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1
Zakharova, M. A., D. S. Gorin, L. A. Marinova, and A. G. Kriger. "X-ray-negative pancreatic dust stones in patients with chronic pancreatiti." Khirurgiya. Zhurnal im. N.I. Pirogova, no. 12 (2019): 137. http://dx.doi.org/10.17116/hirurgia2019121137.
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Risse, O., C. Arvieux, J. Abba, and C. Létoublon. "Chirurgia delle complicanze delle pancreatiti acute." EMC - Tecniche Chirurgiche Addominale 19, no. 1 (March 2013): 1–14. http://dx.doi.org/10.1016/s1283-0798(13)63954-6.
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Hadjiangelis, Nicos P., and Doreen J. Addrizzo-Harris. "Cryptic Miliary Tuberculosis With a Prodrome Resembling Pancreatiti." Chest 124, no. 4 (January 2003): 330S. http://dx.doi.org/10.1378/chest.124.4_meetingabstracts.330s.
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Shaikh, Danial H., Ahmed Alemam, Jennifer von Ende, Haider Ghazanfar, Anil Dev, and Bhavna Balar. "Ansa Pancreatica, an Uncommon Cause of Acute, Recurrent Pancreatitis." Case Reports in Gastroenterology 15, no. 2 (July 1, 2021): 587–93. http://dx.doi.org/10.1159/000516686.
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The pancreatic duct is vulnerable to developmental anomalies which may produce variations in its course and/or its configuration. Ansa pancreatica is the least common anatomic variant. It is characterized by the formation of an “S-shaped loop” from the main pancreatic duct to the minor papilla. Ansa pancreatica has been implicated as a cause of recurrent acute pancreatitis. We review existing literature on pancreatitis secondary to the ansa deformity and present a case of recurrent acute pancreatitis in a patient who was ultimately found to have the ansa deformity on endoscopic ultrasound.
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Bhattacharyya, B. K., S. Chowdhury, S. Das, S. Mukherjee, and D. Bhattacharjee. "Treatment of Pancreatic Exocrine Insufficiency with Enteric Coated Pancreatin Formulations: An Overview." International Journal of Pharmaceutical Sciences and Nanotechnology 6, no. 3 (November 30, 2013): 2125–30. http://dx.doi.org/10.37285/ijpsn.2013.6.3.3.
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Pancreatin is a mixture of several digestive enzymes produced by the exocrine cells of the pancreas. It is composed of amylase, lipase and protease. It is used to treat conditions in which pancreatic secretions are deficient, such as surgical pancreatectomy, pancreatitis and cystic fibrosis. Pancreatin products contain the pancreatic enzymes trypsin, amylase and lipase. The patients with pancreatic diseases often suffer from pancreatic exocrine insufficiency. In such condition pancreas does not secrete required amount of digestive enzymes for proper digestion to occur. Severe pancreatic insufficiency occurs in cystic fibrosis, chronic pancreatitis, tumors or after surgical resection. Thus pancreatic exocrine insufficiency may result in clinical manifestation of malnutrition, weight loss and steatorrhea leading towards the increased risk of morbidity and mortality. For the improvement of clinical symptoms, restriction of fat intake and pancreatic enzyme replacement therapy are recommended. The enzyme substitution therapy is very much challenging because the optimal enzyme dose is highly variable to mimic the physiological pattern of pancreatic exocrine secretion. Regulatory authorities have approved several pancreatic enzyme formulations in the form of enteric coated minimicrosphere which are now available commercially. This review focuses on the physiological considerations of pancreatic exocrine insufficiency and its treatment with enteric coated pancreatin formulations.
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Adibelli, Zehra Hilal, Mustafa Adatepe, Cetin Imamoglu, Ozgur Sipahi Esen, Nazif Erkan, and Mehmet Yildirim. "Anatomic variations of the pancreatic duct and their relevance with the Cambridge classification system: MRCP findings of 1158 consecutive patients." Radiology and Oncology 50, no. 4 (December 1, 2016): 370–77. http://dx.doi.org/10.1515/raon-2016-0041.
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Abstract Background The study was conducted to evaluate the frequencies of the anatomic variations and the gender distributions of these variations of the pancreatic duct and their relevance with the Cambridge classification system as morphological sign of chronic pancreatitis using magnetic resonance cholangiopancreatography (MRCP). Patients and methods We retrospectively reviewed 1312 consecutive patients who referred to our department for MRCP between January 2013 and August 2015. We excluded 154 patients from the study because of less than optimal results due to imaging limitations or a history of surgery on pancreas. Finally a total of 1158 patients were included in the study. Results Among the 1158 patients included in the study, 54 (4.6%) patients showed pancreas divisum, 13 patients (1.2%) were defined as ansa pancreatica. When we evaluated the course of the pancreatic duct, we found the prevalence 62.5% for descending, 30% for sigmoid, 5.5% for vertical and 2% for loop. The most commonly observed pancreatic duct configuration was Type 3 in 528 patients (45.6%) where 521 patients (45%) had Type 1 configuration. Conclusions Vertical course (p = 0.004) and Type 2 (p = 0.03) configuration of pancreatic duct were more frequent in females than males. There were no statistically significant differences between the gender for the other pancreatic duct variations such as pancreas divisium, ansa pancreatica and course types other than vertical course (p > 0.05 for all). Variants of pancreas divisum and normal pancreatic duct variants were not associated with morphologic findings of chronic pancreatitis by using the Cambridge classification system. The ansa pancreatica is a rare type of anatomical variation of the pancreatic duct, which might be considered as a predisposing factor to the onset of idiopathic pancreatitis.
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Bragado, M. J., J. I. San Roman, A. González, L. J. García, M. A. López, and J. J. Calvo. "Impairment of Intracellular Calcium Homoeostasis in the Exocrine Pancreas after Caerulein-Induced Acute Pancreatitis in the Rat." Clinical Science 91, no. 3 (September 1, 1996): 365–69. http://dx.doi.org/10.1042/cs0910365.
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1. We have measured intracellular calcium concentrations in basal conditions and in response to cholecystokinin-octapeptide and acetylcholine in pancreatic acini isolated from rats with caerulein-induced acute pancreatitis and compared them with those in control rats. 2. We also measured amylase secretion in basal conditions and in response to cholecystokinin-octapeptide in both groups. 3. In pancreatic acini from rats with pancreatitis the basal intracellular calcium concentration was significantly increased (134.9±7.1 nmol/l compared with 71.8 ± 2.9 nmol/l, P < 0.001). Moreover, the maximum values of intracellular calcium attained during the stimulation period were equivalent in acini from control and pancreatitic rats with no statistically significant differences. 4. In acini from control rats the differences between the resting levels of intracellular calcium and the maximum intracellular calcium values (Δ[Ca2+]i) in response to several concentrations of cholecystokinin-octapeptide showed a clear dose—response relationship, with a half-maximal increase at 0.1 nmol/l and a maximal difference (Δ[Ca2+]i = 259 ±50 nmol/l) at 1 nmol/l. In contrast, a right-shifted response, with a statistically significant smaller increase, was observed in acini from pancreatitic rats. 5. Basal amylase release was significantly higher in acini from rats with pancreatitis (11.7 ±1.0% of total compared with 5.9 ±1.1% of total, P < 0.001). In contrast, cholecystokinin-octapeptide and acetylcholine-evoked amylase secretion was reduced by more than 85% in acini from pancreatitic rats. 6. In conclusion, calcium homoeostasis in pancreatic acinar cells from rats with caerulein-induced pancreatitis seems to be impaired. These results suggest excessive release of acinar free ionized calcium, or damage to the integrity of mechanisms that restore low resting levels of intracellular free ionized calcium, and the consequent calcium toxicity could be the key trigger in caerulein-induced acute pancreatitis.
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Sommer, Camille Anne, and C. Mel Wilcox. "Pancreatico-pericardial fistula as a complication of chronic pancreatitis." F1000Research 3 (January 29, 2014): 31. http://dx.doi.org/10.12688/f1000research.3-31.v1.
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Pancreatico-pericardial fistula is an extremely rare complication of chronic pancreatitis. We present a case of a 58-year-old man who presented with syncope. Transthoracic echocardiogram revealed a pericardial effusion with tamponade physiology. Pericardiocentesis and pericardial fluid analysis demonstrated a lipase level of 2321 U/L. Subsequently, an endoscopic retrograde cholangiopancreatography (ERCP) was performed, confirming the presence of a pancreatico-pericardial fistula (PPF) from the distal body of the pancreas. A pancreatic duct stent was placed across the duct disruption on two separate occasions; however, despite stent placement, the patient continued to re-accumulate pericardial fluid and deteriorated. While rare, PPFs may complicate chronic pancreatitis, may not respond to pancreatic duct stenting and may portend a poor prognosis.
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Mihai, Catalina, Mariana Floria, Radu Vulpoi, Loredana Nichita, Cristina Cijevschi Prelipcean, Vasile Drug, and Viorel Scripcariu. "Pancreatico-Pleural Fistula – from Diagnosis to Management. A Case Report." Journal of Gastrointestinal and Liver Diseases 27, no. 4 (December 31, 2018): 465–69. http://dx.doi.org/10.15403/jgld.2014.1121.274.ple.
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Pancreatic pseudocysts are frequent complications of both acute and chronic pancreatitis. By contrast, pancreatico-pleural fistula is rare. Here we report a case of massive pleural effusion secondary to a fistula in the left hemi-diaphragm, between a pancreatic pseudocyst and the left pleura, in a patient with a right kidney tumor and bilateral massive pulmonary thromboembolism. This fistula developed after several episodes of un-investigated acute pancreatitis. The pleural effusion was treated by three thoracocenteses, without recurrence.
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Sajika Dighe, Raju Shinde, Sangita Shinde, and Mohit Gupte. "A rare case of pancreaticopleural fistula patient presented in surgery OPD." International Journal of Research in Pharmaceutical Sciences 11, SPL4 (December 21, 2020): 1329–32. http://dx.doi.org/10.26452/ijrps.v11ispl4.4301.
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Pancreatico-pleural fistula is rare and infrequent complication of commonly occurring chronic pancreatitis leading to an extra-peritoneal abnormal connection between the pancreatic system and pleural cavity. Diagnosis needs high-level clinical suspicion to avoid delay in the diagnosis as the patient presents with respiratory distress rather than any abdominal symptom and produces large quantities of pleural fluid intractable of pleural tapping or chest drain. Diagnosis of the fistula is clicked by elevated pleural fluid amylase. Various imaging options are available with their unique importance like CECT, ERCP and MRCP. In a low resource, setup CECT becomes a useful modality to delineate the pancreatic parenchymal changes, pancreatic duct anatomy and fluid collection, thus aid in the diagnosis. Treatment modalities depending on structural anatomy of the duct and parenchymal destruction are either Medical, Conservative and Surgical. Here our patient presented with massive left sided pleural effusion resistant to surgical intervention secondary to chronic pancreatitis in a 28-year man later diagnosed as Pancreatico-pleural fistula on CECT. The patient underwent distal pancreatectomy with splenectomy with decortication of the lung with excision of PPF. The patient now is continuous follow-up for chronic pancreatitis and is symptom-free from last 2 years.
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Kulus, Magdalena, Małgorzata Józkowiak, Dorota Bukowska, Jakub Kulus, and Paweł Antosik. "Coexistence of pancreatic adenocarcinoma and a pseudocyst in cat." Medical Journal of Cell Biology 7, no. 1 (July 1, 2019): 25–31. http://dx.doi.org/10.2478/acb-2019-0004.
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AbstractExocrine pancreatic tumors in cats and dogs are very uncommon, with exocrine pancreatic adenocarcinoma described as a particularly rare, malignant tumor in a small animals. It is usually derived from pancreatic ducts, as well as glandular tissue. Very often the disease has a subclinical course and is diagnosed only during post – mortem examination. Adenocarcinoma metastasize to both the surrounding and distant organs. The etiology of the cancer progress in the pancreas remains unknown.Pancreatic pseudocyst (pseudocystis pancreatis) is a very rare disease in domestic animals. Only a few cases of pancreatic pseudocyst in dogs and cats are described in the available literature. On the other hand, in humans it is a common complication of pancreatitis. The pancreatic pseudocyst can be a result of pancreatitis, as well as be a secondary condition to acute pancreatitis, trauma or chronic inflammation. It is a capsule made of fibrous or granulation tissue, containing sterile pancreatic juice. The pathogenesis of pancreatic pseudocyst is still unknown. Clinical signs are not specific and may resemble symptoms of pancreatitis. The ultrasound examination shows a cyst in the pancreas.This paper describes the case of pancreatic adenocarcinoma in a cat that occurred simultaneously with the pancreatic pseudocyst. Currently, literature indicates the necessity to differentiate the above cancer from cystic lesion. Due to the simultaneous occurrence of both pathologies, extremely rare diagnosis and spectacular picture of changes, it was decided to present this case.
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Aswani, Yashant, Shehbaz MS Ansari, Ulhaas S. Chakraborty, Priya Hira, and Sudeshna Ghosh. "Where there is pancreatic juice, there is a way: Spontaneous fistulization of severe acute pancreatitis-associated collection into urinary bladder." Indian Journal of Radiology and Imaging 30, no. 04 (October 2020): 529–32. http://dx.doi.org/10.4103/ijri.ijri_349_20.
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AbstractPancreatic fluid collections (PFC) are notorious for their extension beyond the normal confines of the pancreatic bed. This distribution is explained by dissection along the fascial planes in retroperitoneum due to the digestive enzymes within the PFC. In genitourinary track, PFCs have been described to involve the kidneys and the ureters. We report a case of severe acute necrotizing pancreatitis in a 28-year-old male, chronic alcoholic, who on readmission developed features of cystitis. The urine was turbid but did not show significant bacteriuria. Close location of the PFC near the urinary bladder (UB) prompted evaluation of urinary lipase and amylase. Elevated urinary enzyme levels suggested a Pancreatico-vesical fistula, conclusive demonstration of which was established by CT cystography. Percutaneous drainage of the necrosum and stenting of pancreatic duct led to spontaneous healing of the pancreatico-vesical fistula. Our case reiterates the remarkable property of pancreatic enzymes to dissect the fascial planes which is demonstrated by decompression of PFC via UB causing spontaneous Pancreatico-vesical fistula. Further, presence of main pancreatic duct fistulization should prompt endoscopic-guided stenting to obliterate the communication with the fistula and accelerate healing.
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Prasad, Mythraeyee, Sipra Rout, Tharani Putta, Reuben Thomas Kurien, Sudipta Dhar Chowdhury, Anu Eapen, Y. S. Hepsy, and Suganthy Rabi. "Anatomical Patterns of the Pancreatic Ductal System – A Cadaveric and Magnetic Resonance Cholangiopancreatography Study." Journal of Morphological Sciences 36, no. 04 (December 2019): 279–85. http://dx.doi.org/10.1055/s-0039-1698371.
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Abstract Introduction Morphological variants of the pancreatobiliary system can predispose to chronic pancreatitis. The goal of the present study is to assess the prevalence of pancreatic duct patterns in the Indian population, both by cadaveric dissection and by magnetic resonance cholangiopancreatography (MRCP). Materials and Methods A total of 15 adult pancreas specimens of unknown age and gender, and 5 fetal pancreas specimens of different gestational ages with the intact second part of duodenum, were dissected by the piecemeal method. For clinical relevance, MRCP images of 103 clinically-diagnosed chronic pancreatitis patients irrespective of their etiology were obtained retrospectively from the existing database and studied. The anatomical patterns were classified as five different types based on the course of the main pancreatic duct and the accessory pancreatic duct and their openings into the duodenal wall, including variants like pancreas divisum and ansa pancreatica. Results In the cadaveric study, the main pancreatic duct was single with a straight course in 46.67% of the adult specimens, and in the MRCP study, the main pancreatic duct showed a descending course in 77.66% of the cases. The most common pattern was type III in both the cadaveric (80%) and radiological (55.33%) studies, and the accessory duct was absent on the MRCP in all type-III cases, while it ended blindly in the cadaveric specimens. Ansa pancreatica (type V) was observed in 1 adult specimen (6.7%), but not in the radiological study. Pancreas divisum (type IV) was observed in the 8 cases (7.76%) cases in the radiological study. Conclusion Knowledge of the anatomical variants of the pancreatic ductal system may be helpful for the radiologists during diagnostic and therapeutic interventional procedures.
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Imran, Mohammad Abu, Karma Sherub, Sonam Tshering, Prabhat Pradhan, and Thukten Chophel. "Post-Operative Complications of Pancreatico Jejunostomy in Patients with Pancreatic Calculi." EAS Journal of Medicine and Surgery 4, no. 6 (June 9, 2022): 130–33. http://dx.doi.org/10.36349/easjms.2022.v04i06.002.
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Background: Pancreatic calculi are a condition characterised by irreversible destruction and fibrosis of the exocrine parenchyma, leading to exocrine pancreatic insufficiency and progressive endocrine failure leading to diabetes. Tropical calcific pancreatitis, an inflammatory condition of the pancreas, is usually associated with the pancreatic duct stones for which lateral pancreatico jejunostomy provides excellent results with acceptable early morbidity and mortality. Objective: To assess the post-operative complications of pancreatico jejunostomy in patients with pancreatic calculi. Methods: This was a descriptive type of prospective study. A total of 26 patients were included in the study between July 2011 to December 2011 in a BSMMU and other private hospitals of Dhaka who underwent lateral pancreatico jejunostomy for pancreatic calculi. Data were collected using a structured questionnaire and presented in tables by number, percentage, mean±SD, median. Results: This study was conducted to find out the efficacy and safety of lateral pancreatico jejunostomy in cases of pancreatic calculi. Highest proportion of the patients (n=26) are in the age group of 30-40 years (13 out of 26 number of patients. The mean age of the patients is 36.74. More than 64% of the patients were male. Female was found in 35% cases. Revealed that 3.84% of the patients were alcoholic. 96.15% of the patients (25 out of 26 patients) were non alcoholic. 30.76% (8 patients out of 26) is associated with gallstone disease.69.23% (18 patients out of 26) is not associated with gallstone disease. Upper abdominal pain was present in 100% patients. Steatorrhoea was present in 15.38% of the patients (4 patients out of 26).Jaundice predominated in 3.85% of the patients (1 patient out of 26). Shows that 34.61% of the patients (9 patients out of 26) developed post-operative morbidity, death occurred in 3.85% (1 patient out of 26). In our study 11.54% of the patients (3 patients out of 26) ............
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Fan, Yu-Ting, Guo-Jian Yin, Wen-Qin Xiao, Lei Qiu, Ge Yu, Yan-Ling Hu, Miao Xing, et al. "Rosmarinic Acid Attenuates Sodium Taurocholate-Induced Acute Pancreatitis in Rats by Inhibiting Nuclear Factor-κB Activation." American Journal of Chinese Medicine 43, no. 06 (January 2015): 1117–35. http://dx.doi.org/10.1142/s0192415x15500640.
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Rosmarinic Acid (RA), a caffeic acid ester, has been shown to exert anti-inflammation, anti-oxidant and antiallergic effects. Our study aimed to investigate the effect of RA in sodium taurocholate ( NaTC )-induced acute pancreatitis, both in vivo and in vitro. In vivo, RA (50 mg/kg) was administered intraperitoneally 2 h before sodium taurocholate injection. Rats were sacrificed 12 h, 24 h or 48 h after sodium taurocholate injection. Pretreatment with RA significantly ameliorated pancreas histopathological changes, decreased amylase and lipase activities in serum, lowered myeloperoxidase activity in the pancreas, reduced systematic and pancreatic interleukin-1 β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) levels, and inhibited NF-κB translocation in pancreas. In vitro, pretreating the fresh rat pancreatic acinar cells with 80 μ mol/L RA 2 h before 3750 nmol/L sodium taurocholate or 10 ng/L TNF-α administration significantly attenuated the reduction of isolated pancreatic acinar cell viability and inhibited the nuclear activation and translocation of NF-κB. Based on our findings, RA appears to attenuate damage in sodium taurocholate-induced acute pancreatitis and reduce the release of inflammatory cytokines by inhibiting the activation of NF-κB. These findings might provide a basis for investigating the therapeutic role of RA in managing acute pancreatits.
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Rabbi, Hashim, Md Mamunur Rashid, AHM Tanvir Ahmed, HM Sabbir Raihan, Sarder Rizwan Nayeem, Mohammad Ali, HA Nazmul Hakim, Ajmal Quader Chowdhury, and Mahmud Mohammad Sarder. "Outcome of Pancreatic Head Coring in as Key Surgical Treatment in Head Dominant Chronic Pancreatitis in Tertiary Referral Centers of Bangladesh." BIRDEM Medical Journal 8, no. 2 (May 16, 2018): 151–58. http://dx.doi.org/10.3329/birdem.v8i2.36647.
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Background: Pancreatic head coring procedure, an organ preserving surgery in which diseased head of pancreas is cored with drainage of main pancreatic duct by lateral pancreatico-jejunostomy. Chronic pancreatitis is a persistently occurring inflammatory disease that causes pancreatic duct stones or calcification, stricture, dilatation of pancreatic duct and irreversible morphological changes resulting intractable pain and losses of exocrine and endocrine function. Appropriate management protocol recognizing underlying pathology, can prevent complications and improves the quality of life. Apart from ductal decompression, in Frey’s’ procedure resection of the “pacemaker of pain” (Head of the pancreas) gives excellent outcome.Methods: In this prospective observational study, we have intended to further validate the Frey’s procedure an effective surgical method in head dominant severe chronic pancreatitis. The study was carried out on 106 Bangladeshi patients who underwent Frey’s Procedure with Lateral Pancreaticojejunostomy from January 2000 to December 2017.Result: The study revealed 51 patients (48.11%) were in 3rd decade of life with 45 male and 61 female. We found 77 patients presented with diabetes mellitus, mostly on insulin. Steatorrhoea was noted in 39 patients and Malnutrition in 79 patients. Visual Analog Scale (VAS) was used for scoring pain. Postoperative morbidity was noted in 29 patients 27.35 % cases, but there was no anastomotic leakage or mortality in the immediate postoperative period in our series.Conclusion: Quality of life has always been the most important decisive factor for patients with severe chronic Pancreatitis. Pain is the predominant clinical feature and very difficult to control. Correction of diabetes and malnutrition are major challenges too. This study revealed, Frey’s procedure with adequate ductal clearance with wide pancreato-jejunal anastomosis in head dominant severe chronic pancreatitis is key to better pain control, improves quality of life and prevents recurrence.Birdem Med J 2018; 8(2): 151-158
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Ohtani, Naoko, Kunihiko Kimoto, Shunichi Yoshida, Tsuguo Tanaka, Hideto Inokuchi, and Keiichi Kawai. "Pancreatic arteriovenous malformation with pancreatitis involving a pancreatico-venous fistula." Gastroenterologia Japonica 27, no. 1 (February 1992): 115–20. http://dx.doi.org/10.1007/bf02775073.
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Drozdov, V. N., E. V. Shikh, A. A. Astapovskiy, Yu V. Kotlyachkova, L. E. Dobrovolskaya, A. K. Starodubtsev, I. A. Komissarenko, and S. Y. Serebrova. "Clinical and pharmacological approaches to the management of exocrine pancreatic insufficiency in chronic pancreatitis." Meditsinskiy sovet = Medical Council, no. 15 (October 19, 2021): 58–67. http://dx.doi.org/10.21518/2079-701x-2021-15-58-67.
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Chronic pancreatitis is a multifactorial disease in which repeated episodes of inflammation of the pancreas contribute to the development of fibrous tissue, leading to chronic pain, as well as exocrine and endocrine insufficiency. The incidence and prevalence of chronic pancreatitis in the world are growing, as evidenced by current statistics. In addition, the annual costs associated with the treatment of exocrine and endocrine insufficiency are also increasing. In the United States alone, the annual cost of treating these complications is $ 75.1 million. Exocrine insufficiency is one of the most frequent complications, which is characterized by a deficiency of pancreatic enzymes, leading to the development of malabsorption syndrome (impaired absorption of nutrients, vitamins and minerals). Due to the increased incidence and deterioration of the quality of life associated with this condition, the goal of treatment is to compensate for the deficiency of exocrine enzymes with oral pancreatic enzyme replacement therapy. The core of this therapy is to deliver activated, unbroken enzymes directly to the small intestine during a meal. Many studies have shown that prescribing enzyme replacement therapy improves symptoms associated with exocrine insufficiency, reduces the progression of osteopenia, and improves survival in such patients. The use of pancreatin contributes to the correction of exocrine insufficiency in patients with chronic pancreatitis. The data presented in the article indicate that the drug is a safe and effective agent, meets all modern standards and requirements, and can be used to correct enzymatic pancreatic insufficiency.
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Heo, Jun. "Infected Pancreatic Necrosis Mimicking Pancreatic Cancer." Case Reports in Gastroenterology 14, no. 2 (August 26, 2020): 436–42. http://dx.doi.org/10.1159/000510161.
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Although infected pancreatic necrosis can develop as a result of rare conditions involving trauma, surgery, and systemic infection with an uncommon pathogen, it usually occurs as a complication of pancreatitis. Early phase of acute pancreatitis can be either edematous interstitial pancreatitis or necrotizing pancreatitis. The late complications of pancreatitis can be divided into pancreatic pseudocyst due to edematous interstitial pancreatitis or walled-off necrosis due to necrotizing pancreatitis. During any time course of pancreatitis, bacteremia can provoke infection inside or outside the pancreas. The patients with infected pancreatic necrosis may have fever, chills, and abdominal pain as inflammatory symptoms. These specific clinical presentations can differentiate infected pancreatic necrosis from other pancreatic diseases. Herein, I report an atypical case of infected pancreatic necrosis in which abdominal pain, elevation of white blood cell, and fever were not found at the time of admission. Rather, a 10-kg weight loss (from 81 to 71 kg) over 2 months nearly led to a misdiagnosis of pancreatic cancer. The patient was finally diagnosed based on endoscopic ultrasound-guided fine-needle aspiration. This case highlights that awareness of the natural course of pancreatitis and infected pancreatic necrosis is important. In addition, endoscopic ultrasound-guided fine-needle aspiration should be recommended for the diagnosis and treatment of indeterminate pancreatic lesions in selected patients.
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Zheng, Yufan, Wenrui Sun, Zhengyang Wang, Jiaying Liu, Cong Shan, Chenxi He, Borui Li, et al. "Activation of Pancreatic Acinar FXR Protects against Pancreatitis via Osgin1-Mediated Restoration of Efficient Autophagy." Research 2022 (November 2, 2022): 1–15. http://dx.doi.org/10.34133/2022/9784081.
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Pancreatitis is the leading cause of hospitalization in gastroenterology, and no medications are available for treating this disease in current clinical practice. FXR plays an anti-inflammatory role in diverse inflammatory diseases, while its function in pancreatitis remains unknown. In this study, we initially observed a marked increase of nuclear FXR in pancreatic tissues of human patients with pancreatitis. Deleting the FXR in pancreatic acinar cells (FXRacinarΔ/Δ) led to more severe pancreatitis in mouse models of caerulein-induced acute and chronic pancreatitis, while the FXR agonist GW4064 significantly attenuated pancreatitis in caerulein or arginine-induced acute pancreatitis and caerulein-induced chronic pancreatitis. FXR deletion impaired the viability and stress responses of pancreatic exocrine organoids (PEOs) in vitro. Utilizing RNA-seq and ChIP-seq of PEOs, we identified Osgin1 as a direct target of FXR in the exocrine pancreas, which was also increasingly expressed in human pancreatitis tissues compared to normal pancreatic tissues. Pancreatic knockdown of Osgin1 by AAV-pan abolished the therapeutic effects of FXR activation on pancreatitis, whereas pancreatic overexpression of Osgin1 effectively alleviated caerulein-induced pancreatitis. Mechanistically, we found that the FXR-OSGIN1 axis stimulated autophagic flux in the pancreatic tissues and cell lines, which was considered as the intrinsic mechanisms through which FXR-OSGIN1 protecting against pancreatitis. Our results highlight the protective role of the FXR-OSGIN1 axis in pancreatitis and provided a new target for the treatment of this disease.
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Whitcomb, David C. "Inflammation and Cancer V. Chronic pancreatitis and pancreatic cancer." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 2 (August 2004): G315—G319. http://dx.doi.org/10.1152/ajpgi.00115.2004.
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Pancreatic inflammation appears to increase the risk of pancreatic cancer. This observation is striking in the hereditary pancreatitis kindreds but also occurs in alcoholic, idiopathic, and tropical chronic pancreatitis and cystic fibrosis. However, the mutations associated with hereditary pancreatitis or cystic fibrosis are not found in sporadic pancreatic adenocarcinomas, suggesting that the effects are indirect by causing recurrent pancreatitis and chronic inflammation. The process of mutation accumulation and clonal expansion that is required for development of invasive pancreatic adenocarcinoma must therefore be accelerated in chronic pancreatitis to account for the high incidence of pancreatic cancer in these patients.
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Hao, Ying, Jing Wang, Ningguo Feng, and Anson W. Lowe. "Determination of Plasma Glycoprotein 2 Levels in Patients With Pancreatic Disease." Archives of Pathology & Laboratory Medicine 128, no. 6 (June 1, 2004): 668–74. http://dx.doi.org/10.5858/2004-128-668-dopgli.
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Abstract Context.—Blood tests possessing higher diagnostic accuracy are needed for all the major pancreatic diseases. Glycoprotein 2 (GP2) is a protein that is specifically expressed by the pancreatic acinar cell and that has previously shown promise as a diagnostic marker in animal models of acute pancreatitis. Objective.—This study describes the development of an assay for GP2, followed by the determination of plasma GP2 levels in patients with acute pancreatitis, chronic pancreatitis, and pancreatic cancer. Design.—Rabbit polyclonal antisera and mouse monoclonal antibodies were generated against human GP2 and used to develop an enzyme-linked immunosorbent assay. The assay was tested in patients with an admitting diagnosis of pancreatic disease at 2 tertiary care facilities. The diagnosis of acute or chronic pancreatitis and pancreatic cancer was determined using previously established criteria that incorporated symptoms, radiology, pathology, and serology. Plasma GP2 levels were determined in 31 patients with acute pancreatitis, 16 patients with chronic pancreatitis, 36 patients with pancreatic cancer, and 143 control subjects without pancreatic disease. Amylase and lipase levels were also determined in patients with acute pancreatitis. Results.—The GP2 assay's sensitivity values were 0.94 for acute pancreatitis, 0.81 for chronic pancreatitis, and 0.58 for pancreatic cancer, which were greater than the 0.71 for acute pancreatitis and 0.43 for chronic pancreatitis (P = .02) observed for amylase. The lipase assay sensitivity for acute pancreatitis was 0.66. The accuracy of the GP2 assay was greater than that of the amylase or lipase assays for acute pancreatitis (GP2 vs lipase, P = .004; GP2 vs amylase, P = .003) when analyzed using receiver operator characteristic curves. When daily serial blood samples were obtained for 13 patients with acute pancreatitis, GP2 levels remained abnormally elevated for at least 1 day longer than the amylase or lipase levels. Conclusion.—The GP2 assay is a useful new marker for acute and chronic pancreatitis.
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Munirathinam, Manoj, Pugazhendhi Thangavelu, and Ratnakar Kini. "Pancreatico‑pleural Fistula: Case Series." Journal of Digestive Endoscopy 09, no. 01 (January 2018): 026–31. http://dx.doi.org/10.4103/jde.jde_23_17.
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ABSTRACTPancreatico‑pleural fistula is a rare but serious complication of acute and chronic pancreatitis. The pleural effusion caused by pancreatico‑pleural fistula is usually massive and recurrent. It is predominately left‑sided but right‑sided and bilateral effusion does occur. We report four cases of pancreatico‑pleural fistula admitted to our hospital. Their clinical presentation and management aspects are discussed. Two patients were managed by pancreatic endotherapy and two patients were managed conservatively. All four patients improved symptomatically and were discharged and are on regular follow‑up. Most of these patients would be evaluated for their breathlessness and pleural effusion delaying the diagnosis of pancreatic pathology and management. Hence, earlier recognition and prompt treatment would help the patients to recover from their illnesses. Pancreatic pleural fistula diagnosis requires a high index of suspicion in patients presenting with chest symptoms or pleural effusion. Extremely high pleural fluid amylase levels are usual but not universally present. A chest X‑ray, pleural fluid analysis, and abdominal imaging (magnetic resonance cholangiopancreatography/magnetic resonance imaging abdomen more useful than contrast‑enhanced computed tomography abdomen) would clinch the diagnosis. Endoscopic retrograde cholangiopancreatography with stent or sphincterotomy should be considered when pancreatic duct (PD) reveals a stricture or when medical management fails in patients with dilated or irregular PD. Surgical intervention may be indicated in patients with complete disruption of PD or multiple strictures.
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de Clerck, F., P. Laukens, V. De Wilde, L. Vandeputte, M. Cabooter, J. Van Huysse, and H. Orlent. "A Suspicious Pancreatic Mass in Chronic Pancreatitis: Pancreatic Actinomycosis." Case Reports in Oncological Medicine 2015 (2015): 1–3. http://dx.doi.org/10.1155/2015/767365.
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Introduction. Pancreatic actinomycosis is a chronic infection of the pancreas caused by the suppurative Gram-positive bacteriumActinomyces. It has mostly been described in patients following repeated main pancreatic duct stenting in the context of chronic pancreatitis or following pancreatic surgery. This type of pancreatitis is often erroneously interpreted as pancreatic malignancy due to the specific invasive characteristics ofActinomyces.Case. A 64-year-old male with a history of chronic pancreatitis and repeated main pancreatic duct stenting presented with weight loss, fever, night sweats, and abdominal pain. CT imaging revealed a mass in the pancreatic tail, invading the surrounding tissue and resulting in splenic vein thrombosis. Resectable pancreatic cancer was suspected, and pancreatic tail resection was performed. Postoperative findings revealed pancreatic actinomycosis instead of neoplasia.Conclusion. Pancreatic actinomycosis is a rare type of infectious pancreatitis that should be included in the differential diagnosis when a pancreatic mass is discovered in a patient with chronic pancreatitis and prior main pancreatic duct stenting. Our case emphasizes the importance of pursuing a histomorphological confirmation.
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Varabei, A. V., A. Ch Shuleika, T. E. Vladimirskay, I. A. Shved, Y. I. Vizhinis, and M. Y. Makki. "Hypoxia of pancreas in pathogenesis of fibrosis in chronic pancreatitis." Proceedings of the National Academy of Sciences of Belarus, Medical series 15, no. 4 (January 14, 2019): 391–404. http://dx.doi.org/10.29235/1814-6023-2018-15-4-391-404.
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The pathogenesis of chronic pancreatitis and pain syndrome had not been fully studied. The aim of the study was to evaluate the interrelation of fibrotic and ischemic changes in the parenchyma of pancreas, and pancreatic duct pressure in the pathogenesis of chronic pancreatitis. In a prospective study, a morphological, the immunohistochemical study of pancreatic preparations was performed, and the indicators of tissue oximetry and pancreatic duct pressure were studied intraoperatively in 40 patients operated for chronic pancreatitis. It was found that with the progression of fibrotic changes in the pancreatic tissue of patients with chronic pancreatitis, there was an increase in TGF-β1 expression (р < 0.001), an increase in the number of pancreatic stellate cells (r = 0.32, р < 0.05), a decrease in glycogen (ischemia marker). The intraoperative direct measurement revealed a high pancreatic duct pressure: 34.2 (26.6; 45.3) mm Hg, a decrease in oxygenation of the pancreatic tissue that correlate with a degree of fibrosis. The pancreatic tissue in chronic pancreatitis has chronic hypoxia associated with fibrosis and increased pancreatic ductal hypertension. So, secondary pancreatic ischemia can be a significant factor in the progression of fibrosis and chronic pain syndrome in chronic pancreatitis.
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Siby, Jayas, Preetha S, and Sindhu R.S. "Proportion of Pancreatic Necrosis among Patients with Acute Pancreatitis and Association between High-Density Lipoprotein (HDL Cholesterol) and Pancreatic Necrosis – A Prospective Observational Study from Kerala, South India." Journal of Evidence Based Medicine and Healthcare 8, no. 20 (May 17, 2021): 1489–94. http://dx.doi.org/10.18410/jebmh/2021/282.
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BACKGROUND Acute pancreatitis is a very common disease and severe acute pancreatitis is life threatening and needs early identification. Current severity predicting indices in acute pancreatitis are cumbersome. There have been previous reports of low HDL cholesterol in life threatening acute pancreatitis. Previous studies in this regard were done in a single ethnicity population and needed to be validated in other ethnic groups. We wanted to estimate the proportion of pancreatic necrosis among the patients with acute pancreatitis attending Government Medical College, Thiruvananthapuram. We also wanted to compare the mean HDL values in those who developed pancreatic necrosis and those who didn’t develop pancreatic necrosis and evaluate the association between HDL value measured 48 – 72 hours of onset of symptoms and pancreatic necrosis. METHODS This was a prospective observational study conducted among 271 patients diagnosed with acute pancreatitis in Government Medical College Hospital, Thiruvananthapuram. Consecutive sampling method was used. RESULTS There were 42 cases of pancreatic necrosis out of 271 cases. The mean HDL of those patients with pancreatic necrosis was found to be less than those without necrosis (P < 0.001). Mean HDL value among those having pancreatic necrosis was 17.7 whereas those without necrosis was 34.9. CONCLUSIONS Proportion of pancreatic necrosis was 15.5 %. The mean HDL measured at 48 hours of symptom onset among the necrotising pancreatitis patients was significantly low when compared to the non-necrotic group (17.7 vs 34.9). All the patients with pancreatic necrosis had their HDL less than 40. Thus, an inference that low HDL at 48 hours of symptom onset was associated with higher incidence of pancreatic necrosis and severe pancreatitis could be made. KEYWORDS Pancreatitis, HDL, Pancreatic Necrosis
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Yan, Jingxin, Zheheng Zhang, Zhixin Wang, Wenhao Yu, Xiaolei Xu, Yaxuan Wang, and Haining Fan. "Pancreatic pseudocyst, pancreatitis, and incomplete pancreas divisum in a child treated with endotherapy: a case report." Journal of International Medical Research 49, no. 5 (May 2021): 030006052110143. http://dx.doi.org/10.1177/03000605211014395.
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Pancreatic divisum (PD) is caused by the lack of fusion of the pancreatic duct during the embryonic period. Considering the incidence rate of PD, clinicians lack an understanding of the disease, which is usually asymptomatic. Some patients with PD may experience recurrent pancreatitis and progress to chronic pancreatitis. Recently, a 13-year-old boy presented with pancreatic pseudocyst, recurrent pancreatitis, and incomplete PD, and we report this patient’s clinical data regarding the diagnosis, medical imagining, and treatment. The patient had a history of recurrent pancreatitis and abdominal pain. Magnetic resonance cholangiopancreatography was chosen for diagnosis of PD, pancreatitis, and pancreatic pseudocyst, followed by endoscopic retrograde cholangiopancreatography, minor papillotomy, pancreatic pseudocyst drainage, and stent implantation. In the follow-up, the pseudocyst lesions were completely resolved, and no recurrent pancreatitis has been observed.
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Patel, Milan R., Amanda L. Eppolito, and Field F. Willingham. "Hereditary pancreatitis for the endoscopist." Therapeutic Advances in Gastroenterology 6, no. 2 (January 3, 2013): 169–79. http://dx.doi.org/10.1177/1756283x12467565.
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Hereditary pancreatitis shares a majority of clinical and morphologic features with chronic alcoholic pancreatitis, but may present at an earlier age. The term hereditary pancreatitis has primarily been associated with mutations in the serine protease 1 gene (PRSS1) which encodes for cationic trypsinogen. PRSS1 mutations account for approximately 68–81% of hereditary pancreatitis. Mutations in other genes, primarily serine protease inhibitor Kazal type 1 (SPINK1) and the cystic fibrosis transmembrane conductance regulator (CFTR) are also associated with hereditary pancreatitis. While chronic alcoholic pancreatitis may develop in the fourth or fifth decades, patients with hereditary pancreatitis may develop symptoms in the first or second decades of life. Hereditary pancreatitis is diagnosed either by detecting a causative gene mutation or by the presence of chronic pancreatitis in two first-degree or three second-degree relatives, in two or more generations, without precipitating factors and with a negative workup for known causes. Patients with hereditary pancreatitis may have recurrent acute pancreatitis and may develop pancreatic exocrine and endocrine insufficiency. Hereditary pancreatitis may involve premature trypsinogen activation or decreased control of trypsin. Recurrent inflammation can lead to acute pancreatitis and subsequently to chronic pancreatitis with parenchymal calcification. There is a markedly increased risk of pancreatic carcinoma compared with the general population. Patients are often referred for evaluation of pancreatitis, biliary or pancreatic ductal dilatation, jaundice, biliary obstruction, pancreatic duct stone or stricture, pancreatic pseudocysts, and for evaluation for malignancy. Medical treatment includes pancreatic enzyme supplementation, nutritional supplementation, diabetes management, and palliation of pain. Patients should avoid tobacco use and alcohol exposure. Hereditary pancreatitis is reviewed and recommendations for genetic testing are discussed.
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Huang, Can, Juan Iovanna, and Patricia Santofimia-Castaño. "Targeting Fibrosis: The Bridge That Connects Pancreatitis and Pancreatic Cancer." International Journal of Molecular Sciences 22, no. 9 (May 7, 2021): 4970. http://dx.doi.org/10.3390/ijms22094970.
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Pancreatic fibrosis is caused by the excessive deposits of extracellular matrix (ECM) and collagen fibers during repeated necrosis to repair damaged pancreatic tissue. Pancreatic fibrosis is frequently present in chronic pancreatitis (CP) and pancreatic cancer (PC). Clinically, pancreatic fibrosis is a pathological feature of pancreatitis and pancreatic cancer. However, many new studies have found that pancreatic fibrosis is involved in the transformation from pancreatitis to pancreatic cancer. Thus, the role of fibrosis in the crosstalk between pancreatitis and pancreatic cancer is critical and still elusive; therefore, it deserves more attention. Here, we review the development of pancreatic fibrosis in inflammation and cancer, and we discuss the therapeutic strategies for alleviating pancreatic fibrosis. We further propose that cellular stress response might be a key driver that links fibrosis to cancer initiation and progression. Therefore, targeting stress proteins, such as nuclear protein 1 (NUPR1), could be an interesting strategy for pancreatic fibrosis and PC treatment.
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Simeonov, Simeon. "TREATMENT OF SEVERE FORM OF “ACUTE PANCREATITIS”." KNOWLEDGE INTERNATIONAL JOURNAL 31, no. 6 (June 5, 2019): 2023–28. http://dx.doi.org/10.35120/kij31062023s.
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The clinical approach with acute pancreatitis is controversial. Generally, it is accepted concervative treatment of the acute edematosic pancreatitis and operative treatment of the infected pancreatic necrosis. Within this frame is the field of discussion of different therapeutic approcaches. The acute pancreatitis manifests itself with differentl clinical models from light to severe necrotizing disorder with local and systematic complications. The acute pancreatitis involves systematic immuno- inflammatory response to a local process of self-digestion of the pancreatic gland with various involvement of peri-pancreatic tissue and remote organs and systems. The overconsumption of alcohol with men and gallstone disease with women are the most popular cause of acute pancreatitis. The main pathologic processes with acute pancreatitis are the inflammation, edema and necrosis of pancreatic tissue as well as the inflammation and injury of extrapancreatic organs. The acute pancreatitis occurs in two forms as they are diagnosed when the patient is hospitalized and they are evaluated in the process of treatment in progress. The foundation of the correspondent treatment is the accurate diagnostic evaluation of the types of pancratiitis in two aspects – clinnical (light, severe acute pancreatitis) and morphologic (edematous, necrotic). The conservative treatment of acute pancreatitis is the main one, the operative intervention is used with patients with acute pancreatitis – it is not shown for severe acute pancreatitis with sterile pancreatic necrosis, as it is admissible in a limited number of cases. The severe acute pancreatitis with infectous pancreatic necrosis is an indicator for operative intervention. Regardless of the bacterial status of pancreatic necrosis, operative treatment should be initiated in a later stage of the disorder.
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Shirai, Yoshihiro, Tomoyoshi Okamoto, Masaru Kanehira, Shinji Onda, Fumitake Suzuki, Ryusuke Ito, Shuichi Fujioka, and Katsuhiko Yanaga. "Pancreatic Follicular Lymphoma Presenting as Acute Pancreatitis: Report of a Case." International Surgery 100, no. 6 (June 1, 2015): 1078–83. http://dx.doi.org/10.9738/intsurg-d-14-00132.1.
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Pancreatic B-cell lymphoma is rare; it accounts for 0.2% to 2.0% of extranodal non-Hodgkin lymphoma, and constitutes less than 0.5% of all pancreatic malignancies. Most histologic types of the pancreatic lymphoma are diffuse large B-cell lymphoma, and follicular lymphoma is quite rare. We report here a case of pancreatic follicular lymphoma that was initially detected by acute pancreatitis. This is the first reported case of pancreatic follicular lymphoma presenting with acute pancreatitis. A 71-year-old woman had epigastric and left upper quadrant abdominal pain. Computed tomography (CT) revealed features of acute pancreatitis. After standard therapy for pancreatitis, enhanced CT showed a pancreatic tumor (50 × 35 mm) in the body of the pancreas with gradual enhancement. Endoscopic retrograde cholangiopancreatography and magnetic resonance cholangiopancreatography showed a complete interruption of the pancreatic duct in the body, with mild dilation of the duct in the tail of the pancreas. Endoscopic ultrasonography revealed hypervascularity of the pancreatic tumor. The patient underwent distal pancreatectomy to remove the cause of pancreatitis and to disclose the diagnosis. Histologic examination revealed follicular lymphoma of pancreas. Despite recent improvement in clinical strategies, differential diagnosis between pancreatic lymphoma and pancreatic cancer is still difficult without histologic information. Pancreatic lymphoma should be considered as a differential diagnosis in a patient who initially presents with acute pancreatitis.
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Romac, Joelle M. J., Rafiq A. Shahid, Steve S. Choi, Gamze F. Karaca, Christoph B. Westphalen, Timothy C. Wang, and Rodger A. Liddle. "Pancreatic secretory trypsin inhibitor I reduces the severity of chronic pancreatitis in mice overexpressing interleukin-1β in the pancreas." American Journal of Physiology-Gastrointestinal and Liver Physiology 302, no. 5 (March 1, 2012): G535—G541. http://dx.doi.org/10.1152/ajpgi.00287.2011.
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IL-1β is believed to play a pathogenic role in the development of pancreatitis. Expression of human IL-1β in pancreatic acinar cells produces chronic pancreatitis, characterized by extensive intrapancreatic inflammation, atrophy, and fibrosis. To determine if activation of trypsinogen is important in the pathogenesis of chronic pancreatitis in this model, we crossed IL-1β transgenic [Tg( IL1β)] mice with mice expressing a trypsin inhibitor that is normally produced in rat pancreatic acinar cells [pancreatic secretory trypsin inhibitor (PTSI) I]. We previously demonstrated that transgenic expression of PSTI-I [Tg( Psti1)] increased pancreatic trypsin inhibitor activity by 190%. Tg( IL1β) mice were found to have marked pancreatic inflammation, characterized by histological changes, including acinar cell loss, inflammatory cell infiltration, and fibrosis, as well as elevated myeloperoxidase activity and elevated pancreatic trypsin activity, as early as 6 wk of age. In contrast to Tg( IL1β) mice, pancreatitis was significantly less severe in dual-transgenic [Tg( IL1β)-Tg( Psti1)] mice expressing IL-1β and PSTI-I in pancreatic acinar cells. These findings indicate that overexpression of PSTI-I reduces the severity of pancreatitis and that pancreatic trypsin activity contributes to the pathogenesis of an inflammatory model of chronic pancreatitis.
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Ectors, N., B. Maillet, R. Aerts, K. Geboes, A. Donner, F. Borchard, P. Lankisch, et al. "Non-alcoholic duct destructive chronic pancreatitis." Gut 41, no. 2 (August 1, 1997): 263–68. http://dx.doi.org/10.1136/gut.41.2.263.
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Background—The pathology of non-alcoholic chronic pancreatitis has not yet been sufficiently studied.Aims—To identify the major changes of pancreatic tissue in patients surgically treated for non-alcoholic chronic pancreatitis.Patients—Pancreatectomy specimens from 12 patients with non-alcoholic chronic pancreatitis, including four patients with autoimmune or related diseases (Sjögren’s syndrome, primary sclerosing cholangitis, ulcerative colitis, and Crohn’s disease), were reviewed.Methods—Morphological changes were studied histologically and immunohistochemically (to type inflammatory cells) and compared with the pancreatic alterations found in 12 patients with alcoholic chronic pancreatitis.Results—In patients with non-alcoholic chronic pancreatitis, with or without associated autoimmune or related diseases, pancreatic inflammation particularly involved the ducts, commonly resulting in duct obstruction and occasionally duct destruction. None of these features was seen in alcoholic chronic pancreatitis which, however, showed pseudocysts and calcifications.Conclusion—The pancreatic changes in patients with non-alcoholic chronic pancreatitis clearly differ from those with alcoholic chronic pancreatitis. The term chronic duct destructive pancreatitis is suggested for this type of pancreatic disease.
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Lahiri, Rajiv P., and Nariman D. Karanjia. "Acute necrotising pancreatitis – early management in the district general hospital and tertiary hepato-pancreatico-biliary unit." Journal of the Intensive Care Society 20, no. 3 (June 21, 2018): 263–67. http://dx.doi.org/10.1177/1751143718783605.
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Acute pancreatitis is a common general surgical emergency presentation. Up to 20% of cases are severe and can involve necrosis with high associated morbidity and mortality. It is most commonly due to gallstones and excess alcohol consumption. All patients with acute pancreatitis need to be scored for severity and patients with severe acute pancreatitis should be managed on the high dependency unit. The mainstay of early treatment is supportive, with care to ensure strict fluid balance and optimisation of end organ perfusion. There is no role for early antibiotic use in acute necrotising pancreatitis and antibiotics should only be used in the presence of positive cultures. Nutritional support is vitally important in improving outcomes in necrotising pancreatitis. This should ideally be provided enterally using an naso-jejunal tube if the patient cannot tolerate oral intake. Patients with significant early necrosis, persisting organ dysfunction, infected walled off necrosis requiring intervention or haemorrhagic pancreatitis should be referred to a regional hepato-pancreatico-biliary unit for advice or transfer. Percutaneous and endoscopic necrosectomy has replaced open surgery due to improved outcomes. Acute necrotising pancreatitis remains a complex surgical emergency with high morbidity and mortality that requires a multidisciplinary approach to attain optimum outcomes. The mainstay of treatment is supportive care and nutritional support. Patients with significant pancreatic necrosis or infected collections requiring drainage require input from a tertiary HPB unit to guide management.
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Kohli, Divyanshoo, Bikram Bal, and Martin Bashir. "Acute Pancreatitis from Prophylactic Pancreatic Stent in Patient with Ansa Pancreatica." American Journal of Gastroenterology 107 (October 2012): S326—S327. http://dx.doi.org/10.14309/00000434-201210001-00792.
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Kemik, Ozgur, Ahu Sarbay Kemik, Aziz Sumer, Hüseyin Beğenik, Ahmet Cumhur Dülger, Sevim Purisa, and Sefa Tuzun. "Serum procarboxypeptidase A and carboxypeptidase A levels in pancreatıc disease." Human & Experimental Toxicology 31, no. 5 (April 18, 2011): 447–51. http://dx.doi.org/10.1177/0960327111405864.
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Background and objectives: To determine the serum levels of procarboxypeptidase A (pro-CPA) and carboxypeptidase A (CPA) in patients with acute and chronic pancreatitis and pancreatic cancer. Materials and methods: Serum samples obtained from 96 patients with acute pancreatitis, 101 patients with chronic pancreatitis, 98 patients with pancreatic cancer and 96 control groups were assayed for biochemical parameters and serum pro-CPA and CPA. Results: Serum pro-CPA and CPA levels were significantly higher in acute and in chronic pancreatic cancer patients compared to control group ( p < 0.001). Pancreatic cancer patients had significantly higher serum pro-CPA and CPA levels when compared with acute and chronic pancreatitis cases ( p < 0.001). Conclusion: These data prove for increased pro-CPA and CPA levels as a biomarker for the diagnosis of pancreatitis and pancreatic cancer.
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Sunami, Yoshiaki, Yijun Chen, Bogusz Trojanowicz, Matthias Sommerer, Monika Hämmerle, Roland Eils, and Jörg Kleeff. "Single Cell Analysis of Cultivated Fibroblasts from Chronic Pancreatitis and Pancreatic Cancer Patients." Cells 11, no. 16 (August 19, 2022): 2583. http://dx.doi.org/10.3390/cells11162583.
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Cancer-associated fibroblasts (CAFs) play a major role in the progression and drug resistance of pancreatic cancer. Recent studies suggest that CAFs exhibit functional heterogeneity and distinct transcriptomic signatures in pancreatic cancer. Pancreatic fibroblasts also form an integral component in pancreatic diseases such as chronic pancreatitis named disease-associated fibroblasts (DAFs). However, intra-tumoral heterogeneity of CAFs in pancreatic cancer patients and their pivotal role in cancer-related mechanisms have not been fully elucidated. Further, it has not been elucidated whether CAF subtypes identified in pancreatic cancer also exist in chronic pancreatitis. In this study, we used primary isolated fibroblasts from pancreatic cancer and chronic pancreatitis patients using the outgrowth method. Single-cell RNA sequencing (scRNA-seq) was performed, and bioinformatics analysis identified highly variable genes, including factors associated with overall survival of pancreatic cancer patients. The majority of highly variable genes are involved in the cell cycle. Instead of previously classified myofibroblastic (myCAFs), inflammatory (iCAFs), and antigen-presenting (ap) CAFs, we identified a myCAFs-like subtype in all cases. Most interestingly, after cell cycle regression, we observed 135 highly variable genes commonly identified in chronic pancreatitis and pancreatic cancer patients. This study is the first to conduct scRNAseq and bioinformatics analyses to compare CAFs/DAFs from both chronic pancreatitis and pancreatic cancer patients. Further studies are required to select and identify stromal factors in DAFs from chronic pancreatitis cases, which are commonly expressed also in CAFs potentially contributing to pancreatic cancer development.
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Yegorov, V. I., V. A. Koubyshkin, G. G. Karmazanovsky, A. I. Schegolev, N. I. Yashina, Yu A. Stepanova, Ye N. Solodinina, and N. S. Izmailova. "Cystic duodenal dystrophy. Typical case as an example of diagnosticsand surgical tactics." Bulletin of Siberian Medicine 6, no. 3 (September 30, 2007): 65–70. http://dx.doi.org/10.20538/1682-0363-2007-3-65-70.
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Duodenal dystrophy, a chronic inflammation of the aberrant pancreatic tissue in the duodenal wall, is a relatively rare disease in the practice of physicians. The heterotopic pancreas is usually functioning, and the development of acute and chronic pancreatitis in it is even more probable than in the orthotopic gland as a result of an underdeveloped duct system. The progression of ectopic pancreatitis associated with increasing cystic formation could lead to a blockade of the major or minor duodenal papilla and subsequent chronic pancreatitits in the pancreas proper. Furthermore, a malignant transformation of the aberrant pancreas is not a rare occurrence. It is essential to carry out a timely and sharp diagnosis of this condition as it often defines the surgical tactics. The purpose of this report is to present a typical case of cystic duodenal dystrophy.
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Huang, Haojie, Jiaxiang Chen, Lisi Peng, Yao Yao, Defeng Deng, Yang Zhang, Yan Liu, et al. "Transgenic expression of cyclooxygenase-2 in pancreatic acinar cells induces chronic pancreatitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 1 (January 1, 2019): G179—G186. http://dx.doi.org/10.1152/ajpgi.00096.2018.
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Replacement of the exocrine parenchyma by fibrous tissue is a main characteristic of chronic pancreatitis. Understanding the mechanisms of pancreatic fibrogenesis is critical for the development of preventive and therapeutic interventions. Cyclooxygenase-2 (COX-2), a rate-limiting enzyme for prostaglandin synthesis, is expressed in patients with chronic pancreatitis. However, it is unknown whether COX-2 can cause chronic pancreatitis. To investigate the roles of pancreatic acinar COX-2 in fibrogenesis and the development of chronic pancreatitis, COX-2 was ectopically expressed specifically in pancreatic acinar cells in transgenic mice. Histopathological changes and expression levels of several profibrogenic factors related to chronic pancreatitis were evaluated. COX-2 was expressed in the pancreas of the transgenic mice, as detected by Western blot analysis. Immunohistochemical staining showed COX-2 was specifically expressed in pancreatic acinar cells. COX-2 expression led to progressive changes in the pancreas, including pancreas megaly, persistent inflammation, collagen deposition, and acinar-to-ductal metaplasia. Quantitative RT-PCR and immunostaining showed that profibrogenic factors were upregulated and pancreatic stellate cells were activated in the COX-2 transgenic mice. Expression of COX-2 in pancreatic acinar cells is sufficient to induce chronic pancreatitis. Targeting this pathway may be valuable in the prevention of chronic pancreatitis. NEW & NOTEWORTHY COX-2 expression is observed in pancreatic tissues of human chronic pancreatitis. In this study, we showed that COX-2 expression caused the development of chronic pancreatitis in transgenic mice, supporting the idea that COX-2 inhibition may be an effective preventive and therapeutic strategy.
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Kim, Daejin, Hanjun Ryu, Hyunsoo Kim, Changkeun Park, Jaekwon Jung, Jongmin Kim, Wooseob Lee, Jiwon Lee, and Jeongin Kim. "Visible Chronic Pancreatitis and Pseudocyst after Drinking Water and Changing Position." Clinical Ultrasound 7, no. 2 (November 30, 2022): 103–7. http://dx.doi.org/10.18525/cu.2022.7.2.103.
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Chronic pancreatitis represents the result of a continuous, prolonged, inflammatory, and fibrosing process that affects the pancreas. Pseudocysts are common sequelae of acute pancreatitis or chronic pancreatitis and the most common cystic lesion of the pancreas. Abdominal ultrasonography is limited in detecting pancreatic disease, especially that located in the pancreatic tail. A 60-year-old woman presented to our institute with upper abdominal discomfort. We visualized pancreatic calcification and pseudocyst after filling the stomach with water by drinking and changing her body position. The patient was diagnosed with chronic pancreatitis and pseudocyst of the pancreatic tail.
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Fousekis, F. S., V. I. Theopistos, K. H. Katsanos, and D. K. Christodouloua. "Pancreatic involvement in inflammatory bowel disease: a review." Herald of Pancreatic Club 44, no. 3 (July 16, 2019): 23–32. http://dx.doi.org/10.33149/vkp.2019.03.02.
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Inflammatory bowel disease (IBD) is a multisystemic disease, and pancreatic manifestations of IBD are not uncommon. The incidence of several pancreatic diseases in Crohn’s disease and ulcerative colitis is more frequent compared to the general population. Pancreatic manifestations in IBD include a wide heterogenic group of disorders and abnormalities of the pancreas and range from mild self-limited diseases to severe disorders. Acute pancreatitis, chronic pancreatitis, autoimmune pancreatitis, pancreatic autoantibodies, exocrine pancreatic insufficiency and asymptomatic imaging and laboratory abnormalities are included in related-IBD pancreatic manifestations. Involvement of the pancreas in IBD may be the result of IBD itself or of medications used.
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Gubergrits, N. B., N. V. Byelyayeva, A. Ye Klochkov, G. M. Lukashevich, P. G. Fomenko, and E. V. Berezhnaya. "Evidence-based pancreatology 2018 (review of research results on diseases and exocrine pancreatic insufficiency)." Herald of Pancreatic Club 43, no. 2 (May 3, 2019): 4–14. http://dx.doi.org/10.33149/vkp.2019.02.01.
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The article presents a detailed review of the research results in the field of pancreatology published in 2018. Certain parts of the review are devoted to the pathogenesis, diagnostics, course of pancreatitis, its treatment, as well as autoimmune, hereditary pancreatitis, pancreatic pathology in children, as well as treatment.
In studying the pathogenesis of pancreatitis, attention is paid to genetic markers of pancreatitis along with a role of bacterial overgrowth syndrome in the small intestine, both in terms of worsening of the course of pancreatitis and the lack of effectiveness of enzyme replacement therapy. The study of the role of alcohol abuse and smoking in the pathogenesis of pancreatic pathology is still in progress.
Diagnostics is going on. Endosonography remains the most informative method.
A number of studies have been devoted to the studying of exocrine and endocrine pancreatic insufficiency both upon pancreatitis, pancreatic tumors, and in functional dyspepsia and HIV infection.
Autoimmune pancreatitis is increasingly being diagnosed, a number of studies are devoted to its diagnostics and treatment.
Pancreatic diseases in children develop mainly on the background of genetic predisposition, while functional pancreatic insufficiency occurs in adult patients.
The study of the peculiarities of the effect of enzyme replacement therapy continues. The immediate and remote results of the surgical treatment of pancreatic pathology are assessed.
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He, Yang, Weijin Fang, Zuojun Li, Linli Sun, Yulu Zhou, Cuifang Wu, Wei Sun, and Chunjiang Wang. "Analysis of the clinical characteristics of olanzapine-induced acute pancreatitis." Therapeutic Advances in Psychopharmacology 12 (January 2022): 204512532210799. http://dx.doi.org/10.1177/20451253221079971.
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Numerous case reports of acute pancreatitis (AP) induced by olanzapine have been published. Little is, however, known about the clinical features of olanzapine-induced AP. The aim of the study was to explore the clinical characteristics of olanzapine-induced AP. We collected literature on AP cases induced by olanzapine from 1996 to April 2021 for retrospective analysis in Chinese and English. The median time to onset of olanzapine-induced acute pancreatic symptoms was 12 (range = 0.86–216) weeks in 25 patients. The clinical features of AP range from asymptomatic elevation of blood amylase/lipase levels to digestive system symptoms (abdominal pain, vomiting, and nausea) and even death in a small number of patients. Laboratory tests showed varying degrees of elevated serum amylase and lipase levels, along with high blood sugar and high triglyceride levels in some patients. Computed tomography showed acute edematous pancreatitis, acute hemorrhagic pancreatitis, and acute necrotizing pancreatitis in the patients. The patients’ symptoms were completely relieved and high triglyceride levels gradually returned to normal levels after olanzapine was stopped. Some patients with hyperglycemia still needed hypoglycemic therapy. AP is a rare adverse effect of olanzapine. Clinicians should be aware of such complications and monitor pancreatin.
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Damian, Raluca, Cristina Oana Mărginean, Nicoleta Suciu, Maria Oana Mărginean, Simona Mocan, and Lorena Elena Meliţ. "METAPLAZIA PANCREATICĂ A MUCOASEI GASTRICE LA COPIL." Romanian Journal of Pediatrics 65, no. 3 (September 30, 2016): 321–23. http://dx.doi.org/10.37897/rjp.2016.3.18.
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Metaplazia pancreatică este definită drept apariţia ţesutului pancreatic într-o locaţie anormală şi fară conectare directă la pancreas. Ţesutul pancreatic heterotopic este cel mai frecvent observat la nivelul mucoasei antrale gastrice, în duoden şi jejun. Prezentăm cazul unei paciente în vârstă de 13 ani care s-a internat în Clinica Pediatrie 1 Târgu-Mureş pentru dureri abdominale recurente şi pirozis. Investigaţiile de laborator efectuate au evidenţiat limfocitoză (41%) cu monocitoză (8,9%), eozinofilie (4,9%), un număr crescut de reticulocite (20%), un nivel seric scăzut al trigliceridelor şi o valoare peste limita superioară a calciului şi magneziului. Ecografia abdominală nu a pus în evidenţă modificări patologice. Endoscopia digestivă superioară a evidenţiat o mucoasă gastrică granulară. Astfel, s-a prelevat un fragment de biopsie de la nivel antral, iar examenul histopatologic a evidenţiat prezenţa unui focar de metaplazie pancreatică la nivelul mucoasei antrale gastrice. Evoluţia a fost favorabilă cu dietă şi tratamentul leziunilor asociate. Particularitatea cazului constă în prezenţa metaplaziei pancreatice a mucoasei gastrice la o pacientă cu dureri abdominale recurente şi pirozis, fără antecedente heredo-colaterale sau personale semnificative.
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Kaliev, A. A. "Clinical and morphologic comparison of pancreatic damage in acute destructive pancreatitis." Kazan medical journal 94, no. 4 (December 15, 2013): 464–68. http://dx.doi.org/10.17816/kmj1950.
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Aim. To compare structural changes revealed at autopsy with clinical data, allowing to clinically predict the pancreatic damage in patients with acute destructive pancreatitis. Methods. Case histories and post-mortem pancreatic tissue samples from 12 patients who died of acute destructive pancreatitis, were examined. Results. Autopsies revealed the similar frequency of pancreatic anterior and posterior surface damage. Three types of pancreatic damage were observed: (1) total or extensive necrosis - 5 cases; (2) pancreatic fatty degeneration - 3 cases; (3) inflammatory changes with local necrotic lesions - 4 cases. Pancreatic morphologic changes were matched with clinical data and results of laboratory and instrumental tests that were performed in the patients who died from pancreatitis. The most significant clinical and laboratory changes were seen in patients with extensive necrosis, while in patients with pancreatic fatty degeneration and local necrotic lesions clinical presentations and changes in laboratory and instrumental tests were not so severe. Conclusion. Macro- and microscopic changes in pancreas observed in patients with acute destructive pancreatitis can be characterized as total or extensive necrosis, pancreatic fatty degeneration and acute inflammation with local necrotic lesions; matching the clinical and morphologic data revealed the relation between the extent of the pancreatic damage and clinical severity of acute destructive pancreatitis.
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Yasunaga, Kohei, Tetsuhide Ito, Masami Miki, Keijiro Ueda, Takashi Fujiyama, Yuichi Tachibana, Nao Fujimori, Ken Kawabe, and Yoshihiro Ogawa. "Using CRISPR/Cas9 to Knock out Amylase in Acinar Cells Decreases Pancreatitis-Induced Autophagy." BioMed Research International 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/8719397.
Full textAbstract:
Pancreatic cancer is a malignant neoplasm that originates from acinar cells. Acinar cells get reprogrammed to become duct cells, resulting in pancreatic cancer. Pancreatitis is an acinar cell inflammation, leading to “impaired autophagy flux”. Pancreatitis promotes acinar-to-ductal transdifferentiation. Expression of amylase gets eliminated during the progression of pancreatic cancer. Amylase is considered as an acinar cell marker; however, its function in cells is not known. Thus, we investigated whether amylase affects the acinar cell autophagy and whether it plays any role in development of pancreatitis. Here, we knocked outATG12in a pancreatic cancer cells and acinar cells using CRISPR/Cas9. Autophagy inhibition led to an increase in the expression of duct cell markers and a simultaneous decrease in that of acinar cell markers. It also caused an increase in cell viability and changes in mitochondrial morphology. Next, we knocked out amylase in acinar cells. Amylase deficiency decreased autophagy induced by pancreatitis. Our results suggest that amylase controls pancreatitis-induced autophagy. We found that eliminating amylase expression contributes to pancreatic cancer etiology by decreasing autophagy. Furthermore, our results indicate that amylase plays a role in selective pancreatitis-induced autophagy of pancreatic enzyme vesicles.
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Plotnikova, E. Yu, K. A. Krasnov, and O. A. Krasnov. "Exocrine insufficiency in pancreatic diseases and other digestive disorders: diagnosis and management." Russian Medical Inquiry 6, no. 5 (2022): 266–71. http://dx.doi.org/10.32364/2587-6821-2022-6-5-266-271.
Full textAbstract:
This paper reviews recent data on exocrine pancreatic insufficiency (EPI). The authors describe in detail the etiology and pathogenesis of both pancreatogenic EPI (resulting from chronic pancreatitis, pancreatic cancer, cystic fibrosis) and EPI resulting from celiac disease or diabetes. Current tests for assessing exocrine function of the pancreas are discussed. This article focuses on the available and informative test to measure pancreatic (fecal) elastase 1 levels in moderate-to-severe EPI. Its advantages are the lack of the effect of diet or fasting on test results and the possibility of performing this test in the setting of pancreatic enzyme replacement therapy. The authors also uncover the rules of correcting EPI using enzymes and management strategies in pancreatic enzyme replacement therapy non-responders involving, in particular, acid suppression therapy. Timely prescription of enzymes in adequate doses to address maldigestion and malabsorption and improvement of strategies to overcome gastric and intestinal pH barriers to guarantee proper enzyme delivery in the duodenum are important. KEYWORDS: pancreas, exocrine pancreatic insufficiency, pancreatic cancer, diabetes, celiac disease, cystic fibrosis, pancreatic (fecal) elastase 1, pancreatin, omeprazole. FOR CITATION: Plotnikova E.Yu., Krasnov K.A., Krasnov O.A. Exocrine insufficiency in pancreatic diseases and other digestive disorders: diagnosis and management. Russian Medical Inquiry. 2022;6(5):266–271 (in Russ.). DOI: 10.32364/2587-6821-2022-6-5-266-271.
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Otani, Taiichi, Akira Matsukura, Takeshi Takamoto, Yasuji Seyama, Yasuhito Shimizu, Michiyo Shinomiya, Hiroshi Usui, Fred S. Gorelick, and Masatoshi Makuuchi. "Effects of pancreatic duct ligation on pancreatic response to bombesin." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 4 (April 2006): G633—G639. http://dx.doi.org/10.1152/ajpgi.00377.2005.
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To examine mechanisms that might be related to biliary pancreatitis, we examined the effects of pancreatic duct ligation (PDL) with pancreatic stimulation in vivo. PDL alone caused no increase in pancreatic levels of trypsinogen activation peptide (TAP), trypsin, or chymotrypsin and did not initiate pancreatitis. Although bombesin caused zymogen activation within the pancreas, the increases were slight and it did not cause pancreatitis. However, the combination of PDL with bombesin resulted in prominent increases in pancreatic TAP, trypsin, chymotrypsin, and the appearance of TAP in acinar cells and caused pancreatitis. Disruption of the apical actin network in the acinar cell was observed when PDL was combined with bombesin but not with PDL or bombesin alone. These studies suggest that when PDL is combined with pancreatic acinar cell stimulation, it can promote zymogen activation, the retention of active enzymes in acinar cells, and the development of acute pancreatitis.
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Derrick, Derrick, Frandy Frandy, and Antonius Dian Wirawan. "Acute Pancreatitis – Etiology, Pathogenesis, Pathophysiology and The Current Trend in Its Management and Prevention." Indonesian Journal of Gastroenterology, Hepatology, and Digestive Endoscopy 20, no. 1 (July 22, 2020): 27–37. http://dx.doi.org/10.24871/201201927-37.
Full textAbstract:
Acute pancreatitis is an episode of cellular injury and inflammation of the pancreas parenchyma triggered by autodigestion of pancreatic parenchyma by abnormally activated pancreatic enzymes, its manifestations ranges from mild, moderate-severe and severe pancreatitis. Most episode of acute pancreatitis resolved completely while some develop recurrent acute pancreatitis and in turn progressing to chronic pancreatitis and its sequelae. While many etiologies known may cause acute pancreatitis, current theories propose three mechanism that may be involved in the pathogenesis of acute pancreatitis i.e. duct obstruction, direct acinar injury and defective intracellular transport. Recommendations from current guidelines are very useful to treat acute pancreatitis, few groundbreaking changes from the previously dated guidelines on treating acute pancreatitis are also made,providing us dated evidence-based approach to treat acute pancreatitis. Judicious and aggressive treatment are needed to minimize the damaged area of involved pancreatic parenchyma. Holistic prevention is neededto minimize the incidence of acute pancreatitis, pushing down the numbers of recurrent acute pancreatitis and ultimately may decrease the incidence of chronic pancreatitis and its sequelae.
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Udd, M., L. Kylänpää, and A. Kokkola. "The Role of Endoscopic and Surgical Treatment in Chronic Pancreatitis." Scandinavian Journal of Surgery 109, no. 1 (March 2020): 69–78. http://dx.doi.org/10.1177/1457496920910009.
Full textAbstract:
Chronic pancreatitis is a long-term illness leading to hospital admissions and readmission. This disease is often caused by heavy alcohol consumption and smoking. Patients with chronic pancreatitis suffer from acute or chronic pain episodes, recurrent pancreatitis, and complications, such as pseudocysts, biliary duct strictures, and pancreatic duct fistulas. Pancreatic duct strictures and stones may increase intraductal pressure and cause pain. Endoscopic therapy is aiming at decompressing the pressure and relieving the pain, most commonly with pancreatic duct stents and pancreatic duct stone retrieval. Early surgery is another option to treat the pain. In addition, endotherapy has been successful in treating complications related to chronic pancreatitis. The therapy should be individually chosen in a multidisciplinary meeting. Endoscopic therapy and surgery as treatment options for chronic pancreatitis are discussed in this review.