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• W2006608857 abstract "Background & Aims: The incidence of Crohn’s disease in Scottish children has increased steadily over 30 years. Many studies have investigated genetic influence or possible links with childhood events. We aimed to study sociodemographic and/or geographic distribution of juvenile=onset Crohn’s disease in Scotland. Methods: Using a previously established and validated database covering the entire Scottish population, 580 Scottish children (<16 years of age at symptom onset) with inflammatory bowel disease incident between 1981 and 1995 were identified. Postcodes of incident cases were classed for geographic location and material deprivation. Incidence rates (/100,000/year) were sex standardized to the 1991 census population. The effects of sex, geographic location, time, and deprivation category were estimated from a multifactorial Poisson regression model. Results: The incidence of juvenile-onset Crohn’s disease was 2.3 (95% CI: 2.0–2.5) for the time period 1981 to 1995 and was significantly higher in northern (3.1, 95% CI: 2.6–3.8) than in southern Scotland (2.1, 95% CI: 1.9–2.4, P < 0.001). The incidence of juvenile-onset ulcerative colitis did not show north/south variation (P = 0.677). The relative risks of developing CD were significantly lower in postcode areas with deprivation categories 2–7 as compared with deprivation score 1 (most affluent, P = 0.033). This pattern was not seen for UC. Conclusions: There was an increased incidence of juvenile-onset Crohn’s disease in northern compared with southern Scotland. Children from more affluent areas had a higher relative risk of developing Crohn’s disease. Juvenile onset ulcerative colitis did not show north/south variation in incidence or association with affluence. Background & Aims: The incidence of Crohn’s disease in Scottish children has increased steadily over 30 years. Many studies have investigated genetic influence or possible links with childhood events. We aimed to study sociodemographic and/or geographic distribution of juvenile=onset Crohn’s disease in Scotland. Methods: Using a previously established and validated database covering the entire Scottish population, 580 Scottish children (<16 years of age at symptom onset) with inflammatory bowel disease incident between 1981 and 1995 were identified. Postcodes of incident cases were classed for geographic location and material deprivation. Incidence rates (/100,000/year) were sex standardized to the 1991 census population. The effects of sex, geographic location, time, and deprivation category were estimated from a multifactorial Poisson regression model. Results: The incidence of juvenile-onset Crohn’s disease was 2.3 (95% CI: 2.0–2.5) for the time period 1981 to 1995 and was significantly higher in northern (3.1, 95% CI: 2.6–3.8) than in southern Scotland (2.1, 95% CI: 1.9–2.4, P < 0.001). The incidence of juvenile-onset ulcerative colitis did not show north/south variation (P = 0.677). The relative risks of developing CD were significantly lower in postcode areas with deprivation categories 2–7 as compared with deprivation score 1 (most affluent, P = 0.033). This pattern was not seen for UC. Conclusions: There was an increased incidence of juvenile-onset Crohn’s disease in northern compared with southern Scotland. Children from more affluent areas had a higher relative risk of developing Crohn’s disease. Juvenile onset ulcerative colitis did not show north/south variation in incidence or association with affluence. Crohn’s disease (CD) and ulcerative colitis (UC) are the 2 main clinical entities of inflammatory bowel disease (IBD). Both are chronic relapsing inflammatory conditions of the gastrointestinal tract and are now a common cause of morbidity in Western Europe and North America.1Rubin G.P. Hungin A.P. Chinn D.J. Dwarakanath D. Quality of life in patients with established inflammatory bowel disease a UK general practice survey.Aliment Pharmacol Ther. 2004; 19: 529-535Crossref PubMed Scopus (89) Google Scholar CD commonly presents during childhood or adolescence (juvenile onset),2Griffiths A.M. Buller H.B. Inflammatory bowel disease.in: Walker W.A. Durie P.R. Hamilton J.R. Walker-Smith J.A. Watkins J.B. Paediatric gastrointestinal disease. 3rd edition. Decker Inc, New York2000: 613-652Google Scholar and growth, pubertal development, education, employment potential, and quality of life may all suffer. The cause of CD remains unclear. The incidence of juvenile-onset (J-O) CD in northern Europe has increased steadily over the last 3 decades,3Armitage E. Drummond H. Ghosh S. Ferguson A. Incidence of juvenile-onset Crohn’s disease in Scotland.Lancet. 1999; 353: 1496-1497Abstract Full Text Full Text PDF PubMed Scopus (82) Google Scholar, 4Hildebrand H. Finkel Y. Grahnquist L. Lindholm J. Ekbom A. Askling J. Changing pattern of paediatric inflammatory bowel disease in northern Stockholm 1990–2001.Gut. 2003; 52: 1432-1434Crossref PubMed Scopus (199) Google Scholar and Scotland now has the highest incidence in the British Isles.5Sawczenko A. Sandhu B.K. Logan R.F. Jenkins H. Taylor C.J. Mian S. Lynn R. Prospective survey of childhood inflammatory bowel disease in the British Isles.Lancet. 2001; 357: 1093-1094Abstract Full Text Full Text PDF PubMed Scopus (315) Google Scholar Familial clustering and twin studies have confirmed the importance of genetic susceptibility, but the rapid increase in incidence is not clearly explained by shifts in frequency of susceptibility genes. Coupled with the lack of complete concordance in monozygotic twin pairs,6Halfvarson J. Bodin L. Tysk C. Lindberg E. Jarnerot G. Inflammatory bowel disease in a Swedish twin cohort a long-term follow-up of concordance and clinical characteristics.Gastroenterology. 2003; 124: 1767-1773Abstract Full Text Full Text PDF PubMed Scopus (310) Google Scholar these data strongly implicate environmental factors as having a critical role in disease etiology. Cigarette smoking,7Bridger S. Lee J.C. Bjarnason I. Jones J.E. Macpherson A.J. In siblings with similar genetic susceptibility for inflammatory bowel disease, smokers tend to develop Crohn’s disease and non-smokers develop ulcerative colitis.Gut. 2002; 51: 21-25Crossref PubMed Scopus (118) Google Scholar diet,8Mahmud N. Weir D.G. The urban diet and Crohn’s disease is there a relationship?.Eur J Gastroenterol Hepatol. 2001; 13: 93-95Crossref PubMed Scopus (52) Google Scholar immunization,9Thompson N.P. Montgomery S.M. Pounder R.E. Wakefield A.J. Is measles vaccination a risk factor for inflammatory bowel disease?.Lancet. 1995; 345: 1071-1074Abstract PubMed Google Scholar altered domestic hygiene,10Gent A.E. Hellier M.D. Grace R.H. Swarbrick E.T. Coggon D. Inflammatory bowel disease and domestic hygiene in infancy.Lancet. 1994; 343: 766-767Abstract PubMed Scopus (312) Google Scholar and refrigeration11Hugot J.P. Alberti C. Berrebi D. Bingen E. Cezard J.P. Crohn’s disease the cold chain hypothesis.Lancet. 2003; 362: 2012-2015Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar have all been proposed as important determinants. In addition to the rapid temporal changes in incidence, geographic and sociodemographic variations have been reported. The north-south gradient in CD incidence was first described in Europe.12Shivananda S. Lennard-Jones J. Logan R. Fear N. Price A. Carpenter L. van Blankenstein M. Incidence of inflammatory bowel disease across Europe: is there a difference between north and south? Results of the European Collaborative Study on Inflammatory Bowel Disease (EC-IBD).Gut. 1996; 39: 690-697Crossref PubMed Scopus (845) Google Scholar In the United States, the incidence of CD is higher in the north compared with the south.13Sonnenberg A. McCarty D.J. Jacobsen S.J. Geographic variation of inflammatory bowel disease within the United States.Gastroenterology. 1991; 100: 143-149Abstract PubMed Google Scholar There is also evidence for epidemiologic variability within countries. Significant differences were found in the incidence of CD and UC between 4 counties in Norway.14Moum B. Vatn M.H. Ekbom A. Aadland E. Fausa O. Lygren I. Stray N. Sauar J. Schulz T. The Inflammatory Bowel South-Eastern Norway (IBSEN) Study Group of GastroenterologistsIncidence of Crohn’s disease in four counties in southeastern Norway, 1990–93. A prospective population-based study.Scand J Gastroenterol. 1996; 31: 355-361Crossref PubMed Scopus (147) Google Scholar, 15Moum B. Vatn M.H. Ekbom A. Aadland E. Fausa O. Lygren I. Sauar J. Schulz T. Stray N. The Inflammatory Bowel South-Eastern Norway (IBSEN) Study Group of GastroenterologistsIncidence of ulcerative colitis and indeterminate colitis in four counties of southeastern Norway, 1990–93. A prospective population-based study.Scand J Gastroenterol. 1996; 31: 362-366Crossref PubMed Scopus (180) Google Scholar An increased incidence of CD has been shown in higher income families,16Blanchard J.F. Bernstein C.N. Wajda A. Rawsthorne P. Small-area variations and sociodemographic correlates for the incidence of Crohn’s disease and ulcerative colitis.Am J Epidemiol. 2001; 154: 328-335Crossref PubMed Scopus (129) Google Scholar although, in contrast, a recent study of socioeconomic status in adult IBD found that IBD patients were not of a higher economic status than the general population.17Bernstein C.N. Kraut A. Blanchard J.F. Rawsthorne P. Yu N. Walld R. The relationship between inflammatory bowel disease and socioeconomic variables.Am J Gastroenterol. 2001; 96: 2117-2125Crossref PubMed Google Scholar The reasons for the observed geographic (north/south and interregional) and socioeconomic variations in these previous studies are not clear, but these may reflect variations in the distribution of important environmental etiologic agents. Alternatively, they may be largely due to regional variations in the sociodemographic characteristics or early life events of populations that may have important etiologic influences. By closely studying patterns in incidence, new hypotheses may be generated about underlying etiologic factors. This present study has investigated geographic and sociodemographic patterns of J-O CD incidence in Scotland. Scotland (latitude 55°–60° north) has a total area of 30,405 square miles (77,837 km2) and includes 4 urban centers with populations over 100,000. The population aged 0–15 years declined by 12.8% from 1,188,465 in 1981 to 1,035,762 in 1995.181991 Scottish Census Data. Annual Report of the Registrar General for Scotland. 1999. General Register Office for Scotland.Google Scholar In 1991, 98% of the 0–15-year-old population were white Caucasian, and there was a net 0.03% outward migration from the whole Scottish population. The Scottish Hospital Discharges-Linked Database followed by case-note verification was used to identify all children less than 16 (<16) years of age with a diagnosis of CD or UC, between January 1981 and December 1995.3Armitage E. Drummond H. Ghosh S. Ferguson A. Incidence of juvenile-onset Crohn’s disease in Scotland.Lancet. 1999; 353: 1496-1497Abstract Full Text Full Text PDF PubMed Scopus (82) Google Scholar Briefly, all case notes were reviewed, and diagnoses of CD or UC were confirmed using the Lennard-Jones criteria. The postcode and age at time of onset of IBD symptoms were recorded. This database had been used previously to look at IBD incidence rates for Scotland19Armitage E. Drummond H.E. Wilson D.C. Ghosh S. Increasing incidence of both juvenile-onset Crohn’s disease and ulcerative colitis in Scotland.Eur J Gastroenterol Hepatol. 2001; 13: 1439-1447Crossref PubMed Scopus (141) Google Scholar in the 0–16 years of age population. This current study used only those children 0–15 years of age because population data concerning postcode areas and socioeconomic status were more readily available for this age group, and direct comparison of standardized incidence rates is possible with other studies using this age range. Ethical approval was obtained from The Paediatrics/Reproductive Medicine Research Ethics Subcommittee along with permission from medical directors of all hospitals prior to case-note review. All incident cases were classified by their postcode at symptom onset in 3 ways: (1) residence in northern or southern Scotland. The division between north and south being at the southern border of the DD and PH postcode areas with PA80-PA86 (Western Isles) also classified as north (see map, Figure 1). This division results in 2 northern and 2 southern urban centers. (2) area of residence using postcode areas. (3) socioeconomic status of the postcode sector (covering approximately 300 households) using the Carstairs score. The Carstairs score20Carstairs V. Morris R. Deprivation and Health in Scotland.Health Bull (Edinb). 1990; 48: 162-175PubMed Google Scholar is a classification of social/material deprivation, originally calculated for 1981 census data. It takes into account levels of male unemployment, car ownership, overcrowding (over 1 person per room), and head of household’s social class categories IV and V.20Carstairs V. Morris R. Deprivation and Health in Scotland.Health Bull (Edinb). 1990; 48: 162-175PubMed Google Scholar The Carstairs score is then ascribed a numeric value as a measure of deprivation for each Scottish postcode sector: 1 being most affluent and 7 being most deprived.20Carstairs V. Morris R. Deprivation and Health in Scotland.Health Bull (Edinb). 1990; 48: 162-175PubMed Google Scholar These deprivation scores (depcat scores) have been updated using 1991 census data: (http://census.ac.uk/cdu/). For children whose date of onset of symptoms occurred between 1981 and 1988, the deprivation scores from 1981 census data were used. For children whose date of onset of symptoms was between 1989 and 1995, postcodes were classed according to the 1991 deprivation scores. There was little change in depcat scores between the 2 census dates: Of 987 sectors, 560 (56.7%) did not change at all, 356 (36%) changed by only 1 category, and just 68 (7%) changed by more than 1 category. Of those areas with depcat scores that did change, 158 (16%) became “more affluent” and 266 (27%) became “more deprived.” The distribution of depcat scores in north and south Scotland did not change by more than 3% between the census dates, and the proportion of the total 0–15 years of age population falling into each depcat score remained constant. To calculate age-specific incidence rates, all children aged 0–15 years between 1981 and 1995 were considered to be at risk of either UC or CD. Annual population data by age, sex, and year were obtained from the General Register Office for Scotland. They were derived or projected from decennial Scottish census figures (1981, 1991) using annual data on births, deaths, and migration. Population data by age, sex, postcode area, and depcat score were obtained for 1981 and 1991 from Scottish census figures. All incidence rates were calculated per 100,000 population per year and were sex standardized to the 1991 Scottish population21Fay M.P. Feuer E.J. Confidence intervals for directly standardized rates a method based on the gamma distribution.Stat Med. 1997; 16: 791-801Crossref PubMed Scopus (340) Google Scholar with 95% confidence intervals (CI) calculated using a gamma approximation to the exact Poisson distribution of cases.21Fay M.P. Feuer E.J. Confidence intervals for directly standardized rates a method based on the gamma distribution.Stat Med. 1997; 16: 791-801Crossref PubMed Scopus (340) Google Scholar Temporal trends were assessed using 2 distinct time periods 1981–1988 and 1989–1995, relating to the census years of 1981 and 1991, respectively. A Poisson regression model was created adding the independent variables of sex, region, time, and depcat score in a stepwise fashion, and relative risks were calculated. P values for each variable were calculated by the usual analysis of deviance method, and all possible interactions between the independent variables were examined for possible significance. A total of 580 affected children aged 0–15 years (383 CD [224 males, 159 females], 197 UC [94 males, 103 females]) were identified. This resulted in age-specific sex-standardized incidences of 2.3 per 100,000 per year for CD (95% CI: 2.0–2.5), 3.4 for IBD (95% CI: 3.2–3.7), and 1.2 per 100,000 per year for UC (95% CI: 1.0–1.3) for Scotland. Postcode data were either missing or incomplete for 7 CD patients (6 males, 1 female), and these were omitted from the subsequent data analyses. The standardized age-specific (0–15 years of age) incidence rates for CD were significantly higher in northern Scotland (3.1 [95% CI: 2.6–3.8]) than in southern Scotland (2.1 [95% CI: 1.9–2.4]) (Table 1). This pattern held if the division for north and south was moved further south to the southern borders of PA, FK, and KY postcode areas (CD north, 2.7 [95% CI: 2.4–3.2], CD south, 2.1 [95% CI: 1.8–2.4]). This relationship was mirrored for IBD but not for UC (Table 1). As can be seen from the map (Figure 1), there was considerable geographic heterogeneity between postcode areas but with more of the areas of higher incidence of CD in the northern region of Scotland.Table 1Age Specific (<16 years), Sex Standardized Incidence of CD, UC, and IBD in Northern and Southern Scotland With 95% Confidence IntervalsDiseaseStandardized incidence 1981–1988 (95% CI)Standardized incidence 1989–1995 (95% CI)Standardized incidence 1981–1995 (95% CI)NorthSouthNorthSouthNorthSouthCD2.8 (2.1–3.6)1.8 (1.5–2.1)3.5 (2.6–4.5)2.5 (2.1–2.9)3.1 (2.6–3.8)2.1 (1.9–2.4)UC0.9 (0.5–1.4)0.9 (0.7–1.1)1.8 (1.2–2.6)1.6 (1.3–2.0)1.3 (1.0–1.8)1.2 (1.1–1.5)IBD3.7 (2.9–4.6)2.6 (2.3–3.0)5.2 (4.2–6.5)4.1 (3.6–4.7)4.4 (3.8–5.2)3.4 (3.0–3.7)NOTE. Data are per 100,000 persons per year. Open table in a new tab NOTE. Data are per 100,000 persons per year. These findings were confirmed by the multifactorial model, in which region (i.e., north) was an independent risk factor for developing IBD and CD but not UC. The relative risk of CD in the south compared with the north was 0.73 (95% CI: 0.58–0.92, P < 0.001) and for IBD, 0.82 (95% CI: 0.68–0.99, P = 0.003). UC did not show this north/south variation (P = 0.677) (Figure 2A, Table 2).Table 2Relative Risks Derived From the Poisson Model for Time Period, 1989–1995 Relative to 1981–1988; Region, South Relative to North; and Sex, Females Relative to MalesParameterCDUCIBDRelative risk95% CIRelative risk95% CIRelative risk95% CITime1.251.02–1.531.7881.35–2.381.411.20–1.66Region0.7330.58–0.921.0320.74–1.450.8200.68–0.99Sex0.7710.63–0.951.1530.87–1.520.8860.75–1.04 Open table in a new tab From the multifactorial analysis, calendar period had an independent influence on the incidence of IBD. The relative risk in the 1989–1995 time period compared with the 1981–1988 time period was 1.25 (95% CI: 1.02–1.53) for CD (P = 0.034), 1.41 (95% CI: 1.2–1.66) for IBD (P < 0.001), and 1.78 (95% CI: 1.35–2.38) for UC (P < 0.001), indicating a continued increase in incidence of IBD (Table 2, Figure 2A). This confirms our previous findings that incidence of juvenile onset IBD increased over this time period.19Armitage E. Drummond H.E. Wilson D.C. Ghosh S. Increasing incidence of both juvenile-onset Crohn’s disease and ulcerative colitis in Scotland.Eur J Gastroenterol Hepatol. 2001; 13: 1439-1447Crossref PubMed Scopus (141) Google Scholar From the multifactorial analysis, the relative risk (RR = 0.77) of developing CD was significantly less in females than males (P = 0.01). This confirms our finding of a male predominance of J-O CD in Scotland.19Armitage E. Drummond H.E. Wilson D.C. Ghosh S. Increasing incidence of both juvenile-onset Crohn’s disease and ulcerative colitis in Scotland.Eur J Gastroenterol Hepatol. 2001; 13: 1439-1447Crossref PubMed Scopus (141) Google Scholar The relative risk of developing the disease in deprivation scores 2–7, compared with the most affluent areas (deprivation score 1), significantly decreased with increasing deprivation for both IBD (P = 0.016) and CD (P = 0.033). (Table 3, Figure 2B). This suggests an inverse association with deprivation for CD and IBD. This pattern was not seen for UC (P = 0.17).Table 3Incidence Case Numbers and Relative Risks Derived From the Poisson Model for Postcode Areas, With Deprivation scores 2–7 Compared With Those With Depcat 1 for CD, UC, and IBDDepcat scoreCDUCIBDn Case No.Relative Risk to Depcat 195% CIn Case No.Relative Risk to Depcat 195% CIn Case No.Relative Risk to Depcat 195% CI13811114912560.8660.57–1.31382.0931.07–4.10941.1400.81–1.613890.8670.59–1.27451.5470.80–2.991341.0200.74–1.424950.8080.55–1.18471.3640.71–2.631420.9330.67–1.295530.8000.53–1.22241.1810.58–2.41770.8840.62–1.276250.4620.28–0.77181.0910.51–2.31430.6060.40–0.917200.5760.33–0.99141.2800.58–2.83340.7380.48–1.15Depcat, deprivation score. Open table in a new tab Depcat, deprivation score. This study shows a definite north-south difference in the incidence of J-O CD (0–15 years of age) in Scotland, which was maintained throughout the period 1981–1995. In addition, these results confirm increasing incidence of J-O IBD (UC and CD) in the 0–15 years age range over the same time period.5Sawczenko A. Sandhu B.K. Logan R.F. Jenkins H. Taylor C.J. Mian S. Lynn R. Prospective survey of childhood inflammatory bowel disease in the British Isles.Lancet. 2001; 357: 1093-1094Abstract Full Text Full Text PDF PubMed Scopus (315) Google Scholar To explain these patterns, we hypothesise that simultaneous etiologic factors may exist, one which is constant with time but exhibits a north-south variation (e.g., genetic susceptibility, which is generally constant in homogeneous populations but may change slowly over time) and a second, which has an equal influence throughout Scotland but is increasing over time (e.g., a more rapidly changing environmental factor). The north-south gradient in IBD incidence was first described in Europe, but it was based on observations from individual studies.22Kyle J. Crohn’s disease in the northeastern and northern Isles of Scotland an epidemiological review.Gastroenterology. 1992; 103: 392-399PubMed Google Scholar, 23Ruiz O.V. Epidemiologic study of Crohn’s disease in Galicia from 1976 to 1983.Rev Esp Enferm Apar Dig. 1984; 66: 273-279PubMed Google Scholar, 24Sinclair T.S. Brunt P.W. Mowat N.A. Nonspecific proctocolitis in northeastern Scotland a community study.Gastroenterology. 1983; 85: 1-11Abstract Full Text PDF PubMed Scopus (177) Google Scholar, 25Lanfranchi G.A. Michelini M. Brignola C. Campieri M. Cortini C. Marzio L. Epidemiological study on intestinal inflammatory diseases in the Province of Bologna.G Clin Med. 1976; 57: 235-245PubMed Google Scholar The conclusions reached by the comparison of these studies are hampered by variations in study design. The European collaborative study on IBD incidence was set up to overcome these methodologic problems and concluded that the “magnitude of the observed excess in north is less than expected on the basis of previous studies …—this may reflect increases in incidence of IBD in Southern Europe whilst north may have stabilised.”12Shivananda S. Lennard-Jones J. Logan R. Fear N. Price A. Carpenter L. van Blankenstein M. Incidence of inflammatory bowel disease across Europe: is there a difference between north and south? Results of the European Collaborative Study on Inflammatory Bowel Disease (EC-IBD).Gut. 1996; 39: 690-697Crossref PubMed Scopus (845) Google Scholar In contrast to this conclusion, we have shown that the rise in incidence of J-O CD is independent of region (north or south) and that the north-south variation is constant throughout this rise. In North America, significant geographic variation also appears to exist. In the United States, a hospital-based study of Medicare beneficiaries (>65 years of age) found that there was a higher prevalence of IBD in the north compared with the south and in urban than in rural areas.13Sonnenberg A. McCarty D.J. Jacobsen S.J. Geographic variation of inflammatory bowel disease within the United States.Gastroenterology. 1991; 100: 143-149Abstract PubMed Google Scholar The cohort of patients in our study was also examined for associations with urban or rural living, but, because of a small number of incident cases within the rural group, the analysis was inconclusive. Although Scotland has a relatively small population and geographic area, this has actually been a great advantage and has resulted in a comprehensive study of the entire Scottish population. Both the previous European and the North American studies were based in vast geographic areas, and neither was population based. The European study applied standardized study criteria and looked at several distinct areas, usually only involving 1 urban center,12Shivananda S. Lennard-Jones J. Logan R. Fear N. Price A. Carpenter L. van Blankenstein M. Incidence of inflammatory bowel disease across Europe: is there a difference between north and south? Results of the European Collaborative Study on Inflammatory Bowel Disease (EC-IBD).Gut. 1996; 39: 690-697Crossref PubMed Scopus (845) Google Scholar and the United States study included only hospital admissions for patients aged 65 years and over.13Sonnenberg A. McCarty D.J. Jacobsen S.J. Geographic variation of inflammatory bowel disease within the United States.Gastroenterology. 1991; 100: 143-149Abstract PubMed Google Scholar A potential criticism of the hospital-based case identification method used in this study has been that ascertainment may be incomplete, if patients with CD or those with mild ulcerative proctitis have never required admission. However in the Scottish pediatric population, during the time period of this study, there was an almost universal admission policy for investigation of IBD. In our previous experience,19Armitage E. Drummond H.E. Wilson D.C. Ghosh S. Increasing incidence of both juvenile-onset Crohn’s disease and ulcerative colitis in Scotland.Eur J Gastroenterol Hepatol. 2001; 13: 1439-1447Crossref PubMed Scopus (141) Google Scholar less than 2% of children with J-O IBD were managed exclusively as outpatients. Other diseases have been shown to exhibit geographic variations in incidence. For multiple sclerosis, prevalence increased with latitude, both north and south of the equator, and it has been suggested that it may be highest in those countries with a high proportion of people of Scottish or Scandinavian ancestry, the latitudinal gradient partly reflecting differences in genetic susceptibility.26Compston D.A.S. Ebers G.C. The genetics of MS.in: Cook S.D. Handbook of neurology. Decker, New York1990: 25-39Google Scholar Thus, the north-south incidence pattern for J-O CD may also reflect differential genetic contributions from ancestral genes from founder populations settled within Scotland. Immigration rates to Scotland have been relatively low in more recent times, but, between the 8th and 11th centuries, Norse peoples from Scandinavia (“Vikings”) raided and then settled in Shetland and Orkney, then along the Scottish coastline and Western Isles,27Davis N. The isles. Macmillan, London1999Google Scholar leading to a north-south axis of Nordic ancestry throughout Scotland. Indeed, admixture analyses looking at mitochondrial DNA lineages from Scandinavia showed ancestral contributions of 35.5% for Orkney, 13.5% for the NW Scottish coast, 11.5% for the Western Isles, and 12.5% for Skye, indicating a greater “Viking” influence further north.28Helgason A. Hickey E. Goodacre S. Bosnes V. Stefansson K. Ward R. Sykes B. mtDNA and the islands of the North Atlantic estimating the proportions of Norse and Gaelic ancestry.Am J Hum Genet. 2001; 68: 723-737Abstract Full Text Full Text PDF PubMed Scopus (170) Google Scholar The postcode areas of higher CD incidence followed this pattern of Nordic ancestry, although we did not look for any direct evidence of association. In addition to the north-south regional difference, we have demonstrated a higher incidence of CD in the more affluent areas of Scotland, as defined by postcode sector. This pattern was independent of temporal, sex, or regional trends and was therefore not purely a reflection of the geographic distribution of deprivation. The relationship to affluence was seen in CD, but not in UC; thus, it is unlikely that the association was simply because of a higher reporting of symptoms to primary care in affluent areas. The Carstairs deprivation scores used in this study were first used to look at social deprivation and ischemic heart disease in Britain.29Carstairs V. Morris R. Deprivation explaining differences in mortality between Scotland and England and Wales.Br Med J. 1989; 299: 886-889Crossref PubMed Scopus (401) Google Scholar They are a proxy guide for the material deprivation of the population for each postcode sector (which covers approximately 300 households). They are not an actual measure of the parental socioeconomic status; such case-specific data were not collected in this study. The deprivation score of the area of residence at symptom onset reflects the general affluence and socioeconomic status of the population living in the area.20Carstairs V. Morris R. Deprivation and Health in Scotland.Health Bull (Edinb). 1990; 48: 162-175PubMed Google Scholar Previous studies have shown increased incidence of CD in higher income families.16Blanchard J.F. Bernstein C.N. Wajda A. Rawsthorne P. Small-area variations and sociodemographic correlates for the incidence of Crohn’s disease and ulcerative colitis.Am J Epidemiol. 2001; 154: 328-335Crossref PubMed Scopus (129) Google Scholar Gent et al.10Gent A.E. Hellier M.D. Grace R.H. Swarbrick E.T. Coggon D. Inflammatory bowel disease and domestic hygiene in infancy.Lancet. 1994; 343: 766-767Abstract PubMed Scopus (312) Google Scholar reported an increased risk of CD in subjects who, as infants, lived in greater degrees of domestic hygiene. It has been suggested that higher incidence rates among those of higher socioeconomic status may be due to a delayed and/or low level of exposure to common infectious agents during childhood because of improved domestic hygiene, resulting in persistent infection or altered immune responses in genetically susceptible hosts.30Montgomery S.M. Pounder R.E. Wakefield A.J. Infant mortality and the incidence of inflammatory bowel disease.Lancet. 1997; 349: 472-473Abstract Full Text Full Text PDF PubMed Scopus (46) Google Scholar This has been termed the hygiene hypothesis. The extent of poverty has traditionally been higher in Scotland than other regions of the United Kingdom but is now broadly similar.31Heaney D.C. MacDonald B.K. Everitt A. Stevenson S. Leonardi G.S. Wilkinson P. Sander J.W. Socioeconomic variation in incidence of epilepsy prospective community based study in southeast England.Br Med J. 2002; : 1013-1016Crossref PubMed Scopus (153) Google Scholar Therefore, a rapid rise in living standards including domestic hygiene, as poverty rates fall, has occurred in Scotland. Similarly, there are direct parallels with the relationship between domestic hygiene and the development of IDDM.32Evans J.M. Newton R.W. Ruta D.A. MacDonald T.M. Morris A.D. Socio-economic status, obesity and prevalence of type 1 and type 2 diabetes mellitus.Diabet Med. 2000; 17: 478-480Crossref PubMed Scopus (259) Google Scholar Recent data have highlighted the role of intestinal flora in perpetuating intestinal inflammation: The identification of the NOD2/CARD15 gene underscores the importance of the host-bacterial interaction. Geographic differences in the NOD2/CARD15 contribution to CD within Europe are now clearly emerging.33Helio T. Halme L. Lappalainen M. Fodstad H. Paavola-Sakki P. Turunen U. Farkkila M. Krusius K. CARD 15/NOD2 gene variants are associated with familially occuring and complicated forms of Crohn’s disease.Gut. 2003; 52: 558-562Crossref PubMed Scopus (229) Google Scholar, 34Arnott I.D. Nimmo E.R. Drummond H.E. Fennell J. Smith B.R. MacKinlay E. Morecroft J. Anderson N. Kelleher D. O’Sullivan M. McManus R. Satsangi J. NOD2/CARD15, TLR4 and CD14 mutations in Scottish and Irish Crohn’s disease patients evidence for genetic heterogeneity within Europe?.Genes Immun. 2004; 5: 417-425Crossref PubMed Scopus (187) Google Scholar Recently Hugot’s intriguing “cold chain” hypothesis also provides a link with hygiene by implicating psychrotrophic bacteria, whose presence is maintained in refrigerated foodstuff.11Hugot J.P. Alberti C. Berrebi D. Bingen E. Cezard J.P. Crohn’s disease the cold chain hypothesis.Lancet. 2003; 362: 2012-2015Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar Our finding of an association with affluence may add weight to the hygiene hypothesis for J-O CD. We could postulate that other environmental factors, e.g., passive smoking or diet, may contribute to this inverse relationship with deprivation. The present data are notable for a well-defined dissociation between CD and UC pattern of incidence distribution. The north-south variation is not significant for UC, and there is no association with deprivation score. This is the first time that such a marked dissociation has been noted and is contrary to that seen in the study of geographic variation in the United States13Sonnenberg A. McCarty D.J. Jacobsen S.J. Geographic variation of inflammatory bowel disease within the United States.Gastroenterology. 1991; 100: 143-149Abstract PubMed Google Scholar in which patterns for UC and CD were found to be similar but subjects were 65 years of age or older. Our findings may simply be due to the smaller incident case number for UC (197 compared with 383 for CD) or may be real for this pediatric subgroup of the IBD population. These findings may have implications as to the etiologic relationship between CD and UC with regard to distinct genetic or environmental factors. In summary, we have shown that the incidence of J-O CD is high in Scotland, that there has been a constant north-south difference in incidence between 1981 and 1995, and that incidence rates are highest in more affluent areas of the country. The influence of genetic or environmental factors on these patterns of incidence now requires detailed investigation. The authors thank Robin Rice (Edinburgh University Data Librarian), who updated discrepant postcodes to relate them to those previously used for the Deprivation Scores and from whom we obtained the computer files for Carstairs scores for both sets of census data." @default.
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