Several reports have described the usefulness of tumor markers detected in pancreatic juice for diagnosis of pancreatic cancer. We performed this study to evaluate the usefulness of tumor markers in pure pancreatic juice collected by duodenoscopic cannulation of pancreatic duct before and after injection of secretin. From April 1993 to July 1995, 8 cases of pancreatic cancer, 5 cases of benign pancreatic lesions, and 5 cases of benign biliary diseases without pancreatic lesion were involved. CEA and CA 19-9 immunoreactivity were measured by radioimmunoassay. Concentrations of CA 19-9 in pure pancreatic juice were significantly higher in patients with pancreatic cancer(median value; 3582, range 88.4-10410 IU/ml) than in control patients(median value 231, range 30.4-682 IU/ml)(p<0.05). Concentrations of CEA in pure pancreatic juice were not significantly different between patients with pancreatic cancer(median value: 6,5, range 1.0-152ng/ml) and control patients(median value: 4.0, range 1-17.2 ng/ml)(p>0.05). There was no significant correlation between levels of CA19-9, CEA in pancreatic juice and those levels in serum. The amounts of juice collected by duodenoscopic cannulation in patients with pancreatic cancer were 1.5+/- 0.9ml during 5 minutes before infusion of secretin, 11.3+/- 3.9ml, 10.8+/- 4.0ml, 10.6+/- 4.0ml in 5 minute interval after infusion of secretin. These results indicated that measurement of CA19-9 in pure pancreatic juice may be used as a marker for pancreatic cancer. Adequate amount of pancreatic juice was collected by duodenoscopic cannulation for evaluation of tumor marker, enzyme studies and cytology.
Catheterization ; Diagnosis ; Humans ; Pancreatic Diseases ; Pancreatic Ducts ; Pancreatic Juice* ; Pancreatic Neoplasms ; Radioimmunoassay ; Secretin ; Biomarkers, Tumor

PURPOSE: This research was done to confirm the effect of secretin on pepsin secretion and to study whether or not feeding can depress the secretin-stimulated pepsin secretion (SSPS) with its related factors. METHODS: Heidenhain (HP) and Pavlov pouches (PP) were made in 6 dogs and cannulae were then inserted into the pouches. The fluids were collected through the cannula every 10 minutes for 3 hours in various conditions, including resting, feeding, secretin perfusion, acidification of the stom-ach and, gastric distension. A modified Anson's hemoglobin method was used to check the amount of pepsin. RESULTS: When secretin was perfused in the HP, there was no increase of pepsin secretion at 0.1 and 0.2 CU/kg/hr, but the pepsin secretion increased at 0.4 and 1.0 CU/kg/hr. Compared to the control, ANOVA showed significant differences for secretin 0.4 CU/kg/hr (P<0.01) and for secretin 1.0 CU/kg/hr (P<0.001). When milk was administered through the gastric cannula after secretin stimulation, pepsin production increased in the PP, but pepsin secretion in the HP dropped close to the basal level after administering milk. This depression was not related to acidity of the milk. ANOVA showed significant differences for secretin with milk vs milk alone (P<0.0005) and vs secretin alone (P<0.0025). The inhibition of SSPS was not observed with any gastric distension or acid perfusion. CONCLUSION: In the HP, secretin increased the pepsin secretion and the vagus nerve has an inhibitory effect on pepsin secretion under secretin stimulation. Milk feeding depressed the SSPS, and that depression was not related to pH of the food and gastric distension. Further study is needed in order to clarify the mechanism of depression.
Animals ; Catheters ; Depression ; Dogs ; Hydrogen-Ion Concentration ; Milk ; Pepsin A* ; Perfusion ; Secretin* ; Vagus Nerve

To clarify the roles of gonadal steroids on pancreatic exocrine secretion, effects of progesterone and estradiol-17beta on spontaneous and secretagogue-induced exocrine response of isolated perfused rat pancreas were investigated. Intra-arterial infusion of progesterone resulted in significant increase of the spontaneous pancreatic fluid and amylase secretion dose-dependently. However, estradiol-17beta did not exert any influence on spontaneous pancreatic exocrine secretion. Exogenous secretin, cholecystokinin (CCK), and acetylcholine markedly stimulated pancreatic fluid and amylase secretion. Progesterone initially enhanced secretin-induced amylase secretion, but this stimulatory response declined thereafter to basal value. Moreover, secretin-induced fluid secretion was not affected by infusion of progesterone. Therefore, initial increase of secretion-induced amylase secretion by progesterone seems to be a non-specific action by washout effect of secretin. Estradiol-17beta failed to change the secretin-induced fluid and amylase secretion. Both progesterone and estradiol-17beta did not exert any influence on CCK-induced fluid and amylase secretion. Acetylcholine-induced exocrine secretion of isolated perfused pancreas also was not affected by intra-arterial infusion of progesterone or estradiol-17beta. It is concluded from the above results that progesterone could enhance the spontaneous pancreatic fluid and amylase secretion of isolated perfused rat pancreas through non-genomic short- term action, and that these effects could be masked by more potent stimulants such as secretin, CCK, and acetylcholine.
Acetylcholine ; Amylases ; Animals ; Cholecystokinin ; Estradiol ; Gonads* ; Infusions, Intra-Arterial ; Masks ; Pancreas* ; Progesterone ; Rats* ; Secretin ; Steroids*

This study was performed to investigate the pancreatic exocrine dysfunction in streptozotocin- induced diabetic rats. Changes in pancreatic enzymes secretion and in pancreatic enzymes content were observed. The output and the tissue content of amylase were significantly reduced in diabetic rats, while the output and the content of lipase were increased. Plasma secretin and cholecystokinin (CCK) concentrations of diabetic rats were significantly increased compared to those of normal rats. The altered pancreatic exocrine function was abolished by the exogenous insulin administration. The exogenous insulin also restored the increased plasma secretin and CCK concentrations. From the above results, it is suggested that, in streptozotocin-induced diabetic rats, anticoordinated changes in pancreatic enzymes secretion as well as pancreatic enzymes content are attributable to insulin deficiency and that the insulin deficiency is responsible for the increased plasma concentrations of both secretin and CCK. However, it is not clear whether the elevated plasma secretin and CCK concentrations played a direct role in changes of pancreatic exocrine function.
Amylases ; Animals ; Cholecystokinin ; Gastrointestinal Hormones* ; Insulin ; Lipase ; Plasma ; Rats* ; Secretin ; Streptozocin

BACKGROUND: The aims of this study were to evaluate the diagnostic value of pancreatic elastase-1(PE-1) in patients with pancreatic diseases and compare the significance of PE-1 with that of pancreatic exocrine function test by pure pancreatic juice (PPJ) collection. METHODS: For evaluation of PE-1, seventy nine patients with pancreatic diseases were examined. For evaluation of exocrine pancreatic function by PPJ, twenty three patients with Chronic pancreatitis(CP) were examined. PPJ was collected by endoscopic cannulation of main pancreatic duct under the intravenous bolus injection of secretin (0.25 CU/kg body weight) and cholecystokinin (CCK, 40 ng/kg body weight). RESULTS: Pancreatic exocrine functions were significantly decreased in patients with CP showing moderate and severe ductal changes on pancreatogram. The mean concentration of fecal PE-1 was significantly decreased in patients with CP and pancreatic cancer, but not in patients with acute pancreatitis. When we analyzed the PE-1 concentration according to Cambridge classification, the concentration of fecal PE-1 was significantly decreased only in patients with moderate and severe CP. With a cut off of 200 ug fecal PE-1/g, the sensitivity of PE-1 was 25%, 60%, and 100%, respectively, for mild, moderate and severe CP, and the specificity was 88.1%. The mean concentration of serum PE-1 was increased both in patients with acute and chronic pancreatitis, but there was no difference between both group. CONCLUSION: Fecal PE-1 is useful for diagnosis of pancreatic exocrine insufficiency in patients with CP, especially in moderate and severe grade of pancreatic exocrine insufficiency. The diagnostic value of fecal PE-1 was also similar to secretin-CCK test in pancreatic exocrine insufficiency.
Catheterization ; Cholecystokinin ; Classification ; Diagnosis ; Humans ; Pancreatic Diseases* ; Pancreatic Ducts ; Pancreatic Juice ; Pancreatic Neoplasms ; Pancreatitis ; Pancreatitis, Chronic ; Secretin ; Sensitivity and Specificity

BACKGROUND/AIMS: The duodenal intubation test (duodenal secretin test; DST) is now considered the 'gold standard' test of exocrine pancreatic function in detecting exocrine pancreatic dysfunction in patients with chronic pancreatitis. However, the DST has not been widely used, because it is time-consuming, invasive, and labor-intensive. On the other hand, intraductal secretin test (IDST) with endoscopic retrograde cannulation of the main pancreatic duct has been showed similar diagnostic efficiency compared with DST. We assessed the clinical usefulness of IDST and investigated parameters for assessing impaired pancreatic function of IDST. METHODS: Pure pancreatic juices were collected from 12 patients with chronic pancreatitis by endoscopic cannulation after a bolus intravenous injection of secretin 100 U, for 15min in three 5-min intervals. Five parameters of IDST were measured, and the sensitivity, specificity, and accuracy of IDST evaluated compared with ERP. RESULTS: When we regarded mean-1.5 SD as the lower limits of IDST, the diagnostic sensitivity, specificity, and accuracy of five parameters to detect chronic pancreatitis were 91.7-100%, 75-87.5%, and 85-90%, respectively. Among five parameters, pancreatic juice secretory volume, bicarbonate concentration, and amylase output showed the highest diagnostic accuracy, followed by lipase output and bicarbonate output. A 10-min collection showed as much information as a 15-min collection. CONCLUSIONS: 10-min intraductal secretin test is useful as the conventional exocrine pancreatic function test in detecting exocrine pancreatic dysfunction in patients with chronic pancreatitis and the most discriminatory parameters are pancreatic juice secretory volume, bicarbonate concentration, and amylase output.
Amylases ; Catheterization ; Hand ; Humans ; Injections, Intravenous ; Intubation ; Lipase ; Pancreatic Ducts ; Pancreatic Function Tests ; Pancreatic Juice ; Pancreatitis, Chronic* ; Secretin* ; Sensitivity and Specificity

gamma-Aminobutyric Acid (GABA) is contained in pancreatic islet beta-cells although its physiological role in pancreatic exocrine function is completely unknown at the present time. Recently, we have reported that exogenous GABA enhances secretagogue-evoked exocrine secretion in the isolated, perfused rat pancreas. This study was aimed to investigate an effect of exogenous GABA on pancreatic exocrine secretion in vivo evoked by intestinal stimulation. Rats were anesthetized with urethane (1.4 g/kg) after 24-h fast with free access to water. GABA (10, 30 and 100micromol/kg/h), given intravenously, did not change spontaneous pancreatic amylase secretion but dose-dependently elevated the amylase secretion evoked by intraduodenal sodium oleate (0.05 mmol/h). GABA (30micromol/kg/h) also further increased the amylase secretion stimulated by CCK+(30 pmol/kg/h) plus secretin (20 pmol/kg/h) but failed to modify the amylase secretion induced by secretin alone. GABA (10, 30 and 100micromol/kg/h) also dose-dependently elevated pancreatic amylase secretion evoked by CCK+alone. Bicuculline (100micromol/kg/h), a GABAA-receptor antagonist, markedly reduced the GABA-enhanced pancreatic responses to sodium oleate, CCK+plus secretin or CCK+alone. The results indicate that GABA enhances the sodium oleate-evoked pancreatic amylase secretion via GABAA-receptors in anesthetized rats, which may account for elevating the action of CCK+released by sodium oleate.
Amylases* ; Animals ; Bicuculline ; Cholecystokinin ; gamma-Aminobutyric Acid* ; Islets of Langerhans ; Oleic Acid* ; Pancreas ; Rats* ; Secretin ; Sodium* ; Urethane ; Water

Autism spectrum disorder (ASD) is characterized by persistent deficits within two core symptom domains: social communication and restricted, repetitive behaviors. Although numerous studies have reported psychopharmacological treatment outcomes for the core symptom domains of ASD, there are not enough studies on fundamental treatments based on the etiological pathology of ASD. Studies on candidate medications related to the pathogenesis of ASD, such as naltrexone and secretin, were conducted, but the results were inconclusive. Oxytocin has been identified as having an important role in maternal behavior and attachment, and it has been recognized as a key factor in the social developmental deficit seen in ASD. Genetic studies have also identified associations between ASD and the oxytocin pathway. As ASD has its onset in infancy, parents are willing to try even experimental or unapproved treatments in an effort to avoid missing the critical period for diagnosis and treatment, which can place their child in an irreversible state. While therapeutic application of oxytocin for ASD is in its early stages, we have concluded that oxytocin would be a promising therapeutic substance via a thorough literature review focusing on the following: the relationship between oxytocin and sociality; single nucleotide polymorphisms as a biological marker of ASD; and validity verification of oxytocin treatment in humans. We also reviewed materials related to the mechanism of oxytocin action that may support its potential application in treating ASD.
Autistic Disorder* ; Child ; Autism Spectrum Disorder* ; Critical Period (Psychology) ; Diagnosis ; Humans ; Maternal Behavior ; Naltrexone ; Oxytocin* ; Parents ; Pathology ; Polymorphism, Single Nucleotide ; Secretin ; Social Change ; Biomarkers

In clinical practice, pharmacological treatment is mostly focused on behavioral symptoms in everyday life. Nevertheless, persistent effort continues to develop medication for causal treatment. Recent changes in diagnostic criteria from Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision (DSM-IV-TR) to DSM-5 would affect not only diagnosing approaches, but also therapeutic approaches. Because previous pervasive developmental disorders have been integrated into a single entity, the autism spectrum disorder (ASD), we have to prepare for what medications are valuable for the ASD. In this article, we reviewed the following etiological treatment: acetylcholine and glutamate related medicine; amino acid medicine such as secretin, endogenous opioid, and oxytocin; complementary and alternative medicine such as chelating agents, vitamins, and omega-3; promising drugs related to the scope of pharmacogenetics currently under study.
Acetylcholine ; Behavioral Symptoms ; Chelating Agents ; Child ; Autism Spectrum Disorder* ; Complementary Therapies ; Diagnostic and Statistical Manual of Mental Disorders ; Drug Therapy* ; Glutamic Acid ; Oxytocin ; Pharmacogenetics ; Secretin ; Vitamins

Pancreatic polypeptie (PP) is released from the pancreas in response to vagal stimulation. Amongst other effects, PP has been reported to inhibit pancreatic exocrine function. Apart from any potential physiological role, such inhibition could have important consequences for in vitro studies of pancreatic function employing acetylcholine as a stimulus. We have therefore tested the effect of bovine PP on two in vitro pancreatic preparations: the incubated, uncinate pancreas of young rats and the perfused cat pancreas. In the former, PP (10(-10)-10(-8)M) had little or no effect on enzyme discharge or45Ca efflux under basal conditions or during stimulation with caerulein, CCK-PZ or acetylcholine. In the perfused cat pancreas, similar concentrations of PP were also without effect on fluid secretion evoked by secretin infusion, or enzyme discharge evoked by CCK-PZ injection or infusion. We conclude that bovine PP has no direct effects on the cellular mechanisms responsible for pancreatic electrolyte secretion or enzyme discharge in the species studied.
Acetylcholine/pharmacology ; Amylases/secretion* ; Animal ; Caerulein/pharmacology ; Calcium/metabolism* ; Cats ; Cholecystokinin/pharmacology ; Electrolytes/secretion* ; In Vitro ; Pancreas/drug effects ; Pancreas/metabolism* ; Pancreatic Polypeptide/pharmacology* ; Perfusion ; Rats ; Secretin/pharmacology