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and a subsequent risk of developing HL NS (Table 1).Our findings are important for several reasons.We show for the first time that the risk for HL following a personal history of autoimmune disease may vary by HL subtype.Autoimmunity was associated with a significantly elevated risk for MC HL, but there were no significant associations with NS HL and the risk estimates were generally lower.Interestingly, we found a long latency from the date of autoimmune diagnosis to the date of MC HL (mean time =15.4 years) suggesting that long-term chronic immune stimulation may play a role in the causation of MC HL.Taken together, our observations support the hypothesis that the etiology of HL might differ by HL subtype.Also, we confirmed that Sjögren's syndrome is associated with a highly increased risk of HL.We used high-quality data, 11 however, the nature of this study is hypothesis-generating and one has to interpret our findings with caution due to the low numbers of cases by subtype, hampering further stratified analyses.In conclusion, our findings support a role for chronic immune stimulation in the etiology of HL.Our novel finding of a different risk pattern by HL subtypes suggests the operation of separate pathogenetic mechanisms and needs to be supported by other study groups.
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Mustjoki et al. (2009) studied this question.
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