Relevant bibliographies by topics / Pancreatiti

Academic literature on the topic 'Pancreatiti'

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Published: 1 April 2023

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Journal articles on the topic "Pancreatiti"

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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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Dissertations / Theses on the topic "Pancreatiti"

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Fernandes, Cátia Conceição da Encarnação. "Clínica médica e cirúrgica em animais de companhia: pancreatite em animais de companhia." Master's thesis, Universidade de Évora, 2015. http://hdl.handle.net/10174/18224.

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Este relatório apresenta a conclusão de seis meses de estágio curricular incorporado no Mestrado Integrado em Medicina Veterinária e descreve as atividades médico-veterinárias realizadas e assistidas num Hospital e Clínica de referência. Tem como parte integrante uma revisão bibliográfica médica atual do estado de arte da Pancreatite em Animais de Companhia e posterior discussão de casos clínicos. A pancreatite é uma doença inflamatória de particular importância. O seu comportamento dinâmico e as espécies animais atingidas determinam a sua imprevisibilidade. Nos gatos, a possível associação de outras co morbilidades inflamatórias toma, por vezes, a pancreatite um desafio. Estudos recentes conferem uma nova visão sobre esta doença que até então era turva, pouco compreendida e assente em alguns aspetos que hoje se confirmam totalmente paradoxais e erráticos. O foco dirige-se para a nutrição enteral precoce e à combinação da mensuração da lipase pancreática e ecografia como os meios de diagnóstico de eleição; ABSTRACT: This Report presents the conclusion of a six months of internship incorporated into Veterinary Medicine Master's degree and is intended to describe the medical and Veterinary activities done and assisted in a hospital and reference clinic. lt includes a review of current medical literature on state of the science regarding Pancreatitis in Companion Animals and further discussion of clinical cases. Pancreatitis is an inflammatory disease of particular importance. lts dynamic behavior and the affected animal species determine its unpredictability. In cats due to the possible association of the other comorbidities of inflammatory nature make sometimes pancreatitis a challenge. Recent studies provide new insight into this disease, which until now was blurred, poorly understood and based on some aspects that today are considered completely paradoxical and erratic. Currently the focus is directed to the early enteral nutrition and in what concerns the diagnosis of pancreatitis, measurement of pancreatic lipase and ultrasound are preferred tools/methods.
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Fitzsimmons, Deborah. "Quality of life in pancreatic cancer and chronic pancreatitis." Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326844.

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Malluta, Éverson Fernando. "Avaliação do pâncreas através da ecoendoscopia em pacientes portadores de Doença de Crohn." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5147/tde-28012009-151207/.

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INTRODUÇÃO: O comprometimento pancreático em pacientes com Doença de Crohn (DC) é objeto de poucos estudos, porém as poucas séries sobre o assunto indicam um acometimento de uma parcela significativa dos pacientes, variando de 1,2% a 58%. O ultra-som endoscópico (EUS) apresenta a vantagem de apresentar uma sensibilidade muito maior que o ultra-som abdominal e a tomografia computadorizada. Quando comparado à colangiopancreatografia retrógrada endoscópica, este possui, além de uma maior sensibilidade, um índice de complicações significativamente menor. OBJETIVOS: Avaliar a incidência de alterações pancreáticas ao ultra-som endoscópico em pacientes com Doença de Crohn, correlacionando com fatores clínicos, bioquímicos e endoscópicos. MÉTODOS: Cinqüenta e um pacientes com DC, com idade entre 18 e 60 anos (média de 38 anos), sem história prévia de doença pancreática, diabetes mellitus ou alcoolismo, foram submetidos ao exame de EUS. O grupo controle foi formado por 20 pacientes submetidos ao EUS e que não apresentavam história de doença pancreato-biliar ou de Crohn. Dados clínicos, endoscópicos e laboratoriais foram coletados para posterior correlação. Onze variáveis ecoendoscópicas foram analisadas, tanto ductais quanto parenquimatosas. Os pacientes com três ou mais alterações foram submetidos à colangiorressonância magnética (CRNM). Para análise da função pancreática, foi realizado dosagens de elastase fecal em 39 pacientes. RESULTADOS: Dos pacientes analisados, 56% pertenciam ao sexo feminino, com tempo médio de diagnóstico da enfermidade de 7 anos e índice de atividade da doença (CDAI) médio de 102. Dois pacientes, (3,9%) apresentaram quatro alterações ecoendoscópicas, três pacientes, (5,9%) possuíram três alterações, 11 pacientes, (21,5%) tiveram duas alterações e 13 pacientes, (25,5%) apresentaram apenas uma alteração ao EUS. As alterações parenquimatosas totalizaram 39 achados, contra 11 alterações ductais. Apenas três pacientes (16%) do grupo controle apresentaram uma alteração ecoendoscópica (p<0,001). Os pacientes com três ou mais alterações ao EUS realizaram a CRNM, que não mostrou alterações em nenhum dos casos. Quatro pacientes, (10%) apresentaram dosagens de elastase fecal compatíveis com insuficiência pancreática exócrina, sem apresentar correlação com a ecoendoscopia. O único fator preditivo correlacionado com o número de alterações ao EUS foi doença ileal exclusiva. CONCLUSÕES: Os pacientes com DC possuíram uma alta incidência de anormalidades na morfologia pancreática (aproximadamente 10% com três ou mais alterações no EUS). Estas alterações foram localizadas predominantemente em parênquima, o que pode justificar a falta de correlação com a CRNM
BACKGROUND: Pancreas injury usually is not mentioned as an extra-intestinal manifestation of Crohns disease, but the few available series suggest pancreatic injury in a significant proportion of these patients, ranging from 1.2% to 58% in this series. Endoscopic ultrasound (EUS) presents the advantage of having a much higher sensitivity than the abdominal ultrasound or computadorized tomography in evaluating pancreas abnormalities. Compared to the endoscopic retrograde cholangiopancreatography, EUS has at least an equal sensitivity, with a lower complication rate. AIMS: To evaluate the incidence of pancreatic alterations by means of the EUS in Crohns disease, correlating them with clinical, endoscopic and biochemical data. METHODS: Fifty one patients with Crohns disease, age between 18 and 60 years-old (mean = 38), without previous history of pancreatic disease, diabetes mellitus or alcoholism, were submitted to EUS. The control-group was formed by 20 patients submitted to EUS with no previous history of pancreatic or Crohns disease. Clinical, endoscopic and biochemical data were collected in order to determine possible predictive factors. Eleven variables were analyzed, both in pancreatic parenchyma and ducts. The patients with 3 or more alterations were submitted to magnetic resonance. Pancreatic function was determined using fecal elastase assay in 39 patients. RESULTS: Of the 51 analyzed patients, 56% were female, with mean diagnosis time of seven years (1-25) and Crohns disease Activity Index (CDAI) of 102 (20-419). Two patients (3.9%) presented 4 alterations in the EUS exam, 3 (5.9%) presented 3 alterations, 11 (21.5%) had 2 alterations and 13 (25.5%) had 1 alteration in the EUS, which were statistically significant when compared to the control-group, in whom only 16% presented 1 exam alteration (p<0.001). The parenchymal abnormalities were more common, totalizing 39 findings when compared to 11 ductal abnormalities. The patients with 3 or more alterations in the exam were submitted to magnetic resonance; however, pancreatic lesions were not detected. Four patients (10%) had low fecal elastase measurement, suggestive of exocrine pancreatic insufficiency. None of these patients had significant pancreatic alterations in EUS. The only predictive factor that correlated with the number of alterations in EUS was isolated ileal disease. CONCLUSIONS: Patients with Crohns disease had a higher incidence of pancreatic abnormalities (10% with 3 or more alterations in endoscopic ultrasound) in comparison to the control-group. These alterations were found most frequently in the pancreatic parenchyma, which might explain the lack of correlation with the magnetic resonance, which is more prone to detect duct abnormalities. The only predictive factor to these alterations on EUS was ileal disease
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Sampaio, Cristina Cardoso. "Pancreatite alcoólica." Master's thesis, [s.n.], 2014. http://hdl.handle.net/10284/4842.

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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas
A pancreatite alcoólica é uma das principais complicações do consumo excessivo de álcool. O risco de desenvolver a doença aumenta com a ingestão de doses crescentes de álcool, sugerindo que os efeitos tóxicos estão relacionados com a quantidade de álcool ingerida. No entanto, apenas uma minoria dos alcoólicos desenvolve pancreatite, o que indica a necessidade de um fator desencadeador adicional para iniciar a lesão pancreática clinicamente evidente. A pancreatite alcoólica começa como um processo agudo necroinflamatório/ autodigestivo, progredindo com repetidos episódios de necroinflamação. O seu espectro clínico inclui pancreatite aguda (dor abdominal aguda e elevados níveis séricos das enzimas pancreáticas) e pancreatite crónica (dor abdominal, má digestão e diabetes). Têm sido feitos avanços significativos que fornecem uma visão sobre os mecanismos moleculares da lesão pancreática provocada pelo álcool, principalmente no que diz respeito aos seus efeitos tóxicos sobre as células acinares pancreáticas e recentemente, nas células estreladas pancreáticas (PSCs), que desempenham um papel fundamental na fibrose, caraterística da pancreatite crónica alcoólica. Alcoholic pancreatitis is a major complication of alcohol abuse. The risk of developing pancreatitis increases with increasing doses of alcohol, suggesting that alcohol exerts dose-related toxic effects on the pancreas. However, it is also clear that only a minority of alcoholics develop the disease, indicating that an additional trigger may be required to initiate clinically evident pancreatic injury. Alcoholic pancreatitis is thought to begin as an acute necroinflammatory/autodigestive process in a susceptible individual and to progress with repeated episodes. The clinical spectrum of the disease includes acute pancreatitis (acute abdominal pain and raised sérum levels of pancreatic enzymes) and chronic pancreatitis (abdominal pain, maldigestion, diabetes). Significant advances have been made in recent years that provide an insight into the molecular mechanisms of alcohol-related pancreatic injury, particularly with respect to the direct toxic effects of alcohol on pancreatic acinar cells and on the recently characterized PSCs, with may play a key role in the fibrosis of alcoholic chronic pancreatitis.
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Шевченко, Володимир Порфирович, Владимир Порфирьевич Шевченко, Volodymyr Porfyrovych Shevchenko, V. O. Bratushka, Y. I. Sobolev, I. A. Myslovsky, O. V. Kravez, et al. "The results of surgical treatment of pancreatic pseudocysts following acute pancreatitis." Thesis, Видавництво СумДУ, 2012. http://essuir.sumdu.edu.ua/handle/123456789/27527.

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Ikuta, Kozo. "Nardilysin inhibits pancreatitis and suppresses pancreatic ductal adenocarcinoma initiation in mice." Kyoto University, 2019. http://hdl.handle.net/2433/242408.

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Wilson, Benjamin Gregg. "Feline pancreatic lipase: purification and validation of a clinically significant radioimmunoassay for the diagnosis of feline pancreatitis." Texas A&M University, 2003. http://hdl.handle.net/1969.1/1581.

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Serum lipase activity has traditionally been used for diagnosis of pancreatitis in human beings and dogs. However, serum lipase activity is not specific for exocrine pancreatic function and many cell types other than pancreatic acinar cells also synthesize lipases. Recently, an immunoassay for the measurement of canine pancreatic lipase immunoreactivity has been developed and validated. This assay has shown to be specific for exocrine pancreatic function and sensitive for the diagnosis of canine pancreatitis. The objectives of this project were to purify feline pancreatic lipase (fPL), have antibodies against fPL (anti-fPL antibodies) produced, and develop a radioimmunoassay (RIA) for the diagnosis of feline pancreatitis. Pancreatic lipase was purified from feline pancreatic tissue by delipidation, anion-exchange chromatography, size-exclusion chromatography, and cation-exchange chromatography. Antiserum against fPL was raised in rabbits. Tracer was produced by iodination (125I) of fPL using the chloramine T method. An RIA was established and validated by determination of sensitivity, dilutional parallelism, spiking recovery, intraassay variability, and inter-assay variability. A control range for fPLI in cat serum was established from 30 clinically healthy cats using the central 95th percentile. The sensitivity of the fPLI assay was 1.2 μg/L. Observed to expected ratios for serial dilutions ranged from 58.0 to 164.3% for 4 different serum samples at dilutions of 1 in 2, 1 in 4, and 1 in 8. Observed to expected ratios for spiking recovery ranged from 76.0 to 156.5% for 4 different serum samples and 6 different spiking concentrations. Coefficients of variation for intra-assay variability for 4 different serum samples were 10.1, 4.5, 2.2, and 3.9%. Coefficients of variation for inter-assay variability for 4 different serum samples were 24.4, 15.8, 16.6, and 21.3%. The control range for serum fPLI concentration was established as 1.2 to 3.8 μg/L. All of the objectives outlined above were successfully met, leading to the development of an RIA for the measurement of fPLI in cat serum. The RIA for fPLI described here is sufficiently accurate and precise, but has a limited linearity and reproducibility in the lower and higher end of the working range.
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Abou, Khalil Jad. "Pancreatic fistulas after pancreatico-duodenectomies: are pancreatico-gastrostomies safer than pancreatico-jejunostomies? a quasi-experiment and propensity-score adjusted analysis." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=122998.

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BACKGROUND Pancreatic fistula (PF) is a major contributor to morbidity and mortality after pancreaticoduodenectomy (PD). There remains a debate as to whether reestablishing pancreaticoenteric continuity through a Pancreatico-Gastrostomy (PG,) compared to a Pancreatico-Jejunostomy(PJ,) can decrease the risk of PF and total complications. GOAL: We compared the outcomes of patients undergoing PG or PJ after PD at the McGill University Health Centers, where patient assignment to PG or PJ fulfills most of the criteria for a Quasi-Experiment. METHODS Data on pre-operative factors and post- operative complications was collected for patients undergoing PD in our database between 1999 and 2011 and receiving either a PG or PJ reconstruction. We performed a propensity-score adjusted logistic regression to identify the effect of surgical technique on outcomes of PF, delayed gastric emptying (DGE), and total complications. We used the ISGPF and Strasberg and Linehan definition and classification for PF and the ISGPS definition for DGE. The total morbidity experience was assessed using the Clavien-Dindo classification and the Comprehensive Comorbidity Index (CCI) for all complications. RESULTS 23/103 and 20/103 (p=0.49) of patients had PF and 74/103 and 55/103 patients had all-grades DGE in the PG and PJ groups respectively (p=0.02). The groups did not differ with regards to Clavien-Dindo grade of complications (p=0.29) but did differ with regards to the CCI (38.4 vs. 31.4 for PG vs. PG respectively, p=0.02.) Propensity-score adjusted multivariate analysis showed no effect of surgical technique on PF (p=0.89), DGE grades B/C (p=0.9) or CCI (p=0.41) but there remained an effect on all-grades DGE (p=0.012.) CONCLUSION Patients undergoing PG reconstruction did not have less PF than those reconstructed with PJ after PD at our institution; Though Patients in both groups experienced a similar burden of complications, the odds of all- grade DGE were higher in the PG group.
CONTEXTE les fistules pacreatiques (PF) constituent une cause significative de la morbiditée et mortalité subie par les patients qui recoivent une pancreaticoduodenectomie (PD). La technique ideale pour retablir la continuité pancreatico-enterique est inconnue. Il n'est pas donné que les Pancreatico-Gastrostomies (PG) donne moi de PF et de complications post-operatives que les Pancreatico-Jejunostomies(PJ). BUT: Nous avons comparé le profile de complications post-operatoire chez les patients ayant subi une PG or PJ apres PD au Centre Universitaire de Sante McGill. METHODOLOGIE: Nous avons collecté des données pre-operatoires ainsi que les complications post- operatoires pour les patients ayant subi une PD dans notre base de données entre 1999 et 2011 et ayant subi une reconstruction par PG ou PJ. Nous avons performé une regression logistique ajustée pour un" propensity-score" pour identifier l'effet de la technique chirurgicale sur les PF, les delais de la motilitée gastrique (DGE), et les complications totales. nous avons utilisé les classifications ISGPF et Strasberg et Linehan pour PF et la definition ISGPS pour DGE. La morbidité totale a été evaluée par la classification Clavien-Dindo et l'Index Comprehensif de Morbidité (CCI). RESULTATS 23/103 et 20/103 (p=0.49) des patients ont developpé une PF et 74/103 et 55/103 patients ont eu DGE en periode post operatoire dans les groupes PG et PJ respectivement (p=0.02). Le grade Clavien-Dindo des complications n'etait pas different entre les groupes (p=0.29) mais le CCI l'etait (38.4 vs. 31.4 for PG vs. PG respectivement, p=0.02.) l'analyse multivariable ajustée pour le "Propensity-score" n'a pas montré d'effet de la technique chirurgical sur PF (p=0.89), DGE grades B/C (p=0.9) ou CCI (p=0.41) mais il restait un effet sur le DGE de toutes les grades de severité (p=0.012.) CONCLUSION Les patients ayant recu une PG n'avaient pas moins de PF que ceux ayant recu une PJ aprés PD a notre institution; Les deux groupes ont souffert du meme profile de complications, mais le groupe PG avait plus de DGE de toutes grades.
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Camargo, Enilton Aparecido. "Caracterização da pancreatite aguda induzida por fosfolipases 'A IND. 2' secretorias." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308940.

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Orientador: Edson Antunes
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A pancreatite aguda e uma doença inflamatória do pâncreas caracterizada por intensa necrose pancreática e efeitos sistêmicos secundários como lesão pulmonar, os quais são a principal causa da mortalidade observada nessa doença. Ha evidencia de que as fosfolipases A2 (PLA2) tem um importante papel na fisiopatologia da pancreatite aguda. O objetivo deste trabalho foi investigar a capacidade de PLA2s de induzir pancreatite em ratos e os mecanismos envolvidos nesse fenômeno. As seguintes PLA2s foram utilizadas: piratoxina-I (homologo Lys-49 de PLA2 desprovido de atividade catalitica), bothropstoxina-II (homologo Asp-49 de PLA2 com baixa atividade catalítica) e a PLA2 proveniente do veneno de Naja moçambique moçambique (que possui alta atividade catalítica). Ratos Wistar machos (200-250 g) provenientes do CEMIB/UNICAMP foram utilizados. As PLA2s foram injetadas no ducto biliopancreatico de animais anestesiados e apos diferentes tempos experimentais foram avaliados o extravasamento de proteínas plasmáticas no pâncreas, infiltrado de neutrofilos no pâncreas e pulmão e amilase serica. A analise histológica do pâncreas e pulmão também foi realizada em alguns grupos experimentais. Piratoxina-I foi capaz de causar extravasamento de proteínas plasmáticas no pâncreas, infiltrado de neutrofilos no pulmão e os níveis sericos de amilase. Alem disso, a piratoxina-I causou alterações histológicas nos tecidos pancreático (infiltrado de neutrofilos, necrose de células acinares e edema intersticial) e pulmonar (edema intersticial e diminuição do espaço alveolar), que foram mais evidentes nos tempos iniciais da pancreatite (4-12h). Bothropstoxina-II e a PLA2 do veneno de Naja moçambique moçambique, a semelhança da Piratoxina-I, também foram capazes de aumentar o extravasamento de proteínas plasmáticas e o influxo de neutrofilos no tecido pancreático por mecanismos nao relacionados a sua atividade catalítica. Entretanto, o influxo de neutrofilos para o pulmão e o aumento dos níveis sericos de amilase causados por essas PLA2s foi dependente de sua atividade catalítica. As PLA2s também causaram secreção deamilase de acinos pancreáticos isolados, que foi dependente da atividade catalítica dessas enzimas. Adicionalmente, com o objetivo de entender o mecanismo envolvido na pancreatite induzida pela PLA2 de Naja mocambique mocambique animais foram tratados com os seguintes agentes farmacológicos: pentoxifilina (inibidor da sintese de TNF-á), SR140333 (antagonista de receptor NK1), icatibant (antagonista de receptor B2), L-NAME (inibidor não seletivo das NOS), aminoguanidina (inibidor preferencial da NOS induzivel), indometacina (inibidor não seletivo de COX), celecoxib (inibidor seletivo de COX-2), PCA4248 (antagonista dos receptores de PAF) e AA861 (inibidor da 5-lipoxigenase). Em conjunto, nossos dados mostraram que os efeitos locais e secundários são multimediados, envolvendo a participação de bradicinina, substancia P, NO, TNF-á, PAF e metabolitos das COXs. Em conclusão, demonstramos que as PLA2s secretorias são capazes de induzir pancreatite aguda em ratos quando injetadas no ducto biliopancreatico, um quadro caracterizado por efeitos inflamatórios locais e secundários cuja mediação farmacológica envolve vários fatores. Alem disso, a pancreatite aguda induzida pelas PLA2s reproduz algumas alterações observadas na pancreatite aguda em humanos, representando uma nova estratégia de estudo da fisiopatologia da pancreatite aguda
Abstract: Acute pancreatitis is an inflammatory disease of the pancreas that is characterized by intense pancreatic necrosis and remote systemic effects such as the lung injury that is the main cause of death during acute pancreatitis. There are evidences that phospholipases A2 (PLA2) have an important role in the acute pancreatitis pathophysiology. The aim of this work was to investigate the ability of PLA2 to induce acute pancreatitis in rats, and the mechanisms underlying this phenomenon. The following PLA2s were used: piratoxin-I (a Lys-49 PLA2 homologue devoid of catalytic activity), bothropstoxin-II (an Asp-49 PLA2 homologue with low catalytic activity) and PLA2 from Naja mocambique mocambique venom (high catalytic activity). Male Wistar rats (200-250g) provided by CEMIBUNICAMP have been used. The PLA2s were injected into the common bile duct of anesthetized rats, after which pancreatic plasma protein extravasation, pancreatic and lung neutrophil infiltration and serum levels of amylase were measured. Histology of the pancreatic and lung tissue has also been carried out in some experimental group. Piratoxin-I was able to increase the pancreatic plasma protein extravasation, lung neutrophil infiltration and serum amylase levels. In addition, Piratoxin-I caused histological changes in the pancreatic (neutrophil infiltration, areas of acinar cell necrosis and interstitial edema) and lung (interstitial edema and diminuition of alveolar space) tissues, which were more evident in the early periods (4-12h) after the injection. Bothropstoxin-II and PLA2 from Naja mocambique mocambique venom were also able to increase the plasma protein extravasation and neutrophil influx in the pancreatic tissue by mechanisms unrelated to their catalytic activity. However, the remote lung neutrophil influx caused by these PLA2s was shown to depend on their catalytic activity. The enhancement of serum amylase levels was also dependent on the catalytic activity of these enzymes. The PLA2s also caused amylase secretion from isolated pancreatic acini, which was dependent on their catalytic activity. Next, in order to further understand the mechanisms involved in pancreatitis induced by PLA2 Naja mocambique mocambique, animals were treated with the following pharmacological agents: pentoxifylline (TNF-á synthesis inhibitior), SR140333 (NK1receptor antagonist), icatibant (B2 receptor antagonist), L-NAME (non-selective NOS inhibitor), aminoguanidine (preferential inducible NOS inhibitor), indomethacin (nonselective COX inhibitor), celecoxib (selective COX-2 inhibitor), PCA4248 (PAF receptor antagonist) and AA861 (5-lipoxygenase inhibitor). Taken together our data showed that local and remote effects are multimediated, involving the participation of bradykinin, substance P, NO, TNF-á, PAF and COXs metabolites. In conclusion, we have shown that secretory PLA2s are able to induce acute pancreatitis in rats when injected into the common bile duct. Therefore, PLA2-induce acute pancreatitis reproduces some aspects of the human disorder representing a new strategy to study the pathophysiology of acute pancreatitis
Doutorado
Farmacologia
Doutor em Farmacologia
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Karjula, H. (Heikki). "Diagnosis, treatment and prophylaxis of pancreatic fistulas in severe necrotizing pancreatitis and the long-term outcome of acute pancreatitis." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526224312.

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Abstract Acute infected necrotizing pancreatitis (ANP) is a very complex disease with a high risk of complications and death. ANP is difficult to treat and is often associated with poor outcomes. Despite the increasing data on the technical details required to perform a mini-invasive necrosectomy for walled-off necrosis (WON), relatively few studies have focused on the presence and consequences of pancreatic duct disruption in the context of APN. Moreover, the long-term prognosis of patients with acute pancreatitis (AP) is scant. The aim of this study was to examine the diagnosis, treatment and prophylaxis of pancreatic fistulas (PFs) associated with APN. In addition, the long-term prognosis of AP was evaluated. The study population consists of the patients with AP treated at Oulu University Hospital, Finland (Studies I–IV) and Copenhagen University Hospital, Denmark (Study II) during 1995–2015. In the first part of the study, all consecutive patients following open necrosectomy for infected ANP were demonstrated to have PF. Endoscopic transpapillary pancreatic stenting (ETPS) was attempted and proven to be an effective and safe treatment for patients with PF. In Study II, prophylactic pancreatic stenting in the early stage of the disease was tested in a randomized controlled trial to the patients with ANP to prevent PFs associated with the disease. However, the study showed that the patients with ANP did not benefit from early prophylactic pancreatic ductal stenting (PPDS); instead, it seemed to be harmful for the patients. The results of Study III showed that single drain amylase level measurement after surgical necrosectomy is unreliable. According to this study, serial measurements are recommended to diagnose PFs after necrosectomy. Study IV including 1644 patients showed that AP, especially alcohol AP, was associated with a high long-term mortality. On the other hand, AP without an alcohol aetiology had a minimal impact on survival. In conclusion, in patients with infected ANP, a PF has to be considered in treatment, but the prevention of ductal leak with PPDS is not recommended. In addition, the poor long-term outcome among alcohol AP patients was due to alcohol-related diseases
Tiivistelmä Akuutti nekrotisoiva haimatulehdus ja erityisesti siihen liittyvä bakteeri-infektio on sairaus, johon liittyy korkea komplikaatio- ja kuolleisuusriski. Tautia usein komplisoi infektion lisäksi nekroosiin liittyvä haimafisteli, joka tekee hoidosta entistä haasteellisemman. Viime aikaisissa tutkimuksissa on käsitelty runsaasti mini-invasiivista nekrosektomiaa, mutta suhteellisen vähän on tutkimuksia nekrotisoivaan haimatulehdukseen liittyvästä fisteliongelmasta. Haimatulehdus-potilaiden pitkäaikaisennuste on myös epäselvä. Tämän väitöskirjatutkimuksen tavoitteena oli selvittää nekrotisoivaan haimatulehdukseen liittyvän haimafistelin yleisyyttä, diagnostiikkaa, ehkäisyä ja hoitoa. Lisäksi tarkasteltiin akuuttiin haimatulehdukseen sairastuneiden potilaiden pitkäaikaisennustetta. Ensimmäisessä osatyössä ilmeni, että kaikille potilaille, joille suoritettiin haiman nekrosektomia kehittyi fisteli ja endoskooppinen transpapillaarinen haimateiden stenttaus (ETPS) osoittautui hyväksi ja turvalliseksi hoidoksi fistelin hoidossa. Toisessa prospektiivisessa randomoidussa kontrolloidussa osatyössä tutkittiin profylaktista haimateiden stenttausta nekrotisoivassa haimatulehduksessa. Tutkimus osoitti, etteivät potilaat hyötyneet stenttauksesta: toimenpiteestä oli enemmän haittaa kuin hyötyä. Tämän tutkimuksen mukaan protetisointia ei suositella tehtäväksi taudin alkuvaiheessa. Kolmannessa osatyössä selvitettiin haiman nekrosektomian jälkeisen haimafistelin diagnosointia. Tutkimustuloksen mukaan haimafistelin osoittamiseksi dreenieritteen amylaasitasoa mittaamalla tarvitaan useita mittauskertoja, koska yksittäisen mittauksen sensitiivisyys on matala. Neljännessä osatyössä analysoitiin Oulun yliopistollisessa sairaalassa 1995–2012 akuutin haimatulehduksen sairastaneiden työikäisten potilaiden pitkäaikaisennustetta ja kuolinsyitä. Noin kymmenen vuoden seurannassa tutkimusryhmän (n = 1 644) kuolleisuus oli yli nelinkertainen verrattuna ikä- ja sukupuolivakioituihin verrokeihin (n = 8 220). Merkittävin kuolleisuutta lisäävä tekijä oli alkoholi. Tutkimuksemme osoitti, että infektoituneen haimanekroosiin liittyvä haimafisteli on huomioitava hoidossa. Varhaisesta profylaktisesta haimateiden protetisoinnista ei tutkimuksessa osoitettu olevan hyötyä. Alkoholin aiheuttaman haimatulehduksen pitkäaikaisennusteen mortaliteetti on korkea johtuen alkoholin käytöstä ja siihen liittyvistä sairauksista
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Books on the topic "Pancreatiti"

1

V, Balakrishnan, Kumar Harish, S. Sudhindran, and A. G. Unnikrishnan. Chronic pancreatitis and pancreatic diabetes in India. Edited by Indian Pancreatitis Study Group. Cochin, India]: Indian Pancreatitis Study Group, 2006.

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G, Beger H., Büchler Markus 1955-, and Malfertheiner P. 1950-, eds. Standards in pancreatic surgery. Berlin: Springer-Verlag, 1993.

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Kanojia, Ravi P. Laparoscopic lateral pancreatico-jejunostomy for chronic pancreatitis in children. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-7849-4.

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C, Langley William, ed. Pancreatitis research advances. New York: Nova Biomedical Books, 2007.

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1952-, Johnson C. D., and Imrie C. W, eds. Pancreatic disease: Towards the year 2000. 2nd ed. London: Springer, 1999.

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1932-, Burns Gerard P., and Bank S, eds. Disorders of the pancreas: Current issues in diagnosis and management. New York: McGraw-Hill, Health Professions Division, 1992.

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Lankisch, P. G., and Peter A. Banks. Pancreatitis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80320-8.

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Adams, David B., Peter B. Cotton, Nicholas J. Zyromski, and John Windsor, eds. Pancreatitis. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781118924907.

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A, Banks Peter, ed. Pancreatitis. Berlin: Springer, 1998.

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C, Carter David, and Warshaw Andrew L. 1939-, eds. Pancreatitis. Edinburgh: Churchill Livingstone, 1989.

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Book chapters on the topic "Pancreatiti"

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Tuan, Le Quan Anh, and Pham Minh Hai. "Laparoscopic Internal Drainage of Pancreatic Pseudocysts." In Mastering Endo-Laparoscopic and Thoracoscopic Surgery, 345–48. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-3755-2_50.

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AbstractAccording to revised Atlanta criteria, pancreatic pseudocyst (PP) is a chronic (>4 weeks) fluid collection within pancreatic parenchyma or adjacent space of pancreas which has no solid debris [1]. Pancreatic pseudocyst is consequence of acute pancreatitis in most cases. However, it may be consequence of chronic pancreatitis, pancreatic trauma, or pancreatic operation [2].
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Forsmark, Chris E. "Pancreatitis-Related Pancreatic Masses: Chronic Pancreatitis." In Pancreatic Masses, 75–84. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-19677-0_6.

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Al-Salem, Ahmed H. "Pancreatitis and Pancreatic Pseudocyst." In Atlas of Pediatric Surgery, 221–27. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-29211-9_25.

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Arshad, Ali, and Ashley Dennison. "Acute Pancreatitis, Chronic Pancreatitis and Pancreatic Neoplasms." In Gastroenterology For General Surgeons, 103–17. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-92768-8_10.

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Carter, D. C. "Pancreatico-duodenectomy for Chronic Pancreatitis." In Aktuelle Pankreaschirurgie, 149–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75265-0_21.

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Badalov, Nison, and Scott Tenner. "Chronic Pancreatitis and Pancreatic Pseudocysts." In Practical Gastroenterology and Hepatology: Small and Large Intestine and Pancreas, 420–26. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444328417.ch57.

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Guarise, Alessandro, Niccolò Faccioli, Giovanni Morana, and Alec J. Megibow. "Chronic Pancreatitis vs Pancreatic Tumors." In Imaging of the Pancreas, 329–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-68251-6_18.

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Sunderland, G. T., and C. W. Imrie. "Pancreatic Fistulas in Acute Pancreatitis." In Pancreatic Fistulas, 61–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77418-8_4.

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Vesentini, S. "Pancreatic Fistulas in Chronic Pancreatitis." In Pancreatic Fistulas, 70–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77418-8_5.

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Hindy, Pierre, and Scott Tenner. "Chronic Pancreatitis and Pancreatic Pseudocysts." In Practical Gastroenterology and Hepatology Board Review Toolkit, 378–82. Oxford, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119127437.ch63.

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Conference papers on the topic "Pancreatiti"

1

Hasanova, S. Y. k. "To the question of the treatment of pancreatic necrosis." In General question of world science. Наука России, 2021. http://dx.doi.org/10.18411/gq-31-07-2021-06.

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The results of surgical treatment of pancreatic necrosis using stem cells, the structure of mortality and complications for the period 2013-2019 were analyzed. It has been shown that the use of cordon blood stem cells after laparotomy in the treatment of pancreatic necrosis can reduce the mortality rate associated with complications of infected pancreatic necrosis and improve the overall results of treatment of acute pancreatitis.
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Thomas, David, Emma Bermingham, Mark Roberts, and Wayne Young. "An investigation into the effect of high fat and carbohydrate diets on a range of biomarkers associated with pancreatitis in dogs." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/uvdt4784.

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Studies suggest that dogs preferentially choose fat as their major dietary energy source (59-63% of the total metabolisable energy (ME) content of the diet). However, high fat diets have been linked to the development of pancreatitis in dogs. This study investigated several biomarkers associated with pancreatitis in dogs fed either a high fat (HF; Protein: Fat: Carbohydrate content; 35%:63%:2% ME; n= 10 dogs) or high carbohydrate (HC; Protein: Fat: Carbohydrate content; 17%:32%:51% ME) diet.A high fat meal tolerance test (MTT) was undertaken on dogs (n=20) at baseline consuming a commercial dry food diet (Protein: Fat: Carbohydrate content; 23%:25%:52% on an ME basis) and then again after 8 weeks consuming either a HF (n=10) or HC (n=10) diet. Briefly, after an overnight fast, dogs were fed a single meal containing 100% of their daily requirements (P: F: C content; 35%:63%:2% ME). Each dog was then blood sampled 1, 2, 3, 4, 5, 6, 12, and 24 hours post-prandially. Samples were analysed for plasma triglycerides and markers of pancreatitis (i.e., pancreatic lipase, endotoxin, C-reactive protein, Interleukin 1-alpha, Interleukin 6 and Tumour necrosis factor-alpha). The postprandial peak plasma concentration of triglycerides (Cmax) were higher (p less than 0.001) at baseline, compared to after feeding of the either the HC or HF diets for 8 weeks. This suggests dietary components such as moisture level, specific ingredients, level of diet processing, and possibly apparent nutrient digestibility were potential factors driving this response. There was no effect of feeding either HF or HC diets on Cmax values (P >0.05) during the final MTT. This study suggests that feeding a HF diet for 8 weeks does not elevate blood markers associated with pancreatitis, with the serum biochemistry and complete blood count indicating the dogs remained clinically healthy.
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Clark, K., and K. E. Gross. "Pancreatico-Pleural Fistula and Pancreatico-Pericardial Fistula: Unusual Complications of Pancreatitis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6439.

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MARINGHINI, A., R. PATTI, A. TERMINI, M. CIAMBRA, and P. BIFFARELLA. "PANCREATIC FUNCTION TESTS IN DIAGNOSIS OF CHRONIC PANCREATITIS." In Proceedings of the 92nd Course of the International School of Medical Sciences. WORLD SCIENTIFIC, 1999. http://dx.doi.org/10.1142/9789814447249_0012.

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Budzinskiy, S., S. Shapovalianz, E. Fedorov, M. Zakharova, and E. Platonova. "ENDOSCOPIC PANCREATIC DUCT STENTING IN MANAGEMENT OF CHRONIC PANCREATITIS." In ESGE Days. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1704663.

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Ruud, T. E., W. Müller-Esterl, H. Fritz, J. O. Stadaas, and A. O. Aasen. "RELATIONS BETWEEN APROTININ CONCENTRATIONS AND HEMODYNAMICS IN EXPERIMENTAL ACUTE PANCREATITIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644333.

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Acute pancreatitis (AP) was induced in juvenil pigs by injection of Na-taurocholate into the pancreatic duct. Eight animals remained untreated (group A), while 7 pigs (group B) received 60000 KIU/kg aprotinin (Tras-ylol, Bayer AG Leverkusen, West Germany) intravenously during 30 min before the induction of AP, thereafter 10000 KIU/kg/h during a 6 h observation period. Seven pigs (group C) received 60000 KIU/kg aprotinin during 30 min starting 3 h after the induction of AP, thereafter 10000 KIU/kg/h. The total infusion volume was the same in all 3 groups (5 ml/kg/h). Using an enzym-linked immunosorbent assay for aprotinin, maximum plasma concentration of aprotinin in group B was found 30 min after start of the infusion (2.8(1.9-5.4)umol/l). The aprotinin concentration thereafter remained elevated for the rest of the observation period (1.4(0.4-1.9) umol/1 after 6 h). The aprotinin concentration gradually increased in the peritoneal exudate during ongoing aprotinin infusion. After 1 h the aprotinin conc. in plasma and the exudate were within the same range. Similar results were observed in group C experiments, where the aprotinin conc. in plasma and peritoneal exudate both were approximately 2 umol/1 1 h after start of the infusion. Assayed by the chromogenic peptide substrate S-2302 (Kabi Vitrum AB, Stockholm, Sweden), markedly elevated values of plasma kallikrein inhibition were detected both in plasma and peritoneal exudate after start of aprotinin infusion in group B and C.In group A, 5 out of 8 animals died in a circulatory collapse, while the animals in group B and C remained hemodynamic stable and all survived the observation.Aprotinin concentrations of 1-3 umol/1 in plasma and peritoneal exudate improves the outcome during experimental acute pancreatitis in pigs.
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Malinka, T., B. Globke, L. Timmermann, F. Klein, J. Pratschke, and M. Bahra. "Necrotising pancreatitis of the pancreatic remnant (NECROREMNANTITIS): A new definition of severe pancreatitis after pancreatectomy." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695503.

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BOCKMAN, DALE E. "PATHOLOGY OF CHRONIC PANCREATITIS: RELATIONSHIP TO PANCREATIC ANATOMY AND NERVES." In Proceedings of the 92nd Course of the International School of Medical Sciences. WORLD SCIENTIFIC, 1999. http://dx.doi.org/10.1142/9789814447249_0001.

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LAYER, PETER, and JUTTA KELLER. "HUMAN EXOCRINE PANCREATIC SECRETION IN NORMAL PANCREAS AND CHRONIC PANCREATITIS." In Proceedings of the 92nd Course of the International School of Medical Sciences. WORLD SCIENTIFIC, 1999. http://dx.doi.org/10.1142/9789814447249_0010.

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Li, Lisha, Heping Wang, and Yulin Li. "Network Analysis Reveals the Connection Between Chronic Pancreatitis and Pancreatic Cancer." In International Conference on Biomedical and Biological Engineering. Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/bbe-16.2016.59.

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Reports on the topic "Pancreatiti"

1

Research, Gratis. Gallstone Pancreatitis. Gratis Research, January 2020. http://dx.doi.org/10.47496/gr.blog.08.

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2

Alseidi, Adnan. Pancreatic Anatomy. Touch Surgery Simulations, 2018. http://dx.doi.org/10.18556/touchsurgery/2018.s0111.

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Jayasinghe, Ravindri, Sonali Ranasinghe, Chandrani Kuruppu, Umesh Jayarajah, and Sanjeewa Seneviratne. Clinical characteristics and outcomes of acute pancreatitis following spinal surgery: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0017.

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Abstract:
Review question / Objective: This study reviews the current evidence on clinical characteristics and outcome of Acute Pancreatitis following spinal surgery. Condition being studied: Acute pancreatitis in spinal surgery. Information sources: All articles were searched electronically using PubMed/Medline, Scopus, EMBASE, Cochrane CENTRAL, and Latin American & Caribbean Health Sciences Literature (LILACS) before May 2020 without any restriction in the language or status of publication. Key words related to acute pancreatitis and its complications and various types of spinal surgeries were searched in the title and abstract fields.
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Sahin-Toth, Miklos. Mouse Model of Human Hereditary Pancreatitis. Fort Belvoir, VA: Defense Technical Information Center, September 2015. http://dx.doi.org/10.21236/ada624309.

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Miller, George. Divergent Effects of Dendritic Cells on Pancreatitis. Fort Belvoir, VA: Defense Technical Information Center, September 2015. http://dx.doi.org/10.21236/ada624310.

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Beatty, Gregory, Patrick Guirnalda, and Santiago L. Luque. Listeria Vaccines for Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada600605.

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Lu, Lei, Hangbin Jin, Jing Yang, Jianfeng Yang, and Xiaofeng Zhang. Early versus delayed cholecystectomy for mild gallstone pancreatitis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0033.

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Wang, Lei. Molecular Probes for Pancreatic Cancer Imaging. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.3105.

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Yu, David. The Replication Stress Response in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada599228.

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Yu, Davis S. The Replication Stress Response in Pancreatic Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada621841.

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