Radiofrequency-assisted transection of the pancreas vs stapler in distal pancreatectomy: a propensity score matched cohort analysis.

To demonstrate the efficacy of radiofrequency for pancreatic stump closure in reducing the incidence of postoperative pancreatic fistula (POPF) in distal pancreatectomy (DP) compared with mechanical transection methods. Despite all the different techniques of pancreatic stump closure proposed for DP, best practice for avoiding POPF remains an unresolved issue, with an incidence of up to 30% regardless of center volume or surgical expertise. DP was performed in a cohort of patients by applying radiofrequency to stump closure (RF Group) and compared with mechanical closure (Control Group). A propensity score (PS) matched cohort study was carried out to minimize bias from nonrandomized treatment assignment. Cohorts were matched by PS accounting for factors significantly associated with either undergoing RF transection or mechanical closure through logistic regression analysis. The primary end-point was the incidence of clinically relevant POPF (CR-POPF). Of 89 patients included in the whole cohort, 13 case patients from the RF-Group were 1:1 matched to 13 control patients. In both the first independent analysis of unmatched data and subsequent adjustment to the overall propensity score-matched cohort, a higher rate of CR-POPF in the Control Group compared with the RF-Group was detected (25.4% vs 5.3%, p = 0.049 and 53.8% vs 0%; p = 0.016 respectively). The RF Group showed better outcomes in terms of readmission rate (46.2% vs 0%, p = 0.031). No significant differences were observed in terms of mortality, major complications (30.8% vs 0%, p = 0.063) or length of hospital stay (5.7 vs 5.2 days, p = 0.89). Findings suggest that the RF-assisted technique is more efficacious in reducing CR-POPF than mechanical pancreatic stump closure.

Gallbladder disease and pancreatic cancer risk: a multicentric case-control European study.

BACKGROUND AND AIMS: The overall evidence on the association between gallbladder conditions (GBC: gallstones and cholecystectomy) and pancreatic cancer (PC) is inconsistent. To our knowledge, no previous investigations considered the role of tumour characteristics on this association. Thus, we aimed to assess the association between self-reported GBC and PC risk, by focussing on timing to PC diagnosis and tumour features (stage, location, and resection). METHODS: Data derived from a European case-control study conducted between 2009 and 2014 including 1431 PC cases and 1090 controls. We used unconditional logistic regression models to estimate odds ratios (ORs) and corresponding 95% confidence intervals (CIs) adjusted for recognized confounders. RESULTS: Overall, 298 (20.8%) cases and 127 (11.6%) controls reported to have had GBC, corresponding to an OR of 1.70 (95% CI 1.33-2.16). The ORs were 4.84 (95% CI 2.96-7.89) for GBC diagnosed <3 years before PC and 1.06 (95% CI 0.79-1.41) for ≥3 years. The risk was slightly higher for stage I/II (OR = 1.71, 95% CI 1.15-2.55) vs. stage III/IV tumours (OR = 1.23, 95% CI 0.87-1.76); for tumours sited in the head of the pancreas (OR = 1.59, 95% CI 1.13-2.24) vs. tumours located at the body/tail (OR = 1.02, 95% CI 0.62-1.68); and for tumours surgically resected (OR = 1.69, 95% CI 1.14-2.51) vs. non-resected tumours (OR = 1.25, 95% CI 0.88-1.78). The corresponding ORs for GBC diagnosed ≥3 years prior PC were close to unity. CONCLUSION: Our study supports the association between GBC and PC. Given the time-risk pattern observed, however, this relationship may be non-causal and, partly or largely, due to diagnostic attention and/or reverse causation.

PET/TC imaging with somatostatin analogues for assessment of neuroendocrine tumors, initial experience. / PET/TC con análogos de la somatostatina en el estudio de tumores neuroendocrinos, experiencia inicial.

PET with somatostatin analogues (SSA PET/CT) enables the detection of cells with overexpression of somatostatin receptors, especially subtypes 2 and 5; this detection is variable depending on the type of molecule used. This is the basis for its use in the study of neuroendocrine tumours (NETs), which are characterized by an overexpression of these receptors in more than 80% of the subtypes. This PET is now being used in our country supported by the good results published by other groups, that were superior to those of other imaging techniques. We present two of the first cases of SSA-PET/CT with 68Ga-edotreotide (SomaKit TOC®) performed in our centre. SSA-PET/CT was the test that finally determined the clinical management of both patients.

Risk of pancreatic cancer associated with family history of cancer and other medical conditions by accounting for smoking among relatives.

Background: Family history (FH) of pancreatic cancer (PC) has been associated with an increased risk of PC, but little is known regarding the role of inherited/environmental factors or that of FH of other comorbidities in PC risk. We aimed to address these issues using multiple methodological approaches. Methods: Case-control study including 1431 PC cases and 1090 controls and a reconstructed-cohort study (N = 16 747) made up of their first-degree relatives (FDR). Logistic regression was used to evaluate PC risk associated with FH of cancer, diabetes, allergies, asthma, cystic fibrosis and chronic pancreatitis by relative type and number of affected relatives, by smoking status and other potential effect modifiers, and by tumour stage and location. Familial aggregation of cancer was assessed within the cohort using Cox proportional hazard regression. Results: FH of PC was associated with an increased PC risk [odds ratio (OR) = 2.68; 95% confidence interval (CI): 2.27-4.06] when compared with cancer-free FH, the risk being greater when ≥ 2 FDRs suffered PC (OR = 3.88; 95% CI: 2.96-9.73) and among current smokers (OR = 3.16; 95% CI: 2.56-5.78, interaction FHPC*smoking P-value = 0.04). PC cumulative risk by age 75 was 2.2% among FDRs of cases and 0.7% in those of controls [hazard ratio (HR) = 2.42; 95% CI: 2.16-2.71]. PC risk was significantly associated with FH of cancer (OR = 1.30; 95% CI: 1.13-1.54) and diabetes (OR = 1.24; 95% CI: 1.01-1.52), but not with FH of other diseases. Conclusions: The concordant findings using both approaches strengthen the notion that FH of cancer, PC or diabetes confers a higher PC risk. Smoking notably increases PC risk associated with FH of PC. Further evaluation of these associations should be undertaken to guide PC prevention strategies.

Inflammatory Bowel Disease and Eating Disorders: A systematized review of comorbidity.

OBJECTIVE: Research has shown that there is an association between Inflammatory Bowel Disease, anxiety and mood disorders, however little is known about their association with Eating Disorders. In this paper we will present a case of a young female with a comorbid diagnosis of Inflammatory Bowel Disease and Eating Disorder, and then discuss the results from a systematic review of the literature, describing published cases of patients with the same condition. METHODS: A systematized review of the literature was conducted according to MOOSE guidelines. A computerized literature search of MEDLINE, PsycINFO and EMBASE, and a manual search through reference lists of selected original articles were performed to identify all published case-reports, case series and studies of Inflammatory Bowel Disease and Eating Disorders. RESULTS: Fourteen articles were included, encompassing 219 cases, including ours. The vast majority were females ranging from 10 to 44years old. Anorexia Nervosa (n=156) and Crohn's Disease (n=129) was the most frequent combination (n=90) reported in the literature. These cases present a poor prognosis because of corticoid refusal, medication abandon and/or deliberate exacerbation of IBD symptoms, in the context of trying to lose weight. CONCLUSION: Recent evidence suggests there is a possible association between Inflammatory Bowel Disease and Eating Disorders, although the mechanisms involved in its ethiopathogenesis are still unknown. To be aware of this association is important because a delayed diagnosis of this comorbidity may lead to worse prognosis. Further research and a multidisciplinary approach could facilitate earlier diagnosis and provide therapeutic interventions.

A systems approach identifies time-dependent associations of multimorbidities with pancreatic cancer risk.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is usually diagnosed in late adulthood; therefore, many patients suffer or have suffered from other diseases. Identifying disease patterns associated with PDAC risk may enable a better characterization of high-risk patients. METHODS: Multimorbidity patterns (MPs) were assessed from 17 self-reported conditions using hierarchical clustering, principal component, and factor analyses in 1705 PDAC cases and 1084 controls from a European population. Their association with PDAC was evaluated using adjusted logistic regression models. Time since diagnosis of morbidities to PDAC diagnosis/recruitment was stratified into recent (<3 years) and long term (≥3 years). The MPs and PDAC genetic networks were explored with DisGeNET bioinformatics-tool which focuses on gene-diseases associations available in curated databases. RESULTS: Three MPs were observed: gastric (heartburn, acid regurgitation, Helicobacter pylori infection, and ulcer), metabolic syndrome (obesity, type-2 diabetes, hypercholesterolemia, and hypertension), and atopic (nasal allergies, skin allergies, and asthma). Strong associations with PDAC were observed for ≥2 recently diagnosed gastric conditions [odds ratio (OR), 6.13; 95% confidence interval CI 3.01-12.5)] and for ≥3 recently diagnosed metabolic syndrome conditions (OR, 1.61; 95% CI 1.11-2.35). Atopic conditions were negatively associated with PDAC (high adherence score OR for tertile III, 0.45; 95% CI, 0.36-0.55). Combining type-2 diabetes with gastric MP resulted in higher PDAC risk for recent (OR, 7.89; 95% CI 3.9-16.1) and long-term diagnosed conditions (OR, 1.86; 95% CI 1.29-2.67). A common genetic basis between MPs and PDAC was observed in the bioinformatics analysis. CONCLUSIONS: Specific multimorbidities aggregate and associate with PDAC in a time-dependent manner. A better characterization of a high-risk population for PDAC may help in the early diagnosis of this cancer. The common genetic basis between MP and PDAC points to a mechanistic link between these conditions.

Meal size can be decreased in obese subjects through pharmacological acceleration of gastric emptying (The OBERYTH trial).

BACKGROUND: Entry of nutrients into the small intestine activates neuro-hormonal signals that regulate food intake through induction of satiation. OBJECTIVE: To evaluate whether caloric intake can be decreased by pharmacologically accelerating gastric emptying (GE) of nutrients into the small intestine. METHODS: Subjects were tested in 2 days, at baseline (day1) and after randomly receiving, in a double-blind manner, a 1 h infusion of erythromycin (3 mg Kg(-1), to accelerate GE) or placebo (day 2). Ad libitum caloric intake and postprandial gastrointestinal symptoms were evaluated using a validated nutrient drink test, simultaneously measuring gastric emptying [corrected] by scintigraphy. Plasma levels of satiation factors were also measured to evaluate their role in the modification of caloric intake and postprandial symptoms. Acceleration of GE was assessed as the difference in percentage emptied between day 2 and day 1 (DGE). The effects of DGE on caloric intake and symptoms were evaluated using multiple (lineal) regression. RESULTS: Among 30 overweight/obese subjects (24F and 6 M), 15 received erythromycin and 15 placebo. The overall median age was 36 years (IQR: 30-42) and body mass index was 30 Kg m(-2) (IQR: 27-36). Subjects receiving erythromycin on day 2 presented accelerated GE as compared with placebo (P = 0.0002). DGE at 15 min after initiating eating had a significant effect on prospective caloric intake (P = 0.004). From the best-fitted regression model (R (2) = 81%, P < 0.0001), a 10% increase in GE at 15 min induced on an average a 135 ± 43.5 Kcal decrease in caloric intake. Postprandial increase in cholecystokinin (CCK) (P = 0.03) and insulin (P = 0.02) was associated with decreased caloric intake. Acceleration of GE at 60 min after initiating eating increased postprandial symptom scores measured 30 min after the completion of food consumption (P = 0.01). Postprandial increase in CCK (P = 0.002) and PP (P = 0.02) was associated with postprandial symptoms. CONCLUSION: Meal size can be reduced in overweight/obese subjects by pharmacologically accelerating GE. This may be a reasonable target in obesity management.