Background: The subsidence of cow's milk allergy (CMA) has been a subject of controversy. In this study the authors examined whether children with this condition in infancy developed full tolerance or whether they continue to have vague gastrointestinal (GI) symptoms relating to the consumption of milk or dairy products and/or signs of mucosal lesion in the GI tract.
Methods: The authors reexamined 56 10-year-old subjects who manifested CMA before 1 year of age, and compared the results with a group of 204 randomly selected age-matched school children. Fifty-three and 90 subjects respectively attended a reexamination and were evaluated for growth, lactose tolerance, and immunoglobulin A (IgA)- and IgG-class antibodies to whole cow's milk. The subjects reporting milk-related GI symptoms were encouraged to do a 4-week blind elimination-challenge test with 1 week of low-lactose milk flour. Sixteen of the 25 children were able to complete the trial.
Results: Approximately half the study subjects (45%) reported milk-related GI symptoms, whereas the respective figure among the control subjects was 10%. Three of six study subjects and seven of 10 control subjects, although completing the challenge, responded with intestinal symptoms. The growth of the former CMA subjects was retarded compared with the control subjects, and the difference in height was most striking in those subjects still reporting milk-related GI symptoms. However, all subjects had normal hemoglobin and whole-blood folic acid levels. The CMA subjects had significantly (P = 0.014) lower concentrations of milk antibodies compared with the control subjects. Lactose malabsorption, defined as high counts in a hydrogen breath test and related clinical symptoms, was found in eight CMA subjects (14%) and six control subjects (3%).
Conclusions: In a certain proportion of subjects with CMA in infancy, GI intolerance seems to persist even after small-dose tolerance has been achieved. The intestinal symptoms and the increased prevalence of lactose intolerance may be caused by a disturbance of the surface epithelial cells—a state to which the authors refer as residual intestinal disease.
Departments of Pediatrics, University Hospital, *Oulu and †Helsinki, Finland
Received February 24, 2000: accepted October 25, 2000.
Address correspondence and reprint requests to Dr. Jorma Kokkonen, Department of Pediatrics, University of Oulu, FIN-90220 Oulu, Finland.