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- Grodzinsky, Ewa, 1958-, et al.
(author)
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IgA endomysium antibodies : an early predictor for celiac disease in children without villous atrophy
- 2008
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In: Acta Paediatrica. - : Wiley. - 0803-5253 .- 1651-2227. ; 97:7, s. 972-976
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Journal article (peer-reviewed)abstract
- Aim: To evaluate possible differences between children with anti-endomysium antibodies (EMA) positivity and normal small bowel mucosa and children with positive EMA and an enteropathy diagnosed as celiac disease (CD).Methods: Children with suspected CD and positive EMA (≥1/10) undergoing small bowel biopsy during 1996 to 2002, were investigated (n = 133). Data registered were: year and month of birth, timing of the first biopsy, sex, heredity for CD, dermatitis herpetiformis and diabetes mellitus and outcome of the anti-gliadin antibody test (AGA). The case group, with EMA positivity and normal histology (n = 39; 59% female, mean age at the first biopsy 7.3 years, range 1.4–16), was compared with the disease control group, with positive EMA and a biopsy suggestive and further on diagnosed as CD (n = 94; 56% female; mean age 7.6 years at the first biopsy, range 0.70–17).Results: AGA positivity and heredity for CD were found to predict the outcome of a pathological jejunal mucosa. Nineteen of the 39 children in the case group were rebiopsied of whom 11 had developed an enteropathy during a follow-up period of 2–7 years (median 4.5 years).Conclusions: EMA positivity in the absence of small bowel enteropathy could be a very early predictor for later overt CD, and necessitates further follow-up, especially if the child is AGA positive and there is a family history of CD.
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| 3. |
- Laurin, Pia, 1969-
(author)
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Clinical and epidemiological aspects of childhood celiac disease
- 2002
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Doctoral thesis (other academic/artistic)abstract
- Background: Celiac disease (CD) is one of the most common chronic diseases in childhood in many countries. It is a small intestinal disease, caused by gluten in genetically predisposed individuals, but underlying immunological mechanisms are not exactly known. Gluten is found in wheat, rye and barley, and possibly in oats. The clinical presentation of CD varies from overt to no symptoms at all. Treatment with gluten free diet (GFD) heals the mucosa and symptoms disappear. The varying clinical presentation makes the evaluation of the "true" prevalence difficult. When screening with serum antibodies, similar prevalence is found in several countries. The reported increase of clinically detected cases among Swedish children in the mid 1980s attracted much interest and was publicly debated. Infant feeding changes was focused on, but new diagnostic tools were also introduced during this period.Aims: To describe epidemiological changes in the county of Östergötland from 1980 to 2001. To analyse the possible influence of diagnostic activity and accuracy and the possible influence of certain infant feeding patterns on disease occurrence. To study gluten intake, clinical, histological and immunological parameters during gluten challenge. To evaluate the practical usefulness of the nitric oxide (NO) analysis in CD.Material and methods: All children (0-17.9 years) investigated for suspected CD in the county of Östergötland 1980-2001 were studied regarding disease occurrence, diagnostic activity and accuracy. Data on infant feeding were analysed in 72 CD children and 288 agematched referents. During gluten challenge 25 children were studied regarding gluten intake, serum antibodies, NO products in the urine, clinical symptoms and mucosal histology. NO products were also measured at different stages of CD investigation in !37 children.Results: The incidence rate of CD in small children has fluctuated over the study period. How, or whether, infant feeding and/or diagnostic tools have influenced this is not known.CD children were significantly shorter breastfed, more seldom breastfed at gluten introduction, and started more often with follow-up formula than porridge. This could be interpreted in two ways. Breastfeeding per se could protect against CD, but it is also known that a breastfed baby consumes lower amounts of gluten at the time of introduction. The lower exposure can make symptoms more vague in early childhood and thus postpone the diagnosis.Gluten intake during challenge varied a lot. Some CD children reacted to minute amounts of gluten. Despite the small amounts given, all children showed signs of relapse at a clinical, serological, or histological level.CD children on a gluten containing diet have significantly higher levels of NO products in the urine, compared to reference children and to CD children on a GFD. NO products increased during gluten challenge, and doubled within four weeks of challenge. This is probably caused by iNOS activation and increased NO production in the diseased intestinal mucosa.Conclusions: How, or whether, changes in infant feeding and/or new diagnostic tools influenced the fluctuating incidence of the disease is not known. Very small amounts of gluten caused relapse in CD children. NO products in the urine were elevated in CD children on a gluten diet, and doubled within four weeks of gluten challenge. NO analysis is simple and non-traumatic for the child, and could be of value as a diagnostic tool in celiac disease.
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| 4. |
- Laurin, Pia, 1969-, et al.
(author)
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Even small amounts of gluten cause relapse in children with celiac disease
- 2002
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In: Journal of Pediatric Gastroenterology and Nutrition - JPGN. - : Ovid Technologies (Wolters Kluwer Health). - 0277-2116 .- 1536-4801. ; 34:1, s. 26-30
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Journal article (peer-reviewed)abstract
- Background: Previously, a gluten challenge was customary to establish the diagnosis of celiac disease in children. There are no clear recommendations on how to perform this challenge or what markers to rely on for timing the biopsy after the challenge. The authors' aim was to monitor gluten intake, clinical symptoms, and antibody kinetics to evaluate the influence of gluten exposure during the challenge.Methods: Twenty-five children under investigation for suspected celiac disease were challenged. One child was excluded because blood samples, food records, or biopsy was lacking. Median age at the postchallenge biopsy was 3.8 (2.7-8.8) years. The families kept daily records of the children's gluten intake and of symptoms that occurred. Blood samples were taken monthly for analysis of antigliadin and endomysium antibodies and total immunoglobulin A (IgA). A third biopsy was performed when clinical symptoms suggested a relapse.Results: All 24 children showed deterioration of the mucosa or elevated antibodies during gluten challenge. Median duration of the challenge was 13 (5-51) weeks, and mean gluten intake was 1.7 (0.2-4.3) g/d and 0.1 (0.02-0.26) g/kg daily.Conclusions: Gluten intake during the challenge varied widely, and the parents were unable to give their children the recommended amount. Despite the small amounts given, all children showed signs of relapse at a clinical, laboratory, or histologic level. Much smaller amounts of gluten than previously suggested seem sufficient to cause relapse during gluten challenge in children.
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| 5. |
- Laurin, Pia, 1969-, et al.
(author)
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Increase in nitric oxide urinary products during gluten challenge in children with coeliac disease
- 2003
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In: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 38:1, s. 55-60
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Journal article (peer-reviewed)abstract
- Background: Coeliac disease is a gluten-sensitive enteropathy where pro-inflammatory cytokines and excess nitric oxide (NO) production can contribute to mucosal damage. NO urinary products are elevated in coeliac children on a gluten diet, but it is not known how rapidly this increase develops after gluten exposure.Methods: Oral gluten challenge was performed in 25 children whose families kept a daily record of gluten intake and symptoms. Blood was analysed monthly for antigliadin (AGA) and endomysium antibodies (EMA). Urine was analysed every second week for NO products, i.e. the sum of nitrite and nitrate was measured with a colorimetric method. We performed a third biopsy when clinical symptoms indicated a relapse. Median age at the post-challenge biopsy was 3.8 (2.7-8.8) years.Results: Signs of morphological or serological relapse were seen in all children. Mean daily gluten intake was 0.10 (range 0.02-0.26) g/kg bodyweight. Median NO level was doubled and significantly higher after 4 weeks of challenge but not after 2 weeks. EMA, but not AGA levels, correlated positively with NO. Intraepithelial lymphocyte count was significantly higher in the post-challenge biopsy, but did not correlate with the NO levels.Conclusions: NO products in urine increased during gluten challenge. EMA levels reflected severity of mucosal damage, and NO products reflected the inflammatory response, which was doubled after 4 weeks of challenge. The NO analysis is simple and non-traumatic for the child. It can be performed repeatedly during investigation of children with suspected coeliac disease.
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| 6. |
- Laurin, Pia, 1969-, et al.
(author)
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Increasing prevalence of coeliac disease in Swedish children : influence of feeding recommendations, serological screening and small intestinal biopsy activity
- 2004
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In: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 39:10, s. 946-952
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Journal article (peer-reviewed)abstract
- Background: The prevalence of coeliac disease (CD) in Swedish children has attracted considerable interest over the past few decades, and especially the influence of feeding habits on the increased incidence. A national study has reported a trend towards a decrease in incidence after a change in infant feeding recommendations was introduced in 1996. The aim of this study was to evaluate, in a geographically defined area, the change in incidence with time and the influence of the introduction of antibody analysis.Methods: Cases of suspected paediatric CD between 1980 and 2003 were studied for prevalence, biopsy findings and antibody analyses.Results: A total of 2029 children were investigated by small intestinal biopsy, yielding 554 CD cases. The area initially showed the same trend as the national study, but the annual incidence rate is now increasing again. Median age at diagnosis has increased significantly since 1997 from less than 2 years of age to above 5 years. Cumulative incidence at 2 years of age is much higher for the birth cohorts 1983–96 than 1980–82 or 1997–2001. Diagnostic accuracy was significantly higher after the introduction of antigliadin (AGA) analysis, and especially after antiendomysium (EMA) analysis.Conclusions: The incidence rate of CD in small children in our region has varied widely over the 24‐year period observed. Feeding practice and methods of investigation have changed during this period. The annual incidence rate for the total child population in 2003 was almost equal to the peak value observed in 1994. There were no conclusive results on whether antibody analysis had an influence on diagnostic activity, but this seems to have increased diagnostic accuracy.
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