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PubMed1996

Effect of pregnancy on the clinical course of a cohort of women with inflammatory bowel disease.

The incidence of relapses of inflammatory bowel disease in pregnancy ranges from 20 to 35%. The effect of pregnancy on Crohn's disease and ulcerative colitis after pregnancy has been investigated here. During the survey period, 29 pregnancies occurred in 18 Crohn's patients, and 25 in 19 ulcerative colitis patients. Incidence of relapses during pregnancy and post-partum was 14 and 17% in Crohn's, and 36 and 12% in ulcerative colitis. Fourteen Crohn's patients (17 pregnancies) and 17 ulcerative colitis patients (19 pregnancies) were followed for 3 years before pregnancy and for 4 years after delivery. During the 3 years after pregnancy, the number of relapses/year was significantly lower compared to the 3 years before pregnancy and to the incidence in controls, both in Crohn's (p < 0.05) and ulcerative colitis (p < 0.005). Changes in nutritional status were recorded in 41% of Crohn's, but in none of the ulcerative colitis patients. The reduced incidence of relapses following delivery in Crohn's patients was more marked in the 10 with normal nutritional status at the time of conception (70% reduction in number of relapses, p < 0.05), while in the 7 significantly underweight patients, the reduction was slight (27% reduction in number of relapses, p = NS). In conclusion, the incidence of relapses in the first 3 years after pregnancy is lower than in the pre-pregnancy period. In Crohn's disease, the effect is more evident in patients with normal nutritional status at the time of conception than in malnourished patients.

Abortion, Spontaneous↗
PubMed1998

[Necessary diagnosis before and reliable examinations after surgical interventions in chronic inflammatory bowel diseases].

The primary diagnosis of chronic inflammatory bowel disease (Crohn's disease, ulcerative colitis) is performed by standardized procedures in specialized Gastroenterology Departments or Ambulances. For the assessment of disease activity the clinical presentation of the patient is most important. This is also true for the indication for surgical interventions. In certain instances laboratory markers, endoscopic and histologic examinations, ultrasound, X-ray, and cross-sectional imaging like computed tomography (CT) or magnetic resonance imaging (MRI) give important additional informations. Depending on the clinical situation surgeons and gastroenterologists decide on the most useful technical examinations for planning the operative strategy. After surgery, diagnostic procedures focus on disease progression and complications. Disturbances of intestinal function as consequence of the operation have also to be considered in the routine diagnostic program.

Colitis, Ulcerative↗
PubMed2003

Malignancies in inflammatory bowel disease.

The risk of luminal gastrointestinal tract, hepatobiliary tract, and non-gastrointestinal tract cancers in inflammatory bowel disease remains of great interest. The purpose of this review is to report on studies published in 2002 that have addressed several important questions related to the biology, natural history, and risk factors for colonic and extracolonic cancers. Two studies reported conflicting results on the natural history of low-grade dysplasia in patients with ulcerative colitis. Other investigators focused on the safety of medications used to treat inflammatory bowel disease, one noting no increased risk of cancer with azathioprine, another suggesting that anti-tumor necrosis factor therapy may increase the risk of lymphoma. Studies of patients after total proctocolectomy and ileoanal pouch anastomosis suggest that these patients continue to have a small risk of bowel cancer. A novel observation from studies focusing on the subgroup of patients with inflammatory bowel disease and primary sclerosing cholangitis was the identification of an increased risk of pancreatic cancer. Finally, many investigators continue to pursue potential biomarkers of malignancy for use in inflammatory bowel disease cancer surveillance programs. These studies have added to our knowledge of the risk of malignancy in inflammatory bowel disease and have set the stage for future long-term studies to better delineate the risk of lymphoma with the use of anti-tumor necrosis factor therapy and the fate of low-grade dysplasia in flat mucosa. Clinical application of potential biomarkers of malignancy in inflammatory bowel disease cancer surveillance is anticipated in the near future.

Journal Article↗
PubMed1999

The relationship between habits of food consumption and reported reactions to food in people with inflammatory bowel disease--testing the limits.

Anecdotally, people with inflammatory bowel disease (IBD) report that some foods make them feel better and some foods make them feel worse. This paper reports about the relationship between food habits and reactions to foods in people with IBD. A database was designed to incorporate the date of data collection, the IBD disease, food habits, the quantity consumed and a response rating of the subjects' reactions to each food. For each of 122 foods, subjects were asked simultaneously about these five categories. Thirty three subjects with Crohn's disease and 27 with ulcerative colitis completed the questionnaire in two seasons. The focus of the examination was directed to the upper and lower limit of reactions to foods. Foods that affect people negatively and foods that affect people positively were identified in relation to habits of consumption. Foods that affect people negatively were among those never consumed while foods that affect people positively were among the regularly consumed foods. Findings included an increased number of foods that caused problems for people with Crohn's disease when compared with people with ulcerative colitis. Problems with chocolate, dairy products, fats and artificial sweeteners were documented in both groups of IBD. A standard food list generated without the input of individuals with a chronic illness may be inadequate to collect data about their consumption since many of the foods on the list were reportedly never consumed and there may be other foods not on the list that are consumed by this chronically ill population.

Colitis, Ulcerative↗
PubMed2006

A comprehensive analysis of 12 thrombophilic mutations and related parameters in patients with inflammatory bowel disease: data from Turkey.

BACKGROUND: Possible association of inflammatory bowel disease (IBD) with the most common inherited prothrombotic conditions has been the focus of many investigations. Advance in modern molecular biology is expanding the thrombophilia evaluation steadily. We tried to put forward a comprehensive thrombophilic profile in IBD and to see the probable role of this profile in pathogenesis. METHODS: A total of 60 adults (33 patients and 27 healthy controls) were included. We used the CVD-StripAssay which is based on the reverse-hybridization principle to identify a total of 12 thrombophilic gene mutations: Factor V R506Q, Factor V H1299R, prothrombin G20210A, Factor XIII V34L, beta-Fibrinogen-455 G-A, PAI-1 4G/5G, platelet GPIIIa L33P, MTHFR C677T, MTHFR A1298C, ACE I/D, Apo B R3500Q and Apo E2/E3/E4, respectively. Besides, we evaluated many related blood parameters such as protein C, protein S, AT-III, IL-6, TNF-alpha, Apo-A1, Apo-B100, homocysteine (tHcy) etc. using commercially available assays. RESULTS: The frequencies of genetic polymorphisms were found to be statistically insignificant among patients and controls, except for three: Beta-Fibrinogen-455G-A, MTHFR A1298C and ACE-I/D. Two patients with a history of deep venous thrombosis had more than one polymorphism. Patients with MTHFR C677T and MTHFR A1298C gene mutations had a similar mean tHcy levels with controls. Patients with Apolipoprotein B R3500Q and Apolipoprotein E4 gene mutations had similar mean LDL-cholesterol levels. Mean total cholesterol and triglyceride levels were similar in patients and controls of Apo E2, E3, E4 alleles. CONCLUSION: Predominantly, the presence of genetic mutations that predispose to hypercoagulable states does not appear to be in correlation with IBD. There was a statistical difference between the proportions of the mutated allele frequencies of Beta-Fibrinogen-455G-A, MTHFR A1298C and ACE-I/D in IBD.

Adolescent↗
PubMed2006

Relapse of inflammatory bowel disease associated with use of nonsteroidal anti-inflammatory drugs.

To determine whether an association exists between relapse in inflammatory bowel disease and use of nonsteroidal anti-inflammatory drugs (NSAIDs), a retrospective records review was conducted of patients with Crohn's disease, ulcerative colitis, or indeterminate colitis examined at an outpatient tertiary care center between July 17, 2000, and November 1, 2001. Extracted data collected during the patient's last visit included medication use, maintenance therapy, disease activity, and smoking status. Use of NSAIDs was defined as a daily dose or more of any type the month before relapse. Of 60 patients (22, relapse; 38, remission), 9 (41%) in relapse and 10 (26%) in remission used NSAIDs. Maintenance therapy varied from 68% (relapse) to 92% (remission). The adjusted odds ratio between medication use and relapse was 6.31 (95% confidence interval, 1.16-34.38; P = .03). Use of NSAIDs was associated with relapse. A prospective cohort study that corrects for maintenance therapy is needed to evaluate this relationship.

Adult↗
PubMed2005

Environmental risk factors in paediatric inflammatory bowel diseases: a population based case control study.

BACKGROUND: Environmental exposures in early life have been implicated in the aetiology of inflammatory bowel disease. OBJECTIVE: To examine environmental risk factors prior to the development of inflammatory bowel disease in a paediatric population based case control study. METHODS: A total of 222 incident cases of Crohn's disease and 60 incident cases of ulcerative colitis occurring before 17 years of age between January 1988 and December 1997 were matched with one control subject by sex, age, and geographical location. We recorded 140 study variables in a questionnaire that covered familial history of inflammatory bowel disease, events during the perinatal period, infant and child diet, vaccinations and childhood diseases, household amenities, and the family's socioeconomic status. RESULTS: In a multivariate model, familial history of inflammatory bowel disease (odds ratio (OR) 4.3 (95% confidence interval 2.3-8)), breast feeding (OR 2.1 (1.3-3.4)), bacille Calmette-Guerin vaccination (OR 3.6 (1.1-11.9)), and history of eczema (OR 2.1 (1-4.5)) were significant risk factors for Crohn's disease whereas regular drinking of tap water was a protective factor (OR 0.56 (0.3-1)). Familial history of inflammatory bowel disease (OR 12.5 (2.2-71.4)), disease during pregnancy (OR 8.9 (1.5-52)), and bedroom sharing (OR 7.1 (1.9-27.4)) were risk factors for ulcerative colitis whereas appendicectomy was a protective factor (OR 0.06 (0.01-0.36)). CONCLUSIONS: While family history and appendicectomy are known risk factors, changes in risk based on domestic promiscuity, certain vaccinations, and dietary factors may provide new aetiological clues.

Adolescent↗
PubMedDate not supplied

Sexual health issues in inflammatory bowel disease.

Alterations in sexual health caused by inflammatory bowel disease (IBD) may affect quality of life and disease status. IBD usually strikes adolescents or young adults, who are also facing developmental milestones important to sexual health. Issues include growth and development, body image, intimacy and sexual functioning, fertility, and pregnancy. A review of published research regarding these issues, in addition to suggestions for nursing assessment and interventions, is included in this article. Nurses must offer sensitive support and suggestions for coping. Nurses must be aware of the issues influencing sexual health when providing total care to clients with IBD.

Adult↗
PubMed2003

IgA antiglomerular basement membrane nephritis associated with Crohn's disease: a case report and review of glomerulonephritis in inflammatory bowel disease.

A case of glomerulonephritis in a 35-year-old man with Crohn's disease is described here. The patient presented with severe diarrhea, nephrotic range proteinuria, hematuria, microangiopathic hemolytic anemia, thrombocytopenia, hypocomplementemia, acute renal failure requiring hemodialysis, cryoglobulinemia, and extensive thrombotic gangrene of the distal upper and lower limbs. The patient did not respond to plasmapheresis and steroid therapy and died of upper gastrointestinal bleeding. Renal tissue obtained at autopsy showed IgA-mediated antiglomerular basement membrane crescentic glomerulonephritis. Linear staining of the glomerular basement membrane by non-IgG antibodies is quite unusual with only 11 cases previously reported in the worldwide literature, 8 caused by IgA. Glomerulonephritis is a rarely reported extraintestinal manifestation of inflammatory bowel disease, and there are only 24 previously described cases that are reviewed and summarized in this report. Glomerulonephritis occurred in the setting of active bowel inflammation in all cases, circulating immune complexes were found in nearly half the cases, and serum complements usually were normal. Renal insufficiency and nephrotic range proteinuria were typically present at the time of diagnosis of glomerulonephritis and most often improved in parallel with treatment of the gastrointestinal disorder. The histologic findings were varied and included membranoproliferative glomerulonephritis, mesangioproliferative glomerulonephritis, membranous nephropathy, IgA nephropathy, and IgM nephropathy. Thus, the authors present the first case of glomerulonephritis caused by antiglomerular basement membrane disease in association with inflammatory bowel disease.

Adult↗
PubMedDate not supplied

The genetic background of inflammatory bowel disease.

Available evidence indicates that genetic factors are essential in providing the susceptibility to the majority of the various forms of inflammatory bowel disease occurring in man. It is also clear that the genetic susceptibility to these diseases is complex, and that more than one gene may predispose (the concept of multilocus/oligogenic inheritance), and likely in different etiologic combinations (the concept of genetic heterogeneity). Paradigms are now available that should lead to the identification of a number of these predisposing genes. These paradigms include the candidate gene approach, systematic genome wide scans, and mouse human synteny. While genome wide scans are currently limited to multiplex family linkage studies, both candidate genes and mouse human synteny can be approached in either linkage or association paradigms. Eventually whole genome association studies will be available as well. Identification of inflammatory bowel disease predisposing genes should lead to their incorporation in studies of natural history, investigation of environmental risk factors, and especially utilization of genetic markers in clinical trials. This will allow us to identify the best therapy available for the individual patient based on their unique genetic constitution. With advances in molecular technology, the search for genes influencing traits and diseases with a complex genetic background, such as the inflammatory bowel diseases, has become a realistic task. Although exogenous or infectious agents may contribute to the pathogenesis or may trigger the onset of disease, and the immune system almost certainly mediates the tissue damage, it is clear from available data that genetic factors determine the susceptibility of a given individual to inflammatory bowel disease (reviewed below). Thus, genetic studies are essential for the delineation of the basic etiologies of the various forms of inflammatory bowel disease and thus can aid in the development of radically new and specific therapies. In this review, we will discuss the importance and complexity of genetic factors in inflammatory bowel disease, methods and problems in the genetic dissection of complex traits, and future directions of genetic studies in inflammatory bowel disease.

Animals↗
PubMed2003

Hypothalamic digoxin, hemispheric chemical dominance, and inflammatory bowel disease.

The isoprenoid pathway produces three key metabolites--endogenous digoxin, dolichol, and ubiquinone. It was considered pertinent to assess the pathway in inflammatory bowel disease (ulcerative colitis and regional ileitis). Since endogenous digoxin can regulate neurotransmitter transport, the pathway and the related cascade were also assessed in individuals with differing hemispheric dominance to find out the role of hemispheric dominance in its pathogenesis. All the patients with inflammatory bowel disease were right-handed/left hemispheric dominant by the dichotic listening test. The following parameters were measured in patients with inflammatory bowel disease and in individuals with differing hemispheric dominance: (1) plasma HMG CoA reductase, digoxin, dolichol, ubiquinone, and magnesium levels; (2) tryptophan/tyrosine catabolic patterns; (3) free-radical metabolism; (4) glycoconjugate metabolism; and (5) membrane composition and RBC membrane Na+-K+ ATPase activity. Statistical analysis was done by ANOVA. In patients with inflammatory bowel disease there was elevated digoxin synthesis, increased dolichol and glycoconjugate levels, and low ubiquinone and elevated free radical levels. There was also an increase in tryptophan catabolites and a reduction in tyrosine catabolites. There was an increase in cholesterol:phospholipid ratio and a reduction in glycoconjugate level of RBC membrane in these groups of patients. Inflammatory bowel disease is associated with an upregulated isoprenoid pathway and elevated digoxin secretion from the hypothalamus. This can contribute to immune activation, defective glycoprotein bowel antigen presentation, and autoimmunity and a schizophreniform psychosis important in its pathogenesis. The biochemical patterns obtained in inflammatory bowel disease is similar to those obtained in left-handed/right hemispheric dominant individuals by the dichotic listening test. But all the patients with peptic ulcer disease were right-handed/left hemispheric dominant by the dichotic listening test. Hemispheric chemical dominance has no correlation with handedness or the dichotic listening test. Inflammatory bowel disease occurs in right hemispheric chemically dominant individuals and is a reflection of altered brain function.

Adult↗
PubMed1984

Correlation of histopathologic evidence of disease activity with the presence of immunoglobulin-containing cells in the colons of patients with inflammatory bowel disease.

Immunofluorescence of formalin-fixed, paraffin-embedded tissues was performed to study the plasma cell population in 114 colonic specimens from 58 patients. Correlation of the histopathologic stage of disease activity with the isotypes and numbers of immunoglobulin-containing cells in the lamina propria demonstrated highly significant (P less than 0.001) increases in the mean numbers of IgG- (18-fold), IgA- (twofold) and IgM- (sixfold) containing cells in specimens from patients with active inflammatory bowel disease as compared with control specimens. Increased numbers of immunoglobulin-containing cells were uncommon in inactive inflammatory bowel disease and in reactive mucosa. No deposition of immunoglobulin-containing immune complexes was found at any stage of disease activity. These findings suggest that immune complex-mediated damage does not play a major role in the epithelial damage in inflammatory bowel disease. In future studies, it will be of importance to determine whether the antibody from immunoglobulin-containing cells seen in patients with inflammatory bowel disease can effect damage via an antibody-dependent cell-mediated cytotoxicity mechanism.

Antigen-Antibody Complex↗
PubMed2003

Emerging biotherapies for inflammatory bowel disease.

The immunological and genetic pathogeneses of inflammatory bowel disease (IBD) have been well studied, but not well elucidated in recent years. Accordingly, the pharmacological treatment of IBD is focusing upon the individual pathologic step (targeting therapy). It has recently become apparent that new drugs such as biological immunomodulating agents and anti-inflammatory cytokines have better short-term effects in some respects than conventional drugs, and they could change the treatment strategy of IBDs in the near future. Many options are now available to treat IBD. The choice depends on the type of IBD, the location of inflammation and the severity of symptoms. Many key processes in the inflammatory cascade have been targeted by cytokine and anticytokine therapies ranging from antigen presentation, T cell activation, overproduction of pro-inflammatory cytokines and migration of inflammatory cells to blockade of effector signals. TNF-alpha plays an important role in the induction of other cytokines as well as in the upregulation of adhesion molecules in chronic IBDs, Crohn's disease (CD) and ulcerative colitis. In fact, the most successful approaches so far in the treatment of IBD have been anti-TNF strategies. In contrast, the use of antiadhesion molecules strategies has been demonstrated to be ineffective in IBD.

Clinical Trials as Topic↗
PubMed1992

Autoantibodies to neutrophil cytoplasmic (ANCA) and endothelial cell surface antigens (AECA) in chronic inflammatory bowel disease.

Sera from 103 patients with chronic inflammatory bowel disease (IBD) were tested prospectively for antibodies against neutrophil cytoplasmic antigens (anti-neutrophil cytoplasm antibodies, ANCA) and endothelial cell surface antigens (anti-endothelial cell antibodies, AECA) by indirect immunofluorescence (IIF) and assays based on whole fixed neutrophils, purified neutrophil enzyme substrates and human umbilical vein endothelial cells. Using IIF, ANCA were found in 26 IBD sera (25%) and in none of 51 controls. Twenty-two positive sera (85%) were from patients with ulcerative colitis (UC). The pattern of distribution of immunofluorescence was always perinuclear (P-ANCA). A majority of UC patients positive for these autoantibodies (68%) had active colitis, but none had evidence of vasculitis. Using a whole neutrophil ELISA, binding was demonstrable in 73% of UC sera compared to 27% of Crohn's (CD) sera and only 4% of controls. Unlike vasculitis sera, UC sera with P-ANCA did not bind strongly to myeloperoxidase (MPO). Forty-five per cent of IBD sera tested positive for IgG AECA in an endothelial cell ELISA, compared to seven of 51 (14%) controls. Binding correlated with both active and extensive colitis. A type of P-ANCA, in most cases distinct from MPO-specific P-ANCA observed in vasculitis, is detected in a significant proportion of patients with UC, but rarely Crohn's colitis and therefore may be of differential diagnostic value. IgG AECA are also frequent in CIBD sera but are less disease specific than ANCA.

Adolescent↗
PubMed2001

6-mercaptopurine metabolite levels in children with inflammatory bowel disease.

OBJECTIVES: Some authors suggest that efficacy of 6-mercaptopurine (6-MP) in patients with inflammatory bowel disease correlates with circulating 6-thioguanine (6-TG) levels more than 235 pmol/8 x 10(8) red blood cells. The authors evaluated the relation between 6-MP metabolite levels and disease activity in children and adolescents with inflammatory bowel disease. METHODS: Clinical status and hematologic and hepatic parameters were determined in 101 children with inflammatory bowel disease from a single center and compared with 6-MP metabolite levels. RESULTS: There was a trend for higher 6-TG levels among patients in remission than among those with active disease (217 vs. 173); however the difference was not statistically significant ( P = 0.09). The likelihood of therapeutic response did not increase significantly at 6-TG levels greater than 235 pmol/8 x 10(8) red blood cells (odds ratio 1.7; P = 0.1). In the current study, 58% of patients in remission had 6-TG levels less than 235. However, serial measurements of 6-MP metabolite levels in 50 patients with active disease showed that increasing 6-TG levels correlated significantly with disease remission in patients followed up longitudinally ( P = 0.04). Leukopenia was significantly associated with high 6-TG levels ( P = 0.03) but not with clinical response ( P = 0.2). CONCLUSIONS: These data suggest that the target range of 6-TG levels previously described by others did not apply to 58% of the pediatric patients with IBD in remission. However, serial monitoring of 6-MP metabolite levels in individual patients with active disease should allow dose escalation and induction of remission while minimizing the risk of toxicity.

Adolescent↗
PubMed1999

Current pharmacotherapy for inflammatory bowel disease.

Ulcerative colitis (UC) and Crohn's disease (CD), collectively termed inflammatory bowel disease (IBD), are chronic spontaneously relapsing enteropathies of unknown aetiology. Pharmacotherapy for IBD has essentially been unchanged for over twenty years, with therapy based around 5-aminosalicylic acid (5-ASA) preparations, corticosteroids, antibiotics and immunosuppression. Much of the controversy surrounding optimal use of these drugs in IBD arises as a consequence of methodological deficiencies in many of the early trials combined with the difficulty in consistent patient selection due to the heterogeneous nature of both UC and CD. More recently, well-designed clinical trials have attempted to provide an 'evidence based' approach to managing IBD which, in time, will allow optimisation of current therapies and accurate evaluation of novel agents. Over the past two decades, improved research methodology has considerably increased our molecular understanding of the aetiopathogenesis of IBD which has ultimately lead to the development of specific mediator directed or 'designer' drug therapy for IBD. This review evaluates the literature on current IBD therapy, summarises the important recent studies which have made an impact on clinical practice, and examines the risks and benefits of the novel agents which are currently under investigation in clinical trials of IBD therapy.

Clinical Trials as Topic↗
PubMed2006

Frequency and characteristics of pancreatitis in patients with inflammatory bowel disease.

BACKGROUND AND AIMS: Clinical symptoms of inflammatory bowel disease (IBD)-associated pancreatitis are found in approximately 2% of patients, but the frequency of the disease could be much higher since IBD-associated pancreatitis could be mainly a silent disease. The aim of this study was to describe the radiological and biological features of IBD-associated pancreatitis and assess its frequency by comparing data from IBD patients with or without a history of pancreatitis. METHODS: 79 patients were prospectively enrolled (median age 36 years). Symptoms of pancreatitis had been previously recorded in 30 of them (group P; the other 49 patients (group C) had no history of pancreatitis. Pancreatic ductal changes were investigated by pancreato-MRI. Exocrine function was assessed by the fecal elastase test and by assaying serum amylase, lipase, C-reactive protein, PAP, IgG4 and pancreatic autoantibodies. RESULTS: Increased levels of amylase and lipase occurred in 11% of IBD patients, that frequency being significantly higher in group P (23%) than in group C (4%) (p = 0.01). Low fecal elastase reflecting impaired exocrine function was observed in 30% of patients and again significantly more in group P (50%) than in group C (17%) (p = 0.04). The frequency of elevated values varied from 12% for amylase and lipase to 18% for PAP, 20% for pancreatic autoantibodies and 45% for CRP, without a difference between groups P and C. Silent exocrinopathy was observed in both groups, pancreatic autoantibodies and pancreatic duct alterations being found in 20 and 11% of patients, respectively. CONCLUSION: Finding pancreatic insufficiency in about 30% of the included patients and in 50% of those with a previous history of pancreatitis suggests that IBD might be associated with chronic pancreatic alteration. Episodes of mild acute pancreatitis observed in some patients are not always due to adverse effects of treatments and can be acute manifestations of the chronic disease.

Adult↗
PubMedDate not supplied

Validity and completeness of the General Practice Research Database for studies of inflammatory bowel disease.

PURPOSE: The objective of this study was to evaluate the validity and completeness of the General Practice Research Database (GPRD) as a tool for research into inflammatory bowel disease epidemiology. METHODS: Patients diagnosed with inflammatory bowel disease were identified from GPRD. Mailed surveys were sent to the general practitioner caring for a stratified random sample of 170 of these patients and collected information on the diagnosis of inflammatory bowel disease and the most recent surgery and hospitalization. RESULTS: Usable surveys were returned for 157 patients (92%). The inflammatory bowel disease diagnosis was highly probable or probable in 144 (92%, 95% CI 86 to 96%). Among the 53 patients with a potentially incident inflammatory bowel disease diagnosis, 33 (62%) had the first recorded diagnosis in GPRD within 30 days of the date reported in the survey (median difference -8 days; interquartile range 0 to -81 days). Of 12 surgeries and 25 hospitalizations reported in the survey, 11 (92%) and 19 (76%) were identified in GPRD, respectively. CONCLUSIONS: The diagnosis of inflammatory bowel disease in GPRD appears reliable for most patients. Important medical events such as hospitalizations and surgery are recorded at a high rate, although algorithms to identify these events are complex.

Cohort Studies↗