The mean age of the children in the study was 11 years 3 months and the range was 6 years 5 months-16 years 5 months. Each of the children in the recurrent abdominal pain group met the criteria outlined by Apley,4 which included at least three attacks of pain occurring over a period longer than 3 months, with no known organic cause, and severe enough to affect the child's participation in his normal activities. They underwent a thorough physical examination and rectal examination including immediate microscopy of stools for ova and parasites, with no positive results. Laboratory investigations included blood count and in most cases urine analysis and culture. All test results were within normal limits. In addition, all the children with recurrent abdominal pain were followed up for at least 18 months and none developed an organic pathology that would account for their pain. A structured interview was conducted with each child and at least one parent to provide comparison information between children with recurrent abdominal pain and control children with no history of abdominal pain. The Quay-Peterson behaviour checklist6 was completed independently by each of the child's parents and the child's teacher. The Poznanski depression scale7 was completed by the interviewer and the Birleson self report scale8 was completed by the child. Each parent independently completed the Locke-Wallace marital adjustment scale.9 Sociodemographic measures were taken for each child's family along with a measure of the amount of life stress each child had experienced, and a family history of pain. A complete medical and pain history was also determined for each child. In addition, 25 of the children with recurrent abdominal 388 copyright.

Studies by Thompson, 1 Carter et al, 2 MacDonald et al. and McCrae 4 have all shown a high familial frequency of coeliac disease (CD). The diagnostic criteria differed in each study; in Thompson's patients the diagnosis was based on clinical or historical data alone; in Carter's study response to a gluten-free diet was required, while in MacDonald's and McCrae's studies the diagnostic criteria included the demonstration of the lesion of CD by small bowel biopsy. In MacDonald's study some asymptomatic cases were discovered and a few of these had normal fat balance results. No hereditary pattern emerged from these studies though MacDonald postulated a dominant gene with variable penetrance while McCrae suggested that susceptibility to CD is inhereited multifactorially and that enviromental factors other than dietary gluten are of aetiological importance. Hoffman et al. 5, on the other hand, have described discordance for CD in identical twins.

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