Interstitial cajal-like cells and bile lithogenicity in the pathogenesis of gall-stone disease.

UNLABELLED

Gall-stone disease constitutes a serious clinical problem and is the most frequent cause of elective cholecystectomies. There are many etiopatogenic factors however; lithogenic bile and its stasis due to gall-bladder hypomotility seem to be the most important. In recent years discovery of pacemaker function of Interstitial Cells of Cajal changed our understanding of smooth muscle physiology and helped to disclose many gastrointestinal motility disorders.

THE AIM OF THE STUDY

was identification and quantification of interstitial Cajal-like cells (ICLCs) in gall-bladder muscle wall from patients with cholelithiasis and in gall-stone-free controls, as well as determination of the relationship between the number of ICLCs and Cholesterol Saturation Index (CSI) of bile in both analyzed groups.

MATERIAL AND METHODS

20 patients operated for symptomatic cholelithiasis were enrolled into the study group. The control group consisted of 20 patients operated for pancreatic head tumors, with no pre- and intraoperative signs of gall-stones. Identification of ICLCs in the gall-bladder was performed by means of double immunofluorescence technique with anti c-Kit and anti-mast cell tryptase antibodies. Quantitative analysis was carried out under fluorescence microscopy conjoined with image analysis software. Bile samples were used for calculation of CSI.

RESULTS

ICLCs were detected within gall-bladder muscle wall. Number of ICLCs was statistically significantly lower in patients from the study group as compared to control. The study also revealed statistically significantly higher CSI in the study group.

CONCLUSIONS

The quantity of ICLCs is diminished in the gall-bladder from patients with cholelithiasis and there is negative correlation between the number of ICLCs and CSI of bile. Regarding the role of ICCs in regulation of GI tract motility, it appears that reduction in their number may be important etiopatogenic factor of cholelithiasis.