© 2017, © 2017 American Federation for Medical Research. A middle-aged man presents with acute pancreatitis of unknown etiology and is found to have a presentation consistent with the diagnosis of type 2 autoimmune pancreatitis (AIP). AIP is a group of rare heterogeneous diseases that are challenging to diagnose. There are 2 types of AIP. Type 1 disease is the more common worldwide than type 2 AIP. While type 1 AIP is associated with IgG4-positive antibodies, type 2 AIP is IgG4 antibody negative. Both types of AIP are responsive to corticosteroid treatment. Although type 1 AIP has more extrapancreatic manifestations and more commonly relapses, this is a case of a patient with type 2 AIP with inflammatory bowel disease and relapsing course.

Background: Pancreatic disease is a global problem. Severe acute pancreatitis (AP) carries a 30-50% mortality. Current scoring systems fall short in predictive accuracy, sensitivity, specificity and availability. Pancreatic cancer (PC) is a leading cause of cancer-related mortality, most patients die within one year of diagnosis. Late presentation and lack of effective oncological treatment determine a desperate need to focus on early detection of the pancreatic cancer. Current biomarkers fall short in accessibility, sensitivity and specificity and ability to distinguish malignant from benign conditions. Metabolomics aims to decipher molecular signatures that will distinguish disease from controls, ultimately leading to novel targets for diagnosis and treatment. Initial studies are discovery-based, hypothesis-generating and typically aim to establish a snapshot of the metabolism of an individual by metabolite profile. Aims: Establish a prospective phenotypic and demographic database of patients with acute pancreatitis. Determine urinary and serum metabolomic profiles of AP and PC in comparison to controls and establish if metabolomic profiling can distinguish severity of each disease in order to identify potential novel bio-markers. Methods: Urine and serum samples from 73 AP, 32 PC, 62 Healthy Controls, 8 Chronic pancreatitis and 8 Benign jaundice participants were analysed using GC-MS and UPLCMS. Metabolite identification was subject to univariate and multivariate analysis (p<0.05). Results: The differentiation of metabolite profiles was most distinct with AP. There was no differentiation by AP aetiology. AP severity was distinquished by metabolite profile. Profiles of resectable patients were distinct form non-resectable PC. Fatty acids(FA), glycerophoshocholines, eicosanoids, TCA cycle intermediates and melatonin levels were altered in AP. PC was defined by altered concentrations of FAs, eicosanoids, glycerophoshocholines, sphingomyelins, folates and amino acids and peptides (e.g. glutamine). Altered levels of UFAs, neuromedins, Vitamin D3 determined stage of PC. Conclusion: Urinary and serum metabolomic signatures may provide future biomarker panels for grading AP and PC.

Se reporta dos casos de pancreatitis secundaria a la infección por citomegalovirus confi rmado por reacción en cadena de la polimerasa en tiempo real (PCR-RT) en pacientes portadores del virus de la inmunodefi - ciencia humana (VIH). Se descartaron otras causas mediante exámenes auxiliares. Ambos pacientes fueron tratados con ganciclovir y se obtuvo una mejoría tanto clínica como en los exámenes auxiliares. Esta patología no debe pasar desapercibida en pacientes VIH positivos a pesar de no presentar la característica clínica de pancreatitis aguda / We report two cases of pancreatitis secondary to cytomegalovirus infections which were tested by reverse transcription polymerase chain reaction (RT-PCR) in patients with human immunodefi ciency virus (HIV). Other causes were ruled out by laboratory fi ndings. Both patients were treated with ganciclovir and improved clinically and as indicated by laboratory fi ndings. This condition should not be ignored in HIV-positive patients in spite of the absence of the clinical characteristics of acute pancreatitis.

La pancreatitis aguda es una enfermedad inflamatoria del páncreas exocrino; el rango de incidencia es de 10 a 80 / 100,000 habitantes por año y el rango de mortalidad varia de 2 a 10%. Las causas más comunes son la litiasis biliar y el alcohol. Los pacientes con pancreatitis aguda se presentan con dolor en el hemiabdomen superior y/o diferentes grados de insuficiencia orgánica. El diagnostico se sospecha por una presentación clínica típica y una amilasa serica elevada más de tres veces su valor normal. En presentaciones atípicas podrían requerir confirmación con tomografía axial computarizada. El manejo inmediato es hidratación endovenosa, analgésicos y monitoreo continuo. La mayoría de los pacientes presentan pancreatitis leve y se recuperan sin tratamiento adicional. En 20% de los pacientes la enfermedad es severa y esta asociada con una mortalidad de aproximadamente 20-40%; Estos pacientes requieren un manejo en cuidados intensivos o podrían requerir transferencia a una unidad especializada.

Objetivo principal: Determinar la prevalencia de pacientes adultos hospitalizados por pancreatitis aguda en el Servicio de Medicina del Hospital Vitarte durante el periodo Enero – Julio 2015. Materiales y Métodos: Estudio descriptivo, retrospectivo, transversal con un total de 114 pacientes hospitalizados en el periodo enero – julio 2015 en el servicio de medicina del hospital de vitarte con el diagnostico de pancreatitis agudo. Los datos fueron recabados mediante revisión de historias clínicas y trabajadas mediante el programa de SPSS versión 23. Resultados: Del análisis y discusión de los resultados obtenidos se estableció que la prevalencia de pacientes adultos hospitalizados por pancreatitis aguda en el Servicio de Medicina del Hospital Vitarte durante el periodo Enero – Julio 2015 fue de 21.39%. Hubo 96% de mujeres y 18% entre los pacientes. La edad media fue de 40,48 años. La etiología de mayor frecuencia fue la biliar en el 97.4% de los casos. La estancia hospitalaria promedio fue de 4 – 6 días. La manifestación clínica más frecuentes fue el dolor abdominal. La presencia de falla orgánica según la escala de Marshall es de 9.6%. Conclusión: La prevalencia de pacientes hospitalizados por Pancreatitis Aguda en el servicio de Hospitalización de Medicina del Hospital Vitarte en el periodo Enero – Julio 2015 fue de 21.39%. La presencia de falla orgánica según la escala de Marshall es de 9.6%.

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Tsang, Siu Wai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 107-121). / Abstracts in English and Chinese. / Abstract --- p.i / 摘要 --- p.iii / Acknowledgements --- p.v / Table of Contents --- p.vi / List of Abbreviations --- p.x / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- Renin-angiotensin system (RAS) --- p.1 / Chapter 1.1.1 --- Circulating RAS --- p.2 / Chapter 1.1.2 --- Tissue-specific RAS --- p.5 / Chapter 1.2 --- RAS inhibitors --- p.7 / Chapter 1.2.1 --- Angiotensin converting enzyme inhibitor --- p.8 / Chapter 1.2.2 --- Non-specific angiotensin II receptor blocker --- p.9 / Chapter 1.2.3 --- Specific AT1 receptor antagonist --- p.10 / Chapter 1.2.4 --- Specific AT2 receptor antagonist --- p.11 / Chapter 1.3 --- Pancreas and functions of exocrine pancreas --- p.14 / Chapter 1.3.1 --- Structure of pancreas --- p.14 / Chapter 1.3.2 --- Exocrine secretions and pancreatic enzymes --- p.16 / Chapter 1.3.3 --- Regulation of exocrine secretions --- p.17 / Chapter 1.4 --- Pancreatic RAS --- p.18 / Chapter 1.4.1 --- Expression and localization --- p.18 / Chapter 1.4.2 --- Regulation --- p.19 / Chapter 1.4.3 --- Clinical relevance to the pancreas --- p.20 / Chapter 1.5 --- Acute pancreatitis --- p.21 / Chapter 1.5.1 --- Pathogenesis --- p.21 / Chapter 1.5.2 --- Experimental models of acute pancreatitis --- p.22 / Chapter 1.5.3 --- Criteria of acute pancreatitis --- p.23 / Chapter 1.5.4 --- Oxidative stress in acute pancreatitis --- p.24 / Chapter 1.6 --- RAS and acute pancreatitis in exocrine pancreas --- p.26 / Chapter 1.6.1 --- RAS and acute pancreatitis --- p.26 / Chapter 1.6.2 --- RAS and pancreatic microcirculation --- p.26 / Chapter 1.6.3 --- RAS and tissue injury --- p.27 / Chapter 1.6.4 --- Exocrine pancreatic RAS and acute pancreatitis-induced injury --- p.28 / Chapter 1.7 --- Aims of study --- p.29 / Chapter Chapter 2 --- Materials and Methods / Chapter 2.1 --- Animal models and RAS inhibitors --- p.30 / Chapter 2.1.1 --- Cerulein-induced acute pancreatitis --- p.30 / Chapter 2.1.2 --- Prophylactic treatment with RAS inhibitors --- p.31 / Chapter 2.1.3 --- Therapeutic treatment with RAS inhibitors --- p.32 / Chapter 2.2 --- Evaluation of pancreatic injury --- p.32 / Chapter 2.2.1 --- Assessment of pancreatic water content --- p.33 / Chapter 2.2.2 --- Measurement of α-amylase activity in plasma --- p.33 / Chapter 2.2.3 --- Measurement of lipase activity in plasma --- p.34 / Chapter 2.3 --- Histopathological examinations --- p.34 / Chapter 2.3.1 --- Preparation of paraffin blocks --- p.35 / Chapter 2.3.2 --- Hematoxylin and eosin staining --- p.35 / Chapter 2.4 --- Biochemical assay of pancreatic oxidative status --- p.37 / Chapter 2.4.1 --- Sample preparation --- p.37 / Chapter 2.4.2 --- Quantification of protein content --- p.37 / Chapter 2.4.3 --- Measurement of glutathione levels --- p.38 / Chapter 2.4.4 --- Assessment of protein oxidation --- p.38 / Chapter 2.4.5 --- Assessment of lipid peroxidation --- p.39 / Chapter 2.4.6 --- Measurement of NADPH oxidase activity --- p.40 / Chapter 2.5 --- Studies of pancreatic digestive enzyme secretions from isolated acini --- p.40 / Chapter 2.5.1 --- Dissociation of acini from pancreatic tissue --- p.40 / Chapter 2.5.2 --- Treatment with peptides and RAS inhibitors --- p.42 / Chapter 2.5.3 --- Quantification of protein and DNA contents --- p.43 / Chapter 2.5.4 --- Measurement of a-amylase and lipase secretions --- p.44 / Chapter 2.5.5 --- RT-PCR analysis of RAS components in acinar cells --- p.44 / Chapter 2.6 --- Studies of RAS inhibitors on acute pancreatitis-induced systemic inflammation --- p.45 / Chapter 2.6.1 --- Systemic inflammation treatment --- p.45 / Chapter 2.6.2 --- Measurement of myeloperoxidase activity in lung and liver --- p.46 / Chapter 2.7 --- Statistical analysis --- p.47 / Chapter Chapter 3 --- Results / Chapter 3.1 --- Time-course experiment of acute pancreatitis model --- p.48 / Chapter 3.1.1 --- Effect of acute pancreatitis on tissue injury --- p.48 / Chapter 3.1.2 --- Effects of acute pancreatitis on oxidative status --- p.48 / Chapter 3.2 --- Evaluation of ramiprilat and saralasin on changes of acute pancreatitis- induced pancreatic injury --- p.50 / Chapter 3.2.1 --- Changes in tissue injury and histopathology --- p.50 / Chapter 3.2.2 --- Changes in oxidative status --- p.57 / Chapter 3.3 --- Evaluation of losartan and PD123319 on changes of acute pancreatitis- induced pancreatic injury --- p.61 / Chapter 3.3.1 --- Changes in tissue injury and histopathology --- p.61 / Chapter 3.3.2 --- Changes in oxidative status --- p.68 / Chapter 3.4 --- Evaluation of acinar secretions of digestive enzymes --- p.71 / Chapter 3.4.1 --- Cholecystokinin octapeptide-induced acinar secretions --- p.71 / Chapter 3.4.2 --- Angiotensin II-induced acinar secretions --- p.71 / Chapter 3.4.3 --- Effects of losartan and PD 123319 on α-amylase secretion --- p.74 / Chapter 3.5 --- Existence and regulation of acinar RAS by acute pancreatitis --- p.75 / Chapter 3.5.1 --- Expression of angiotensinogen and its regulation by acute pancreatitis in acini --- p.76 / Chapter 3.5.2 --- Expression of AT1 receptor and its regulation by acute pancreatitis in acini --- p.76 / Chapter 3.5.3 --- Expression of AT2 receptor and its regulation by acute pancreatitis in acini --- p.76 / Chapter 3.5.4 --- Evaluation of RAS inhibitors in acute pancreatitis-induced acinar cells --- p.80 / Chapter 3.6 --- Preliminary data on acute pancreatitis-induced systemic inflammation --- p.81 / Chapter 3.6.1 --- Time-course experiment on lung injury --- p.81 / Chapter 3.6.2 --- Time-course experiment on liver injury --- p.83 / Chapter 3.6.3 --- Evaluation of losartan on systemic inflammation --- p.85 / Chapter Chapter 4 --- Discussion / Chapter 4.1 --- "Actions of RAS inhibitors on the changes of tissue injury, oxidative status and histopathology in acute pancreatitis-induced pancreas" --- p.87 / Chapter 4.1.1 --- Differential effects of ramiprilat and saralasin --- p.88 / Chapter 4.1.2 --- Differential effects of losartan and PD123319 --- p.92 / Chapter 4.2 --- Potential functions of RAS in pancreatic acinar secretions --- p.95 / Chapter 4.2.1 --- Potential role of AT1 receptor --- p.96 / Chapter 4.2.2 --- Potential role of AT2 receptor --- p.98 / Chapter 4.3 --- Regulation of RAS in acute pancreatitis-induced acini --- p.98 / Chapter 4.3.1 --- Regulation of RAS components in acinar cells --- p.99 / Chapter 4.3.2 --- Differential actions of losartan and PD123319 --- p.100 / Chapter 4.4 --- Potential role of RAS in acute pancreatitis --- p.102 / Chapter 4.4.1 --- Regulation of RAS components by acute pancreatitis --- p.102 / Chapter 4.4.2 --- Differential functions of AT1 and AT2 receptors in acute pancreatitis --- p.103 / Chapter 4.5 --- Conclusion --- p.104 / Chapter 4.6 --- Further studies --- p.105 / Chapter Chapter 5 --- Bibliography --- p.107

Establece la utilidad de los puntajes BISAP y APACHE II como predictores de severidad de pancreatitis aguda (PA) en pacientes del Hospital Nacional Dos de Mayo. Se realiza un estudio analítico, retrospectivo y transversal entre enero y diciembre de 2016 de pacientes con diagnóstico de PA según la nueva clasificación Atlanta 2012 y se define severidad como falla orgánica persistente mediante puntaje Marshall modificado ≥ 2 a las 48 horas. Selecciona puntos de corte apropiados con los que se calcula la sensibilidad, especificidad, VPP y VPN; y confecciona la curva ROC para los puntajes BISAP y APACHE-II. / Tesis

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 &#956;g/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 &#956;g/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.

No description available.