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1.  Moderate activation of IKK2-NF-kB in unstressed adult mouse liver induces cytoprotective genes and lipogenesis without apparent signs of inflammation or fibrosis 
BMC Gastroenterology  2015;15:94.
Background
The NF-kB signaling, regulated by IKK1-p52/RelB and IKK2-p65, is activated by various stresses to protect or damage the liver, in context-specific manners. Two previous studies of liver-specific expression of constitutive active IKK2 (IKK2ca) showed that strong activation of IKK2-NF-kB in mouse livers caused inflammation, insulin resistance, and/or fibrosis. The purpose of this study was to understand how moderate activation of IKK2-NF-kB in adult mouse livers alters hepatic gene expression and pathophysiology.
Method
We generated mice with adult hepatocyte-specific activation of Ikk2 (Liv-Ikk2ca) using Alb-cre mice and Ikk2ca Rosa26 knockin mice in which a moderate expression of Ikk2ca transgene was driven by the endogenous Rosa26 promoter.
Results
Surprisingly, compared to wild-type mice, adult male Liv-Ikk2ca mice had higher hepatic mRNA expression of Ikk2 and classical NF-kB targets (e.g. Lcn2 and A20), as well as IKK1, NIK, and RelB, but no changes in markers of inflammation or fibrosis. Blood levels of IL-6 and MCP-1 remained unchanged, and histology analysis showed a lack of injury or infiltration of inflammatory cells in livers of Liv-Ikk2ca mice. Moreover, Liv-Ikk2ca mice had lower mRNA expression of prooxidative enzymes Cyp2e1 and Cyp4a14, higher expression of antioxidative enzymes Sod2, Gpx1, and Nqo1, without changes in key enzymes for fatty acid oxidation, glucose utilization, or gluconeogenesis. In parallel, Liv-Ikk2ca mice and wild-type mice had similar levels of hepatic reduced glutathione, endogenous reactive oxygen species, and lipid peroxidation. Additionally, Liv-Ikk2ca mice had higher Cyp3a11 without down-regulation of most drug processing genes. Regarding nuclear proteins of NF-kB subunits, Liv-Ikk2ca mice had moderately higher p65 and p50 but much higher RelB. Results of ChIP-qPCR showed that the binding of p50 to multiple NF-kB-target genes was markedly increased in Liv-Ikk2ca mice. Additionally, Liv-Ikk2ca mice had moderate increase in triglycerides in liver, which was associated with higher lipogenic factors Pparγ, Lxr, Fasn, Scd1, and CD36.
Conclusion
In summary, moderate activation of IKK2-NF-kB in unstressed adult mouse hepatocytes produces a cytoprotective gene expression profile and induces lipogenesis without apparent signs of inflammation or fibrosis, likely due to strong activation of the anti-inflammatory IKK1-RelB alternative NF-kB pathway as well as the Lxr.
Electronic supplementary material
The online version of this article (doi:10.1186/s12876-015-0325-z) contains supplementary material, which is available to authorized users.
doi:10.1186/s12876-015-0325-z
PMCID: PMC4518658  PMID: 26219821
IKK2; IKK1; NF-kB; RelB; Lxr; Liver; Mice; Lipogenesis; Inflammation; Fibrosis
2.  “And then you start to loose it because you think about Nutella”: The significance of food for people with inflammatory bowel disease - a qualitative study 
BMC Gastroenterology  2015;15:93.
Background
Many patients with inflammatory bowel disease strongly believe that food or certain food products heavily influence the symptoms or even trigger acute flare-ups. Unfortunately, there is no generalizable information for these patients, and therefore no effective diet has been identified to date.
Methods
The narrative interviews we used for this study provide the basis for the German website www.krankheitserfahrungen.de. Maximum-variation sampling was used to include a broad range of experiences and a variety of different factors that might influence people’s experiences. The sample included men and women of different age groups and social and ethnic backgrounds from across Germany. The interviews were analyzed using grounded theory.
Results
Four interrelated categories emerged: managing uncertainty, eating: between craving and aversion, being different and professional help as a further source of uncertainty. The most important issue for our responders was the handling of uncertainty and to find a way between desire for, and aversion against, eating. Many participants described difficulties during formal social occasions such as weddings, birthdays, or when going out to a restaurant.
Conclusions
Many of the experiences the participants reported in their daily struggle with food and their illness, such as cravings for and abstaining from certain foods, were rather unusual and often stressful. Because they decided not to go out in public any longer, some of the interviewees experienced even more social isolation than they did before. Health professionals need to become more involved and not only advice about food and eating, but also help their patients find strategies for avoiding social isolation.
doi:10.1186/s12876-015-0322-2
PMCID: PMC4518859  PMID: 26219642
Inflammatory bowel disease; Diet; Narration; Qualitative research
3.  Intrahepatic cholestasis of pregnancy: observational study of the treatment with low-dose ursodeoxycholic acid 
BMC Gastroenterology  2015;15:92.
Background
To exam the biochemical, obstetric management and pregnancy outcome in women with intrahepatic cholestasis of pregnancy (ICP) and treatment with ursodeoxycholic acid (UDCA).
Methods
Pregnancy outcome in patients with ICP (N = 307) was studied and patients treated with UDCA (N = 208) vs. no UDCA were compared. The data of the antenatal visits, deliveries and neonatal outcome of 307 pregnancies with ICP was collected from the hospital computerized delivery room log book. UDCA was used in 208 pregnancies. The diagnosis was made by maternal pruritus and elevation of total fasting bile acid (BA) (>6 μmol/l) and elevation of serum alanine aminotransferases (ALT) (>45 U/l). Maternal and neonatal data was analysed and data of the patients who used UDCA during pregnancy was analysed separately and compared with the data from patients without medication.
Results
UDCA was well tolerated. Mothers receiving UDCA had ICP diagnosed five weeks earlier than mothers without medication. At the diagnosis, levels of total BA and ALT were higher in the group using UDCA compared to the group without medication. Most deliveries were induced and perinatal outcome was good. Apgar scores at 5 min were significantly lower in UDCA group (p < 0.05), but fetal umbilical artery pH values were similar in both groups (p > 0.05). There were 30 patients with total BA > 40 μmol/l at diagnosis, 24 with UDCA and 6 without medication and those deliveries were induced soon after diagnosis. The preterm labour was also more common in these patents (p < 0.05). Women with preterm babies had significantly early onset pruritus and ICP was diagnosed earlier. Serum ALT and total BA levels were significantly higher in those pregnancies at diagnosis and also at first control.
Conclusions
Preterm labour was associated in severe ICP (total BA > 40 μmol/l), ALT levels were also significantly higher and ICP was diagnosed earlier (p < 0.05). Apgar scores were lower in preterm babies (p < 0.05), but umbilical artery pHvalues were not significantly lower. UDCA was well tolerated by pregnant women. With low-dose UDCA treatment the obstetric outcome was good. We still recommend careful obstetrical follow-up.
doi:10.1186/s12876-015-0324-0
PMCID: PMC4517361  PMID: 26215400
Pregnancy; Intrahepatic cholestasis; Ursodeoxycholic acid
4.  Associations of coffee consumption with markers of liver injury in the insulin resistance atherosclerosis study 
BMC Gastroenterology  2015;15:88.
Background
Coffee consumption has been associated with reduced risk of developing type 2 diabetes mellitus (T2DM) however, the mechanism for this association has yet to be elucidated. Non-alcoholic fatty liver disease (NAFLD) characterizes and predicts T2DM yet the relationship of coffee with this disorder remains unclear. Our aim was to investigate the associations of coffee with markers of liver injury in 1005 multi-ethnic, non-diabetic adults in the Insulin Resistance Atherosclerosis Study.
Methods
Dietary intake was assessed using a validated 114-item food frequency questionnaire. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and fetuin-A were determined in fasting blood samples and the validated NAFLD liver fat score was calculated. Multivariate linear regression assessed the contribution of coffee to variation in markers of liver injury.
Results
Caffeinated coffee showed significant inverse associations with ALT (β = −0.08, p = 0.0111), AST (β = −0.05, p = 0.0155) and NAFLD liver fat score (β = −0.05, p = 0.0293) but not with fetuin-A (β = 0.04, p = 0.17). When the highest alcohol consumers were excluded, these associations remained (ALT β = −0.11, p = 0.0037; AST β = −0.05, p = 0.0330; NAFLD liver fat score β = −0.06, p = 0.0298). With additional adjustment for insulin sensitivity, the relationship with ALT remained significant (ALT β = −0.08, p = 0.0400; AST β = −0.03, p = 0.20; NAFLD liver fat score β = −0.03, p = 0.27). There were no significant associations of decaffeinated coffee with liver markers.
Conclusions
These analyses indicate a beneficial impact of caffeinated coffee on liver morphology and/or function, and suggest that this relationship may mediate the well-established inverse association of coffee with risk of T2DM.
Electronic supplementary material
The online version of this article (doi:10.1186/s12876-015-0321-3) contains supplementary material, which is available to authorized users.
doi:10.1186/s12876-015-0321-3
PMCID: PMC4515880  PMID: 26215323
Coffee; Caffeine; Decaffeinated; Type 2 diabetes; ALT; AST; NAFLD liver fat score; Fetuin-A; Liver enzymes; Insulin resistance atherosclerosis study
5.  Multicenter study on hemorrhagic risk of heparin bridging therapy for periendoscopic thromboprophylaxis 
BMC Gastroenterology  2015;15:89.
Background
For endoscopic interventions, heparin bridging therapy is recommended in patients who are at high risk from interruption of antithrombotic therapy. Although heparin bridging has been reported to be effective in preventing thrombosis, several reports have raised concerns about increased risk of bleeding. The aim of this study was to clarify complications of hepari  bridging therapy in therapeutic endoscopy.
Methods
A nationwide multicenter survey using questionnaire was performed about patients undergoing therapeutic endoscopy with heparin bridging. Patients who underwent therapeutic endoscopy without heparin bridging therapy were considered as controls. Compliance scores of heparin bridging therapy guideline were employed, and association was analyzed between the score and occurrence of post-procedural bleeding.
Results
The incidence of post-procedural bleeding was significantly higher (13.5 %, 33/245) in the heparin group compared with the control group (2.7 %, 299/11102)(p < 0.001). Thrombosis occurred in 1 patient each in the two groups. In the heparin group, post-procedural bleeding was more likely to be delayed bleeding. Dose adjustment of heparin was a significant factor contributing to bleeding. The compliance score of heparin bridging therapy guideline was significantly higher in those who suffered bleeding.
Conclusions
Heparin bridging therapy significantly increased the risk of post-procedural bleeding compared with the control. The bleeding risk was associated with greater adherence with guidelines for heparin bridging therapy.
doi:10.1186/s12876-015-0315-1
PMCID: PMC4515926  PMID: 26215103
Endoscopic treatment; Post-procedural bleeding; Thrombosis; Antithrombotic therapy
6.  A novel mutation within the lactase gene (LCT): the first report of congenital lactase deficiency diagnosed in Central Europe 
BMC Gastroenterology  2015;15:90.
Background
Congenital lactase deficiency is an extremely rare gastrointestinal disorder characterized by neonatal-onset watery diarrhoea and failure to thrive. We present the first genetically confirmed case of congenital lactase deficiency in Central Europe.
Case presentation
After an uneventful pregnancy and birth, a male newborn of consanguineous parents of Turkish origin presented with watery diarrhoea. On day 17, he was admitted to hospital with weight loss, hypertonic dehydration, and metabolic acidosis. Additionally, the patient showed an elevated calcium concentration in blood and urine as well as nephrocalcinosis. Diarrhoea stopped during intravenous rehydration and when feeding a glucose-, galactose-, and lactose-free formula. Therefore, glucose-galactose-malabsorption was assumed. However, genetic testing of the SGLT1 (SLC5A1) gene was negative and, indeed, feeding maltodextrine did not result in recurrence of diarrhoea. In contrast, lactose feeding immediately caused watery diarrhoea, suggesting congenital lactase deficiency. Genetic testing of the LCT gene revealed homozygosity for a 1-bp deletion in exon 8 (c.3448delT). Because of the nature of the mutation, causing a frame shift and a premature termination of translation, congenital lactase deficiency was confirmed and intestinal biopsies were unnecessary. The patient’s general condition improved substantially on a lactose-free diet, including hypercalcaemia, hypercalciuria, and nephrocalcinosis which, however, only disappeared after months.
Conclusion
This case demonstrates (a) that congenital lactase deficiency should be considered in cases of severe neonatal diarrhoea, (b) that intestinal biopsies can be avoided in typical cases that are confirmed by genetic testing, and (c) that the associated nephrocalcinosis can be reversed on diet and an appropriate fluid management.
doi:10.1186/s12876-015-0316-0
PMCID: PMC4515929  PMID: 26215149
Congenital lactase deficiency; CLD; LCT gene; Nephrocalcinosis
7.  Access to primary care is associated with better autoimmune hepatitis outcomes in an urban county hospital 
BMC Gastroenterology  2015;15:91.
Background
Autoimmune hepatitis causes chronic hepatitis and often leads to cirrhosis and death without treatment. We wanted to see if having access to primary care or insurance prior to diagnosis is associated with better outcomes for patients in an urban, public hospital with mostly socioeconomically disadvantaged Hispanic patients.
Methods
We did a retrospective study at our institution. Kaplan Meier survival analysis was done looking at transplant-free overall survival for patients diagnosed at our institution. The log-rank test was done to compare survival between patients with and without prior access to primary care, and between patients with and without insurance at diagnosis.
Results
Overall 5- and 10-year transplant-free overall survival was 91 % (95 % CI, 83-100 %) and 75 % (95 % CI, 50-99 %), respectively. Patients with primary care prior to diagnosis had significantly better transplant-free overall survival than those without (log rank test p = 0.019). Patients with primary care also had better clinical markers at diagnosis. Having insurance at diagnosis was not associated with better outcomes.
Conclusions
Outcomes of autoimmune hepatitis are poor in our setting but access to primary care prior to diagnosis was associated with better outcomes. This is likely due to the important role that primary care plays in detecting disease and initiating treatment earlier. With the expansion of access to healthcare that the Affordable Care Act provides, future patients are likely to do better with even rare diseases like autoimmune hepatitis.
doi:10.1186/s12876-015-0318-y
PMCID: PMC4517362  PMID: 26215250
Autoimmune hepatitis; County; Safety-net; Hispanic
8.  Comparison of clinical course and outcome of acute pancreatitis according to the two main etiologies: alcohol and gallstone 
BMC Gastroenterology  2015;15:87.
Background
Studies concerning clinical course and outcome of acute pancreatitis (AP) according to etiologies were rare, especially after year 2000. This study was designed to investigate the difference between the clinical course of alcoholic and biliary AP.
Methods
Of the 153 patients diagnosed as AP with a first attack between January 2011 and January 2013, extensive clinical data of 50 patients with AP caused by alcohol and 76 patients with AP caused by gallstone were analyzed retrospectively. We compared the severity of AP defined by revised Atlanta classification in 2012, local complications, severity scores, and computed tomography severity index (CTSI) between alcoholic and biliary AP. We also evaluated the length of hospital stay, duration of NPO, and in-hospital mortality in each group.
Results
Hemoglobin, hematocrit, and serum C-reactive protein level measured after admission for 24 h were significantly higher in the alcohol group than in the biliary group. Incidence of pseudocyst formation was significantly higher in the alcohol group than in the biliary group (20.0 % vs. 6.6 %, P = 0.023). Among prognostic scoring systems, only CTSI showed significant difference (P < 0.001) with a mean score of 3.0 ± 0.9 in the alcohol group and 1.7 ± 1.2 in the biliary group. Severe AP with organ failure persisting beyond 48 h was observed in 12 patients (24.0 %) in the alcohol group and one patient (1.3 %) in the biliary group (P < 0.001). There were 4 mortalities in the alcohol group only (P = 0.012).
Conclusion
More severe forms of AP and local complication, such as pseudocyst formation, are associated with alcoholic AP compared with biliary AP.
doi:10.1186/s12876-015-0323-1
PMCID: PMC4513750  PMID: 26209440
Acute pancreatitis; Etiology; Alcohol; Gallstone; Clinical course
9.  Early stage signet ring cell carcinoma of the colon examined by magnifying endoscopy with narrow-band imaging: a case report 
BMC Gastroenterology  2015;15:86.
Background
Signet ring cell carcinoma of the colon and rectum is rare, and most cases are detected at an advanced stage. We present a case of primary signet ring cell carcinoma detected at an early stage by magnifying endoscopy with narrow-band imaging (NBI) and crystal violet staining.
Case presentation
A 73-year-old man visited our hospital for screening colonoscopy. Six years previously, he had undergone endoscopic submucosal dissection (ESD) for early gastric cancer. The pathological diagnosis was a well-differentiated adenocarcinoma, invading into the mucosa without lymphovascular invasion. Colonoscopy revealed a flat elevated lesion with a slightly depressed area, 20 mm in diameter, in the cecum. Further, magnifying endoscopy with NBI revealed that the surface pattern was slightly irregular and microvessels had a regular diameter and distribution in the margin of the lesion, but in the central part of the lesion, irregularity in the tumor surface pattern and form as well as in the diameter and distribution of microvessels was noted. Additionally, due to mucus, avascular areas were also observed. Magnifying endoscopy combined with 0.05 % crystal violet staining showed IIIL and VI pit patterns in the margin of the lesion, and a VI pit pattern in the central part of the lesion; however, due to mucus exudate, this finding could not be established with certainty. The lesion was successfully removed en bloc using ESD without complications. The tumor was composed mainly of signet ring cell carcinoma, partially mixed with moderately differentiated (tub2) and well-differentiated (tub1) adenocarcinomas. The tumor cells infiltrated 250 μm into the submucosal layer and involved lymphatic vessels. Therefore, the patient underwent an additional laparoscopic ileocecal resection, and the resected specimen revealed no residual carcinoma or lymph node metastasis.
Conclusion
In this case report, we present a case of primary signet ring cell carcinoma detected at an early stage and identified by magnifying endoscopy with NBI and crystal violet staining.
doi:10.1186/s12876-015-0317-z
PMCID: PMC4512161  PMID: 26205810
Signet ring cell carcinoma; Colon cancer; Narrow band imaging; Pit pattern
10.  Rectal indomethacin versus placebo to reduce the incidence of pancreatitis after endoscopic retrograde cholangiopancreatography: results of a controlled clinical trial 
BMC Gastroenterology  2015;15:85.
Background
Acute pancreatitis is the most common major complication after endoscopic retrograde cholangiopancreatography (ERCP). Many drugs have been evaluated for prophylaxis, including nonsteroidal anti-inflammatory drugs (NSAIDs), which are potent inhibitors of phospholipase A2 and play a role in the pathogenesis of acute pancreatitis. Rectal NSAIDs have been shown in prospective studies to decrease the incidence of this complication, but the indication is not generalized in clinical practice. The aim of this study was to evaluate the efficacy of rectal administration of indomethacin in reducing the incidence of post-ERCP pancreatitis in high-risk patients.
Methods
This was a controlled clinical trial where patients with an elevated risk of developing post-ERCP pancreatitis were assigned to receive 100 mg of rectal indomethacin or a 2.6 g suppository of glycerin immediately after ERCP, without placement of a pancreatic stent. The patients were determined to be at high risk based on validated patient- and procedure-related risk factors. Post-ERCP pancreatitis was defined as the presence of new upper abdominal pain, hyperamylasemia/hyperlipasemia (at least three times the upper limit) 2 hours after the procedure and hospitalization at least 48 hours because of the complication. Pancreatitis severity was defined according to Cotton’s criteria.
Results
One hundred sixty-six patients were included; 82 in the study group and 84 in the placebo group. Patients had at least one major and/or two minor risk factors for developing post-ERCP pancreatitis. The incidence of the complication was 4.87 % (4/82) in the study group and 20.23 % (17/84) in the placebo group; this difference was significant (P = 0.01). According to Cotton’s criteria, 17 patients (80.9 %) developed mild pancreatitis and 4 (19.1 %) had moderate pancreatitis; 3 of these 4 patients belonged to the placebo group (P = 0.60). Based on these results, an absolute risk reduction of 0.15 (15 %), a relative risk reduction of 0.75 (75 %) and a number needed to treat of 6.5 patients were calculated to prevent an episode of post-ERCP pancreatitis. There was no mortality.
Conclusions
Rectal indomethacin reduced the incidence of post-ERCP pancreatitis among patients at high risk of developing this complication.
Trial registration
National Clinical Trials NCT02110810. Date April 7, 2014.
doi:10.1186/s12876-015-0314-2
PMCID: PMC4508969  PMID: 26195123
Prophylaxis; Rectal indomethacin; Postendoscopic retrograde cholangiopancreatography pancreatitis
11.  Desmoid tumors complicating Familial Adenomatous Polyposis: a meta-analysis mutation spectrum of affected individuals 
BMC Gastroenterology  2015;15:84.
Background
Desmoid tumors are a group of benign, invasive, solid tumors that are relatively rare in the general population, but can occur in up to 21 % of patients with Familial Adenomatous Polyposis (FAP). They can be difficult to treat and have high rates of recurrence even after resection. Our goal with this study was to identify the genetic mutations that put certain patients with FAP at high risk for desmoid tumors and could be future targets for research.
Methods
We performed a search in Pubmed, Ovid Medline and Embase to identify subjects with desmoid tumors and FAP. As a reference group for APC mutations in the unselected FAP population, we used the UMD-APC database referenced in the Orphanet portal which includes APC mutation data on 2040 individuals with FAP.
Results
Mutations were able to be broken down into 7 regions based on previously published data. Mutations in the APC gene from codons 1310 to 2011 were the most common region encompassing 48 % of published desmoid cases and 40 % of the reference population. It had a slightly elevated odds ratio of 1.4 that was statistically significant along with codon region 543-713 that had an odds ratio of 2.0. Using a combination of p-value and CI, the remaining 5 regions did not meet statistical significance as either the p >0.05 or the CI included 1.0. The most common point mutation found was codon 1309 (13.1 %), but it was also the most commonly found mutation in our reference population (12.9 %) and had an odds ratio of 1.0.
Conclusions
There is an increased risk for desmoid tumors in individuals with APC mutations between codons 543-713 and 1310-2011 when compared to a reference population. These patients may benefit from further study to develop surveillance protocols that could improve outcomes.
Electronic supplementary material
The online version of this article (doi:10.1186/s12876-015-0306-2) contains supplementary material, which is available to authorized users.
doi:10.1186/s12876-015-0306-2
PMCID: PMC4504176  PMID: 26179480
Familial adenomatous polyposis; FAP; Desmoid tumors; Solid tumors; Intra-abdominal tumors; Adenomatous polyposis gene mutation; APC
12.  Activation of transcription factor AP-1 in response to thermal injury in rat small intestine and IEC-6 cells 
BMC Gastroenterology  2015;15:83.
Background
Our previous studies indicated that heat stress can cause significant damage to the intestinal epithelium and induce differential expression of many genes in rat small intestine. The transcription factors AP-1 and NF-κB, which act as important mediators by binding to specific DNA sequences within gene promoters, regulate the transcription of genes associated with immune regulation, stress response and cell fate.
Methods
To determine whether AP-1 and NF-κB are involved in hyperthermia-induced injury in rat small intestine and IEC-6 cells, we investigated their activity, and the expression of related proteins, by electrophoretic mobility shift assays and western blotting, respectively.
Results
Heat stress resulted in severe damage to the epithelium of the small intestine. The cell morphology and viability were obviously altered when IEC-6 cell was exposed to hyperthermia. AP-1 was activated in the small intestine of heat-stressed rats, as was phosphorylation of the JNK signaling pathway. In IEC-6 cell line, AP-1 activation in groups exposed to 42 °C for 1 h, 2 h and 4 h was significantly increased. In contrast, NF-κB was not activated in both in vivo and in vitro models.
Conclusion
These results reveal that AP-1 is likely to play an important role in regulating gene transcription in rat small intestine and IEC-6 cells during exposure to heat stress.
Electronic supplementary material
The online version of this article (doi:10.1186/s12876-015-0309-z) contains supplementary material, which is available to authorized users.
doi:10.1186/s12876-015-0309-z
PMCID: PMC4498520  PMID: 26162907
AP-1; NF-κB; Heat stress; Rat small intestine; IEC-6
13.  Frequent co-occurrence of high-grade dysplasia in large flat colonic polyps (>20 mm) and synchronous polyps 
BMC Gastroenterology  2015;15:82.
Background
Large colonic polyps are associated with advanced dysplasia, but prevalence and characteristics of synchronous polyps in patients with large flat colonic polyps are poorly investigated. This study aims to characterize clinicopathological features of large flat colonic polyps and their impact on occurrence and characteristics of synchronous polyps.
Methods
A total of 802 patients that underwent endoscopic mucosal resection (EMR) of flat colonic polyps >20 mm from 2003 to 2014 in an academic endoscopy unit were retrospectively analyzed for size, location and histology of large polyps and synchronous polyps.
Results
Average size of large polyps was 34.1 mm (range 20–150 mm, standard deviation 16.1 mm). Histology included 52.5 % adenomas with low-grade dysplasia (LGD), 26.7 % with high-grade dysplasia (HGD), 9.6 % serrated polyps and 11.2 % adenocarcinomas. The majority of large polyps were localized in the proximal colon (61 %). 72.2 % of adenocarcinomas were found in the distal colon, while 80.5 % of all serrated polyps were detected in the proximal colon. Increase in polyp size, advanced age and location in the distal colon were associated with presence of HGD/adenocarcinoma in large polyps, as identified by multivariate analysis. Synchronous polyps were detected in 67.2 % of patients undergoing complete colonoscopy during EMR. Presence of HGD/adenocarcinoma in the large polyp, localization of any synchronous polyp in the rectosigmoid colon and occurrence of multiple synchronous polyps were associated with presence of HGD/adenocarcinoma in synchronous polyps.
Conclusions
Synchronous polyps are frequently found in patients with large flat colonic polyps. The prevalence of synchronous polyps with high grade dysplasia is highest in patients with large flat polyps containing HGD/adenocarcinoma.
Electronic supplementary material
The online version of this article (doi:10.1186/s12876-015-0312-4) contains supplementary material, which is available to authorized users.
doi:10.1186/s12876-015-0312-4
PMCID: PMC4498525  PMID: 26160557
Colonic polyp; Colonoscopy; Adenoma; Synchronous polyps; Endoscopic mucosal resection
14.  High expression of carbonic anhydrase IX is significantly associated with glandular lesions in gastroesophageal junction and with tumorigenesis markers BMI1, MCM4 and MCM7 
BMC Gastroenterology  2015;15:80.
Background
Carbonic anhydrase IX (CA9) is a transmembrane glycoprotein related to hypoxia. Increased CA9 expression has been associated with decreased survival and cancer progression and has been targeted as a potential therapy for several cancers, including esophageal cancer. The reported percentages of expression of CA9 in esophageal adenocarcinoma vary, and CA9 expression in precancerous esophageal lesions has not been well studied.
Methods
In this study, we investigated CA9 expression in esophageal cancers and in precancerous lesions and explored the association of CA9 expression with prognostic factors and with stem cell and tumorigenesis-related markers including BMI1, cyclin E, ki67, MCM4 and MCM7 expression. Previously constructed tissue microarrays consisting of samples of 7 tissue types (columnar cell metaplasia, Barrett esophagus, low- and high-grade dysplasia, esophageal adenocarcinoma, squamous epithelium, and squamous cell carcinoma) were used for the immunostaining of CA9, BMI1, cyclin E, Ki67, MCM4 and MCM7.
Results and discussion
CA9 high expression occurred more frequently in glandular mucosa with or without dysplasia than in squamous epithelium or squamous cell carcinoma. Survival duration of esophageal adenocarcinoma did not significantly differ between patients with high CA9 expression and those with low expression. High CA9 expression is significantly associated with BMI1, cyclin E, Ki67, MCM4 and MCM7 expression.
Conclusions
High CA9 expression may be related to the acidic environment caused by gastroesophageal reflux disease in the gastroesophageal junction and associated with tumorigenesis through BMI1, MCM4 and MCM7.
doi:10.1186/s12876-015-0310-6
PMCID: PMC4495619  PMID: 26156831
CA9; Esophageal adenocarcinoma; Esophageal squamous cell carcinoma; Barrett’s esophagus; Gastroesophageal reflux disease; BMI1
15.  Efficacy and safety of B-mode ultrasound-guided percutaneous transhepatic gallbladder drainage combined with laparoscopic cholecystectomy for acute cholecystitis in elderly and high-risk patients 
BMC Gastroenterology  2015;15:81.
Background
Standards in treatment of acute cholecystitis (AC) in the elderly and high-risk patients has not been established. Our study evaluated the efficacy and safety of B-mode ultrasound-guided percutaneous transhepatic gallbladder drainage (PTGD) in combination with laparoscopic cholecystectomy (LC) for acute cholecystitis (AC) in elderly and high-risk patients.
Methods
Our study enrolled 35 elderly and high-risk AC patients, hospitalized between January 2010 and April 2014 at the Wenzhou People's Hospital. The patients underwent B-mode ultrasound-guided PTGD and LC (PTGD + LC group). As controls, a separate group of 35 elderly and high-risk AC patients who underwent LC alone (LC group) during the same period at the same hospital were randomly selected from a pool of 186 such cases. The volume of bleeding, surgery time, postoperative length of stay, conversion rate to laparotomy and complication rates (bile leakage, bleeding, incisional hernia, incision infection, pulmonary infarction and respiratory failure) were recorded for each patient in the two groups.
Results
All patients in the PTGD + LC group successfully underwent PTGD. In the PTGD + LC group, abdominal pain in patients was relieved and leukocyte count, alkaline phosphatase level, total bilirubin and carbohydrate antigen 19-9 (CA19-9) decreased to normal range, and alanine aminotransferase and aspartate aminotransferase levels improved significantly within 72 h after treatment. All patients in the PTGD + LC group underwent LC within 6–10 weeks after PTGD. Our study revealed that PTGD + LC showed a significantly higher efficacy and safety compared to LC alone in AC treatment, as measured by the following parameters: duration of operation, postoperative length of hospital stay, volume of bleeding, conversion rate to laparotomy and complication rate (operation time of LC: 55.6 ± 23.3 min vs. 91.35 ± 25.1 min; hospitalized period after LC: 3.0 ± 1.3 d vs. 7.0 ± 1.7 d; intraoperative bleeding: 28.7 ± 15.2 ml vs. 60.38 ± 16.4 ml; conversion to laparotomy: 3 cases vs. 10 cases; complication: 3 cases vs. 8 cases; all P < 0.05 ).
Conclusion
Our results suggest that B-mode ultrasound-guided PTGD in combination with LC is superior to LC alone for treatment of AC in elderly and high-risk patients, showing multiple advantages of minimal wounding, accelerated recovery, higher safety and efficacy, and fewer complications.
doi:10.1186/s12876-015-0294-2
PMCID: PMC4496925  PMID: 26156691
Percutaneous transhepatic gallbladder drainage; Laparoscopic cholecystectomy; Acute cholecystitis; B-mode ultrasound; Efficacy; Safety
16.  IGF-1 decreases portal vein endotoxin via regulating intestinal tight junctions and plays a role in attenuating portal hypertension of cirrhotic rats 
BMC Gastroenterology  2015;15:77.
Background
Intestinal barrier dysfunction is not only the consequence of liver cirrhosis, but also an active participant in the development of liver cirrhosis. Previous studies showed that external administration of insulin-like growth factor 1 (IGF-1) improved intestinal barrier function in liver cirrhosis. However, the mechanism of IGF-1 on intestinal barrier in liver cirrhosis is not fully elucidated. The present study aims to investigate the mechanisms of IGF-1 improving intestinal barrier function via regulating tight junctions in intestines.
Methods
We used carbon tetrachloride induced liver cirrhotic rats to investigate the effect of IGF-1 on intestinal claudin-1 and occludin expressions, serum alanine transaminase (ALT) and aspartate transaminase (AST) levels, severity of liver fibrosis, portal pressures, enterocytic apoptosis and lipopolysaccharides (LPS) levels in portal vein. The changes of IGF-1 in serum during the development of rat liver cirrhosis were also evaluated. Additionally, we assessed the effect of IGF-1 on claudin-1 and occludin expressions, changes of transepithelial electrical resistance (TEER) and apoptosis in Caco-2 cells to confirm in vivo findings.
Results
Serum IGF-1 levels were decreased in the development of rat liver cirrhosis, and external administration of IGF-1 restored serum IGF-1 levels. External administration of IGF-1 reduced serum ALT and AST levels, severity of liver fibrosis, LPS levels in portal vein, enterocytic apoptosis and portal pressure in cirrhotic rats. External administration of IGF-1 increased the expressions of claudin-1 and occludin in enterocytes, and attenuated tight junction dysfunction in intestines of cirrhotic rats. LPS decreased TEER in Caco-2 cell monolayer. LPS also decreased claudin-1 and occludin expressions and increased apoptosis in Caco-2 cells. Furthermore, IGF-1 attenuated the effect of LPS on TEER, claudin-1 expression, occludin expression and apoptosis in Caco-2 cells.
Conclusions
Tight junction dysfunction develops during the development of liver cirrhosis, and endotoxemia will develop subsequently. Correspondingly, increased endotoxin in portal system worsens tight junction dysfunction via decreasing intestinal occludin and claudin-1 expressions and increasing enterocytic apoptosis. Endotoxemia and intestinal barrier dysfunction form a vicious circle. External administration of IGF-1 breaks this vicious circle. Improvement of tight junctions might be one possible mechanism of the restoration of intestinal barrier function mediated by IGF-1.
doi:10.1186/s12876-015-0311-5
PMCID: PMC4495682  PMID: 26152281
Liver cirrhosis; IGF-1; Tight junction; Intestinal barrier; Apoptosis
17.  HBV genotypes and response to tenofovir disoproxil fumarate in HIV/HBV-coinfected persons 
BMC Gastroenterology  2015;15:79.
Background
Hepatitis B virus (HBV) genotypes can influence treatment outcome in HBV-monoinfected and human immunodeficiency virus (HIV)/HBV-coinfected patients. Tenofovir disoproxil fumarate (TDF) plays a pivotal role in antiretroviral therapy (ART) of HIV/HBV-coinfected patients. The influence of HBV genotypes on the response to antiviral drugs, particularly TDF, is poorly understood.
Methods
HIV/HBV-co-infected participants with detectable HBV DNA prior to TDF therapy were selected from the Swiss HIV Cohort Study. HBV genotypes were identified and resistance testing was performed prior to antiviral therapy, and in patients with delayed treatment response (>6 months). The efficacy of TDF to suppress HBV (HBV DNA <20 IU/mL) and the influence of HBV genotypes were determined.
Results
143 HIV/HBV-coinfected participants with detectable HBV DNA were identified. The predominant HBV genotypes were A (82 patients, 57 %); and D (35 patients, 24 %); 20 patients (14 %) were infected with multiple genotypes (3 % A + D and 11 % A + G); and genotypes B, C and E were each present in two patients (1 %). TDF completely suppressed HBV DNA in 131 patients (92 %) within 6 months; and in 12 patients (8 %), HBV DNA suppression was delayed. No HBV resistance mutations to TDF were found in patients with delayed response, but all were infected with HBV genotype A (among these, 5 patients with genotype A + G), and all had previously been exposed to lamivudine.
Conclusion
In HIV/HBV-coinfected patients, infection with multiple HBV genotypes was more frequent than previously reported. The large majority of patients had an undetectable HBV viral load at six months of TDF-containing ART. In patients without viral suppression, no TDF-related resistance mutations were found. The role of specific genotypes and prior lamivudine treatment in the delayed response to TDF warrant further investigation.
doi:10.1186/s12876-015-0308-0
PMCID: PMC4495698  PMID: 26152237
18.  Intraductal papillary mucinous carcinoma of the pancreas associated with pancreas divisum: a case report and review of the literature 
BMC Gastroenterology  2015;15:78.
Background
Pancreas divisum, the most common congenital anomaly of the pancreas, is caused by failure of the fusion of the ventral and dorsal pancreatic duct systems during embryological development. Although various pancreatic tumors can occur in patients with pancreas divisum, intraductal papillary mucinous neoplasm is rare.
Case presentation
A 77-year-old woman was referred to our hospital because she was incidentally found to have a cystic tumor in her pancreas at a regular health checkup. Contrast-enhanced abdominal computed tomography images demonstrated a cystic tumor in the head of the pancreas measuring 40 mm in diameter with slightly enhancing mural nodules within the cyst. Endoscopic retrograde pancreatography via the major duodenal papilla revealed a cystic tumor and a slightly dilated main pancreatic duct with an abrupt interruption at the head of the pancreas. The orifice of the major duodenal papilla was remarkably dilated and filled with an abundant extrusion of mucin, and the diagnosis based on pancreatic juice cytology was “highly suspicious for adenocarcinoma”. Magnetic resonance cholangiopancreatography depicted a normal, non-dilated dorsal pancreatic duct throughout the pancreas. The patient underwent a pylorus-preserving pancreaticoduodenectomy under the diagnosis of intraductal papillary mucinous neoplasm with suspicion of malignancy arising in the ventral part of the pancreas divisum. A pancreatography via the major and minor duodenal papillae on the surgical specimen revealed that the ventral and dorsal pancreatic ducts were not connected, and the tumor originated in the ventral duct, i.e., the Wirsung’s duct. Microscopically, the tumor was diagnosed as intraductal papillary mucinous carcinoma with microinvasion. In addition, marked fibrosis with acinar cell depletion was evident in the ventral pancreas, whereas no fibrotic change was noted in the dorsal pancreas.
Conclusion
Invasive ductal carcinomas of the pancreas associated with pancreas divisum usually arise from the dorsal pancreas, in which the occurrence of pancreatic cancer may link to underlying longstanding chronic pancreatitis in the dorsal pancreas; however, the histopathogenesis of intraductal papillary mucinous neoplasm in this anomaly is a critical issue that warrants further investigation in future.
doi:10.1186/s12876-015-0313-3
PMCID: PMC4495851  PMID: 26152300
Intraductal papillary mucinous carcinoma; Pancreas; Pancreas divisum; Ventral pancreas
19.  Laparoscopic colonic resection for splenic flexure cancer: our experience 
BMC Gastroenterology  2015;15:76.
Background
The treatment of colon cancer located in splenic flexure is not standardized. Laparoscopic approach is still considered a challenging procedure. This study reviews two Institutions experience in laparoscopic treatment of left colonic flexure cancer. Intraoperative, pathologic and postoperative data from patients undergoing laparoscopic splenic flexure resection were analyzed to assess oncological safety as well as early and medium-term outcomes.
Methods
From October 2005 to May 2014 laparoscopic splenic flexure resection was performed in 23 patients.
Results
Conversion rate was nihil. In 7 cases the anastomosis was performed intracorporeally. Specimen mean length was 21.2 cm, while the distance of distal and proximal resection margin from tumor site was 6.5 and 11.5 respectively. The mean number of harvested lymph nodes was 20.8. Mean operative time was 190 min and mean estimated blood loss was equal to 55 ml. As regard major postoperative complications, one case of postoperative acute pancreatitis and one case of postoperative bleeding from the anastomotic suture line were reported.
Conclusions
Although our experience is limited and appropriate indications must be set by future randomized studies, we believe that laparoscopic resection with intracorporeal anastomosis appears feasible and safe for patients affected by splenic flexure cancer.
doi:10.1186/s12876-015-0301-7
PMCID: PMC4494171  PMID: 26148781
Laparoscopic resection; Colon cancer; Splenic flexure; Intracorporeal anastomosis
20.  Lamina propria macrophage phenotypes in relation to Escherichia coli in Crohn’s disease 
BMC Gastroenterology  2015;15:75.
Background
Abnormal handling of E. coli by lamina propria (LP) macrophages may contribute to Crohn’s disease (CD) pathogenesis. We aimed to determine LP macrophage phenotypes in CD, ulcerative colitis (UC) and healthy controls (HC), and in CD, to compare macrophage phenotypes according to E. coli carriage.
Methods
Mucosal biopsies were taken from 35 patients with CD, 9 with UC and 18 HCs. Laser capture microdissection was used to isolate E. coli-laden and unladen LP macrophages from ileal or colonic biopsies. From these macrophages, mRNA was extracted and cytokine and activation marker expression measured using RT-qPCR.
Results
E. coli-laden LP macrophages were identified commonly in mucosal biopsies from CD patients (25/35, 71 %), rarely in UC (1/9, 11 %) and not at all in healthy controls (0/18). LP macrophage cytokine mRNA expression was greater in CD and UC than healthy controls. In CD, E. coli-laden macrophages expressed high IL-10 & CD163 and lower TNFα, IL-23 & iNOS irrespective of macroscopic inflammation. In inflamed tissue, E. coli-unladen macrophages expressed high TNFα, IL-23 & iNOS and lower IL-10 & CD163. In uninflamed tissue, unladen macrophages had low cytokine mRNA expression, closer to that of healthy controls.
Conclusion
In CD, intra-macrophage E. coli are commonly found and LP macrophages express characteristic cytokine mRNA profiles according to E. coli carriage. Persistence of E. coli within LP macrophages may provide a stimulus for chronic inflammation.
doi:10.1186/s12876-015-0305-3
PMCID: PMC4490755  PMID: 26137941
Crohn’s disease; Escherichia coli; Macrophages
21.  Plasma osteopontin is a biomarker for the severity of alcoholic liver cirrhosis, not for hepatocellular carcinoma screening 
BMC Gastroenterology  2015;15:73.
Background
Implementation of surveillance programs for at-risk populations and identification of biomarkers for early hepatocellular carcinoma (HCC) detection are a major public health goal. Recently, osteopontin (OPN) has attracted attention as a promising biomarker, with some potential advantages compared to alpha-fetoprotein (AFP), but its role in the context of alcoholic cirrhosis has never been assessed. The aims of this study are to assess the utility of plasma OPN in the diagnosis of HCC in alcoholic cirrhotic patients and to investigate whether increased values are due to the tumor or underlying liver disease severity.
Methods
A total of 90 consecutively alcoholic cirrhosis patients, observed between Jun 2013 and May 2014 at a Liver Disease Unit, were included and divided into two groups: 45 without (group I) and 45 with HCC (group II). Plasma levels of OPN (ELISA, Immuno-Biological Laboratories, Gunma, Japan) and AFP (IMMULITE® 2000 AFP, Siemens Healthcare Diagnostics, Tarrytown, New York) were assessed. The diagnostic accuracy of each marker was evaluated using Receiver-Operating Characteristic (ROC) curve analysis (AUC) and its 95 % Confidence Interval (CI).
Results
Plasma OPN levels in group I patients (1176.28 +/–744.59 ng/mL) weren’t significantly different from those of group II (1210.75 +/–800.60 ng/mL) (p = 0.826). OPN levels significantly increased with advancing BCLC tumor stage and with advancing Child-Pugh class, in both groups. Comparing the two groups, AUC for OPN and AFP were 0.51 (95 % CI: 0.39–0.63) and 0.79 (95 % CI: 0.70–0.89), respectively. Based on the ROC analysis, there were no satisfactory cut-off values for OPN that would distinguish patients with from those without tumour.
Conclusions
Despite having a correlation with BCLC stage, the same was observed with progressive deterioration of underlying liver function in terms of Child-Pugh class and MELD score, and isn’t a useful diagnostic biomarker for HCC in alcoholic cirrhotic patients, particularly in the early stages. AFP confirms the performance evidenced in other studies, being superior to OPN. Searching more specific biomarkers for early diagnosis of HCC in alcoholic cirrhosis is still warranted.
doi:10.1186/s12876-015-0307-1
PMCID: PMC4487194  PMID: 26122937
22.  Relation of cholesterol metabolism to pediatric gallstone disease: a retrospective controlled study 
BMC Gastroenterology  2015;15:74.
Background
Cholesterol metabolism may be involved in pediatric gallstone disease. We aimed to reveal cholesterol metabolites and phytosterols and their relation to stone composition of sterols in children having black pigment and cholesterol stones.
Methods
We performed retrospective controlled clinical study, in which we examined parameters of cholesterol metabolism and liver function values in serum (n = 28) and gallstones (n = 46) of consecutively cholecystectomized children. Serum values of age-, body mass index- and sex-matched children (n = 82) and adult gallstones (n = 187) served as controls.
Results
Surrogate markers of cholesterol synthesis in serum (squalene/cholesterol, cholestenol/cholesterol and lathosterol/cholesterol) were 26–52 % higher in both stone subclasses compared to controls (p < 0.05 for all). Respectively, cholestanol/cholesterol and plant sterols campesterol/cholesterol and sitosterol/cholesterol (cholesterol absorption markers) had decreasing order in serum: black pigment stone group > controls > cholesterol stone group (p < 0.05 for all). In black pigment stone group, stone cholestanol/cholesterol was associated with serum bile acids (r = 0.620, p = 0.018). In cholesterol stone group, surrogate markers of cholesterol synthesis in serum (e.g., lathosterol/cholesterol) inversely reflected those of absorption (r-range -0.633–-0.706, p-range 0.036–0.015). In cholesterol stone group, serum and stone lathosterol/cholesterol and cholestanol/cholesterol were positively interrelated (r-range 0.727–0.847, p < 0.05 for both).
Conclusions
Gallstone subclasses shared enhanced cholesterol synthesis. Cholesterol stone children were low cholesterol absorbers with intact homeostasis of cholesterol metabolism. Black pigment stone group was characterized by deteriorated cholesterol metabolism, and accumulation of cholestanol, campesterol and sitosterol in serum and stones suggesting their participation in pathogenesis.
doi:10.1186/s12876-015-0304-4
PMCID: PMC4487209  PMID: 26122832
Black pigment gallstones; Cholesterol gallstones; Non-cholesterol sterols; Plant sterols
23.  Differential hepatotoxicity of dietary and DNL-derived palmitate in the methionine-choline-deficient model of steatohepatitis 
BMC Gastroenterology  2015;15:72.
Background
Saturated fatty acids are toxic to liver cells and are believed to play a central role in the pathogenesis of non-alcoholic steatohepatitis. In experimental steatohepatitis induced by feeding mice a methionine-choline-deficient (MCD) diet, the degree of liver damage is related to dietary sugar content, which drives de novo lipogenesis and promotes the hepatic accumulation of saturated fatty acids. The objective of this study was to determine whether dietary palmitate exerts the same toxicity as carbohydrate-derived palmitate in the MCD model of fatty liver disease.
Methods
We fed mice custom MCS and MCD formulas containing 4 different carbohydrate-fat combinations: starch-oleate, starch-palmitate, sucrose-oleate and sucrose-palmitate.  After 3 wk, we compared their metabolic and disease outcomes.
Results
Mice fed the custom MCD formulas developed varying degrees of hepatic steatosis and steatohepatitis, in the order starch-oleate < starch-palmitate < sucrose-oleate < sucrose-palmitate. Liver injury correlated positively with the degree of hepatic lipid accumulation. Liver injury also correlated positively with the amount of palmitate in the liver, but the relationship was weak. Importantly, mice fed MCD starch-palmitate accumulated as much hepatic palmitate as mice fed MCD sucrose-oleate, yet their degree of liver injury was much lower. By contrast, mice fed MCD sucrose-palmitate developed severe liver injury, worse than that predicted by an additive influence of the two nutrients.
Conclusion
In the MCD model of steatohepatitis, carbohydrate-derived palmitate in the liver is more hepatotoxic than dietary palmitate. Dietary palmitate becomes toxic when combined with dietary sugar in the MCD model, presumably by enhancing hepatic de novo lipogenesis.
doi:10.1186/s12876-015-0298-y
PMCID: PMC4479079  PMID: 26103964
Liver; Fatty liver; Lipotoxicity; Saturated fat; De novo lipogenesis; Macronutrient
24.  Genetic mutations in SPINK1, CFTR, CTRC genes in acute pancreatitis 
BMC Gastroenterology  2015;15:70.
Background
Explanation of the ultimate causes of acute and chronic pancreatitis is challenging. Hence, it is necessary to seek various etiological factors, including genetic mutations that may be of importance in triggering recurrence and progression of acute to chronic pancreatitis. The aim of this study was to determine the frequency of genetic mutations in patients with acute pancreatitis and to investigate their relationship with the etiology and clinical course.
Methods
The study included 221 patients treated for acute pancreatitis and 345 healthy subjects as a control group. Peripheral blood samples were collected from each study participant and genomic DNA was isolated. Genotyping of common mutations in the SPINK1 (p.N34S and p.P55S) and CTRC (p.I259V, p.V235I, p.K247_R254del, p.E225A) genes was performed using the high-resolution melting method. Mutations in the CFTR p.F508del (delF508_CTT) were genotyped using allele-specific amplification polymerase chain reaction. All detected mutations were confirmed with direct capillary DNA sequencing.
Results
Mutations in SPINK 1, CFTR and CTRC were detected in 6.3 %, 2.3 % and 1.8 % of patients with acute pancreatitis versus 3.2 %, 3.8 % and 1.2 % of volunteers in the control group. No relationship was found between the detected mutations and severity of acute pancreatitis: mild acute pancreatitis, mutation of CFTR in 4 (2.8 %) and CTRC in 2 (1.4 %) patients; severe acute pancreatitis, mutation of CFTR and CTRC in 1 (2.6 %) case each. The SPINK1 mutation was significantly more frequent in 8 (10.4 %) severe cases than in 6 (4.2 %) mild cases (P < 0.05), and was observed in 5/70 (7.1 %) patients with alcohol-related AP, 5/81 (6.2 %) with biliary AP, and 4/63 (6.3 %) in those without any established cause of the disease.
Conclusions
Mutation p.N34S in SPINK1 may predispose patients to acute pancreatitis, especially in those abusing alcohol, and may promote a more severe course of the disease.
doi:10.1186/s12876-015-0302-6
PMCID: PMC4476205  PMID: 26100556
Acute pancreatitis; Etiology; SPINK1 mutations; CFTR mutations; CTRC mutations
25.  Massive mesenteric panniculitis due to fibromuscular dysplasia of the inferior mesenteric artery: a case report 
BMC Gastroenterology  2015;15:71.
Background
Fibromuscular dysplasia (FMD) is a nonatheromatous, noninflammatory arterial disorder of unknown etiology resulting in vessel stenosis and/or aneurysm formation. The renal and cephalocervical (mainly carotid arteries) arterial beds are classically involved; involvement of visceral arteries is rare. Mesenteric panniculitis (MP) is an inflammatory process of mesenteric fat considered to be of unknown etiology. The majority of cases involve the small bowel mesentery; colorectal MP is rare. To our knowledge, no example of MP due to FMD has been described.
Case presentation
A 52 year old man presented with steadily worsening lower abdominal pain. Investigation revealed ischemic rectosigmoid mucosa associated with a large mesenteric mass of unknown nature. Angiography showed the disease was limited to the distribution of the inferior mesenteric artery. Subsequent symptoms of large bowel obstruction necessitated a left hemicolectomy. Pathologic examination showed bowel wall necrosis and massive panniculitis of the rectosigmoid due to FMD. Subsequent angiographic imaging of other vascular beds was negative.
Conclusions
Several features of this case are noteworthy: FMD limited to the inferior mesenteric artery has not been previously reported, FMD has not previously been implicated as a cause of MP, and the massive extent of panniculitis. An accompanying literature review of cases of visceral FMD, traditionally believed to almost exclusively affect females, highlights a greater than anticipated number of males (33 %), and a gender difference regarding concomitant involvement of cephalocervical and/or renal vascular beds (32 % in males versus 80 % in females). The latter observation may have implications regarding the value of radiologic screening of other vascular beds, particularly in asymptomatic males, in patients presenting with visceral artery FMD.
Electronic supplementary material
The online version of this article (doi:10.1186/s12876-015-0303-5) contains supplementary material, which is available to authorized users.
doi:10.1186/s12876-015-0303-5
PMCID: PMC4477478  PMID: 26100669
Mesentery; Panniculitis; Fibromuscular dysplasia; Visceral; Inferior mesenteric artery

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