C J Groves

St. Mark's Hospital, Harrow, England, United Kingdom

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Publications (9)95.7 Total impact

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    ABSTRACT: Ileal inflammation in ulcerative colitis can occur as backwash ileitis or prestomal ileitis. After restorative proctocolectomy (RPC), ileal inflammation may be present in the pouch (pouchitis) but inflammation proximal to the pouch in the neo-terminal ileum, so called pre-pouch ileitis (PI), has also been observed. As pouchitis is increasingly common and PI can mimic it, our aim was to characterize this condition. A review of prospectively collected data on 571 inflammatory bowel disease patients undergoing follow-up after RPC in a single centre over 22 years was performed. The histology of biopsy material was reviewed and staining for colonic mucosal phenotypic changes was undertaken. It was not routine practice to prospectively assess all patients for pre-pouch ileitis when the database was constructed. Of 19 patients with inflammation of the pre-pouch neo-terminal ileum (NTI) identified three had Crohn's disease and one a NSAID stricture. The remaining 15 had a characteristic diffuse inflammation extending from the NTI-pouch junction proximally: pre-pouch ileitis. The inflammation extended proximally for up to 50 cm. Fistula formation was seen in only one. Seven (47%) of 15 had pouchitis but only two had suffered backwash ileitis pre-operatively. Seven responded to medical therapy and four to surgery. The histological appearances including staining for colonic phenotypic change were similar in PI and pouchitis. Pre-pouch ileitis is uncommon. As the patients' previous diagnosis of UC was confirmed and there was no radiological or histological evidence of Crohn's disease, PI appears to have a distinct pathogenesis from Crohn's disease.
    Full-text · Article · Jul 2006 · Colorectal Disease
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    ABSTRACT: In familial adenomatous polyposis, the long-term risk of pouch polyposis and potential for pouch cancer are unknown. Our aim was to evaluate prospectively the prevalence, nature, and etiology of pouch ileal adenomas with that of nonpouch ileal adenomas in familial adenomatous polyposis. Sixty patients with familial adenomatous polyposis pouch, 47 familial adenomatous polyposis patients with ileorectal anastomosis, and 20 younger patients with familial adenomatous polyposis who had prophylactic colectomy were examined with videoendoscopy. Adenomatous polyps were found in the pouches of 34 patients (57 percent). A total of 362 polyps were identified (range, 0-50 per patient). A logistic regression model confirmed that there was a significant association between the increasing age of the patient and the presence of pouch adenomas (P < 0.02) and the length of follow-up since pouch surgery (P < 0.05). There was no apparent relationship between the development of pouch adenomas and the severity of either colonic or duodenal polyposis and there were no clear genotype or phenotype correlations. Most polyps were tubular adenomas with mild dysplasia, but 11 patients had more advanced histology, including two patients with large villous adenomas. Nonpouch ileal mucosa was spared from visually observed adenomas, with only 1 of 48 (2 percent) patients with ileorectal anastomosis adenomas and 0 of 20 (0 percent) younger, precolectomy patients having terminal ileal adenomas. However, microadenomas were present on random biopsy in 4 percent to 5 percent of nonpouch ileum. The risk of pouch cancer in familial adenomatous polyposis is unclear, but follow-up periods since surgery remain relatively short. Long-term endoscopic surveillance of familial adenomatous polyposis pouches is thus recommended along with evaluation of potential therapeutic options for pouch adenomas.
    No preview · Article · May 2005 · Diseases of the Colon & Rectum
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    ABSTRACT: Although only 5 per cent of patients with familial adenomatous polyposis (FAP) die from duodenal cancer, a recent study indicated that the mortality rate is much higher in patients with Spigelman stage IV disease. This has prompted an increased rate of referral for excisional surgery and an analysis of the results. Between January 1994 and June 2002, 16 patients with FAP (mean age 55 years; eight men) were referred to a single surgeon for pylorus-preserving pancreaticoduodenal resection for Spigelman stage IV duodenal adenomatosis. One patient died from multiple organ failure after relaparotomy for haemorrhage and a jejunal perforation; other major complications included anastomotic leak (one), primary haemorrhage (one), lymphatic leak (one), chylous ascites (one), pulmonary embolus (two) and prolonged delayed gastric emptying that required total parenteral nutrition (three). Overall there were 11 major complications in eight patients. Two patients developed insulin-dependent diabetes and one postprandial dumping. Postoperative histological examination revealed five unsuspected cancers, which led to four deaths within 3 years of surgery. One patient died 2 months after surgery from pulmonary thromboembolism and another at 5 months from an inoperable brain tumour. Nine of the 16 patients were alive and well at a mean of 38 months after surgery. The choice between continued endoscopic surveillance and excisional surgery for Spigelman stage IV duodenal disease remains finely balanced.
    Full-text · Article · Sep 2004 · British Journal of Surgery
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    ABSTRACT: Studies of adenomatous polyposis coli (APC) mutations in familial adenomatous polyposis (FAP) have focused on large bowel disease. It has been found that: 1) germline APC mutations around codon 1300 are associated with severe colorectal polyposis; 2) somatic APC mutations in colorectal tumors tend to cluster approximately between codons 1250 and 1450; and 3) patients with germline mutations close to codon 1300 tend to acquire somatic mutations (second hits) in their colorectal polyps by allelic loss, whereas the tumors of other FAP patients have truncating second hits. Using new and published data, we have investigated how germline and somatic APC mutations influence the pathogenesis of upper gastrointestinal polyps in FAP. We have compared the results with those from colorectal disease. We found that somatic mutations in upper gastrointestinal polyps cluster approximately between codons 1400 and 1580. Patients with germline APC mutations after codon 1400 tend to show allelic loss in their upper gastrointestinal polyps; the tumors of other patients have truncating somatic mutations after codon 1400. Finally, patients with germline mutations after codon 1400 tend to have more severe duodenal polyposis (odds ratio, 5.72; 95% confidence interval, 1.13 to 28.89; P = 0.035). Thus, in both upper gastrointestinal and colorectal tumors, a specific region of the APC gene is associated with severe disease, clustering of somatic mutations, and loss of the wild-type allele. However, the region concerned is different in upper gastrointestinal and colorectal disease. The data suggest that loss of all APC SAMP repeats is probably necessary for duodenal and gastric tumorigenesis in FAP, as it is in colonic tumors. Compared with colonic tumors, however, retention of a greater number of beta-catenin binding/degradation repeats is optimal for tumorigenesis in upper gastrointestinal FAP.
    Full-text · Article · Jul 2002 · American Journal Of Pathology
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    ABSTRACT: Duodenal cancer is one of the leading causes of death in familial adenomatous polyposis (FAP) patients. An endoscopic surveillance programme was therefore initiated in 1988, the outcome of which is described in this paper. We report the 10 year follow up of 114 patients with FAP who were prospectively screened for the presence and severity of duodenal adenomas. Six of 114 patients (median age 67 years) developed duodenal adenocarcinoma. Four of these were from 11 patients who originally had Spigelman stage IV disease (advanced duodenal polyposis), which gives a 36% risk within this group of developing cancer. One case of duodenal cancer arose from 41 patients who originally had stage III disease (2%) and one cancer arose from 44 patients with original stage II disease (2%). All six patients have died: five were inoperable and one had recurrence three years after a pancreaticoduodenectomy. There was no association between duodenal cancer and site of germline mutation of the APC gene. Surveillance for duodenal adenocarcinoma and subsequent early referral for curative surgery has not been effective. Selection of patients with advanced but benign (Spigelman stage IV) duodenal polyposis for prophylactic pancreaticoduodenectomy should therefore be considered and can now be justified on the basis of these results. More comprehensive endoscopic surveillance of high risk (stage III and IV) patients is needed in an attempt to avoid underestimating the severity of duodenal polyposis, and to evaluate the role of endoscopic therapy in preventing advanced disease.
    Full-text · Article · Jun 2002 · Gut
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    C J Groves
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    ABSTRACT: Background: Duodenal cancer is one of the leading causes of death in familial adenomatous polyposis (FAP) patients. An endoscopic surveillance programme was therefore initiated in 1988, the outcome of which is described in this paper. Methods: We report the 10 year follow up of 114 patients with FAP who were prospectively screened for the presence and severity of duodenal adenomas. Results: Six of 114 patients (median age 67 years) developed duodenal adenocarcinoma. Four of these were from 11 patients who originally had Spigelman stage IV disease (advanced duodenal polyposis), which gives a 36% risk within this group of developing cancer. One case of duodenal cancer arose from 41 patients who originally had stage III disease (2%) and one cancer arose from 44 patients with original stage II disease (2%). All six patients have died: five were inoperable and one had recurrence three years after a pancreaticoduodenectomy. There was no association between duodenal cancer and site of germline mutation of the APC gene. Conclusions: Surveillance for duodenal adenocarcinoma and subsequent early referral for curative surgery has not been effective. Selection of patients with advanced but benign (Spigelman stage IV) duodenal polyposis for prophylactic pancreaticoduodenectomy should therefore be considered and can now be justified on the basis of these results. More comprehensive endoscopic surveillance of high risk (stage III and IV) patients is needed in an attempt to avoid underestimating the severity of duodenal polyposis, and to evaluate the role of endoscopic therapy in preventing advanced disease.
    Preview · Article · May 2002 · Gut
  • CJ Groves · IG Beveridge · RK Phillips

    No preview · Article · Apr 2001 · Gastroenterology
  • IG Beveridge · CJ Groves · K Neale · RKS Phillips

    No preview · Article · Apr 2001 · Gastroenterology
  • CJ Groves · BP Saunders · AD Spigelman · RK Phillips

    No preview · Article · Apr 2001 · Gastroenterology