Patterns of autoimmunity and subsequent chronic lymphocytic leukemia in Nordic countries
A population-based case-control study was conducted to evaluate risk of developing chronic lymphocytic leukemia (CLL) associated with personal and/or family history of autoimmune and related diseases. Data were obtained for all (n = 7764) patients diagnosed with CLL in Sweden and Denmark over a 40-y...
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Published in | Blood Vol. 108; no. 1; pp. 292 - 296 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Washington, DC
Elsevier Inc
01.07.2006
The Americain Society of Hematology The American Society of Hematology |
Subjects | |
Online Access | Get full text |
ISSN | 0006-4971 1528-0020 |
DOI | 10.1182/blood-2005-11-4620 |
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Summary: | A population-based case-control study was conducted to evaluate risk of developing chronic lymphocytic leukemia (CLL) associated with personal and/or family history of autoimmune and related diseases. Data were obtained for all (n = 7764) patients diagnosed with CLL in Sweden and Denmark over a 40-year period and with linkable relatives, 16 658 matched control subjects, and first-degree relatives of patients (n = 17 991) and control subjects (n = 39 388). Odds ratios (ORs) were calculated to quantify risk of CLL in relation to personal/family history of 32 autoimmune and related disorders. The risk of CLL was significantly increased among subjects with a personal history of pernicious anemia (OR = 1.94; 1.18-3.18), mainly in the 0- to 1-year latency period. A significantly decreased risk of CLL was found among individuals with a personal history of chronic rheumatic heart disease (OR = 0.55; 0.33-0.93), particularly persons with a long latency (10+ years) between the 2 conditions. We found no association between personal or familial occurrence of other autoimmune or related disorders and CLL. If our results are confirmed, mechanistic studies examining how pernicious anemia might promote increased occurrence of CLL and how chronic rheumatic heart disease protects against CLL, perhaps related to long-term antibiotics use, may provide insights to the as-yet-unknown etiology of CLL. (Blood. 2006;108:292-296) |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 O.L., E.A.E., M.S.L., and L.R.G. designed the study; M.S.L., G.G., L.R.G., L.M., and K.H. obtained data; O.L. and E.A.E. analyzed data; O.L., E.A.E., N.E.C., G.G., L.M., K.H., M.S.L., and L.R.G. were involved in the interpretation of the results; O.L. initiated this work and wrote the report. All authors read, gave comments, and approved the final version of the manuscript. O.L., E.A.E., and L.R.G. had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked “advertisement” in accordance with 18 U.S.C. section 1734. Supported by the Intramural Research Program of the National Institutes of Health, National Cancer Institute. Prepublished online as Blood First Edition Paper, March 9, 2006; DOI 10.1182/blood-2005-11-4620. Reprints: Ola Landgren, Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd, Bldg EPS/Rm 7110, Bethesda, MD 20892-7236; e-mail: landgreo@mail.nih.gov. |
ISSN: | 0006-4971 1528-0020 |
DOI: | 10.1182/blood-2005-11-4620 |