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PubMedDate not supplied

Adenocarcinoma of the duodenum: factors influencing long-term survival.

This single-institution retrospective analysis reviews the management and outcome of patients with surgically treated adenocarcinoma of the duodenum. Between February 1984 and August 1996, fifty-five patients with adenocarcinoma of the duodenum underwent surgery at The Johns Hopkins Hospital. Univariate analysis was performed to identify possible prognostic indicators. Curative resection was performed in 48 patients (87%): 35 of these patients (73%) underwent a pancreaticoduodenectomy (PD), whereas 27% (n = 13) underwent a pancreas-sparing duodenectomy (PSD). Patients undergoing PD were comparable to those undergoing PSD with respect to demographic factors, presenting symptoms, and tumor pathology. The remaining 13% of patients (n = 7) were deemed unresectable at the time of surgery and underwent biopsy and/or palliative bypass. PD was associated with an increase in postoperative complications when compared to PSD (57% vs. 30%), but this difference was not statistically significant. One perioperative death occurred following PD (mortality 2.9%). The overall 5-year survival rate for the 48 patients undergoing potentially curative resection was 53%. Negative resection margins (P <0.001), PD (P <0.005), and tumors in the first and second portions of the duodenum (P <0.05) were favorable predictors of long-term survival by univariate analysis. Nodal status, tumor diameter, degree of differentiation, and the use of adjuvant chemoradiation therapy did not influence survival. These data support an aggressive role for resection in patients with adenocarcinoma of the dueodenum

Adenocarcinoma↗
PubMed2000

Effect of somatostatin on electrogenic ion transport in the duodenum and colon of the mouse, Mus domesticus.

In this study, we have used the mouse intestine and the Ussing short circuit technique to compare the effects and mechanism of action of somatostatin (SST, 0.1 microM) on cAMP- and Ca(2+)-mediated ion secretion in the duodenum and colon of the Swiss-Webster mouse. The cAMP-dependent secretagogues, prostaglandin E(2) (1 microM) and dibutyryl-cAMP (150 microM) increased short circuit current (I(sc)) in both regions, but only the colonic response was inhibited by SST. This inhibition was independent of enteric nerves, suggesting a direct action on the epithelial cells. The Ca(2+)-dependent secretagogue carbachol (10 microM) stimulated a transient increase in I(sc) in both intestinal segments. In the duodenum, SST partially inhibited this increase in I(sc) and both the responses to carbachol and SST were independent of enteric nerves. In the colon, while SST inhibited the carbachol induced increase in I(sc), pre-treatment with tetrodotoxin (750 nM) profoundly inhibited the carbachol induced increase in I(sc), thus markedly reducing the inhibitory effect of SST. This indicates an involvement of the enteric nervous system in the response to carbachol and the action of SST in the colon. These data indicate marked regional differences within the mouse intestine of the effects of SST on ion secretion and demonstrate different mechanisms of action of SST in the duodenum and colon.

Animals↗
PubMed2001

Developmental changes in heme-oxygenase-2 and bNOS expression in enteric neurons in the pig duodenum.

There exists much parallelism between carbon monoxide- and nitric oxide-generating systems. Therefore, we wondered whether developmental and functional differences along the duodenum similarly affect, part of them, namely, heme oxygenase-2-(HO-2) and neural isoform of nitric oxide synthase- (nNOS) expressing neurons. By applying NADPH diaphorase histochemistry and HO-2 immunohistochemistry on whole-mount preparations and by using stereologic methods, a qualitative and quantitative description of HO-2 and nNOS expression was obtained. Examinations were carried out on the duodenum of fetal, neonatal and weaned pigs. At all ages, three enteric plexuses were readily distinguished. The presence of both enzymes fits in with other morphological and physiological reports. However, the expression of both enzymes significantly changed during development. The number of HO-2-IR neurons increased approximately 20-fold in the inner submucous and almost doubled in the myenteric plexus. In addition, the number of nNOS-expressing neurons displayed a significant decrease in the outer submucous plexus after weaning. High levels of glucocorticoids may cause the perinatally increased HO-2 expression, whereas an influence on nNOS expression is doubtful. Therefore, it seems that notwithstanding the high similarity between both systems, their expression is regulated differently in the pig duodenum.

Animals↗
PubMed2003

Clinical efficiency of Epigam in patients with exacerbation of peptic ulcer disease of the stomach and duodenum.

Clinical efficiency and safety of Epigam containing antibodies to histamine in ultralow doses were studied during the therapy of patients with exacerbation of peptic ulcer disease of the stomach and duodenum associated with Helicobacter pylori infection. We examined 20 patients (18-50 years) with ulcerative lesions of the mucosal layer in the stomach and duodenum and H. pylori infection. Epigam (1 tablet, 6 times a day) or H2 receptor blocker ranitidine (150 mg, 2 times a day) were given in combination with amoxicillin (500 mg, 3 times a day, 14 days) and metronidazole (500 mg, 2 times a day, 14 days) for 28 days. The efficiency of treatment was determined before and 1, 2, 3, and 4 weeks after the start of therapy. The symptoms of peptic ulcer disease and time of ulcer healing underwent similar changes in patients of both groups. However, after ranitidine therapy pain syndrome disappeared more rapidly than in patients receiving Epigam. Epigam did not cause undesirable side effects. Our results indicate that Epigam is an efficient and safe preparation that may be used for combination therapy of patients with peptic ulcer disease of the stomach and duodenum.

Adolescent↗
PubMed2001

Glycoconjugate histochemistry in the duodenum of fetal and adult fallow deer.

This work aimed to characterize the complex carbohydrates in the duodenum of fetal and adult fallow deer. The proximal parts of the duodenum were removed from the intestine of 12- and 16-week-old fetuses and of adult fallow deer. Sections were assessed by conventional carbohydrate histochemistry combined with glycosidase digestions and treatment with KOH. During development, there was an increase in the acid carboxylated components of the glycoconjugates in goblet cells, while the duodenal glands expressed high quantities of sulphated glycoconjugates at the beginning of development but, in the adult. mainly secreted neutral and carboxylated glycoconjugates containing sialic acid. Sulphated components, probably represented by chondroitin sulphate B-like and heparan sulphate-like glycosaminoglycans may play a role in the morphofunctional differentiation of the duodenum.

Animals↗
PubMed1998

Nervous control of alkaline secretion in the duodenum as studied by the use of cholera toxin in the anaesthetized rat.

There is experimental evidence for an axon reflex control of alkaline secretion in the rat duodenum. We have investigated if there is also an intramural reflex control of alkaline secretion similar to that demonstrated with regard to the control of the fluid transport in the rat jejunum. Alkaline secretion in the duodenum of an anesthetized rat was continuously monitored using an in situ titration technique. The segment was extrinsically denervated. Exposing the duodenal segment to 80 microg cholera toxin markedly increased alkaline secretion. This response was abolished by hexamethonium (28 micromol (10 mg) kg(-1) body wt), a nicotinic receptor blocker, lidocaine (0.5 mL of a 1% solution on the serosal surface), a local anaesthetic, and nifedipine (5.75 micromol (2 mg) kg(-1) body wt i.v.), a calcium channel blocker. The response to cholera toxin was partially abolished by granisetron (0.11 micromol (40 microg) kg(-1) body wt i.v.), a 5-HT3 receptor blocker. Atropine (1.7 micromol (0.5 mg) kg(-1) body wt i.v.), a muscarinic receptor blocker, had no effect. We therefore conclude that the alkaline secretion in the rat jejunum evoked by cholera toxin exhibits the same pharmacological properties as the fluid secretion caused by the toxin in the jejunum. This suggests that the alkaline secretion in the rat duodenum is controlled not only by an axon reflex but also by an intramural secretory reflex similar to that controlling fluid transport in the rat jejunum.

Alkalies↗
PubMed1999

Bradykinin elevates cytosolic Ca2+ concentration in smooth muscle cells isolated from rat duodenum.

The effect of bradykinin on the cytosolic Ca2+ concentration were measured in single, Fura-2 loaded, smooth muscle cells isolated from rat duodenum. All cells responded with a Ca2+ signal when exposed to bradykinin. The bradykinin response consisted of an initial Ca2+ spike followed by a plateau. Pre-treatment of single muscle cells with either the phospholipase C blocker U-73122 or thapsigargin, which is a potent inhibitor of the endoplasmic reticulum Ca2+-ATPase, inhibited the response to bradykinin. Pre-treatment of the cells with EGTA or La3+ to inhibit the Ca2+ influx, abolished the response induced by bradykinin. We conclude that bradykinin applied to single smooth muscle cells from rat duodenum, increases cytosolic Ca2+ by emptying intracellular Ca2+ stores, and by contribution from extracellular Ca2+. In contrast to bradykinin-induced response in isolated rat duodenum (a relaxation followed by a contraction), we did not observe a biphasic effect of bradykinin on cytosolic Ca2+ in single muscle cells. Bradykinin may thus cause relaxation of duodenal smooth muscle indirectly through an effect on neighbouring cells as dilatation is brought about by this agent in blood vessels.

Animals↗
PubMed1999

Effect of hydroquinone, hydroxocobalamin and carboxy-PTIO on non-adrenergic non-cholinergic nerve mediated relaxations of the rat duodenum.

Relaxation induced by NANC-nerve stimulation is reduced by nitric oxide synthase (NOS) inhibitors but not by superoxide generators or NO scavengers, casting doubts on the precise nature of the neurotransmitter being released by these nerves. The lack of effect of superoxide anion generators to inhibit nitrergic nerve-mediated relaxations has been attributed to the protective action of high tissue levels of superoxide dismutase (SOD). The effects of hydroquinone, hydroxocobalamin and carboxy-PTIO, three NO inactivators which do not depend on superoxide anion generation, upon nitrergic nerve-mediated relaxations of the rat proximal duodenum were determined in order to elucidate whether they are mediated by free NO. GABA and nicotine caused relaxations of isolated segments of the rat proximal duodenum in a concentration-dependent manner that were abolished by tetrodotoxin (TTX). Similarly, transmural electrical stimulation (TES) caused frequency-dependent relaxations that were also abolished by TTX. The NOS inhibitors L-NAME and L-NOARG reduced in a concentration-dependent manner nerve-mediated relaxations elicited by TES, nicotine and GABA. The effect of NOS inhibitors was prevented by L-arginine but not D-arginine. NO caused concentration-dependent relaxations that were not affected by TTX or L-NOARG but were abolished by hydroquinone, hydroxocobalamin and carboxy-PTIO. In contrast, these compounds failed to affect TES-, nicotine- and GABA-induced relaxations. The lack of effect of hydroquinone, hydroxocobalamin and carboxy-PTIO upon nerve-mediated relaxations was unaltered by pretreatment with the SOD irreversible inhibitor DETCA. The present findings show that nitrergic nerve-mediated relaxations of the rat duodenum are unaffected by NO inactivators that do not generate superoxide anion. It is suggested that either a NO-containing molecule that is unreactive with the inactivators tested is the inhibitory neurotransmitter released by nitrergic nerves or that NOS activity fulfills another role in nitrergic nerves which could be related to the release of an still unidentified transmitter.

Animals↗
PubMed1999

Effects of diabetes on non-adrenergic, non-cholinergic relaxation induced by GABA and electrical stimulation in the rat isolated duodenum.

1. The effects of streptozotocin (STZ)-induced experimental diabetes on nitrergic-mediated responses to GABA and electrical field stimulation (EFS) have been evaluated in rat isolated duodenum. 2. In the presence of noradrenergic and cholinergic blockade, EFS (60 V, 1 ms, 0.1-32 Hz) induced frequency dependent relaxations of the preparation. GABA also caused submaximal relaxation of the rat duodenum. The relaxations induced by GABA and EFS were reduced in duodenal tissues from diabetic rats compared with control rats. 3. Neither ATP- nor sodium nitroprusside-induced relaxations were altered in diabetic duodenal tissues. GABA- and EFS-induced relaxations were inhibited by NG-nitro-L-arginine methyl ester (L-NAME; 300 mmol/L) in both diabetic and control rats. Although the inhibition caused by L-NAME of GABA- and EFS-induced relaxation was partially reversed by L-arginine (1 mmol/L), L-arginine alone had no effect on GABA- and EFS-induced relaxation in diabetic rats. 4. These results suggest that STZ-induced diabetes impairs non-adrenergic, non-cholinergic relaxation induced by EFS and GABA. Impairment of nitrergic innervation of the rat duodenum may contribute to the abnormalities of intestinal motility abnormalities associated with diabetes.

Animals↗
PubMed2002

An alternate pathway of cAMP-stimulated Cl secretion across the NKCC1-null murine duodenum.

BACKGROUND & AIMS: Adenosine 3',5'-cyclic monophosphate (cAMP)-stimulated anion secretion across the duodenal epithelium requires the cystic fibrosis transmembrane conductance regulator (CFTR) in the apical membrane and anion uptake proteins in the basolateral membrane. NKCC1, the epithelial Na(+)/K(+)/2Cl(-) cotransporter, is the major protein responsible for Cl(-) uptake. In this study, we evaluate the role of NKCC1 in determining the relative rates of transepithelial Cl(-) and HCO(3)(-) secretion during cAMP stimulation of the duodenum. METHODS: Bicarbonate and chloride secretion across duodenal mucosa was measured in Ussing chambers by pH stat and (36)Cl flux methods using mice with either gene-targeted deletion of NKCC1 (NKCC1-/-) or bumetanide blockade of NKCC1. RESULTS: Total anion secretion stimulated by forskolin treatment of NKCC1-null duodenum resulted from approximately equivalent rates of electrogenic chloride, electrogenic bicarbonate, and electroneutral bicarbonate secretion. Evaluation of the alternate chloride secretory pathway indicated chloride uptake by a basolateral membrane anion exchange process with characteristics consistent with the anion exchanger isoform AE2. CONCLUSIONS: Chloride uptake by basolateral anion exchanger activity (AE2) supports intracellular cAMP-stimulated chloride secretion in the NKCC1-null duodenum. A model for the alternate chloride secretion pathway is proposed whereby chloride uptake via AE2 is coupled to basolateral NaHCO(3) cotransport to support CFTR-mediated chloride and bicarbonate secretion.

Animals↗
PubMed2002

[Arterial port-catheter dislocation into the duodenum].

Arterial port-catheter dislocations into the duodenum are rare complications. We report on a 64-year-old male with sigmoid-resection for carcinoma, left hemihepatectomy and arterial port-catheter implantation into the common hepatic artery for liver metastases in both lobes and partial dislocation of the port system into the duodenum. Therefore, the port-catheter system had to be explanted after 8 cycles of cytostatic therapy and the duodenum had to be closed by a suture. Six months after surgery the patient felt well, a new singular metastasis in the right liver lobe could be treated successfully by laserinduced thermotherapy. At present the patient has no evidence for another metastasis.

Catheters, Indwelling↗
PubMed2006

Endoscopic and histological findings in the duodenum of adults with celiac disease before and after changing to a gluten-free diet: a 2-year prospective study.

BACKGROUND AND STUDY AIMS: Published follow-up data on small-intestinal recovery in patients with celiac disease are scarce and contradictory. This is especially the case for adult patients, who often show incomplete histological recovery after starting a gluten-free diet (GFD). We conducted a 2-year prospective study to evaluate the effectiveness of a GFD in improving the endoscopic and histological duodenal findings in adults with celiac disease. PATIENTS AND METHODS: We studied 42 consecutive adults with newly diagnosed celiac disease (13 men, 29 women; mean age 32.7 years, range 15 - 72 years). All the patients underwent esophagogastroduodenoscopy and small-bowel biopsy. We devised our own grading system for the endoscopic appearance of the duodenum, which ranged from "normal" appearance to "mild", "moderate", or "severe" alterations. Small-bowel biopsies were obtained from the second part of the duodenum (and from the duodenal bulb when it had a micronodular appearance). The histopathological appearances were described according to modified Marsh criteria. RESULTS: A normal endoscopic appearance in the duodenum was found in 5/42 patients (11.9 %) at entry and in 32/42 patients (76.2 %) after 2 years on a GFD. Subdividing the patients according to age, patients aged from 15 years to 60 years showed significant improvement within 12 months ( P < 0.0001 for patients aged from 15 years to 45 years; P < 0.003 for patients in the 46 years to 60 years group), whereas the improvement in endoscopic findings in patients older than 60 years was not statistically significant, even 24 months after starting the GFD. "Normal" histology was reported in none of the patients at entry, but in 25 patients (59.5 %) after 24 months on a GFD, but this parameter did not show a significant improvement until the patients had been on the GFD for 12 months ( P < 0.0001). Only the younger patients (5 - 30 years) showed significant improvement of histology within 12 months ( P < 0.034); older patients (>30 years) showed histological improvement but this was not statistically significant, even after 24 months on a GFD. CONCLUSIONS: This study shows for the first time that endoscopic recovery is faster than histological recovery in adults with celiac disease who go on a GFD. Moreover, older patients showed incomplete endoscopic and histological recovery even 24 months after starting a GFD. We therefore advise, as a minimum recommendation, that follow-up biopsies should be taken 1 - 2 years after starting a GFD in adults with celiac disease.

Adolescent↗
PubMed1991

The duodenum in liver cirrhosis: endoscopic, morphological and clinical findings.

Endoscopic studies were performed to determine whether changes occurred in the duodenum related to portal hypertension in patients with liver cirrhosis. The total of 271 patients studied were subdivided into three groups: 83 patients with liver cirrhosis and portal hypertension, 53 with liver cirrhosis but no portal hypertension, and 135 controls. In the duodenum of cirrhotic patients with portal hypertension several changes were observed on endoscopy that were also present in the other two groups. Atrophy and vascular malformations, however, were present only in the duodenum of cirrhotic patients with portal hypertension, although in only a few patients and with statistical significance only for vascular malformations (p less than 0.01, phi = 0.21). Eleven percent of the patients had more than one endoscopic finding, but the associations of findings were without statistical significance. No statistically significant correlation was observed between the clinical severity of cirrhosis or the severity of esophageal varices and the endoscopic findings. Finally, there was no statistically significant difference between the histological findings of duodenitis in the three groups of patients.

Aged↗
PubMed1992

[A villous adenoma of the duodenum].

X-ray contrast examination of the upper gastrointestinal tract in a 73-year-old man with nocturnal heartburn demonstrated a constant filling defect in the duodenum. Gastroduodenoscopy revealed a 4 x 3 cm polypoid mucosal change of the duodenal wall adjacent to the pancreas. Histological examination of an endoscopically obtained biopsy showed a tubulovillous adenoma with severe mucosal dysplasia. The affected segment of duodenum was resected. Serial sections showed extensive focal carcinomatous degeneration of an adenoma. The postoperative course was unremarkable. At endoscopy 30 months later, when the patient was free of any symptoms, there was no macroscopic or microscopic evidence of recurrence. Experience so far indicates that villous adenoma of the duodenum should be treated by radical surgery.

Adenoma↗
PubMed2002

Iron uptake from plasma transferrin by the duodenum is impaired in the Hfe knockout mouse.

Hereditary hemochromatosis (HH) is a disorder of iron metabolism in which enhanced iron absorption of dietary iron causes increased iron accumulation in the liver, heart, and pancreas. Most individuals with HH are homozygous for a C282Y mutation in the HFE gene. The function of HFE protein is unknown, but it is hypothesized that it acts in association with beta(2)-microglobulin and transferrin receptor 1 to regulate iron uptake from plasma transferrin by the duodenum, the proposed mechanism by which body iron levels are sensed. The aim of this study was to test this hypothesis by comparing clearance of transferrin-bound iron in Hfe knockout (KO) mice with that observed in C57BL/6 control mice. The mice were fed either an iron-deficient, control, or iron-loaded diet for 6 weeks to alter body iron status. The mice then were injected i.v. with (59)Fe-transferrin, and blood samples were taken over 2 h to determine the plasma (59)Fe turnover. After 2 h, the mice were killed and the amount of radioactivity in the duodenum, liver, and kidney was measured. In both Hfe KO and C57BL/6 mice, plasma iron turnover and iron uptake from plasma transferrin by the duodenum, liver, and kidney correlated positively with plasma iron concentration. However, duodenal iron uptake from plasma transferrin was decreased in the Hfe KO mice compared with the control mice. Despite this difference in duodenal uptake, the Hfe KO mice showed no decrease in iron uptake by the liver and kidney or alteration in the plasma iron turnover when compared with C57BL/6 mice. These data support the hypothesis that HFE regulates duodenal uptake of transferrin-bound iron from plasma, and that this mechanism of sensing body iron status, as reflected in plasma iron levels, is impaired in HH.

Animals↗
PubMed2001

Pdx-1 is required for activation in vivo from a duodenum-specific enhancer.

The purine metabolic gene adenosine deaminase (ADA) is expressed along a defined spatiotemporal pattern in the developing mammalian small intestine, where high-level expression is limited to the villous epithelium of the duodenum. This activation is observed in rodents as the intestine completes the final maturation resulting in adult crypt-villus structures at 2-3 weeks postpartum. A regulatory module responsible for this pattern of expression has been identified in the second intron of the human ADA gene. Of the multiple duodenal proteins that can interact with this small duodenal enhancer region, the studies contained in this work describe the identification of five of these proteins as the dispersed homeobox protein PDX-1. This transcription factor exhibits a profile of expression in the small intestine similar to that observed for ADA, making it an ideal candidate factor for the duodenum-specific ADA enhancer. Loss of PDX-1 binding, via a PDX-1 mutated enhancer transgenic construction, resulted in complete loss of high-level activation in the duodenum, demonstrating the absolute requirement for this factor in vivo. However, co-transfection experiments suggest that other proteins that bind the enhancer are also required for enhancer function because PDX-1 alone was incapable of significant transactivation.

Adenosine Deaminase↗
PubMed2002

Cis elements of the villin gene control expression in restricted domains of the vertical (crypt) and horizontal (duodenum, cecum) axes of the intestine.

Villin, an actin bundling protein found in the apical brush border of absorptive tissues, is one of the first structural genes to be transcriptionally activated in the embryonic intestinal endoderm. In the adult, villin is broadly expressed in every cell of the intestinal epithelium on both the vertical axis (crypt to villus tip) and the horizontal axis (duodenum through colon) of the intestine. Here, we document that a 12.4-kilobase region of the mouse villin gene drives high level expression of two different reporter genes (LacZ and Cre recombinase) within the entire intestinal epithelium of transgenic mice. Deletion of a portion of this transgene results in reduction of beta-galactosidase activity in restricted domains of the small intestine (duodenum) and large intestine (cecum). In addition, expression is reduced in the crypt compartment throughout the intestine. Thus, the global expression pattern of villin in the intestine is apparently the consequence of an amalgam of distinct and individual domain-specific control processes. That is, expression of villin in the duodenum and cecum requires different regulatory sequences than the rest of the intestine, and the expression of villin in crypts is regulated by different circuitry than expression of villin on villus tips.

Animals↗
PubMed1977

The enhancement by dietary zinc deficiency of the susceptibility of the rat duodenum to colchicine.

1. The incidence of colchicine-induced lesions in the germinal epithelium oof the rat duodenum was studied in young rats in an early stage of zinc deficiency and in their pair-fed controls. At both dose levels of colchicine used, a marked increase in the amount of cell damage was observed in the duodenum of Zn-deficient rats as compared with the pair-fed, control (Zn-supplemented) rats. 2. No statistical interaction between Zn and colchicine was demonstrable, and no lesions were found in the duodenum of animals that had not been treated with colchicine. 3. The results are discussed in relation to the effects of Zn deficiency in animals and the possible involvement of Zn in the maintenance of the integrity of microtubular structures.

Animals↗