PURPOSE: To investigate the risk of cancer in individuals with IgA deficiency compared with the general population. METHODS: Prospective nationwide population-based cohort study. We identified 2320 individuals with IgA deficiency (IgA levels < 0.07 g/L) diagnosed between 1980 and 2010 in six Swedish university hospitals. Individuals with IgA deficiency were then matched on age, sex, place of residence, and year of diagnosis with up to 10 general population controls (n = 23,130). Through linkage with the Swedish Cancer Register we calculated conditional hazard ratios (HRs) for cancer diagnosed after IgA deficiency diagnosis in patients without a previous cancer diagnosis. RESULTS: During follow-up, 125 individuals with IgA deficiency (61/10,000 person-years) and 984 controls (47/10,000 person-years) developed cancer (HR 1.31; 95%CI = 1.09-1.58). In cause-specific analyses, we found an increased risk of any gastrointestinal cancer (HR = 1.64; 95%CI = 1.07-2.50), but not for lymphoproliferative malignancy (HR 1.68; 95%CI = 0.89-3.19). Relative risk estimates for overall cancer were very high in the first year of follow-up (overall: HR = 2.80; 95%CI = 1.74-4.49), but failed to reach statistical significance thereafter. IgA deficiency diagnosed in childhood (n = 487) was not associated with overall cancer (HR = 3.26; 0.88-12.03). CONCLUSIONS: Individuals with IgA deficiency are at a moderately increased risk of cancer, with excess risks of gastrointestinal cancer. This excess risk is highest just after diagnosis suggesting a degree of surveillance bias. Children with IgA deficiency were at no increased risk of cancer but the statistical power was limited in subanalyses.
PURPOSE: To investigate the risk of cancer in individuals with IgA deficiency compared with the general population. METHODS: Prospective nationwide population-based cohort study. We identified 2320 individuals with IgA deficiency (IgA levels < 0.07 g/L) diagnosed between 1980 and 2010 in six Swedish university hospitals. Individuals with IgA deficiency were then matched on age, sex, place of residence, and year of diagnosis with up to 10 general population controls (n = 23,130). Through linkage with the Swedish Cancer Register we calculated conditional hazard ratios (HRs) for cancer diagnosed after IgA deficiency diagnosis in patients without a previous cancer diagnosis. RESULTS: During follow-up, 125 individuals with IgA deficiency (61/10,000 person-years) and 984 controls (47/10,000 person-years) developed cancer (HR 1.31; 95%CI = 1.09-1.58). In cause-specific analyses, we found an increased risk of any gastrointestinal cancer (HR = 1.64; 95%CI = 1.07-2.50), but not for lymphoproliferative malignancy (HR 1.68; 95%CI = 0.89-3.19). Relative risk estimates for overall cancer were very high in the first year of follow-up (overall: HR = 2.80; 95%CI = 1.74-4.49), but failed to reach statistical significance thereafter. IgA deficiency diagnosed in childhood (n = 487) was not associated with overall cancer (HR = 3.26; 0.88-12.03). CONCLUSIONS: Individuals with IgA deficiency are at a moderately increased risk of cancer, with excess risks of gastrointestinal cancer. This excess risk is highest just after diagnosis suggesting a degree of surveillance bias. Children with IgA deficiency were at no increased risk of cancer but the statistical power was limited in subanalyses.
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