Coeliac disease has emerged as a public health problem. The aim of the present study was to analyse trends in the occurrence of symptomatic coeliac disease in Swedish children from 1973 to 1997, and to explore any temporal relationship to changes in infant dietary patterns. We established a population-based prospective incidence register of coeliac disease in 1991, and, in addition, retrospective data from 1973 were collected. A total of 2151 cases fulfilled the diagnostic criteria. Furthermore. We collected national data on a yearly basis on duration of breastfeeding, intake of gluten-containing cereals and recommendations on when and how to introduce gluten into the diet of infants. From 1985 to 1987 the annual incidence rate in children below 2 y of age increased fourfold to 200-240 cases per 100000 person years, followed from 1995 by a sharp decline to the previous level of 50-60 cases per 100000 person years. This epidemic pattern is quite unique for a chronic disease of immunological pathogenesis, suggesting that prevention could be possible. The ecological observations made in this study are compatible with the epidemic being the result, at least in part, of a change in and an interplay among three factors within the area of infant feeding, i.e. amount of gluten given, age at introduction of gluten, and whether breastfeeding was ongoing or not when gluten was introduced. Other factor(s) may also have contributed, and the search for these should be intensified.

Coeliac disease has emerged as a public health problem. The aim of the present study was to analyse trends in the occurrence of symptomatic coeliac disease in Swedish children from 1973 to 1997, and to explore any temporal relationship to changes in infant dietary patterns. We established a population‐based prospective incidence register of coeliac disease in 1991, and, in addition, retrospective data from 1973 were collected. A total of 2151 cases fulfilled the diagnostic criteria. Furthermore, we collected national data on a yearly basis on duration of breastfeeding, intake of gluten‐containing cereals and recommendations on when and how to introduce gluten into the diet of infants. From 1985 to 1987 the annual incidence rate in children below 2 y of age increased fourfold to 200‐240 cases per 100 000 person years, followed from 1995 by a sharp decline to the previous level of 50‐60 cases per 100 000 person years. This epidemic pattern is quite unique for a chronic disease of immunological pathogenesis, suggesting that prevention could be possible. The ecological observations made in this study are compatible with the epidemic being the result, at least in part, of a change in and an interplay among three factors within the area of infant feeding, i.e. amount of gluten given, age at introduction of gluten, and whether breastfeeding was ongoing or not when gluten was introduced. Other factor(s) may also have contributed, and the search for these should be intensified.

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1 Bchildrm vlu fullfilled the criteria of chrrnic mn-gzcific diarrhea of i n f q wre evaluated for intestinal bacterial ow?qmdh as a use of *their diarrka.& children e r e -zed into gm@ I (=lo), rto were treated with trirrethprim wlfm?thmazole (TW) SKI -11 (~5 1 , three childrm were excllxled becase of Yersinia entemlitica infect~n)treated with lau lirtase diet cnly. The aim of the st* as to investigate hther mlmlzatim of the d l intestire with w r respiratory tract micmflora was related to the d i a r h ard if treatrmt rnth R.0( resolved the diai-rka. MTHDS. Strlngtest (Enterntest Pediatri&) ove-of the snall intestine (>105cfu/ml) with W r rrspiratory t x t micruflora. Alpha hasrolytic streptrmcci dminated in all but ale string. In nine of ten childm~ in gru&~ I the diarrhea resolved irmediately khile the diarrhea persisted in all childrm in -11. All childrm i both graps M d e q~t e calorie d fat inM. CO\CLVSICNS. The results injicate that bafterial oveqmvth of thz d l intestire ~ith pper respiratory tract micmflora my t~ a cause of chrrnlc mrcspeciflc djar rka ad that this d i a r M c m be treated m f u l l y with W.There are several causes to infantile colic. We have shown that bovine whey protein via the mother's milk can provoke infantile colic in breast-fed infants, and that formula-fed colicky infants can become symptom free on CM-free diet. The aim of this study was to evaluate,under controlled conditions, the effect of bovine whey protein given to colicky infants. We found in 24 out of 27 infants with severe colic that the symptoms disappeared when they were given a CM-Free diet (~utramigenj.' The mean age for colic debut was 6.4 weeks. These 24 infants were entered into a double-blind cross-over study. The infants (on CM-free diet) were given the contents of identical capsules with each meal, during day 6 . The same procedure was repeated on day 10. The capsules contained either whey protein (with Nutramigen added) or human albumin powder (with Nutramigen added). We found that 18 infants reacted wlth colic on the whey protein challenge, 2 infants reacted with colic on placebo (p< 0.001) and 4 infants did not react at all. Crying hours per day for the 24 infants were 5.5 h on formula feeding and 1.0 h on Nutramigen (p< 0.001). Crying hours per day were 3.2 h on whey protein challenge and 0.96 h on placebo (p< 0.001). In conclusion: Bovine whey proteln can give colic symptoms in infants with severe infantile colic. Small intestinal villous enterOCyteS express Class 11 molecules Testing of intestinal permeability appears to be a n whereas crypt cells do not. The role of such molecules in the gut objective means of diagnosing food allergy. Permeabiis unknown but it has been suggested that they may be involved in lity by the differential absorption of maintaining tolerance to oral antigens. In some children with IPD, mannit01 and lactulose in 1 7 healthy children aged circulating EcAbs are present together with other autoimmune mani-1-38 months, and 1 1 aged 2-46 months,with milk allergy festations. Jejuna...

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