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This is the published version of a paper published in Journal of Crohn's & Colitis.
Citation for the original published paper (version of record):
Zhulina, Y., Udumyan, R., Henriksson, I., Tysk, C., Montgomery, S. et al. (2014)
Temporal trends in non-stricturing and non-penetrating behaviour at diagnosis of Crohn's disease
in Örebro, Sweden: a population-based retrospective study.
Journal of Crohn's & Colitis, 8(12): 1653-1660
http://dx.doi.org/10.1016/j.crohns.2014.07.006
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Temporal trends in non-stricturing and
non-penetrating behaviour at diagnosis of
Crohn's
disease
in
Örebro,
Sweden:
A
population-based retrospective study
Yaroslava Zhulina
a,b, Ruzan Udumyan
c, Ida Henriksson
a, Curt Tysk
a,b,
Scott Montgomery
c, Jonas Halfvarson
a,b,⁎
aDepartment of Internal Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden b
School of Health and Medical Sciences, Örebro University, Örebro, Sweden
cClinical Epidemiology and Biostatistics Unit, Örebro University Hospital, Örebro, Sweden
Received 22 May 2014; received in revised form 1 July 2014; accepted 19 July 2014 KEYWORDS Crohn's disease; Epidemiology; Incidence; Prevalence; Phenotype Abstract
Background and aim: The incidence of Crohn's disease (CD) is continuing to rise in several countries and in others it appears to have already levelled off after a period of increase. We updated our previous population-based study, by re-extraction of all information on patients diagnosed with CD between 1963 and 2010. Our aim was to assess temporal trends in incidence, prevalence and disease phenotype at diagnosis.
Methods: Patients of all ages with a potential diagnosis of CD were identified retrospectively by evaluation of medical notes of all current and previous patients at the colitis clinic, Örebro University Hospital amended by computerised search in the inpatient, outpatient, primary care and histopathological records. Diagnosis was confirmed by subsequent evaluation of medical notes. Disease phenotype was defined according to the Montreal classification.
Results: The incidence increased over time, especially among Crohn's disease, A1 and A3.
SaTScan model revealed a statistically significant high incidence during 1991–2010 (p = 0.0001).
The median age at diagnosis increased from 28 (3–79) years to 37 (5–87) years (p = 0.0002). The
point prevalence increased from 21/105 (14–32) in 1965 to 267/105 (244–291) in 2010.
Non-stricturing and non-penetrating disease at diagnosis increased from 12.5% in 1963–1965 to
82.3% in 2006–2010 (p b 0.0001).
⁎ Corresponding author at: Department of Internal Medicine, Division of Gastroenterology, Örebro University Hospital, SE-70185 Örebro, Sweden. Tel.: + 46 19 6022361; fax: + 46 19 6021774.
E-mail addresses:Yaroslava.Zhulina@orebroll.se(Y. Zhulina),Ruzan.Udumyan@orebroll.se(R. Udumyan),Ida.Henriksson@orebroll.se
(I. Henriksson),Curt.Tysk@orebroll.se(C. Tysk),Scott.Montgomery@orebroll.se(S. Montgomery),Jonas.Halfvarsson@orebroll.se
(J. Halfvarson).
http://dx.doi.org/10.1016/j.crohns.2014.07.006
1873-9946/© 2014 European Crohn's and Colitis Organisation. Published by Elsevier B.V. All rights reserved. A v a i l a b l e o n l i n e a t w w w . s c i e n c e d i r e c t . c o m
ScienceDirect
Conclusion: The incidence of CD increased over time, although it seemed to be plateauing during the most recent decades. A striking increase in non-stricturing, non-penetrating disease at diagnosis was observed, suggesting earlier diagnosis or phenotypic change. The observed point prevalence in 2010 is among the highest reported.
© 2014 European Crohn's and Colitis Organisation. Published by Elsevier B.V. All rights reserved.
1. Introduction
An increasing incidence of Crohn's disease has been reported since the mid-1900s, especially in Northern Europe and North America.1 A recent meta-analysis points towards
continuous increase in the incidence of Crohn's disease even beyond 1980 in the majority of studies throughout the world.2However, a plateau or even declining incidence has
been observed in some of the high-incidence cohorts.3–5
These observations suggest that the incidence may soon level off in some of the areas with early rising incidence rates.
Although clinically Crohn's disease is regarded as one diagnosis, the diagnostic entity comprises a broad clinical spectrum. Progression to complicated disease behaviour, i.e. stricturing and penetrating disease, has been reported in a high proportion of patients with non-stricturing, non-penetrating disease,6and is associated with an increased need for surgical
interventions and poor quality of life. Modern therapy algorithms aim to rapidly achieve and maintain clinical and endoscopic remission and in theory, this strategy can reduce progression to complicated disease behaviour and need of surgery. Diagnostic delay has also been associated with increased risk for progression to stricturing disease and surgery.7 However, longitudinal data regarding diagnostic
delay in the diagnosis of Crohn's disease are sparse.7
Retro-spective assessment of diagnostic delay is difficult, since self-reported data on onset of symptoms might be influenced by recall bias. Yet, non-stricturing, non-penetrating disease represents a plausible marker of early disease, since it most often represent a temporary disease status.6However, if there
has been a temporal trend in the proportion with non-stricturing, non-penetrating disease at diagnosis remains unknown.
In a previous study from our catchment area, Lindberg et al. reported incidence and prevalence rates over the period 1963–1987. We re-extracted all information on patients diagnosed with Crohn's disease between 1963 and 1987,8and
extracted data on patients diagnosed with Crohn's disease from 1st of January 1988 up to 31st of December 2010. Our aim was to study temporal trends over the almost five decades long observation period. More specifically, we wanted to assess trends in incidence, prevalence and disease phenotype at diagnosis.
2. Material and methods
2.1. Study area and population
The primary catchment area of Örebro University Hospital covers 3998 km2 and includes five municipalities. The
population lives in a mix of urban and rural settings. The number of inhabitants increased from 164 972 in 1987 to 189 603 in 2010, with an average of 51.1% of the population being women. In addition to Örebro University hospital there are 17 primary health care clinics, some private general practitioners but no private gastroenterologists within the area. Since the late 1970s cases with inflammatory bowel disease (IBD), suspected or verified, have been referred to the hospital. All colonoscopy procedures within the catch-ment area were performed at the Endoscopy unit, Örebro University Hospital and all histopathological examinations were performed by the Department of Pathology of the same hospital. Information about the age and sex distributions of the general population in the catchment area was obtained from Statistics Sweden.9
The Uppsala Regional Ethics Committee approved the study (2010/304).
2.2. Patient population
Patients of all ages with a potential diagnosis of Crohn's disease were identified retrospectively by evaluation of medical notes of all present and previous patients at the Colitis Clinic, Department of internal medicine, Örebro University Hospital. In addition the ICD10 codes: K500-K509; Crohn's disease, K528-K529; colitis UNS, M074-M076, IBD associated arthropa-thy, M091-M092, IBD associated juvenile arthritis and the ICD9 codes: 555; regional enteritis, 556; ulcerative colitis, and 558, other and unspecified non-infectious gastroenteritis and colitis were searched for in the county council's computerised inpatient, outpatient and primary care records, covering diagnoses since 2000, and Örebro University Hospital's old local computerised records, covering inpatients and outpa-tients between 1988 and 2000. The old local computerised records were linked with the histopathological records at the Department of Pathology, Örebro University Hospital (search terms; Crohn's disease, inflammation, fistula or ulcer in gastric, small bowel, large bowel or rectal mucosa).
2.3. Diagnostic criteria and measures
The medical notes of all patients with potential Crohn's disease were reviewed by YZ to verify the diagnosis. Patients were included if they lived within the catchment area at any time during their disease course, were diagnosed between 1963 and 2010 and fulfilled the Lennard–Jones criteria for Crohn's disease.10Records for patients where
diagnosis was uncertain were jointly reviewed by YZ, CT and JH.
Date of the diagnosis was defined as the date of the first examination consistent with Crohn's disease. In patients where the diagnosis had been changed from ulcerative
colitis or IBD-unclassified to Crohn's disease the date of the first IBD diagnosis was used. In any patient where precise date of diagnosis could not be obtained retrospectively, the date was approximated to the 15th of the month where possible, otherwise to the 30th of June of the year of diagnosis. Location and behaviour of the disease were defined in all patients according to the Montreal classification.11 Thus, data for
patients diagnosed during the previously reported period, 1963–1987,8were re-extracted for information on diagnosis
and disease phenotype. We have previously reported patients diagnosed with IBD during 2010 as a part of the European Crohn's and Colitis Organisation's (ECCO) Epidemiological Committee (EpiCom) inception cohort. Patients with Crohn's disease within this cohort were included among patients diagnosed 1988–2010 in the present study.
2.4. Statistical analysis
Age at diagnosis is presented as median and range. Incidence rates were calculated as crude (all ages) and age standardised aggregated over 5-year periods by the direct method to allow for a changing population age structure over time. The age and sex characteristics of the Örebro population for each year of the study period were used for standardisation, while the Örebro population for 1999 was used as the standard comparison population. The 95% confidence intervals (CI) of the incidence rates were computed assuming a Poisson distribution. Time-trends in incidence were assessed using Poisson regression models. Possible temporal clusters in incidence rates were prospectively analysed based on discreet Poisson model analysis with a time aggregation length of five years, adjusted for age and sex, using SaTScan v 9.3 for Windows (http://www.satscan.org). The chi-squared test was used to compare sex distributions as well as distribution of disease phenotypes within patient population in 5-year periods. Point prevalence was calculated for the end of each 5-year period. Stata version 12 SE for Windows (Stata Corporation, College Station, TX) was used for these analyses.
3. Results
One thousand and twenty-six potential cases of Crohn's disease were identified by assessment of all current and previous patients at the Colitis clinic, department of internal medicine, Örebro University Hospital and by computerised search within the inpatient, outpatient and primary care records as well as histopathological records. In total, 786 of the 1026 potential cases fulfilled the diagnostic criteria, and of these 535 were diagnosed between 1963 and 2010 as incident cases, i.e. living within the catchment area of Örebro University Hospital at the time of Crohn's disease diagnosis. The remaining 240 cases were excluded due to diagnoses other than Crohn's disease (ulcerative colitis; n = 15, inflammatory bowel disease unclassified; n = 31, microscopic colitis; n = 1, non-IBD diagnoses; n = 193).
Of the 535 incident cases, 285 were female, yielding a female to male ratio of 1.1:1. The difference in sex distribution (adjusted for age) was not statistically significant (p = 0.7).
3.1. Incidence rates by 5-year periods over 1963–2010
Crude and age standardised incidence rates (IR) in 5 year study periods for the entire study period are shown in
Table 1. Incidence rate ratios (IRR) increased with time,
when comparing IR over the 5 year intervals (Supplement Table 2). Trend analysis, using Poisson regression models, revealed statistically significant linear and quadratic trends with increasing incidence rate estimates over time, although the estimates successively levelled off. A SaTScan model revealed a statistically significant high incidence during 1991–2010 (p = 0.0001).
The sex distribution over the 5-year intervals did not vary within the patient population. However the age distribution varied significantly (pb 0.0001) and median age at diagnosis increased with time. Especially the incidence of Crohn's disease, A1 and A3 appears to increase over time (Fig. 1).
3.2. Disease phenotypes at diagnosis
Information regarding disease location and behaviour at diagnosis was available in 534 (99.8%) and 532 (99.4%) patients, respectively. Disease characteristics at diagnosis according to the Montreal classification for patients diagnosed within each 5-year period are presented in Supplement Table 1. Age distribution varied significantly over time (Chi2 = 64.6, DF = 18, pb 0.0001). An increasing proportion of A3, i.e. patients diagnosedN40 years of age, was observed between 1963 and 2010 (Fig. 2, panel a). The proportion of patients in the A3 category increased from 0% in 1963–1965 to 32.3% in 2006–2010. Disease location at diagnosis in 5-year intervals appears rather stable during the 47-year period (p = 0.086), especially during the later decades (Fig. 2, panel b). Sex was not associated with disease location (data not shown). The proportion of patients with non-stricturing, non-penetrating disease (B1) at diagnosis increased from 12.5% in 1963–1965 to 82.3% in 2006–2010 (Fig. 2, panel c). That is a statistically significant increase by 69.8% (95% CI for the difference is 44.9% to 94.6%, pb 0.0001).
3.3. Point prevalence by 5-year periods
The point prevalence of Crohn's disease gradually increased in the Örebro catchment area from 21/105(95% CI, 14–32) on the 31st of December 1965 to 267/105(244–291) on the 31st of December 2010. On 31 December 2010, 506 patients with Crohn's disease lived in the area, and corresponding point prevalence figures for men and women were 236/105 (206–269) and 297/105 (263–333), respectively. Age standardised incidence rates in 5-year study periods and point prevalence at the end of each 5-year study period are shown inFig. 3.
4. Discussion
This population based study revealed possible plateauing in the incidence of Crohn's disease during the last decades following an initial increase. We also observed an increased proportion of patients diagnosed with non-stricturing and
non-penetrating disease (B1) over time, suggesting that patients with Crohn's disease receive a diagnosis earlier in their disease course, or phenotypic change over time. Our data are strengthened by thorough case ascertainment, where cases with potential Crohn's disease were identified retrospectively by assessment of all patients at the Colitis clinic amended by computerised searches of the inpatient, outpatient and primary care records as well as the histopathological records. The medical notes of all patients with potential Crohn's disease, including all re-extracted cases during the previously reported period, 1963–1987,8
were then reviewed to confirm or refute the diagnosis of Crohn's disease and to classify the phenotype of the disease. A long-term history of referral of all patients with possible IBD to secondary care, absence of private gastroenterolo-gists, centralized endoscopic and histopathological assess-ment within the catchassess-ment area further suggests almost complete inclusion. These factors make our catchment area relatively well suited for this epidemiological study. We observed a pronounced rise in incidence rates and subse-quent levelling off, as demonstrated by trend analysis. Application of a SaTScan model confirmed the existence of a temporal increase in incidence during 1991–2010. The observed rise in incidence could not be explained by an increased number of smokers. Conversely, the proportion of smokers seemed to decrease over time. Whether a temporal trend in smoking habits influenced the observed plateauing in incidence rate, can only be speculated on.
Probably the increased rates can to some extent be explained by improved diagnostic methods. Colonoscopy, magnetic resonance imaging, computer tomography, bowel ultrasound and capsule enteroscopy have been introduced and replaced barium X-ray of large and small bowel. This could influence assessment of location (not seen in our study) but is unlikely to explain the observed change in disease behaviour. The proportion of individuals aged 40 years and above in the general population increased numerically from 47.7% in 1963 to 49.4% in 2010. We, therefore, age-standardised the incidence rates and rate ratios to account for the shift in age composition during the study period. Our incidence seems to be slightly lower than the reported figures in the Uppsala region of Sweden. Sjöberg et al. observed a mean annual incidence of 9.9/105 during 2005–2009,12 which is higher than those previously
reported.13However, our findings are consistent with some
recent reports from high incidence areas.14 Chouraki et al.
reported a plateau in the incidence rate of Crohn's disease in Northern France from 1988 to 2007,15,16and even declining
incidence of Crohn's disease has been reported from a Canadian high-incidence area.3Although Crohn's disease has
been the subject of numerous epidemiological studies, there are very few population-based studies with long-term data on incidence, prevalence and phenotype characteristics over time.17,18 The observed point prevalence of 267 per
105 in 2010 is substantially higher than that of previously observed in 1987 and is among the highest reported.1,19
Similar to the incidence plateau, prevalence possibly may level off during the latter part of the study period, although a longer observation period is required to assess these temporal trends in incidence and prevalence with certainty. Early identification and diagnosis of Crohn's disease are of great importance, since diagnostic delay is associated with
Table 1 Crude and age-standardised incidence rate of Crohn's disease per 100,000 inhabitants (with 95% CI) aggregated over 5-year periods by direct method. a Period Males and females Males Females Median age (years) b No. of incident CD cases Crude IR (95% CI) Age-standardised IR (95% CI) a No. of incident CD cases Crude IR (95% CI) Age-standardised IR (95% CI) a No. of i ncident CD cases Crude IR (95% CI) Age-standardised IR (95% CI) a 1963 – 1965 20.5 8 2.3 (0.1 – 4.5) 2.1 (0.6 – 3.6) 4 2.4 (0.1 – 6.0) 2.2 (0.0 – 4.4) 4 2.2 (0.6 – 5.6) 2.0 (0.0 – 4.1) 1966 – 1970 23 36 5.0 (3.5 – 7.0) 4.6 (3.1 – 6.1) 16 4.6 (2.6 – 7.4) 4.1 (2.1 – 6.1) 20 5.5 (3.3 – 8.4) 5.1 (2.8 – 7.3) 1971 – 1975 27 35 4.3 (3.0 – 6.0) 4.3 (2.9 – 5.8) 18 4.5 (2.7 – 7.2) 4.6 (2.5 – 6.8) 17 4.1 (2.4 – 6.6) 4.1 (2.1 – 6.1) 1976 – 1980 26 57 7.0 (5.3 – 9.0) 6.9 (5.1 – 8.7) 26 6.5 (4.3 – 9,6) 6.4 (3.9 – 8.9) 31 7.4 (5.0 – 10.5) 7.4 (4.8 – 10.0) 1981 – 1985 32 62 7.6 (5.8 – 9.7) 7.6 (5.7 – 9.5) 28 7.0 (4.7 – 10.1) 7.1 (4.4 – 9.9) 34 8.1 (5.6 – 11.3) 8.0 (5.3 – 10.8) 1986 – 1990 40.5 56 6.7 (5.1 – 8.8) 6.7 (4.9 – 8.5) 29 7.2 (4.8 – 10.3) 7.0 (4.4 – 9.7) 27 6.3 (4.2 – 9.2) 6.4 (4.0 – 8.9) 1991 – 1995 33 67 7.8 (6.0 – 9.9) 7.7 (5.8 – 9.6) 29 6.9 (4.6 – 9.9) 6.9 (4.4 – 9.4) 38 8.6 (6.1 – 11.8) 8.5 (5.8 – 11.2) 1996 – 2000 41.5 62 7.0 (5.4 – 9.0) 7.1 (5.3 – 8.8) 31 7.2 (4.9 – 10.2) 7.2 (4.7 – 9.8) 31 6.9 (4.7 – 9.8) 6.9 (4.5 – 9.3) 2001 – 2005 41.5 90 10.0 (8.1 – 12.3) 9.9 (7.8 – 11.9) 41 9.3 (6.7 – 12.6) 9.2 (6.3 – 12.0) 49 10.7 (7.9 – 14.2) 10.5 (7.6 – 13.5) 2006 – 2010 27 62 6.7 (5.1 – 8.5) 6.7 (5.0 – 8.3) 27 5.9 (3.9 – 8.6) 6.0 (3.7 – 8.3) 35 7.4 (5.2 – 10.3) 7.3 (4.8 – 9.7) IR; incidence rate, No; number, 95% CI; 95% confidence interval, CD; Crohn's disease. a Örebro population in 1999 was used as standard population. b Median age at diagnosis of persons with Crohn's disease. 4 Y. Zhulina et al.
progression to stricturing disease and increased need of surgery.7In addition, the possibility to achieve endoscopic
remission, and thereby improved long-term prognosis, seems to be greater in patients with shorter disease duration.20,21
However, information on date of onset of symptoms was incomplete, due to the retrospective design. The incom-plete information was particularly pronounced in patients diagnosed in the earlier years of the study. This problem is illustrated by the limited amount of contemporaneous information on awareness of Crohn's disease, including
patient's and doctor's delay, in the literature.22–25
Non-stricturing, non-penetrating disease represents a plausible marker of early disease, although it may also present variation in disease phenotype. Interestingly, we observed a striking increase in non-stricturing, non-penetrating disease during the years 1963–2010. More than 80% of the patients had non-stricturing, non-penetrating disease at diagnosis during the last years of the observation period. This figure is consistent with a recently reported data from the Uppsala region of Sweden, as well as from the
0
5
10
15
Incidence/100000 person years
1963−1965 1966−1970 1971−1975 1976−1980 1981−1985 1986−1990 1991−1995 1996−2000 2001−2005 2006−2010
Period
A1 A2 A3
Age−specific incidence rate of Crohn´s disease per 100,000 inhabitants in Örebro county
Figure 1 Age-specific incidence rate of Crohn's disease, A1, A2 and A3, per 100,000 inhabitants, 1963–2010. A1; below ≤16 years old,
A2; between 17 and 40 years old, A3; above≥40 years old.
0 20 40 60 80 Percentage 1963−1965 1966−1970 1971−1975 1976−1980 1981−1985 1986−1990 1991−1995 1996−2000 2001−2005 2006−2010 Period A1 A2 A3 Age 0 20 40 60 80 Percentage 1963−1965 1966−1970 1971−1975 1976−1980 1981−1985 1986−1990 1991−1995 1996−2000 2001−2005 2006−2010 Period L1 L2 L3 L4 Location 0 20 40 60 80 Percentage 1963−1965 1966−1970 1971−1975 1976−1980 1981−1985 1986−1990 1991−1995 1996−2000 2001−2005 2006−2010 Period B1 B2 B3 Behaviour
Figure 2 Disease phenotype at diagnosis 1963–2010. A1; below ≤16 years old, A2; between 17 and 40 years old, A3; above ≥40 years
old, L1; ileal, L2; colonic, L3; ileocolonic, L4; isolated upper gastrointestinal, B1; non-stricturing non-penetrating, B2; stricturing, B3; penetrating.
ECCO-EpiCom European inception cohort.12,26This temporal
trend suggests that patients are diagnosed earlier in their disease course today than in the past and it can be hypothesized that this could have improved treatment outcomes in the recent years. This is supported by the observed decreasing diagnostic delay in Denmark, a country with a health care system similar to Sweden.27,28In contrast
to some previous studies we did not observe an increase in the proportion of colonic disease at diagnosis over time.29,30
However, the literature is inconsistent and a stable phenotypic profile over time in terms of disease location at diagnosis has been reported.16 In addition, disease
behav-iour has not been included in several of the previous studies and it can be questioned if reported temporal trends in disease location at diagnosis reflect a shift in disease behaviour rather than a true change in disease location at diagnosis.
Another strength of our study is the inclusion of all patients with Crohn's disease, irrespective of age at diagnosis. We observed an increasing incidence and proportion of patients diagnosed at age≥40 years during the study period. These findings are supported by a recent data in other cohorts31–33
Similarly, the incidence of Crohn's disease, A1 (paediatric Crohn's disease) rose over time, although the proportion of patients diagnosed at an age≤16 years did not increase. The observed rise in incidence of paediatric Crohn's disease is supported by several recent reports on paediatric Crohn's disease,34,35 including data from Sweden,29,36 although the
literature is inconsistent.31,37
The retrospective design is a potential limitation of the study. To limit the influence of possible information bias, assessment of all case notes at the Colitis clinic, Örebro University Hospital was amended by identification through computerised system. The histopathological records were included in this computerised search, as there was no single source of electronic records that covered the entire study
period. Yet, the retrospective design might have introduced selection bias, since the computerised systems covered patients from 1988 only and early indolent cases with a single episode of inflammation might more easily have been overlooked. Furthermore, the improved diagnostic methods might have introduced a time dependent bias in terms of disease phenotype at diagnosis. Primarily this would influence assessment of location (temporal trends were not seen in our study) but less likely to influence assessment of non-stricturing, non-penetrating behaviour, which we observed to vary over time. The absence of information about immigrants is another potential limitation of the study. It is difficult to predict how migration would influence the results since an increased incidence of IBD has not been observed in first generation immigrants but there may be an increase among second-generation immigrants.38,39It seems
unlikely that immigrants without a previous diagnosis would have increased the proportion of Crohn's disease, B1 over time. Conversely, a diagnostic delay would have increased the proportion of Crohn's disease, B2 and B3, and could theoretically influence the age at diagnosis and contribute to the observed increasing proportion of Crohn's disease, A3. The analyses of Crohn's disease in one county only, and the limited number of inhabitants in our primary catchment area, are two further possible limitations of the study. Therefore, possible geographic variations within Sweden cannot be ruled out and some of the statistical analyses might lack power, due to the low number of patients with some Crohn's disease characteristics within our catchment area. In line with current recommendations,40 we applied
Lennard–Jones criteria for the diagnosis of Crohn's disease in this study,10in contrast to our previous study where Garland
diagnostic criteria were used.8,41In short, criteria of Garland
classify patients into: definite, probable and possible Crohn's disease, depending on findings for histology, endoscopy and radiology as well as the discharge diagnosis, where only
2 4 6 8 10
Age−standardised incidence rate per 100,000 inhabitants
1963−1965 1966−1970 1971−1975 1976−1980 1981−1985 1986−1990 1991−1995 1996−2000 2001−2005 2006−2010 Period 50 100 150 200 250 300
Point prevalence per 100,000 inhabitants
31 Dec 1965 31 Dec 1970 31 Dec 1975 31 Dec 1980 31 Dec 1985 31 Dec 1990 31 Dec 1995 31 Dec 2000 31 Dec 2005 31 Dec 2010 Date
Figure 3 Age-standardised incidence rate with 95% confidence interval (left panel) and point prevalence with 95% confidence interval
(right panel) for the study period 1963–2010.
definite and probable diagnoses were included in our previous study. To our knowledge there are no direct comparisons between the criteria of Garland and the Lennard–Jones criteria. However, definite and probable Crohn's disease according to the criteria of Garland seem to depend more on histological and surgical findings and pay less attention to the overall clinical picture compared to that of Lennard–Jones criteria. We could not identify individual patients that were included in the previous study,8 since the raw data are no
longer available. Therefore, all data from the previously reported study period (1963–1987) had to be re-extracted. The difference in patient identification procedures, diagnostic criteria, access to demographic information and length of the observation period influenced the observed point prevalence value. Lindberg et al.8reported a point prevalence of 146 per
105 individuals in 1987, which is somewhat lower than our figure for the same year.
In conclusion, we observed an increasing incidence of Crohn's disease in the Örebro catchment area, although the incidence rate seemed to be plateauing during the most recent decades. The incidence figures were notably higher among those aged 40 years and above as well as among paediatric Crohn's disease. An increasing proportion of patients were diagnosed with non-stricturing, non-penetrating disease over time, possibly suggesting that patients with Crohn's disease are diagnosed in an earlier point in the disease course than in previous years, alternatively it may reflect the change in disease phenotype. The observed point prevalence in 2010 is among the highest reported.
Supplementary data to this article can be found online at
http://dx.doi.org/10.1016/j.crohns.2014.07.006.
Conflict of interest
None.Acknowledgements
We acknowledge Åsa Ekblom, Birgitta Meijer and Ann-Britt Löf for secretarial assistance; Mia Lagerroos, Anders Dahl, Michael Lundberg and Mats Granberg for their IT support with this project.
This project was supported by the Karlskoga Hospital Reseach Foundation (grant AE-37256) and by grants from the Bengt Ihre's Foundation (grant SLS-254051), Örebro University Hospital Research Foundation (grant OLL-256371), Örebro County Research Foundation (grants OLL-93671, OLL-172601, OLL-200541, OLL-256771), the Swedish Foundation for Gas-trointestinal Research (grant 2009) and Swedish Research Council (521-2011-2764).
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