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OBJECTIVE: To describe the frequency of symptoms and associated conditions among screening-detected celiac disease (CD) cases and non-CD children and to evaluate questionnaire-based case-finding targeting the general population. METHODS: In a population-based CD screening of 12-year-olds, children and their parents completed questionnaires on CD-associated symptoms and conditions before knowledge of CD status. Questionnaire data for those who had their CD detected in the screening (n = 153) were compared with those of children with normal levels of CD markers (n = 7016). Hypothetical case-finding strategies were also evaluated. Questionnaires were returned by 7054 (98%) of the children and by 6294 (88%) of their parents. RESULTS: Symptoms were as common among screening-detected CD cases as among non-CD children. The frequency of children with screening-detected CD was similar when comparing the groups with and without any CD-related symptoms (2.1% vs 2.1%; P = .930) or CD-associated conditions (3.6% vs 2.1%; P = .07). Case-finding by asking for CD-associated symptoms and/or conditions would have identified 52 cases (38% of all cases) at a cost of analyzing blood samples for 2282 children (37%) in the study population. CONCLUSIONS: The current recommended guidelines for finding undiagnosed CD cases, so-called active case-finding, fail to identify the majority of previously undiagnosed cases if applied in the general population of Swedish 12-year-olds. Our results warrant further studies on the effectiveness of CD case-finding in the pediatric population, both at the clinical and population-based levels.

OBJECTIVES. Sweden experienced a unique epidemic of celiac disease in children METHODS. A population-based incidence register of celiac disease in children covering the entire nation from 1998 to 2003 and part of the country back to 1973 was analyzed. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition diagnostic criteria for celiac disease were used. The annual incidence rate for each age group and the cumulative incidence according to age for each birth cohort were calculated. RESULTS. A considerable difference in cumulative incidences of celiac disease at comparable ages was demonstrated between birth cohorts from the epidemic and postepidemic periods. The difference persisted during the preschool years, although it decreased somewhat with age. During the last years of the follow-up period, there was again a successive increase in incidence rate among children CONCLUSIONS. The difference in celiac disease risk between birth cohorts at comparable ages suggests an opportunity for primary prevention. This highlights the importance of further exploring the role of infant feeding and exogenous factors besides dietary gluten that might initiate or prevent disease development. Moreover, on the basis of postepidemic incidence trends, we speculate that the Swedish epidemic might not have been as unique as thought previously, although its magnitude was striking.

Objective. The study was designed to investigate the prevalence of celiac disease (CD) among 2.5-year-old children in a Swedish urban population with a high incidence of CD. Material and Methods. Six hundred ninety apparently healthy children, born in the 12-month period of July 1992 through June 1993, were screened for immunoglobulin A (IgA) antigliadin antibodies and IgA antiendomysium antibodies, and those antibody-positive at repeated testing were further investigated with intestinal biopsy. Results. Of the 690 children, 6 were both IgA antigliadin antibody- and IgA antiendomysium antibody-positive, and 7 were antiendomysium antibody-positive but antigliadin antibody-negative. Jejunal biopsy, performed in 12 cases, manifested partial or total villous atrophy in 8 cases. Thus, together with an additional child whose parents declined the offered biopsy, but whose response to a gluten-free diet confirmed the presence of CD, the prevalence of CD in the study series was 1.3% (9/690; 95% confidence interval: .4–2.2). However, independent of the study, an additional 22 cases of symptomatic, biopsy-verified CD have already been detected in the birth cohort of 3004 children. Conclusions. The prevalence of CD in our study series was high, at least 1.0%, but may be as high as 2.0% if the frequency of silent CD is as high as we have found in the remaining unscreened cohort. These findings confirm that CD is one of the most common chronic disorders.

Objective. This study was conducted to investigate the prevalence of celiac disease (CD) in children and adolescents at diagnosis of insulin-dependent diabetes mellitus (IDDM) before insulin treatment was started. Material and Methods. At diagnosis of IDDM, and before treatment was started, 115 children and adolescents were screened for IgA- antiendomysium (EMA) and IgA-antigliadin antibodies (AGA). Those found to be EMA-positive and/or AGA-positive were investigated further with intestinal biopsy. Results. Of the 115 patients, 2 had known CD at diagnosis of IDDM; of the remainder of patients, 6% (7/113) were found to be EMA-positive and 9% (10/113) were found to have AGA levels above normal. Of the 6 patients who underwent biopsy, 5 manifested villous atrophy. In addition, 2 patients with high EMA and AGA antibody titers refused biopsy, and 4 patients with low EMA and/or AGA titers were found to have normal titers at control before biopsy decision. Conclusion. Because the prevalence of CD at diagnosis of IDDM would seem to be 6% to 8%, screening for CD seems to be justified among patients with newly diagnosed IDDM.

Objective. This study was undertaken to investigate the prevalence of celiac disease in children and adolescents with Down syndrome. Material and Methods. Forty-three children and adolescents with Down syndrome were screened for IgA-antigliadin antibodies (AGA) and IgA-antiendomysium antibodies (EMA). Patients found to be either AGA- or EMA-positive were investigated further with intestinal biopsy. Results. None of the 43 patients had known celiac disease at entry into the study; 37% (16/43) were found to have AGA levels above normal, and 16% (7/43) to be EMA-positive. Of the 15 patients who underwent biopsy, 8 manifested villous atrophy. Villous atrophy was present in all 7 of the EMA-positive patients, whereas the villi were normal in 7 of the 13 AGA-positive patients who underwent biopsy. Conclusions. EMA is a good immunologic marker for use in screening for celiac disease, and screening is justified in patients with Down syndrome.

OBJECTIVES: Between 1984 and 1996, Sweden experienced an “epidemic” of clinical celiac disease in children METHODS: A 2-phase cross-sectional screening study was performed in which 13 279 children from 2 birth cohorts participated: children born during the epidemic (1993) and children born after the epidemic (1997). Previously diagnosed cases were reported and confirmed. Blood samples were analyzed for serological markers and children with positive values were referred for small intestinal biopsy. Infant feeding practices in the cohorts were ascertained via questionnaires. Prevalence comparisons were expressed as prevalence ratios. RESULTS: The total prevalence of celiac disease was 29 in 1000 and 22 in 1000 for the 1993 and 1997 cohorts, respectively. Children born in 1997 had a significantly lower risk of having celiac disease compared with those born in 1993 (prevalence ratio: 0.75; 95% confidence interval: 0.60–0.93; P = .01). The cohorts differed in infant feeding (specifically, in the proportion of infants introduced to dietary gluten in small amounts during ongoing breastfeeding). CONCLUSIONS: A significantly reduced prevalence of celiac disease in 12-year-olds indicates an option for disease prevention. Our findings suggest that the present infant feeding recommendation to gradually introduce gluten-containing foods from 4 months of age, preferably during ongoing breastfeeding, is favorable.

OBJECTIVES: To investigate if changes in the national Swedish vaccination program coincided with changes in the celiac disease (CD) incidence rate in infants (ie, the Swedish CD Epidemic), and to assess the potential association between these vaccinations and CD risk. METHODS: All studies were based on the National Swedish Childhood Celiac Disease Register. Using an ecological approach, we plotted changes over time in the national vaccination program in the graph displaying CD incidence rate. A population-based incident case-referent study of invited infants was performed. Exposure information was received through a questionnaire and child health clinic records. Vaccines explored were diphtheria/tetanus, pertussis (acellular), polio (inactivated), Haemophilus influenzae type b (conjugated), measles/mumps/rubella, and live attenuated bacillus Calmette-Guérin (BCG) in children with increased tuberculosis risk. Findings were subjected to a birth cohort analysis. RESULTS: Introduction of pertussis vaccine coincided in time with decreasing CD incidence rates. In the infant case-referent study, however, neither vaccination against pertussis (odds ratio 0.91; 95% confidence interval 0.60–1.4), nor against Haemophilus influenzae type b or measles/mumps/rubella was associated with CD. Coverage for the diphtheria/tetanus and polio vaccines was 99%. BCG was associated with reduced risk for CD (adjusted odds ratio 0.54; 95% confidence interval 0.31–0.94). Discontinuation of general BCG vaccination did not affect the cumulative incidence of CD at age 15 years. CONCLUSIONS: Early vaccinations within the national Swedish program were not associated with CD risk, nor could changes in the program explain the Swedish epidemic. A protective effect by BCG was suggested, which could be subject to further studies.

Objective. This study was designed to determine whether a relationship exists between previ- ous exposure to measles, mumps, and rubella (MMR) by natural infection or vaccination or by new immunization with MMR vaccine, and either the presence or levels of autoantibodies against thyroid cell and pancreatic b-cell antigens. Methods. Antibodies against MMR and autoantibod- ies against thyroglobulin, thyroid peroxidase, pancreas islet cells (ICA), islet cell surface, glutamic acid decar- boxylase 65k autoantibodies, and insulin were studied before, and 3 months after, vaccination with combined MMR vaccine in 386 school children between 11 and 13 years of age. Results. The vaccination changed neither the preva- lence nor the level of autoantibodies. Children with ru- bella antibodies before vaccination had higher levels of ICA than did the rubella seronegative children. In con- trast, thyroid autoantibody levels and prevalence were lower in children with antibodies against measles, mumps, or both before vaccination than in children with- out those antibodies. Conclusions. Previous natural infection or vaccina- tion against measles, mumps, or both seemed to have an inhibitory effect on the development of thyroid autoan- tibodies. In contrast, children with previous exposure to rubella had higher levels of ICA. No evidence was found that MMR vaccination during adolescence may trigger autoimmunity. Pediatrics 1999;104(1). URL: http://www. pediatrics.org/cgi/content/full/104/1/e12; autoantibodies, thyroiditis, type 1 diabetes mellitus, vaccination, virus. ABBREVIATIONS. AIT, autoimmune thyroiditis; Tg-ab, thyro- globulin autoantibodies; TPO-ab, thyroid peroxidase autoantibod- ies; ICA, pancreas islet cell autoantibodies; GAD65Ab, glutamic acid decarboxylase autoantibodies; IAA, insulin autoantibodies; CRS, congenital rubella syndrome; ICSA, islet cell surface autoan- tibodies; GAD65Ab, glutamic acid decarboxylase 65k autoanti- bodies; MMR, measles, mumps, and rubella; JDF, Juvenile Diabe- tes Foundation; IgG, immunoglobulin G. n the majority of cases, children with autoim- mune diseases such as autoimmune thyroiditis (AIT) or insulin-dependent type 1 diabetes melli- tus are characterized by the absence of any first degree relative with the disease in question. 1 The prevalence of autoimmune markers associated with these disorders in children is higher than the preva- lence of the respective diseases. It is unclear when and why autoantibodies are acquired and what in- duces the progress of disease in the individual pa- tient. At clinical diagnosis of AIT, 93% to 95% of the patients have at least one of the thyroglobulin auto- antibodies (Tg-ab) or thyroid peroxidase autoanti- bodies (TPO-ab). 2,3 Of patients with newly diagnosed type 1 diabetes mellitus, 80% to 90% have islet cell

Microcephaly and its etiology were studied in an unselected Swedish urban infant population. Virtually, all live-born infants (14,724) born between October 1977 and December 1983 in the city of Malmö, Sweden, were included in the study. Special attention was given to the role of congenital infections, particularly to cytomegalovirus infection. The infant population was studied from two points of view. One part of the study was prospective and based on regular cytomegalovirus isolation in urine within the first week of life. About 80% of the newborns were adequately studied by this test. None of 56 infants shown to be cytomegalovirus excreters (congenitally infected) and followed up were born with or developed microcephaly (head circumference smaller than 3 SD below the mean for age and sex) during the first 1 to 7 years of life. However, two of the 56 infants had a head circumference of –2 SD. In the beginning of 1985, an inventory was made of the presence of symptomatic microcephaly in the abovementioned population still living in the city or deceased there. Of about 10,000 such children, 12 were found to have symptomatic microcephaly. By studies of personal, clinical, and laboratory data and by retrospective serologic studies of frozen pre- and postconceptional maternal sera, a possible explanation or a recognized syndrome was obtained in ten of the 12 cases. In one of them, the mother had a primary cytomegalovirus infection, possibly in early pregnancy. Although the infant had symptoms compatible with a congenital infection, no laboratory evidence of transmitted infection was found. In no case were congenital rubella virus or Toxoplasma gondii infections suspected.

A prospective study of congenital cytomegalovirus infection in Malmö, Sweden, was performed from 1977 through 1985. The diagnosis was based on isolation of cytomegalovirus soon after birth. Congenital cytomegalovirus infection was identified in 76 infants, and as of September 1986 CNS symptoms have been experienced by nine of them. In at least seven of these infants, the disturbances can be referred to the cytomegalovirus infection. The strains from eight of the nine infants have been further studied by restriction endonuclease analysis of cytomegalovirus DNA. The cleavage patterns obtained with BamHI, EcoRI, and HindIII showed a unique pattern for each one of the eight strains. No common pattern could be associated with these eight strains in comparison with strains from postnatally infected children.