Pancreatic Abnormalities Research Articles

Valoración de la grasa hepática y pancreática como biomarcadores de imagen en el síndrome metabólico

ObjectiveTo objectively evaluate hepatic and pancreatic involvement in metabolic syndrome through magnetic resonance imaging (MRI) biomarkers. Material and methodsFrom an initial retrospective sample of 407 patients diagnosed with metabolic syndrome studied by MRI in a single center during a 2-year period, 154 were excluded because of a lack of clinical and/or laboratory data, pancreatic abnormalities, or inadequate quality of MRI studies. To measure hepatic and pancreatic fat, we used chemical shift imaging (in-phase and out-of-phase), measuring the fat fraction (%) in regions of interest in the pancreas and liver. Associations between the fat fraction and selected clinical and laboratory variables were assessed with beta regression models. ResultsIn the end, 253 patients were included. The hepatic fat fraction was 4.9% and the pancreatic fat fraction was 7.9%. We found no significant associations between the hepatic fat fraction and any of the clinical or laboratory variables. However, the pancreatic fat fraction was positively associated with age (OR=1.025, p<0.001) and baseline glucose (OR=1.005, p<0.001). Patients with diabetes had higher values of pancreatic fat fraction (OR=2.64, p=0.038). Pancreatic fat fraction and hepatic fat fraction were positively associated (OR=69.44, p<0.001). ConclusionsPancreatic steatosis can be considered a marker of metabolic syndrome and diabetes. Quantitative MRI enables the diagnosis and grading of fatty pancreas through simple chemical shift techniques.

GATA6 mutations: Characterization of two novel patients and a comprehensive overview of the GATA6 genotypic and phenotypic spectrum.

The first human mutations in GATA6 were described in a cohort of patients with persistent truncus arteriosus, and the phenotypic spectrum has expanded since then. This study underscores the broad phenotypic spectrum by presenting two patients with de novo GATA6 mutations, both exhibiting complex cardiac defects, pancreatic, and other abnormalities. Furthermore, we provided a detailed overview of all published human genetic variation in/near GATA6 published to date and the associated phenotypes (n = 78). We conclude that the most common phenotypes associated with a mutation in GATA6 were structural cardiac and pancreatic abnormalities, with a penetrance of 87 and 60%, respectively. Other common malformations were gallbladder agenesis, congenital diaphragmatic hernia, and neurocognitive abnormalities, mostly developmental delay. Fifty‐eight percent of the mutations were de novo, and these patients more often had an anomaly of intracardiac connections, an anomaly of the great arteries, and hypothyroidism, compared with those with inherited mutations. Functional studies mostly support loss‐of‐function as the pathophysiological mechanism. In conclusion, GATA6 mutations give a wide range of phenotypic defects, most frequently malformations of the heart and pancreas. This highlights the importance of detailed clinical evaluation of identified carriers to evaluate their full phenotypic spectrum.

Ameliorative Activity of Pumpkin (Cucurbita maxima) Fruit and Seeds Powders on Diabetic, Oxidative and Pancreatic Status in Rats

Background: Diabetes mellitus is the one of the most common endocrine diseases that is characterized by hyperglycemia, altered metabolism with an increased risk of much complications. Besides drugs classically used for the treatment of diabetes several species of plants have been described as having a hypoglycemic activity with decreased side effects.&#x0D; Aim of the Work: This work aimed to investigate the possible anti-diabetic effect of oral administration of pumpkin (Cucurbita maxima) fruit flesh and seeds powders on Streptozotocin induced diabetic rats via studying blood glucose levels, oxidative biomarkers as well as islets of Langerhans structure changes.&#x0D; Materials and Methods: 60 adult albino rats of Sprague-Dawely strains (200±5 gm) were classified into five groups of ten animals each except diabetic control group was composed of twenty rats as follow Group I: healthy control; Group II: diabetic control ,Group III, IV and V: diabetic rats received 2 g pumpkin fruit, seeds, fruit and seeds mixture powders respectively /kg body weight daily by oral intubation.&#x0D; Results: The results of present study showed that pumpkin powders caused significant improvements (P≤0.05) in blood glucose, insulin levels and glycated hemoglobin percent compared to diabetic control group. Also pumpkin powders improved antioxidants activities and healed Langerhans islets by increasing their number and size in comparison with diabetic control group. Conclusion: The present study showed that pumpkin powders may normalize the various biochemical and pancreatic tissues abnormalities resulted due to diabetes metabolic disorders and it is a source of potent anti-diabetic agent. The diabetic rats that were administered with the pumpkin fruit powder, exhibited the highest improvements.

Tu1312 – Camostat Mesilate, Pancrelipase and Rabeprazole Combination Therapy Improves Epigastric Pain in Early Chronic Pancreatitis and Functional Dyspepsia with Pancreatic Emzyme Abnormalities

Tu1312 – Camostat Mesilate, Pancrelipase and Rabeprazole Combination Therapy Improves Epigastric Pain in Early Chronic Pancreatitis and Functional Dyspepsia with Pancreatic Emzyme Abnormalities

Pancreatic Cysts and Intraductal Papillary Mucinous Neoplasm in Autosomal Dominant Polycystic Kidney Disease.

Pancreatic lesions in autosomal dominant polycystic kidney disease (ADPKD) are primarily cysts. They are increasingly recognized, with isolated reports of intraductal papillary mucinous neoplasia (IPMN). Retrospective study to determine prevalence, number, size, and location of pancreatic abnormalities using abdominal magnetic resonance imaging (MRI) of genotyped ADPKD patients (seen February 1998 to October 2013) and compared with age- and sex-matched non-ADPKD controls. We evaluated presentation, investigation, and management of all IPMNs among individuals with ADPKD (January 1997 to December 2016). Abdominal MRIs were examined for 271 genotyped ADPKD patients. A pancreatic cyst lesion (PCL) was detected in 52 patients (19%; 95% confidence interval, 15%-23%). Thirty-seven (71%) had a solitary PCL; 15 (28%) had multiple. Pancreatic cyst lesion prevalence did not differ by genotype. Intraductal papillary mucinous neoplasia was detected in 1% of ADPKD cases. Among 12 IPMN patients (7 branch duct; 5 main duct or mixed type) monitored for about 140 months, 2 with main duct IPMNs required Whipple resection, and 1 patient died of complications from small-bowel obstruction after declining surgical intervention. With MRI, PCLs were detected in 19% and IPMNs in 1% of 271 ADPKD patients with proven mutations, without difference across genotypes. Pancreatic cyst lesions were asymptomatic and remained stable in size.

SUN-LB033 New Onset Diabetes in a Post-Renal Transplant Pediatric Patient with a Mutation of the Hepatocyte Nuclear Factor-1β Gene

Background: Maturity onset diabetes of the young (MODY) 5 is a rare type of dominantly inherited diabetes mellitus (DM). It is caused by mutations of the hepatocyte nuclear factor-1beta (HNF-1 beta) gene. Most are missense mutations that produce truncated proteins resulting in a variable clinical spectrum that may include kidney, genital and pancreatic abnormalities. We describe a case of a young patient diagnosed with DM after renal transplant; also, his diagnosis disclosed extensive family history of DM. Case: Six-year-old African-American patient with history of end stage renal disease due to bilateral cystic dysplasia presented with significant hyperglycemia three days after renal transplant. Polycystic kidney disease observed in prenatal ultrasound led to genetic testing. He was found to have a 1.0-1.8Mb deletion on chromosome microarray at 17q12 that included TCF2/HNF1B genes. His HbA1C was 5.8% at time of endocrine evaluation. He received one time high dose steroids in operating room and was started on tacrolimus after transplant. Pancreatic ultrasound showed normal pancreatic head, body not visualized. He was sent home with intensive insulin management on day 20 after renal transplant. Patient’s family history revealed mother with diagnosis of type 2 diabetes mellitus (T2DM) at age 19, maternal grandmother and great-grandmother diagnosed at early age with T2DM as well. Discussion: HNF-1 beta gene encodes a transcription factor that regulates nephron and embryonic pancreas development. MODY 5 is clinically heterogeneous disorder and the degree of insulin deficiency is variable, some family members who carry the gene remain free of diabetes into later adult life. The mean age of diagnosis of DM is 26 years with a range of 10–61 years. Our patient is only six years old and he may have presented earlier due post-transplant status, high dose steroids and tacrolimus use, all factors known to be triggers for hyperglycemia but the persistence of insulin requirement and levels of HbA1C being on pre-diabetes range at time of evaluation might be a sign of early deterioration of pancreatic function. Diagnosis of MODY5 has important implications for treatment, prognosis, and genetic counseling. Diabetes in these patients requires early use of insulin. Patient’s family members were advised to undergo genetic testing and screening for renal abnormalities and DM. Further studies on the correlation of phenotypes and genotypes will help delineate the clinical course of MODY 5. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. s presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.

Chronic Asymptomatic Pancreatic Hyperenzymemia (CAPH): Meta-analysis of pancreatic findings at second-level imaging

Background/ObjectivesData estimating the prevalence of significant findings during the investigation of patients with Chronic Asymptomatic Pancreatic Hyperenzymemia (CAPH) are scanty and heterogeneous, and the diagnostic approach is therefore uncertain. The aim of this study was to meta-analyze pancreatic abnormalities detected at second-level imaging in patients with CAPH. MethodsPubmed database was searched until September 2018 for articles evaluating CAPH patients through MRI-Cholangio-Pancreatography with/without secretin (MRCP or s-MRCP) or Endoscopic Ultrasound (EUS). The methodology was developed from PRISMA checklist. Pooled prevalences of pancreatic findings were calculated, with subgroup analyses according to imaging modality. Quality of the studies, publication bias and heterogeneity were analyzed. ResultsIn 8 articles describing 521 patients with CAPH, pooled prevalence of normal imaging was 56.6% [95%CI (CI) 41.9–70.2; I2 = 88.6%). Prevalences of neoplasia, chronic pancreatitis, pancreatic cysts and benign abnormalities were 2.2% [CI1.2–4.1; I2 = 0%], 16.2% [CI10.2–24.8; I2 = 71.5%], 12.8% [CI8.2–19.3; I2 = 64.7%] and 17.2% [CI11.9–24.2; I2 = 71.5%] respectively. In sub-analyses, EUS and s-CPRM were less frequently normal and diagnosed more “early” chronic pancreatitis, while neoplastic lesions were still rare. ConclusionsIn CAPH patients, second-level pancreatic imaging is normal in 56% of the cases, neoplastic lesions are rare and the rate of pancreatic cysts is similar to that seen as incidental findings. More than one third of patients are diagnosed with abnormalities whose prognostic significance is uncertain. Despite the superior sensitivity of EUS or s-CPRM, the less costly/invasive and more available contrast-enhanced MRCP does not seem to miss relevant findings in this setting.

Are BRCA1 and BRCA2 gene mutation patients underscreened for pancreatic adenocarcinoma?

Breast cancer (BRCA) mutations account for the highest proportion of hereditary causes of pancreatic ductal adenocarcinoma (PDAC). Screening is currently recommended only for patients with one first-degree relative or two family members with PDAC. We hypothesized that screening all BRCA1/2 patients would identify a higher rate of pancreatic abnormalities. All BRCA1/2 patients at a single academic center were retrospectively reviewed (2005-2015). Pancreatic abnormalities were defined on cross-sectional imaging as pancreatic neoplasm (cystic/solid) or main-duct dilation. Two hundred and four patients were identified with BRCA mutations. Forty-seven (40%) had abdominal imaging (20 computerized tomography and 27 magnetic resonance imaging). Twenty-one percent had pancreatic abnormalities (PDAC [n = 2] and intraductal papillary mucinous neoplasm [IPMN; n = 8]). The prevalence of pancreatic abnormalities and IPMN was higher in BRCA2 patients than in the general population (21% vs 8% and 17% vs 1%; P = 0.0007 and P < 0.0001, respectively), with no influence of family history. Similarly, BRCA1 patients had an increased prevalence of IPMN (8.3% vs 1%; P < 0.0001). In this series, 4% and 17% of BRCA2 patients developed PDAC and IPMN, respectively. Eight percent of BRCA1 patients developed IPMN. Under current recommended screening, 60% of BRCA1/2 patients had incompletely pancreatic assessment. With no influence of family history, this study suggests all BRCA1/2 patients should undergo a high-risk screening protocol that will identify a higher rate of precancerous pancreatic neoplasms amenable to curative resection.

Streptococcus bovis Group Bacteremia in the 21st Century

Introduction Advanced phenotypic, genomic, and proteomic laboratory techniques have recently modified Streptococcus bovis group (SBG) nomenclature. We wished to determine if physicians continue to recognize the importance of SBG and its association with gastrointestinal (GI) tract abnormalities and infective endocarditis amid the changes in microbiologic identification and nomenclature of these organisms. Methods We reviewed the medical records of adult patients (≥18 years of age) with positive blood cultures for SBG organisms admitted to our 510-bed teaching hospital from January 1, 2006, to December 31, 2017. We report the epidemiology, sources of bacteremia, comorbid conditions, courses of treatment, and the mortality for these patients. We also assess the hospital treatment team's (HTT's) knowledge of SBG nomenclature and of the associations of SBG bacteremia and underlying GI disease and infective endocarditis amid the changes in nomenclature of these organisms. Results There were 42 cases of SBG bacteremia during the 12-year study period: 22 in women (52.4%) and 20 in men (47.6%). Patient ages ranged from 51 to 96 years (mean age, 74.3 years; median age, 72.0 years). All but 2 patients had multiple comorbid conditions. Diabetes mellitus was the most common comorbidity. Colonoscopy was performed during hospitalization in 22 (52.5%) of 42 patients. The identifiable sources of bacteremia were as follows: lower GI tract in 19 patients (45.2%), upper GI tract in 5 patients (11.9%), Laennec cirrhosis in 3 patients (7.1%), and pancreatic disorders in 2 patients (4.6%). Eleven patients (26.2%) had primary bacteremia. Two patients with primary bacteremia had prior splenectomy. The historic association between SBG bacteremia and underlying GI tract disease was recognized by 37 (88.1%) of 42 HTTs, but all available provider progress notes mention only “colon carcinoma” as the possibly associated GI tract pathology. The historic association of SBG bacteremia with infective endocarditis was recognized in writing by 32 (76.2%) of 42 HTTs. Endocarditis was diagnosed in 12 patients (28.6%): 9 definite endocarditis and 3 possible endocarditis. The mitral valve was the most commonly involved valve. Four SBG isolates were intermediately susceptible to penicillin G with minimum inhibitory concentrations of 0.125 μg/mL or greater. Twenty-three (54.8%) of 42 SBG strains were resistant or intermediately susceptible to clindamycin. Twenty-four (57.1%) of 42 strains were resistant or intermediately susceptible to erythromycin. All strains were tested for susceptibility to ceftriaxone and vancomycin and retained susceptibility to both antimicrobial agents throughout the study period. Six of 42 patients died, for a mortality rate of 11.9%. Infectious disease consultation was obtained in 35 (80.0%) of 42 patients. Infectious disease consultation was positively associated with survival (P = 0.0041, Fisher exact test). The new nomenclature schemes for prior members of the SBG were recognized by all HTTs because our microbiology laboratory reported each member of the group, regardless of new name, with “bovis group” added to the identification on all positive culture reports. Conclusions Streptococcus bovis group bacteremia is a disease of older adults with all but 3 patients 60 years or older and a mean age at onset of 73.4 years. Most HTTs considered colon carcinoma as a possible source for and infective endocarditis as a potential complication of SBG bacteremia. However, most HTTs were not aware that SBG bacteremia could be associated with nonmalignant colonic lesions especially polyps, Laennec cirrhosis, or with pancreatic, biliary, and upper GI tract anatomic abnormalities. Of our SBG isolates, 54.8% were not sensitive to clindamycin. Clindamycin should not be used for empiric treatment of SBG bacteremia. The ID service should be consulted on all patients with SBG bacteremia because such consultation had a positive correlation with patient survival (P = 0.0041).

Repercussions of low fructose-drinking water in male rats.

Fructose consumption has increased worldwide, and it has been associated with the development of metabolic diseases such as insulin resistance (IR) and steatosis. The aim was to evaluate if lower fructose concentrations may cause pancreatic structural abnormalities, leading to a glucose intolerance without steatosis in male rats. Young male rats orally received 7% fructose solution for 12 weeks. Body weight, food, water, and energy intake were measured. An oral glucose tolerance test (OGTT) was performed. After final experimental period, all rats were anaesthetized and killed. Blood samples were collected for biochemical analyses and organs (liver and pancreas) were processed for morphological analyses. Fructose consumption was not associated with lipid accumulation in liver. However, fructose administration was associated with an increased area under curve from OGTT and an increased percentage of insulin-positive cells, high beta cell mass and reduced pancreatic islet area. Fructose supplementation (7%) did not cause steatosis, but it led to abnormal morphology and function of pancreatic islet cells, contributing for glucose intolerance development. Our findings demonstrate that even low fructose concentrations may cause deleterious effects in animals.

Pancreatic endosonographic findings and clinical correlation in Crohn's disease

OBJECTIVES:We aimed to evaluate the incidence of pancreatic alterations in Crohn's disease using endoscopic ultrasound (EUS) and to correlate the number of alterations with current clinical data.METHODS:Patients diagnosed with Crohn's disease (n=51) were examined using EUS, and 11 variables were analyzed. A control group consisted of patients with no history of pancreatic disease or Crohn's disease. Patients presenting with three or more alterations underwent magnetic resonance imaging (MRI). Pancreatic function was determined using a fecal elastase assay.RESULTS:Two of the 51 patients (3.9%) presented with four EUS alterations, 3 (5.9%) presented with three, 11 (21.5%) presented with two, and 13 (25.5%) presented with one; in the control group, only 16% presented with one EUS alteration (p<0.001). Parenchymal abnormalities accounted for 39 of the EUS findings, and ductal abnormalities accounted for 11. Pancreatic lesions were not detected by MRI. Low fecal elastase levels were observed in 4 patients, none of whom presented with significant pancreatic alterations after undergoing EUS. Ileal involvement was predictive of the number of EUS alterations.CONCLUSION:A higher incidence of pancreatic abnormalities was found in patients with Crohn's disease than in individuals in the control group. The majority of these abnormalities are related to parenchymal alterations. In this group of patients, future studies should be conducted to determine whether such morphological abnormalities could evolve to induce exocrine or endocrine pancreatic insufficiency and, if so, identify the risk factors and determine which patients should undergo EUS.

Intricate interplay between endrocrine and exocrine pancreas

The pancreas is a vital organ of the human body that plays a dual role as both endocrine and exocrine organ. The endocrine part of the pancreas is responsible for maintaining blood glucose homeostasis and the exocrine part aids in the digestion of food. The exocrine and the endocrine pancreas mediate their functions by secreting digestive enzymes and islet hormones respectively. It is possible to assess abnormalities in the function of pancreas with assays that detect exocrine and endocrine secretions to assist in predicting pancreatic dysfunction. Although individual assays exist for each of the hormones, it was not the same for the endocrine hormone somatostatin. We have developed a new ELISA assay for the quantification of somatostatin, a pancreatic islet hormone that can be used along with other hormonal assays to examine the pancreatic health. Abnormalities in pancreatic health can be predicted early especially through genetic risk factors, some of the genetic risk factors like Cyclin Dependent Kinase Inhibitor 2A (CDKN2A) are reported to be linked with both diabetes and Pancreatic Ductal Adenocarcinoma (PDAC). Therefore, evaluating the secretory profile of the pancreas in individuals with these genetic risk factors becomes essential to detect initial signs of disorders like diabetes and pancreatic cancer. Exploiting the secretion assays combined with screening for genetic risk factors might help in understanding the intricate interplay between PDAC and diabetes. Overall, this would help in early detection of pancreatic abnormalities enabling intervention to mitigate risk of diabetes and pancreatic cancer.

DWI of Pancreatic Ductal Adenocarcinoma: A Pilot Study to Estimate the Correlation With Metastatic Disease Potential and Overall Survival.

The purpose of this study is to analyze the relationship between the apparent diffusion coefficient (ADC) of pancreatic ductal adenocarcinoma (PDAC) and the presence or development of metastasis and overall survival (OS). Of 290 consecutive patients with histopathologically proven PDAC from January 2013 to December 2014, staging DWI was performed for 124 patients. Image quality was adequate in 112 studies. Sixty-five patients were treatment naïve, but 17 of the 65 were excluded because of the presence of other associated pancreatic pathologic abnormalities. Data for the remaining 48 patients (24 men and 24 women; median age, 65.5 years; interquartile range, 56-77 years) were obtained during a 4-year follow-up period (mean [± SD], 397 ± 415.1 days). The correlation between ADC and the presence or development of metastasis was assessed using descriptive statistics. OS was determined and mortality analysis was performed using Pearson correlation and Kaplan-Meier curves. Of 48 patients, 10 had metastases at staging MRI, and 12 later developed metastatic disease. Among the latter, the mean time from staging MRI to metastasis was 258 ± 274.1 days. Most (86%) metastases were hepatic (n = 19). During the follow-up period, the remaining 26 patients (54%) never developed metastases. Patients with metastatic disease (n = 22) had significantly lower mean ADCs than did those without metastases (1.27 × 10-3 vs 1.43 × 10-3 mm2/s; p = 0.047). The ADC of PDAC had a positive correlation with survival: patients with PDAC with lower ADCs (< 1.36 × 10-3 mm2/s) had significantly worse 4-year OS rates than did patients with higher ADC values (p = 0.036). Pretreatment ADC values of PDAC may be significantly lower in patients who have or will develop metastatic disease and may correlate with worse OS.

Clinical and Genetic Characteristics of Patients with Shwachman-Diamond Syndrome in Japan

▪Background: Shwachman-Diamond syndrome (SDS) is an inherited bone marrow failure syndrome (IBMFS) characterized by bone marrow failure and pancreatic insufficiency. Patients with SDS have propensity to develop myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Although it is the third most common IBMFS following Fanconi anemia and Diamond-Blackfan anemia in western countries, the incidence of SDS has been considered to be much lower in Japan. Patients and methods:In addition to the cases of SDS diagnosed by SBDSgene mutation analysis at Kyoto University, we captured those from the central review system of the Japanese Society of Pediatric Hematology and Oncology and the targeted sequencing system for IBMFS at Nagoya University as well as the previous Japanese nationwide survey for SDS that was conducted in 2010. Results:A total of 47 cases from 43 families with biallelic SBDSgene mutation were captured. After the previous nationwide survey, 21 cases were accumulated in the past 8 years: 2.6 cases per year in average. Median age at presentation is 0 year, and median age at diagnosis is two years. Male-female ratio of the patients was 2.1:1. Birth weight was less than 2500g in approximately half of the patients. Most common mutation was 183-184TA>CT/258+2T>C (73%) followed by 258+2T>C/258+2T>C (6.6%). Notably, a patient with heterozygous 258+2T>C mutation was shown to have exon 3 deletion in the SBDS gene by whole exome sequencing. Clinical features at initial visit were various kinds of cytopenia, failure to thrive, steatorrhea, liver dysfunction, short stature, and skeletal abnormalities. Pancreatic insufficiency and/or pancreatic abnormality in imaging studies were found in almost all patients. Neutropenia was documented in one-third of the cases at initial visit; however, eventually 89% of the patients had neutropenia. Other hematological abnormalities were anemia (64%), thrombocytopenia (69%), and pancytopenia (40%). Bone marrow examination revealed hypoplasia (60%), dysplasia (36%), and chromosome abnormalities (23%) including del(20q), i(7q), and complex chromosome abnormalities. Four male patients (8.5%) of the cohort were documented to develop AML. Age at onset of AML was more than 18 years in three patients. Three patients complicated with AML and two patients with severe bone marrow failure underwent hematopoietic stem cell transplantation (HSCT). Interestingly, one patient with AML harboring normal karyotype is alive without relapse 20 years after HSCT. Three patients (6%) died; the cause of death was AML in two and complication of HSCT in one. Conclusion: Along with growing recognition of the disease among physicians and establishment of mutation analysis system, newly diagnosed cases of SDS were accumulated constantly. SDS may be more common than previously thought in our country. Clinical characteristics are similar to those that were reported in previous studies. As shown in a recent study on a large MDS cohort from an international registry of HSCT, patients with SDS may develop AML in adulthood and have very poor prognosis. The SDS cohort in Japan may provide a platform to investigate clinical and genetic factors associated with severity and phenotypes of the disease under a relatively uniform ethnic background. DisclosuresNo relevant conflicts of interest to declare.

Comparison of clinical symptoms, gastric motility and fat intake in the early chronic pancreatitis patients with anti-acid therapy-resistant functional dyspepsia patients.

BackgroundThere was no available data concerning the clinical differentiation between the updated definition of early chronic pancreatitis (ECP) and anti-acid therapy-resistant functional dyspepsia (RFD).AimsWe aimed to determine whether clinical symptoms, gastric motility, psychogenic factors and fat intake can help distinguish early chronic pancreatitis (ECP) from anti-acid therapy-resistant functional dyspepsia patients with pancreatic enzyme abnormalities (RFD-P) and anti-acid therapy-resistant functional dyspepsia (RFD) patients using endosonography.MethodsWe enrolled 102 consecutive patients presenting with typical symptoms of RFD patients (n = 52), ECP patients (n = 25) and RFD-P patients (n = 25). ECP patients were diagnosed based on the criteria recommended by the Japan Pancreatic Association. Gastric motility was evaluated by 13C-acetate breath tests. Severity of duodenal inflammation was examined.Results24.5% of RFD patients were determined as ECP using endosonography. Abdominal pain score in Gastrointestinal Symptom Rating Scale (GSRS) in the patients with ECP was significantly lower compared to that in the patients with RFD-P. There were no significant differences in State-Trait Inventory (STAI)-state/-trait scores, Self-Rating Questionnaire for Depression (SRQ-D) scores and clinical symptoms for fat intake among three groups. The early phase of gastric emptying (AUC5; AUC15) in ECP and RFD-P patients were significantly disturbed compared to those in RFD patients.ConclusionsEvaluation of severity of abdominal pain and measurement of the early phase of gastric emptying will be useful tools to distinguish ECP patients from RFD patients. Accurate diagnosis of ECP patients may contribute to the prevention from advancing of chronic pancreatitis.

Camostat Mesilate, Pancrelipase, and Rabeprazole Combination Therapy Improves Epigastric Pain in Early Chronic Pancreatitis and Functional Dyspepsia with Pancreatic Enzyme Abnormalities

Background/Aims: The aims of the study are to clarify the pathophysiological differences among early chronic pancreatitis (ECP), functional dyspepsia with pancreatic (FD-P) enzyme abnormalities and FD patients and to determine whether camostat mesilate, pancrelipase, and rabeprazole triple therapy improve FD symptoms in the ECP patients and FD-P patients in cross-over way. Methods: We enrolled 84 consecutive patients presenting with typical symptoms of FD patients (n = 42), ECP patients (n = 15), and FD-P patients (n = 27). Gastric emptying was assessed by the ¹³C-acetate breath test. ECP was diagnosed based on the criteria recommended by the Japan Pancreatic Association. Results: The proportions of female in ECP patients and FD-P were significantly higher compared to that in FD patients. The early phase of gastric emptying in ECP and FD-P patients was significantly disturbed compared to that in FD patients. The primary outcome of this study is that 4 weeks of camostat mesilate, pancrelipase, and rabeprazole triple therapy significantly ameliorated epigastric pain in ECP patients compared to acotiamide and rabeprazole combination therapy. Conclusion: Although there were no significant differences in pathophysiology between ECP patients and FD-P patients, triple therapy can significantly ameliorate epigastric pain in ECP patients. Further studies will be needed to clarify why triple therapy can improve epigastric pain in ECP patients.

Type 1 and Type 2 Autoimmune Pancreatitis: Distinctive Clinical and Pathological Features, But Are There Any Differences at Magnetic Resonance? Experience From a Referral Center.

This study aimed to evaluate magnetic resonance imaging findings of autoimmune pancreatitis (AIP) and to find radiological patterns that could differentiate type 1 and type 2 AIP. Eighty-four patients with diagnosis of AIP were enrolled. Image analysis included pancreatic signal intensity abnormalities, enhancement pattern, extrapancreatic involvement, and main pancreatic duct alterations. Pancreatic parenchyma resulted in hypointensity on T1-weighted images in 65 (98.5%) of 66 cases in type 1 and in 17 (94.5%) of 18 in type 2 (P > 0.05) and in hyperintensity on T2-weighted images in 41 (62%) of 66 and in 15 (83.4%) of 18, respectively (P > 0.05). Lesions were hypovascular in 64 (97%) of 66 cases in type 1 and in 16 (88.9%) of 18 in type 2 with delayed contrast retention in 56 (84.8%) of 66 and in 17 (94.5%) of 18, respectively (P > 0.05). Autoimmune cholangitis was found in 29 (43.9%) of 66 patients with type 1 and in 3 (16.7%) of 18 with type 2 (P = 0.02); renal involvement was observed in 20 (30.3%) of 66 and 1 (5.5%) of 18, respectively (P = 0.02). Both subtypes presented with multiple stenoses (P > 0.05). Dilation of upstream duct was more frequent in type 1 (P = 0.02). Magnetic resonance imaging is useful in detecting extrapancreatic involvement, typically seen in type 1. Dilation of the upstream duct suggests type 1 AIP.

English

Several studies highlight beneficial effect of glabridin as an anti-hyperglycemic agent. However, the protective mechanisms of glabridin on improvement of pancreatic islets damage due to streptozotocin (STZ) exposure have not been adequately investigated. In the present study, we aimed to elucidate the effects of glabridin on restoration of pancreatic islet architecture, at least in part by restoring collagen I and fibronectin, through an activation of protein kinase Cs (PKCs) and transforming growth factor (TGF)-&beta;1 in STZ-induced pancreatic &beta;-cell injuries. Glabridin (40 mg/kg b.wt./day) was administrated to STZ-exposed rats for 8 weeks. The effects of glabridin were then investigated by measuring body weight, blood glucose level, pancreatic morphology, and protein expressions of PKCs, TGF-&beta;1, collagen I, and fibronectin. The results revealed that glabridin prevented weight loss and significantly decreased blood glucose level. Physical distortion and impairment with irregular outline was clearly observed in untreated STZ islets. Nevertheless, rat islets showed nearly normal architecture with a high &beta;-cell number after glabridin treatment. Glabridin also ameliorated the expression levels of PKCs, TGF-&beta;1, collagen I, and fibronectin in STZ-rat pancreas. These results provide novel evidence that glabridin significantly reduced pancreatic islets abnormalities in STZ-exposed rats and these effects could be associated with its hypoglycemic activity and with restoration of normal levels of PKCs, TGF-&beta;1, collagen I and fibronectin, which could subsequently contribute to maintaining islet structure and function. Key words: Glabridin, pancreas, diabetes mellitus, anti-hyperglycemia, anti-oxidant activity, streptozotocin.

Prevalence of cystic lesions and other morphological pancreatic abnormalities in type 2 diabetes mellitus patients

Life history (LH) theory provides an evolutionary account of individual differences in various traits, including wellbeing. The theory distinguishes between a fast LH strategy, indicated by a short-term perspective (e.g., impulsivity), versus a slow LH strategy, indicated by a long-term perspective (e.g., more constraint behavior). Previous studies have reported an association between a fast LH strategy and more stress, but much of the mediating mechanisms are still unknown. Accordingly, we present three studies testing 1) whether LH strategy is directly associated with the number of disruptive life events and coping strategies, and 2) whether life events and coping mediate the LH-strategy-stress relationship. The results of the three studies converged: Faster LH strategists reported more disrupted life events, showed a less effective coping pattern, and life events and coping both partially mediated the LH strategy-stress association. These results point to several factors that can explain why LH strategy relates to stress.

Modified breath-hold compressed-sensing 3D MR cholangiopancreatography with a small field-of-view and high resolution acquisition: Clinical feasibility in biliary and pancreatic disorders.

Compressed-sensing (CS) accelerated 3D MR cholangiopancreatography (MRCP) could be acquired in both navigator-triggered (NT) and breath-hold (BH) mode, but the latter has been considered inferior in depicting pancreatic duct and diagnosing pancreatic duct-related diseases. To prospectively evaluate the clinical feasibility of a modified 3D BH-CS-MRCP prototype protocol with small field-of-view (FOV) and higher spatial resolution, and to compare its performance to the original BH-CS-MRCP and NT-CS-MRCP. Prospective cohort study. Eighty-two patients with suspected pancreaticobiliary diseases (46 male, median age, 55 years, range, 16-79 years), including seven noncooperative patients. 3T, CS-MRCP. Three protocols were performed in random order in each patient. Acquisition time of each protocol was recorded. Image quality, background suppression, duct visibility, and diagnostic confidence with duct anatomic variations and duct-related pathologies were rated on a 5-point scale by two blinded radiologists independently. The Wilcoxon signed-rank test was used to compare the intraindividual difference. Interobserver agreement was determined using kappa coefficients. The diagnostic performance was calculated using receiver operating characteristic curves. Acquisition time was 17 seconds for both BH-CS-MRCP protocols, and 127.5 ± 36.9 seconds for NT-CS-MRCP. In 75 cooperative patients, the incidence of major artifacts was low for all protocols (5.3-8.0%). Background suppression was similar with the two BH-CS-MRCP protocols (3.67 ± 0.77 for original BH-CS-MRCP and 3.70 ± 0. 57 for modified BH-CS-MRCP, respectively), both inferior to the NT-CS-MRCP protocol (4.41 ± 0.68, P < 0.001 for both). Modified BH-CS-MRCP and NT-CS-MRCP depicted pancreatic duct and second-level branches of biliary duct better than original BH-CS-MRCP (all P < 0.01). The diagnostic performance for detecting bile duct abnormalities was similar for all protocols (P = 0.53-0.87), whereas for detecting pancreatic duct abnormalities, modified BH-CS-MRCP and NT-CS-MRCP had significantly better performance compared to original BH-CS-MRCP (both P < 0.01). In seven noncooperative patients, NT-CS-MRCP had superior image quality than both BH protocols (both P < 0.01). Modified BH-CS-MRCP is feasible for pancreatic and biliary disorders. NT-CS-MRCP might be more useful in noncooperative patients. 2 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2018;47:1389-1399.