Duodenal Origin Research Articles

Relationship between entero-hepatic bile acid circulation and interdigestive migrating myoelectrical activity in rats

To investigate the effects of entero-hepatic bile acid circulation on the inter-digestive migrating myoelectrical complex (MMC) in rats. Thirty-two rats were divided into four groups. Three pairs of bipolar silver electrodes were chronically implanted in the antrum, duodenum and jejunum. Three groups of them were ligated around the upper part of common bile duct (CBD). The experiments were performed in conscious and fasting state. The gastrointestinal myoelectrical activity was recorded. Ursodeoxycholic acid (UDCA) and saline were then perfused into stomachs of two groups with CBD obstruction and the effects of them on the MMC were observed. A typical pattern of MMC was observed in normal fasting rats. MMC of antral and duodenal origin disappeared temporarily in earlier stage of CBD obstruction. While MMC of jejunum origin appeared. increased MMC cycle duration was seen after 4 d in rats with CBD obstruction. The MMC after CBD obstruction was characterized by an increased duration of phase II-like activity and decreased duration of phase I and III activity. Perfusion into stomachs with UDCA resulted in a shorter MMC cycle duration and a longer duration of phase III of duodenal origin compared to the normal group. Entero-hepatic bile acid circulation initiates inter-digestive MMC of duodenal origin.

Effects of motilin and ursodeoxycholic acid on gastrointestinal myoelectric activity of different origins in fasted rats.

To investigate gastrointestinal migrating myoelectric complex (MMC) and the effects of porcine motilin and ursodeoxycholic acid (UDCA) on MMC of gastrointestinal tract of different origins in fasted rats. Three bipolar silver electrodes were chronically implanted on the antrum, duodenum and jejunum. Seven days later 24 experimental rats were divided into 2 groups. One group was injected with porcine motilin via sublingual vein at a dose of 20 microg/kg, the other group was perfused into stomach with UDCA. The gastrointestinal myoelectric activity was recorded 1 h before and 2 h after the test substance infusions into the rats. In all fasted rats a typical pattern of MMC was observed. Among the totally 68 activity fronts recorded in fasted rats under control, 67% started in duodenum, and 33% in antrum. MMC cycle duration and duration of phase III of antral origin were longer than those of duodenal origin. Administration of 20 microg/kg porcine motilin induced a premature antral phase III of antral origin. But perfusion into stomach with UDCA resulted in shorter MMC cycle duration, longer duration of phase III of duodenal origin, which were followed with shorter cycle duration and duration of antral phase III. In fasted rats, MMC could originate from antrum and duodenum respectively. The characteristics of MMC of different origins may contribute to the large variations within subjects. The mechanisms of different origins of phase III may be different. Porcine motilin and UDCA could affect MMC of different origins of the gastrointestinal tract in fasted state, respectively.

Xenin-immunoreactive cells and extractable xenin in neuroendocrine tumors of duodenal origin

Background & Aims: Xenin is a 25–amino acid peptide produced by specific endocrine cells of the duodenal mucosa. We investigated whether xenin is expressed in neuroendocrine tumors. Methods: Seventy-two foregut and midgut neuroendocrine tumors were examined by means of immunohistochemistry, confocal laser microscopy with an antibody against the C-terminus of xenin, and high-pressure liquid chromatography after acidic extraction, assessed by radioimmunoassay. Results: We found xenin-immunoreactive cells in 23 of 26 duodenal neuroendocrine tumors, including gastrinomas, somatostatinomas, and nonfunctioning and enterochromaffin cell tumors. In these tumors, up to 20% of the endocrine cells were xenin immunoreactive, and xenin immunoreactivity was concentrated in secretory granules. Xenin was coexpressed with chromogranin A. We found no xenin expression in gastrin-, somatostatin-, and serotonin-immunoreactive cells. High-pressure liquid chromatography after acidic extraction revealed 497 ± 285 pmol of xenin per gram of tissue in 5 duodenal gastrinomas. The other neuroendocrine tumors, such as bronchial carcinoids, gastric enterochromaffin-like cell carcinoids, gastric and ileal enterochromaffin cell carcinoids, insulinomas, and gastrinomas of pancreatic origin, did not contain immunoreactive xenin. Conclusions: Xenin is a peptide marker specific to neuroendocrine tumors of the duodenum. This finding may be useful in tumor classification and in the differential diagnosis of neuroendocrine tumors of the upper gut.GASTROENTEROLOGY 2002;123:1616-1626

Migrating motor complex cycle duration is determined by gastric or duodenal origin of phase III.

The migrating motor complex (MMC) shows large variations within an individual and between individuals. This study aimed to investigate, with respect to this variability, the importance of gastric or duodenal origin of phase III activity. Interdigestive 6- to 10-h stationary antroduodenal motility recordings of 19 healthy male subjects were analyzed for MMC cycle durations and duration of phases I, II, and III, all with respect to the place of origin of each phase III. Data are given for the duodenal recording site as means +/- SE. Mean MMC cycle duration was 117.3 +/- 13.9 min, regardless of the place of origin of phase III. Seventy-two phase III cycles were observed in total, 35 and 37 starting in the "antrum" and duodenum, respectively. After a phase III of "antral" origin, MMC cycle duration was 156.1 +/- 11.0 min, significantly longer than MMC cycle duration following a phase III of duodenal origin, 80.5 +/- 10.7 min (P < 0.001). Phase III duration was longer when of "antral" origin than when starting in the duodenum (7.6 +/- 0.4 and 5.3 +/- 0.4 min, respectively; P < 0.001). MMC cycle duration and duration of phases I, II, and III depend on the place of origin of phase III ("antral" or duodenal) and on the origin of the preceding phase III. This factor explains part of the MMC variability observed within individuals. Mean MMC cycle duration in healthy subjects or patients should therefore also include information on the origin of phase III.

Thirty-Year Survival with an Untreated Malignant Duodenal Somatostatinoma.

Gastrointestinal somatostatinomas are rare. Only 56 cases with duodenal origin have been reported in the literature. The long-term course of an untreated tumor like this is unknown. We report a case of a male patient who lived 30 yr with an untreated metastatic duodenal somatostatinoma. This case suggests that a duodenal somatostatinoma may be of low malignant potential and that expectancy when treating this tumor might be indicated.

Mixed reflux of gastric and duodenal juices is more harmful to the esophagus than gastric juice alone. The need for surgical therapy re-emphasized.

The author's goal was to determine the role of duodenal components in the development of complications of gastroesophageal reflux disease. There is a disturbing increase in the prevalence of complications, specifically the development of Barrett's esophagus among patients with gastroesophageal reflux disease. Earlier studies using pH monitoring and aspiration techniques have shown that increased esophageal exposure to fluid with a pH above 7, that is, of potential duodenal origin, may be an important factor in this phenomenon. The presence of duodenal content in the esophagus was studied in 53 patients with gastroesophageal reflux disease confirmed by 24-hour pH monitoring. A portable spectrophotometer (Bilitec 2000, Synectics, Inc.) with a fiberoptic probe was used to measure intraluminal bilirubin as a marker for duodenal juice in the esophagus. Normal values for bilirubin monitoring were established for 25 healthy subjects. In a subgroup of 22 patients, a custom-made program was used to correlate simultaneous pH and bilirubin absorbance readings. Fifty-eight percent of patients were found to have increased esophageal exposure to gastric and duodenal juices. The degree of mucosal damage increased when duodenal juice was refluxed into the esophagus, in that patients with Barrett's metaplasia (n = 27) had a significantly higher prevalence of abnormal esophageal bilirubin exposure than did those with erosive esophagitis (n = 10) or with no injury (n = 16). They also had a greater esophageal bilirubin exposure compared with patients without Barrett's changes, with or without esophagitis. The correlation of pH and bilirubin monitoring showed that the majority (87%) of esophageal bilirubin exposure occurred when the pH of the esophagus was between 4 and 7. Reflux of duodenal juice in gastroesophageal reflux disease is more common than pH studies alone would suggest. The combined reflux of gastric and duodenal juices causes severe esophageal mucosal damage. The vast majority of duodenal reflux occurs at a pH range of 4 to 7, at which bile acids, the major component of duodenal juice, are capable of damaging the esophageal mucosa.

Mixed Reflux of Gastric and Duodenal Juices Is More Harmful to the Esophagus than Gastric Juice Alone

Objective The author's goal was to determine the role of duodenal components in the development of complications of gastroesophageal reflux disease. Summary and Background Data There is a disturbing increase in the prevalence of complications, specifically the development of Barrett's esophagus among patients with gastroesophageal reflux disease. Earlier studies using pH monitoring and aspiration techniques have shown that increased esophageal exposure to fluid with a pH above 7, that is, of potential duodenal origin, may be an important factor in this phenomenon. Methods The presence of duodenal content in the esophagus was studied in 53 patients with gastroesophageal reflux disease confirmed by 24-hour pH monitoring. A portable spectrophotometer (Bilitec 2000, Synectics, Inc.) with a fiberoptic probe was used to measure intraluminal bilirubin as a marker for duodenal juice in the esophagus. Normal values for bilirubin monitoring were established for 25 healthy subjects. In a subgroup of 22 patients, a custom-made program was used to correlate simultaneous pH and bilirubin absorbance readings. Results Fifty-eight percent of patients were found to have increased esophageal exposure to gastric and duodenal juices. The degree of mucosal damage increased when duodenal juice was refluxed into the esophagus, in that patients with Barrett's metaplasia (n = 27) had a significantly higher prevalence of abnormal esophageal bilirubin exposure than did those with erosive esophagitis (n = 10) or with no injury (n = 16). They also had a greater esophageal bilirubin exposure compared with patients without Barrett's changes, with or without esophagitis. The correlation of pH and bilirubin monitoring showed that the majority (87%) of esophageal bilirubin exposure occurred when the pH of the esophagus was between 4 and 7. Conclusions Reflux of duodenal juice in gastroesophageal reflux disease is more common than pH studies alone would suggest. The combined reflux of gastric and duodenal juices causes severe esophageal mucosal damage. The vast majority of duodenal reflux occurs at a pH range of 4 to 7, at which bile acids, the major component of duodenal juice, are capable of damaging the esophageal mucosa.

Cytogenetically detected clonal heterogeneity in a duodenal adenocarcinoma

A primary duodenal adenocarcinoma, a tumor type for which no previous chromosome data existed, was cytogenetically analyzed after short-term culture. The main tumor mass was localized in the pancreatic head, but the histopathologic examination revealed its duodenal origin. A total of six abnormal, karyotypically unrelated, clones were identified. The largest exhibited clonal evolution and consisted of two subclones with massively rearranged karyotypes in the hypodiploid and hypotetraploid range. Chromosome imbalances brought about by these complex changes were gain of 1q, losses of chromosomes 6 and 9, and total or partial losses of 1p, 3p, 3q, 9p, 10p, 17p, 17q, 18q, 20p, and 20q. The remaining five smaller clones had 1–2 numerical or balanced structural chromosome aberrations. The present study thus revealed yet another epithelial tumor type characterized by karyotypically unrelated clones. For this as for other tumors, the pathogenetic significance of such cytogenetic polyclonality remains uncertain.

Pathologic aspects of gastrinomas in patients with Zollinger-Ellison syndrome with and without multiple endocrine neoplasia type I.

During the three decades since the recognition of the Zollinger-Ellison syndrome (ZES), major progress has been made in the diagnosis and treatment of this disease. However, the many failed operations in patients with ZES, the existence of primary lymph node gastrinomas, and the surgical approach of patients with ZES and multiple endocrine neoplasia type I (MEN-I) have remained controversial issues. In this review, our experience with the pathology of immunocytochemically identified gastrinomas in 44 patients with ZES is presented and related to the relevant literature. (1) Gastrinomas occur frequently in the duodenum (> 40%) and are commonly small (< 1 cm). They can therefore easily be missed at surgical exploration; lymph node metastases from such occult gastrinomas may be mistaken for primary tumors. (2) Most pancreatic gastrinomas reside in the head of the gland and have a diameter of 1 to 3 cm. (3) Gastrinomas associated with MEN-I are predominantly of duodenal origin and frequently multicentric; sporadic gastrinomas are single and more often pancreatic. Because MEN-I associated pancreatic tumors seldom contain gastrin, ZES in MEN-I patients is almost never cured by resection of the pancreatic tumors. (4) The metastatic potential of most small duodenal gastrinomas seems to be restricted to the regional lymph nodes.

Duodenal preabsorptive origin of gustatory alliesthesia in rats.

Facial consummatory responses reflecting ingestive and aversive perceptions were studied and quantified in rats chronically implanted with gastric, duodenal, and oral catheters. A gustatory stimulus of 50 microliters of 1.75 mol/l sucrose was injected into the mouth every 5 min for 65 min. At time 0, 0.5 ml containing 0.3 g glucose was injected into the stomach or into the duodenum. Typical ingestive facial consummatory responses were observed in response to sweet stimuli prior to the load. Aversive consummatory responses were observed in response to sweet stimuli after the glucose duodenal load (negative alliesthesia). The gastric load of glucose was not followed by negative alliesthesia in response to sweet oral stimuli. In the last part of the experiment the rats were vagotomized. When the rats were subjected again to the same gustatory sessions, the duodenal load was followed by weak and delayed negative alliesthesia in response to sweet stimuli. These results in rats parallel results obtained in human subjects and reinforce the hypothesis of the existence of a duodenal preabsorptive signal for alimentary alliesthesia. They also suggest that the vagus nerve plays a part in the perception of satiety.

Regional characteristics of intestinal iron absorption in the guinea-pig.

Features of iron absorption by the upper small intestine and ileum in the adult guinea-pig have been compared. Autoradiographic methods have revealed that whilst only upper villus enterocytes in the duodenum-jejunum are involved in brush-border uptake, the entire villus epithelium in the ileum displays this function. Consistent with these results was the finding that brush-border membrane vesicles prepared from ileal mucosa demonstrated a higher capacity for iron uptake (expressed per mg protein) compared to vesicles of duodenal origin. Iron transport to blood following 30 min exposure of mucosa to 59Fe-ascorbate was some elevenfold higher in upper, compared to lower, small intestine. The relevance of these findings to our knowledge of the cellular processes involved in intestinal iron absorption and its regional localization is discussed.

Entrainment of duodenal activity to periodic feeding.

The electrical activity of the antrum and proximal duodenum was recorded simultaneously with bar pressing for food in various feeding conditions. During restricted feeding (RF; food available from 1200 to 1600 hr; lights-on from 0800 to 2000 h), large-amplitude slow potentials of duodenal origin were observed 3-5 hr preceding food access. These potentials occurred in short trains at irregular intervals of approximately 1 min and appeared to be associated with the active phase of the migrating motility complex. At least 8-10 days on RF were required before these irregular contractions (ICs) reliably preceded food access. The distribution of ICs showed a circadian variation during food deprivation, and transients lasting 4-6 days were observed in response to 6- or 8-hr phase delays of food access. These observations suggest that ICs are modulated by a circadian mechanism. On the average, the increase in ICs occurred about 2 hr earlier than bar pressing in anticipation of food, and there was no specific relation between individual ICs and bar pressing. However, bar pressing frequently occurred 0.5 min or longer after an increase in electromyogram (EMG) amplitude. Unreinforced bar pressing was never observed during a quiescent EMG.

The sonographic appearance of duodenal lesions.

The sonographic findings in 17 patients with duodenal tumors and in one patient with a benign ulcer and stricture of the duodenum were reviewed. An abdominal mass was detected sonographically in all patients; in 15 of 18 cases, such lesions presented high-level central echoes and hypoechoic periphery. Identification of the duodenal origin of the disease was possible by sonography in only 16 of 18 patients: by evaluation of the relationship of the mass with abdominal vessels in eight patients; by demonstrating that the lesion was continuous with a normal duodenum in seven patients; or by demonstrating the mass within the duodenum itself in one patient. Signs and symptoms of duodenal tumors are usually nonspecific, and sonography can be used as the first imaging method in these cases. A careful analysis of the relationship of the tumor to surrounding structures may allow correct identification of its origin.

Carcinoid-islet cell tumors of the duodenum: Report of twenty-one cases

A series of twenty-one carcinoid-islet cell tumors of the duodenum is reported. Eighteen were found at operation, and three were found incidentally at autopsy. Among those patients who came to operation, thirteen had duodenal ulcers, four had polypoid lesions of the duodenum, and one had obstructive jaundice due to an invasive tumor at the ampulla of Vater. Nine patients with duodenal ulcer had evidence of endocrine activity, eight of these had the Zollinger-Ellison syndrome, and one had an elevated level of 5-hydroxyindoleacetic acid in the urine. Six patients had multiple endocrine adenomatosis or evidence of neural ectodermal dysplasia. Seven tumors behaved in a malignant fashion and six of these had endocrine activity. The malignancy of only one tumor could be determined on histologic grounds alone. The remainder were diagnosed by lymph node metastasis or local recurrence. Endocrine activity, mucosal ulceration overlying the tumor, and continued secretion of highly acid gastric contents after excision of the tumor suggested the presence of metastases or multiple tumors. Tumors not associated with a duodenal ulcer were treated by simple excision if they had not metastasized and by pancreaticoduodenectomy if malignant. Tumors associated with an uncomplicated duodenal ulcer were treated by subtotal gastrectomy and excision of the tumor. Although two patients in this series were cured of the Zollinger-Ellison syndrome by partial gastrectomy and excision of the tumor, two patients died after partial gastrectomy. Six of the eight patients with gastrin-producing tumors had either lymph node metastasis or associated pancreatic tumors. For this reason, unless gastrin levels can be shown to fall to normal after resection of a duodenal tumor, we believe total gastrectomy is the procedure of choice in patients with the Zollinger-Ellison syndrome of duodenal origin just as it is with ulcerogenic tumors of the pancreas.

The Treatment in Massive Hemorrhage of Gastric or Duodenal Origin

The Treatment in Massive Hemorrhage of Gastric or Duodenal Origin

The formation of concretions of aluminum salts of fatty acids after the use of aluminum hydroxide

Following a hemorrhage of duodenal ulcer origin in a patient using aluminum hydroxide as an antacid, small concretions were found in the stool. The passage of these concretions through the intestinal tract was accompanied by severe intermittent cramps and pain.

CARCINOMA OF THE SUPRAPAPILLARY PORTION OF THE DUODENUM

The purpose of this communication is to report six cases of carcinoma of the suprapapillary segment of the duodenum and to analyze and summarize the data obtained from the reported cases of this condition. Reports of one hundred and four cases were abstracted from the literature, thirty-five1of which were regarded as acceptable on the basis of the data presented, a clinical history and gross and microscopic studies of the primary lesion being presented in each report. Twelve2additional cases, although probably authentic examples of this condition, could not be included in the present analysis because of insufficient clinical or pathologic data. Fifty-seven more reported cases were discarded, nineteen because, owing to involvement of the stomach, pancreas or bile passages in the malignant process,3the duodenal origin of the lesion was not established with certainty and thirty-eight4because the histologic studies were not reported, the diagnosis

Correlation of in vitro Activity of Normal Human Gastric Juice on Casein at pH 7.4 with Gastric Intrinsic Factor

The administration of mixtures of normal human gastric juice (intrinsic factor) and beef muscle (extrinsic factor) at pH 5 or 7 to patients with pernicious anemia results in increased blood production and clinical improvement,1,2In 1930, in association with Dr. C. W. Heath, unsuccessful attempts were made to show that gastric juice at pH 7.4 caused the production of amino acid from beef muscle. Griffiths3 showed that gastric juice incubated with beef muscle globulin at pH 6 produced certain chemical changes. Emerson and Helmer4 could not confirm his results. However, the present observations show that when casein was substituted for beef muscle, gastric juice at pH 7.4 did produce progressive changes in the casein.Normal human gastric juice was obtained free from bile after injection of histamine, filtered through gauze and placed in the ice box. A one percent solution of A. H. Thomas & Company washed casein was prepared at pH 7.4, avoiding excess of acid or alkali. To 50 ml. of this solution were added 5...