Emilsson, Louise

Background and aims: Clinical experience suggests that patients with coeliac disease (CD) are more prone to develop herpes zoster (HZ), but robust studies are lacking. Methods: We identified 29,064 patients with CD 1969−2008 using biopsy report data from Sweden’s 28 pathology departments. CD was equalled to villous atrophy (Marsh histopathology grade III). Each patient was matched on age, sex, calendar year and county of residence to up to five reference individuals ( n=144,342) from the general population. We then used Cox regression to estimate hazard ratios (HRs) for future HZ (defined as having a hospital-based inpatient or outpatient record of this diagnosis in the Swedish Patient Register). Results: During follow-up, 154 (0.53%) individuals with CD and 499 (0.35%) reference individuals developed HZ. Among individuals aged ≥60 years, 1.06% of CD individuals and 0.85% of reference individuals had a lifetime record of HZ. Overall, CD was associated with a 1.62-fold increased risk of HZ (95% CI=1.35−1.95), and was seen also when we considered comorbidity with lymphoproliferative disease, systemic lupus erythematosus, type 1 diabetes, thyroid disease, rheumatoid disease and excluded individuals with a record of dermatitis herpetiformis. The increased risk remained significant after more than five years of follow-up (1.46; 1.16−1.84) Conclusions: CD is associated with HZ, the increased relative risk persists over time from celiac diagnosis but the absolute risk is small.

Background Patients with celiac disease (CD) are at increased risk of certain infections, but it is unknown if mucosal healing influences this risk. Methods We collected data on 29,096 individuals with CD (equal to villous atrophy) through Sweden’s 28 pathology departments undergoing biopsy 1969–2008. Through the Swedish Patient Register we obtained information on any infection and specifically sepsis, streptococcal infection, influenza, Clostridium difficile, herpes zoster and pneumococcal infection up until December 2009. We used Cox regression to calculate hazard ratios (HRs) for the risk of future diagnosis of infection according to mucosal healing on follow-up biopsy (persistent villous atrophy vs mucosal healing). Results Of 5598 CD individuals with no record of any infections before follow-up biopsy, 45% had persistent villous atrophy, 619 (24%) of them had a later infection, compared to 579 (19%) in those with mucosal healing ( p < 0.01); the yearly incidence was 2.1% in both groups. Adjusting for age, sex, calendar period, time between biopsies and education, persistent villous atrophy was however not associated with later infection overall (HR = 0.99; 95% CI = 0.88–1.11) or with any of the specific infections. Conclusions In CD, mucosal healing does not influence the risk of serious infection requiring hospital-based medical attention.

Background and Aims: A recent study found a 10-fold increased risk of celiac disease (CD) in individuals with Henoch-Schonlein purpura (HSP), but the confidence interval (CI) was wide. Methods: The retrospective cohort study of all patients with CD in Sweden, diagnosed through small intestinal biopsy from 1969 to 2008 (n=29,077). Each individual with CD was matched to up to 5 controls (n=144,433). Data on study participants were linked to diagnostic codes for HSP in the National Patient Registry. Through Cox regression we estimated hazard ratios for CD and later HSP. Through logistic regression we calculated odds ratios for HSP preceding CD. Results: During follow-up 19 individuals with CD and 99 controls developed HSP. This corresponded to a hazard ratio of 0.96 (95% CI, 0.59-1.56). Looking backward, we found no increased risk of earlier HSP in patients with CD (odds ratio=1.02; 95% CI, 0.60-1.72). Conclusions: In this study of more than 29,000 patients with CD, we found no increased risk of HSP before or after CD.