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61.
  • Ludvigsson, Jonas F., 1969-, et al. (författare)
  • Risk of Infections Among 2100 Individuals with IgA Deficiency : a Nationwide Cohort Study
  • 2016
  • Ingår i: ; 36:2, s. 134-140
  • Tidskriftsartikel (refereegranskat)abstract
    • To explore the risk of infections in individuals with IgA deficiency compared to general population controls.In this nationwide prospective population-based cohort study, we used data on IgA levels (< 0.07 g/L) from six university hospitals in Sweden to identify 2100 individuals with IgA deficiency. Individuals were diagnosed between 1980 and 2010. For each patient with IgA deficiency we identified 10 controls from the general population, matched on age, sex, and place of residence (n = 18,653). Data on infections were obtained from the Swedish National Patient Register (including inpatient and hospital-based outpatient care) between 2001 and 2010. We defined infections as having a record of a relevant international classification of disease (ICD) code. Prevalences and prevalence ratios (PRs) were calculated.Individuals with IgA deficiency were more likely to have a record of any infection (36.1 vs. 18.8 % in controls) corresponding to a PR of 2.4 (95%CI 2.2-2.6). We also noted statistically significant associations with IgA deficiency (all P-values < 0.05) and respiratory tract infections (17.8 vs. 6.3 % in controls; PR = 3.2), gastrointestinal infections (6.0 vs. 1.8 % in controls; PR = 3.5), skin infections (4.1 vs. 2.2 % in controls; PR = 1.9), joint infections (0.48 vs. 0.24 % in controls; PR = 2.0; P = 0.052), sepsis (1.5 vs. 0.45 % in controls; PR = 3.4), meningitis (0.38 vs. 0.12 %, PR = 3.2), mastoiditis/otitis (2.1 vs. 1.1 % in controls; PR = 2.0), and urinary tract infections (6.1 vs. 3.4 % in controls; PR = 1.8).Individuals with IgA deficiency are at an increased risk of infections requiring hospital care.
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62.
  • Ludvigsson, Jonas F., et al. (författare)
  • Small-intestinal histopathology and mortality risk in celiac disease
  • 2009
  • Ingår i: Journal of the American Medical Association (JAMA). - 0098-7484 .- 1538-3598. ; 302:11, s. 1171-1178
  • Tidskriftsartikel (refereegranskat)abstract
    • CONTEXT: Studies of mortality in celiac disease have not taken small-intestinal pathology into account. OBJECTIVE: To examine mortality in celiac disease according to small-intestinal histopathology. DESIGN, SETTING, AND PATIENTS: Retrospective cohort study. We collected data from duodenal/jejunal biopsies taken between July 1969 and February 2008 on celiac disease (Marsh stage 3: villous atrophy; n = 29,096 individuals) and inflammation (Marsh stage 1-2; n = 13,306) from all 28 pathology departments in Sweden. A third cohort consisted of individuals with latent celiac disease from 8 university hospitals (n = 3719). Latent celiac disease was defined as positive celiac disease serology in individuals with normal mucosa (Marsh stage 0). Through linkage with the Swedish Total Population Register, we estimated the risk of death through August 31, 2008, compared with age- and sex-matched controls from the general population. MAIN OUTCOME MEASURE: All-cause mortality. RESULTS: There were 3049 deaths among patients with celiac disease, 2967 with inflammation, and 183 with latent celiac disease. We found an increased hazard ratio (HR) for death in celiac disease (HR, 1.39; 95% confidence interval [CI], 1.33-1.45; median follow-up, 8.8 years), inflammation (HR, 1.72; 95% CI, 1.64-1.79; median follow-up, 7.2 years), and latent celiac disease (HR, 1.35; 95% CI, 1.14-1.58; median follow-up, 6.7 years). The absolute mortality rate was 10.4 (95% CI, 10.0-10.8) per 1000 person-years in celiac disease, 25.9 (95% CI, 25.0-26.8) in inflammation, and 6.7 (95% CI, 5.7-7.6) in latent celiac disease. Excess mortality was 2.9 per 1000 person-years in celiac disease, 10.8 in inflammation, and 1.7 in latent celiac disease. This risk increase was also seen in children. Excluding the first year of follow-up, HRs decreased somewhat. CONCLUSION: Risk of death among patients with celiac disease, inflammation, or latent celiac disease is modestly increased.
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63.
  • Ludvigsson, Jonas F., et al. (författare)
  • Symptoms and signs in individuals with serology positive for celiac disease but normal mucosa
  • 2009
  • Ingår i: BMC Gastroenterology. - 1471-230X .- 1471-230X. ; 9, s. 57-
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Antibody serology is an important tool in the investigation of celiac disease (CD), but does not always correlate with mucosal appearance in the small intestine. Patients with positive CD serology but normal mucosa (Marsh 0) are at increased risk of future CD. In this study we describe a model for identifying and characterizing individuals with normal mucosa but positive CD serology. Such individuals are sometimes referred to as having latent CD. METHODS: The records of ten Swedish pathology departments were used to identify individuals with biopsies indicating normal duodenal/jejunal mucosa. Using the national personal identification number, these data were linked with CD serology data (antigliadin, antiendomysial and tissue transglutaminase antibodies); and we thereby identified 3,736 individuals with normal mucosa but positive CD serology. Two independent reviewers then manually reviewed their biopsy reports to estimate comorbidity. We also randomly selected 112 individuals for validation through patient chart review. RESULTS: The majority of the 3,736 individuals were females (62%). Children (0-15 years) made up 21.4%. The median number of biopsy specimen was 3. Our review of biopsy reports found that other gastrointestinal comorbidity was rare (inflammatory bowel disease: 0.4%; helicobacter pylori infection: 0.2%). Some 22% individuals selected for patient chart review had a relative with CD. The most common symptoms among these individuals were diarrhea (46%) and abdominal pain (45%), while 26% had anemia. Although 27% of the individuals selected for validation had been informed about gluten-free diet, only 13% were adhering to a gluten-free diet at the end of follow-up. CONCLUSION: Individuals with positive CD serology but normal mucosa often have CD-like symptoms and a family history of CD.
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64.
  • Ludvigsson, Jonas F., et al. (författare)
  • Validation study of villous atrophy and small intestinal inflammation in Swedish biopsy registers
  • 2009
  • Ingår i: BMC Gastroenterology. - 1471-230X .- 1471-230X. ; 9, s. 19-
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Small intestinal biopsy with villous atrophy (VA) is the gold standard for the diagnosis of celiac disease (CD). We validated VA (Marsh 3) and small intestinal inflammation without VA (Marsh 1+2) in Swedish regional biopsy registers. METHODS: All pathology departments in Sweden (n = 28) were searched to identify individuals with VA or duodenal/jejunal inflammation. The validation consisted of blinded examination of biopsy samples, manual review of biopsy reports, web surveys, and patient chart reviews of 121 individuals with VA and 39 with inflammation. RESULTS: We identified 29,148 individuals with VA and 13,446 individuals with inflammation. In a blinded examination, Swedish pathologists correctly classified 90% of biopsies with VA. Manual screening of 1,534 biopsy reports (performed by co-author JFL and a research assistant) found that comorbidity other than CD was rare. IBD was the most common comorbidity and occurred in 0.3% of biopsies with VA (1.6% in inflammation). Among 114 patients with VA and available data, 108 (95%) had a clinical diagnosis of CD. 79% of the validated individuals with VA and 64% of those with inflammation had documented gastrointestinal symptoms prior to biopsy. 88% of the validated individuals with VA had positive CD serology before their first biopsy. 172/180 (96%) of Swedish gastroenterologists and 68/68 (100%) of pediatricians perform a small intestinal biopsy in at least 9 out of 10 individuals prior to diagnosis of CD. CONCLUSION: Regional biopsy data are feasible to identify individuals with CD and small-intestinal inflammation. The specificity of CD is high in villous atrophy.
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65.
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66.
  • Mollazadegan, Kaziwe, et al. (författare)
  • Increased risk of uveitis in coeliac disease : a nationwide cohort study
  • 2012
  • Ingår i: ; 96:6, s. 857-861
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Case reports suggest a potential association between coeliac disease (CD) and uveitis, but larger well-controlled studies are lacking. The aim of this study was therefore to examine the risk of uveitis in patients with biopsy-verified CD.Methods: Small intestinal biopsy reports performed between July 1969 and February 2008 were collected from all (n-28) pathology departments in Sweden. From these reports, 29 044 patients with CD (equals villous atrophy, Marsh 3) were identified. Uveitis was defined according to relevant International Classification of Disease codes in the Swedish National Patient Register. Cox regression was used to estimate HR for uveitis in individuals with CD compared with those in reference individuals matched for age, sex, county and calendar year.Results: During follow-up, 148 patients with CD developed uveitis (expected count 112), corresponding to a HR of 1.32 (95% CI 1.10 to 1.58). The absolute risk of uveitis was 50/100 000 person-years in CD. The risk estimate did not change more than marginally when adjusted for type 1 diabetes, rheumatoid arthritis and autoimmune thyroid disease (HR 1.30; 95% CI 1.08 to 1.56). The risk of uveitis remained significantly increased even 5 years after CD diagnosis (HR 1.31; 95% CI 1.04 to 1.64).Conclusion: A moderately increased risk of uveitis was found in patients with biopsy- verified CD. CD might be considered in patients with uveitis of unknown aetiology.
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67.
  • Nordwall, Maria, et al. (författare)
  • Early diabetic complications in a population of young patients with Type 1 diabetes mellitus despite intensive treatment
  • 2006
  • Ingår i: Journal of Pediatric Endocrinology & Metabolism. - 0334-018X. ; 19:1, s. 45-54
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: To describe the prevalence of early complications in an unselected population of patients with type 1 diabetes mellitus (DM1) diagnosed in childhood with intensive insulin treatment from diagnosis.Methods: Eighty children and adolescents with DM1, age 7-22 years and DM1 duration >3 years, were studied. Neuropathy was defined as abnormal nerve conduction finding in ≥2 of 4 nerves (sural and peroneal nerves), nephropathy as albumin excretion rate ≥20 μg/min and retinopathy as all grades of retinal changes in fundus photographs.Results: The prevalence of neuropathy was 59%, of retinopathy 27% and of nephropathy 5% after 13 years DM1 duration. Mean (SD) long-term HbA1c was 8.4 (0.9)% (DCCT-corrected value).Conclusion: Even in a population with intensive insulin treatment from the beginning and fairly good metabolic control, the prevalence of subclinical neuropathy was high, while other diabetic complications were lower than usually reported.
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68.
  • Ortqvist, E., et al. (författare)
  • Temporary preservation of beta-cell function by diazoxide treatment in childhood type 1 diabetes
  • 2004
  • Ingår i: Diabetes Care. - 0149-5992. ; 27:9, s. 2191-7
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: We examined the effect of diazoxide, an ATP-sensitive K(+) channel opener and inhibitor of insulin secretion, on beta-cell function and remission in children at clinical onset of type 1 diabetes. RESEARCH DESIGN AND METHODS: A total of 56 subjects (21 girls and 35 boys, age 7-17 years) were randomized to 3 months of active treatment (diazoxide 5-7.5 mg/kg in divided doses) or placebo in addition to multiple daily insulin injections and were followed for 2 years. RESULTS: Diazoxide decreased circulating C-peptide concentrations by approximately 50%. After cessation of the treatment, basal and meal-stimulated C-peptide concentrations increased to a maximum at 6 months, followed by a decline. Meal-stimulated C-peptide concentration was significantly higher at 12 months (0.43 +/- 0.22 vs. 0.31 +/- 0.26 nmol/l, P = 0.018) and tended to fall less from clinical onset to 24 months in the diazoxide- vs. placebo-treated patients (-0.05 +/- 0.24 vs. -0.18 +/- 0.26 nmol/l, P = 0.064). At 24 months, the meal-stimulated C-peptide concentrations were 0.24 +/- 0.20 and 0.20 +/- 0.17 nmol/l, respectively. Side effects of diazoxide were prevalent. CONCLUSIONS: This study demonstrates that partial inhibition of insulin secretion for 3 months at onset of childhood type 1 diabetes suspends the period of remission and temporarily preserves residual insulin production. Further evaluation of the full potential of beta-cell rest will require compounds with less side effects as well as protocols optimized for sustained secretory arrest.
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69.
  • Sherry, Nicole, et al. (författare)
  • Teplizumab for treatment of type 1 diabetes (Protege study): 1-year results from a randomised, placebo-controlled trial
  • 2011
  • Ingår i: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 378:9790, s. 487-497
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Findings of small studies have suggested that short treatments with anti-CD3 monoclonal antibodies that are mutated to reduce Fc receptor binding preserve beta-cell function and decrease insulin needs in patients with recent-onset type 1 diabetes. In this phase 3 trial, we assessed the safety and efficacy of one such antibody, teplizumab. less thanbrgreater than less thanbrgreater thanMethods In this 2-year trial, patients aged 8-35 years who had been diagnosed with type 1 diabetes for 12 weeks or fewer were enrolled and treated at 83 clinical centres in North America, Europe, Israel, and India. Participants were allocated (2:1:1:1 ratio) by an interactive telephone system, according to computer-generated block randomisation, to receive one of three regimens of teplizumab infusions (14-day full dose, 14-day low dose, or 6-day full dose) or placebo at baseline and at 26 weeks. The Protege study is still underway, and patients and study staff remain masked through to study closure. The primary composite outcome was the percentage of patients with insulin use of less than 0.5 U/kg per day and glycated haemoglobin A(1c) (HbA(1c)) of less than 6-5% at 1 year. Analyses included all patients who received at least one dose of study drug. This trial is registered with ClinicalTrials.gov, number NCT00385697. less thanbrgreater than less thanbrgreater thanFindings 763 patients were screened, of whom 516 were randomised to receive 14-day full-dose teplizumab (n=209), 14-day low-dose teplizumab (n=102), 6-day full-dose teplizumab (n=106), or placebo (n=99). Two patients in the 14-day full-dose group and one patient in the placebo group did not start treatment, so 513 patients were eligible for efficacy analyses. The primary outcome did not differ between groups at 1 year: 19.8% (41/207) in the 14-day full-dose group; 13.7% (14/102) in the 14-day low-dose group; 20.8% (22/106) in the 6-day full-dose group; and 20.4% (20/98) in the placebo group. 5% (19/415) of patients in the teplizumab groups were not taking insulin at 1 year, compared with no patients in the placebo group at 1 year (p=0.03). Across the four study groups, similar proportions of patients had adverse events (414/417 [99%] in the teplizumab groups vs 98/99 [99%] in the placebo group) and serious adverse events (42/417 [10%] vs 9/99 [9%]). The most common clinical adverse event in the teplizumab groups was rash (220/417 [53%] vs 20/99 [20%] in the placebo group). less thanbrgreater than less thanbrgreater thanInterpretation Findings of exploratory analyses suggest that future studies of immunotherapeutic intervention with teplizumab might have increased success in prevention of a decline in beta-cell function (measured by C-peptide) and provision of glycaemic control at reduced doses of insulin if they target patients early after diagnosis of diabetes and children.
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70.
  • Song, Mingyang, et al. (författare)
  • Risk of colorectal cancer incidence and mortality after polypectomy : a Swedish record-linkage study
  • 2020
  • Ingår i: The Lancet Gastroenterology & Hepatology. - : Elsevier. - 2468-1253. ; 5:6, s. 537-547
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Long-term colorectal cancer incidence and mortality after colorectal polyp removal remains unclear. We aimed to assess colorectal cancer incidence and mortality in individuals with removal of different histological subtypes of polyps relative to the general population.Methods: We did a matched cohort study through prospective record linkage in Sweden in patients aged at least 18 years with a first diagnosis of colorectal polyps in the nationwide gastrointestinal ESPRESSO histopathology cohort (1993-2016). For each polyp case, we identified up to five matched reference individuals from the Total Population Register on the basis of birth year, age, sex, calendar year of biopsy, and county of residence. We excluded patients and reference individuals with a diagnosis of colorectal cancer either before or within the first 6 months after diagnosis of the index polyp. Polyps were classified by morphology codes into hyperplastic polyps, sessile serrated polyps, tubular adenomas, tubulovillous adenomas, and villous adenomas. Colorectal cancer cases were identified from the Swedish Cancer Registry, and cause-of-death data were retrieved from the Cause of Death Register. We collected information about the use of endoscopic examination before and after the index biopsy from the Swedish National Patient Registry, and counted the number of endoscopies done before and after the index biopsies. We calculated cumulative risk of colorectal cancer incidence and mortality at 3, 5, 10, and 15 years, and computed hazard ratios (HRs) and 95% CIs for colorectal cancer incidence and mortality using a stratified Cox proportional hazards model within each of the matched pairs.Findings: 178 377 patients with colorectal polyps and 864 831 matched reference individuals from the general population were included in our study. The mean age of patients at polyp diagnosis was 58.6 (SD 13.9) years for hyperplastic polyps, 59.7 (14.2) years for sessile serrated polyps, 63.9 (12.9) years for tubular adenomas, 67.1 (12.1) years for tubulovillous adenomas, and 68.9 (11.8) years for villous adenomas. During a median of 6.6 years (IQR 3.0-11.6) of follow-up, we documented 4278 incident colorectal cancers and 1269 colorectal cancer-related deaths in patients with a polyp, and 14 350 incident colorectal cancers and 5242 colorectal cancer deaths in general reference individuals. The 10-year cumulative incidence of colorectal cancer was 1.6% (95% CI 1.5-1.7) for hyperplastic polyps, 2.5% (1.9-3.3) for sessile serrated polyps, 2.7% (2.5-2.9) for tubular adenomas, 5.1% (4.8-5.4) for tubulovillous adenomas, and 8.6% (7.4-10.1) for villous adenomas compared with 2.1% (2.0-2.1) in reference individuals. Compared with reference individuals, patients with any polyps had an increased risk of colorectal cancer, with multivariable HR of 1.11 (95% CI 1.02-1.22) for hyperplastic polyps, 1.77 (1.34-2.34) for sessile serrated polyps, 1.41 (1.30-1.52) for tubular adenomas, 2.56 (2.36-2.78) for tubulovillous adenomas, and 3.82 (3.07-4.76) for villous adenomas (p<0.05 for all polyp subtypes). There was a higher proportion of incident proximal colon cancer in patients with serrated (hyperplastic and sessile) polyps (52-57%) than in those with conventional (tubular, tubulovillous, and villous) adenomas (30-46%). For colorectal cancer mortality, a positive association was found for sessile serrated polyps (HR 1.74, 95% CI 1.08-2.79), tubulovillous adenomas (1.95, 1.69-2.24), and villous adenomas (3.45, 2.40-4.95), but not for hyperplastic polyps (0.90, 0.76-1.06) or tubular adenomas (0.97, 0.84-1.12).Interpretation: In a largely screening-naive population, compared with individuals from the general population, patients with any polyps had a higher colorectal cancer incidence, and those with sessile serrated polyps, tubulovillous adenomas, and villous adenomas had a higher colorectal cancer mortality.
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