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1.  Lymphocyte subset infiltration patterns and HLA antigen status in colorectal carcinomas and adenomas. 
Gut  1996;38(1):85-89.
Fifty eight large bowel adenocarcinomas and 20 adenomas were studied immunohistochemically, using fresh frozen tissue sections, with regard to lymphocyte subpopulations (CD3, CD4, CD8, CD19, and CD20) in the inflammatory infiltrate and to expression of human leucocyte antigens (HLA-ABC, HLA-A2, and HLA-DR). The findings were related to differentiation and Duke's stage of carcinoma. The inflammatory infiltrate was found to have a phenotype that remained constant irrespective of the intensity of the inflammation. CD4 and CD3 positive cells predominated with fewer CD8 positive cells and a scanty diffuse CD19/20 positive cell population. CD19/20 follicular aggregates were common at the advancing margin of the carcinomas. There was no significant association with Duke's stage, differentiation or HLA status. HLA changes (ABC loss, A2 loss, and DR gain) were associated with differentiation, being more common and more extensive in poorly differentiated carcinomas. HLA-A2 loss was also associated with stage of progression of carcinoma. Inflammation associated with adenomas was found to have a similar phenotype to that associated with carcinomas. HLA changes in adenomas were uncommon, being seen in only one of our 20 cases.
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PMCID: PMC1382984  PMID: 8566865
2.  Cell proliferation in the gastric corpus in Helicobacter pylori associated gastritis and after gastric resection. 
Gut  1995;36(3):351-353.
Patients who have undergone gastric resection are at higher risk of developing gastric carcinoma than normal subjects, and bile reflux is believed to play a role in carcinogenesis. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging, particularly where there is chronic epithelial injury associated with bile reflux. Helicobacter pylori is considered a major risk factor for gastric cancer in the intact stomach. It has been shown previously that antral cell proliferation is increased in H pylori gastritis and falls to normal levels after eradication of the organism. Little is known of corpus cell proliferation in H pylori gastritis or after gastric resection. Using in vitro bromodeoxyuridine labelling of endoscopic biopsy specimens we have found that corpus cell proliferation is increased in H pylori gastritis. Cell proliferation was greater in corpus biopsy specimens of resected stomachs than in H pylori gastritis. Subgroup analysis of patients who had undergone gastric resection indicated that those positive for H pylori had higher levels of cell proliferation than those negative for the organism. These findings provide further evidence that H pylori and bile have a role in gastric carcinogenesis and suggest that their presence has a synergistic effect on gastric epithelial cell proliferation.
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PMCID: PMC1382443  PMID: 7698691
3.  Cell proliferation in Helicobacter pylori associated gastritis and the effect of eradication therapy. 
Gut  1995;36(3):346-350.
Helicobacter pylori causes chronic (type B) gastritis. The 'intestinal' form of gastric cancer arises against a background of chronic gastritis, and prospective epidemiological studies have shown that H pylori is a major risk factor for this. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging where there is chronic epithelial cell injury associated with H pylori gastritis. In vitro bromodeoxyuridine labelling of endoscopic antral biopsy specimens was used to measure mucosal cell proliferation in H pylori associated gastritis before and after therapy for H pylori triple infection. Cell proliferation was increased in H pylori associated gastritis patients compared with normal controls and patients with H pylori negative chronic gastritis (p = 0.0001; Tukey's Studentised range). There was no difference in antral epithelial cell proliferation between duodenal ulcer and non-ulcer subjects infected with H pylori (p = 0.62; Student's t test). Antral mucosal cell proliferation fell four weeks after completing triple therapy, irrespective of whether or not H pylori had been eradicated (p = 0.0001). At retesting six to 18 months later (mean = 12 months), however, those in whom H pylori had not been successfully eradicated showed increased mucosal proliferation compared with both H pylori negative subjects at a similar follow up interval and all cases (whether H pylori positive or negative) four weeks after completion of triple therapy (p = 0.024). These findings suggest that H pylori infection causes increased gastric cell proliferation and in this way may play a part in gastric carcinogenesis.
PMCID: PMC1382442  PMID: 7698690
4.  Prevalence of Helicobacter pylori infection and its effect on symptoms and non-steroidal anti-inflammatory drug induced gastrointestinal damage in patients with rheumatoid arthritis. 
Gut  1993;34(12):1677-1680.
Non-steroidal anti-inflammatory drugs (NSAIDs) and Helicobacter (H pylori) are both associated with an increased risk of peptic ulceration and gastropathy. It is not known, however, if there is an interaction between these two agents, and thus whether or not screening for H pylori before NSAID treatment is of value. The aim of this study was to find out if H pylori potentiates the damaging effects of NSAIDs. Fifty two patients with rheumatoid arthritis requiring longterm NSAID treatment were studied. Dyspeptic symptoms were assessed according to a standardised questionnaire. Gastroscopy was performed after a one week washout period during which NSAIDs were discontinued. Gastric and duodenal mucosal damage was graded endoscopically. H pylori was identified by biopsy urease test and by histological tests. Investigations were repeated after one month's treatment with an NSAID. Patients with H pylori infection (n = 26) had a higher dyspeptic symptom score (p < 0.05). One patient with duodenal ulcer (H pylori +ve) and two with endoscopic gastritis (both H pylori +ve) were excluded from further study. Forty two subjects completed the study. After treatment there was a rise in the gastric damage score both in the H pylori +ve (p = 0.06) and the H pylori -ve (p < 0.005) groups. There was no difference in the extent of increase in grade or the final grade at the end of the treatment period between the H pylori +ve and -ve patients. It is concluded that H pylori infection is associated with increased dyspeptic symptoms in patients receiving NSAIDs but that it does not potentiate NSAID gastropathy.
PMCID: PMC1374461  PMID: 8282254
5.  Ultrasound scanning and 99mTc sulphur colloid scintigraphy in diagnosis of Budd-Chiari syndrome. 
Gut  1986;27(12):1502-1506.
Ultrasound scanning and 99mTc sulphur colloid scintigraphy are widely used in the diagnosis of the Budd-Chiari syndrome and have been compared at the time of presentation in 18 patients in whom the diagnosis was subsequently confirmed by histology and hepatic venography. Ultrasound was diagnostic in 16 (87%). The findings seen most often included hepatic vein abnormalities, caudate lobe hypertrophy with decreased reflectivity and compression of the inferior vena cava. Additional information not shown by scintigraphy included intracaval tumour, or thrombosis, and concomitant portal vein thrombosis. Although scintigraphic abnormalities were present in all patients, only in three (17%) was the 'classical' appearance of increased uptake and/or enlargement of the caudate lobe present. In one patient with nonspecific abnormalities on ultrasound, scintigraphy gave a positive diagnosis and it is in such cases that scintigraphy should continue to be used.
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PMCID: PMC1433960  PMID: 3542741
6.  Budd-Chiari syndrome presenting as fulminant hepatic failure. 
Gut  1986;27(9):1101-1105.
Two cases of the Budd-Chiari syndrome are described in whom the diagnosis was finally confirmed at necropsy. The presentation was with encephalopathy, occurring within eight weeks of first symptoms and coming therefore within the definition of fulminant hepatic failure. In one, thought to have non-A, non-B hepatitis, encephalopathy progressed to grade 4 coma with death 12 days after presentation. In the other, mistakenly thought to have intra-abdominal malignancy, an exploratory laparotomy exacerbated the encephalopathy with death three weeks later. In neither case were non-invasive investigations, such as ultrasound and isotope scanning, carried out which might have facilitated an earlier diagnosis and consideration for orthotopic liver transplantation, probably the most appropriate form of therapy for these very severe cases.
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PMCID: PMC1433808  PMID: 3758822
7.  Hepatotoxicity to sodium valproate: a review. 
Gut  1984;25(6):673-681.
PMCID: PMC1432377  PMID: 6428980

Results 1-7 (7)