Abstract 648
Background and objective. A multifactorial etiology has been suggested for infantile colic. The high level of serum motilin and urine serotonin metabolite as well as the gallbladder hypocontractility found in earlier studies support a gastrointestinal etiology, Cholecystokinin (CCK) is the primary hormone causing the postprandial contraction of the gallbladder. It also has calming and satiating behavioral effects. We therefore measured the fasting plasma level of CCK and the CCK responses to feeding in colicky and non-colicky infants to test the hypothesis of deficient secretion or action of CCK as an etiological factor of infantile colic. Methods. Three blood samples were taken; before feeding (after a four-hours fast), immediately after, and 60 minutes after feeding. Plasma CCK concentrations were determined by a CCK specific RIA. The gallbladder response to feeding was evaluated ultrasonographically by calculating a contractility index (CI), which was a percentual decrease of the gallbladder planimetric ellipsoid size from the fasting size in an hour after the start of the feeding. Results. Forty colicky and 40 non-colicky age-matched infants were studied at the mean age of 37 (range 20-48) days. The mean daily duration of crying was 4.0 (SD 1.8) hours in colicky and 0.9 (1.0) hours in non-colicky infants. The mean fasting plasma CCK concentration was 3.4 (range 0.4 - 8.5) pmol/L in colicky and 5.2 (1.1 - 24.0) pmol/L in non-colicky infants (p = 0.03, t-test). Immediately after feeding, the CCK concentration was 32.7 (2.4-87.4) pmol/L in colicky and 42.6 (9.2-95.4) pmol/L in non-colicky infants, respectively (p = 0.079), and the CCK concentrations were 23.1 (2.8 - 75.2) pmol/L and 33.6 (9.4 - 96.4) pmol/l one hour after feeding, respectively (p = 0.042). No differences in the CCK responses were found between the two groups of infants. The gallbladder CI was 55 (SD 28) % in colicky and 63(SD 23) % in non-colicky infants (p = ns). There was a significant linear correlation (r = 0.38, p = 0.025) between the CI and the CCK concentration immediately after the feeding in non-colicky, but not in colicky infants, while there was a significant linear correlation (r = 0.43, p = 0.019) between the CI and the CCK concentration one hour after the feeding in colicky, but not in non-colicky infants. Conclusions. Both the fasting and the postprandial CCK concentrations of colicky infants were significantly lower than those of the non-colicky infants. The results let us suggest that colicky infants may differ from other infants in the regulation of the CCK secretion or kinetics.
