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1.  Chronic diarrhoea 
Gut  2007;56(12):1756-1757.
PMCID: PMC2095683  PMID: 17998327
2.  When even people at high risk do not take up colorectal cancer screening 
Gut  2007;56(12):1648-1650.
Despite the most intense efforts by medical professionals, a significant fraction of people who we believe “should” be screened are not being screened
PMCID: PMC2095684  PMID: 17998319
4.  Menstrual and reproductive factors and gastric cancer risk in a large prospective study of women 
Gut  2007;56(12):1671-1677.
Gastric cancer incidence rates are consistently lower in women than men in both high and low‐risk regions worldwide. Sex hormones, such as progesterone and estrogen, may protect women against gastric cancer.
To investigate the association of menstrual and reproductive factors and gastric cancer risk.
These associations were prospectively investigated in 73 442 Shanghai women. After 419 260 person‐years of follow‐up, 154 women were diagnosed with gastric cancer. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated using Cox proportional hazards models adjusted for age, body mass index, education, income, and cigarette use.
No associations were observed between gastric cancer risk and age of menarche, number of children, breast feeding, or oral contraceptive use. In contrast, associations were observed with age of menopause (HR 0.80 per five‐year increase in menopausal age, 95% CI 0.66–0.97), years of fertility (participants with less than 30 years of fertility were at increased risk compared with those with 30–36 years of fertility, HR 1.90, 95% CI 1.25–2.90), years since menopause (HR 1.26 per five years, 95% CI 1.03–1.53), and intrauterine device use (HR for users 1.61, 95% CI 1.08–2.39).
These results support the hypothesis that female hormones play a protective role in gastric cancer risk.
PMCID: PMC2095686  PMID: 17627962
stomach neoplasms; cohort studies; prospective studies; hormones
5.  [No title available] 
Gut  2007;56(12):1705.
PMCID: PMC2095687
6.  Haematemesis with mediastinal lymphadenopathy 
Gut  2007;56(12):1684.
PMCID: PMC2095688  PMID: 17998324
7.  Optimising corticosteroid treatment for autoimmune pancreatitis 
Gut  2007;56(12):1650-1652.
Unanswered questions
PMCID: PMC2095689  PMID: 17998320
8.  Clinical gastrointestinal endoscopy 
Gut  2007;56(12):1800.
PMCID: PMC2095690
9.  Long‐term prognosis of autoimmune pancreatitis with and without corticosteroid treatment 
Gut  2007;56(12):1719-1724.
Autoimmune pancreatitis (AIP) is a unique form of chronic pancreatitis, and has a favourable response to corticosteroid treatment (CST). Little is known, however, about the long‐term outcome of AIP. This study aimed to document the prognosis without and with CST, and to examine the indication for CST.
Patients and methods
The prognosis and clinical features of 23 patients without CST and 19 patients treated with CST from onset were investigated. In addition, factors concerning the late occurrence of unfavourable events related to AIP were examined.
The patients without CST were 19 men and four women, with an average age of 66 years. After an average observation period of 25 months, 16 patients (70%) developed unfavourable events including obstructive jaundice as a result of distal bile duct stenosis in four, growing pseudocyst in one, sclerogenic changes of extrapancreatic bile duct in nine, hydronephrosis as a result of retroperitoneal fibrosis in one, and interstitial nephritis in one. Patients with obstructive jaundice at onset showed a higher cumulative event occurrence rate (p = 0.025). The patients treated with CST were 16 men and three women, with an average age of 64 years. After an average observation period of 23 months, six patients (32%) developed unfavourable events consisting of interstitial pneumonia in three, and a recurrence of obstructive jaundice in three. In multivariate analysis, CST (HR 0.33, 95% CI 0.12–0.89, p = 0.029) and obstructive jaundice at onset (HR 3.09, 95% CI 1.14–8.32, p = 0.026) were significant predictive factors for unfavourable events.
CST could reduce AIP‐related unfavourable events. The early introduction of CST is recommended especially for patients with obstructive jaundice.
PMCID: PMC2095691  PMID: 17525092
autoimmune pancreatitis; corticosteroid; prognosis; sclerosing cholangitis; obstructive jaundice
10.  Correlations between magnetic resonance spectroscopy alterations and cerebral ammonia and glucose metabolism in cirrhotic patients with and without hepatic encephalopathy 
Gut  2007;56(12):1736-1742.
Hepatic encephalopathy is considered to be mainly caused by increased ammonia metabolism of the brain. If this hypothesis is true, cerebral glucose utilisation, which is considered to represent brain function, should be closely related to cerebral ammonia metabolism. The aim of the present study was to analyse whether cerebral ammonia and glucose metabolism in cirrhotic patients with early grades of hepatic encephalopathy are as closely related as could be expected from current hypotheses on hepatic encephalopathy.
13N‐ammonia and 18F‐fluorodesoxyglucose positron emission tomography, magnetic resonance imaging and magnetic resonance spectroscopy (MRS) were performed in 21 cirrhotic patients with grade 0–1 hepatic encephalopathy. Quantitative values of cerebral ammonia uptake and retention rate and glucose utilisation were derived for several regions of interest and were correlated with the MRS data of the basal ganglia, white matter and frontal cortex.
A significant correlation between plasma ammonia levels and cerebral ammonia metabolism, respectively, and MRS alterations could be shown only for white matter. In contrast, MRS alterations in all three regions studied were significantly correlated with the glucose utilisation of several brain regions. Cerebral ammonia and glucose metabolism were not correlated.
Increase of cerebral ammonia metabolism is an important but not exclusive causal factor for the development of hepatic encephalopathy.
PMCID: PMC2095692  PMID: 17660226
liver cirrhosis; early hepatic encephalopathy; magnetic resonance spectroscopy; positron emission tomography
11.  Gut in 2007 
Gut  2007;56(12):1645.
Editor's report for past year
PMCID: PMC2095693  PMID: 17998317
12.  A large‐scale, multicentre, double‐blind trial of ursodeoxycholic acid in patients with chronic hepatitis C 
Gut  2007;56(12):1747-1753.
Combined pegylated interferon and ribavirin has improved chronic hepatitis C (CH‐C) therapy; however, sustained virological response is achieved in only about half of the patients with a 1b genotype infection. We assessed oral ursodeoxycholic acid (UDCA) on serum biomarkers as a possible treatment for interferon non‐responders.
CH‐C patients with elevated alanine aminotransferase (ALT) were assigned randomly to 150 (n = 199), 600 (n = 200) or 900 mg/day (n = 197) UDCA intake for 24 weeks. Changes in ALT, aspartate aminotransferase (AST) and gamma‐glutamyl transpeptidase (GGT) were assessed. This study is registered at, identifier NCT00200343.
ALT, AST and GGT decreased at week 4 and then remained constant during drug administration. The median changes (150, 600 and 900 mg/day, respectively) were: ALT, −15.3, −29.2 and −36.2%; AST, −13.6, −25.0 and −29.8%; GGT, −22.4, −41.0 and −50.0%. These biomarkers decreased significantly less in the 150 mg/day than in the other two groups. Although changes in ALT and AST did not differ between the 600 and 900 mg/day groups, GGT was significantly lower in the 900 mg/day group. In subgroup analysis, ALT decreased significantly in the 900 mg/day group when the baseline GGT exceeded 80 IU/l. Serum HCV‐RNA did not change in any group. Adverse effects were reported by 19.1% of the patients, with no differences between groups.
A 600 mg/day UDCA dose was optimal to decrease ALT and AST levels in CH‐C patients. The 900 mg/day dose decreased GGT levels further, and may be preferable in patients with prevailing biliary injuries.
PMCID: PMC2095694  PMID: 17573387
13.  Faecal S100A12 as a non‐invasive marker distinguishing inflammatory bowel disease from irritable bowel syndrome 
Gut  2007;56(12):1706-1713.
S100A12 is a pro‐inflammatory protein that is secreted by granulocytes. S100A12 serum levels increase during inflammatory bowel disease (IBD). We performed the first study analysing faecal S100A12 in adults with signs of intestinal inflammation.
Faecal S100A12 was determined by ELISA in faecal specimens of 171 consecutive patients and 24 healthy controls. Patients either suffered from infectious gastroenteritis confirmed by stool analysis (65 bacterial, 23 viral) or underwent endoscopic and histological investigation (32 with Crohn's disease, 27 with ulcerative colitis, and 24 with irritable bowel syndrome; IBS). Intestinal S100A12 expression was analysed in biopsies obtained from all patients. Faecal calprotectin was used as an additional non‐invasive surrogate marker.
Faecal S100A12 was significantly higher in patients with active IBD (2.45 ± 1.15 mg/kg) compared with healthy controls (0.006 ± 0.03 mg/kg; p<0.001) or patients with IBS (0.05 ± 0.11 mg/kg; p<0.001). Faecal S100A12 distinguished active IBD from healthy controls with a sensitivity of 86% and a specificity of 100%. We also found excellent sensitivity of 86% and specificity of 96% for distinguishing IBD from IBS. Faecal S100A12 was also elevated in bacterial enteritis but not in viral gastroenteritis. Faecal S100A12 correlated better with intestinal inflammation than faecal calprotectin or other biomarkers.
Faecal S100A12 is a novel non‐invasive marker distinguishing IBD from IBS or healthy individuals with a high sensitivity and specificity. Furthermore, S100A12 reflects inflammatory activity of chronic IBD. As a marker for neutrophil activation, faecal S100A12 may significantly improve our arsenal of non‐invasive biomarkers of intestinal inflammation.
PMCID: PMC2095695  PMID: 17675327
14.  Ursodeoxycholic acid in chronic hepatitis C 
Gut  2007;56(12):1652-1653.
Cytoprotective but anti‐apoptotic
PMCID: PMC2095696  PMID: 17998321
15.  A rare complication of peptic ulcer disease 
Gut  2007;56(12):1664.
PMCID: PMC2095697  PMID: 17998322
16.  [No title available] 
Gut  2007;56(12):1800.
PMCID: PMC2095698
17.  Digest 
Gut  2007;56(12):1645.
PMCID: PMC2095699
18.  Crohn's disease or abdominal tuberculosis? 
Gut  2007;56(12):1757-1758.
PMCID: PMC2095700  PMID: 17998328
Gut  2007;56(12):1677.
PMCID: PMC2095701
20.  [No title available] 
Gut  2007;56(12):1800.
PMCID: PMC2095702
21.  Mucosal T‐cell immunoregulation varies in early and late inflammatory bowel disease 
Gut  2007;56(12):1696-1705.
Background and aims
Crohn's disease is a life‐long form of inflammatory bowel disease (IBD) mediated by mucosal immune abnormalities. Understanding of the pathogenesis is limited because it is based on data from adults with chronic Crohn's disease. We investigated mucosal T‐cell immunoregulatory events in children with early Crohn's disease.
Mucosal biopsies and T‐cell clones were derived from children experiencing the first attack of Crohn's disease, children with long‐standing Crohn's disease, infectious colitis, and children without gut inflammation.
As in acute infectious colitis, interleukin (IL) 12 induced T cells from early Crohn's disease to acquire a strongly polarised T helper (Th) type 1 response characterised by high IFN‐γ production and IL12Rβ2 chain expression. Th1 polarisation was not induced in clones from late Crohn's disease. Mucosal levels of IL12p40 and IL12Rβ2 messenger RNA were significantly higher in children with early than late Crohn's disease. These results demonstrate that susceptibility to IL12‐mediated modulation is strongly dependent on the stage of Crohn's disease.
At the onset of Crohn's disease mucosal T cells appear to mount a typical Th1 response that resembles an acute infectious process, and is lost with progression to late Crohn's disease. This suggests that mucosal T‐cell immunoregulation varies with the course of human IBD. Patients with the initial manifestations of IBD may represent an ideal population in which immunomodulation may have optimal therapeutic efficacy.
PMCID: PMC2095703  PMID: 17682002
22.  JournalScan 
Gut  2007;56(12):1759.
PMCID: PMC2095704
23.  Fat transforms ascorbic acid from inhibiting to promoting acid‐catalysed N‐nitrosation 
Gut  2007;56(12):1678-1684.
The major potential site of acid nitrosation is the proximal stomach, an anatomical site prone to a rising incidence of metaplasia and adenocarcinoma. Nitrite, a pre‐carcinogen present in saliva, can be converted to nitrosating species and N‐nitroso compounds by acidification at low gastric pH in the presence of thiocyanate.
To assess the effect of lipid and ascorbic acid on the nitrosative chemistry under conditions simulating the human proximal stomach.
The nitrosative chemistry was modelled in vitro by measuring the nitrosation of four secondary amines under conditions simulating the proximal stomach. The N‐nitrosamines formed were measured by gas chromatography–ion‐trap tandem mass spectrometry, while nitric oxide and oxygen levels were measured amperometrically.
In absence of lipid, nitrosative stress was inhibited by ascorbic acid through conversion of nitrosating species to nitric oxide. Addition of ascorbic acid reduced the amount of N‐nitrosodimethylamine formed by fivefold, N‐nitrosomorpholine by >1000‐fold, and totally prevented the formation of N‐nitrosodiethylamine and N‐nitrosopiperidine. In contrast, when 10% lipid was present, ascorbic acid increased the amount of N‐nitrosodimethylamine, N‐nitrosodiethylamine and N‐nitrosopiperidine formed by approximately 8‐, 60‐ and 140‐fold, respectively, compared with absence of ascorbic acid.
The presence of lipid converts ascorbic acid from inhibiting to promoting acid nitrosation. This may be explained by nitric oxide, formed by ascorbic acid in the aqueous phase, being able to regenerate nitrosating species by reacting with oxygen in the lipid phase.
PMCID: PMC2095705  PMID: 17785370
cancer; diet, gastro‐oesophageal junction, nitrite; nitrosation
24.  Multiple sessile polypoid lesions in the stomach 
Gut  2007;56(12):1754.
PMCID: PMC2095706  PMID: 17998325
25.  Benefits of lifestyle modification in NAFLD 
Gut  2007;56(12):1760-1769.
PMCID: PMC2095707  PMID: 17911352

Results 1-25 (1343)