Chifumi Yamamoto

Treatment of herpes simplex esophagitis in an immunocompetent patient with intravenous acyclovir: a case report and review of the literature.

A 35-yr-old, immunocompetent male was admitted complaining of severe odynophagia. He was diagnosed as having herpes simplex esophagitis and was started on intravenous acyclovir 5 mg/kg every 8 h on the day of admission. His response was dramatic. Within 24 h he was virtually asymptomatic. Acyclovir therapy in immunocompetent adults with esophagitis has been described in only a handful of cases in the literature, although the therapy is well established in immunocompromised patients. We review the English literature and discuss the efficacy of the therapy. Acyclovir therapy may be beneficial in immunocompetent patients with particularly severe odynophagia.

Calcitonin gene-related peptide affords gastric mucosal protection by activating potassium channel in Wistar rat

BACKGROUND & AIMS Calcitonin gene-related peptide (CGRP) protects the gastric mucosa against injurious stimuli in various experimental models. The underlying mechanism could be the increase in gastric mucosal blood flow (GMBF). A number of endogenous vasodilators exert their effects through the activation of adenosine triphosphate (ATP)-sensitive potassium (KATP) channels on vascular smooth muscle. The present experiments were performed to elucidate whether CGRP increases GMBF through the activation of KATP channels and whether the channels are involved in the protection by CGRP of gastric mucosa. METHODS GMBF was determined by the hydrogen-clearance technique in male Wistar rats. Mucosal lesions were produced by intragastric superfusion with 0.15N HCland 15% ethanol for 40 minutes. Effects of an agonist (Y-26763, intra-arterially) and an inhibitor (glibenclamide, intravenously) of KATP channels were tested. RESULTS Y-26763 increased GMBF, which was abolished by glibenclamide, and a CGRP-induced increase in GMBF was attenuated by glibenclamide. Macroscopic and microscopic lesions were exacerbated by human CGRP-(8-37) (a CGRP-1 receptor antagonist; intra-arterially) and glibenclamide but were ameliorated by exogenous CGRP (intra-arterially). CONCLUSIONS CGRP protects the gastric mucosa against ulcerogenic stimuli, at least in part, through the activation of KATP channels in rats.

Oral administration of mesalazine protects against mucosal injury and permeation in dextran sulfate sodium-induced colitis in rats

Abstract Objective. Mesalazine, from which 5-aminosalicylic acid is released, is a therapeutic drug for inflammatory bowel disease. There has been no study concerning the effect of orally administered mesalazine on dextran sodium sulfate (DSS)-induced colitis in the rat model of ulcerative colitis. Material and methods. Colitis was evaluated by means of the length of the colon, white blood cell count (WBC), tissue myeloperoxidase (MPO) activity, and histological inflammation scores. Colonic mucosal permeation was evaluated using Evans blue. The localization of a tight junction protein, occludin, was evaluated immunohistochemically and examined using confocal laser scanning microscopy. Results. Mesalazine significantly improved changes in the length of the colon, tissue MPO activity, WBC, and the histological inflammation score as compared with DSS-induced colitis. Furthermore, the drug completely inhibited the increased permeation in DSS-induced colitis in rats. The immunofluorescence signals of occludin were disrupted and irregularly distributed in DSS-induced colitis, while the signals appeared as a typical reticular pattern but with reduced intensity by the administration of mesalazine, without any reduction in the protein content. In addition, the oral administration of mesalazine significantly improved mucosal permeation, thereby protecting the intestinal mucosa against injury in DSS-induced colitis in rats. Conclusions. These findings suggest that the recovery of mucosal impairment due to treatment with mesalazine may be associated with the protection of the tight junction protein occludin in DSS-induced colitis.

Double doses of secretin contribute to diagnosis of Zollinger-Ellison syndrome in secretin and selective arterial secretion injection tests- : A case report

Zollinger–Ellison syndrome (ZES) involves hypergastrinemia produced by a gastrin-secreting tumor of the pancreas or duodenum. A fasting gastrin level higher than 1000 pg/ml and a basal acid output greater than 15 mEq/hr in patients with recalcitrant peptic ulcers are diagnostic for ZES (1). In the absence of these data, provocative testing, such as the secretin and calcium tests, may be required. The secretin test offers the greatest sensitivity and specificity. Unfortunately secretin tests can be negative in a significant population of patients with ZES (2, 3). Previous studies demonstrated that the secretin test is positive in 87 to 93% of all patients diagnosed with ZES (1). In the standard secretin test, an intravenous bolus of 2 μg/kg of secretin, where 1 μg is equivalent to 2 U, is infused (1). However, Matsui et al. reported that a secretin dose of 6 U/kg proved more useful than the standard 3 U/kg dose in four patients diagnosed with ZES (4). The selective arterial secretion injection test (SASI) is useful in localizing gastrinomas (5–8). The standard dose of secretin for the SASI is usually 3 U/kg (5, 6) or 30 U (7, 8). In our patient, diagnosed with hypergastrinemia and recalcitrant peptic ulcer, the secretin and SASI tests yielded negative outcomes using 3 U/kg of secretin but were positive when 6 U/kg of secretin was

A case of Meckel's diverticulum adherent to the posterior abdominal wall: the efficacy of small-bowel radiography coupled with barium enema examination

with mild chronic inflammatory infiltrates and foci of ectopic gastric mucosa. The patient’s postoperative course was uneventfull, and he was discharged without complications after the surgical resection. Meckel’s diverticulum is the most common congenital anomaly of the gastrointestinal tract.1 In children, 99mTc scanning is proposed be a sensitive and specific diagnostic procedure, as most bleeding diverticula contain gastric mucosa.2 However, even with bleeding, this method has high false-positive and false-negative rates in adult patients.3 Moreover, a CT scan cannot clearly distinguish a Meckel’s diverticulum from a bowel loop in the abdomen and is thus not practical for preoperative diagnosis. In our patient, the Meckel’s diverticulum was adherent to the posterior abdominal wall, and findings on CT scan alone were insufficient to make the diagnosis of a Meckel’s diverticulum. However, on small-bowel radiography coupled with barium enema examination, the rounded collection of barium at the anal side of the stricture strongly suggested a Meckel’s diverticulum. In adults, obstruction (36.5%) is the most common complication of a Meckel’s diverticulum, followed by intussusception (13.7%), inflammation (12.7%), and hemorrhage (12%).4 Obstructive symptoms may occur when either (1) the diverticulum is attached by a fibrous band to the umbilicus, abdominal wall, or other viscera; or (2) the diverticulum is free and unattached.5 However, in our patient, the findings corresponded to neither situation, as the diverticulum had no fibrous band, but was attached to the posterior abdominal wall. We suggest that chronic inflammation of the Meckel’s diverticulum may have extended to the adjacent intestine, producing the ileal stricture and adhesion.

Effect of diet on changes in small intestinal blood flow following intracolonic administration of indomethacin to rats.

Liquid diet (LD) is known to be protective against indomethacin-induced enteropathy, which is thought to be associated with ischemic change. We tested the hypothesis that the solid component of diet modulates small intestinal blood flow (SIBF) following indomethacin administration. In the first experiment, male Wistar rats were divided into 18-hr-fasted and normal diet groups. Indomethacin (20 mg/kg) or vehicle was administered intracolonically. SIBF was measured on both the mesenteric and antimesenteric sides of the intestine, using the hydrogen gas clearance method. In the second experiment, rats were given LD alone or LD with increasing concentration of soluble/insoluble fiber for seven days. The baseline SIBF was significantly higher in the groups with normal diet and LD with fiber than in the fasting and LD groups. Following indomethacin administration, SIBF gradually decreased in the groups with normal diet and LD with insoluble fiber, while neither liquid diet nor fasting reduced SIBF. There was no difference in SIBF between the mesenteric and antimesenteric sides of the intestine in any group. Our findings suggest that solid components of diet increase basal SIBF and decrease SIBF following indomethacin administration.

The Effect of Polyethylene Glycol-Electrolyte on Dextran Sulfate Sodium-Induced Colitis in Rats

The Effect of Polyethylene Glycol-Electrolyte on Dextran Sulfate Sodium-Induced Colitis in Rats Chifumi Yamamoto, Kunihiko Aoyagi, Yoshihiro Hayashi, Isamu Morita, Shotaro Sakisaka Background & Aims: Polyethylene glycol-electrolyte (PEG-EL) is the most commonly used agent for mechanical bowel cleansing. Adverse events related to PEG-EL have included serum electrolyte disturbance, gastrointestinal discomfort and rectal mucosal abnormalities. However, there have been few studies evaluating the effect of PEG-EL on colitis, such as ulcerative colitis. The aim of this study was to evaluate the safety of PEG-EL in cases of both normal colon and dextran sulfate sodium (DSS)-induced colitis. Methods: Exp. 1; Twenty Male Wistar rats were divided into two groups, the DSS-induced colitis group and the normal colon group. Colitis was induced by administering 3% DSS in drinking water over a period of 6 days. Following the administration of DSS or distilled water, each group received either PEG-EL (Niflec , Ajinomoto Pharma, Tokyo, Japan) or distilled water for 14 hours (each group, n Z 5). Colitis was evaluated by tissue myeloperoxidase (MPO) activity and by the inflammation score as described by Cooper. A blood sample was taken from the portal vein to measure WBC, RBC and Hb. Exp. 2; The effect of PEG-EL in the DSS-induced colitis group (each group, n Z 5) was evaluated in the same way as in Exp. 1, 12, 24 and 48 hours after the administration of either PEG-EL or distilled water. Results: Exp. 1; PEG-EL did not change the inflammation score in either the normal colon group (0 vs. 0) or the DSS-induced colitis group (2.15 G 0.6 vs. 2.2 G 0.6, p Z 0.89). Similarly, MPO activity, RBC and Hb showed no significant change. However, WBC was significantly increased in the DSS-induced colitis group which received PEG-EL (69,440 G 1971 vs. 51,040 G 2288, p Z 0.019). Exp. 2; At 12, 24 and 48 hours, there was no significant difference in either the inflammation score or MPO activity in any of the groups (see Table). However, there was a tendency to be a delay in decreasing MPO activity at 12 hrs in the DSS-induced colitis group which received PEG-EL (see Table). Conclusions: The present study shows that PEG-EL histologically affected neither the normal colon nor DSS-induced colitis. However, the improvement in colitis showed an inclination to be delayed in the DSS-induced colitis group which received PEG-EL. Consequently, it is essential that adequate care is taken when we use PEG-EL for patients with colitis.