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Volume 20, Issue 3, Pages 217-222 (March 2010)


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Subsequent Autoimmune or Related Disease in Asthma Patients: Clustering of Diseases or Medical Care?

Kari Hemminki, MD, PhDabcCorresponding Author Informationemail address, Xinjun Li, MD, PhDc, Jan Sundquist, MD, PhDcd, Kristina Sundquist, MD, PhDbc

Received 7 August 2009; accepted 25 November 2009. published online 28 December 2009.

Purpose

Asthma includes immunological components that may share mechanisms with autoimmune diseases. We analyzed the subsequent occurrence of any of 22 autoimmune and related conditions in hospitalized asthma patients.

Methods

A nationwide study was conducted in Sweden on subsequent diseases of asthma patients on the basis of the Hospital Discharge Register. Standardized incidence ratios (SIRs) were calculated for subsequent autoimmune diseases.

Results

A total of 4006 patients were hospitalized for an autoimmune condition after last hospitalization for asthma. The SIRs were increased for 11 subsequent autoimmune conditions, diagnosed at least 5 years after asthma. The highest SIRs were noted for polyarteritis nodosa (4.29) and Addison disease (3.62). SIRs for these diseases and others, including the most common autoimmune disease rheumatoid arthritis, were increased even when the follow-up was started 5 years after the last asthma hospitalization. Addison disease and Crohn disease were increased in asthma patients hospitalized at various ages, whereas young asthma patients presented with celiac disease and immune thrombocytopenic purpura.

Conclusions

Hospitalized asthma patients presented with a number of subsequent autoimmune and related diseases. Although we were unable to exclude the effects of environmental factors, the data suggest that shared genetic factors or gene-environment interactions may explain coexistence of some of these diseases.

a Division of Molecular Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany

b Center for Family and Community Medicine, Karolinska Institute, Huddinge, Sweden

c Center for Primary Health Care Research, Lund University, Malmö, Sweden

d Stanford Prevention Research Center, Stanford University School of Medicine, Stanford, CA

Corresponding Author InformationAddress correspondence to: K. Hemminki, DKFZ, Im Neuenheimer Feld 580, D-69120 Heidelberg, Germany. Tel: 49-6221-421800; Fax 49-6221-421810.

 This work was supported by the National Institutes of Health (Grant No. R01-H271084-1), the Swedish Research Council (Grant No. K2001-27X-11651-06C), and the Swedish Council for Working Life and Social Research (Grant No. 2001-2373).

PII: S1047-2797(09)00363-9

doi:10.1016/j.annepidem.2009.11.007


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