bluuebunny/crossref_metadata_2025_split huggingface dataset:
Treatment of Peptic Ulcer
Authors: Tytgat Guido N.J. 
Published: April 2003

The current therapy of choice for all <i>Helicobacter pylori</i>-associated ulcer disease is eradication therapy. Although adequate therapeutic regimens are currently available, often still ineffective therapies are tried. Cure of the infection essentially eliminates the ulcer diathesis. Cure of the infection is especially indicated in complicated/recalcitrant ulcer disease. Sadly, at present only a minority of peptic ulcer disease patients receive adequate eradication therapy. Cure of the infection does not equal full resolution of dyspeptic symptoms. A variable percentage of patients continues acid suppressant therapy for ongoing or newly developed dyspeptic or reflux symptoms. Acid-suppressant therapy, both for healing and for maintenance, remains the cornerstone of peptic ulcer therapy in all other circumstances (<i>H. pylori</i>-negative ulcer, aspirin/NSAID-induced ulceration, hyperacidity related ulcer etc.). Proton pump inhibitors are superior to H<sub>2</sub>RA<sub>S</sub> both for healing and for maintenance. Whether higher doses are occasionally necessary in <i>H. pylori</i>-negative ulcers, requires further study. Acid-suppressant therapy, even when prolonged, so far appears safe and well tolerated.
Malabsorption Syndromes
Authors: Bai Julio C. 
Published: April 2003

<b>Background/Aims:</b> Malabsorption syndromes commonly result from a pathological interference of the normal digestive process. There have been major advances in the last 4 years. The purpose of this review is to highlight in the form of a brief summary the most outstanding information available. <b>Methods:</b> The review was performed based on a medical literature search using MEDLINE (1993–1997), bibliographic reviews of book chapters and review articles. As a consequence of the extensive information incorporated in the period and the limited scope of this review, the review will focus in three aspects: (1) an overview on some clinical aspects of malabsorption; (2) diseases in which predominates the disturbed mucosal phase of the digestive process, and (3) providing information on diagnostic testing regarding malabsorption. <b>Results:</b> Major advances on celiac disease, Whipple’s disease, giardiasis, tropical sprue, malabsorption of oligo- and disaccharides, vitamin B<sub>12</sub> and bile salts are discussed. New aspects on diagnostic procedures for malabsorption are also presented. <b>Conclusion:</b> Although major advances have given a great support to the investigation of malabsorption, yet the syndrome remains a major diagnostic dilemma. Based on the limited availability of most diagnostic tests, a simple and practical diagnostic algorithm is presented.
Medical Treatment of Portal Hypertension
Authors: Bosch Jaime 
Published: April 2003

The medical treatment of portal hypertension has experienced marked progress in the past decade due to the production of effective portal hypertension therapy. This has been possible because of the better understanding of the pathophysiological mechanisms leading to portal hypertension. A major step forward was the introduction of beta-blockers for the prevention of bleeding and rebleeding from gastroesophageal varices. Effective therapy requires the reduction of the hepatic venous pressure gradient (HVPG) to 12 mm Hg or below, or at least by 20% of baseline values. Unfortunately, this is only achieved in <sup>1</sup>/<sub>3</sub>–<sup>1</sup>/<sub>2</sub> of patients. The combination therapy associated with isosorbide-5-mononitrate and propranolol or nadolol administration enhances the fall in portal pressure and increases the number of patients in whom HVPG decreases more than 20% and below 12 mm Hg. Randomized trials (RCTs) support the fact that combination therapy is more effective than propranolol or nadolol alone and better than sclerotherapy. In the treatment of acute variceal bleeding, pharmalogical therapy offers the unique advantage of permitting the provision of specific therapy immediately after arrival to hospital, or even during transferral to hospital by ambulance, since it does not require sophisticated personnel. Terlipressin has proved to be effective and to decrease mortality from bleeding. RCTs have shown that this drug is as effective and safer than emergency sclerotherapy. Therapy should be maintained for five days to prevent early rebleeding. Somatostatin is probably as effective as terlipressin.
Medical Therapy of Achalasia: A Benefit Reserved for Few
Authors: Bortolotti M. 
Published: April 2003

<i>Background:</i> The rationale for medical therapy of initial achalasia and the results obtained over the last 20 years in our laboratory are presented. <i>Methods:</i> Achalasic patients were selected as candidates for medical therapy on the basis of the presence of a slight esophageal dilation (<5 cm) on X-rays and a good manometric response to nifedipine administration. These patients were asked to take 10–20 mg of nifedipine sublingually 30–45 min before each meal for 2 weeks. Chronic medical therapy was continued only in those with an ‘excellent’ or ‘good’ clinical response to nifedipine and a lack of severe side effects. X-ray controls were planned every 6 months and manometric examination after the first 6 months. <i>Results:</i> Of the 56 patients selected in the above-mentioned manner, 17 had an insufficient clinical response or severe side effects during the initial trial and did not continue medical therapy. Of the 39 patients who started chronic medical treatment, 13 are still on therapy and 26 stopped after an average of 2.8 years: 17 because they underwent dilation or myotomy; 4 for unknown reasons, and 5 apparently recovered. Esophageal manometry was carried out in 4 of the latter patients and revealed that the achalasic motor pattern had been replaced by a near-normal pattern. <i>Conclusions:</i> We believe that medical treatment of achalasia should be carried out not only in those patients who cannot undergo invasive procedures or do not respond well to them, but also in patients with initial achalasia selected using the above-mentioned criteria, because regression of the disease could take place in some of them.
Pseudomembranous Colitis: Causes and Cures
Authors: Surawicz ChristinaM. , McFarland LynneV. 
Published: April 2003

Clostridium difficile is the most common nosocomial pathogen of the gastrointestinal tract and has increased in frequency over time. Typical symptoms of C. difficile infection include diarrhea, which is usually nonbloody, or colitis associated with severe abdominal pain, fever and/or gross or occult blood in the stools. Pseudomembranous colitis (PMC), the severest form of this disease, occurs as a result of a severe inflammatory response to the C. difficile toxins. This review focuses on PMC, as this severe form is associated with the greatest medical concern. Diagnosis rests on detection of C. difficile in the stool, either by culture, tissue culture assay for cytotoxin B or detection of antigens in the stool by rapid enzyme immunoassays. Oral therapy with metronidazole 250 mg 4 times a day for 10 days is the recommended first-line therapy. Vancomycin is also effective, but its use must be limited to decrease the development of vancomycin-resistant organisms such as enterococci. Vancomycin (125–500 mg 4 times a day for 10 days) should be limited to those who cannot tolerate or have not responded to metronidazole, or when metronidazole use is contraindicated, as in the first trimester of pregnancy. A therapeutic response within a few days is usual. Recurrence of symptoms after antibiotics occurs in 20% of cases and is associated with persistence of C. difficile in the stools. Further recurrences then become more likely. Therapy with antibiotics in a pulsed or tapered regimen is often effective as are efforts to normalize the fecal flora. The yeast Saccharomyces boulardii has been proven in controlled trials to reduce recurrences when given as an adjunct to antibiotic therapy. Careful hand washing and environmental decontamination are necessary to prevent epidemics.
Establishment and Characterization of a Human Rectal Neuroendocrine Carcinoma Xenograft into Nude Mice
Authors: Tanaka Noritake , Onda Masahiko , Seya Tomoko , Kanazawa Yoshikazu , Naito Zenya , Asano Goro , Oguro Tatsuo 
Published: April 2003

<i>Background:</i> Carcinoid tumor has been recognized as having a much wider spectrum than was previously thought. Now the term ‘neuroendocrine carcinoma’ (NEC) has been suggested to describe malignant epithelial tumors of neuroendocrine differentiation. Its biological behavior has not been well characterized because of the lack of in vivo models. <i>Materials and Methods:</i> A metastatic inguinal lymph node from rectal NEC was used for heterotransplantation into nude mice. Histochemical and immunohistochemical stainings were performed in addition to ultrastructural investigations. Hormonal peptides were measured in both xenograft tumor tissue and serum. <i>Results:</i> We succeeded in heterotransplantation of human rectal NEC into nude mice. To date tumorigenicity has been retained for approximately 38 months. The xenograft tumor was a histopathologically identical tumor. The immunohistochemical expression of the various hormonal peptides in the xenograft was essentially the same as that of the primary rectal tumor. Tissue and serum hormonal peptides in the xenografted tumor were measured. Serum glucagon and serotonin were significantly higher than in control mice. <i>Conclusions:</i> The expression of various hormonal peptides in NEC may vary depending on the surrounding environment. The establishment of NEC in xenografts provides a model for further study of the biological behavior of NEC, as well as the in vivo effects of chemotherapeutic agents on tumor growth and the release of hormonal peptides.
Role of Endothelins in Trinitrobenzene Sulfonic Acid-Induced Colitis in Rats
Authors: Gulluoglu Bahadır M. , Kurtel Hızır , Gulluoglu Mine G. , Yegen Cumhur , Aktan A. Özdemir , Dizdaroglu Ferhunde , Yalin Rıfat , Yegen Berrak Ç. 
Published: April 2003

To determine the role of endothelins (ET) on experimental colitis, following intracolonic trinitrobenzene sulfonic acid administration, rats were given orally either bosentan (BS), a nonselective ET receptor antagonist (100 mg/kg in 5% arabic gum), or arabic gum by gavage for 2 or 14 days. Macroscopic damage scores obtained in the vehicle (1.4 ± 0.4), acute (4.8 ± 0.6) and chronic (3.8 ± 0.3) colitis groups were significantly higher than in the control group (0). BS treatment reduced the scores in both acute (3 ± 0.5) and chronic (2.3 ± 0.5) colitis groups. Myeloperoxidase (MPO) activities of colonic tissues were elevated in acute and chronic colitis groups (325.1 ± 44.9 and 431.8 ± 54.6 U/g wet weight) as compared with the control group (73.6 ± 11 U/g wet weight). Plasma protein oxidation levels were found to be significantly increased in the chronic colitis group (1,158.1 ± 63.4 nmol/ml) compared with the control, ethanol and acute colitis groups (274.3 ± 23.1, 490 ± 52.2 and 422.2 ± 50.5 nmol/ml). BS treatment significantly reduced both the protein oxidation level (375.5 ± 46.9 nmol/ml) and MPO activity (167.5 ± 35.8 U/g wet weight). The results of the present study suggest the involvement of ETs in the pathogenesis of colonic injury in this animal model of colitis.
Increased Susceptibility of Diabetic Rat Gastric Mucosa to Food Deprivation during Cold Stress
Authors: Korolkiewicz Roman , Tashima Kimihito , Kubomi Masafumi , Kato Shinichi , Takeuchi Koji 
Published: April 2003

<i>Background:</i> We investigated the mechanisms responsible for the increased susceptibility of diabetic rat gastric mucosa to damage inflicted by overnight food deprivation (18 h) and its worsening by the cold restraint stress (4°C, 3 h). <i>Methods:</i> Gastric damage was measured in fasted animals, some of which were rendered diabetic by a single intraperitoneal injection of streptozotocin (STZ; 70 mg/kg) 5 weeks before experiments (STZ 5W). <i>Results:</i> STZ 5W rodents showed a number of hemorrhagic lesions in corpus mucosa (26.8 ± 5.2 mm<sup>2</sup>) which could be prevented by insulin or nitric oxide synthase (NOS) inhibitors: aminoguanidine or L-NAME (N<sup>ω</sup>-nitro-L-arginine methyl ester). Mucosal injury was further aggravated by low temperature (51.1 ± 7.8 mm<sup>2</sup>), the damage ameliorated by insulin, aminoguanidine, or L-NAME. The salutary actions of L-NAME were L-arginine sensitive. Low temperature and L-NAME did not significantly influence the gastric secretory parameters in normal rats. On the other hand, L-NAME and aminoguanidine counteracted the attenuation of gastric juice acidity and acid output in STZ 5W rodents. Blood plasma nitrite and nitrate levels and outputs in gastric juice were augmented in STZ 5W animals in comparison to controls. The total activities of NOS including inducible NOS but not constitutive NOS were markedly enhanced by fasting and cold restraint in gastric mucosa of STZ 5W animals (2.2- and 3.7- or 2.4- and 17.9-fold respectively). <i>Conclusions:</i> Stressful stimuli, such as food bereavement and cold challenge contribute to the elevated susceptibility of diabetic gastric mucosa to damage, even though the main aggressive factor, i.e., gastric acid secretion, is attenuated. The enhanced production of nitric oxide by inducible NOS during food deprivation and cold exposure seems to play an important role in gastric mucosal integrity disturbances during diabetes.
Tumor Necrosis Factor-Alpha in Ileal Mast Cells in Patients with Crohn’s Disease
Authors: Lilja I. , Gustafson-Svärd C. , Franzén L. , Sjödahl R. 
Published: April 2003

<i>Background:</i> Reports that both intestinal and extraintestinal Crohn’s disease (CD) had healed successfully after treatment with anti-tumor necrosis factor-alpha (TNF-α) antibody have strengthened the hypothesis that it has a role in the treatment of CD. The macrophage is one source of TNF-α. Intestinal mast cells are also thought to have a role in CD, but it is not known if human ileal mast cells express TNF-α. <i>Aim:</i> To find out whether TNF-α is expressed by mast cells in the ileal wall in CD patients and controls. <i>Methods:</i> TNF-α was sought immunohistochemically in full thickness specimens of ileal wall from patients with CD (histologically normal, n = 9; inflamed, n = 6) and controls (patients with colonic cancer, n = 8). Mast cells were identified by metachromasia and anti-mast cell tryptase immunoreactivity. <i>Results:</i> In all layers of the ileal wall, and in every specimen investigated, mast cells were the main cell type that expressed TNF-α immunoreactivity out of the TNF-α-labelled cells. The number of TNF-α- labelled mast cells was greater in the muscularis propria in patients compared with controls, both in uninflamed (1.7-fold, p < 0.05) and in inflamed bowel (4.6-fold, p < 0.002); greater in the submucosa in inflamed compared with uninflamed CD (1.6-fold, p < 0.01), and less in the lamina propria in inflamed compared with uninflamed CD (0.4-fold, p < 0.05). <i>Conclusion:</i> Mast cells are an important source of TNF-α in all layers of the ileal wall, and the increased density of TNF-α-positive mast cells in the submucosa and muscularis propria may contribute to the tissue changes and symptoms in CD.
Role of Vascular Endothelial Growth Factor in Portal Hypertensive Gastropathy
Authors: Tsugawa Kouji , Hashizume Makoto , Migou Shinichirou , Kishihara Fumiaki , Kawanaka Hirofumi , Tomikawa Morimasa , Sugimachi Keizo 
Published: April 2003

<i>Background and Aims: </i>Portal hypertensive gastropathy (PHG) is now recognized as a distinct entity; however, the angiogenesis in the portal hypertensive gastric mucosa has yet to be elucidated. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor involved in both physiological and pathological angiogenesis. The aim of this study was thus to examine the function of VEGF in the portal hypertensive and non-portal hypertensive gastric mucosa. <i>Method:</i> Forty-five cirrhotic patients were divided into 3 groups as follows. Group I included 15 patients without PHG who were treated with 1.5 g teprenone/day for 8 weeks: PHG(–)-t. Group II included 15 patients with PHG who were not treated with teprenone: PHG(+)-n. Group III included 15 patients with PHG who were treated with teprenone for 8 weeks: PGH(+)-t. The gastric mucosal blood flow (GMBF), the concentration of gastric mucosal VEGF and hexosamine and the endoscopic findings were studied both before and after medication. <i>Results:</i> Before teprenone treatment, the GMBF in the antrum, fundus, fornix were significantly higher in PHG(+)-n than PHG(–)-t. After treatment, the GMBF in the fundus and fornix significantly decreased more than before treatment in the PHG(+)-t. After treatment, the GMBF in the antrum increased significantly more than before treatment in PHG(–)-t. The gastric VEGF and hexoxamine concentration in the antrum were significantly higher in PHG(+)-n than in PHG(–)-t. After treatment, the gastric VEGF and hexosamine concentration in the antrum significantly decreased in PHG(+)-t while no change in concentration was recognized in PHG(+)-n. In the endoscopic findings, a decrease in the PHG score was recognized in 2 patients in PHG(+)-t. <i>Conclusion:</i> Portal hypertensive gastric mucosal change was thus found to trigger a high concentration of VEGF and hexosamine. Such increased activity of VEGF and hexosamine may thus account for the presence of active congestion in PHG.
Starvation, Leptin and Epithelial Cell Proliferation in the Gastrointestinal Tract of the Mouse
Authors: Chaudhary M. , Mandir N. , FitzGerald A.J. , Howard J.K. , Lord G.M. , Ghatei M.A. , Bloom S.R. , Goodlad R.A. 
Published: April 2003

<i>Background/Aims:</i> Leptin, the ob/ob gene product, is a recently discovered peptide hormone, secreted by adipocytes, which can act as a satiety factor to regulate food intake. Its levels thus will be related to the presence of food in the lumen of the gut, and food intake is one of the most potent stimuli for intestinal epithelial cell proliferation. Leptin has a variety of other actions and the aim of this study was to see if one of these was to stimulate mucosal growth. <i>Methods: </i>Three groups of mice were fed ad libitum, starved for 48 h or starved for 48 h and given twice-daily intraperitoneal injections of recombinant leptin (1 μg/g). <i>Results:</i> Starvation led to a 20% decrease in body weight and a similar decrease in the weights of the intestines. Starvation also markedly inhibited intestinal epithelial cell proliferation. Leptin had little effect on the small intestine and did not stimulate proliferation. However, in the hind gut it was associated with small but significant decreases in caecal weight, distal colon mitotic counts (p = 0.036) and in colonic crypt area (approximately 20%, p < 0.001). <i>Conclusion:</i> Leptin did not stimulate intestinal cell proliferation, however it did have a paradoxical inhibitory action on the caecum and colon.
An Audit of the Perceived Efficacy and Tolerability of Gabapentin Therapy in an Out-Patient Cohort with Chronic Epilepsy
Authors: Langan Y. , Duncan J.S. , Sander J.W.A.S. 
Published: April 2003

A retrospective audit of the perceived efficacy and tolerability of adjunctive gabapentin (GBT) therapy in patients with intractable epilepsy was carried out. The case-notes of 263 consecutive patients attending a tertiary referral centre in whom GBT had been added to concomitant anti-epileptic drugs were reviewed. There were 119 males (45%); the median age was 35 years (range 15–81 years) and the median duration of epilepsy was 20 years. The median dose of GBT administered was 1,600 mg (range 300–4,800 mg). Twenty-nine patients (11%) had a reduction in seizure frequency of greater than 50% and 7 (3%) achieved seizure freedom of 6 months’ duration at least while taking GBT. Side-effects were reported by 169 patients (61%) and in 40 (15%) an increase in seizure frequency of 50% occurred, this being the commonest reason for GBT withdrawal. The median duration of treatment was 4 months (range 0.03–47 months). Ten patients, in whom GBT therapy had proven ineffective in doses of 900–1,800 mg, were rechallenged with doses of 300–4,800 mg. One individual experienced a 50% reduction in seizure frequency and 1 an increase in seizures of at least 50%. GBT was generally well tolerated at high doses and rechallenge of a small number with GBT in doses up to 4,800 mg did not result in further improvement in seizure frequency in the majority.
Measurement of (1→3)-β-<i>D</i>-Glucan in an Experimental Model of Systemic Candidiasis
Authors: Kawagoe T. , Nakao A. , Kanbe T. , Tamura H. , Tanaka S. , Takagi H. 
Published: April 2003

To investigate the utility of measuring blood concentrations of (1→3)-β-<i>D</i>-glucan, a component of the fungal cell wall, as an auxiliary diagnostic method for systemic candidiasis, rats were inoculated with <i>Candida albicans</i> and the number of <i>C. albicans</i> in the viscera and glucan in the blood were quantitated. The concentration of blood glucan and the number of <i>C. albicans</i> in the viscera were also measured both under leukopenia and with deteriorated reticuloendothelial system cell function, and when the liver and spleen had been excised. As a result, systemic candidiasis appeared in the group with leukopenia, and the number of living <i>C. albicans</i> increased in the kidney and liver. Together with this increase in the number of <i>C. albicans</i>, there was an increase in blood (1→3)-β-<i>D</i>-glucan. Measurements of blood (1→3)-β-<i>D</i>-glucan well reflect a proliferation of <i>C. albicans</i> in vivo, which would make this a useful auxiliary for the clinical diagnosis of systemic mycosis.
Metabolism of Superoxide Dismutase during the Adynamic Ileus of Endotoxemia
Authors: Cullen J.J. , Ephgrave Kimberly S. , Hemann Lynda L. , Hinkhouse Marilyn , Conklin J.L. 
Published: April 2003

Endotoxemia is accompanied by gastrointestinal motor disturbances while administration of oxygen free radical scavengers following endotoxemia ameliorates these motor disturbances. We hypothesized that the motor disturbance produced by endotoxemia may be associated with a change in the activity or production of superoxide dismutase (SOD). Strain gauge transducers were placed on the stomach and small bowel of dogs to determine fasting gastrointestinal motility. Manganese and copper/zinc SOD enzyme activities in gut smooth muscle were measured and protein expression was analyzed by Western blotting. Following completion of the baseline studies, dogs were given a single dose of <i>Escherichia coli</i> lipopolysaccharide, 200 µg/kg i.v., and the studies repeated for the next 3 days. Following endotoxin bolus, the migrating motor complex (MMC) was delayed for 2 days while gastric and jejunal smooth muscle levels of Cu/Zn SOD activity were decreased for 1 day in the stomach and for 2 days in the jejunum. Western blotting indicated that endotoxin did not change the amount of SOD enzyme produced. We conclude that endotoxemia results in a temporary prolongation of the MMC and a decrease in Cu/Zn SOD activity. Expression of Cu/Zn SOD and Mn SOD does not seem suppressed by endotoxin as measured by Western blotting. However, the impairment of Cu/Zn SOD activity may contribute to ileus associated with sepsis by altering oxygen-free metabolism in both the stomach and jejunum.