Guidelines for colonic diverticular bleeding and colonic diverticulitis: Japan gastroenterological association

Colonic diverticular disease has been increasing in prevalence in Japan due to the rapidly aging population. Colonic diverticular bleeding can result in hemorrhagic shock requiring blood transfusion, and it carries a high risk of recurrence within 1 year. Colonic diverticulitis can cause abscess, fistula formation, and perforation of the colon that may require surgery, and it often recurs. As a result, patients with colonic diverticular disease are often bothered by required frequent examinations, re-hospitalization, and a consequent decrease in quality of life. However, the management of diverticular disease differs between Japan and Western countries. For example, computed tomography (CT) is readily accessible at Japanese hospitals, so urgent CT may be selected as the first diagnostic procedure for suspected diverticular disease. Endoscopic clipping or band ligation may be preferred as the first endoscopic procedure for diverticular bleeding. Administration of antibiotics and complete bowel rest may be considered as first-line therapy for colonic diverticulitis. In addition, diverticula occur mainly in the sigmoid colon in Western countries, whereas the right side or bilateral of the colon is more commonly involved in Japan. As such, diverticular disease in the right-side colon is more prevalent in Japan than in Western countries. Against this background, concern is growing about the management of colonic diverticular disease in Japan and there is currently no practice guideline available. To address this situation, the Japanese Gastroenterological Association decided to create a clinical guideline for colonic diverticular bleeding and colonic diverticulitis in collaboration with the Japanese Society of Gastroenterology, Japan Gastroenterological Endoscopy Society, and Japanese Society of Interventional Radiology. The steps taken to establish this guideline involved incorporating the concept of the GRADE system for rating clinical guidelines, developing clinical questions (CQs), accumulating evidence through a literature search and review, and developing the Statement and Explanation sections. This guideline includes 2CQs for colonic diverticulosis, 24 CQs for colonic diverticular bleeding, and 17 CQs for diverticulitis.

Effectiveness of modified oral steroid administration for preventing esophageal stricture after entire circumferential endoscopic submucosal dissection.

Esophageal stricture occurs at a high rate after endoscopic submucosal dissection, especially after entire circumferential dissection, leading to poor quality of life. This retrospective cohort study evaluated the stricture rate in circumferential mucosal defect cases following modified steroid administration. We enrolled 22 consecutive patients who underwent entire circumferential endoscopic submucosal dissection for superficial esophageal cancer between April 2010 and April 2015 at our hospital. Until January 2013, a systemic steroid-prednisolone-was administered at 30 mg/day and tapered over 8 weeks in the original method group (original group). From February 2013, 30 mg of prednisolone was administered orally for 3 weeks and then the dose was reduced in 5 mg decrements every 3 weeks. This group was classified as the modified method group (modified group). We retrospectively compared the stricture rates between the two groups. The postoperative stricture rate was significantly lower in the modified group (36.4%; 4/11 patients) than in the original group (82%; 9/11 patients; P = 0.04). The mean number of endoscopic balloon dilatation procedures was significantly lower in the modified group (6.2 ± 11.3) than in the original group (19.4 ± 15.3; P = 0.023). Pneumonia and oral herpes infection, which are adverse events potentially associated with steroid administration, were observed in the original group. Candida esophagitis, arthritis, and steroid-related myopathy were observed in the modified group. This modified systemic steroid administration was effective for patients with entire circumferential mucosal defect. The safety of this method was also demonstrated.

Polyglycolic acid sheet and fibrin glue for preventing esophageal stricture after endoscopic submucosal dissection: a historical control study.

There have been several reports that steroid administration is effective at preventing strictures after endoscopic submucosal dissection (ESD). However, adverse events after steroid use are of great concern. We have reported that shielding with a polyglycolic acid (PGA) sheet and fibrin glue can be useful for prevention of stricture after ESD. We conducted a retrospective analysis of efficiency of shielding with a PGA sheet and fibrin glue for prevention of esophageal stricture compared with intralesional steroid injection. ESD was performed on a total of 489 lesions in 400 patients for superficial esophageal cancer from January 2012 to July 2016. Of these, 39 lesions were enrolled in the study group (PGA sheet and fibrin glue) and 31 lesions were enrolled in the control group. The incidence of postoperative stricture at 6 weeks and the number of sessions of endoscopic balloon dilatation (EBD) required to resolve any strictures were evaluated. The post-ESD stricture rate was 9.1% in the study group (3/33 patients), which was not significantly lower than the stricture rate of 10.3% in the historical control group (3/29 patients; p = 1.00). The mean number of EBD was 0.057 ± 0.24 in the study group and 1.9 ± 5.1 in the control group, which was not significant (P = 0.95). PGA sheet and fibrin glue appear to be a promising option for the prevention of esophageal stricture similar to the effect of intralesional steroid injection.

Vascular density of superficial esophageal squamous cell carcinoma determined by direct observation of resected specimen using narrow band imaging with magnifying endoscopy.

Observation of the microvasculature using narrow band imaging (NBI) with magnifying endoscopy is useful for diagnosing superficial squamous cell carcinoma. Increased vascular density is indicative of cancer, but not many studies have reported differences between cancerous and noncancerous areas based on an objective comparison. We observed specimens of endoscopic submucosal dissection (ESD) using NBI magnification, and determined the vascular density of cancerous and noncancerous areas. A total of 25 lesions of esophageal squamous cell carcinoma that were dissected en bloc by ESD between July 2013 and December 2013 were subjected to NBI magnification. We constructed a device that holds an endoscope and precisely controls the movement along the vertical axis in order to observe submerged specimens by NBI magnification. NBI image files of both cancerous (pathologically determined invasion depth, m1/2) and surrounding noncancerous areas were created and subjected to vascular density assessment by two endoscopists who were blinded to clinical information. The invasion depth was m1/2 in 20, m3/sm1 in four and sm2 in one esophageal cancer lesion. Mean vascular density was significantly increased in cancerous areas (37.6 ± 16.3 vessels/mm2) compared with noncancerous areas (17.6 ± 10.0 vessels/mm2) (P < 0.05). The correlation coefficients between vascular density determined by two endoscopists were 0.86 and 0.81 in cancerous and noncancerous areas, respectively. Receiver operating curve (ROC) analysis revealed that the area under the curve (AUC) of vascular density was 0.895 (95% CI, 0.804-0.986). For this ROC curve, sensitivity was 78.3% and specificity was 87.0% when the cutoff value of vascular density was 26 vessels/mm2. NBI magnification confirmed significant increases in vascular density in cancerous areas compared with noncancerous areas in esophageal squamous cell carcinoma. The rates of agreement between vascular density values determined by two independent operators were high.

A pilot study of EUS-guided hot saline injection for induction of pancreatic tissue necrosis.

BACKGROUND AND STUDY AIMS: Hot saline may be potentially useful for inducing necrosis of pancreatic tissue. However, the local and systemic effects are largely unknown. This pilot study aimed to evaluate the feasibility and safety of EUS-guided injection of hot saline into the pancreas in the porcine model. METHODS: Boiling hot saline was injected into the tail of normal porcine pancreas under EUS guidance in six pigs via a transgastric approach. Three pigs were killed 4 hours later to study the acute effect of the hot saline injection (acute study). The remaining three pigs were killed after 7 days of clinical observation (survival study). RESULT: Injection of 5 mL, 2 mL and 1 mL of hot saline produced localized necrosis (7 - 10 mm) of pancreatic tissue in the acute study. However, there was pooling of hot saline on the surface of the pancreas when 5mL was injected. On the basis of the results of the acute study, the volume of hot saline injected in the survival study was 1 mL. One milliliter of hot saline produced localized or sporadic necrosis of pancreatic tissue without any signs of pancreatitis in all three pigs in the survival study; hot saline was observed to pool on the pancreatic surface of one pig. There was no histological evidence of necrosis in the pancreatic tissue adjacent to the pooled hot saline in either the acute or the survival study. CONCLUSION: EUS-guided hot saline injection of pancreatic tissue in the porcine model was technically successful and led to localized necrosis of pancreatic tissue without any sign of pancreatitis.

Magnifying endoscopy combined with narrow-band imaging for differential diagnosis of superficial depressed gastric lesions.

BACKGROUND AND AIM: Magnifying endoscopy combined with narrow-band imaging (ME-NBI) has been used for differential diagnosis of various focal lesions. The aim of our study was to evaluate ME-NBI criteria for cancer diagnosis in superficial depressed gastric lesions in comparison to conventional white light endoscopy (WLE). PATIENTS AND METHODS: ME-NBI and WLE images of 100 superficial gastric depressions (55 depressed cancers, 45 benign depressions) were independently evaluated by 11 endoscopists blinded to the diagnosis in each case. The presence or absence of predefined ME-NBI findings relating to microvasculature and fine mucosal structure (FMS) was recorded. A general diagnosis of benign or malignant also had to be given on the basis of a general assessment of features of color and shape as shown in the ME-NBI and WLE images, respectively, without regard to any prespecified criteria. RESULTS: Multivariate and ROC analysis demonstrated that the triad of FMS disappearance, microvascular dilation, and heterogeneity appeared to be the best combination for diagnosis of gastric cancer. ME-NBI diagnosis with the triad attained a good specificity (85 %, theoretically calculated if all of the triad were positive), which was significantly ( P < 0.001) superior to WLE general diagnosis (65 %), and comparable with ME-NBI general diagnosis (80 %). The sensitivities of the three diagnoses (ME-NBI with the triad 69 %, WLE general diagnosis 71 %, ME-NBI general diagnosis 72 %) were comparably moderate. The kappa values (interobserver concordance) for ME-NBI diagnosis with the triad (0.47) and ME-NBI general diagnosis (0.48) were superior to the kappa value for WLE diagnosis (0.34). CONCLUSION: The triad of FMS disappearance, microvascular dilation, and heterogeneity has good specificity for the diagnosis of superficial depressed gastric carcinoma, but the sensitivity needs to be improved.

Magnifying endoscopy with narrow band imaging for predicting the invasion depth of superficial esophageal squamous cell carcinoma.

The invasion depth of superficial esophageal squamous cell carcinoma is important in determining therapeutic strategy. The aim of this study was to prospectively investigate the clinical utility of magnifying endoscopy with narrow band imaging compared with that of non-magnifying high-resolution endoscopy or high-frequency endoscopic ultrasonography in predicting the depth of superficial esophageal squamous cell carcinoma. The techniques were carried out in 72 patients with 101 superficial esophageal squamous cell carcinomas, which were then resected by either endoscopic mucosal resection or esophagectomy. The histological invasion depth was divided into two: mucosal or submucosal carcinoma. We investigated the relationship between endoscopic staging and histology of tumor depth. Non-magnifying high-resolution endoscopy, magnifying endoscopy with narrow band imaging, and high-frequency endoscopic ultrasonography had overestimation/underestimation rates of 7/5, 4/4 and 8/3%, respectively. The sensitivity rates for the three techniques were 72, 78, and 83%, respectively, and the specificity rates were 92, 95, and 89%, respectively. There were no statistically significant differences among the three endoscopic techniques. Clinical utility of magnifying endoscopy with narrow band imaging does not seem to be significantly different from that of non-magnifying high-resolution endoscopy or high-frequency endoscopic ultrasonography in predicting the depth of superficial esophageal squamous cell carcinoma. Magnifying endoscopy with narrow band imaging may have potential to reduce overestimation risks of non-magnifying high-resolution endoscopy or high-frequency endoscopic ultrasonography.

Autofluorescence endoscopy versus conventional white light endoscopy for the detection of superficial gastric neoplasia: a prospective comparative study.

BACKGROUND AND STUDY AIMS: Preliminary studies have suggested autofluorescence endoscopy (AFE) to be accurate in the diagnosis of gastric tumors. Our prospective blinded study systematically compared AFE with white light endoscopy (WLE) for the detection of superficial gastric neoplasia. PATIENTS AND METHODS: An enriched population included 33 patients with superficial gastric neoplasia referred for endoscopic submucosal dissection (ESD), and 18 control patients undergoing follow-up endoscopy after curative ESD. At the direction of a study coordinator, two endoscopists who were blinded to the patient's history and to each other's findings, performed WLE followed by AFE or performed AFE alone, in random order. Both endoscopists independently recorded the presence of lesions seen at AFE and WLE. All lesions identified in either test were biopsied and the pathological results were used as the gold standard. RESULTS: 39 gastric neoplasias were histologically confirmed and 52 non-neoplastic lesions were found to be either WLE- and/or AFE-positive. Sensitivities of WLE and AFE alone were 74 % vs. 64 % (n. s.) and specificities were 83 % vs. 40 % ( P = 0.0003), respectively. WLE followed by AFE had a sensitivity of 69 % (n. s.) and a specificity of 64 % ( P = 0.046 compared with WLE alone). Of all neoplasias finally diagnosed, 13 % (or in the case of elevated neoplasias, 23 %) were detected by AFE but not by WLE. CONCLUSIONS: Although one quarter of elevated gastric neoplasias were detected only by AFE, its specificity is poor; therefore its clinical value is limited.

A novel double-channel therapeutic endoscope ("R-scope") facilitates endoscopic submucosal dissection of superficial gastric neoplasms.

BACKGROUND AND STUDY AIM: Endoscopic submucosal dissection (ESD) is a new and radical treatment for superficial gastrointestinal neoplasms that provides high rates of en bloc resection compared with treatment by conventional mucosal resection. However, ESD is a complex procedure that is associated with long operating times and a higher complication rate. This feasibility study assessed the use of a novel double-channel therapeutic endoscope for performing en-bloc ESD in order to assess whether the procedure time could be shortened. PATIENTS AND METHODS: The therapeutic endoscope we used (the "R-scope") is equipped with a multibending system and has two movable instrument channels: one moves a grasping forceps vertically for lesion countertraction; the other swings a cutting knife horizontally for dissection. Twenty consecutive patients (18 men, 2 women; mean age 63 years, range 54 - 80 years) with superficial gastric neoplasms in the distal two-thirds of the stomach underwent resection of their tumor by ESD using the R-scope. Forty size- and location-matched gastric neoplasms resected by conventional ESD were reviewed retrospectively for the purposes of comparison. RESULTS: The rates of curative en-bloc resection, complications, and local recurrence using the two ESD methods were comparable. The mean +/- SD operating time was significantly shorter for ESD using the R-scope than for conventional ESD (57.9 +/- 29.7 minutes vs. 92.8 +/- 58.9 minutes, P = 0.016). CONCLUSION: The R-scope appears to shorten the operating time of ESD with comparable efficacy and complication rates.

Clinical and endoscopic characterization of depressed gastric adenoma.

BACKGROUND AND STUDY AIM: Depressed gastric adenoma remains poorly characterized because it is rare, and is infrequently detected by endoscopy. The aim of this study was to elucidate clinical and endoscopic characteristics of depressed adenoma of the stomach. PATIENTS AND METHODS: 95 consecutive patients who underwent endoscopic resection of gastric adenomas were studied. Gastric adenomas, diagnosed according to the Vienna classification, were endoscopically classified into two types: depressed and protruding adenomas. In order to clarify endoscopic features of gastric adenomas, we performed indigo carmine chromoendoscopy as well as magnifying endoscopy with narrow band imaging, which yields clear images of mucosal microvasculature. RESULTS: 12% of 100 gastric adenomas resected from 95 patients were depressed adenomas. Age and gender were comparable between patients with each type. Depressed adenomas (15.9 +/- 6.2 mm) were significantly larger in diameter than protruding adenomas (10.6 +/- 8.0 mm) (P = 0.01). Half of depressed adenomas were reddish in color, whereas only 18% of protruding adenomas were reddish. Magnifying endoscopy with narrow band imaging showed that 71% of depressed adenomas had a regular ultrafine network pattern of mucosal microvasculature, which was not seen in protruding adenomas. Intramucosal carcinomas were more frequently found in depressed adenomas (25%) than in protruding adenomas (4.5%). CONCLUSIONS: In comparison with protruding adenomas, depressed adenomas were rare and appeared endoscopically as large and reddish with a specific regular ultrafine network pattern of mucosal microvasculature. Depressed adenomas should be endoscopically resected because intramucosal carcinomas were found in a quarter of them.

Magnifying endoscopy combined with narrow band imaging system for early gastric cancer: correlation of vascular pattern with histopathology (including video).

BACKGROUND AND STUDY AIMS: The narrow band imaging (NBI) system consists of a sequential electronic endoscope system and a source of light equipped with new narrow band filters, yielding very clear images of microvessels on mucosal surfaces. The aim of this prospective study was to measure the correlation between the magnified images obtained with the NBI system and the histological findings, especially with regard to the vascular pattern. In addition, three-dimensional images of microvessels were reconstructed using a laser scanning microscope. PATIENTS AND METHODS: Between July 2001 and August 2003, 165 patients with depressed-type early gastric cancer lesions were enrolled in the study. The lesions were carefully observed with magnification using the NBI system. The images, the pathological characteristics of the lesions, and three-dimensionally reconstructed images of the microvascular networks in biopsied specimens were carefully analyzed. The microvascular patterns were classified into three groups: A, fine network; B, corkscrew; and C, unclassified pattern. The endoscopic images were compared with the histological findings. RESULTS: Of the three types of filter available for use with the NBI system, microvascular formation was best enhanced in B mode images produced using short wavelengths, which focus on the superficial mucosal layer. Among 109 cases of differentiated adenocarcinoma, the group A microvascular pattern was observed in 72 cases (66.1 %). Among 56 cases of undifferentiated adenocarcinoma, the group B pattern was observed in 48 cases (85.7 %; P = 0.0011) The microvascular structure observed using the NBI system corresponded with the superficial mucosal layer in the three-dimensional images obtained using laser scanning microscopy and the resected specimens. CONCLUSIONS: Magnifying endoscopy performed in combination with the NBI system is not sufficient to replace conventional histology, but is capable of predicting the histological characteristics of gastric cancer lesions.

Improvement in gastric histology following Helicobacter pylori eradication therapy in Japanese peptic ulcer patients.

We aimed to determine if successful or failed eradication of Helicobacter pylori with triple therapy causes any difference in gastric mucosal histology. Japanese H. pylori-positive patients with a healed peptic ulcer received high (n = 112) or low (n = 113) doses of triple therapy (omeprazole, amoxicillin and clarithromycin) for 1 week. Biopsies from the greater curvature of the central antrum and upper corpus were taken 6 weeks and 30 weeks after treatment completion, and gastric mucosal histology compared between successful (n = 171) and failed (n = 34) eradication groups. Morphological variables of gastritis were graded according to the updated Sydney System. Successful eradication therapy was defined as improvement in inflammation, neutrophil activity and atrophy; failed eradication therapy as improvement in inflammation and neutrophil activity only. Gastric mucosal atrophy gradually improved (in addition to improvements in inflammation and neutrophil activity) with successful eradication of H. pylori infection.

Ab initio study of reactions between halogen atoms and various fuel molecules by Gaussian-2 theory.

Ab initio calculations by using Gaussian-2 theory have been carried out for the reactions between halogen atoms and various fuel molecules, i.e. fluorine, chlorine, and bromine atoms vs. hydrogen, methane, ethane, ethylene, acetylene, ammonia, silane, dichlorosilane and phosphine. The activation energy for the reaction between a halogen atom and a fuel molecule seems to indicate whether the reaction between the fuel gas and the corresponding halogen gas occurs spontaneously when they are brought into contact to each other at room temperature.

Canine H(+)-K(+)-ATPase alpha-subunit gene promoter: studies with canine parietal cells in primary culture.

H(+)-K(+)-adenosinetriphosphatase (H(+)-K(+)-ATPase) is the principal enzyme responsible for the process of gastric acid secretion. This enzyme is expressed in a cell-type-specific manner in gastric parietal cells. To explore the mechanisms regulating its expression, we transfected differentiated canine parietal cells in primary culture with H(+)-K(+)-ATPase-luciferase reporter genes and assessed transcriptional activities. Deletional analysis of the 5'-flanking region of this gene demonstrated a remarkable increment in transcriptional activity associated with a segment between bases -54 to -45 (5' GCTCCGCCTC 3') relative to the transcriptional initiation site. Gel shift assays with competition and supershift analysis demonstrated that this segment is specifically bound by the transcription factor Sp1. A point mutation, eliminating Sp1 binding, diminished basal transcriptional activity by 80%, indicating that this Sp1 binding site is important for constitutive transcriptional activity. Although these studies indicate that Sp1 is required to maintain a high concentration of the H(+)-K(+)-ATPase gene in the parietal cell, its cell-type-specific expression must rely on other elements because Sp1 is a ubiquitously expressed transcription factor.

Epidermal growth factor induces H+,K+-ATPase alpha-subunit gene expression through an element homologous to the 3' half-site of the c-fos serum response element.

Epidermal growth factor (EGF) acutely inhibits acid secretion; however, prolonged administration of EGF has been reported to increase acid production. We undertook these studies to examine whether the physiological effects of EGF on acid secretion are mediated by regulation of gastric H+,K+-ATPase, the principle enzyme responsible for acid secretion. EGF in concentrations equivalent to those in plasma increased H+,K(+)-ATPase alpha-subunit mRNA levels. Using H+,K(+)-ATPase-luciferase constructs transfected into primary cultured parietal cells, a significant step up in EGF inducibility was observed between bases -162 and -156 (5'-GACATGG-3') relative to the cap site. This EGF response element (ERE) conferred EGF inducibility when linked to homologous and heterologous promoters. The ERE is homologous to the 3' half-site of the c-fos serum response element to which rNFIL-6, rE12, and SRE-ZBP bind. Electrophoretic mobility shift assays using an ERE probe and parietal cell nuclear extracts revealed a specific DNA-protein complex, the formation of which was changed by neither E12 and NFIL-6 consensus oligonucleotides nor antibodies for NFIL-6, SRE-ZBP, and E12. Our studies indicate that EGF induces gastric H+,K(+)-ATPase alpha-subunit gene expression via an interaction between a specific ERE and a novel transcriptional factor and that this may be a physiologic mechanism by which EGF regulates acid secretion.

Glycine-extended progastrin processing intermediates induce H+,K(+)-ATPase alpha-subunit gene expression through a novel receptor.

Biologically active amidated gastrin is synthesized by carboxyl-terminal alpha-amidation of a glycine-extended progastrin post-translational processing intermediate (G-Gly). Although plasma levels of G-Gly are equivalent to those of gastrin, G-Gly has essentially no acute effect on gastric acid secretion. However, we have observed that inhibition of gastrin amidation leads to increased plasma concentrations of G-Gly and enhanced gastric acid secretion. We hypothesized, therefore, that G-Gly might have a chronic effect to increase H+,K(+)-ATPase expression in gastric parietal cells. In the present studies, we observed that a 2-day preincubation with G-Gly significantly enhanced histamine-stimulated [14C]aminopyrine uptake by isolated canine gastric parietal cells but acutely administered G-Gly had no effect. On Northern blot analysis, both G-Gly and gastrin dose-dependently increased H+,K(+)-ATPase alpha-subunit gene expression with maximal induction (225 +/- 35 and 170 +/- 29% of basal, mean +/- S.E.) achieved at concentrations of 10(-9) M G-Gly and 10(-8) M gastrin, respectively. Using an H+,K(+)-ATPase alpha-subunit gene-luciferase chimeric reporter construct transfected into primary cultured parietal cells, we observed that both G-Gly and gastrin increased luciferase activity in a manner similar to that obtained by Northern blot analysis. L365,260, a specific gastrin/CCKB receptor antagonist, completely reversed the stimulation of luciferase activity induced by gastrin but had no effect on G-Gly-stimulated activity. Gastrin increased [Ca2+]i, although G-Gly did not, however, genistein (a tyrosine kinase inhibitor) significantly reduced induction of luciferase activity by both G-Gly and gastrin. Specific binding of 125I-Leu15-G2-17-Gly to gastric parietal cells was dose-dependently displaced by G2-17-Gly but not by gastrin nor L365,260. Gastrin peptides truncated at the carboxyl- (G1-13) and amino terminus (G5-17-Gly) both induced H+,K(+)-ATPase alpha-subunit gene expression and inhibited 125I-Leu15-G2-17-Gly binding, but were less potent than G2-17-Gly. These data indicate that G-Gly may have a functional role in potentiating gastric acid secretagogue action via enhanced expression of the gene responsible for H+ generation through action at a novel receptor that can be distinguished from the gastrin/CCKB receptor. Thus, both the substrate and product of the terminal progastrin processing reaction appear to have complementary functions in regulation of gastric acid secretion.

Catecholamine concentrations in biopsied gastroduodenal tissue specimens of patients with duodenal ulcer.

We measured dopamine and norepinephrine concentrations in the biopsied gastroduodenal mucosa obtained from 12 ulcer-free dyspeptic patients, nine patients with active duodenal ulcer, and eight patients with inactive (or healed) duodenal ulcer using a high-performance liquid chromatography with electrochemical detection method. Biopsy specimens were taken from endoscopically normal-appearing mucosa in the gastric body and antrum as well as in the duodenal bulb. Additional specimens were obtained from the outer edge of the ulcer margin in patients with active duodenal ulcer. The mean (+/- SD) mucosal dopamine concentrations in the gastric body and duodenum (7.6 +/- 2.8 and 6.8 +/- 2.6 pg/mg tissue) obtained from patients with inactive duodenal ulcer were significantly (P < 0.05) lower than those from dyspeptic patients (13.6 +/- 6.9 and 10.9 +/- 3.5 pg/mg tissue, respectively). In contrast, no significant differences were observed in the mean norepinephrine concentrations in these gastroduodenal tissues among the three study groups. However, the mean mucosal norepinephrine concentration in the outer edge of duodenal ulcer (86.2 +/- 125.6 pg/mg tissue) was significantly (P < 0.05 and 0.01) reduced as compared with that in the ulcer-free area of duodenum obtained from patients with inactive duodenal ulcer (257.1 +/- 188.2 pg/mg tissue) and from dyspeptic patients (276.8 +/- 138.3 pg/mg tissue). The results suggest that an alteration in the catecholaminergic system may be associated with one of the pathogenic factors of duodenal ulcer.

Dopaminergic control of gastric mucosal blood flow in humans. A study with endoscopic laser Doppler flowmetry coupled with gastric submucosal drug injection.

We studied the dopaminergic regulation of the gastric mucosal blood flow (GMBF) measured with an endoscopic laser Doppler flowmetry in 27 healthy volunteers. They were randomly assigned to receive an endoscopic gastric submucosal injection (0.5 ml) of physiological saline (control group, N = 10), 50 micrograms of dopamine (DA) hydrochloride (N = 8), and 500 micrograms of a DA antagonist, metoclopramide (MCP) (N = 9). The drugs were dissolved in the same saline volume (0.5 ml) as used in control group and were injected via the mucosal area where the baseline GMBF was measured and the postdose GMBF was monitored until 5 min postdose. There was no significant difference in the mean (+/- SEM) baseline laser Doppler signals among the control, DA, and MCP groups (92.6 +/- 9.3, 81.8 +/- 9.0 and 96.9 +/- 13.3 mV, respectively). In the control group, no significant postdose changes in the laser Doppler signals occurred until 5 min postinjection. In contrast, the DA group exhibited a significant (P < 0.05 or 0.01) increase in the laser Doppler signals at 2, 3, 4, and 5 min postdose (118.9 +/- 18.8, 128.5 +/- 16.9, 146.6 +/- 18.6, and 131.2 +/- 14.2 mV, respectively), whereas the MCP group exhibited a significant (P < 0.05 or 0.01) decrease in the signals at 4 and 5 min postdose (67.9 +/- 5.3 and 64.8 +/- 3.5 mV, respectively), as compared not only with the respective baseline values but also with those obtained from other two groups at the corresponding postinjection periods.(ABSTRACT TRUNCATED AT 250 WORDS)

[Hypergastrinemia and type A gastritis in Basedow's disease].

Hypergastrinemia is a very important clinical condition for the reason that a growing body of evidence obtained from animal and human experiments has revealed gastric carcinoids induced by hypergastrinemia. We investigated 35 patients with Basedow's disease (BD) to elucidate the mechanism of hypergastrinemia associated with BD as well as the relationship between type A gastritis and BD. Fasting serum gastrin levels in BD (296.1 +/- 251.4 pg/ml; mean +/- S.D.) were significantly (p less than 0.001) higher than those in age-matched 27 healthy subjects (106.1 +/- 69.2), and in the BD group, significant positive correlation was detected between fasting serum gastrin levels and thyroid hormones (i.e. T3 and free T4). In the hyperchlorhydria group in BD with hypergastrinemia, the levels of fasting serum gastrin were normalized after euthyroidism was attained due to antithyroidal drugs. On the other hand, in the achlorhydria group in BD significant hypergastrinemia was persisted in spite of normalization of thyroid function. Twenty % of the BD patients had histologically proved type A gastritis with achlorhydria, and all patients with type A gastritis were older than 60 years old. Endoscopic examination revealed that one patient with type A gastritis had an early gastric cancer. However, no gastric carcinoids were demonstrated in this study. In conclusion, the results described as above suggested, 1) hypergastrinemia observed in patients with BD may be induced by gastrin hypersecretion due to hyperthyroidism as well as type A gastritis, 2) BD patients with type A gastritis were recommended to undertake regular endoscopic examination for detecting gastric cancers as well as gastric carcinoids.

A case of phacomatosis pigmentovascularis accompanied with esophageal varices due to hypoplasia of the portal veins.

Phacomatosis pigmentovascularis is a rare complex nevus accompanied with various types of developmental abnormalities. We experienced a case of phacomatosis pigmentovascularis with esophageal varices due to hypoplasia of the portal veins. Although computed tomography demonstrated marked atrophy of the right hepatic lobe and compensatory hypertrophy of the left hepatic lobe, laparoscopy revealed no signs of chronic parenchymal liver disease on the liver surface. In addition, no microscopically identifiable pathological findings were observed in the needle-biopsied liver specimens. Angiographic study revealed vascular hypoplasia not only in the portal veins of the right hepatic lobe but also in bilateral iliac veins. To our knowledge, this is the first case of phacomatosis pigmentovascularis accompanied with vascular hypoplasia in the portal veins as well as in systemic veins. It is suggested that the disorders associated with mesodermal developmental abnormalities (e.g. phacomatosis pigmentovascularis, Klippel-Trenaunay-Weber syndrome) may be complicated with developmental vascular abnormalities in the portal veins.