Neutrophil signaling alteration: an adverse inflammatory response after burn shock

BACKGROUND: Perinuclear antineutrophil cytoplasmic antibodies occur frequently in adult patients with chronic pouchitis after colectomy and ileal pouch-anal anastomosis for ulcerative colitis. The purpose of the study was to determine the prevalence of perinuclear antineutrophil cytoplasmic antibodies and cytoplasmic antineutrophil cytoplasmic antibody in children and adolescents who undergo colectomy and ileal pouch-anal anastomosis for ulcerative colitis and familial adenomatous polyposis. METHODS: Five groups of children and adolescents (age, <20 years) were studied, with the following histories: acute pouchitis and history of ulcerative colitis; chronic pouchitis and history of ulcerative colitis; pouchitis with Crohn's disease features and a history of ulcerative colitis; no pouchitis and a history of ulcerative colitis; and familial adenomatous polyposis, with or without pouchitis. Antineutrophil cytoplasmic antibody levels and titers were detected in postoperative sera by enzyme-linked immunosorbent assay, and positive results were subtyped by indirect immunofluorescence. RESULTS: The frequency of perinuclear antineutrophil cytoplasmic antibodies and cytoplasmic antineutrophil cytoplasmic antibody in patients with a history of ulcerative colitis were 67% and 15%, compared with a 0% presence in patients with familial adenomatous polyposis (p < 0.001). There was no significant correlation between the frequency of perinuclear antineutrophil cytoplasmic antibodies and ulcerative colitis patient subgroups (patients with and without pouchitis, 66% and 75%). Similarly, there was no significant correlation between the frequency of cytoplasmic antineutrophil cytoplasmic antibodies among ulcerative colitis patient subgroups (patients with and without pouchitis, 19% and 8%). The frequency of cytoplasmic antineutrophil cytoplasmic antibody in patients with Crohn's disease features (50%), was increased, but this difference was not significant. CONCLUSIONS: There is a high frequency of perinuclear antineutrophil cytoplasmic antibodies in children and adolescents who undergo ileal pouch-anal anastomosis for ulcerative colitis, whether or not they have pouchitis. The frequency of cytoplasmic antineutrophil cytoplasmic antibody is lower in this patient population. Additional studies will be required to determine whether the presence of cytoplasmic antineutrophil cytoplasmic antibody is associated with the postoperative development of features of Crohn's disease.     

Evaluation of various screening and surveillance methods in colorectal carcinoma

Colorectal cancer is a common disease which is almost wholly preventable by early removal of adenomatous polyps. Screening should be offered to all persons without risk factors from the age of 50. Selection of the appropriate screening programme should take into account personal preference, local expertise and insurance coverage. Endoscopic screening and surveillance investigations should be strongly encouraged in all persons wit risk factors such as (1) previous treatment of colorectal adenomatous polyps or cancers, (2) ulcerative colitis, (3) patients with hereditary colorectal cancer syndromes and (4) first degree relatives of patients with colorectal cancer. The following four strategies are available for candidates > 50 years without risk factors: (1) faecal occult blood testing (annually), (2) flexible sigmoidoscopy (every 5 years), (3) a combination of both (1 + 2) strategies and (4) coloscopy (every 10 years). Coloscopy should be performed after a positive test result in strategy programs 1-3. Results from prospective randomized trials are available only for faecal occult blood testing, showing an approximately 15% reduction of mortality in the screening group. The potential for reduction of colorectal cancer mortality has been estimated at 30-70% and 60-90% for flexible sigmoidoscopy and coloscopy respectively. However, no results from prospective randomized trials are presently available. Cost-effectiveness analysis has not shown relevant differences between the four different screening strategies.     

Recent advances in surgery for colon and rectal cancer

Surgery is the mainstay of therapy for colon and rectal cancer. Over the past several decades, there have been important advances both in the understanding of the biology of colon and rectal cancer and in the preoperative and operative techniques for treating this disease. Although it appears in some studies that we have made a difference in the survival rates in the treatment of colon and rectal cancer, in actual fact, this phenomenon may only be secondary to better staging and, therefore, a greater ability to prognosticate a particular patient's chance of cure. What has been learned in the past 20 to 30 years is that most colon and rectal carcinomas start as polyps of the colon and rectum. Most often, polyps are sporadic, but there are certain high-risk groups that produce polyps and, consequently, colon and rectal cancer at a much higher rate. The goal of a practicing physician is to identify these high-risk individuals and to recommend frequent screenings so as to intervene before a polyp has had a chance to become a deeply invasive cancer. These high-risk groups are best typified by familial adenomatous polyposis, which if left untreated will, in 100% of cases, lead to the death of a patient from colon or rectal cancer. Other diseases that lead to an increase in colon and rectal cancer but may not go through the usual adenoma-to-carcinoma sequence include inflammatory bowel disease such as Crohn's colitis and ulcerative colitis. Most patients with colorectal carcinoma are asymptomatic at the time of diagnosis. This phenomenon has led to efforts to screen the general population for polyps and for cancer. Screening techniques such as the detection of occult blood in the stool and endoscopic procedures are currently the most popular. It is unclear at this time exactly what the efficacy of these techniques is in improving the survival of the general population from colorectal carcinoma. The surgical techniques to remove colon and rectal carcinomas have recently expanded to include a more aggressive local excision policy for small tumors of the rectum and the application of laparoscopic techniques, new stapling techniques, and new anastomosing techniques for tumors of the colon and rectum. These techniques have become possible in part through advances in surgical instrumentation and also in part from our increasing understanding of the biology of the disease. Both have allowed for more creative approaches to diagnosing and treating colon and rectal cancer.(ABSTRACT TRUNCATED AT 400 WORDS)     

Inflammatory bowel disease

Although ulcerative colitis and Crohn's disease are relatively uncommon disorders, most primary care practices include a number of individuals with these diagnoses. Much of the initial evaluation and long-term care of these patients is managed or coordinated by their primary care physicians. A familiarity with current principles of diagnosis and treatment is essential. Ulcerative colitis and Crohn's disease are related, immunologically mediated disorders of unknown cause. Both are characterized by chronic relapsing courses, frequent need for surgical intervention, and increased colorectal cancer risk. Significant differences are seen between these two inflammatory bowel disease syndromes, in their histopathologic features, clinical manifestations, and response to treatment. This review focuses on the colorectal manifestations of inflammatory bowel disease, emphasizing clinical presentation, approach to diagnosis, medical and surgical management, and long-term prognosis.     

Does colonoscopic polypectomy reduce the incidence of colorectal carcinoma?

The study's objective was to examine whether there is evidence that colonoscopic polypectomy reduces the incidence of colorectal cancer. The records of all patients who underwent colonoscopic polypectomy by a single surgeon between 1974 and 1991 were reviewed. Patients with colorectal cancer diagnosed at the initial colonoscopy, with a history of colorectal cancer, inflammatory bowel disease or familial adenomatous polyposis or with only hyperplastic polyps were excluded. There were 1008 remaining patients, of whom 645 have attended at least one follow-up colonoscopic examination, and these 645 patients from the basis of the study, because the incidence of cancer is known exactly in this group. The mean period of follow up was 4.4 years and the mean number of follow-up colonoscopic examinations was 2.2. There was a total of 2847 person-years of colonoscopic follow up. The expected incidence of cancer, age and sex adjusted, is calculated using Australian epidemiological figures. The observed incidence of cancer was 3 cases (all asymptomatic) per 2847 person-years, which is indistinguishable from the general population's risk of 3.75 cases per 2847 person-years. Analysis of previous publications suggests that patients with adenomas are at an increased risk of developing colorectal cancer of about 2.5 times the general population's risk. If correct, then the observed incidence of 3 cases per 2847 person-years is less than the expected incidence of 9.4 cases per 2847 person-years. This analysis suggests colonoscopic polypectomy does reduce the incidence of colorectal cancer.     

Inflammatory fibroid polyp in a continent ileo-anal pouch after colectomy for ulcerative colitis--case report

The most frequent complication occurring in continent ileo-anal pouches after colectomy for ulcerative colitis (UC) is pouchitis. Recurrences of adenomas or carcinomas in pouches of familial adenomatous polyposis (FAP) patients are exceptional, whereas in those with ulcerative colitis dysplasia it is a very rare occurrence. We describe the case of a young woman who developed a mass in a J pouch three years after its construction following colectomy for ulcerative colitis. Histological and immunohistochemical studies showed that this mass had the features of an inflammatory fibroid polyp. A review of the literature of lesions observed in continent ileo-anal pouches after colectomy for UC would suggest that this lesion is an exceedingly rare complication of those devices.     

Inherited colorectal polyposis and cancer risk of the APC I1307K polymorphism

Germ-line and somatic truncating mutations of the APC gene are thought to initiate colorectal tumor formation in familial adenomatous polyposis syndrome and sporadic colorectal carcinogenesis, respectively. Recently, an isoleucine-->lysine polymorphism at codon 1307 (I1307K) of the APC gene has been identified in 6%-7% of the Ashkenazi Jewish population. To assess the risk of this common APC allelic variant in colorectal carcinogenesis, we have analyzed a large cohort of unselected Ashkenazi Jewish subjects with adenomatous polyps and.or colorectal cancer, for the APC I1307K polymorphism. The APC I1307K allele was identified in 48 (10.1%) of 476 patients. Compared with the frequency in two separate population control groups, the APC I1307K allele is associated with an estimated relative risk of 1.5-1.7 for colorectal neoplasia (both P=.01). Furthermore, compared with noncarriers, APC I1307K carriers had increased numbers of adenomas and colorectal cancers per patient (P=.03), as well as a younger age at diagnosis. We conclude that the APC I1307K variant leads to increased adenoma formation and directly contributes to 3%-4% of all Ashkenazi Jewish colorectal cancer. The estimated relative risk for carriers may justify specific clinical screening for the 360,000 Americans expected to harbor this allele, and genetic testing in the setting of long-term-outcome studies may impact significantly on colorectal cancer prevention in this population.     

A prospective evaluation of the safety and efficacy of methohexital in the emergency department

OBJECTIVE: Knowledge of a possible correlation between distal polyps found at screening sigmoidoscopy and proximal colonic lesions is important for deciding whether to perform total colonoscopy or not. PATIENTS: A prospective analysis of 2439 consecutive patients with colorectal polyps. Of these, 304 were asymptomatic subjects who underwent complete colonoscopy for screening and were found to have adenomatous or hyperplastic polyps in the distal colorectum. RESULTS: Ten (15%) out of 65 patients with distal hyperplastic polyps only and 86 (36%) out of 239 with distal adenomatous polyps were found to have adenomatous polyps in the proximal colon as well (P < 0.001). The frequency of synchronous proximal adenomas in patients with small (< or = 5 mm) or large distal adenomas (> 5 mm) was comparable (37% and 35%, respectively). However, patients with small distal adenomas had significantly smaller proximal adenomas (P = 0.004) containing less villous component (P = 0.017) than those with large distal adenomas. Neither the patient's age nor the presence of multiple distal adenomas increased the prevalence of proximal adenomas. CONCLUSION: Hyperplastic polyps found on rectosigmoidoscopy do not indicate a need for a complete colorectal examination, as 15% of patients with distal hyperplastic polyps will have proximal adenomatous polyps, a figure that is comparable with that of asymptomatic patients having no distal polyps, either hyperplastic or adenomatous. When only small distal adenomas are found at screening sigmoidoscopy in asymptomatic persons the decision to do a total colonoscopy should be based on individual considerations, as in such cases only small polyps are to be expected in the proximal colon.     

The majority of myeloid-antigen-positive (My+) childhood B-cell precursor acute lymphoblastic leukaemias express TEL-AML1 fusion transcripts

BACKGROUND & AIMS: Crohn's disease and ulcerative colitis show a familial aggregation. In both diseases, anti-goblet cell autoantibodies (GABs) have been described. The aim of this study was to define the role of GABs in the pathogenesis of inflammatory bowel disease. METHODS: The study population comprised 61 patients with ulcerative colitis, 76 patients with Crohn's disease, 101 first-degree relatives of patients with ulcerative colitis, and 105 first-degree relatives of patients with Crohn's disease. Thirty-five patients with infectious enterocolitis and 56 healthy unrelated subjects served as controls. Autoantibodies were detected by indirect immunofluorescence. RESULTS: Thirty-nine percent of patients with ulcerative colitis (24 of 61) and 30% of patients with Crohn's disease (23 of 76) were positive for GABs. GABs were detected in 21% (21 of 101) of first-degree relatives of patients with ulcerative colitis and in 19% (20 of 105) of first-degree relatives of patients with Crohn's disease. In patients with infectious enterocolitis and in healthy controls, GABs were seen in 3% (1 of 35) and 2% (1 of 56), respectively. The differences between control groups and both groups of patients or their first-degree relatives were significant. CONCLUSIONS: The high prevalence in first-degree relatives suggests that GABs may represent a marker characterizing susceptibility to inflammatory bowel disease.     

Multiple adenomatous papillary colonic polyps in a family with frequent cases of stomach carcinoma--a new phenotype of familial colonic polyposis]

A kindred of "minor adenomatous polyposis" associated with a high incidence of gastric cancer is described. Five out of 14 mainly asymptomatic individuals in 2 generations of kindred examined clinically, by panendoscopy and coloscopy exhibited multiple polyps of colon or/and stomach and jejunum. Single or multiple papillary adenomas were detected mainly in the right or middle colon (3 times or in the jejunum (once). Hyperplastic polyps were found in the stomach (3 times) and in the colon (twice of these 5 individuals. Our findings suggest that "minor adenomatous polyposis" associated with gastric cancer may represent another, hitherto unrecognized, phenotype of familial multiple polyposis.     

Colorectal cancer in idiopathic inflammatory bowel disease

The development of colorectal cancer is the most serious long-term problem faced by patients with extensive ulcerative colitis and Crohn's colitis, with an incidence 20-fold higher and an average age of onset 20 years younger than colorectal cancer in the general population. This report summarizes the epidemiology, pathology, and recent advances in the molecular pathogenesis of colorectal cancer in inflammatory bowel disease and of its acknowledged precursor, mucosal dysplasia. It also reviews the rationale behind the use of endoscopic surveillance for dysplasia as a means of reducing cancer mortality, as well as some of the issues involved in its effective implementation.     

Incidence of neoplastic polyps in the ileal pouch of patients with familial adenomatous polyposis after restorative proctocolectomy

PURPOSE: Although adenomatous polyps and even adenocarcinomas have been found in the terminal ileum of patients with familial adenomatous polyposis, the prevalence of neoplastic changes in the pouches of patients who have undergone restorative proctocolectomy is unknown. The objective of this study was to determine the frequency of pelvic pouch neoplasia in familial adenomatous polyposis patients after restorative proctocolectomy. METHODS: Patients in a polyposis registry who had undergone restorative proctocolectomy were recruited. Demographic, surgical, pathologic, and endoscopic data were obtained from patient records. Video pouchoscopy was done after two enemas and representative biopsies were taken. RESULTS: Of 102 eligible patients, 26 (17 males and 9 females) participated. Median age at ileal pouch-anal anastomosis was 31 (range, 12-58) years. Median follow-up period was 66 (11-156) months. Adenomas were found in the pouch of 11 (42 percent) patients, in the terminal ileum above the pouch in 1 patient, and in the anal canal of 4 patients. Among patients with pouch polyps, three patients had one lesion, three patients had two lesions, and five patients had more than ten lesions. The incidence of polyps increased steadily with time from restorative proctocolectomy. There was no relation between the incidence of pouch polyposis and the severity of colonic or duodenal disease. CONCLUSIONS: Proctocolectomy and ileal pouch-anal anastomosis is associated with a significant risk of pouch neoplasia in familial adenomatous polyposis patients. The severity of pouch adenomas was not related either to the severity of colonic or duodenal disease. The pelvic pouches of all patients with familial adenomatous polyposis who have undergone restorative proctocolectomy should be examined periodically.     

Molecular biology of colorectal cancer

Colorectal cancer is a significant cause of morbidity and mortality in Western populations. This cancer develops as a result of the pathologic transformation of normal colonic epithelium to an adenomatous polyp and ultimately an invasive cancer. The multistep progression requires years and possibly decades and is accompanied by a number of recently characterized genetic alterations. Mutations in two classes of genes, tumor-suppressor genes and proto-oncogenes, are thought to impart a proliferative advantage to cells and contribute to development of the malignant phenotype. Inactivating mutations of both copies (alleles) of the adenomatous polyposis coli (APC) gene--a tumor-suppressor gene on chromosome 5q--mark one of the earliest events in colorectal carcinogenesis. Germline mutation of the APC gene and subsequent somatic mutation of the second APC allele cause the inherited familial adenomatous polyposis syndrome. This syndrome is characterized by the presence of hundreds to thousands of colonic adenomatous polyps. If these polyps are left untreated, colorectal cancer develops. Mutation leading to dysregulation of the K-ras protooncogene is also thought to be an early event in colon cancer formation. Conversely, loss of heterozygosity on the long arm of chromosome 18 (18q) occurs later in the sequence of development from adenoma to carcinoma, and this mutation may predict poor prognosis. Loss of the 18q region is thought to contribute to inactivation of the DCC tumor-suppressor gene. More recent evidence suggests that other tumor-suppressor genes--DPC4 and MADR2 of the transforming growth factor beta (TGF-beta) pathway--also may be inactivated by allelic loss on chromosome 18q. In addition, mutation of the tumor-suppressor gene p53 on chromosome 17p appears to be a late phenomenon in colorectal carcinogenesis. This mutation may allow the growing tumor with multiple genetic alterations to evade cell cycle arrest and apoptosis. Neoplastic progression is probably accompanied by additional, undiscovered genetic events, which are indicated by allelic loss on chromosomes 1q, 4p, 6p, 8p, 9q, and 22q in 25% to 50% of colorectal cancers. Recently, a third class of genes, DNA repair genes, has been implicated in tumorigenesis of colorectal cancer. Study findings suggest that DNA mismatch repair deficiency, due to germline mutation of the hMSH2, hMLH1, hPMS1, or hPMS2 genes, contributes to development of hereditary nonpolyposis colorectal cancer. The majority of tumors in patients with this disease and 10% to 15% of sporadic colon cancers display microsatellite instability, also know as the replication error positive (RER+) phenotype. This molecular marker of DNA mismatch repair deficiency may predict improved patient survival. Mismatch repair deficiency is thought to lead to mutation and inactivation of the genes for type II TGF-beta receptor and insulin-like growth-factor II receptor. Individuals from families at high risk for colorectal cancer (hereditary nonpolyposis colorectal cancer or familial adenomatous polyposis) should be offered genetic counseling, predictive molecular testing, and when indicated, endoscopic surveillance at appropriate intervals. Recent studies have examined colorectal carcinogenesis in the light of other genetic processes. Telomerase activity is present in almost all cancers, including colorectal cancer, but rarely in benign lesions such as adenomatous polyps or normal tissues. Furthermore, genetic alterations that allow transformed colorectal epithelial cells to escape cell cycle arrest or apoptosis also have been recognized. In addition, hypomethylation or hypermethylation of DNA sequences may alter gene expression without nucleic acid mutation.     

Incidence of inflammatory bowel diseases in the department of Puy-de-D?me in 1993 and 1994. EPIMICI. Epidémiologie des Maladies Inflammatoires Cryptogenetiques de l'Intestin group

The aim of this prospective epidemiological study was to investigate the incidence of Inflammatory Bowel Disease in the Puy-de-D?me county using the same methodology as EPIMAD's registry. METHODS: From 01/01/93 to 31/12/94, each gastroenterologist (n = 22) collected patients consulting for the first time with clinical symptoms compatible with inflammatory bowel disease. Data were reported on a questionnaire by an interviewer practitioner. The final diagnosis of Crohn's disease and ulcerative colitis was made in a blind manner by two expert gastroenterologists and recorded according to the Calkin's criteria as definite, probable, or possible diagnosis, or unclassifiable chronic colitis or acute colitis. RESULTS: 167 new cases were identified: 112 (67.1%) inflammatory bowel disease for the combined group of definite and probable cases with 79 Crohn's disease (70.5%), 29 ulcerative colitis (25.9%) of which 11 ulcerative proctitis (37.9%), 4 unclassifiable chronic colitis (3.6%) and 55 acute colitis (32.9%). The crude and age-adjusted incidence (per 10(5)/year) was respectively 6.6 and 5.7 for Crohn's disease and 2.4 and 1.9 for ulcerative colitis. The highest age-specific incidence rate for Crohn's disease was between 40-49 years (14.1) and for ulcerative colitis between 80-89 years (6.8). The female/male ratio was 0.8 for Crohn's disease and 1.1 for ulcerative colitis. The median age at the time of diagnosis was 42.6 years for Crohn's disease and 35.3 years for ulcerative colitis. CONCLUSIONS: These preliminary findings revealed a high incidence of Crohn's disease and low of ulcerative colitis in this county. However, these results must be managed carefully because these data were recorded only on two years and the inflammatory bowel disease classified possible and acute colitis require a follow-up.     

Primary sclerosing cholangitis--an ulcerative colitis-associated illness with surgical consequences

Primary sclerosing cholangitis (PSC) is generally associated with ulcerative colitis (UC). The disease typically progresses slowly, but ultimately, and leads to cirrhosis, liver failure or bile duct cancer. PSC patients with simultaneous ulcerative colitis are also at higher risk for colorectal cancer. At the present time, there is no effective treatment for PSC, although preliminary data show encouraging results after treatment with ursodeoxycholic acid. However, there are no data concerning the delay or prevention of progress of the disease with this drug, because follow-up time is not yet long enough. Isolated bile duct strictures should be treated endoscopically. The possible effect of proctocolectomy on the course of PSC is controversial. Liver transplantation is the therapy of choice for PSC in its final stage. The 5-year survival rate (89%) is significantly better than after transplantation for other indications. Patients with ulcerative colitis have to be followed up by lifelong colonoscopy. Although the course of UC after transplantation is mostly asymptomatic, these patients are at higher risk for colorectal cancer.     

Flow cytometry and in vitro tritiated thymidine labeling in normal rectal mucosa of patients at high risk of colorectal cancer

OBJECTIVES: To compare two different methods to evaluate rectal epithelial cell proliferation as a biomarker of risk of developing colon cancer. METHODS: Samples of normal rectal mucosa from 26 patients at increased risk for colorectal cancer (22 patients with adenoma, three with adenocarcinoma of the large bowel, and one with longstanding ulcerative colitis) were examined by means of in vitro labeling with tritiated thymidine and flow cytometry. RESULTS: We found a significant correlation between thymidine-labeling index and the percentage of cells in S-phase, measured by flow cytometry both in formalin-fixed, paraffin-embedded specimens and in frozen specimens (respectively, r = 0.7647, p < 0.001, and r = 0.4503, p < 0.01). However, using flow cytometry, the percentage of cells in S-phase was significantly higher than the thymidine-labeling index in both fixed-embedded and frozen specimens (p < 0.01). Proliferative parameters were not higher in patients with colon carcinoma, and were not related to the degree of dysplasia, the number of adenomas, or familial occurrence of colorectal cancer. Two specimens taken from normal rectal mucosa of two patients with adenomas showed aneuploidy. No aneuploidy was found in normal rectal specimens of patients with adenocarcinoma. CONCLUSIONS: These results show that the calculation of cells in S-phase with in vitro tritiated thymidine labeling or by flow cytometry produces different results. However, the significant correlation between corresponding parameters obtained with these techniques support the use of either method as "intermediate biomarkers" of colorectal cancer risk and prognosis.     

Enhanced intestinal adenomatous polyp formation in Pms2-/-;Min mice

Analysis of two human familial cancer syndromes, hereditary nonpolyposis colorectal cancer and familial adenomatous polyposis, indicates that mutations in either one of four DNA mismatch repair gene homologues or the adenomatous polyposis coli (APC) gene, respectively, are important for the development of colorectal cancer. To further investigate the role of DNA mismatch repair in intestinal tumorigenesis, we generated mice with mutations in both Apc and the DNA mismatch repair gene, Pms2. Whereas Pms2-deficient mice do not develop intestinal tumors, mice deficient in Pms2 and heterozygous for Min, an allele of Apc, develop approximately three times the number of small intestinal adenomas and four times the number of colon adenomas relative to Min and Pms2+/-;Min mice. Although Pms2 deficiency clearly increases adenoma formation in the Min background, histological analysis indicated no clear evidence for progression to carcinoma.     

Cigarette smoking and the colorectal adenoma-carcinoma sequence: a hypothesis to explain the paradox

As recognized precursor lesions to colorectal cancer, colorectal adenomatous polyps have been studied to enhance knowledge of colorectal cancer etiology. Although most of the known risk factors for colorectal cancer are also associated with the occurrence of colorectal adenomas, cigarette smoking has had a strong, consistent relationship with colorectal adenomas but is generally not associated with colorectal cancer. The explanation for this paradox is unknown. With data collected in 1986-1988 during a large case-control study based on colonoscopy results in New York City, New York, the authors investigated the possibility that the paradox may arise because subjects with colorectal adenomas were included in the control group of cancer case-control studies. The authors found a statistically significant increased risk between heavy cigarette smoking (smokers with > or = 40 pack-years of smoking) and risk of adenoma (odds ratio (OR) = 1.61, 95% confidence interval (CI) 1.06-2.44). They saw no increased colorectal cancer risk from heavy cigarette smoking (OR = 1.02, 95% CI 0.52-1.99) using a "manufactured" control group to simulate a typical unscreened, population-based control group. When the authors compared these colorectal cancer cases with an adenoma-free control group examined by colonoscopy in a polytomous model with several case groups (newly diagnosed adenomas, carcinoma in situ, intramucosal carcinoma, and colorectal cancer), they found that the risk for 20-39 pack-years of smoking was elevated, although not statistically significant, and was similar for all four case groups. The risk for the highest smoking category (> or = 40 pack-years) was more strongly elevated in all four case groups, although it was statistically significant for only the newly diagnosed adenoma and the carcinoma in situ cases (adenomas, OR = 1.59, 95% CI 1.05-2.42; carcinoma in situ, OR = 2.05, 95% CI 1.01-4.15; intramucosal carcinoma, OR = 1.30, 95% CI 0.61-2.77; and colorectal cancer, OR = 1.30, 95% CI 0.64-2.65). While the authors' study is weakened by the lack of statistical significance concerning risk for colorectal cancer, these data offer some support for the hypothesis that the association between cigarette smoking and risk of colorectal cancer may have been masked by inclusion in the control group of subjects with adenomas. They also suggest that the major effect of smoking on the colorectal adenoma-carcinoma sequence occurs in the earlier stages of the formation of adenoma and the development of carcinoma in situ.     

Current status of ileoanal reservoirs: 1992

Restorative proctocolectomy with ileoanal reservoir has been a significant development in the surgical treatment of mucosal ulcerative colitis and familial adenomatous polyposis. It enables excision of the diseased colorectal mucosa with preservation of continence and avoidance of a permanent stoma. The surgical techniques, criteria for patient selection, and understanding of the physiology and outcome of the procedure, however, continue to evolve.     

Incidence of inflammatory bowel disease in northern France (1988-1990)

There were no data concerning the incidence of inflammatory bowel disease (IBD) in France. The aim of this study was to investigate the incidence of Crohn's disease and ulcerative colitis in northern France. This prospective population based study was realised through the gastroenterologists of the region Nord-Pas de Calais and the Somme Department. Each gastroenterologist referred patients consulting for the first time with clinical symptoms compatible with IBD. Data were collected by an interviewer practitioner present at the gastroenterologist's consulting room. Two independent expert gastroenterologists assessed each case in a blind manner and made a final diagnosis of Crohn's disease, ulcerative colitis, ulcerative proctitis, or unclassifiable chronic colitis. From 1988 to 1990, 1291 cases of IBD were recorded: 674 (52%) Crohn's disease, 466 (36%) ulcerative colitis including 162 proctitis (35%), and 151 (12%) unclassifiable chronic colitis. The mean annual incidence was 4.9 per 100,000 for Crohn's disease and 3.2 for ulcerative colitis. The sex ratio F/M was 1.3 for Crohn's disease and 0.8 for ulcerative colitis. The highest age specific incidence rate for Crohn's disease was between 20 and 29 years: 13.1 for women and 9.8 for men. The highest age specific incidence rate for ulcerative colitis was between 20 and 39 years: 5.5 for women and 6.5 for men. This first French prospective study has shown an incidence rate for Crohn's disease comparable with that seen in north European studies but lower than that seen for ulcerative colitis. These results could be related to the different environmental factors or the genetic background of the population studied, or both.