vasoactive-intestinal-peptide and Pancreatitis

Somatostatin is a peptide synthesized in many tissues that can act as a neurotransmitter, a systemic hormone, or a local hormone, and inhibits the secretion of hormones or other cell products. A long-acting synthetic analogue of somatostatin (SMS 201-995) has been developed which when administered subcutaneously has a biologic half-life of 90 to 120 minutes and can be administered 2 or 3 times per day. SMS 201-995 can lower plasma concentrations of growth hormone and somatomedin-C in patients with pituitary acromegaly, but no controlled trials to assess symptomatic response or change in tumor size have been done. In patients with pituitary thyrotropin-producing pituitary tumors, SMS 201-995 has been remarkably effective in producing biochemical and clinical responses and is the drug of first choice in this syndrome when tumor resection is not possible. In patients with the carcinoid syndrome, SMS 201-995 effectively reduces diarrhea, is the best available drug for treatment of carcinoid flush (effective in approximately 90% of cases), and is useful in treating carcinoid crisis. Eighty-five percent of patients with pancreatic islet cell tumors that produce vasoactive intestinal peptide will respond to SMS 201-995 with a reduction in diarrhea that often has been resistant to all other therapy. SMS 201-995 may also be useful in treating the symptoms in some patients with glucagonomas, growth hormone releasing hormone-producing tumors and insulinomas. Whether SMS 201-995 has a significant effect on gut neuroendocrine tumor growth remains uncertain. Certain nonmalignant diseases of the gut respond to somatostatin, including secretory diarrhea and fistulas of unknown cause. In general, SMS 201-995 has proved safe with few significant side effects, but whether the long-term use of the drug will result in an iatrogenic form of the somatostatinoma syndrome is uncertain.

Topics: Acromegaly; Adenoma, Islet Cell; Diarrhea; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Gastrointestinal Neoplasms; Growth Hormone; Humans; Intestinal Fistula; Malignant Carcinoid Syndrome; Octreotide; Pancreatic Neoplasms; Pancreatitis; Pituitary Neoplasms; Thyrotropin; Vasoactive Intestinal Peptide

To investigate the therapeutic effect and mechanism of electroacupuncture (EA) in treating gastrointestinal disorder in acute pancreatitis (AP) patients.. A total of 94 cases of AP patients were divided into acupuncture group (n=56) and control group (n=38). The severity of AP was evaluated according to APACHE II and Balthazar CT scoring system. EA (4 Hz, 4-6 V) was applied to bilateral Zusanli (ST 36), Shangjuxu (ST 37), Xuanzhong (GB 39), Taichong (LR 3), and Gongsun (SP 4) for 60 min, twice a day, 5 days altogether. Total and segmental colonic transit time (CTT) were determined by using ingestion of radiopaque markers (SITZMARKS) according to the modified Metcalf's method, serum motilin (MTL), cholecystokinin (CCK), vasoactive intestinal peptide (VIP) contents were assayed using enzyme linked immunosorbent assay (ELISA).. Compared with normal values, total and segmental CTT of AP patients (control group) increased apparently (P < 0.05), especially in right colon, serum MTL and CCK contents in both control and treatment groups on the 1st day decreased considerably (P < 0.05), while serum VIP levels of both control and treatment groups on the 1st day increased markedly (P < 0.05). In comparison with control group, total and segmental CTT of treatment group decreased significantly (P < 0.05). Auto-comparison of both control and treatment groups showed that serum MTL and CCK contents on day 9 were significantly higher than those on day 1 (P < 0.05), while serum VIP contents on day 9 in these two groups were both obviously lower than those on day 1 (P < 0.05). No significant differences were found between treatment group and control group in serum MTL, CCK and VIP levels on the 9th day after the treatment (P > 0.05).. Acupuncture is able to enhance the gastrointestinal dynamics, improve its motor activity.

Topics: Acute Disease; Adult; Aged; Cholecystokinin; Electroacupuncture; Female; Gastrointestinal Transit; Humans; Male; Middle Aged; Motilin; Pancreatitis; Vasoactive Intestinal Peptide

To investigate the effect of treatment with several vasodilatory substance on the changes in mean arterial pressure (MAP) of severe acute pancreatitis.. Pancreatitis was induced in rats by 5% sodium taurocholate retrograde infusion through the pancreatic duct, which produces a significant decrease in arterial blood pressure.. Three hours after the induction of pancreatitis, a fall of approximately 25 mm Hg in MAP was observed, with no changes of MAP in untreated controls. The administration of the nitric oxide synthesis inhibitor, N-nitro-L-arginine methyl ester (25 mg/kg), previously to the induction of pancreatitis, produced a marked fall in MAP leading to the death of all the animals. When several vasodilatory substances, S-nitroso-N-acetylpenicillamine (200 microg x kg x h), calcitonin gene-related peptide (10 microg/kg), and vasoactive intestinal polypeptide (8 microg x kg x h) were administered previously to the induction of pancreatitis, the MAP fall induced by pancreatitis was not observed. The improvement of physiological conditions observed in vasodilator-treated animals is in agreement with histological data, which show only minor structural changes in the pancreas from these animals, in contrast with the severe alterations observed in untreated pancreatitic rats.. : Vasodilation confers protection against the systemic circulatory derangement derived from the development of severe acute pancreatitis.

Topics: Acute Disease; Amylases; Animals; Blood Pressure; Calcitonin Gene-Related Peptide; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Pancreatitis; Penicillamine; Rats; Rats, Wistar; Shock; Vasoactive Intestinal Peptide; Vasodilator Agents

VIP receptor has been clarified to exist on immune cells, indicating its possible involvement in immunity and inflammatory response. Therefore, we investigated the effects of VIP and selective agonists for 2 subtypes of VIP receptor (VPAC1-R and VPAC2-R agonist) on acute pancreatitis.. Acute pancreatitis was induced in mice by 4 intraperitoneal injections of cerulein and an injection of LPS. VIP, VPAC1-R agonist, VPAC2-R agonist, or secretin (5 nmol/body) was administered 30 minutes before and after the administration of LPS. Serum amylase and cytokine levels were determined, and histologic changes were evaluated. In vitro, IL-6 and TNF-alpha production by monocytes from the spleen was determined under the stimulation of LPS with VIP, VPAC1-R agonist, or VPAC2-R agonist, and the expression of VPAC1-R and VPAC2-R mRNA in monocytes was examined.. VPAC1-R agonist significantly decreased serum amylase, IL-6, and TNF-alpha, whereas VPAC2-R agonist markedly increased serum amylase. Histologically, VIP and VPAC1-R agonist attenuated the severity of pancreatitis, although VPAC2-R agonist or secretin showed no significant effect. In vitro, VPAC1-R and VPAC2-R mRNA were obviously expressed in monocytes. Under the stimulation with LPS, VIP presented a biphasic pattern that once decreased IL-6 production from monocytes and then enhanced at high concentration. VPAC1-R agonist reduced IL-6 levels, whereas VPAC2-R agonist increased IL-6 dose-dependently. VPAC1-R agonist reduced TNF-alpha levels in a dose-dependent manner.. VIP attenuated the experimental acute pancreatitis enzymatically and morphologically by inhibiting proinflammatory cytokine production from monocytes mainly through the VPAC1-R.

Topics: Acute Disease; Amylases; Animals; Ceruletide; Cytokines; Interleukin-10; Interleukin-6; Lipopolysaccharides; Male; Mice; Mice, Inbred BALB C; Monocytes; Pancreas; Pancreatitis; Receptors, Vasoactive Intestinal Peptide, Type II; Receptors, Vasoactive Intestinal Polypeptide, Type I; RNA, Messenger; Severity of Illness Index; Spleen; Tumor Necrosis Factor-alpha; Vasoactive Intestinal Peptide

Pituitary adenylate cyclase activating-peptide (PACAP) is a late member of the secretin/glucagon/vasoactive intestinal peptide (VIP) family of brain-gut peptides. It is unknown whether PACAP takes part in the development of acute pancreatitis and whether PACAP or its antagonists can be used to suppress the progression of acute pancreatitis. We investigated the actions of PACAP and its receptor antagonists in acute pancreatitis on rats.. Acute pancreatitis was induced in rats with caerulein or 3.5% sodium taurocholate. The rats were continuously infused with 5-30 microg/kg PACAP via jugular vein within the first 90 min, while 10-100 microg/kg PACAP6-27 and (4-Cl-D-Phe6, Leu17) VIP (PACAP receptor antagonists) were intravenously infused for 1 h. Biochemical and histopathological assessments were made at 4 h after infusion. Pancreatic and duodenal PACAP concentrations were determined by enzyme-linked immunosorbent assay (ELISA). Chinese ink-perfused pancreas was fixed, sectioned and cleared for counting the functional capillary density.. PACAP augmented caerulein-induced pancreatitis and failed to ameliorate sodium taurocholate-induced pancreatitis. ELISA revealed that relative concentrations of PACAP in pancreas and duodenum were significantly increased in both sodium taurocholate- and caerulein-induced pancreatitis compared with those in normal controls. Unexpectedly, PACAP6-27 and (4-Cl-D-Phe6, Leu17) VIP could induce mild acute pancreatitis and aggravate caerulein-induced pancreatitis with characteristic manifestations of acute hemorrhagic/necrotizing pancreatitis. Functional capillary density of pancreas was interpreted in the context of pancreatic edema, and calibrated functional capillary density (calibrated FCD), which combined measurement of functional capillary density with dry weight/wet weight ratio, was introduced. Hyperemia or congestion, rather than ischemia, characterized pancreatic microcirculatory changes in acute pancreatitis.. PACAP may take part in the pathogenesis of acute pancreatitis in rats. The two PACAP receptor antagonsits might act as partial agonists. Calibrated functional capillary density can reflect pancreatic microcirculatory changes in acute pancreatitis.

Topics: Acute Disease; Animals; Capillaries; Ceruletide; Cholagogues and Choleretics; Disease Models, Animal; Duodenum; Hormone Antagonists; Male; Nerve Growth Factors; Neuropeptides; Neurotransmitter Agents; Pancreas, Exocrine; Pancreatitis; Peptide Fragments; Pituitary Adenylate Cyclase-Activating Polypeptide; Rats; Rats, Wistar; Receptors, Cell Surface; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide; Taurocholic Acid; Vasoactive Intestinal Peptide

Gut-origin bacterial translocation is one of the major causes of pancreatic necrotic tissue infection in patients with severe acute pancreatitis (SAP). The gastrointestinal dysmotility is supposed to be the fundamental event in this process. To test this hypothesis, alteration of colonic transit time (CTT) in patients with acute pancreatitis (AP) was investigated. In order to evaluate the possible mechanisms involved in gastrointestinal dysmotility, changes of serum motilin (MTL), cholecystokinin (CCK) and vasoactive intestinal peptide (VIP) in patients with AP were also measured.. Twenty-four non-consecutive patients with AP and 25 controls were included in this study. The diagnosis of AP was based upon clinical features, biochemical indices and radiological investigation. The severity of AP at admission was evaluated according to the APACHE-II and Balthazar computed tomography (CT) scoring system. Total and segmental CTT in patients with AP and in controls were determined by ingestion of radiopaque markers (Sitzmarks(R)) according to the modified Metcalf's method. Meanwhile, serum MTL and CCK were assessed using radioimmunoassay (RIA), and serum VIP was measured by using ELISA in this study.. Compared to the controls, the total CTT and segmental CTT (mainly right and left hemicolon) were prolonged significantly in 10 patients with SAP and 14 patients with MAP; P < 0.05. Moreover, the total CTT and segmental CTT were markedly more delayed in patients with SAP than in patients with MAP; P < 0.05. The concentrations of serum MTL and CCK were significantly decreased in both MAP and SAP patients compared with those in controls (P < 0.01). There was no significant differences in serum MTL and CCK levels between the SAP and MAP groups; P > 0.05. In addition, the concentration of serum VIP was increased in AP patients, and it reached statistical significance in patients with SAP (P < 0.05).. In conclusion, gastrointestinal dysmotility often occurred in patients with AP, especially more severely in SAP patients. One of the possible mechanisms might be related to the synergic actions of gut hormones, such as MTL, CCK and VIP.

Topics: Acute Disease; Adult; Cholecystokinin; Colon; Enzyme-Linked Immunosorbent Assay; Female; Gastrointestinal Diseases; Gastrointestinal Motility; Gastrointestinal Transit; Humans; Male; Middle Aged; Motilin; Pancreatitis; Radioimmunoassay; Severity of Illness Index; Vasoactive Intestinal Peptide

The histopathology of Fibrocalculous Pancreatic Diabetes (FCPD) has been extensively studied, but there are no reports on alteration in patterns of hormone secreting cells using immunohistochemistry in islets of FCPD patients. In this study, we report on the histopathology and immunohistochemistry of islets of FCPD patients and its possible correlation with the clinical picture. Pancreatic biopsies were carried out in six patients with FCPD at the time of surgery for abdominal pain. Routine histopathology and immunohistochemistry studies were carried out with six primary antibodies namely insulin, glucagon, pancreatic polypeptide (PP), somatostatin, vasoactive intestinal peptide and gastrin. Histopathology of the pancreas showed a spectrum of changes ranging from moderate to severe atrophy, fibrosis of the parenchyma and degeneration of the ducts. Nesidioblastosis was present in three patients. Immunohistochemical studies showed a decrease in the number of islets but some patients showed evidence of hyperplasia. There was an overall decrease in the percent of insulin cells and the positivity in the islets correlated with plasma C-peptide levels and the duration of diabetes. There was no consistent relationship with glucagon with some patients showing increased and other decreased positivity. There was a marked decrease in PP and somatostatin positivity, the significance of which is not clear. The reduction, but partial preservation of insulin positivity is consistent with the ketosis resistance shown by patients with Fibrocalculous Pancreatic Diabetes.

Topics: Adolescent; Adult; Atrophy; Biopsy; Blood Glucose; Chronic Disease; Diabetes Mellitus; Female; Gastrins; Glucagon; Humans; Hyperplasia; Immunohistochemistry; Insulin; Islets of Langerhans; Male; Middle Aged; Pancreas; Pancreatic Ducts; Pancreatic Polypeptide; Pancreatitis; Vasoactive Intestinal Peptide

The distribution and concentration of calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), and gastrin-releasing peptide (GRP) immunoreactivities in the pancreas of cats with experimentally induced chronic pancreatitis and of age- and sex-matched controls were investigated. By narrowing the main pancreatic duct between the head and the body to approximately 25% of its normal diameter, we induced within 5 weeks chronic pancreatitis restricted to the body and tail. In control animals, peptide immunoreactive nerves were distributed to the islets, acini, and ducts; the latter were predominantly innervated by fibers immunoreactive for NPY, VIP, or CGRP. The vasculature received an abundant supply of NPY-, CGRP-, and, to a lesser extent, SP-containing axons. Within intrapancreatic ganglia, peptide immunoreactivities were identified in fibers and ganglion cells, with the exception of CGRP and SP immunostaining, which could be visualized only in fibers. In animals with chronic pancreatitis, the innervation pattern of each peptidergic system was comparable to that described in controls. However, there was a remarkable increase in the density and staining intensity of VIP and NPY immunoreactive fibers in the exocrine parenchyma and fibrous septa of the body and tail, where chronic pancreatitis developed. Fibers immunoreactive for CGRP and SP also were moderately denser than in controls, whereas those containing GRP immunoreactivity did not show any detectable changes. In addition, a marked increase of the immunostaining for VIP and, to a much lesser extent, for NPY and GRP, was observed in neurites supplying the head of the pancreas, which appeared devoid of histologically detectable pathological alterations. Radioimmunoassay analysis confirmed the immunohistochemical observations. The increased density of distinct peptidergic nerves in the pancreas with induced chronic pancreatitis might be the result of compensatory phenomena in response to the inflammatory process.

Topics: Animals; Calcitonin Gene-Related Peptide; Cats; Chronic Disease; Constriction; Female; Gastrin-Releasing Peptide; Immunohistochemistry; Male; Neuropeptide Y; Neuropeptides; Pancreas; Pancreatic Ducts; Pancreatitis; Peptides; Substance P; Tachykinins; Vasoactive Intestinal Peptide

Gastrin releasing peptide (GRP) is known to stimulate pancreatic enzyme and islet hormone secretion. In the present immunohistochemical study, the localization and distribution of GRP-like immunoreactivity were investigated in the human pancreas using two antisera with different specificities. GRP-like immunoreactivity (GRP-LI) was observed in numerous nerve fibers diffusely distributed to the exocrine pancreas, but was not seen in intrapancreatic nerve cells of normal pancreatic specimens examined. Nerve fibers and terminals with GRP-LI were found in abundance around pancreatic acini and capillaries, with moderate density around ductules and in the walls of arterioles, and a few were seen in islets. This distribution pattern was quite similar to that of vasoactive intestinal polypeptide (VIP)-LI nerve fibers. The study, using the antibody elution method, strongly suggests the co-localization of GRP- and VIP-LIs within a part of VIP-containing nerve fibers. In the chronic pancreatitis specimens, neurons with GRP-LI were frequently found, and > 90% of intrapancreatic nerve cells were VIP-immunoreactive. Immunostainings for GRP and for VIP on serial adjacent sections of intrapancreatic ganglia from chronic pancreatitis specimens suggested the co-localization of the two immunoreactivities in > 70% of intrapancreatic neurons. The present findings may provide a morphological basis for neurotransmitter and/or neuromodulator roles of GRP in the human pancreas.

Topics: Antibody Specificity; Bombesin; Chronic Disease; Gastrin-Releasing Peptide; Humans; Immunoenzyme Techniques; Nerve Fibers; Neurons; Neuropeptides; Pancreas; Pancreatitis; Peptides; Reference Values; Vasoactive Intestinal Peptide

Vasoactive intestinal polypeptide was demonstrated in the nerves of the human normal pancreas and in pancreatitis by light microscope immunohistochemical technique. In specimens of normal pancreas, vasoactive intestinal polypeptide-immunoreactive neuronal cells were present in the autonomic ganglia. These ganglia were found to receive an abundant supply of vasoactive intestinal polypeptide-positive fibre plexuses. Immunoreactive nerve fibres were seen to run in the stroma, in association with secretory acini, ducts and blood vessels. Vasoactive intestinal polypeptide-positive fibres were also seen close to the Langerhans' islets, but no vasoactive intestinal polypeptide-like immunoreactivity was observed in the endocrine cells. In specimens from patients affected by pancreatitis, even in lesioned regions, immunoreactive elements were extremely scarce.

Topics: Connective Tissue; Ganglia, Autonomic; Humans; Immunohistochemistry; Neurons; Pancreas; Pancreatitis; Vasoactive Intestinal Peptide

A study was made with different doses of cerulein (2, 4, 10 and 20 micrograms/kg) administered subcutaneously to rats by four injections at intervals of 1 hr; the aim of this work was to study exocrine pancreatic secretion of the rat under cerulein-induced acute pancreatitis, analyzing enzyme and hydroelectrolyte secretion of pancreatic juice. A further aim was to study the relationship between the dose of cerulein and the plasma levels of peptides controlling hydroelectrolyte secretion of the pancreas, like secretin and vasoactive intestinal peptide (VIP). At the lowest dose schedule, the amounts of total protein and enzymes (amylase and trypsin) in pancreatic juice decreased significantly, plasma amylase increased, and the pancreas became edematous. Higher doses magnified these effects. By contrast, ductular function (flow and HCO3-) was well preserved in cerulein-treated rats, and this was probably due to the significant increase in plasma levels of immunoreactive secretin whereas VIP levels were unchanged. The secretin released by treatment with cerulein is able to palliate the lack of flow from acinar origin that is affected in the process of acute pancreatitis, being a beneficial response to the cerulein treatment.

Topics: Acute Disease; Amylases; Animals; Ceruletide; Drug Administration Schedule; Injections, Subcutaneous; Male; Pancreas; Pancreatitis; Rats; Rats, Inbred Strains; Reproducibility of Results; Secretin; Vasoactive Intestinal Peptide

We sought to identify characteristics of peptidergic innervation that altered in patients with chronic pancreatitis. Pancreatic tissue removed from patients with chronic pancreatitis was analyzed by immunohistochemistry using antisera against neuropeptide Y, tyrosine hydroxylase, vasoactive intestinal polypeptide, peptide histidine isoleucine, calcitonin gene-related peptide, and substance P, respectively. In accordance with recent findings, the number and diameter of intralobular and interlobular nerve bundles were found to be increased as compared with control pancreas from organ donors. The striking change in the peptidergic innervation pattern in chronic pancreatitis concerned these altered nerves. It consisted of an intensification of the immunostaining for calcitonin gene-related peptide and substance P in numerous fibers contained in these nerves. Adjacent sections showed that immunoreactive substance P and immunoreactive calcitonin gene-related peptide coexisted in these fibers. Because both of these peptides are generally regarded as pain transmitter candidates, our findings provide further evidence that changes in pancreatic nerves themselves might be responsible for the long-lasting pain syndrome in chronic pancreatitis.

Topics: Adult; Calcitonin Gene-Related Peptide; Chronic Disease; Female; Humans; Male; Nerve Fibers; Neuropeptide Y; Neuropeptides; Pain; Pancreas; Pancreatitis; Peptide PHI; Substance P; Tyrosine 3-Monooxygenase; Vasoactive Intestinal Peptide

A disturbed intraduodenal milieu and pancreatic scarring in advanced chronic pancreatitis (CP) may lead to changes of gut and pancreatic hormones. In the present study, the gastroduodenal mucosal content of several regulatory peptides was determined in 8 patients with severe calcific CP and 8 healthy volunteers. In addition, hormone release into the bloodstream was estimated after intraduodenal acid/glucose stimulation in the control subjects and 8 CP patients each with or without secondary diabetes mellitus (DM), and in 8 patients with juvenile DM, so that disturbed gut hormone release could be attributed either to CP or DM. While VIP release into the circulation was similar in all participants, mucosal levels of VIP and substance P were significantly elevated in the duodenal bulb and descending duodenum of CP patients. The somatostatin content of gastroduodenal mucosa in CP was at least as high as in normals. Gastrin was significantly more abundant only in the duodenal bulb of CP patients, while plasma gastrin was normal. Duodenal CCK concentrations tended to be elevated in the duodenal bulb, but not significantly. The release of secretin seemed to be higher in type-1 diabetics than in CP patients. The mucosal pattern of GIP was nearly identical in CP patients and controls. Compatible with this finding, the GIP release did not show any peculiarities in CP with or without DM or in DM. Basal and stimulated plasma levels of motilin were abnormally high in CP. Pancreatic polypeptide plasma levels were normal in DM, but significantly reduced in CP, especially in CP with DM. Fasting PP and stimulated pancreatic enzyme outputs were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Chronic Disease; Diabetes Mellitus; Female; Gastric Inhibitory Polypeptide; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptides; Humans; Intestinal Mucosa; Male; Middle Aged; Motilin; Neurotensin; Pancreatic Polypeptide; Pancreatitis; Secretin; Somatostatin; Substance P; Vasoactive Intestinal Peptide

Plasma vasoactive intestinal peptide (VIP) concentrations of normal individuals and patients with pancreatitis were studied using a VIP RIA kit. The inter-assay and intra-assay variation of this kit were between 2.1 and 9.4%. The VIP levels increased in the acute phase of acute pancreatitis and patients with chronic pancreatitis. The VIP concentration increased during the first 30 min of glucose tolerance test, but this increase was much smaller than that in insulin. These results suggest that this kit is useful for physiologic and pathologic changes in the VIP level.

Topics: Diabetes Mellitus; Glucose Tolerance Test; Humans; Insulin; Pancreatic Neoplasms; Pancreatitis; Radioimmunoassay; Vasoactive Intestinal Peptide

Topics: Acute Disease; Adult; Aged; Female; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Insulin; Male; Middle Aged; Pancreatic Polypeptide; Pancreatitis; Vasoactive Intestinal Peptide

Topics: Acute Disease; Adolescent; Adult; Duodenal Ulcer; Female; Gastrointestinal Hormones; Hepatitis; Humans; Liver Cirrhosis, Alcoholic; Male; Pancreatitis; Stomach Neoplasms; Vasoactive Intestinal Peptide

A sensitive and specific radioimmunoassay for the detection of vasoactive intestinal peptide has been used to study patients with the watery diarrhea syndrome. In eleven patients the syndrome was associated with tumors, and plasma levels of vasoactive intestinal peptide were elevated. VIP levels returned towards normal in five treated patients coincident with amelioration of symptoms. Normal values were obtained in patinets with chronic pancreatitis, sprue, medullary carcinoma, Zollinger-Ellison Syndrome and laxative abuse. In six other patients with indistinguishable syndrome and no findings of tumor at laparotomy and autopsy, vasoactive intestinal peptide levels were normal. The results suggest that VIP may be the causative agent in patients with the watery diarrhea syndrome and tumors, but that an indistinguishable syndrome exists for which VIP is not the cause.

Topics: Diarrhea; Female; Gastrointestinal Hormones; Humans; Male; Middle Aged; Pancreatectomy; Pancreatic Neoplasms; Pancreatitis; Streptozocin; Syndrome; Vasoactive Intestinal Peptide; Zollinger-Ellison Syndrome

Topics: Cholecystokinin; Duodenum; Humans; Pancreas; Pancreatitis; Secretin; Somatostatin; Vasoactive Intestinal Peptide

A 32-year old patient presented with recurrent pancreatitis, severe watery diarrhea and elevated serum levels of vasoactive intestinal polypeptide. His diarrhea appeared to respond to intramuscular propantheline. Initially he improved but had another attack of pancreatitis while hospitalized. Evaluation by ultrasound revealed the presence of a pseudocyst and endoscopic retrograde pancreatography demonstrated complete occlusion of the main pancreatic duct. Exploratory laparotomy was performed with drainage of a pseudocyst. Analysis of the pseudocyst fluid revealed an elevated amylase, lipase and vasoactive intestinal polypeptide level. It is believed that this patient's severe diarrhea was related to his pancreatitis and pancreatic pseudocyst with elevated levels of vasoactive intestinal polypeptide.

Topics: Adult; Diarrhea; Gastrointestinal Hormones; Humans; Male; Pancreatic Cyst; Pancreatitis; Propantheline; Syndrome; Vasoactive Intestinal Peptide