Gall stones in Crohn's disease: another hypothesis.

EDITOR,-We read with interest the paper by Hutchinson et al (Gut 1994; 35: 94-7) suggesting that in Crohn's disease postoperative gall bladder hypomotility may be the main risk factor for the development of gall stones. There are indeed several lines of evidence showing that decreased postprandial gall bladder motility participates in gall stone formation. ' Recent data, however, show that filling and emptying of the gall bladder are complex processes. The gall bladder cyclically contracts during fasting to up to 40% of its maximal volume, just before the occurrence of phase III of the migrating motor complex (MMC) in the antroduodenal area.2 3 The mechanism of these cyclic contractions is not clear. Serum motilin peaks just before phase III of the MMC in the antroduodenal area.4 Moreover, exogenous motilin, producing premature MMCs in the gut, causes an increase in gall bladder motility similar to that seen during spontaneous gall bladder cyclic activity in dogs.3 5 It has therefore been suggested that the increment in plasma motilin concentrations may be responsible for the gall bladder contractions.5 We have recently studied 25 patients with uncomplicated, inactive Crohn's disease (mean Crohn's disease activity index 60 7). Gastrointestinal motility was studied during fasting (5 hours) and after a meal (1 hour) by standard perfusional manometry.6 Data obtained were compared with those of 33 healthy controls. The incidence ofphase III of MMC was considerably reduced. In 13 of 25 patients phase III was absent (v 0 of 33 of healthy controls p<0 001). In the other patients phase III was less frequent (one of 140 minutes v one of 99 minutes, p<005), shorter in duration (4-6 (1) minutes v 6-9 (1), p<005), and rarely starting from the stomach (four of 25 v 18 of 33, p<001). Mean motilin values were in the normal range, but lacked a clear peaking during phase III of the MMC. The high prevalence of gall stones in Crohn's disease is well established. The accepted mechanism of disturbed enterohepatic circulation of bile salts in these patients could perhaps be enhanced if a change in gall bladder motility also occurs. Hutchinson et al suggest that gall bladder sludge may occur because of prolonged fasting or parenteral nutrition in the postoperative period. They found a higher incidence of gall stones in patients with previous laparotomy compared with patients who had not had any abdominal surgery (32% v 13%, p<0005). They did not take into account, however, that the age of the patients, duration of the disease, and number of operations are dependent variables. The incidence of gall stones increases with age in Crohn's disease patients; but the incidence of surgery also increases in these patients with the duration of the disease. We hypothesise that in some patients with Crohn's disease a reduction of cyclic phasic contractions of gall bladder occurs because of a decreased incidence of phases III of the MMC in the antroduodenal area. The lack of periodic stirring and agitation of gall bladder bile may lead to supersaturation of bile and increase propensity for precipitation of salts and formation of gall stones in these patients.7 V ANNESE Division of Gastroenterology, (CSS) Hospital IRCCS, San Giovanni Rotondo, Italy