Moderately increased risk of urinary stone disease in patients with biopsy-verified coeliac disease.

BACKGROUND: Urinary stone disease is a mal-absorptive disorder that is a significant health problem because of its high prevalence and incidence. However, there are few population-based studies on the risk of urinary stone disease in patients with coeliac disease (CD). AIM: To examine the risk of urinary stone disease in CD. METHODS: Population-based cohort study. Using small intestinal biopsy report data from 1969 to 2008 obtained from all Swedish pathology departments (n = 28), we identified 28 735 patients with CD (equal to Marsh 3: villous atrophy). Patients were then matched for gender, age, county and calendar year to 142 177 reference individuals from the Swedish general population. We used Cox regression to estimate hazard ratios (HRs) for future urinary stone disease and conditional logistic regression to calculate odds ratios (ORs) for urinary stone disease before diagnosis of CD. Individuals with urinary stone disease were identified through the Swedish National Patient Register that contains data on inpatient care, outpatient care and day surgery. RESULTS: During follow-up, 314 individuals with CD and 1142 reference individuals developed urinary stone disease. This corresponded to a 27% increased risk of urinary stone disease in CD [95% confidence interval (CI) = 1.12-1.44]. CD patients had an absolute risk of urinary stone disease of 107/100 000 person-years (excess risk of 23/100 000). Risk estimates were similar in men and women, and did not differ according to age at CD diagnosis. Conditional logistic regression found that patients with CD were at a slightly increased risk also of prior urinary stone disease (OR = 1.19; 95% CI = 1.06-1.33). CONCLUSION: In this study, coeliac disease was associated with a moderately increased risk of urinary stone disease both before and after coeliac disease diagnosis.

A population-based investigation of the autoantibody profile in mothers of children with atrioventricular block.

The objective of the study was to investigate the antigen specificity and occurrence of individual autoantibodies in mothers of children diagnosed with atrioventricular (AV) block in a nation-wide setting. Patients with AV block detected before 15 years of age were identified using national quality registries as well as a network of pediatric and adult cardiologists and rheumatologists at the six university hospitals in Sweden. Patients with gross heart malformations, surgically or infectiously induced blocks were excluded. Blood samples were obtained from the mothers and maternal autoantibody profile, including the occurrence of antibodies against Ro52, Ro60, La, SmB, SmD, RNP-70k, RNP-A, RNP-C, CENP-C, Scl-70, Jo-1, ribosomal RNP and histones was investigated in 193 mothers of children with AV block by immunoblotting and ELISA. Autoantibody reactivity was detected in 48% (93/193) of the mothers of children with AV block. In autoantibody-positive mothers, the vast majority, 95% (88/93), had antibodies against Ro52, while 63% (59/93) had autoantibodies to Ro60 and 58% (54/93) had autoantibodies to La. In addition, 13% (12/93) of the autoantibody-positive mothers had antibodies to other investigated antigens besides Ro52, Ro60 and La, and of these anti-histone antibodies were most commonly represented, detected in 8% (7/93) of the mothers. In conclusion, this Swedish population-based study confirms that maternal autoantibodies may associate with heart block in the child. Further, our data demonstrate a dominant role of Ro52 antibodies in association with AV block.

Anti-tumour necrosis factor therapy in rheumatoid arthritis and risk of malignant lymphomas: relative risks and time trends in the Swedish Biologics Register.

BACKGROUND: Tumour necrosis factor (TNF) antagonists have proved effective as treatment against rheumatoid arthritis (RA), but the unresolved issue of whether the use of anti-TNF therapy increases the already elevated risk of lymphoma in RA remains a concern. METHODS: Using the Swedish Biologics Register (ARTIS), the Swedish Cancer Register, pre-existing RA cohorts and cross-linkage with other national health and census registers, a national RA cohort (n = 67,743) was assembled and patients who started anti-TNF therapy between 1998 and July 2006 (n = 6604) were identified. A general population comparator (n = 471,024) was also assembled and the incidence of lymphomas from 1999 to 31 December 2006 was assessed and compared in these individuals. RESULTS: Among the 6604 anti-TNF-treated RA patients, 26 malignant lymphomas were observed during 26,981 person-years of follow-up, which corresponded to a relative risk (RR) of 1.35 (95% CI 0.82 to 2.11) versus anti-TNF-naive RA patients (336 lymphomas during 365,026 person-years) and 2.72 (95% CI 1.82 to 4.08) versus the general population comparator (1568 lymphomas during 3,355,849 person-years). RA patients starting anti-TNF therapy in 1998-2001 accounted for the entire increase in lymphoma risk versus the two comparators. By contrast, RR did not vary significantly by time since start of first treatment or with the accumulated duration of treatment, nor with the type of anti-TNF agent. CONCLUSION: Overall and as used in routine care against RA, TNF antagonists are not associated with any major further increase in the already elevated lymphoma occurrence in RA. Changes in the selection of patients for treatment may influence the observed risk.

Risk for malignant lymphoma in ankylosing spondylitis: a nationwide Swedish case-control study.

BACKGROUND: Several inflammatory conditions are associated with an increased risk of lymphoma. The specific features of inflammation that mediate this risk are unknown. There are few studies on whether ankylosing spondylitis increases the risk of lymphoma. Besides inflammation-lymphoma aetiology, information on risk of lymphoma in ankylosing spondylitis is particularly important as a benchmark in the evaluation of, for example, tumour necrosis factor inhibitors. METHODS: The association between ankylosing spondylitis and malignant lymphomas overall, and separately for non-Hodgkin's lymphoma, Hodgkin's lymphoma and chronic lymphocytic leukaemia, was assessed in a nationwide, population-based case-control study of 50 615 cases of lymphoma and 92 928 matched controls by using prospectively recorded data on lymphomas from the Swedish Cancer Register (1964-2000) and data on pre-lymphoma hospitalisations for ankylosing spondylitis from the Swedish Inpatient Register (1964-2000). The odds ratios (ORs) associated with pre-lymphoma hospitalisation for ankylosing spondylitis were calculated using conditional logistic regression. RESULTS: 23 (0.05%) patients with lymphoma and 41 (0.05%) controls had a pre-lymphoma hospitalisation listing ankylosing spondylitis, relative risk = 1.0 (95% confidence interval (CI) 0.6 to 1.7). The number of discharges and the mean latency between ankylosing spondylitis and lymphoma were similar in patients and controls. Analyses restricted to lymphomas diagnosed during the 1990s showed similar results (OR = 1.3, 95% CI 0.6 to 2.5, number of exposed cases/controls = 14/21). CONCLUSIONS: On average and in the absence of tumour necrosis factor inhibitors, patients hospitalised with ankylosing spondylitis do not appreciably show an increased risk of lymphoma.