Familial intraductal papillary mucinous neoplasms of the pancreas

The prevalence of intraductal papillary mucinous neoplasms in patients with a high risk of pancreatic adenocarcinoma was estimated to be 15%. However, a familial form of intraductal papillary mucinous neoplasms was never described.MethodsThree families (8 patients) with intraductal papillary mucinous neoplasms familial forms were described. Diagnosis was made according to radiological criteria and was confirmed by pathological data. Genetic predisposing factors of pancreatic cancer were searched for.ResultsSymptoms related to intraductal papillary mucinous neoplasms were recurrent acute pancreatitis (n = 3) or fortuitous discovery (n = 5). Number of cystic lesions was ≤3 (n = 4) or >3 (n = 4). Intraductal papillary mucinous neoplasms involved branch ducts (n = 7) or both main pancreatic duct and branch duct (n = 1). Severe and moderate dysplasia was found on surgical specimens. No genetic alteration was found (BRCA2, p16 or CDKN2A genes).ConclusionA familial form of intraductal papillary mucinous neoplasms was found in three families. No pancreatic cancer was found in relatives but an attentive survey has to be proposed.     

Polychemotherapy or gemcitabine in advanced pancreatic cancer: A meta-analysis

BackgroundGemcitabine monotherapy is the cornerstone of treatment for advanced pancreatic cancer. To date, no clear survival benefit has been found when combination chemotherapy has been compared with gemcitabine alone, except in a few studies. This meta-analysis compared the efficacy of polychemotherapy with gemcitabine alone in advanced pancreatic cancer.MethodsRandomised trials comparing combination chemotherapy with gemcitabine alone were identified through electronic searches of PubMed, EMBASE, Web of Science, and the Cochrane Central Register of Controlled Trials. Overall survival, reported as the hazard ratio at the 95% confidence interval, was the primary outcome measure.Results29 trials (19 phase III and 10 small randomised trials) that included 8421 patients were identified. Overall, polychemotherapy significantly improved overall survival (hazard ratio = 0.87; 95% CI, 0.81–0.93; P < 0.0001), progression-free survival (hazard ratio = 0.77; 95% CI, 0.70–0.84; P < 0.00001), and response rate (risk ratio = 1.71; 95% CI, 1.42–2.07; P < 0.00001) compared with gemcitabine alone.ConclusionsCompared with gemcitabine monotherapy, combinations of two or more drugs (particularly those with novel agents or associated with >20% response rates and triplets) improved outcomes and response rate in advanced pancreatic cancer, and they could be considered a new standard of care in advanced settings.     

Antiproliferative effects of carbon monoxide on pancreatic cancer

BackgroundCarbon monoxide, the gaseous product of heme oxygenase, is a signalling molecule with a broad spectrum of biological activities. The aim of this study was to investigate the effects of carbon monoxide on proliferation of human pancreatic cancer.MethodsIn vitro studies were performed on human pancreatic cancer cells (CAPAN-2, BxPc3, and PaTu-8902) treated with a carbon monoxide-releasing molecule or its inactive counterpart, or exposed to carbon monoxide gas (500 ppm/24 h). For in vivo studies, pancreatic cancer cells (CAPAN-2/PaTu-8902) were xenotransplanted subcutaneously into athymic mice, subsequently treated with carbon monoxide-releasing molecule (35 mg/kg b.w. i.p./day), or exposed to safe doses of carbon monoxide (500 ppm 1 h/day; n = 6 in each group).ResultsBoth carbon monoxide-releasing molecule and carbon monoxide exposure significantly inhibited proliferation of human pancreatic cancer cells (p < 0.05). A substantial decrease in Akt phosphorylation was observed in carbon monoxide-releasing molecule compared with inactive carbon monoxide-releasing molecule treated cancer cells (by 30–50%, p < 0.05). Simultaneously, carbon monoxide-releasing molecule and carbon monoxide exposure inhibited tumour proliferation and microvascular density of xenotransplanted tumours (p < 0.01), and doubled the survival rates (p < 0.005). Exposure of mice to carbon monoxide led to an almost 3-fold increase in carbon monoxide content in tumour tissues (p = 0.006).ConclusionThese data suggest a new biological function for carbon monoxide in carcinogenesis, and point to the potential chemotherapeutic/chemoadjuvant use of carbon monoxide in pancreatic cancer.     

Colonoscopic perforations in inflammatory bowel disease: A retrospective study in a French referral centre

BackgroundWhether inflammatory bowel disease patients are at increased risk of colonoscopic perforations remains controversial. Aim of this study was to investigate whether these patients are at increased risk of perforations.MethodsElectronic charts of all patients enrolled in the Nancy IBD cohort (1999–2012) were reviewed. All non-inflammatory bowel disease patients who underwent colonoscopy (1999–2012) were used as controls.ResultsOf 17,992 colonoscopies, 2375 (13.2%) were performed for inflammatory bowel disease: 1547 for Crohn's disease and 828 for ulcerative colitis. Four IBD patients (0.168%) experienced perforation. Perforation occurred in the sigmoid colon (n = 3) and right colon (n = 1) during disease monitoring or colonic stenosis dilatation. Three patients underwent surgery (2 stomas and no death). Colonoscopic perforation occurred in 16/15,617 controls (0.102%): colonic cancer diagnosis (n = 5, 31.3%) or dilatation (n = 2, 12.5%), polypectomy (n = 5, 31.3%) or mucosectomy (n = 1, 6.3%), and follow-up after diverticulitis (n = 2, 12.5%). Perforation rate was not different between IBD and controls (p = 0.57). Perforations occurred in the sigmoid colon (n = 10, 62.5%), the right colon (n = 4, 25%) and the rectum (n = 2, 12.5%). Twelve controls underwent surgery (9 stomas and one death).ConclusionIn this referral centre-based cohort, inflammatory bowel disease patients were not at increased risk of colonoscopic perforation compared to non-IBD controls.     

Immunohistochemical analysis of metaplastic non-goblet columnar lined oesophagus shows phenotypic similarities to Barrett's oesophagus: A study in an Asian population

BackgroundBarrett's oesophagus is a premalignant condition, predisposing to oesophageal adenocarcinoma. However, some adenocarcinoma may arise in columnar lined oesophagus without goblet cells. Our aim was to evaluate the biological properties of non-goblet columnar lined oesophagus only and elucidate its relationship with Barrett's oesophagus and associated neoplasia.MethodsEndoscopic biopsies from patients with Barrett's oesophagus (n = 30), non-goblet columnar lined oesophagus (n = 14), Barrett's oesophagus associated high grade dysplasia (n = 6) and adenocarcinoma (n = 4) were selected. Immunostaining for villin, claudin 3 and MUC4 was performed. Statistical analysis was performed and a p value <0.05 was considered significant.ResultsVillin and MUC4 were positive in 42%, 100% each and 50% in non-goblet columnar lined oesophagus, Barrett's oesophagus, high grade dysplasia and adenocarcinoma respectively, while claudin 3 was 100% positive in all the groups. In non-goblet columnar lined oesophagus, six cases that were villin immunopositive, showed positive expression for claudin 3 and/or MUC4 and there was no difference from the high grade dysplasia or adenocarcinoma (p > 0.05).ConclusionOur results indicate that a subset of non-goblet columnar lined oesophagus shows an intestinal phenotype representing an early stage of Barrett's oesophagus. This subset probably harbours the potential to change into adenocarcinoma in the long term.     

Central nervous system infection following allogeneic hematopoietic stem cell transplantation

Objective/backgroundHere, we described the clinical characteristics and outcomes of central nervous system (CNS) infections occurring after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in a single institution over the previous 6 years.MethodsCharts of 353 consecutive allogeneic transplant recipients were retrospectively reviewed for CNS infection.ResultsA total of 17 cases of CNS infection were identified at a median of 38 days (range, 10–1028 days) after allo-HSCT. Causative pathogens were human herpesvirus-6 (n = 6), enterococcus (n = 2), staphylococcus (n = 2), streptococcus (n = 2), varicella zoster virus (n = 1), cytomegalovirus (n = 1), John Cunningham virus (n = 1), adenovirus (n = 1), and Toxoplasma gondii (n = 1). The cumulative incidence of CNS infection was 4.1% at 1 year and 5.5% at 5 years.ConclusionMultivariate analysis revealed that high-risk disease status was a risk factor for developing CNS infection (p = .02), and that overall survival at 3 years after allo-HSCT was 33% in patients with CNS infection and 53% in those without CNS infection (p = .04).     

Rural–urban differences in the long-term risk of colorectal cancer after adenoma removal: A population-based study

BackgroundWe investigated the impact of municipality of residence on colonoscopic surveillance and colorectal cancer risk after adenoma resection in a French well-defined administrative area.MethodsThis registry-based study included all patients residing in Côte d’Or (n = 5769) first diagnosed with colorectal adenomas between January 1, 1990, and December 31, 1999. Information about colonoscopic surveillance and colorectal cancer incidence was collected until December 31, 2003.ResultsA rural place of residence reduced the probability of colonoscopic surveillance in men [HR = 0.89 (95%CI: 0.79–0.99), p = 0.041] and in patients without family history of colorectal cancer [HR = 0.91(0.82–0.99), p = 0.044]. After a median follow-up of 7.7 years, 87 patients developed invasive colorectal cancer. After advanced adenoma removal, the standardized incidence ratio for colorectal cancer was 3.03 (95%CI: 1.92–4.54) for rural patients and 1.87 (95%CI: 1.26–2.66) for urban patients compared with the general population. The risk of colorectal cancer was higher in rural patients than in urban ones only after removal of the initial advanced adenoma [HR = 1.73 (95%CI: 1.01–3.00, p = 0.048)]. Further adjustment for surveillance colonoscopy, physician location, and other confounders had little impact on these results.ConclusionThe increased risk of subsequent colorectal cancer after advanced adenoma removal in French rural patients was not explained by a lower rate of colonoscopic surveillance. The role of socio-economic and environmental factors requires further exploration.     

Prognostic value of neutrophil-to-lymphocyte ratio in patients treated with concurrent chemoradiotherapy for locally advanced oesophageal cancer

BackgroundWe performed a retrospective analysis of Asian patients with locally advanced oesophageal cancer to test the hypothesis that an elevated neutrophil-to-lymphocyte ratio is associated with a poor survival rate after definitive concurrent chemoradiotherapy.MethodsIn total, 138 patients diagnosed with locally advanced oesophageal cancer (TNM classification of malignant tumours stage II or III) who were treated with definitive concurrent chemoradiotherapy between January 2005 and December 2010 were retrospectively analysed. Definitive concurrent chemoradiotherapy was performed using two different chemotherapy regimens.ResultsThe median follow-up duration was 39.5 months (range 1.1–93.4). The median progression-free survival was 14.0 months, and the median overall survival was 19.9 months. Compared with the low (<2.0) neutrophil-to-lymphocyte ratio group (n = 43, 31.2%), the high (≥2.0) neutrophil-to-lymphocyte ratio group (n = 95, 68.8%) exhibited significant decreases in the durations of both progression-free survival and overall survival. Using multivariate analysis, an elevated neutrophil-to-lymphocyte ratio was also significantly associated with decreased progression-free survival (HR 1.799; 95% CI, 1.050–3.083; P = 0.032) and overall survival duration (HR 2.115; 95% CI, 1.193–3.749; P = 0.010).ConclusionsThe pretreatment neutrophil-to-lymphocyte ratio is a useful prognostic marker in patients with locally advanced oesophageal cancer treated with definitive concurrent chemoradiotherapy.     

Use of sulphonylurea and cancer in type 2 diabetes—The Hong Kong Diabetes Registry

BackgroundHyperglycaemia is a risk factor for cancer and some sulphonylureas have anti-oxidant properties. This study examined associations between use of sulphonylureas and cancer.MethodsA consecutive cohort of 6103 Hong Kong Chinese patients with T2DM, free of cancer, was analysed using Cox models. Sulphonylurea usage was defined as use of the drugs at or within 2.5 years before enrolment and/or during follow-up periods. We adjusted for identified risk factors of cancer, use of other drugs, non-linear associations of lipids with cancer and probabilities of use of these drugs at different times and doses where appropriate.ResultsDuring a median of 4.91 years of follow-up, 271 developed cancer. Glibenclamide, gliclazide and glipizide were ever used in 32.5% (n = 1983), 47.8% (n = 2920) and 13.5% (n = 823). After adjustment for covariates, use of gliclazide and glibenclamide was associated with reduced cancer risk in a dose-dependent manner. In addition, there were interactions between metformin and glibenclamide/glipizide use towards lower adjusted cancer risks.ConclusionsIn T2DM, use of glibenclamide and gliclazide may be associated with reduced cancer risk.     

Sorafenib does not improve efficacy of chemotherapy in advanced pancreatic cancer: A GISCAD randomized phase II study

BackgroundThe RAF–MEK–ERK pathway is commonly activated in pancreatic cancer because of a high frequency of KRAS-BRAF mutations. A phase II randomized trial was designed to investigate the activity of sorafenib in combination with chemotherapy in advanced pancreatic cancer.MethodsLocally advanced or metastatic pancreatic adenocarcinoma patients were randomized in a 1:1 ratio to receive cisplatin plus gemcitabine with sorafenib 400 mg bid (arm A) or without sorafenib (arm B).ResultsOne hundred and fourteen patients were enrolled; of these, 43 (74.6%) patients progressed in arm A and 44 (82.4%) in arm B. Median progression-free survival was 4.3 months (95% CI: 2.7–6.5) and 4.5 months (95% CI: 2.5–5.2), respectively (HR = 0.92; 95% CI: 0.62–1.35). Median overall survival was 7.5 (95% CI: 5.6–9.7) and 8.3 months (95% CI: 6.2–8.7), respectively (HR = 0.95; 95% CI: 0.62–1.48). Response rates were 3.4% in arm A and 3.6% in arm B.ConclusionsSorafenib does not significantly enhance activity of chemotherapy in advanced pancreatic cancer patients, and therefore should not be assessed in phase III trials.     

Niveles séricos de IGF-1 e IGFBP-3 en pacientes con esófago de Barrett y adenocarcinoma de esófago. Estudio longitudinal

BackgroundBarrett's esophagus (BE) is an entity with a known histological progression to malignancy. The insulin-like growth factor (IGF) system is involved in the carcinogenesis through obesity-related mechanisms that include IGF and it has been associated with several types of cancer.ObjectivesTo evaluate the serological levels of IGF-1 and IGFBP-3 in patients with BE and esophageal adenocarcinoma.Patients and methodsProspective study of patients with BE and esophageal adenocarcinoma who underwent upper endoscopy between September 2012 and December 2015. A baseline determination of IGF-1 and IGFBP-3 was performed. We included a control group of patients without BE.ResultsOne hundred sixteen patients were included: 36 controls, 62 with BE (42 without dysplasia and 20 with dysplasia) and 18 with adenocarcinoma. IGF-1 and IGF-1/IGFBP-3 molar ratio showed a progression to high levels in BE and adenocarcinoma than in controls (IGF-1: 135.55 ± 66.07 ng/ml, 148.33 ± 81.5 ng/ml, 108.19 ± 46.69 ng/ml, respectively; P = .049) (molar ratio: 0.23 ± 0.91, 0.29 ± 0.11, 0.19 ± 0.06, respectively; P = .001), without differences between the histological types of BE. Fifty-four out of the 65 patients with BE were followed up (median of 58.50 months, range 12–113) and 11 of them (20.4%) presented progression to low-grade dysplasia (n = 8) or high-grade dysplasia/adenocarcinoma (n = 3), without differences in the IGF system compared with patients without progression.ConclusionsPatients with BE and esophageal adenocarcinoma have changes in the IGF system although the serological levels of IGF-1 and IGFBP-3 do not correlate with histological progression of BE.     

Insulin use and cancer risk in patients with type 2 diabetes: A systematic review and meta-analysis of observational studies

AimsTo determine whether data from observational studies supports the hypothesis of an increased risk of overall and site-specific cancer among individuals with diabetes using exogenous insulin therapies.MethodsWe conducted a comprehensive search of nine key biomedical databases for all years up to December 2011, restricted to the English language. Data from cohort and nested case-control studies were included in random effects meta-analyses of site-specific and overall cancer incidence comparing ever use and new use of: (1) insulin to no insulin and; (2) insulin glargine to other insulins.ResultsThe search yielded 3052 unique citations, of which 19 were selected for inclusion, representing data for 1,332,120 people and 41,947 cancers. Pancreatic cancer risk was increased among new users of insulin (RR: 3.18, 95%CI: 3.27–3.71, I² = 32%). New use of insulin glargine was associated with an increased risk of pancreatic cancer (RR: 1.63, 95%CI: 1.05–2.51, I² = 0%) and prostate cancers (RR: 2.68, 95%CI: 1.50–4.79, I² = 0%) but a decreased risk of colorectal cancer (RR: 0.78, 95%CI: 0.64–0.94, I² = 15%).ConclusionNew use of insulin or insulin glargine was associated with an increased risk of pancreatic cancer, possibly due to reverse causality. New use of insulin glargine was associated with a decreased risk of colorectal cancer but an increased risk of prostate cancer. Our results should be interpreted with caution due to limitations of included studies.     

The impact of antiviral therapy for HCV on kidney disease: a systematic review and meta-analysis

BackgroundControversy persists about the role of hepatitis C as a risk factor for developing kidney disease in the general population. Some authors have evaluated the effect of antiviral therapy for HCV on the risk of kidney disease.Study Aims and DesignA systematic review of the published medical literature was performed to assess whether antiviral therapy for HCV has an independent impact on kidney survival in the adult general population. A random effects model was used to generate an overall estimate of the risk of kidney disease after anti-HCV therapy across the published studies. Meta-regression and stratified analysis were also carried out.ResultsFifteen studies were eligible (n = 356, 285 patients) and separate meta-analyses were conducted according to the outcome. Pooling studies based on viral responses (n = 7; 34,763 individual patients) demonstrated a relationship between sustained viral response and lower frequency of kidney disease; the overall estimate for adjusted risk of kidney disease was 2.50 (95% CI, 1.41; 4.41) (p = 0.0016) and between-study heterogeneity was found (p-value by Q test = 0.004). Aggregation of studies comparing treated vs untreated cohorts (n = 8, n = 333,312 patients) revealed an association between anti-HCV therapy and lower risk of kidney disease. The overall estimate for adjusted risk of kidney disease across the eight studies was 0.39 (95% CI, 0.25; 0.612) (p = 0.0001). Meta-regression showed that the effectiveness of antiviral therapy in reducing the frequency of kidney disease diminishes as cirrhosis (p = 0.02) and HBV infection (p = 0.0001) increase among HCV-infected individuals.ConclusionsAntiviral therapy for HCV lowers the risk of kidney disease among HCV-infected individuals. Studies to understand the mechanisms underlying this association are ongoing.     

The relationship between Helicobacter pylori and cancer risk

ObjectivesThis study investigated the correlation between Helicobacter pylori (HP) and cancer risk. We compared the age, sex, and comorbidity of cancer patients both infected and not infected by HP.MethodsIn this study, we compared a comparison cohort (N = 24,088) and an HP cohort (N = 6022), both taken from the NHI database. We performed a statistical analysis with the multivariable Cox proportional model to estimate the risk of developing cancer for a comparison and the HP cohort.ResultsOur results showed that the proportion of peptic ulcers in the HP cohort was nearly 4 times higher than that in the comparison cohort. The HP cohort was significantly associated with increased colorectal (HR = 1.73, 95% CI = 1.08–2.77), stomach (HR = 5.21, 95% CI = 2.46–11.05) and pancreatic (HR = 2.77, 95% CI = 1.04–7.39) cancer risks compared to the comparison cohort. In addition, the cancer risk in the HP cohort was considerably higher than that in the comparison cohort when hypertension was absent in both cohorts.ConclusionsIn this study, we proposed a method to investigate the correlation between HP infection and cancer risk. We found that HP infection is associated with the development of colorectal, stomach, and pancreatic cancers, and could thus be an independent carcinogenic risk factor.     

Prognostic factors in patients with non resectable metastatic colorectal cancer in the era of targeted biotherapies: Relevance of Köhne's risk classification

BackgroundKöhne's prognostic classification has been previously proposed, based on performance status, alkaline phosphatase level, number of metastatic sites and white blood cells count.AimsTo identify prognostic factors for survival and to assess the validity of Köhne's classification, in the era of targeted biotherapies, in patients treated with chemotherapy for non resectable metastatic colorectal cancer.MethodsA total of 290 consecutive patients were retrospectively identified in all gastroenterology units of one French county, between 2004 and 2008. Univariate and multivariate analysis for overall survival were performed using pre-treatment patient characteristics.ResultsAll data were available for prognostic categorization in 133 patients. Median survival was 22.1 months. The distribution and median survival for Köhne's prognostic groups were as following: good (n = 73; 24.8 months), intermediate (n = 35; 24.2 months), and poor (n = 25; 7.0 months). The survival difference was significant between good and poor prognostic groups (p < 0.01) and between intermediate and poor prognostic groups (p < 0.01), but not between good and intermediate prognostic groups (p = 0.5). The two independent prognostic factors of survival in multivariate analysis were performance status 0/1 (p < 0.01) and white blood cells count < 10 × 10⁹/L (p < 0.01).ConclusionsThe relevance of Köhne's classification is questioned. A simplified score could be validated by largest studies, based on white blood cells count and performance status.     

Patient and graft survival in pancreas transplant recipients: The EFISPAN study

Introduction and objectivesGraft outcomes in pancreas transplantation have improved in recent decades, but data are mainly derived from registries or prospective single-centre studies. This large epidemiological study was undertaken to investigate the impact of clinical and demographic factors on graft and patient survival in pancreas transplant recipients in Spain, and to provide robust, country-wide, practice-based data to complement registry findings.Patients and methodsWe conducted a retrospective, longitudinal, epidemiological study to assess risk factors impacting patient and graft survival in pancreas transplant recipients in eight centres in Spain. All patients transplanted between 1 January 2008 and 31 December 2012 were included; data were collected until 31 December 2015. The Kaplan–Meier method was used for all time-to-event analyses, including patient survival, graft survival, acute rejection, and BPAR. For graft survival analysis, in cases of death with functioning graft, patients were censored without any event on the date of death. For acute rejection and BPAR, patients were censored without any event on the date of death or graft loss. Univariable and multivariable analyses (Cox proportional hazards model) were conducted to assess the association between baseline clinical and demographic characteristics and patient/graft survival.ResultsData were included for 241 (80.1%) simultaneous pancreas-kidney transplants, 56 (18.6%) pancreas-after-kidney transplants and 4 (1.3%) pancreas transplants alone. Mean ± standard deviation time from diagnosis until transplantation was 26.1 ± 7.5 years. Nineteen patients died, mainly due to infections (n = 10); the remaining 282 patients (93.7%) survived from transplantation until the end of the study. Among 55 patients (18.3%) with pancreas graft loss, the main reasons were vascular thrombosis (n = 19), chronic rejection (n = 10), acute rejection (n = 6) and death with a functioning graft (n = 5). The overall rate of vascular-related death was 1.3% at 5 years post transplant. Univariable analysis showed that patient age and weight, donor age, previous kidney transplantation, previous cardiovascular events and need for insulin more than 48 h post transplantation were significantly associated with pancreas graft survival. Of these, in multivariable analyses pancreas graft survival was inferior in patients who had received a previous kidney transplant prior to pancreas transplantation (log-rank test, p = 0.0002). Glucose metabolism, renal function and cardiovascular risk factors were generally stable following transplantation.ConclusionsThe results of this multicentre study highlight the excellent patient and graft outcomes following pancreas transplantation, with a notably low incidence of cardiovascular events.     

The role of 18fluoro-deoxyglucose positron emission tomography/computed tomography in resectable pancreatic cancer

BackgroundThe role of ¹⁸fluoro-deoxyglucose positron emission tomography/computed tomography in pancreatic ductal adenocarcinoma is debated. We retrospectively assessed the value of ¹⁸fluoro-deoxyglucose positron emission tomography/computed tomography in addition to conventional imaging as a staging modality in pancreatic cancer.Methods¹⁸Fluoro-deoxyglucose positron emission tomography/computed tomography was performed in 72 patients with resectable pancreatic carcinoma after multi-detector computed tomography positron emission tomography was considered positive for a maximum standardized uptake value >3.ResultsOverall, 21% of patients had a maximum standardized uptake value ≤3, and 60% of those had undergone neoadjuvant treatment (P = 0.0001). Furthermore, 11% of patients were spared unwarranted surgery since positron emission tomography/computed tomography detected metastatic disease. All liver metastases were subsequently identified with contrast-enhanced ultrasound. Sensitivity and specificity of positron emission tomography/computed tomography for distant metastases were 78% and 100%. The median CA19.9 concentration was 48.8 U/mL for the entire cohort and 292 U/mL for metastatic patients (P = 0.112).ConclusionsThe widespread application of ¹⁸fluoro-deoxyglucose positron emission tomography/computed tomography in patients with resectable pancreatic carcinoma seems not justified. It should be considered in selected patients at higher risk of metastatic disease (i.e. CA19.9 > 200 U/mL) after undergoing other imaging tests. Neoadjuvant treatment is significantly associated with low metabolic activity, limiting the value of positron emission tomography in this setting.     

The association between ectopic fat in the pancreas and subclinical atherosclerosis in type 2 diabetes

AimsEvidence that pancreatic fat accumulation has a role in obesity, metabolic syndrome and type 2 diabetes mellitus (DM) is emerging. However, data on the influence of pancreatic steatosis on subclinical atherosclerosis are lacking.MethodsWe examined 198 patients with type 2 DM. Pancreatic computed tomography (CT) attenuations were assessed using CT imaging. Obesity was defined as BMI ≥ 25 kg/m² according to the Asian-specific BMI cut-offs. We defined pancreatic steatosis as pancreatic attenuations below median levels.ResultsThe pancreatic attenuations was significantly correlated with age (r = −0.302, p < 0.001), visceral fat area (r = −0.194, p = 0.006) and vascular stiffness (r = −0.242, p = 0.001). In the non-obese group (BMI < 25 kg/m²), pancreatic steatosis was associated with a higher prevalence of carotid artery plaque and vascular stiffness. In the non-obese group, patients with pancreatic steatosis, compared with those without, had an odds ratio (OR) of 3.1 (95% CI 1.2–8.1) for carotid atherosclerosis, after adjusting for age, gender and BMI. However, significant associations between pancreatic steatosis and atherosclerosis were not found in the obese group.ConclusionEctopic fat in the pancreas is strongly associated with carotid atherosclerosis in non-obese subjects with type 2 DM. This finding highlights the importance of pancreatic fat deposits related to a higher risk of cardiovascular disease, especially in non-obese subjects.     

Incidence and clinical course of Crohn's disease during the first year — Results from the IBD Cohort of the Uppsala Region (ICURE) of Sweden 2005–2009

Background and Aims: As a part of the Swedish ICURE study where the epidemiological results of ulcerative colitis and microscopic colitis recently have been published, we hereby present the corresponding figures for Crohn's disease.Methods: All patients diagnosed with Crohn's disease in Uppsala County (305,381 inhabitants) were prospectively registered during 2005–2006 and the same for all new patients with Crohn's disease in Uppsala Region (642,117 inhabitants) during 2007–2009.Results: 264 patients with Crohn's disease were included. The mean annual incidence was 9.9/100,000/year (95% CI: 7.1–12.6). Incidence among children < 17 years was 10.0/100,000/year (95% CI: 3.8–16.3). 51% of the patients had ileal involvement (L1: n = 73, 28%. L2: n = 129, 49%. L3: n = 62, 23%, L4: n = 47, 18%) and 23% had a stricturing or penetrating disease (B1: n = 204, 77%. B2: n = 34, 13%. B3: n = 26, 10%. p: n = 27, 10%). Intestinal resection rate during the first year was 12.5%. Patients with complicated disease had longer symptom duration before diagnosis compared to patients with non-complicated disease (median months 12.0, IQR: 3.0–24.0 vs 4.0, IQR: 2.0–12.0, p = 0.0032). Patients 40 years or older had an increased risk for surgery (HR: 2.03, 95% CI: 1.01–4.08, p = 0.0457).Conclusions: The incidence of Crohn's disease in a region of Sweden is one of the highest reported in Europe. Long symptom duration precedes stricturing or penetrating behaviour. Old age is an independent risk factor for surgery.     

Exposure to radiotherapy for first primary cancer as a risk factor for second primary thyroid cancer: A case-control study

BackgroundSecond primary neoplasms are associated with high mortality and morbidity rates in cancer survivors successfully treated for the first malignancy. Studies suggested an association between the type of first neoplasm and risk of subsequent thyroid cancer, with part of this risk attributable to exposure to radiotherapy during treatment of the first primary tumor. This study aimed to determine whether radiotherapy is a risk factor for thyroid cancer in patients previously treated for another neoplasm.MethodsThis retrospective case-control study included patients diagnosed with their first cancer between 2007 and 2017. Patients who subsequently developed thyroid cancer as a second primary neoplasm were defined as “cases”, and patients who did not develop a second cancer were defined as “controls”. Exposure to radiotherapy was the primary risk factor of interest; other risk factors were the site to which radiotherapy was delivered and the first neoplasm type.ResultsExposure to radiotherapy was associated with an increased risk of thyroid cancer (odds ratio [OR] = 2.410, 95% confidence interval [CI]: 1.219–4.764), in particular, in women (OR = 3.121, 95% CI: 1.232–7.907) and in patients receiving radiotherapy to the thorax (OR = 6.298, 95% CI: 2.581–15.370). The median survival time from first cancer recovery to thyroid cancer occurrence was 63.80 months; there was no difference in survival between patients who did and did not receive radiotherapy (P = 0.899).ConclusionRadiation to the thorax can increase the risk of thyroid cancer as a second neoplasm among patients with cancer successfully treated for their first cancer.