P. Kuitunen

Supplementary feeding in maternity hospitals and the risk of cow’s milk allergy: A prospective study of 6209 infants ☆ ☆☆ ★

BACKGROUND Early feeding with cows milk (CM) may increase the risk of cows milk allergy (CMA). OBJECTIVE We sought to examine prospectively whether supplementary feeding of CM at the maternity hospital would increase the risk when compared with feeding with pasteurized human milk or hydrolyzed formula. METHODS We studied 6209 unselected healthy, full-term infants, of whom 5385 (87%) required supplementary milk while in the hospital. The infants were randomly assigned to receive CM formula (1789 infants), pasteurized human milk (1859 infants), or whey hydrolysate formula (1737 infants). The comparison group (824 infants) was composed of infants who were exclusively breast-fed. The infants were followed for 18 to 34 months for symptoms suggestive of CMA. The primary endpoint was a challenge-proven adverse reaction to CM after a successful CM elimination diet. RESULTS The cumulative incidence of CMA in the infants fed CM was 2.4% compared with 1.7% in the pasteurized human milk group (odds ratio [OR], 0.70; 95% confidence interval [CI], 0. 44-1.12) and 1.5% in the whey hydrolysate group (OR, 0.61; 95% CI, 0. 38-1.00). In the comparison group, CMA developed in 2.1% of the infants. Among the infants who required supplementary feeding at hospital, both exposure to CM while in the hospital (OR, 1.54; 95% CI, 1.04-2.30; P =.03) and obvious parental atopy (OR, 2.32; 95% CI, 1.53-3.52; P <.001) increased the risk of CMA. CONCLUSIONS Our data indicate that feeding of CM at maternity hospitals increases the risk of CMA when compared with feeding of other supplements, but exclusive breast-feeding does not eliminate the risk.

EUROPEAN SOCIETY FOR PAEDIATRIC GASTROENTEROLOGY

After oral administration, the non-enteropathogenic strain E. coli 083 was detected in the stools of colonized infants from the 2nd day, and remained dominant up to 16 weeks. Serum antibodies against E. coli 083 were found 4 weeks after colonization. At 16 weeks the antibody level did not differ from that of bottle-fed controls, although breast-fed controls still had a low titer. IgG passively transferred from the mother decreased slowly but an increase from the 12th week was probably due to endogenous production. In breast-fed controls no decrease was noticed. The IgA level rose gradually from the 4th week in all groups. Colonization did not significantly influence serum immunoglobulin levels. Coproantibodies were detected in colonized artifically fed infants at 4 weeks and the maximum level persisted to 16 weeks. In breastfed colonized infants the coproantibody level was significantly higher between 2 and 6 weeks than in controls. IgM in low levels was detectable only in the artificially fed colonized group from the 4th to 16th weeks. The secretory IgA level in breast-fed colonized and control infants was high between 1 and 8 weeks. In bottlefed colonized infants the IgA increase started from the 4th week and was significantly higher in the 6th, 12th and 16th week than in controls. No IgG was found in stool filtrates of any group. Artificial colonization induced formation of secretory IgA. Passive transfer masked this effect in the breast-fed infants. In bottle-fed infants artificial colonization caused active formation. Lysozyme feeding did not affect the IgG level up to 16 weeks, but at 5 and 6 months it was even higher than in breast-fed infants. IgM was not affected by lysozyme. IgA was higher ’ in lysozyme-fed infants from the 12th week than in controls, and a t 16 weeks and 5 and 6 months higher than in breast-fed infants. In breast-fed infants high IgA levels were found in stool filtrates from the 1st to the 12th week, i.e. during the time of breast feeding. In lysozyme-fed infants secretory IgA was higher than in controls up to the 16th week. Stool filtrates of lysozyme-fed infants contained only traces of lysozyme. Gastrointestinal infections were less frequent in lysozyme-fed infants than in controls.

THE CONCENTRATIONS OF COPPER AND ZINC IN HUMAN MILK A Longitudinal Study

Abstract. Vuori, E. and Kuitunen, P. (Department of Public Health Science and Childrens Hospital, University of Helsinki, Helsinki, Finland). The concentrations of copper and zinc in human milk—a longitudinal study. Acta Pædiatr Scand, 68: 33, 1979.—Twenty‐seven healthy Finnish mothers were followed during the course of their entire lactation period. A total of 229 individual milk samples, collected in the beginning and at the end of each feed during a 24‐h period, were obtained from the 2nd week to the 9th month of lactation. The copper and zinc concentrations were determined by atomic absorption spectrophotometry. The concentrations of the trace‐elements investigated were dependent on the stage of lactation. The median copper and zinc concentrations decreased during the course of lactation from about 0.60 mgyl and 4.0 mg/l to 0.25 mg/l and 0.5 mg/l, respectively. The importance of considering the stage of lactation in the evaluation of the trace‐element nutrition value of breast milk should be emphasized. The calculated means of the concentrations of these trace‐elements in mature human milk presented in the literature seem to overestimate the actual levels in prolonged lactation.

RESPONSE OF THE JEJUNAL MUCOSA TO COW'S MILK IN THE MALABSORPTION SYNDROME WITH COW'S MILK INTOLERANCE A Light‐ and Electron‐Microscopic Study

Three infants, in whom the malabsorption syndrome, small intestinal. mucosal damage and clinical cows milk intolerance were found, were challenged with cows milk after initial treatment with breast milk. The small intestinal mucosa was investigated with light and electron microscopy both before and after provocation.

Changing pattern of cow's milk intolerance. An analysis of the occurrence and clinical course in the 60s and mid-70s.

ABSTRACT. Verkasalo, M., Kuitunen, P., Savilahti, E. and Tiilikainen, A. (Childrens Hospital, University of Helsinki, Finland). Changing pattern of cows milk intolerance. Acta Paediatr Scand, 70: 289, 1981.–The rapid changeover to commercial adapted infant formulae which took place in Finland between 1973 and 1975 was studied as a factor in the occurrence of severe intestinal cows milk intolerance (CMI). Of infants treated for CMI in 1962‐73, ninety‐three percent (25/27) were on homemade or unadapted formulae. The admission rate for CMI in these years was 0.22/1 000 liveborn infants breast fed less than six months. During 1974‐77 the corresponding figure was 0.56, with 85 % of the patients (18/26) on adapted cows milk formulae. The patients treated before 1974 had a longer symptomatic period before admission, greater growth retardation and more severe intestinal damage than those seen during and after 1974. This is believed to reflect mainly the increasing awareness of CMI on the part of both laymen and the medical profession. In the history of 2/3 of the patients at least one of the following conditions was noted: non‐breast feeding, infectious gastroenteritis, praematurity, 21‐trisomy, prior intra‐abdominal surgery, Hirschsprungs disease, and atopic disease in family members. The long follow‐up averaging over four years revealed four patients with coeliac disease. In one of these the proximal jejunal mucosa was normal after two years on gluten‐containing diet, but he showed a mucosal relapse as late as between 2 to 4 years on normal diet.

Protein Patterns of Brush-Border Fragments in Congenital Lactose Malabsorption and in Specific Hypolactasia of the Adult

Brush-border membrane proteins of the small-bowel mucosa were separated on polyacrylamide gels from intestinal biopsy specimens obtained from four children with congenital lactose malabsorption and from two adults with specific hypolactasia. In three patients with the congenital type of lactase deficiency the protein band corresponding to brush-border lactase was reduced in intensity, but was never completely absent. No difference in gel patterns was detected when this pattern in congenital deficiency was compared to that obtained from the two patients with adult-type selective hypolactasia. In one patient with congenital lactose malabsorption the protein band corresponding to lactase activity was not detectable. The findings suggest that the mechanisms leading to low lactase activity in the congenital and adult forms of lactose intolerance are similar.

INTESTINAL MALABSORPTION: A CLINICAL STUDY OF 22 CHILDREN OVER 2 YEARS OF AGE

A classic clinical picture and steatorrhoea with gluten intolerance are the criteria usually applied in the diagnosis of coeliac disease. Hence, it is difficult to detect the existence of atypical symptomatology in the disease. Nevertheless, more or less atypical forms have been described by many authors, expecially in older children (2, 3, 8). When the finding of villous atrophy of the intestinal mucosa is taken as the diagnostic criterion of coeliac disease, it is possible to evaluate the clinical manifestations in coeliac disease and even detect other conditions associated with intestinal mucosal villous atrophy. This report presents the clinical symptomatology and findings in respect of 22 children over 2 years of age, in whom significant villous atrophy was found. The authors believe that these patients are all suffering from coeliac disease, although this name has not been applied because the diagnosis has not been properly verified in each case. We have previously presented a series of infants with similar findings (11).

Disaccharidases and histology of duodenal mucosa in congenital lactose malabsorption.

A study has been made of the disaccharidase activities and histology of duodenal mucosa in two infants with typical congenital lactose malabsorption. The mucosal samples were taken by means of peroral intestinal biopsy. At the time Of biopsy, the patients were 2½ and 4½ months old and they had been on lactose free diet 39 days and 3 ½ months respectively.

Nemaline myopathy. Report of four cases and review of the literature.

Nemaline myopathy, first described in 1963 by Shy et al. (26), is characterized clinically by congenital nonprogressive or slowly progressive muscular weakness, most prominent in the proximal muscle groups. Histological preparations of a muscle biopsy reveal subsarcolemmal aggregates of minute abnormal rod-shaped or thread-like structures. Because of the thread-like appearance of these structures under the light microscope, the disease is called “nemaline myopathy”. At the ultrastructural level these rods seem to represent an accumulation of Z-band material with axial and cross striae and in cross sections at high magnification they seem to have a crystal lattice structure. Up to now, at least 30 patients with this disorder have been published, 19 of them females, and only 5 patients with late onset (Table 1 and 2). Because there have been no previous reports of nemaline myopathy in the Scandinavian countries, we present 4 cases diagnosed at the Children’s Hospital, University of Helsinki, in 1970.

Malabsorption syndrome in childhood. The occurrence of absorption defects and their clinical significance.

Defective intest,inal absorption is one of the most characteristic findings in coeliac disease. Beside the determination of faecal fat, many new tests have been developed for the assessment of intestinal absorption. Among these, the D-xylose excretion test and the determination of urinary FICLU have come into wide clinical use. Although these tests usually enable a clear differentiation to be made between normals and patients with coeliac disease, abnormal results may be obtained in many other diseases and clinical states, which can all be listed under the title malabsorption syndrome. Furthermore, these indirect tests may give “false positive” results for various reasons [2, 31. Therefore, evaluation of the significance of the results of these absorption tests is difficult and has rarely been carried out in a series of patients suffering from different forms of the malabsorption syndrome. In this study absorption defects have been searched for by means of faecal fat determination, the D-xylose excretion test and the FICLU test in children with symptoms suggestive of the malabsorption