fat necrosis

Advantages of lumboscopy in surgery of peripancreatic fat necrosis

Chronic pancreatitis in dogs: A retrospective study of clinical, clinicopathological, and histopathological findings in 61 cases

The objective of this study was to characterize the clinical, clinicopathological, and histopathological findings of dogs with chronic pancreatitis. The necropsy database at Texas A&M University was searched for reports of dogs with histological evidence of chronic pancreatitis defined as irreversible histologic changes of the pancreas (i.e. fibrosis or atrophy). A reference necropsy population of 100 randomly selected dogs was used for signalment and concurrent disease comparisons. Cases were categorized as clinical or incidental chronic pancreatitis based on the presence of vomiting, decreased appetite, or both vs. neither of these signs. All archived pancreas samples were scored histologically using a published scoring system. Sixty-one dogs with chronic pancreatitis were included. The most frequent clinical signs were lethargy, decreased appetite, vomiting, and diarrhea. Compared to the reference necropsy population, chronic pancreatitis cases were more likely to be older, neutered, of the non-sporting/toy breed group, and to have concurrent endocrine, hepatobiliary, or neurological disease. Clinical cases had significantly higher histological scores for pancreatic necrosis and peripancreatic fat necrosis, and were significantly more likely to have hepatobiliary or endocrine disease as well as increased liver enzyme activities, or elevated cholesterol and bilirubin concentrations. In conclusion, clinical disease resulting from chronic pancreatitis might be related to the presence of pancreatic necrosis and pancreatic fat necrosis. The signalment, presentation, and concurrent diseases of dogs with chronic pancreatitis are similar to those previously reported for dogs with acute pancreatitis.

Severity of Acute Pancreatitis: Impact of Local and Systemic Complications

Severity of Acute Pancreatitis: Impact of Local and Systemic Complications

Specificity of a canine pancreas-specific lipase assay for diagnosing pancreatitis in dogs without clinical or histologic evidence of the disease

To evaluate the specificity of a canine pancreas-specific lipase (cPSL) assay for diagnosing pancreatitis in dogs without clinical or histologic evidence of the disease. 20 dogs from another study with macroscopic evidence of pancreatitis and 44 dogs surrendered for euthanasia or expected to die. Prior to death, physical examination of each dog was performed and blood samples were collected for serum biochemical, serum cPSL, and hematologic analyses. After death, the pancreas was removed, sectioned in 1- to 2-cm slices, and evaluated by a pathologist. Dogs were classified by whether they had clinical or macroscopic pancreatitis. Each pancreatic section was histologically examined, and mean cumulative scores (MCSs) were assigned for 8 histologic characteristics. For each characteristic, comparisons were made between dogs with and without pancreatitis to establish histologic criteria for lack of evidence of pancreatitis. For all histologic characteristics except lymphocytic infiltration, the median MCS differed significantly between dogs with and without pancreatitis. Dogs were categorized as having no histologic evidence of pancreatitis when the MCSs for neutrophilic infiltration, pancreatic necrosis, peripancreatic fat necrosis, and edema were 0.0. On the basis of these criteria, 40 dogs were classified as having no evidence of pancreatitis. The cPSL concentration was within reference limits in 38 of these 40 dogs and was less than the cutoff value for diagnosing pancreatitis (400 μg/L) in 39 of the 40 dogs, resulting in a specificity of 97.5% (95% confidence interval, 86.8% to 99.9%). The cutoff cPSL value used in this study may be useful for diagnosing pancreatitis in dogs with a lack of histologic lesions consistent with pancreatitis and for which pancreatitis is not considered a major differential diagnosis.

ENDOSCOPIC NECROSECTOMY UNDER DIRECT VISION AFTER ENDOSCOPIC ULTRASOUND-GUIDED CYSTGASTROSTOMY FOR ORGANIZED PANCREATIC NECROSIS

A 56-year-old man was referred for an enlarging pancreatic pseudocyst that developed after severe acute pancreatitis with gallstones. Abdominal ultrasound showed a huge cystic lesion with a large amount of solid high echoic components. Arterial phase contrast-enhanced computed tomography scan revealed arteries across the cystic cavity. Stents were placed after endoscopic ultrasound-guided cystgastrostomy; however, the stents were obstructed by necrotic debris, and secondary infection of the pseudocyst occurred. Therefore, the cystgastrostomy was dilated by a dilation balloon, and a forward-viewing endoscope was inserted into the cystic cavity. Many vessels and a large amount of necrotic debris existed in the cavity. Under direct vision, all necrotic debris was safely removed using a retrieval net and forceps. One year after this procedure, there was no recurrence. Our case indicates that peripancreatic fat necrosis can cause exposure of vessels across/along the cystic cavity, and blind necrosectomy should be avoided.

Concentration-Dependent Efficacy of Endoscopic Ultrasound-Guided Ethanol Ablation of Pancreatic Tissue in the Pig

Background: Ethanol is a commonly available agent and has been used to successfully and safely ablate cystic lesions. The aim of this study was to determine the local and systemic long-term effect of EUS-guided injection of ethanol into the pancreas of pigs using 2 ml of ethanol, in increasing concentration of 0% to 100%, diluted with normal saline. Methods: Six pigs were sedated by general anesthesia and ethanol was injected under EUS-guidance with a 22-gauge needle into the tail of the pancreas. The endpoints of this study were gross and microscopic evidence of inflammation of the pancreas and clinical tolerance. The animals were observed by determining the blood levels of amylase and lipase and by an upper abdominal CT scan. Results: Six Yorkshire breed pigs were used for this study. The animals were monitored for 7 days after the injection. CT scanning demonstrated a localized site of non-perfused pancreatic tissue measuring on average 19.4 ( ±10.5) mm in the animals that underwent an injection 40%, 60%, 80% and 100% of ethanol. By CT, there was no evidence of peri-pancreatic fat necrosis. At sacrifice, no gross lesion could be identified in the pancreatic tail of the animals that received normal saline or 20% ethanol. The other animals displayed a visible necrotic area in the tail of the pancreas (figure 1). By histology, the average maximal diameter of the lesions was 20.8 ( ±4.3) mm. The diameter of tissue necrosis correlated with the concentration of injected ethanol. Clinically, the animals appeared to tolerate the procedure well. Blood levels of amylase and lipase were within normal limits. Conclusions: The EUS-guided injection of ethanol into the pig pancreas resulted in localized tissue necrosis. This technique is a potential minimally invasive local treatment option for pancreatic neuroendocrine tumors.

Obesity: an important prognostic factor in acute pancreatitis.

Ninety-nine patients with acute pancreatitis in whom body mass index (BMI = weight (kg)/height2 (m2)) was measured were studied prospectively to determine the importance of obesity as a prognostic factor in this disease. Of 19 obese patients (BMI > or = 30 kg/m2), 12 developed severe pancreatitis; seven had abscesses, of whom five died, and two further patients died. In 80 non-obese patients, the incidence of severe pancreatitis (n = 5), abscess formation (n = 4) and death (n = 4) was significantly less (P = 0.0007). The mean(s.d.) BMI of 17 patients with severe acute pancreatitis was significantly higher than that in 82 patients with mild acute disease (31.2(5.6) versus 23.3(5.6) kg/m2, P < 0.001). As a single prognostic factor, obesity had a sensitivity of 63 per cent and a specificity of 95 per cent for predicting disease severity. When five obese women with gallstone pancreatitis were excluded, the sensitivity of obesity increased to 86 per cent. Severe pancreatitis occurred in all eight obese patients with disease of an alcoholic aetiology. These data suggest that increased fat deposits in the peripancreatic and retroperitoneal spaces in obese patients may increase the risk of peripancreatic fat necrosis, abscess and death. Consideration should be given to including obesity as a prognostic factor in acute pancreatitis.

Case reports

Peripancreatic Fat Necrosis Mimicking Pancreatic Cancer

Relationship of Pancreatic and Peripancreatic Fat Necrosis to Organ Failure in Acute Pancreatitis

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Influência da toxicidade combinada no desenvolvimento da lesão pancreática alcoólica. Ensaio experimental prolongado.

The aim of this study was to evaluate the adverse effects on the exocrine pancreas of ethanol and ethanol with congeners which coexist in alcoholic beverages most commonly consumed by the Portuguese population. Eighteen male Wistar rats were divided into three groups and submitted to a daily intraperitoneal injection of a hydroalcoholic solution of ethanol (SHAE) and a hydroalcoholic solution of ethanol, acetaldehyde, methanol and higher alcohols (SHAF); the third group served as a control and received an equivalent volume of an isocaloric solution of dextrose. All the animals were sacrificed at the end of the 9th week of the experiment. The following histological lesions were considered: acinar cell necrosis and steatosis, ductal dilatation, intraluminal plugs, parenchymal inflammation, fibrosis, peripancreatic fat necrosis and inflammation. Their severity was graded by means of a scoring system. The histopathologic changes which characterize pancreatitis (acinar cell necrosis, parenchymal inflammation, fibrosis and peripancreatic fat necrosis and inflammation) were found in the majority of animals of both study groups, but in none of the control group. The lesions tend to be more frequent and severe in the group treated with ethanol and its congeners (SHAF) than in the SHAE group; these differences are statistically significant when necrosis, ductal dilatation and overall severity of lesions are considered. The results of this study suggest that in the pancreas the toxicity of ethanol is enhanced by interaction with other components of alcoholic beverages.

Free fatty acids in serum of patients with acute necrotizing or edematous pancreatitis

Serum concentrations of free fatty acids (FFA) were assayed in 20 patients with acute necrotizing pancreatitis (ANP). Pancreatic and peripancreatic fat necrosis was verified on operation and/or by contrast-enhanced computed tomography. For comparison, 20 patients with acute edematous pancreatitis (AEP) were examined. On admission, FFA serum levels were 1.14 +/- 0.12 (SEM) mmol/L in ANP and, thus, significantly (p < 0.03) higher than in AEP (0.78 +/- 0.09 mmol/L). The two groups also differed in the later course: in ANP, the FFA values remained raised (d 5-11:0.86 +/- 0.13 mmol/L; p > 0.05 vs day 1), whereas in AEP, the FFA concentrations normalized within 1 wk (d 2-4:0.52 +/- 0.11 mmol/L; d 5-11:0.39 +/- 0.05 mmol/L; p < 0.05 vs day 1 and p < 0.01 vs ANP). Serum FFA correlated positively with C-reactive protein levels (rs = 0.42; p < 0.01), but has less discriminating potency between ANP and AEP. In AEP, the initial peak may correspond to the disease outburst itself and to unspecific stress. In ANP, the higher and sustained elevation of FFA may predominantly mirror the ongoing pancreatic parenchymal and extrapancreatic fat necrosis, and be pathophysiologically relevant, especially in view of significantly reduced serum albumin levels in ANP.

Human acute pancreatitis: its pathogenesis in the light of immunocytochemical and ultrastructural findings in acinar cells.

Human acute pancreatitis results from an autodigestive process frequently associated with alcohol abuse, gall stone disease and shock. Peripancreatic fat necrosis was identified as one of the earliest visible lesions, whereas acinar cell necrosis and haemorrhage were regarded as secondary changes. To examine the alterations in acinar cells in more detail, their enzyme content and fine structural features were studied immunocytochemically using antisera against alpha-amylase, lipase, trypsin, chymotrypsin and pancreatic stone protein, and electronmicroscopically in pancreatic tissues from patients with severe acute pancreatitis. Peripheral acinar cells in the immediate vicinity of fat necrosis were found to be heavily degranulated, while acinar cells at some distance of necrosis fully retained their enzyme content. Other frequent changes of the acinar cells included cuboidal transformation, loss of microvilli, increased occurrence of autophagosomes, and formation of enlarged acinar lumina. As there was no apparent cell membrane leakage or rupture of duct lumina, it is concluded that the acinar cells adjacent to fat necrosis release their granules by undirected basolateral extrusion. The findings thus suggest that one of the basic defects in acute pancreatitis is the uncontrolled release of enzymes from peripheral acinar cells into the interstitial space which, in turn, presumably by the action of lipase, leads to autodigestive fat necrosis.

Steroid-Induced Pancreatitis

THE COMPLICATIONS of therapy with adrenocortical hormones have been reviewed extensively, but the pancreatic abnormalities which occur in association with administration of steroids rarely have been included.¹ A postmortem study by Carone and Liebow²revealed histologic evidence of acute pancreatitis, or peripancreatic fat necrosis, in 16 of 54 patients treated with corticotropin or adrenal steroids. In a control group of 54 patients of comparable age and with similar major diseases, only two had these pathologic changes. The clinical diagnosis of pancreatitis was not made in any of these patients. In 1961 Nelp³reviewed the literature and reported six of his own cases of clinically manifest acute pancreatitis associated with the administration of adrenal steroids. To our knowledge, no additional cases have been reported. In 12 of 14 previously reported instances of symptomatic pancreatitis induced by steroids, the diagnosis was not made until exploratory surgery or autopsy.^3-8