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1.  Hepatolithiasis with biliary ascariasis – a case report 
BMC Gastroenterology  2003;3:35.
Background
Biliary ascariasis is regarded as possible etiological factor for hepatolithiasis. Here we report one case of a patient with hepatolithiasis with biliary ascariasis who developed a liver abscess, which was treated with partial hepatectomy.
Case presentation
A young adult female presented with epigastric pain and vomiting with repeated attacks of cholangitis. ERCP showed evidence of multiple intrahepatic calculi with the development of abscess in the left lobe of liver. The patient underwent partial hepatectomy and was found to have biliary ascariasis on histology. She was treated with antihelmenthic therapy and has had an uneventful postoperative period of 2 years.
Conclusion
Biliary ascariasis with hepatolithiasis, although rare, should be considered in endemic countries.
doi:10.1186/1471-230X-3-35
PMCID: PMC324404  PMID: 14687416
2.  A novel mutation of the calcium sensing receptor gene is associated with chronic pancreatitis in a family with heterozygous SPINK1 mutations 
BMC Gastroenterology  2003;3:34.
Background
The role of mutations in the serine protease inhibitor Kazal type 1 (SPINK1) gene in chronic pancreatitis is still a matter of debate. Active SPINK1 is thought to antagonize activated trypsin. Cases of SPINK1 mutations, especially N34S, have been reported in a subset of patients with idiopathic chronic pancreatitis. However, the inheritance pattern is still unknown. Some cases with N34S heterozygosity have been reported with and without evidence for CP indicating neither an autosomal recessive nor dominant trait. Therefore SPINK1 mutations have been postulated to act as a disease modifier requiring additional mutations in a more complex genetic model. Familial hypocalciuric hypercalcemia (FHH) caused by heterozygous inactivating mutations in the calcium sensing receptor (CASR) gene is considered a benign disorder with elevated plasma calcium levels. Although hypercalcemia represents a risk factor for pancreatitis, increased rates of pancreatitis in patients with FHH have not been reported thus far.
Methods
We studied a family with a FHH-related hypercalcemia and chronic pancreatitis. DNA samples were analysed for mutations within the cationic trypsinogen (N29I, R122H) and SPINK1 (N34S) gene using melting curve analysis. Mutations within CASR gene were identified by DNA sequencing.
Results
A N34S SPINK1 mutation was found in all screened family members. However, only two family members developed chronic pancreatitis. These patients also had FHH caused by a novel, sporadic mutation in the CASR gene (518T>C) leading to an amino acid exchange (leucine->proline) in the extracellular domain of the CASR protein.
Conclusion
Mutations in the calcium sensing receptor gene might represent a novel as yet unidentified predisposing factor which may lead to an increased susceptibility for chronic pancreatitis. Moreover, this family analysis supports the hypothesis that SPINK1 mutations act as disease modifier and suggests an even more complex genetic model in SPINK1 related chronic pancreatitis.
doi:10.1186/1471-230X-3-34
PMCID: PMC317302  PMID: 14641934
chronic pancreatitis; idiopathic chronic pancreatitis; SPINK1 mutation; calcium sensing receptor
3.  Generic and disease-specific health related quality of life in non-cirrhotic, cirrhotic and transplanted liver patients: a cross-sectional study 
BMC Gastroenterology  2003;3:33.
Background
Studies on Health Related Quality of Life (HRQoL) of chronic liver patients were performed in clinical populations. These studies included various disease stages but small variations in aetiology and no transplanted patients. We performed a large HRQoL study in non-cirrhotic, cirrhotic and transplanted liver patients with sufficient variety in aetiology. We compared the generic HRQoL and fatigue between liver patients and healthy controls and compared the disease-specific and generic HRQoL and fatigue between non-cirrhotic, cirrhotic and transplanted liver patients, corrected for aetiology.
Methods
Members of the Dutch liver patient association received the Short Form-36, the Liver Disease Symptom Index and the Multidimensional Fatigue Index-20. Based on reported clinical characteristics we classified respondents (n = 1175) as non-cirrhotic, compensated cirrhotic, decompensated cirrhotic or transplants. We used linear, ordinal and logistic regression to compare the HRQoL between groups.
Results
All liver patients showed a significantly worse generic HRQoL and fatigue than healthy controls. Decompensated cirrhotic patients showed a significantly worse disease-specific and generic HRQoL and fatigue than non-cirrhotic patients, while HRQoL differences between non-cirrhotic and compensated cirrhotic patients were predominantly insignificant. Transplanted patients showed a better generic HRQoL, less fatigue and lower probabilities of severe symptoms than non-cirrhotic patients, but almost equal probabilities of symptom hindrance.
Conclusions
HRQoL in chronic liver patients depends on disease stage and transplant history. Non-cirrhotic and compensated cirrhotic patients have a similar HRQoL. Decompensated patients show the worst HRQoL, while transplanted patients show a significantly better HRQoL than cirrhotic and non-cirrhotic patients.
doi:10.1186/1471-230X-3-33
PMCID: PMC293464  PMID: 14617381
5.  Cytotoxic isolates of Helicobacter pylori from Peptic Ulcer Diseases decrease K+-dependent ATPase Activity in HeLa cells 
BMC Gastroenterology  2003;3:31.
Background
Helicobacter pylori is a Gram negative bacterium that plays a central role in the etiology of chronic gastritis and peptic ulcer diseases. However, not all H. pylori positive cases develop advanced disease. This discriminatory behavior has been attributed to the difference in virulence of the bacteria. Among all virulence factors, cytotoxin released by H. pylori is the most important factor. In this work, we studied variation in H. pylori isolates from Indian dyspeptic patients on the basis of cytotoxin production and associated changes in K+-dependent ATPase (one of its targets) enzyme activity in HeLa cells.
Methods
The patients were retrospectively grouped on the basis of endoscopic and histopathological observation as having gastritis or peptic ulcer. The HeLa cells were incubated with the broth culture filtrates (BCFs) of H. pylori isolates from patients of both groups and observed for the cytopathic effects: morphological changes and viability. In addition, the K+-dependent ATPase activity was measured in HeLa cells extracts.
Results
The cytotoxin production was observed in 3/7 (gastritis) and 4/4 (peptic ulcer) H. pylori isolates. The BCFs of cytotoxin producing H. pylori strains reduced the ATPase activity of HeLa cells to 40% of that measured with non-cytotoxin producing H. pylori strains (1.33 μmole Pi/mg protein and 3.36 μmole Pi/mg protein, respectively, p < 0.05). The decreased activity of ATPase enzyme or the release of cytotoxin also correlated with the increased pathogenicity indices of the patients.
Conclusions
Our results suggest that the isolation of cytotoxic H. pylori is more common in severe form of acid peptic diseases (peptic ulcer) than in gastritis patients from India. Also the cytotoxin released by H. pylori impairs the ion-transporting ATPase and is a measure of cytotoxicity.
doi:10.1186/1471-230X-3-31
PMCID: PMC280654  PMID: 14604441
Helicobacter pylori; Cytotoxin and ATPase
6.  Cystadenocarcinoma of the appendix: an incidental imaging finding in a patient with adenocarcinomas of the ascending and the sigmoid colon 
BMC Gastroenterology  2003;3:30.
Background
Primary adenocarcinomas of the appendix are uncommon. Mucoceles that result from mucinous adenocarcinomas of the appendix may be incidentally detected on imaging.
Case presentation
A case of a mucocele of the appendix, due to cystadenocarcinoma, is presented as an incidental imaging finding in a female, 86-year-old patient. The patient was admitted due to rectal hemorrhage and underwent colonoscopy, x-ray, US and CT. Adenocarcinoma of the ascending colon, adenomatous polyp of the sigmoid colon and a cystic lesion in the right iliac fossa were diagnosed. The cystic lesion was characterized as mucocele. The patient underwent right hemicolectomy, excision of the mucocele and sigmoidectomy. She recovered well and in two-year follow-up is free from cancer.
Conclusions
Preoperative diagnosis of an underlying malignancy in a mucocele is important for patient management, but it is difficult on imaging studies. Small lymph nodes or soft tissue stranding in the surrounding fat on computed tomography examination may suggest the possibility of malignancy.
doi:10.1186/1471-230X-3-30
PMCID: PMC270054  PMID: 14572318
Mucocele of the appendix; Adenocarcinoma of the colon; Ultrasonography; Computed Tomography
7.  Adenoviral expression of a transforming growth factor-β1 antisense mRNA is effective in preventing liver fibrosis in bile-duct ligated rats 
BMC Gastroenterology  2003;3:29.
Background
Transforming growth factor-β (TGF-β) is a key mediator in establishing liver fibrosis. Therefore, TGF-β as a causative agent may serve as a primary target for antifibrotic gene therapy approaches. We have previously shown that the adenoviral delivery of a transgene constitutively expressing a TGF-β1 antisense mRNA blocks TGF-β synthesis in culture-activated hepatic stellate cells and effectively abolishes ongoing fibrogenesis in vitro.
Methods
Ligature of the common bile duct was used to induce liver fibrosis in rats. The effect of the TGF-β1 antisense on fibrogenesis was analyzed in this model of liver injury.
Results
In the present study, we demonstrate that the adenoviral vector directs the synthesis of mRNA quantities that are approximately 8000-fold more abundant than endogenous TGF-β1 mRNA. In experimentally injured rat livers induced by ligature of the common bile duct, a model for persistent fibrogenesis and cirrhosis, administration of the adenoviral vector abrogates TGF-β-enhanced production of collagen and α-smooth muscle actin. Furthermore, the number of cells positive for α-smooth muscle actin resulting from active recruitment of activated hepatic stellate cells around the bile ductular structures was significantly reduced in animals after application of Ad5-CMV-AS-TGF-β1. However, the observed elevated serum levels of aspartate aminotransferase, alanine aminotransferase, and bilirubin induced in this obstructive liver injury model were not significantly altered in the presence of the TGF-β antagonist.
Conclusion
Taken together, our data provides in vivo evidence that the delivery of TGF-β1 antisense mRNA specifically abolishes the diverse effects of direct TGF-β function in ongoing liver fibrogenesis. Therefore, we conclude that the expressed transgene is therapeutically useful for inhibition of TGF-β effects in diverse applications, ranging from clarification of TGF-β function in the course of liver injury to the development of novel gene therapeutic approaches.
doi:10.1186/1471-230X-3-29
PMCID: PMC270053  PMID: 14565855
8.  Anorectal motility in patients with achalasia of the esophagus: recognition of an esophago-rectal syndrome 
BMC Gastroenterology  2003;3:28.
Background
During my study of constipation, I encountered patients who had achalasia of the esophagus (AE) as well. The possibility of an existing relationship between the 2 conditions was studied.
Method
Investigations to study the anorectal motility in 9 AE patients included: the intestinal transit time, anorectal manometry, rectoanal inhibitory reflex, defecography and electromyography (EMG) of external anal sphincter and levator ani muscle. Anorectal biopsy was done. The study comprised 8 healthy volunteers as controls.
Results
6/9 AE patients had constipation presenting as strainodynia (excessive prolonged straining at stool). Rectocele was present in 4 of them. The 6 constipated patients showed significantly high rectal neck pressure (p < 0.05), absent rectoanal inhibitory reflex and aganglionosis in the anorectal biopsy. The EMG revealed diminished activity in 4 of the 6 constipated patients. The remaining 3 patients with AE had normal anorectal function. Heller's myotomy with Nissen's fundoplication improved the dysphagia, but not the constipation which was, however, relieved after performance of anorectal myectomy.
Conclusion
The high incidence of constipation with AE postulates a relationship between the 2 conditions. Both have the same pathologic lesion which is aganglionosis. This study is preliminary and requires further studies on a larger number of patients.
doi:10.1186/1471-230X-3-28
PMCID: PMC270052  PMID: 14563218
Esophagus; Rectum; Achalasia; Constipation; Strainodynia; Myotomy; Myectomy
9.  Clinical and histological features of nonalcoholic steatohepatitis in Iranian patients 
BMC Gastroenterology  2003;3:27.
Background
Although several studies have been performed on risk factors and natural course of NASH, it seems that NASH tends to be more than a disease confined to strict boundaries. The objective of this study was to assess the clinical and paraclinical features and risk factors for non-alcoholic steatohepatitis (NASH) patients in an Iranian population
Methods
Patients with histologically confirmed NASH who had elevated liver aminotransaminases, negative serologic markers of viral or autoimmune hepatitis and no findings in favor of metabolic liver disease were enrolled. A careful history was taken regarding alcohol intake.
Results
53 patients consisting of 32 male and 21 female entered the study. The mean age was 37.8 ± 11.3 years. Twenty-six patients (55.3%) were overweight, 15 (31.9%) obese, 40 (75.5%) dyslipidemic, and three patients (5.7%) were diabetic. Liver biopsy showed mild steatosis in 35.7%, moderate steatosis in 53.6%, and severe forms in 10.7%. In 80.2% of patients, portal inflammation was present, and 9.4% had cirrhosis. The amount of increase in liver enzymes bore no relationship with fibrosis, portal inflammation, and degree of steatosis.
Conclusions
The patients in our study showed a male predominancy and were somewhat younger than other studies.
doi:10.1186/1471-230X-3-27
PMCID: PMC270051  PMID: 14561231
Nonalcoholic steatohepatitis; liver biopsy; Nonalcoholic Fatty liver disease; steatosis; obesity; Epidemiology
10.  Botulinum toxin in gastric submucosa reduces stimulated HCl production in rats 
BMC Gastroenterology  2003;3:26.
Background
Botulinum toxin blocks acetylcholine release from nerve endings and acts as a long term, reversible inhibitor of muscle contraction as well as of salivary, sweat gland, adrenal and prostatic secretions. The aim of the present study is to investigate whether gastric submucosal injection of botulinum toxin type A reduces stimulated gastric production of HCl.
Methods
Sixty-four rats were randomized in two groups and laparotomized. One group was treated with botulinum toxin-A 10 U by multiple submucosal gastric injections, while the second group was injected with saline. Two weeks later, acid secretion was stimulated by pyloric ligation and acid output was measured. Body weight, food and water intake were also recorded daily.
Results
HCl production after pyloric ligation was found to be significantly lower in botulinum toxin-treated rats (657 ± 90.25 micromol HCl vs. 1247 ± 152. P = 0.0017). Botulinum toxin-treated rats also showed significantly lower food intake and weight gain.
Conclusions
Botulinum toxin type A reduces stimulated gastric acidity. This is likely due either to inhibition of the cholinergic stimulation of gastric parietal cells, or to an action on the myenteric nervous plexuses. Reduction of growth and food intake may reflect both impaired digestion and decreased gastric motility.
doi:10.1186/1471-230X-3-26
PMCID: PMC222954  PMID: 12964945
11.  Mice with targeted disruption of p8 gene show increased sensitivity to lipopolysaccharide and DNA microarray analysis of livers reveals an aberrant gene expression response 
BMC Gastroenterology  2003;3:25.
Background
p8 is a DNA-binding protein induced in many tissues in response to LPS treatment. Hence, p8 could be a mediator of LPS-associated effects or, on the contrary, p8 expression may be part of the protective mechanism of the tissues in response to LPS. Finally, p8 expression in response to LPS could also be a simple epiphenomenon.
Methods
To investigate the role of p8 in vivo, we generated p8-deficient mice by gene targeting. Because p8 is a stress protein, we analyzed the response of p8-/- mice to a systemic stress induced by LPS injection. Liver was chosen as model organ to monitor alterations in gene expression.
Results
LPS resulted in higher serum TNF-α concentration and higher mortality rate in p8-deficient mice than in wild-type. Also, liver and pancreas, but not lung, from p8-/- mice showed increased amounts of MPO and HPO. To gain insight into the molecular bases of such susceptibility, we used high density DNA microarrays consisting of ~6000 genes and ESTs to compare gene regulation in response to LPS in p8+/+ and p8-/- livers. In wild-type, 105 genes and 73 ESTs were up-regulated and 232 genes and 138 ESTs down-regulated. By contrast, 212 genes and 125 ESTs were found up-regulated and 90 genes and 85 ESTs down regulated in p8-/- mice. Among them, only 93 (51 induced and 42 repressed) corresponded to the wild-type pattern, demonstrating that p8 deficiency hinders the normal response to LPS, which may account for the increased sensitivity of p8-/-mice to the endotoxin.
Conclusions
The large number of genes showing abnormal regulation after LPS suggests that p8 is an important regulatory factor involved in many cellular defence pathways.
doi:10.1186/1471-230X-3-25
PMCID: PMC212298  PMID: 12959645
p8; LPS; microarray; gene expression; mice
12.  Retreatment of hepatitis C non-responsive to Interferon. A placebo controlled randomized trial of Ribavirin monotherapy versus combination therapy with Ribavirin and Interferon in 121 patients in the Benelux [ISRCTN53821378] 
BMC Gastroenterology  2003;3:24.
Background
Evidence based medicine depends on unbiased selection of completed randomized controlled trials. For completeness it is important to publish all trials. This report describes the first large randomised controlled trial where combination therapy was compared to placebo therapy and to ribavirin monotherapy, which has not been published untill now.
Methods
One hundred and twenty one patients with chronic hepatitis C and elevated transaminases who did not respond to previous treatment with standard interferon monotherapy, were included from 16 centers in Belgium, the Netherlands and Luxembourg between 1992 and 1996. Patient poor-response characteristics were: genotype 1 (69%), HCV RNA above 2 × 106 copies/ml (55%) and cirrhosis (38%). Patients were randomized to 6 months combination therapy with interferon alpha-2b (3 MU tiw) and ribavirin (1000–1200 mg / day), 6 months ribavirin monotherapy (1000–1200 mg / day) or 6 months ribavirin placebo. The study was double blinded for the ribavirin / placebo component. One patient did not fit the entry criteria, and 3 did not start. All 117 patients who received at least one dose of treatment were included in the intention to treat analysis.
Results
At the end of treatment, HCV RNA was undetectable in 35% of patients on combination therapy and in none of the patients treated with ribavirin monotherapy or placebo. The sustained virological response rate at 6 months after therapy was 15% for patients treated with interferon and ribavirin.
During the 6 months treatment period 13% of patients on interferon ribavirin combination therapy, 13% of patients on ribavirin monotherapy and 11% of patients on placebo withdrew due to side effects or noncompliance. At 24 weeks of treatment the mean Hb level was 85% of the baseline value, which means a mean decrease from 9.1 mmol/l to 7.8 mmol/l. The Hb levels at the end of treatment were not significantly different from patients treated with ribavirin monotherapy (p = 0.76). End of treatment WBC was significantly lower in patients treated with combination therapy, compared to ribavirin (p < 0.01) as well as for patients treated with ribavirin monotherapy compared to placebo (p < 0.01).
Discussion
This belated report on the only placebo controlled study of interferon ribavirin combination therapy in non responders to standard doses of interferon monotherapy documents the effectiveness, be it limited, of this approach as well as the dynamics of the effects on blood counts.
doi:10.1186/1471-230X-3-24
PMCID: PMC222984  PMID: 12948399
Hepatitis C; Treatment; Randomised controlled trial; Interferon; Ribavirin; Non-responders; Monotherapy; Placebo
13.  Influence of rectal prolapse on the asymmetry of the anal sphincter in patients with anal incontinence 
BMC Gastroenterology  2003;3:23.
Background
Anal sphincter defects have been shown to increase pressure asymmetry within the anal canal in patients with fecal incontinence. However, this correlation is far from perfect, and other factors may play a role. The goal of this study was to assess the impact of rectal prolapse on anal pressure asymmetry in patients with anal incontinence.
Methods
44 patients, (42 women, mean age: 64 (11) years), complaining of anal incontinence, underwent anal vector manometry, endo-anal ultrasonography (to assess sphincter defects) and pelvic viscerogram (for the diagnosis of rectal prolapse). Resting and squeeze anal pressures, and anal asymmetry index at rest and during voluntary squeeze were determined by vector manometry.
Results
Ultrasonography identified 19 anal sphincter defects; there were 9 cases of overt rectal prolapse, and 14 other cases revealed by pelvic viscerogram (recto-anal intussuception). Patients with rectal prolapse had a significantly higher anal sphincter asymmetry index at rest, whether patients with anal sphincter defects were included in the analysis or not (30 (3) % versus 20 (2) %, p < 0.005). Among patients without rectal prolapse, a higher anal sphincter asymmetry index during squeezing was found in patients with anal sphincter defects (27 (2) % versus 19 (2) %, p < 0.03).
Conclusions
In anal incontinent patients, anal asymmetry index may be increased in case of anal sphincter defect and/or rectal prolapse. In the absence of anal sphincter defect at ultrasonogaphy, an increased anal asymmetry index at rest may point to the presence of a rectal prolapse.
doi:10.1186/1471-230X-3-23
PMCID: PMC194588  PMID: 12925237
14.  Endoscopic sclerotherapy compared with no specific treatment for the primary prevention of bleeding from esophageal varices. A randomized controlled multicentre trial [ISRCTN03215899] 
BMC Gastroenterology  2003;3:22.
Background
Since esophageal variceal bleeding is associated with a high mortality rate, prevention of bleeding might be expected to result in improved survival. The first trials to evaluate prophylactic sclerotherapy found a marked beneficial effect of prophylactic treatment. These results, however, were not generally accepted because of methodological aspects and because the reported incidence of bleeding in control subjects was considered unusually high. The objective of this study was to compare endoscopic sclerotherapy (ES) with nonactive treatment for the primary prophylaxis of esophageal variceal bleeding in patients with cirrhosis.
Methods
166 patients with esophageal varices grade II, III of IV according to Paquet's classification, with evidence of active or progressive liver disease and without prior variceal bleeding, were randomized to groups receiving ES (n = 84) or no specific treatment (n = 82). Primary end-points were incidence of bleeding and mortality; secondary end-points were complications and costs.
Results
During a mean follow-up of 32 months variceal bleeding occurred in 25% of the patients of the ES group and in 28% of the control group. The incidence of variceal bleeding for the ES and control group was 16% and 16% at 1 year and 33% and 29% at 3 years, respectively. The 1-year survival rate was 87% for the ES group and 84% for the control group; the 3-year survival rate was 62% for each group. In the ES group one death occurred as a direct consequence of variceal bleeding compared to 9 in the other group (p = 0.01, log-rank test). Complications were comparable for the two groups. Health care costs for patients assigned to ES were estimated to be higher. Meta-analysis of a large number of trials showed that the effect of prophylactic sclerotherapy is significantly related to the baseline bleeding risk.
Conclusion
In the present trial, prophylactic sclerotherapy did not reduce the incidence of bleeding from varices in patients with liver cirrhosis and a low to moderate bleeding risk. Although sclerotherapy lowered mortality attributable to variceal bleeding, overall survival was not affected. The effect of prophylactic sclerotherapy seems dependent on the underlying bleeding risk. A beneficial effect can only be expected for patients with a high risk for bleeding.
doi:10.1186/1471-230X-3-22
PMCID: PMC194733  PMID: 12919638
15.  Dapsone induced cholangitis as a part of dapsone syndrome: a case report 
BMC Gastroenterology  2003;3:21.
Background
Dapsone can rarely cause a hypersensitivity reaction called dapsone syndrome, consisting of fever, hepatitis, exfoliative dermatitis, lymphadenopathy and hemolytic anemia. Dapsone syndrome is a manifestation of the DRESS (drug rash with eosinophilia and systemic symptoms) syndrome which is a serious condition that has been reported in association with various drugs. Cholangitis in dapsone syndrome has not been reported so far in the world literature.
Case presentation
We report a patient who presented with fever, exfoliative dermatitis, jaundice and anemia within three weeks of starting of dapsone therapy. These features are typical of dapsone syndrome, which is due to dapsone hypersensitivity and is potentially fatal. Unlike previous reports of hepatitic or cholestatic injury in dapsone syndrome we report here a case that had cholangitic liver injury. It responded to corticosteroids.
Conclusion
We conclude that cholangitis, though unusual, can also form a part of dapsone syndrome. Physicians should be aware of this unusual picture of potentially fatal dapsone syndrome.
doi:10.1186/1471-230X-3-21
PMCID: PMC194587  PMID: 12911838
16.  Analysis of antimicrobial susceptibility and virulence factors in Helicobacter pylori clinical isolates 
BMC Gastroenterology  2003;3:20.
Background
In this study, we evaluated the prevalence of primary resistance of Brazilian H. pylori isolates to metronidazole, clarithromycin, amoxicillin, tetracycline, and furazolidone. In addition, the vacA, iceA, cagA and cagE genotypes of strains isolated from Brazilian patients were determined and associated with clinical data in an effort to correlate these four virulence markers and antibiotic resistance.
Methods
H. pylori was cultured in 155 H. pylori-positive patients and MICs for metronidazole, clarithromycin, amoxicillin, tetracycline, and furazolidone were determined by the agar dilution method. Genomic DNA was extracted, and allelic variants of vacA, iceA, cagA and cagE were identified by the polymerase chain reaction.
Results
There was a strong association between the vacA s1/cagA -positive genotype and peptic ulcer disease (OR = 5.42, 95% CI 2.6–11.3, p = 0.0006). Additionally, infection by more virulent strains may protect against GERD, since logistic regression showed a negative association between the more virulent strain, vacA s1/cagA-positive genotype and GERD (OR = 0.26, 95% CI 0.08–0.8, p = 0.03). Resistance to metronidazole was detected in 75 patients (55%), to amoxicillin in 54 individuals (38%), to clarithromycin in 23 patients (16%), to tetracycline in 13 patients (9%), and to furazolidone in 19 individuals (13%). No significant correlation between pathogenicity and resistance or susceptibility was detected when MIC values for each antibiotic were compared with different vacA, iceA, cagA and cagE genotypes.
Conclusion
The analysis of virulence genes revealed a specific association between H. pylori strains and clinical outcome, furthermore, no significant association was detected among pathogenicity and resistance or susceptibility.
doi:10.1186/1471-230X-3-20
PMCID: PMC194586  PMID: 12911839
17.  Over-expression of the mitogen-activated protein kinase (MAPK) kinase (MEK)-MAPK in hepatocellular carcinoma: Its role in tumor progression and apoptosis 
BMC Gastroenterology  2003;3:19.
Background
Hepatocellular carcinoma (HCC) is one of the most common malignancies in South East Asia. Although activation of the MEK-MAPK is often associated with cellular growth, the role of MEK-MAPK in growth and survival of hepatocarcinoma cells has not been established.
Methods
Immuno-histochemistry was used to localize phosphorylated MAPK and MEK1/2 in the tissues. 3-(4,5-Dimethylthiazol-2-y1)-2,5-diphenyltetrazolium bromide (MTT) assay and ELISA were used to determine cell viability and cell proliferation. Deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay was used to detect apoptotic cells. Western blots analysis was performed to determine the levels of proteins involved in the MEK-MAPK and apoptotic pathways. Transfection study was performed to assess the role of MEK-MAPK pathway in growth and survival of liver cancer cells.
Results
We report that phosphorylation of MEK1/2 at Ser217/221 was detected by immuno-histochemistry in 100% (46 of 46) of HCCs examined. A positive signal was localized in the nuclei of hepatocarcinoma cells but not in dysplastic hepatocytes or stromal cells. Over-expression and phosphorylation of MAPK was also detected in 91% (42 of 46) and 69% (32 of 46) of HCCs examined, respectively. The percentage of cells showing positively for phosphorylated MEK1/2 increased with advancing tumor stage. In vitro, treatment of human HepG2 and Hep3B cells with MEK1/2 specific inhibitors U0126 and PD98059 led to growth inhibition and apoptosis. U0126 induced the release of cytochrome c and increased the cleavage of caspase-3, caspase-7, and poly ADP-ribose polymerase (PARP). Inhibition of phosphatidylinositol 3-kinase (PI-3K), c-Jun N-terminal kinase (JNK) and p38 kinase activities caused only a mild apoptosis in HepG2 and Hep3B cells. Activated MEK1-transfected cells were more resistant to UO126-induced apoptosis in vitro and formed larger tumors in SCID mice than mock-transfected cells.
Conclusion
In conclusion, our results demonstrate that MEK-MAPK plays an important role in the growth and survival of liver cancer cells and suggest that blocking MEK-MAPK activity may represent an alternative approach for the treatment of liver cancer.
doi:10.1186/1471-230X-3-19
PMCID: PMC317301  PMID: 12906713
18.  A case of sigmoid endometriosis difficult to differentiate from colon cancer 
BMC Gastroenterology  2003;3:18.
Background
Although endometriosis with sigmoid serosal involvement is not uncommon in women of childbearing age, the mucosal involvement is rare and differential diagnosis from colon cancer may be difficult due to the lack of pathognomonic symptoms and the poor diagnostic yield of colonoscopy and colonic biopsies.
Case presentation
We present a case of a young woman with sigmoid endometriosis, in which the initial diagnostic workup suggested colon cancer. Histologic evidence, obtained from a second colonoscopy, along with pelvic ultrasound findings led to the final diagnosis of intestinal endometriosis which was confirmed by laparoscopy.
Conclusion
Colonic endometriosis is often a diagnostic challenge and should be considered in young women with symptoms from the lower gastrointestinal tract.
doi:10.1186/1471-230X-3-18
PMCID: PMC184504  PMID: 12906714
colon cancer; endometriosis; intestinal bleeding.
19.  Differential gene expression profile in the small intestines of mice lacking pacemaker interstitial cells of Cajal 
BMC Gastroenterology  2003;3:17.
Background
We previously identified eight known and novel genes differentially expressed in the small intestines of wild type and W/WV mice, which have greatly reduced populations of the interstitial cells of Cajal, that are responsible for the generation of electrical slow waves, by using a differential gene display method.
Methods
By using the same method we isolated additional candidate genes that were specifically down- or up-regulated in W/WV mice. Novel transcripts were designated as DDWMEST.
Results
We isolated seven candidates that were specifically down- or up-regulated in W/WV mice. Two novel transcripts, DDWMEST 1 and -91 were increased in both fed and fasted W/WV mice. Expression of another five genes was suppressed in W/WV mice: ARG2 (Arginase II), ONZIN (encoding leukemia inhibitory factor regulated protein), and three novel transcripts: DDWMEST62, -84, and -100. Together with the previous report, we identified fifteen differentially expressed genes in total in the small intestines of W/WV mice. Eight of these genes were reduced in the jejunums of W/WV mice compared to age matched wild type mice, whereas the other seven genes showed an increase in expression. Differential expression was the same in fasted and fed animals, suggesting that the differences were independent of the dietetic state of the animal.
Conclusions
Several known and novel genes are differentially expressed in the small intestines of W/WV mice. Differential gene comparison might contribute to our understanding of motility disorders associated with the loss of the interstitial cells of Cajal.
doi:10.1186/1471-230X-3-17
PMCID: PMC198276  PMID: 12831403
20.  Antral hyperplastic polyp causing intermittent gastric outlet obstruction: Case report 
BMC Gastroenterology  2003;3:16.
Background
Hyperplastic polyps are the most common polypoid lesions of the stomach. Rarely, they cause gastric outlet obstruction by prolapsing through the pyloric channel, when they arise in the prepyloric antrum.
Case presentation
A 62-year-old woman presented with intermittent nausea and vomiting of 4 months duration. Upper gastrointestinal endoscopy revealed a 30 mm prepyloric sessile polyp causing intermittent gastric outlet obstruction. Following submucosal injection of diluted adrenaline solution, the polyp was removed with a snare. Multiple biopsies were taken from the greater curvature of the antrum and the corpus. Rapid urease test for Helicobacter pylori yielded a negative result. Histopathologic examination showed a hyperplastic polyp without any evidence of malignancy. Biopsies of the antrum and the corpus revealed gastritis with neither atrophic changes nor Helicobacter pylori infection. Follow-up endoscopy after a 12-week course of proton pomp inhibitor therapy showed a complete healing without any remnant tissue at the polypectomy site. The patient has been symptom-free during 8 months of follow-up.
Conclusions
Symptomatic gastric polyps should be removed preferentially when they are detected at the initial diagnostic endoscopy. Polypectomy not only provides tissue to determine the exact histopathologic type of the polyp, but also achieves radical treatment.
doi:10.1186/1471-230X-3-16
PMCID: PMC166166  PMID: 12831404
gastric outlet obstruction; pyloric channel; hyperplastic polyp; polypectomy.
21.  Quality control in colorectal cancer screening: Systematic microbiological investigation of endoscopes used in the NORCCAP (Norwegian Colorectal Cancer Prevention) trial 
BMC Gastroenterology  2003;3:15.
Background
Endoscopic colorectal cancer (CRC) screening is currently implemented in many countries. Since endoscopes cannot be sterilised, the transmission of infectious agents through endoscopes has been a matter of concern. We report on a continuous quality control programme in a large-scale randomised controlled trial on flexible sigmoidoscopy screening of an average-risk population. Continuously, throughout a two-year screening period, series of microbiological samples were taken from cleaned ready-to-use endoscopes and cultured for bacterial growth.
Results
8573 endoscopies were performed during the trial period. Altogether, 178 microbiological samples (2%) were taken from the biopsy channels and surfaces from the endoscopes. One sample (0.5%) showed faecal contamination (Enterobacter cloacae), and 25 samples (14%) showed growth of environmental bacteria.
Conclusions
Growth of bacteria occurs in a clinical significant number of samples from ready-to-use endoscopes. Pathogenic bacteria, however, were found only in one sample. Improvement of equipment design and cleaning procedures are desirable and continuous microbiological surveillance of endoscopes used in CRC screening is recommended.
doi:10.1186/1471-230X-3-15
PMCID: PMC166145  PMID: 12803654
22.  Differential gene expression in the murine gastric fundus lacking interstitial cells of Cajal 
BMC Gastroenterology  2003;3:14.
Background
The muscle layers of murine gastric fundus have no interstitial cells of Cajal at the level of the myenteric plexus and only possess intramuscular interstitial cells and this tissue does not generate electric slow waves. The absence of intramuscular interstitial cells in W/WV mutants provides a unique opportunity to study the molecular changes that are associated with the loss of these intercalating cells.
Method
The gene expression profile of the gastric fundus of wild type and W/WV mice was assayed by murine microarray analysis displaying a total of 8734 elements. Queried genes from the microarray analysis were confirmed by semi-quantitative reverse transcription-polymerase chain reaction.
Results
Twenty-one genes were differentially expressed in wild type and W/WV mice. Eleven transcripts had 2.0–2.5 fold higher mRNA expression in W/WV gastric fundus when compared to wild type tissues. Ten transcripts had 2.1–3.9 fold lower expression in W/WV mutants in comparison with wild type animals. None of these genes have ever been implicated in any bowel motility function.
Conclusions
These data provides evidence that several important genes have significantly changed in the murine fundus of W/WV mutants that lack intramuscular interstitial cells of Cajal and have reduced enteric motor neurotransmission.
doi:10.1186/1471-230X-3-14
PMCID: PMC165421  PMID: 12795813
23.  Esophageal and small bowel obstruction by occupational bezoar: report of a case 
BMC Gastroenterology  2003;3:13.
Background
Phytobezoar may be a cause of bowel obstruction in patients with previous gastric surgery. Most bezoars are concretions of poorly digested food, which are usually formed initially in the stomach. Intestinal obstruction (esophageal and small bowel) caused by an occupational bezoar has not been reported.
Case presentation
A 70-year old male is presented suffering from esophageal and small bowel obstruction, caused by an occupational bezoar. The patient has worked as a carpenter for 35 years. He had undergone a vagotomy and pyloroplasty 10 years earlier. The part of the bezoar, which caused the esophageal obstruction was removed during endoscopy, while the part of the small bowel was treated surgically. The patient recovered well and was discharged on the 8th postoperative day.
Conclusions
Since occupational bezoars may be a cause of intestinal obstruction (esophageal and/or small bowel), patients who have undergone a previous gastric surgery should avoid occupational exposures similar to the presented case.
doi:10.1186/1471-230X-3-13
PMCID: PMC165420  PMID: 12795814
24.  The addition of locust bean gum but not water delayed the gastric emptying rate of a nutrient semisolid meal in healthy subjects 
BMC Gastroenterology  2003;3:12.
Background
Most of the previous studies regarding the effects of gel-forming fibres have considered the gastric emptying of liquid or solid meals after the addition of pectin or guar gum. The influence of locust bean gum, on gastric emptying of nutrient semisolid meals in humans has been less well studied, despite its common occurrence in foods. Using a standardised ultrasound method, this study was aimed at investigating if the gastric emptying in healthy subjects could be influenced by adding locust been gum, a widely used thickening agent, or water directly into a nutrient semisolid test meal.
Methods
The viscosity of a basic test meal (300 g rice pudding, 330 kcal) was increased by adding Nestargel (6 g, 2.4 kcal), containing viscous dietary fibres (96.5%) provided as seed flour of locust bean gum, and decreased by adding 100 ml of water. Gastric emptying of these three test meals were evaluated in fifteen healthy non-smoking volunteers, using ultrasound measurements of the gastric antral area to estimate the gastric emptying rate (GER).
Results
The median value of GER with the basic test meal (rice pudding) was estimated at 63 %, (range 47 to 84 %), (the first quartile = 61 %, the third quartile = 69 %). Increasing the viscosity of the rice pudding by adding Nestargel, resulted in significantly lower gastric emptying rates (p < 0.01), median GER 54 %, (range 7 to 71 %), (the first quartile = 48 %, the third quartile = 60 %). When the viscosity of the rice pudding was decreased (basic test meal added with water), the difference in median GER 65 %, (range 38 to 79 %), (the first quartile = 56 %, the third quartile = 71 %) was not significantly different (p = 0.28) compared to the GER of the basic test meal.
Conclusions
We conclude that the addition of locust bean gum to a nutrient semisolid meal has a major impact on gastric emptying by delaying the emptying rate, but that the addition of water to this test meal has no influence on gastric emptying in healthy subjects.
doi:10.1186/1471-230X-3-12
PMCID: PMC165603  PMID: 12793910
Gastric Emptying; Real-time Ultrasound; Healthy humans; Dietary fiber; Viscous fiber; Semisolid meal
25.  Mediastinitis complicating a percutaneous endoscopic gastrostomy: a case report 
BMC Gastroenterology  2003;3:11.
Background
Since its introduction in the early 1980s, percutaneous endoscopic gastrostomy has become the most popular method for performing a gastrostomy for long-term enteral feeding. It has been associated, however, with a lot of minor and major complications.
Case presentation
A case of mediastinitis with concominant sepsis caused by a masked esophageal perforation after percutaneous endoscopic gastrostomy in a multi-traumatized, brain-injured patient is presented. Ten – fourteen days after the procedure, the patient became febrile and gradually septic with tenderness of the sternum and upper abdomen. Computerized tomography of the thorax revealed mediastinitis. An urgent left thoracotomy and laparotomy were performed for drainage of the mediastinum, removal of the gastrostomy and insertion of a jejunostomy tube. The patient improved soon after the surgery. He was successfully weaned off the ventilator and was discharged from the Intensive Care Unit.
Conclusion
Perforating mediastinitis is a rare but potentially lethal complication of percutaneous endoscopic gastrostomy. When diagnosed and properly treated it may have a favourable outcome.
doi:10.1186/1471-230X-3-11
PMCID: PMC165419  PMID: 12791167
Mediastinitis; percutaneous endoscopic gastrostomy; complications; intensive care unit; brain injury

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