Pancreatitis Lesions Research Articles

A deep learning-powered diagnostic model for acute pancreatitis

BackgroundAcute pancreatitis is one of the most common diseases requiring emergency surgery. Rapid and accurate recognition of acute pancreatitis can help improve clinical outcomes. This study aimed to develop a deep learning-powered diagnostic model for acute pancreatitis.Materials and methodsIn this investigation, we enrolled a cohort of 190 patients with acute pancreatitis who were admitted to Sichuan Provincial People’s Hospital between January 2020 and December 2021. Abdominal computed tomography (CT) scans were obtained from both patients with acute pancreatitis and healthy individuals. Our model was constructed using two modules: (1) the acute pancreatitis classifier module; (2) the pancreatitis lesion segmentation module. Each model’s performance was assessed based on precision, recall rate, F1-score, Area Under the Curve (AUC), loss rate, frequency-weighted accuracy (fwavacc), and Mean Intersection over Union (MIOU).ResultsUpon admission, significant variations were observed between patients with mild and severe acute pancreatitis in inflammatory indexes, liver, and kidney function indicators, as well as coagulation parameters. The acute pancreatitis classifier module exhibited commendable diagnostic efficacy, showing an impressive AUC of 0.993 (95%CI: 0.978–0.999) in the test set (comprising healthy examination patients vs. those with acute pancreatitis, P < 0.001) and an AUC of 0.850 (95%CI: 0.790–0.898) in the external validation set (healthy examination patients vs. patients with acute pancreatitis, P < 0.001). Furthermore, the acute pancreatitis lesion segmentation module demonstrated exceptional performance in the validation set. For pancreas segmentation, peripancreatic inflammatory exudation, peripancreatic effusion, and peripancreatic abscess necrosis, the MIOU values were 86.02 (84.52, 87.20), 61.81 (56.25, 64.83), 57.73 (49.90, 68.23), and 66.36 (55.08, 72.12), respectively. These findings underscore the robustness and reliability of the developed models in accurately characterizing and assessing acute pancreatitis.ConclusionThe diagnostic model for acute pancreatitis, driven by deep learning, exhibits excellent efficacy in accurately evaluating the severity of the condition.Trial RegistrationThis is a retrospective study.

Comparing the clinical value of baseline [68Ga]Ga-FAPI-04 PET/CT and [18F]F-FDG PET/CT in pancreatic ductal adenocarcinoma: additional prognostic value of the distal pancreatitis.

Anatomical and molecular staging strategies are needed for the personalized treatment of localized pancreatic ductal adenocarcinoma (PDAC). This study evaluated the performance of [68Ga]Ga-FAPI-04 and [18F]F-FDG PET/CT on the disease staging and prognostic value of patients with localized PDAC on contrast-enhanced (CE)-CT images. Patients with suspected localized PDAC on CE-CT were recruited for static [68Ga]Ga-FAPI-04 and 18[F]F-FDG and PET/CT, and select patients underwent simultaneous 60-min dynamic 68Ga-FAPI-04 PET/CT. The diagnostic and staging performances of the static PET/CT results were evaluated by delineating regions of interest in the primary tumor, whole pancreas, and distal pancreas in both types of scans and then evaluating correlations between the PET/CT findings and clinicopathological characteristics. Furthermore, Kaplan-Meier and hazard ratio (log-rank) methods were used to evaluate the prognostic value of the combined dynamic [68Ga]Ga-FAPI-04 and static [18F]F-FDG PET/CT method. We included 49 patients with histologically confirmed PDAC adenocarcinomas; 32 underwent 60-min dynamic [68Ga]Ga-FAPI-04 PET/CT imaging simultaneously. The static [68Ga]Ga-FAPI-04 method had significantly higher accuracy and uptake values than the static [18F]F-FDG method for primary PDAC lesions, metastatic lymph nodes, and distal metastases. Furthermore, 18.4% and 10.2% of the patients' stages changed after using the [68Ga]Ga-FAPI-04 and [18F]F-FDG PET/CT methodologies, respectively, compared to the CE-CT-designated stage. The Ki values obtained from dynamic [68Ga]Ga-FAPI-04 PET/CT did not differ between PDAC and distal obstructive pancreatitis lesions. Pathologically enlarged tumor size, poor differentiation, and perineural invasion were associated with increased [68Ga]Ga-FAPI-04 uptake but not with [18F]F-FDG uptake. The preoperative prognostic performance of [68Ga]Ga-FAPI-04 was better than that of [18F]F-FDG. Interestingly, combined [68Ga]Ga-FAPI-04 and [18F]F-FDG uptake results in the whole pancreas could further stratify patients based on their postoperative prognosis. 6[68Ga]Ga-FAPI-04 PET/CT was more sensitive and accurate than [18F]F-FDG PET/CT for tumor, node, and metastasis staging of PDAC identified on CE-CT. Additionally, [68Ga]Ga-FAPI-04 uptake was significantly associated with pathologically aggressive tumor features. Combined [68Ga]Ga-FAPI-04 and [18F]F-FDG PET/CT findings improved the prognostic value, potentially providing a non-invasive guide for clinical management. Finally, increased fibroblast activity in PDAC-induced obstructive pancreatitis may be associated with poor patient survival rates.

Radiomics Model Based on MR Images to Discriminate Pancreatic Ductal Adenocarcinoma and Mass-Forming Chronic Pancreatitis Lesions.

BackgroundIt is difficult to identify pancreatic ductal adenocarcinoma (PDAC) and mass-forming chronic pancreatitis (MFCP) lesions through conventional CT or MR examination. As an innovative image analysis method, radiomics may possess potential clinical value in identifying PDAC and MFCP. To develop and validate radiomics models derived from multiparametric MRI to distinguish pancreatic ductal adenocarcinoma (PDAC) and mass-forming chronic pancreatitis (MFCP) lesions.MethodsThis retrospective study included 119 patients from two independent institutions. Patients from one institution were used as the training cohort (51 patients with PDAC and 13 patients with MFCP), and patients from the other institution were used as the testing cohort (45 patients with PDAC and 10 patients with MFCP). All the patients had pathologically confirmed results, and preoperative MRI was performed. Four feature sets were extracted from T1-weighted imaging (T1WI), T2-weighted imaging (T2WI), and the artery (A) and portal (P) phases of dynamic contrast-enhanced MRI, and the corresponding radiomics models were established. Several clinical characteristics were used to discriminate PDAC and MFCP lesions, and clinical model was established. The results of radiologists’ evaluation were compared with pathology and radiomics models. Univariate analysis and the least absolute shrinkage and selection operator algorithm were performed for feature selection, and a support vector machine was used for classification. The receiver operating characteristic (ROC) curve was applied to assess the model discrimination.ResultsThe areas under the ROC curves (AUCs) for the T1WI, T2WI, A and, P and clinical models were 0.893, 0.911, 0.958, 0.997 and 0.516 in the primary cohort, and 0.882, 0.902, 0.920, 0.962 and 0.649 in the validation cohort, respectively. All radiomics models performed better than clinical model and radiologists’ evaluation both in the training and testing cohorts by comparing the AUC of various models, all P<0.050. Good calibration was achieved.ConclusionsThe radiomics models based on multiparametric MRI have the potential ability to classify PDAC and MFCP lesions.

Noninvasive assesment in differentiating benign and malign pancreatic lesions with endosonographic elastography score and strain ratio

Background: We aimed to evaluate the diagnostic capability of endoscopic ultrasound elastography (EUS-EG) and strain ratio (SR) for differentiating benign pancreatic lesions from the malign lesions Material and Method: We retrospectively evaluated well collected data of patients who undergone EUS-EG in a single centre during the period of January 2016-June 2019. Patients who had pancreatic disorders were further evaluated for the study. The final diagnosis of solid pancreatic lesions (SPL) was made by histopathologic examination. Control group consisted of patients with chronic pancreatitis (CP) who diagnosed according to Rosemont criteria. Elastography was evaluated by a qualitative (elastography scores) and a quantitative method SR. Results: A total of 66 patients (42 (63.6%)female/42 (63.6%)male) with mean age of 58.88±15.32 (19- 80) were included in the study. Thirty-eight patients had SLP, remain 28 patients were CP. In SPL group, 32 (84.2%) had adenocarcinomas and 6 (15.8%) had neuroendocrine tumors. Among 28 patients with benign pancreatic lessions, 23 (82.1%) had CP while five (17.9%) had autoimmune pancreatitis. Median SR values were significantly higher in patients with SPL than those with CP (44.0 (10.0-110.0) vs 7.0 (2.6-14.6), p&amp;lt;0.001). Elasticity scores were also significantly different between patients with SLP and CP (p&amp;lt;0.001). Elasticity scores were significantly different between adenocarcinomas and CP (p&amp;lt;0.001). A 14 cut-off value of SR had 97% sensitive and 100% specificity for SPL and receiver-operating characteristic curves showed an area under the curve of 0.99.6. Likelihood Ratio test revealed that SR appears as the best parameter in discrimination of lesion type either as benign or malignant (X2 = 54.031, p&amp;lt;0.001). Conclusion: Our study suggested that EUS-elastography and SR scores are highly effective in differentiating malign-benign pancreatitis lesions

Pancreatic cancer risk in relation to lifetime smoking patterns, tobacco type, and dose-response relationships

Chronic pancreatitis lesions usually embrace both intraduct papillary mucinous neoplasm (IPMN) and pancreatic ductal adenocarcinoma (PDAC). Patients at genetically-determined high risk of PDAC often harbor IPMN and/or chronic pancreatitis, suggesting IPMN, chronic pancreatitis and PDAC may share pathogenetic mechanisms. Chronic autoimmune pancreatitis (AIP) may also herald PDAC. Concurrent IPMN and AIP have been reported in few patients. Here we describe two patients with IPMN who developed type-1 AIP fulfilling the Honolulu and Boston diagnostic criteria. AIP diffusively affected the whole pancreas, as well as peripancreatic lymph nodes and the gallbladder. Previous pancreatic resection of focal IPMN did not show features of AIP. One of the patients carried a CFTR class-I mutation. Of notice, serum IgG4 levels gradually decreased to normal values after IPMN excision. Common risk factors to IPMN and AIP may facilitate its coincidental generation.

Lesions of pancreatitis in obese rats decrease after bariatric surgery

Lesions of pancreatitis in obese rats decrease after bariatric surgery

CTNNB1 mutational analysis of solid-pseudopapillary neoplasms of the pancreas using endoscopic ultrasound-guided fine-needle aspiration and next-generation deep sequencing

Solid-pseudopapillary neoplasm (SPN), a rare neoplasm of the pancreas, frequently harbors mutations in exon 3 of the cadherin-associated protein beta 1 (CTNNB1) gene. Here, we analyzed SPN tissue for CTNNB1 mutations by deep sequencing using next-generation sequencing (NGS). Tissue samples from 7 SPNs and 31 other pancreatic lesions (16 pancreatic ductal adenocarcinomas (PDAC), 11 pancreatic neuroendocrine tumors (PNET), 1 acinar cell carcinoma, 1 autoimmune pancreatitis lesion, and 2 focal pancreatitis lesions) were analyzed by NGS for mutations in exon 3 of CTNNB1. A single-base-pair missense mutations in exon 3 of CTNNB1 was observed in all 7 SPNs and in 1 of 11 PNET samples. However, mutations were not observed in the tissue samples of any of the 16 PDAC or other four pancreatic disease cases. The variant frequency of CTNNB1 ranged from 5.4 to 48.8 %. Mutational analysis of CTNNB1 by NGS is feasible and was achieved using SPN samples obtained by endoscopic ultrasound-guided fine needle aspiration.

Serine protease inhibitor Kazal type 1 and epidermal growth factor receptor are expressed in pancreatic tubular adenocarcinoma, intraductal papillary mucinous neoplasm, and pancreatic intraepithelial neoplasia

Serine protease inhibitor Kazal type 1 (SPINK1) is expressed in normal human pancreatic acinar cells and in a variety of tumors, and binds to the epidermal growth factor receptor (EGFR), mediating cell proliferation through the mitogen-activated protein kinase cascade in pancreatic cancer cell lines. Here, we aimed to assess SPINK1 and EGFR expression in various neoplastic lesions, including tissues demonstrating precancerous changes. Surgical specimens of pancreatic ductal adenocarcinoma (n = 23), intraductal papillary mucinous neoplasm (IPMN;n = 21), pancreatic neoplasms other than ductal adenocarcinoma (n = 8), chronic pancreatitis (n = 11), and pancreatic intraepithelial neoplasia (PanIN) lesions within the resected specimens were analyzed immunohistochemically for SPINK1 and EGFR expression. Sixty-five PanIN-1A, 32 PanIN-1B, 17 PanIN-2, and 6 PanIN-3 were identified. Both SPINK1 and EGFR were expressed in almost all PanIN lesions. All tubular ductal adenocarcinoma, IPMN, and mucinous cystadenocarcinoma samples (neoplasms of ductal origin) expressed SPINK1, whereas acinar cell carcinoma, anaplastic carcinoma, adenosquamous carcinoma, insulinoma, and islet cell carcinoma did not. EGFR was expressed in 87 % of tubular adenocarcinoma and 48 % of IPMN lesions. Among IPMN lesions, malignant lesions (IPMC) expressed EGFR more often than benign lesions (IPMA) did. Scattered expression of EGFR was observed in normal pancreatic ducts and within the tubular complex within chronic pancreatitis lesions. These results indicate that SPINK1 plays a role as a growth factor, signaling through the EGFR pathway in pancreatic ductal adenocarcinoma and neoplasms, and that the EGFR is involved in the malignant transformation of IPMN.

Peri-Vaterian Duodenal Irritation: Main Physiopathogenic Mechanism of Biliary Acute Pancreatitis. Its Mimicking by the “Short-Term” (&lt;20 min) “Closed Duodenal-Loop” The Beneficial Role of Topical Anesthesia of the Trigger Zone

Purpose: We have shown in humans, dogs, opossum and rats that the peri-Vaterian Duodenum (PVD)is the starting point of activation of autonomic arc reflexes(AAR). Three complex nervous systems are involved: the vagal, the splanchnic-celiac, the entero-pancreatic and the sensory afferent. Three types of AAR are elicited: the secretory inhibitor, the sympatho-ischemic(ischemia through opening of arterio-venous shunts), the pseudo-axonic(neurogenic inflammation). The irritation of the afferent, nerve fibers by stones or blood clots in the bile duct outlet; surgical or intemperate maneuvers in the PVD,is the pivotal mechanism of biliary acute pancreatitis(BAP). The aim of this report is to describe our experimental approach to mimick, through a surgical model this frequent entity. Methods: 73 male Wistar rats were studied. Under ip tiopental anesthesia, the left jugular vein was catheterized. Amylasemia, lipasemia and WBC was determined. Through a catheter inserted in the gastric antrum, a duodenal loop,comprised between a ligature at the pylorus and another placed below the bile-pancreatic duct outlet, was filled with sodium taurocholate stained with blue methylene. This allowed to check, de visu, whether or not reflux occurred in the bile duct. This is never observed below a 20'lapse. When occationaly observed, the test was interrupted.In 1° series,n = 21, the changes were evaluated at2h,when a complete autopsy is performed. In the2°series n = 11,the same protocol was performed at 24h. The results were compared with those of a shamgroup,n = 25. In the 1rst series, two subgroups were considered, one control(C)n = 11 and another experimental(E)n = 10, in which lidocaine was instilled into the duodenum previous to the duodenal loop construction. Results: In both the 1°and 2° experimental series, it was microscopic remarkable that the pancreatic ductal tree was free of any extraneous luminal content with an absence of any kind of damage of both bile and pancreatic duct epithelium. This fact coupled to the spotty distribution of the acute pancreatitis lesions gives strong support to our contention that the inflammatory lesions are induced independently of any duodenal content in the bile-pancreatic ducts. These findings do not favor the Opie physiopathogenic mechanism of BAP; in contrast, they provide added support to our hypothesis that the pivotal axis of this entity is centered in the irritation and consequent over activation of the AAR. Conclusion: The fact that topical anesthesia of the PVD, the most sensitive zone of the duodenum, induce a lower leucocyte count,a reduced level of amylasemia and lipasemia, is another suggestive feature that is coherent with our hypothesis of BAPhere delineated.

Sensitivity and Specificity of Canine Pancreas‐Specific Lipase (cPL) and Other Markers for Pancreatitis in 70 Dogs with and without Histopathologic Evidence of Pancreatitis

Pancreatitis is a common disorder in dogs for which the antemortem diagnosis remains challenging. To compare the sensitivity and specificity of serum markers for pancreatitis in dogs with histopathologic evidence of pancreatitis or lack thereof. Seventy dogs necropsied for a variety of reasons in which the pancreas was removed within 4 hours of euthanasia and serological markers were evaluated within 24 hours of death. Prospective study: Serum was analyzed for amylase and lipase activities, and concentrations of canine trypsin-like immunoreactivity (cTLI) and canine pancreas-specific lipase (cPL). Serial transverse sections of the pancreas were made every 2 cm throughout the entire pancreas and reviewed using a semiquantitative histopathologic grading scheme. The sensitivity for the Spec cPL (cutoff value 400 μg/L) was 21 and 71% in dogs with mild (n = 56) or moderate-severe pancreatitis (n = 7), and 43 and 71% (cutoff value 200 μg/L), respectively. The sensitivity for the cTLI, serum amylase, and lipase in dogs with mild or moderate-severe pancreatitis was 30 and 29%; 7 and 14%; and 54 and 71%, respectively. The specificity for the Spec cPL based on 7 normal pancreata was 100 and 86% (cutoff value 400 and 200 μg/L, respectively), whereas the specificity for the cTLI, serum amylase, and lipase activity was 100, 100, and 43%, respectively. The Spec cPL demonstrated the best overall performance characteristics (sensitivity and specificity) compared to other serum markers for diagnosing histopathologic lesions of pancreatitis in dogs.

Pancreatic mucinous cystadenoma in an adult with cystic fibrosis

Cystic fibrosis (CF) is the most frequent genetic disease in the Caucasian population. It seems to be associated with an increased risk of digestive cancer but only few cases of pancreatic tumors have been reported. As pancreatic lesions of the pancreas in CF patients are not rare, their etiological diagnosis is substantial. We report herein a case of a mucinous cystadenoma in a patient with CF. Diagnosis and management of pancreatic cystic tumors in patients at high risk of operative morbidity are challenging. When the potential malignancy of a pancreatic cystic mass cannot be well established in a CF patient, partly because of frequent chronic pancreatitis lesions, we suggest that surgical management should be undertaken instead of radiological surveillance.

Chronic Pancreatitis Is Associated With Disease-Specific Regulatory T-Cell Responses

Chronic pancreatitis is characterized by alternating phases of acute inflammation and quiescent disease. Involvement of T-cell responses has been suggested, but pancreatitis-specific T cells have not been described. We characterized T-cell responses against pancreatitis, pancreatic carcinoma-associated antigens, and tetanus toxoid in the bone marrow, blood, and/or pancreatitis lesions of patients with pancreatitis, pancreatic cancer, and healthy individuals. T cells were functionally characterized by antigen-dependent secretion of interferon (IFN)-gamma, interleukin (Il)-4, and IL-10, which indicate type 1, type 2, or regulatory T-cell responses, respectively. Regulatory T cells were characterized by multicolor flow cytometry. Isolated regulatory T cells were tested for their capacity to recognize pancreatitis-associated antigens and to suppress conventional T cells in an antigen-dependent manner. T cell-derived cytokines in tissue lesions were quantified by enzyme-linked immunosorbent assay. Chronic pancreatitis patients showed similar to pancreatic cancer patients and healthy individuals type 1 T-cell responses against tetanus toxoid; however, they exhibited strong IL-10-based T-cell responses against pancreatitis-associated but not pancreatic carcinoma-associated antigens. T cells from pancreatic cancer patients responded to pancreatic cancer-associated but not pancreatitis-associated antigens with IFN-gamma secretion. Pancreatitis-specific IL-10 responses were mediated by IL-10(+)IFN-gamma(-)FoxP3(+) regulatory T cells, which were expanded in the blood, bone marrow, and pancreatitis lesions and possessed the potential to suppress the proliferation of autologous conventional T cells in an antigen-specific manner. Pancreatitis lesions, in comparison with pancreatic carcinomas, contained increased concentrations of IL-10 and reduced levels of IFN-gamma, suggesting pancreatitis-specific activity of regulatory T cells in situ. Chronic pancreatitis is associated with disease-specific regulatory T-cell responses.

Pathology of Whooper Swans (Cygnus cygnus) Infected with H5N1 Avian Influenza Virus in Akita, Japan, in 2008

Two (1 adult and 1 young bird) of 4 H5N1-highly-pathogenic-avian-influenza (HPAI)-virus-infected whooper swans in Akita, Japan, in 2008 were investigated pathologically. Macroscopically, white spots with hemorrhages were scattered in the pancreas in the adult bird. Histologically, the adult bird had severe necrotizing pancreatitis and mild nonpurulent encephalitis. The young bird had severe nonpurulent encephalitis and nonpurulent enteric ganglionitis, and intestinal venous wall thickening. Virus antigens were detected in the lesions of pancreatitis in the adult bird and of encephalitis in adult and young birds. These findings suggest that the swans died or became moribund due to neurological disorders and necrotizing pancreatitis caused by H5N1 HPAI virus infection.

Is acute recurrent pancreatitis a chronic disease?

Whether acute recurrent pancreatitis is a chronic disease is still debated and a consensus is not still reached as demonstrated by differences in the classification of acute recurrent pancreatitis. There is major evidence for considering alcoholic pancreatitis as a chronic disease ab initio while chronic pancreatitis lesions detectable in biliary acute recurrent pancreatitis (ARP) seem a casual association. Cystic fibrosis transmembrane conductance regulator (CFTR) gene mutation, hereditary and obstructive pancreatitis seem an acute disease that progress to chronic pancreatitis, likely as a consequence of the activation and proliferation of pancreatic stellate cells that produce and activate collagen and therefore fibrosis. From the diagnostic point of view, in patients with acute recurrent pancreatitis Endoscopic ultrasound (EUS) seems the more reliable technique for an accurate evaluation and follow-up of some ductal and parenchymal abnormalities suspected for early chronic pancreatitis.

Pancréatite aiguë compliquée d’une septicémie à Clostridium tertium

Clostridium tertium septicaemia, although usually described in neutropenic patients, can also occur in the absence of neutropenia, as in our case report. A 61 year-old woman presented with pain in the right hypochondrium and epigastrium, constipation and vomiting that led to the diagnosis of acute pancreatitis of biliary origin. During septic shock, analysis of the liquid of an intra-abdominal mass and the results of the blood cultures revealed a Gram positive bacillus identified as C. tertium. During laparotomy, necrotic-hemorrhagic acute pancreatitis lesions were found with subtotal colic necrosis. Analysis of the peritoneal fluid revealed C. tertium. The patient died on D 46 after several nosocomial pneumopathies without identification of C. tertium. Three factors appear related to the onset of C. tertium septicaemia: neutropenia, lesions of the intestinal mucosa and previous treatment with 3rd generation, broad spectrum, cephalosporins. Such septicaemias are rare in immunocompetent patients and do not appear to have been reported before in a context of acute pancreatitis.

Differential diagnosis of pancreatic cancer and focal pancreatitis by using EUS-guided FNA

Despite advances in diagnostic imaging techniques, the differentiation between pancreatic cancer and focal pancreatitis remains difficult. This study evaluated the effectiveness of EUS-guided FNA in the differential diagnosis between pancreatic cancer and focal pancreatitis, with particular reference to detection of the K-ras point mutation. The study included 62 consecutive patients with pancreatic ductal cancer and 15 patients with focal pancreatitis demonstrated as a pancreatic mass lesion by EUS. Sensitivity, specificity, overall accuracy, positive predictive value, and negative predictive value of cytopathologic diagnosis were 82%, 100%, 86%, 100%, and 58%, respectively. Sensitivity, specificity, overall accuracy, positive predictive value, and negative predictive value of histopathologic diagnosis were 44%, 100%, 55%, 100%, and 32%, respectively. The K-ras point mutation was found in 74% of pancreatic cancers and 0% of focal pancreatitis lesions. No complication of EUS-guided FNA was observed. EUS-guided FNA is useful for the differential diagnosis of pancreatic mass lesions caused by pancreatic cancer and focal pancreatitis. Analysis for the K-ras point mutation in specimens obtained by EUS-guided FNA may enhance diagnostic accuracy in indeterminate cases.

Involvement of lipid peroxidation in spontaneous pancreatitis in WBN/Kob rats.

To cast light on the mechanisms underlying development of spontaneous pancreatitis lesions, tissues from WBN/Kob rats at various ages were histopathologically and immunohistochemically investigated with special reference to the existence of the lipid peroxidation products 4-hydroxy-2-nonenal (HNE), 4-hydroxy-2-hexenal (HHE), and malondialdehyde (MDA). Male 4-20-week-old WBN/Kob rats were killed to allow sampling of pancreatic tissues, which were fixed in cold acetone and 10% neutral-buffered formalin. and then processed for routine histopathology as well as immunohistochemistry for proteins modified by HNE, HHE, and MDA. Although no remarkable histologic changes were noted in younger animals, edema, hemorrhage, inflammatory cell infiltration, fibrosis, vacuolation of acinar cells, and ductular proliferation were observed in exocrine pancreatic tissue from animals at 10-15 weeks of age. In animals aged 20 weeks, the lesions had progressed remarkably and deposits of hemosiderin were apparent with fibrosis. Immunohistochemical examination for lipid peroxidation product-modified proteins showed HNE and MDA to be negative in all pancreatic tissues, but HHE was positive in the areas involving atrophy of acinar cells and fibrosis in the islets. The results of the present study thus provide support for the conclusion that lipid peroxidation during spontaneous pancreatitis in WBN/Kob rats may possibly be involved in the development of diabetes in this model.

Avian influenza A virus induced stunting syndrome-like disease in chicks.

Two-day-old specific-pathogen free chicks were inoculated with type A influenza virus (A/whistling swan/Shimane/499/83 (H5N3) through the air sac. Inoculated chicks showed mild to severe diarrhea and lesions of pancreatitis and atrophy of the pancreas, thymus and bursa of Fabricius. One chick died on each of days 4, 6 and 14 postinoculation (PI). Reduced weight gain was conspicuous from day 22 PI. Positive immunoreaction to the virus antigen was detected in the pancreas, kidneys, liver, lungs and air sacs, and cecal lamina propria. Virus recovery persisted longer in the pancreas. Some of these findings conformed to those of stunting syndrome.

Vascular and ductal patterns of pancreas by microradiography and their relation to lesions of pancreatitis.

Histopathological findings of pancreas freshly obtained from 108 autopsy cases were analyzed and individual lesions were correlated with vascular and ductal patterns revealed by microradiography. As the intralobular artery was demon-strated as a terminal artery, its functional and/or organic occlusion was expected to produce focal atrophy, parenchymal necrosis and fibrosis of lobular unit. Atrophy of acinar cells leading to replacement by isolated fat cells developed presumably from disturbance of systemic arterial circulation. Venous stasis seemed to be responsible for the formation of pseudolobules. Organic and/or functional obstructions in any part of the pancreatic duct caused various lesions of pancreatitis. Periductal location of focal necrosis and cell infiltration was regarded as a result of pancreatic juice leakage. Because the peripheral range of the pancreas was abundant in ductules, fat necrosis and fibrosis probably of ductal origin preferred the periphery. It was presumed that the ductal and vascular factors could interact each other in producing pancreatitis and both might even precipitate serious damages of the pancreas.