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Risk of ulcerative colitis and Crohn's disease among offspring of patients with chronic inflammatory bowel disease

AMERICAN JOURNAL OF GASTROENTEROLOGY 1999年第11期94卷 3236-3238页

作者： Orholm, M Fonager, K Sorensen, HT Aarhus Univ Hosp Danish Epidemiol Sci Ctr Dept Epidemiol & Social Med DK-8000 Aarhus Denmark Aarhus Univ Hosp Dept Med 5 DK-8000 Aarhus Denmark Aalborg Hosp Clin Epidemiol Res Unit Dept Med M Aalborg Denmark Elsinore Hosp Dept Internal Med Elsinore Denmark

OBJECTIVE: The incidence of inflammatory bowel disease (IBD) varies among and within countries, but several studies have indicated that genetic factors may play an important role in the etiology of IBD. A Danish regional study has observed an almost 10-fold increased risk for ulcerative colitis (UC) and Crohn's disease (CD) among first-degree relatives of patients with these diseases. To give more precise risk estimates we conducted a nationwide study using population-based data from the Danish National Registry of Patients (NRP). METHODS: All patients from the entire Danish population (5.2 million), who were discharged between 1977 and 1992 with a diagnosis of either UC or CD were extracted from the NRP. The offspring of these patients born in 1958 or later were identified in the Civil Registration System and subsequently linked to the NRP by means of the civil registration number. All Danish citizens alive or born on April 1, 1968 or later no registered in the Civil Registration System by a unique registration number, which includes the data of birth and links the offspring to their parents. The prevalence proportion ratio (PPR) was estimated by dividing the observed number of offspring with UC or CD, respectively, with the expected number of cases from the general population. RESULTS: The PPRs of CD and UC among offspring of patients with UC were 2.6 and 5.1, respectively, and the PPRs of CD and UC among offspring of patients with CD were 12.8 and 4.0, respectively. All ratios were significantly increased. CONCLUSION: The risk for UC and CD among offspring of patients with IBD is 2-13 times higher than the risk within the general population. (C) 1999 by Am. Cell. of Gastroenterology.

关键词：慢性病结肠炎溃疡性/遗传学置信区间 Crohn病/遗传学丹麦发病率炎性肠疾病/遗传学泊松分布人群监测患病率登记危险因素性别因素儿童女(雌)性人类男(雄)性

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Linkage and linkage disequilibrium in chromosome band 1p36 in American Chaldeans with inflammatory bowel disease

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HUMAN MOLECULAR GENETICS 2000年第9期9卷 1425-1432页

作者： Cho, JH Nicolae, DL Ramos, R Fields, CT Rabenau, K Corradino, S Brant, SR Espinosa, R LeBeau, M Hanauer, SB Bodzin, J Bonen, DK Univ Chicago Hosp Martin Boyer Genet Res Lab Gastroenterol Sect Dept Med Chicago IL 60637 USA Univ Chicago Hosp Martin Boyer Genet Res Lab Hematol Oncol Sect Dept Stat Chicago IL 60637 USA Johns Hopkins Univ Sch Med Dept Med Harvey M & Lynn P Meyerhoff Inflammatory Bowel Di Baltimore MD 21205 USA DMC Sinai Hosp Detroit MI USA

The idiopathic inflammatory bowel diseases (IBDs), consisting of Crohn's disease and ulcerative colitis, are complex genetic disorders involving chronic inflammation of the intestines. Multiple genetic loci have been implicated through genome-wide searches, but refinement of localization sufficient to undertake positional cloning efforts has been problematic. This difficulty can be obviated through identification of ancestrally shared regions in genetic isolates, such as the Chaldean population, a Roman Catholic group from Iraq. We analyzed four multiply affected American Chaldean families with inflammatory bowel disease not known to be related. We observed evidence for linkage and linkage disequilibrium in precisely the same region of chromosome band 1p36 reported previously in an outbred population. Maximal evidence for linkage was observed near D1S1597 by multipoint analysis (MLOD = 3.01, P = 6.1 x 10(-5)). A shared haplotype (D1S507 to D1S1628) was observed over 27 cM between two families. There was homozygous sharing of a 5 cM portion of that haplotype in one family and over a <1 cM region in the second family. Homozygous sharing of this haplotype near D1S2697 and D1S3669 was observed in one individual in a third multiply affected family, with heterozygous sharing in a fourth family. Linkage in outbred families as well as in this genetic isolate indicates that a pathophysiologically crucial IBD susceptibility gene is located in 1p36. These findings provide a unique opportunity to refine the localization and identify a major susceptibility gene for a complex genetic disorder.

关键词：染色体人 1对人种群家庭卫生遗传标记疾病遗传易感性单元型原位杂交荧光炎性肠疾病/遗传学连锁(遗传学) 连锁不平衡优势对数记分法中东/人种学表型物理染色体图多态性单核苷酸美国/流行病学女(雌)性人类男(雄)性

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RELP, a novel human REG-like protein with up-regulated expression in inflammatory and metaplastic gastrointestinal mucosa

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AMERICAN JOURNAL OF PATHOLOGY 2003年第1期163卷 11-20页

作者： Kämäräinen, M Heiskala, K Knuutila, S Heiskala, M Winqvist, O Andersson, LC Univ Helsinki Dept Pathol Haartman Inst FIN-00014 Helsinki Finland Univ Helsinki Cent Hosp Diagnost Lab Helsinki Finland Univ Helsinki Dept Med Genet Helsinki Finland RW Johnson Pharmaceut Res & Dev San Diego CA USA

2We screened expressed sequence tag databases for genes with up-regulated expression in inflammatory bowel diseases. A gene encoding a regenerating protein (REG)-like protein called RELP was identified and characterized. The relp gene encodes a major transcript of 1518 nucleotides, and two truncated splice variants. Unlike the reg genes, which form a cluster in chromosome 2, relp maps to chromosome 1p12-13.1. The predicted translation product is a 158-amino acid preprotein, showing 43% to 47% similarity to the REG proteins. It contains a 22-amino acid signal peptide, and a conserved calcium-dependent carbohydrate-recognition domain. Complementary DNA for the orthologous mouse gene was also cloned. The RELP protein is constitutively expressed in epithelial neuroendocrine cells of the small intestine and in parietal cells of the gastric mucosa. An up-regulated expression of RELP was seen in epithelial cells of inflammatory mucosa in ulcerative colitis and Crohn's disease, in regenerating epithelial borders of gastric ulcers, and in metaplastic epithelium in the antrum and the esophagus. Our findings suggest that RELP might be involved in inflammatory and metaplastic responses of the gastrointestinal epithelium.

关键词：碱基序列染色体人 1对数据库遗传学表达的序列标记胃黏膜/细胞学胃黏膜/病理学胃黏膜/生理学原位杂交荧光炎性肠疾病/遗传学炎性肠疾病/代谢肠黏膜/细胞学肠黏膜/病理学肠黏膜/生理学外源凝集素类 C型化生分子序列数据神经组织蛋白质类/遗传学神经组织蛋白质类/代谢蛋白质生物合成序列比对组织分布肿瘤细胞培养的增量调节/生理学动物人类小鼠

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CD4⁺ CD25⁺ regulatory T lymphocytes inhibit microbially induced colon cancer in Rag2-deficient mice

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AMERICAN JOURNAL OF PATHOLOGY 2003年第2期162卷 691-702页

作者： Erdman, SE Poutahidis, T Tomczak, M Rogers, AB Cormier, K Plank, B Horwitz, BH Fox, JG MIT Div Comparat Med Cambridge MA 02139 USA Brigham & Womens Hosp Dept Pathol Div Immunol Res Boston MA 02115 USA Childrens Hosp Div Emergency Med Boston MA 02115 USA

Inflammatory bowel diseases, including ulcerative colitis and Crohn's disease, increase the risk of colorectal cancer in humans. It has been recently shown in humans and animal models that intestinal microbiota and host immunity are integral in the progression of large bowel diseases. Lymphocytes are widely believed to prevent bacterially induced inflammation in the bowel, and lymphocytes are also critical in protecting against primary tumors of intestinal epithelia in mice. Taken together, this raises the possibility that lymphocytes may inhibit colon carcinogenesis by reducing bacterially driven inflammation. To examine the role of bacteria, lymphocytes, and inflammatory bowel disease in the development of colon cancer, 129/SvEv Rag-2-deficient and congenic wildtype mice were orally inoculated with a widespread enteric mouse bacterial pathogen, Helicobacter hepaticus, or sham-dosed with media only. H. hepaticus-infected Rag2-/-, but not sham-dosed Rag2-/- mice, rapidly developed colitis and large bowel carcinoma. This demonstrated a link between microbially driven inflammation and cancer in the lower bowel and suggested that innate immune dysregulation may have an important role in inflammatory bowel disease and progression to cancer. H. hepaticus-infected wild-type mice did not develop inflammation or carcinoma showing that lymphocytes were required to prevent bacterially induced cancer at this site. Adoptive transfer with CD4(+) CD45RB(1o) CD25(+) regulatory T cells into Rag-deficient hosts significantly inhibited H. bepaticus-induced inflammation and development of cancer. These results suggested that the ability of CD4(+) T cells to protect against intestinal cancer was correlated with their ability to reduce bacterially induced inflammatory bowel disease. Further, regulatory T cells may act directly on the innate immune system to reduce or prevent disease. These roles for T cells in protection against colon carcinoma may have implications for new modes of pre

关键词：过继转移抗原 CD4/免疫学结肠肿瘤/遗传学结肠肿瘤/免疫学结肠肿瘤/病理学结肠肿瘤/预防和控制 DNA结合蛋白质类/缺乏 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/生理学疾病模型动物螺杆菌感染/并发症炎性肠疾病/遗传学炎性肠疾病/免疫学炎性肠疾病/病理学淋巴细胞输注小鼠基因敲除受体白细胞介素2/免疫学 T淋巴细胞/免疫学转座酶类/缺乏转座酶类/遗传学转座酶类/生理学动物小鼠

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Genetic factors determine extent of bone loss in inflammatory bowel disease

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GASTROENTEROLOGY 2000年第4期119卷 909-920页

作者： Schulte, CMS Dignass, AU Goebell, H Röher, HD Schulte, KM Univ Essen Gesamthsch Dept Internal Med Div Endocrinol D-45122 Essen Germany Univ Essen Gesamthsch Dept Internal Med Div Gastroenterol D-45122 Essen Germany Univ Dusseldorf Clin Gen Surg D-4000 Dusseldorf Germany

Background & Aims: Although bone loss and osteoporosis are well-known long-term sequelae of inflammatory bowel disease (IBD), the risk factors for increased bone loss have not been identified. Balances of pro- and anti-inflammatory cytokines influence mechanisms of both chronic inflammation and bone resorption. The aim of this study was to identify genetic risk factors for rapid bone loss in IBD patients as a model of disease- and inflammation-associated bone loss. Methods: Multiple clinical parameters, biochemical markers of bone metabolism (vitamin D, parathyroid hormone, N-terminal telopeptide of type-I collagen, desoxypyridinoline, bone alkaline phosphatase), and bone mineral density were prospectively assessed in 83 IBD patients over 1.6 +/- 0.3 years. Eighty-six healthy bone marrow donors sewed as controls for allelotyping. The allele status of the interleukin 1 receptor antagonist (IL-1ra), IL-6, heat shock protein 70-2 (hsp 70-2), and heat shock protein 70-hom (hsp hem) genes was typed and correlated with clinical course of IBD and extent of bone loss. Results: The extent of bone loss was not correlated to clinical severity of disease or application of corticosteroids. Noncarriage of the 240-base pair allele of the IL-1ra gene and carriage of the 130-base pair allele of IL-6 were independently associated with increased bone loss. Genetic variations of the hsp genes were not associated with degree of bone loss. The combined presence of the named risk factors was significantly associated with increasing bone loss. Conclusions: Genetic variations in the IL-6 and IL-1ra gene identify IBD patients at risk for increased bone loss.

关键词：吸收测定法光子碱性磷酸酶/血液等位基因氨基酸类/血液骨密度骨质吸收/病因学骨质吸收/遗传学结肠炎溃疡性/遗传学结肠炎溃疡性/病理生理学胶原/血液胶原Ⅰ型 Crohn病/遗传学 Crohn病/病理生理学 DNA/遗传学 HSP70热休克蛋白质类/遗传学炎性肠疾病/遗传学炎性肠疾病/病理生理学白细胞介素1受体拮抗蛋白质白细胞介素6/遗传学微卫星重复骨质疏松/病因学骨质疏松/遗传学肽类/血液聚合酶链反应多态现象遗传唾液糖蛋白类/遗传学人类

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Clinical phenotype is related to HLA genotype in the peripheral arthropathies of inflammatory bowel disease

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GASTROENTEROLOGY 2000年第2期118卷 274-278页

作者： Orchard, TR Thiyagaraja, S Welsh, KI Wordsworth, BP Gaston, JSH Jewell, DP Univ Oxford Radcliffe Infirm Gastroenterol Unit Oxford OX2 6HE England Churchill Hosp Nuffield Dept Surg Transplant Immunol Lab Oxford OX3 7LJ England John Radcliffe Hosp Musculoskeletal Res Unit Nuffield Dept Med Oxford OX3 9DU England Univ Cambridge Addenbrookes Hosp Dept Rheumatol Cambridge CB2 2QQ England

Background & Aims:The detection of phenotype-determining genes as opposed to disease susceptibility genes requires precise phenotypic characterization of patients. Peripheral arthropathies in inflammatory bowel disease (IBD) are well recognized and are classified with the HL4-B*27-related spondyloarthropathies by the European Spondyloarthropathy Study Group. However, previous HLA studies in IBD have only shown this association with axial disease rather than peripheral arthropathy. We recently reported a clinical classification that describes 2 types of peripheral arthropathy, distinguished by their natural history and articular distribution. We now report the results of immunogenetic studies in these patients and compare them with other spondyloarthropathies. Methods: IBD patients with type 1 (n = 57) and type 2 (n = 45) peripheral arthropathy were identified by case note review and questionnaire. Patients and 603 controls from Oxfordshire were assigned HLA-A, -B, -C, -DR, and -DQ genotypes by sequence-specific primer polymerase chain reaction. Patient results were compared with controls (corrected for multiple comparisons), then with each other in light of existing hypotheses. The results were compared with those of a cohort of 30 patients with postenteric reactive arthritis (ReA) and 16 patients with IBD-associated ankylosing spondylitis (IBD-AS). Results: Type 1 arthropathy was associated with HLA-DRB1*0103 (DR103;a rare subtype of DR1) in 33% (P < 0.0001;relative risk [RR], 12.1), B*35 in 30% (P = 0.01;RR, 2.2), and B*27 in 26% (P = 0.001;RR, 4.0). In contrast, type 2 was associated with HLA-B*44 in 62% (P = 0.01;RR, 2.1). Similar significant associations to type 1 arthropathy were found in ReA, except that the HLA-B*27 association was significantly stronger and an association was found with DRB1*0101 (DR1) in 43%(P = 0.001;RR, 2.2). IBD-AS was associated only with HLA-B*27 and DRB1*0101. Conclusions: These data suggest that the clinical classification into type

关键词：结肠炎溃疡性/遗传学结肠炎溃疡性/免疫学 Crohn病/遗传学 Crohn病/免疫学疾病遗传易感性/遗传学基因型 HLA-A抗原/遗传学 HLA-B抗原/遗传学 HLA-C抗原/遗传学 HLA-D抗原/遗传学 HLA-DR抗原/遗传学 HLA-DRB1链炎性肠疾病/并发症炎性肠疾病/遗传学炎性肠疾病/免疫学关节疾病/并发症关节疾病/遗传学关节疾病/免疫学主要组织相容性复合物表型参考值人类

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Thrombosis, factor V Leiden, and inflammatory bowel disease

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GASTROENTEROLOGY 1999年第3期116卷 778-779页

作者： Shanahan, F Natl Univ Ireland Univ Coll Cork Dept Med Cork Ireland

GASTROENTEROLOGY 1999;116:778-779

关键词：因子Ⅴ/遗传学炎性肠疾病/并发症炎性肠疾病/遗传学点突变回顾性研究危险因素血栓栓塞/并发症血栓栓塞/流行病学血栓性静脉炎/并发症血栓性静脉炎/流行病学血栓性静脉炎/遗传学人类

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NF-κB in IBD:: Does binding to DNA imply transcriptional activity?

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GASTROENTEROLOGY 1999年第6期116卷 1504-1505页

作者： Andresen, L Eugen-Olsen, J Perner, A Rask-Madsen, J Univ Copenhagen Hvidovre Hosp Clin Res Unit Copenhagen Denmark Univ Copenhagen Hvidovre Hosp Dept Gastroenterol Copenhagen Denmark

GASTROENTEROLOGY 1999;116:1504-1505

关键词： DNA/代谢炎性肠疾病/遗传学炎性肠疾病/代谢 NF-κB/代谢转录遗传/生理学人类

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Genetic aspects of inflammatory bowel disease: how far have we come, and where are we heading?

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Current gastroenterology reports 1999年第6期1卷 491-495页

作者： Cho, J. Emma Getz Inflammatory Bowel Disease Research Center Department of Medicine The University of Chicago G705 Gastroenterology Section 5841 South Maryland Avenue Chicago 60637-1521 IL United States

Crohn"s disease and ulcerative colitis are related complex genetic disorders, with gene-gene and gene-environment interactions that are critical to their pathogenesis. Multiple genetic loci have been implicated through genome-wide searches. Of these, a locus on Crohn"s disease has been definitively established in the pericentromeric region of chromosome 16. Multiple candidate gene studies have been forwarded, and functionally significant variants in immune-associated genes will provide additional insight. Characterization of the genetic variation responsible for causing inflammatory bowel disease will result in development of novel therapeutic approaches as well as in tailoring of specific therapies to individual patients based on their specific molecular pathogenesis.

关键词：遗传标记疾病遗传易感性炎性肠疾病/诊断炎性肠疾病/遗传学连锁(遗传学) 人类

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Pediatric inflammatory bowel disease.

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Current gastroenterology reports 1999年第3期1卷 220-222页

作者： Orenstein, S.R. University of Pittsburgh School of Medicine Children's Hospital of Pittsburgh One Children's Place Pediatric Gastroenterology Pittsburgh 15213-2583 PA United States

Pediatric inflammatory bowel disease (IBD) becomes adult inflammatory bowel disease, but several considerations require particular attention when children develop the disease. The disease generally manifests with active inflammation in children, whereas obstruction from "burnt-out" disease may become more prevalent with age. Because children are still growing, avoiding the growth-suppressing affects of the disease (and of steroid pharmacotherapy) is important in pediatric patients, in contrast to adults. Finally, the longer life expectancy of children than adults mandates even more attention to long-term safety issues in young patients.

关键词： 6-巯嘌呤/投药和剂量抗体抗中性白细胞胞质/分析硫唑嘌呤/投药和剂量药物疗法联合因子Ⅴ/遗传学炎性肠疾病/诊断炎性肠疾病/药物疗法炎性肠疾病/遗传学危险因素儿童人类

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