Pancreatic Exocrine Secretion Research Articles

Lack of Pituitary Adenylate-Cyclase Activating Peptide (PACAP) Receptor Leads to Failure of Active-Ghrelin Suppression after Feeding: ACG/AstraZeneca Fellow Award

Purpose: PACAP is a pituitary and gastrointestinal neuropeptide, which binds with high affinity to the PAC1 receptor and has physiological effects on endocrine and exocrine pancreatic secretions. We previously reported that PAC1 null mice exhibit an obese phenotype compared to wild type (WT) mice. We also demonstrated that PACAP injected intra-peritoneally inhibits appetite in WT mice. This led us to hypothesize that PACAP and PAC1 may regulate the secretion of key gastrointestinal hormones that regulate appetite. Methods: A total of 32 age- and weight-matched PAC1 null (n=16) and WT (n=16) male C57BL/6 mice were included in the study. After 16 hours of overnight fast in a controlled environment, 8/16 randomly selected mice from each of the two groups were subjected to fasting blood draw. The other half in both the groups (8/16) were allowed ad-libitum feeding and blood sampling was conducted 30-60 minutes later for a prandial sample. Levels of active-ghrelin (a-ghrelin), glucagon like peptide-1 (GLP-1), glucagon, insulin, amylin, pancreatic polypeptide (PP) and peptide tyrosine tyrosine (PYY) were determined using Luminex x-MAP technology. Results: The median post-prandial levels of a-ghrelin were significantly different in the two groups; 363 (IQR 185.5-607.5) in PAC1 null vs. 7.9 (IQR 1.9-74) pg/mL (p=0.003) in WT mice. There was no difference in median fasting a-ghrelin levels in PAC1 null 552 (IQR 402-924) as compared to WT mice 381 (IQR 299-602) pg/mL. As expected, PAC1 null mice had significantly lower median fasting [58.1 (IQR, 26.5-104.5) vs. 288 (IQR 256-698) pg/mL (p<0.001) and prandial [135.5 (IQR 93.4-210) vs. 2368.5 (IQR 2178.5-3665.5) pg/mL (p<0.001) insulin, and lower median fasting [7.2 (IQR 5.8-12.6) vs. 13.4 (IQR 13.4-35.2) pg/mL (p=0.03) and prandial [12.2 (IQR 6.1-23.6) vs. 29.9 (IQR 13.4-57.3) pg/mL (p=0.03) levels of glucagon than WT mice. No difference was seen in median PYY levels among PAC1 null as compared to WT mice in both fasting 76.9 (IQR 44.4-124.5) vs. 61.3 (13.7-108) pg/mL and feeding state 76.8 (IQR 49.6-109.7) vs. 94.8 (IQR 62.5-181) pg/mL. There was no significant difference in the levels of GLP-1, PP, and amylin between PAC1 null and WT mice. Conclusion: In mice lacking PAC1 receptor, levels of active ghrelin remained elevated in the post-prandial state in contrast to their wild type counterparts which demonstrated a significant fall in their ghrelin levels after feeding. PACAP plays a key role in appetite regulation and energy homeostasis by suppressing the release of major orexigenic hormone ghrelin. PAC-1 receptor agonist may act as potential therapeutic agent for appetite down-regulation in overweight individuals which merits further investigations.

Modulation of pancreatic exocrine and endocrine secretion

Recent advances in the regulation of pancreatic secretion by secretagogues, modulatory proteins and neural pathways are discussed. Downstream events involved in secretagogue stimulation of pancreatic secretion have been elucidated through characterization of the Src kinase pathway. An additional mechanism regulating vagus nerve effects on the pancreas involves Group II and III metabotropic glutamate receptors that are located presynaptically on certain vagal pancreas-projecting neurons. Hypothalamic neurons perceive glucose and regulate insulin release by direct communication with islets, and activation of proopiomelanocortin neurons by leptin enhances insulin secretion and modulates glucose but not energy homeostasis. Ghrelin and somatostatin mediate glucose-stimulated insulin secretion by differential receptor signaling that is dependent on the amount of ghrelin and state of receptor heterodimerization. Endoplasmic reticulum (ER) stress and loss-of-function mutations of a key ER stress protein are associated with disruption of membrane translocation and reduction in insulin secretion. The importance of hormones, neuropeptides, amino acids, cytokines and regulatory proteins in pancreatic secretion and the pathophysiology of type 2 diabetes are also discussed. The biomolecular pathways regulating pancreatic secretions are still not fully understood. New secretagogues and mechanisms continue to be identified and this information will aid in drug discovery and development of new and improved therapy for pancreatic disorders.

Nutritional management of acute pancreatitis

Enteral nutrition has emerged as one of the most effective treatments in the early management of patients with acute pancreatitis. The original rationale for nutrition in acute pancreatitis, dating back to the mid-20th century, was to provide full nutritional requirements but avoid stimulating exocrine pancreatic secretion. The purpose of this article is to review the recent clinical studies of enteral nutrition in acute pancreatitis to revise the rationale and develop a contemporary conceptual framework for nutritional management of this disease. Several recent randomized controlled trials dispel the outdated concept of 'pancreatic rest', which equates with gut neglect, and offer 'gut rousing' as a preferred concept. The new concept postulates that gastrointestinal (dys)function has a discernible impact on the outcomes of patients with acute pancreatitis. Further, timely administration of appropriate intraluminal modalities prevents or mitigates the gastrointestinal dysfunction. Nutritional management in acute pancreatitis should aim primarily at maintaining the gastrointestinal function. Providing full nutritional requirements and avoiding pancreatic exocrine stimulation should be considered as secondary aims.

The development of fibrosis in a novel model of chronic pancreatitis is mediated by complement factor C5

The development of fibrosis in a novel model of chronic pancreatitis is mediated by complement factor C5

Duodenal application of Li+ in a submaximal therapeutic dose inhibits exocrine pancreatic secretion and modulates gastro-duodenal myoelectrical activity in a conscious pig model

This study tested whether duodenal application of lithium inhibits gastroduodenal motility, and whether it suppresses secretion from the exocrine pancreas. Five suckling pigs, 16-18 days old, were surgically fitted with 3 serosal electrodes on the wall of the gastric antrum and the duodenum for electromyography of smooth muscles, and with a pancreatic duct catheter and a duodenal T-cannula for collection and re-entrant flow of pancreatic juice. After the recovery period, on alternative days, each animal was tested once with an intraduodenal infusion of Li+ (100 mmol·L(-1) C3H5LiO3, 10 mL·kg(-1)·h(-1)) for 1 h, and once with an intraduodenal infusion of NaCl (154 mM, 10 ml·kg(-1)·h(-1)), also for 1 h, with the first treatment, i.e., Li+ or NaCl, randomly assigned. Individual pigs served as their own controls, with data recorded prior to a treatment being used as the baseline. Li+ increased the duration of quiescence (P < 0.05) and activity phase (P < 0.05) in the antrum, thus increasing (P < 0.05) the duration of antral myoelectrical cycles. Li+ shortened (P < 0.05) phase I, but it did not affect phase II or phase III or the MMC in the duodenum. Li+ inhibited pancreatic juice outflow as well as pancreatic enzyme and bicarbonate output (P < 0.05 for all pancreatic parameters).

Prospective randomized trial of the effect of octreotide on pancreatic juice output after pancreaticoduodenectomy in relation to histological diagnosis, duct size and leakage

BackgroundOctreotide is generally administered based on the surgeon's interpretation of perceived risk for pancreatic fistula at the time of pancreaticoduodenectomy (PD). MethodsA single‐institution, prospective randomized trial was conducted between April 2009 and December 2011 involving 62 PD patients who were randomized to receive octreotide (100 μg subcutaneously every 8 h; n = 32) or placebo (n = 30). Pancreatic juice output was measured after the operation using a catheter inserted into the pancreatic duct. Postoperative complications were recorded. ResultsNo significant differences in median output were found between the octreotide (82.5 ml) and placebo (77.5 ml) groups (P = 0.538). Median total output was significantly lower in patients with adenocarcinoma compared with those with periampullary tumours (P = 0.004) and in patients with a duct diameter of >5 mm compared with those with a duct diameter of <5 mm (P = 0.001). There were no significant differences in overall morbidity between the octreotide and placebo groups (P = 0.819). Grade B pancreatic fistula (International Study Group for Pancreatic Fistula) was observed in two and three patients in the octreotide and placebo groups, respectively. ConclusionsMorbidity did not differ significantly between the groups. This study did not demonstrate an inhibitory effect of octreotide on exocrine pancreatic secretion. Based on these results, the routine use of octreotide after PD cannot be recommended.

Pancreatic Exocrine Insufficiency (PEI) in chronic pancreatitis (CP) and cystic fibrosis (CF) patients: Combining clinician insights and existing literature to develop a conceptual model to aid in the identification and management of PEI

Pancreatic Exocrine Insufficiency (PEI) in chronic pancreatitis (CP) and cystic fibrosis (CF) patients: Combining clinician insights and existing literature to develop a conceptual model to aid in the identification and management of PEI

Effects of Ghrelin on the Structural Complexity of Exocrine Pancreas Tissue Architecture

Recent studies have shown that ghrelin increases pancreatic exocrine secretion. However, the potential effects of ghrelin on the morphology of exocrine pancreas (EP) remain unknown. In this work, using fractal analysis, we demonstrate that centrally administered ghrelin increases structural complexity and tissue disorder in rat EP. The study was carried out on a total of 40 male Wistar rats divided into four groups (n = 10): ghrelin-treated animals (average age, 1.5 months), ghrelin-treated animals (8.5 months), and controls (1.5 and 8.5 months). The pancreas tissue sections were stained with hematoxylin/eosin and visualized by light microscopy. For each animal, the average values of tissue fractal dimension, lacunarity, as well as parameters of co-occurrence matrix texture, were determined using tissue digital micrographs. The results indicate that ghrelin administration increases EP fractal dimension and textural entropy, and decreases lacunarity, regardless of the age. To our knowledge, this is the first study to investigate the effects of ghrelin on the morphological properties of pancreatic tissue, and also the first to apply fractal and textural analysis methods in quantification of EP tissue architecture.

Sa1855 Group II Metabotropic Glutamate Receptors in the Dorsal Motor Nucleus of the Vagus (DMV) Mediate Changes in Pancreatic Exocrine Secretion in Acute Pancreatitis

flux. Conclusions: Ethanol alone does not stimulate autophagosome formation due to excessive LC3-II delipidation by Atg4. In contrast, ethanol+ low-dose CR pancreatitis decreases Atg4 and stimulates autophagy. Both ethanol and alcoholic pancreatitis cause lysosomal dysfunction resulting in impaired autophagic flux. The results support our 2-hit hypothesis that a combination of 1) autophagy induction, and 2) lysosomal dysfunction causing impaired autophagic flux, are both critical in the mechanism of alcoholic pancreatitis.

Leucine markedly regulates pancreatic exocrine secretion in goats

Four goats (30.1±1.3kg) with common bile duct re-entrant catheter and duodenal catheter were used to evaluate the effects of duodenal leucine infusion on pancreatic exocrine secretion and plasma parameters with two 4×4 Latin square design experiments. In the long-term infusion experiment, goats were fed twice daily [700g/day, dry matter (DM) basis] at 8:00 and 18:00hours and were duodenally infused with 0, 3, 6, 9g/day leucine for 14days. Pancreatic juice and jugular blood samples were collected over 1-h intervals for 6h daily from d 11 to 14days to encompass a 24-h day. In the short-term experiment, goats were infused leucine for 10h continuously at the same infusion rate with Experiment 1 after feed deprivation for 24h repeated every 10days. Pancreatic juice and blood samples were collected at 0, 1, 2, 4, 6, 8 and 10h of infusion. The results showed that the long-term leucine infusion did not affect pancreatic juice secretion, protein output, trypsin and lipase secretion and plasma insulin concentration, but linearly increased α-amylase secretion. No changes in pancreatic protein and lipase secretion were observed in the short-term infusion. Pancreatic juice and α-amylase secretion responded quadratically, with the greatest values observed in the 3 and 6g/day leucine respectively. Trypsin secretion linearly decreased, while plasma insulin concentration increased linearly with increased leucine infusion. The results demonstrated that duodenal leucine infusion dose and time dependently regulated pancreatic enzyme secretion not associated with the change in plasma insulin concentration.

EXOCRINE PANCREATIC INSUFFICIENCY IN CHILDREN WITH TYPE 1 DIABETES MELLITUS: A NEW PROBLEM OF PEDIATRIC GASTROENTEROLOGY

One of the complications of diabetes mellitus is the development of pancreatic exocrine insufficiency. Fecal elastase 1 is a good marker of pancreatic exocrine secretion. The aim of the study was to evaluate the pancreatic exocrine secretion in children with type 1 diabetes mellitus with fecal elastase 1 test to estimate the possible need for exogenous pancreatic enzyme replacement therapy. The exocrine pancreatic function was evaluated in 54 diabetic children on the basis of steatocrite test and a determination of fecal elastase 1 concentrations. Compared to the controls, the diabetic children had significantly lower levels of fecal elastase 1 concentration (p&lt;0,001). Steatorrhoea was registered in all patients with fecal elastase 1 level &lt; 200 µg/g stool. All those patients were treated with pancreatin (creon) for 1 month. A reduction of fat excretion was observed in the pancreatin treated group at the end of the study. Pancreatin replacement therapy can be used safely in children with type 1 diabetes mellitus associated with exocrine pancreatic insufficiency.

Age-associated changes in pancreatic exocrine secretion of the isolated perfused rat pancreas

Gut functions, such as gastrointestinal motility, gastric secretion and pancreatic secretion, were reduced with age. Glucose tolerance is impaired, and the release of insulin and β-cell's sensitivity on glucose are reduced with age. However, a lot of controversial data have been reported as insulin concentrations after glucose ingestion are either higher or no different in elderly and young subjects. Thus, this study was aimed to investigate whether aging could affect pancreatic exocrine secretion and its action mechanisms. An isolated perfused rat pancreatic model was used to exclude the effects of external nerves or hormones. Pancreatic secretion was increased by CCK under 5.6 mM glucose background in the isolated perfused pancreas of young (3 months), 12 months and 18 months aged rats. There was no significant difference between young and aged rats. In 3 months old rats, CCK-stimulated pancreatic secretion was potentiated under 18 mM glucose background. However, the potentiation effects of endogenous insulin and CCK were not observed in 12 and 18 months old rats. Exogenous insulin also potentiated CCK-stimulated pancreatic secretion in 3 months old rats. Similarly, exogenous insulin failed to potentiate CCK-stimulated pancreatic secretion as that of 3 months old rats. Wet weight of pancreas and amylase content in pancreatic tissue were not changed with age. These results indicate that pancreatic exocrine secretion is reduced with age and endogenous insulin secretion and/or action is involved in this phenomenon.

Role of the vagus in the reduced pancreatic exocrine function in copper-deficient rats

Copper plays an essential role in the function and development of the central nervous system and exocrine pancreas. Dietary copper limitation is known to result in noninflammatory atrophy of pancreatic acinar tissue. Our recent studies have suggested that vagal motoneurons regulate pancreatic exocrine secretion (PES) by activating selective subpopulations of neurons within vagovagal reflexive neurocircuits. We used a combination of in vivo, in vitro, and immunohistochemistry techniques in a rat model of copper deficiency to investigate the effects of a copper-deficient diet on the neural pathways controlling PES. Duodenal infusions of Ensure or casein, as well as microinjections of sulfated CCK-8, into the dorsal vagal complex resulted in an attenuated stimulation of PES in copper-deficient animals compared with controls. Immunohistochemistry of brain stem slices revealed that copper deficiency reduced the number of tyrosine hydroxylase-immunoreactive, but not neuronal nitric oxide synthase- or choline acetyltransferase-immunoreactive, neurons in the dorsal motor nucleus of the vagus (DMV). Moreover, a copper-deficient diet reduced the number of large (>11 neurons), but not small, intrapancreatic ganglia. Electrophysiological recordings showed that DMV neurons from copper-deficient rats are less responsive to CCK-8 or pancreatic polypeptide than are DMV neurons from control rats. Our results demonstrate that copper deficiency decreases efferent vagal outflow to the exocrine pancreas. These data indicate that the combined selective loss of acinar pancreatic tissue and the decreased excitability of efferent vagal neurons induce a deficit in the vagal modulation of PES.

Does secretin add value in pediatric magnetic resonance cholangiopancreatography?

Secretin--a hormone that stimulates pancreatic exocrine secretion--is described to improve visualization of the pancreatic duct by magnetic resonance cholangiopancreatography (MRCP). In our pediatric practice, however, we have not observed substantial benefit with the use of secretin. To determine whether secretin dilates and improves visualization of the pancreatic duct in pediatric MRCP. Retrospective evaluation of secretin-enhanced MRCPs performed over a 15-month period. One reviewer measured the pancreatic duct pre- and post-secretin and two reviewers, blinded to the administration of secretin, assessed image quality and subjective duct visibility. Similar assessments of the biliary tree served as internal controls. We reviewed 20 MRCPs in 17 children. Following secretin administration, there was a small (0.3 mm) but statistically significant increase in pancreatic duct diameter (P = 0.002) and small (<0.2 mm) but significant increase in intrahepatic bile duct diameter (P = 0.0104). On subjective review, there was no significant difference in image quality or duct visibility based on the administration of secretin. Secretin induces dilatation of the pancreatic duct but the value of that effect in pediatric MRCP is suspect given the small change in duct diameter and the lack of improvement in image quality and duct visibility.

Valsartan, a specific angiotensin II receptor blocker, inhibits pancreatic fluid secretion via vagal afferent pathway in conscious rats

Background/aimThe renin–angiotensin system (RAS) exists in the pancreas, but the role of RAS in the regulation of pancreatic exocrine secretion under physiological conditions has been little known. The present study addressed the RAS's effect on the pancreatic secretion by using valsartan, a specific angiotensin II receptor blocker, in conscious rats. MethodMale Wistar rats prepared with pancreatic, biliary, duodenal and jugular vein cannulas were used. To examine the role of RAS in the pancreatic secretion, valsartan at 1, 5, or 25mg/kg was administered into the duodenum via cannula, and volume of pancreatic juice and protein concentration were determined. In addition, to examine the role of RAS in hormone-stimulated pancreatic hypersecretion, pancreatic secretion was examined in response to stimulation of secretin or cholecystokinin after intraduodenal infusion of valsartan at 25mg/kg. Furthermore, to examine the mechanism of action of RAS on pancreatic secretion, intravenous infusion of atropine or perivagal application of capsaicin was conducted and then the pancreatic secretion was examined following intraduodenal infusion of valsartan at 25mg/kg. ResultsVolume of pancreatic juice, but not protein output, significantly decreased after administration of valsartan. However, administration of valsartan did not exert significant effects on secretin- or cholesystokinin-stimulated pancreatic secretion. Treatment with atropine and perivagal application of capsaicin completely abolished the suppressive effect of valsartan on pancreatic juice secretion. ConclusionPresent results suggest that RAS plays a stimulatory role in pancreatic juice secretion via cholinergic afferent pathway without affecting protein secretion and hormonally stimulated pancreatic secretion under physiological conditions.

Pancreatic insulin and exocrine secretion are under the modulatory control of distinct subpopulations of vagal motoneurones in the rat

Brainstem vago-vagal neurocircuits modulate upper gastrointestinal functions. Derangement of these sensory-motor circuits is implicated in several pathophysiological states, such as gastroesophageal reflux disease (GERD), functional dyspepsia and, possibly, pancreatitis. While vagal circuits controlling the stomach have received more attention, the organization of brainstem pancreatic neurocircuits is still largely unknown. We aimed to investigate the in vitro and in vivo modulation of brainstem vagal circuits controlling pancreatic secretion. Using patch clamp techniques on identified vagal pancreas-projecting neurones, we studied the effects of metabotropic glutamate receptor (mGluR) agents in relation to the effects of exendin-4, a glucagon-like peptide 1 analogue, cholecystokinin (CCK) and pancreatic polypeptide (PP). An in vivo anaesthetized rat preparation was used to measure pancreatic exocrine secretion (PES) and plasma insulin following microinjection of metabotropic glutamate receptor (mGluR) agonists and exendin-4 in the brainstem. Group II and III mGluR agonists (2R,4R-4-aminopyrrolidine-2,4-dicarboxylate (APDC) and L(+)-2-amino-4-phosphonobutyric acid (L-AP4), respectively) decreased the frequency of miniature inhibitory and excitatory postsynaptic currents (mIPSCs and mEPSCs, respectively) in the majority of the neurones tested. All neurones responsive to L-AP4 were also responsive to APDC, but not vice versa. Further, in neurones where L-AP4 decreased mIPSC frequency, exendin-4 increased, while PP had no effect upon, mIPSC frequency. Brainstem microinjection of APDC or L-AP4 decreased plasma insulin secretion, whereas only APDC microinjections increased PES. Exendin-4 microinjections increased plasma insulin. Our results indicate a discrete organization of vagal circuits, which opens up promising avenues of research aimed at investigating the physiology of homeostatic autonomic neurocircuits.

Faecal elastase-1 is an independent predictor of survival in advanced pancreatic cancer

BackgroundThe relationship between prognosis of advanced pancreatic cancer and exocrine secretion impairment is unknown. AimTo investigate a possible correlation between faecal elastase-1 value and survival in advanced pancreatic cancer. Methods194 patients with advanced pancreatic cancer were prospectively enrolled between 2007 and 2009 and underwent faecal elastase-1 measurement. Exocrine pancreatic secretion was defined as “moderately reduced” (faecal elastase-1: 100–200μg/g), “severely reduced” (faecal elastase-1<100 and >20μg/g) and “extremely reduced” (faecal elastase-1≤20μg/g). ResultsMedian faecal elastase-1 was 204μg/g (interquartile range 19; 489). Overall, 48 patients (25%) had an extremely reduced exocrine pancreatic secretion, 28 (14%) a severely reduced exocrine pancreatic secretion and 21 (11%) a moderately reduced exocrine pancreatic secretion. Patients with extremely reduced exocrine pancreatic secretion had higher rates of pancreatic head localizations (P<0.01) and of jaundice (P<0.01). Median overall survival was 10.5months. Patients with faecal elastase-1≤20μg/g had a worse prognosis (median survival: 7 versus 11months, P=0.031). Presence of metastases (Hazard ratio 1.81, P<0.0001), haemoglobin≤12g/L (Hazard ratio 2.12, P=0.001), albumin≤40g/L (Hazard ratio 1.64, P=0.010) and FE-1≤20μg/g (Hazard ratio 1.59 P=0.023) resulted as independent predictors of survival in advanced pancreatic cancer patients. ConclusionsA low value of faecal elastase-1 is strongly correlated with a poor survival in advanced pancreatic cancer.

TLQP-21, a VGF-derived peptide, stimulates exocrine pancreatic secretion in the rat

The aims of this paper were to study: (1) the effects of TLQP-21 (non-acronic name), the C-terminal region of the VGF (non-acronic name), polypeptide (from residue 557 to 576 of VGF), on in vitro amylase release from rat isolated pancreatic lobules and acinar cells; (2) the mechanism through which TLQP-21 regulates exocrine pancreatic secretion, by using the muscarinic receptor antagonist atropine (10−6M) and the cyclo-oxygenase inhibitor, indomethacin (10−6M). On pancreatic lobules of rats, concentrations of TLQP-21 from 10−7 to 10−5M significantly (p<0.05) induced a 2–3-fold increase of baseline pancreatic amylase release, measured at the end of 60min incubation period. Co-incubation with atropine 10−6M did not antagonise the enzyme outflow induced by the peptide. On the contrary, co-incubation of TLQP-21 (10−7 and 10−6M) with indomethacin, at concentration of 10−6M, which alone did not modify enzyme secretion, completely suppressed the increase of amylase evoked by TLQP-21 on pancreatic lobules. On rat pancreatic acinar cells, TLQP-21, at all the concentrations tested, was unable to affect exocrine pancreatic secretion, indicating an indirect mechanism of action on acinar cells. These results put in evidence, for the first time, that TLQP-21, a VGF-derived peptide, modulates exocrine pancreatic secretion in rats through a stimulatory mechanism involving prostaglandin release. In conclusion, TLQP-21 could be included among the neurohumoral signals regulating pancreatic exocrine secretion, and increases the knowledge concerning the systems controlling this function.

Pancreatic carcinoma mimicking diffuse‐type autoimmune pancreatitis: Important diagnostic role of pancreatic juice cytology using endoscopic naso‐pancreatic drainage

The occurrence of a diffusely swollen pancreas raises the possibility of several diseases in the differential diagnosis, including autoimmune pancreatitis (AIP), pancreatic lymphoma and whole pancreatic cancer (PC). Diffuse-type AIP, in particular, is characterized by a capsule-like rim, without dilation of the main pancreatic duct (MPD). In this article we report a case of PC that mimicked diffuse-type AIP on ultrasonography (US) and computed tomography (CT) images, which was successfully diagnosed by a cytology of pancreatic juice obtained using endoscopic naso-pancreatic drainage (ENPD).

Pancreaticopleural fistula: etiology, treatment and long-term follow-up

Pancreaticopleural fistula (PPF) are uncommon. Complex multidisciplinary treatment is required due to nutritional compromise and sepsis. This is the first description of long-term follow-up of patients with PPF. Eleven patients with PPF treated at a specialist unit were identified. Causation, investigation, treatment and outcomes were recorded. Pancreatitis was the etiology of the PPF in 9 patients, and in the remaining 2 the PPF developed following distal pancreatectomy. Cross-sectional imaging demonstrated the site of duct disruption in 10 cases, with endoscopic retrograde cholangiopancreatography identifying the final case. Suppression of pancreatic exocrine secretion and percutaneous drainage formed the mainstay of treatment.Five cases resolved following pancreatic duct stent insertion and three patients required surgical treatment for established empyema. There were no complications. In all cases that resolved there has been no recurrence of PPF over a median follow-up of 50 months (range 15-62). PPF is an uncommon event complicating pancreatitis or pancreatectomy; pancreatic duct disruption is the common link. A step-up approach consisting of minimally invasive techniques treats the majority with surgery needed for refractory sepsis.