Trends in inflammatory bowel disease and pancreatic cancer: an analysis of the National Inpatient Sample database.

Background: An association between inflammatory bowel disease (IBD) and pancreatic cancer has been suggested in the literature. We aimed to determine the trend in prevalence of pancreatic cancer amongst patients hospitalized for Crohn's disease (CD) or ulcerative colitis (UC) in the United States. Methods: An analysis of the National Inpatient Sample database was performed to identify adults diagnosed with pancreatic cancer and CD or UC, using validated ICD-9 and ICD-10 codes, from 2003-2017. Age, sex, and racial demographics were also collected. Surveillance, Epidemiology and End Results registry (SEER) data were analyzed for trends in the incidence and mortality of pancreatic cancer amongst the general population in the United States. Results: From 2003-2017, there was a significant increase in the hospitalizations related to pancreatic cancer, from 0.11% to 0.19% (PTrend<0.001), representing a 72.73% increase, in CD patients, and from 0.08% to 0.38% (PTrend<0.001), representing a 375.00% increase, in UC patients. According to the SEER 13 data on pancreatic cancer in the general population, the incidence of pancreatic cancer increased from 11.34 per 100,000 cases in 2003 to 12.74 per 100,000 cases in 2017, thus representing only a 12.35% increase over the study period. Conclusions: Our study indicates a trend for increasing prevalence of pancreatic cancer in patients hospitalized with CD and UC from 2003-2017 in the United States. This increasing trend observed in the IBD population parallels the increase in the incidence of pancreatic cancer reported among the general population, but at a much greater rate.

Association of ITM2A rs1751094 polymorphism on X chromosome in Korean pediatric patients with autoimmune thyroid disease.

BACKGROUND: Autoimmune thyroid disease (AITD) manifests with a female predominance, and much attention has been directed towards the integral membrane protein 2 A (ITM2A) gene located on the X chromosome. METHODS: In a study of 166 pediatric patients with autoimmune thyroid disease (AITD), the ITM2A rs1751094 single-nucleotide polymorphism (SNP) was genotyped. The sample comprised 143 females and 23 males, with 67 patients diagnosed with Hashimoto chronic thyroiditis (HD) and 99 with Graves' disease (GD). In the 99 GD patients, 49 (49.5%) exhibited thyroid-associated ophthalmopathy (TAO). Among the 85 GD patients, 70.6% (60/85) were considered intractable GD. The results were compared to those from 198 healthy Korean individuals, including 97 females and 101 males. RESULTS: The frequency of the rs1751094 C allele and CC/AC genotype were higher in AITD, GD and HD patients compared to controls, while the frequency of the A allele and AA genotype were lower. The results were more pronounced in female AITD and GD patients compared to male patients. The association was also found in intractable GD and TAO patients. Target SNP fits Hardy-Weinberg equilibrium. CONCLUSIONS: These findings indicate that the ITM2A gene polymorphism on the X chromosome may contribute to the immunological basis of female-predominant AITD in Korean children.

End-stage renal disease is associated with increased post endoscopic retrograde cholangiopancreatography adverse events in hospitalized patients.

AIM: To determine if end-stage renal disease (ESRD) is a risk factor for post endoscopic retrograde cholangiopancreatography (ERCP) adverse events (AEs). METHODS: We performed a retrospective cohort study using the Nationwide Inpatient Sample (NIS) 2011-2013. We identified adult patients who underwent ERCP using the International Classification of Diseases 9th Revision (ICD-9-CM). Included patients were divided into three groups: ESRD, chronic kidney disease (CKD), and control. The primary outcome was post-ERCP AEs including pancreatitis, bleeding, and perforation determined based on specific ICD-9-CM codes. Secondary outcomes were length of hospital stay, in-hospital mortality, and admission cost. AEs and mortality were compared using multivariate logistic regression analysis. RESULTS: There were 492175 discharges that underwent ERCP during the 3 years. The ESRD and CKD groups contained 7347 and 39403 hospitalizations respectively, whereas the control group had 445424 hospitalizations. Post-ERCP pancreatitis (PEP) was significantly higher in the ESRD group (8.3%) compared to the control group (4.6%) with adjusted odd ratio (aOR) = 1.7 (95%CI: 1.4-2.1, a P < 0.001). ESRD was associated with significantly higher ERCP-related bleeding (5.1%) compared to the control group 1.5% (aOR = 1.86, 95%CI: 1.4-2.4, a P < 0.001). ESRD had increased hospital mortality 7.1% vs 1.15% in the control OR = 6.6 (95%CI: 5.3-8.2, a P < 0.001), longer hospital stay with adjusted mean difference (aMD) = 5.9 d (95%CI: 5.0-6.7 d, a P < 0.001) and higher hospitalization charges aMD = $+82064 (95%CI: $68221-$95906, a P < 0.001). CONCLUSION: ESRD is a risk factor for post-ERCP AEs and is associated with higher hospital mortality. Careful selection and close monitoring is warranted to improve outcomes.

Vipp1 is required for basic thylakoid membrane formation but not for the assembly of thylakoid protein complexes.

Vipp1 (vesicle inducing protein in plastids 1) is found in cyanobacteria and chloroplasts where it is essential for thylakoid formation. Arabidopsis thaliana mutant plants with a reduction of Vipp1 to about 20% of wild type content become albinotic at an early stage. We propose that this drastic phenotype results from an inability of the remaining Vipp1 protein to assemble into a homo-oligomeric complex, indicating that oligomerization is a prerequisite for Vipp1 function. A Vipp1-ProteinA fusion protein, expressed in the Deltavipp1 mutant background, is able to reinstate oligomerization and restore photoautotrophic growth. Plants containing Vipp1-ProteinA in amounts comparable to Vipp1 in the wild type exhibit a wild type phenotype. However, plants with a reduced amount of Vipp1-ProteinA protein are growth-retarded and significantly paler than the wild type. This phenotype is caused by a decrease in thylakoid membrane content and a concomitant reduction in photosynthetic activity. To the extent that thylakoid membranes are made in these plants they are properly assembled with protein-pigment complexes and are photosynthetically active. This strongly supports a function of Vipp1 in basic thylakoid membrane formation and not in the functional assembly of thylakoid protein complexes. Intriguingly, electron microscopic analysis shows that chloroplasts in the mutant plants are not equally affected by the Vipp1 shortage. Indeed, a wide range of different stages of thylakoid development ranging from wild-type-like chloroplasts to plastids nearly devoid of thylakoids can be observed in organelles of one and the same cell.