cholecystokinin and Esophageal-Achalasia

Topics: Anemia, Pernicious; Animals; Cholecystokinin; Esophageal Achalasia; Esophagogastric Junction; Esophagus; Estradiol; Gastric Juice; Gastrins; Glucagon; Humans; Hydrogen-Ion Concentration; In Vitro Techniques; Opossums; Pressure; Progesterone; Secretin; Zollinger-Ellison Syndrome

Topics: Animals; Cholecystokinin; Esophageal Achalasia; Esophagogastric Junction; Gastrins; Gastroesophageal Reflux; Gastrointestinal Motility; Hernia, Diaphragmatic; Humans; Pentagastrin; Pressure; Secretin

Topics: Cholecystokinin; Drug Hypersensitivity; Esophageal Achalasia; Esophagogastric Junction; Gastrins; Gastrointestinal Hormones; Humans; Secretin

Topics: Adult; Aged; Cholecystokinin; Dose-Response Relationship, Drug; Esophageal Achalasia; Esophagogastric Junction; Gastrins; Humans; Middle Aged; Muscle Contraction; Parasympathetic Nervous System

In some patients, the type 3 achalasia (A3) motor pattern may be an effect of chronic use of high-dose opioids. No motor findings have been identified to differentiate opioid-induced A3 (OA3) from idiopathic A3 (IA3). We investigated whether OA3 could be distinguished from IA3 on the basis of differences in esophageal motor responses to amyl nitrite, cholecystokinin, or atropine.. We performed a retrospective study of patients who received pharmacologic provocation during esophageal high-resolution manometry from 2007 through 2017 at a tertiary referral center. We identified 26 patients with IA3 (9 women; mean age, 68 ± 13 years) and 24 patients with OA3 (15 women; mean age, 59 ± 10 years). We compared pressure topography metrics during deglutition and after administration of amyl nitrite, cholecystokinin, or atropine between patients with OA3 vs IA3.. Amyl nitrite induced a similar relaxation response in both groups, but the rebound contraction of the lower esophageal sphincter during amyl nitrite recovery, and the paradoxical esophageal contraction during the first phase of cholecystokinin response, were both significantly attenuated in patients with OA3. The second phase of cholecystokinin response in patients with OA3 was 100% relaxation, when present, in contrast to only 26% of patients with IA3. There was no significant difference between groups in inhibition of lower esophageal sphincter tone or esophageal body contractility by cholinergic receptor blockade.. Nearly half of patients with an A3 pattern of dysmotility are chronic, daily users of opioids with manometry patterns indistinguishable from those of patients with IA3. Patients with OA3 differ from patients with IA3 in responses to amyl nitrite and cholecystokinin. These findings might be used to identify patients with dysmotility resulting from opioid use.

Topics: Aged; Amyl Nitrite; Analgesics, Opioid; Cholecystokinin; Esophageal Achalasia; Esophageal Sphincter, Lower; Female; Humans; Manometry; Middle Aged; Retrospective Studies

Absent esophageal contractility (AC) is distinguished from type 1 achalasia (ACH1) during high-resolution manometry (HRM) on the basis of normal or elevated deglutitive integrated relaxation pressure (IRP) values. However, IRP measurements are subject to pressure recording error. We hypothesized that distinctive responses to pharmacologic provocation using amyl nitrite (AN) and cholecystokinin (CCK) could reliably distinguish AC patients from those with ACH1.. To compare esophageal response with AN and CCK in a well-defined cohort of ACH1 and AC patients.. All available clinical, radiographic, endoscopic, and manometric information in 34 patients with aperistalsis was reviewed to determine the final diagnosis of ACH1 and AC. The differences in response to provocative challenges with the rapid drink challenge (RDC) test and administration of AN and CCK were compared between these two groups.. Eighteen patients were diagnosed with ACH1 and sixteen with AC. While IRP values were significantly higher in ACH1, the standard criterion value misclassified four AC patients as having ACH1 and five ACH1 patients as having AC. IRP values on the RDC did not accurately segregate AC from ACH1, but we were able to identify AN and CCK esophageal motor response criteria that allowed correct classification of ACH1 and AC patients.. Nearly a quarter of AC and ACH1 patients may be misdiagnosed based on manometric IRP criteria alone. Differences in the esophageal motor responses to AN and CCK have the potential to facilitate the correct diagnosis in these challenging patients.

Topics: Adult; Aged; Amyl Nitrite; Cholecystokinin; Diagnosis, Differential; Esophageal Achalasia; Esophageal Motility Disorders; Esophagus; Female; Humans; Male; Manometry; Middle Aged; Muscle Contraction

Because of evidence that the abnormalities in achalasia are not restricted to the distal esophagus, we investigated gallbladder function by cholescintigraphy in the steady state and in response to CCK and the scintigraphic gastric emptying of a liquid caloric meal in 10 individuals with achalasia and 10 normal controls. No abnormalities were found during the filling phase of the gallbladder but seven of the 10 patients showed a 50% reduction in the ejection fraction (39.4% +/- 30.4 vs 80.3 +/- 8.3 of controls, mean +/- SD, P = 0.007) and a slower than normal ejection phase (9.1%/min +/- 6.6 vs 18.1 +/- 4.5, P = 0.02. In eight of the 10 patients, gastric liquid emptying was accelerated with a T1/2 of 41.5 min +/- 15.4 vs 74.7 min +/- 11.5 in the controls (P = 0.007). It is concluded that in some achalasia patients extraesophageal functional abnormalities of the gastrointestinal tract may be found. Whether these findings are promoted by degenerative charges of extraesophageal nerve fibers as well as their clinical significance require further investigations.

Topics: Cholecystokinin; Esophageal Achalasia; Female; Gallbladder; Gastric Emptying; Humans; Imino Acids; Male; Manometry; Middle Aged; Organotechnetium Compounds; Radionuclide Imaging; Technetium Tc 99m Diethyl-iminodiacetic Acid

Autonomic denervation is found throughout the entire length of the digestive tract in Chagas' disease. Anatomic evidence of myenteric ganglia reduction in chagasic gallbladders has been noted; however, the sphincter of Oddi has not been studied. The purpose of this study is twofold: first, to determine sphincter of Oddi pressure in 11 patients with chronic Chagas' disease and megaesophagus, and to compare the results with those obtained in 27 control subjects; and second, to evaluate the effect of cholecystokinin-octapeptide on sphincter of Oddi pressure in both groups of patients. Sphincter of Oddi pressure was recorded continuously via an endoscopically placed triple-lumen catheter inserted into the papilla and directed into the common bile duct. Basal sphincter of Oddi pressure was 12.9 +/- 1.1 mmHg in controls as compared with 44.9 +/- 4.7 mmHg in chagasics with megaesophagus. Mean common bile duct/duodenum gradient pressure was 4.1 +/- 2.4 mmHg in controls as compared with 13.1 +/- 2.7 mmHg in chagasics. Amplitude of sphincter of Oddi phasic contractions in the control group was 102.4 +/- 5.5 mmHg as compared with 140.5 +/- 9.2 mmHg in the chagasic group. Pulse dose of intravenous cholecystokinin-octapeptide produced a decrease of basal sphincter of Oddi pressure with inhibition of sphincter of Oddi phasic contractions in both chagasic and control patients. In chagasic patients, a neural abnormality in the sphincter of Oddi segment could explain the observed high basal pressure and high amplitude of phasic contractions. Chagasic patients with sphincter of Oddi pressure abnormalities, demonstrating sphincter of Oddi relaxation after cholecystokinin-octapeptide, may have neural impairment limited to preganglionic fibers, while the postganglionic inhibitory nerves remain at least partially intact.

Topics: Adolescent; Adult; Ampulla of Vater; Chagas Disease; Cholecystokinin; Common Bile Duct; Esophageal Achalasia; Female; Humans; Male; Manometry; Middle Aged; Peptide Fragments; Pressure; Sincalide; Sphincter of Oddi

Twenty-six patients who had typical symptoms of biliary tract disease, e.g. postprandial right upper quadrant pain, nausea and vomiting, fatty food intolerance and flatulence and who had had two or more normal oral cholecystograms were subjected to cholecytokinin cholescystography. Ten patients showed a normal response to the intravenous administration of cholecystokinin, namely prompt and complete emptying of the gallbladder without producing any adverse reaction or symptoms. Sixteen patients demonstrated either no contraction or incomplete contraction of the gallbladder in response to cholecystokinin; several patients had moderate contraction of the gallbladder accompanied by symptoms of biliary colic. This latter group underwent cholecystectomy and operative cholangiography. Fifteen of the 16 patients are asymptomatic or improved, and only one patient continues to have symptoms. All removed gallbladders had histologic evidence of chronic cholecystitis. It is concluded that in some individuals with continuing symptoms suggesting gallbladder disease but normal oral cholecystograms, cholecystokinin cholecystography may be helpful in identifying physiologic dysfunction of the gallbladder.

Topics: Adult; Aged; Cholecystectomy; Cholecystitis; Cholecystography; Cholecystokinin; Diagnosis, Differential; Esophageal Achalasia; Esophageal Neoplasms; Female; Gallbladder; Gallbladder Diseases; Gastritis; Humans; Male; Middle Aged

Topics: Cholecystokinin; Esophageal Achalasia; Gastrins; Humans; Secretin

Topics: Cholecystokinin; Cholelithiasis; Duodenal Ulcer; Esophageal Achalasia; Gastrins; Gastritis; Gastrointestinal Hormones; Humans; Pancreatic Diseases; Peptic Ulcer; Secretin; Stomach Neoplasms; Stomach Ulcer

Topics: Animals; Calcitonin; Ceruletide; Cholecystokinin; Dogs; Dose-Response Relationship, Drug; Esophageal Achalasia; Esophagogastric Junction; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Manometry; Muscle Tonus; Secretin

Topics: Ampulla of Vater; Animals; Cardia; Cholecystokinin; Dogs; Epinephrine; Esophageal Achalasia; Follicle Stimulating Hormone; Muscle, Smooth; Neostigmine; Norepinephrine; Progesterone; Rabbits; Sensory Receptor Cells; Stimulation, Chemical; Sympathetic Nervous System; Vagotomy