Cholesterosis of the gallblader and clinical and diagnostical characteristics of patients with different body weight

Gallbladder cholesterosis (GBC) has been studied more often in overweight and obese patients, however, this disease is often found in people with normal weight too.

The aim: to study the clinical and metabolic peculiaritiess of GBC patients with normal body mass and overweight.

Material and methods. We examined 100 patients with GBC: 54 with normal (subgroup 1 – 23 male and 31 female patients, median age 39 years) and 46 – with overweight (subgroup 2 – 24 male and 22 female patients, median age 46 years). All participants underwent a general clinical examination, ultrasound of the abdominal organs and brachiocephalic arteries (BCA), diagnostics of H. pylori presence, assessment of the gallbladder contractile function. Patients with dyspepsia underwent fibrogastroscopy.

Results. In patients with GBC, the clinical picture was characterized by syndromes of intestinal dyspepsia (33–47%), biliary dysfunction (30–33%), abdominal pain syndrome and gastric dyspepsia (37–43%). Both subgroups were found to be highly infected with H. pylori (68–76%). In subgroup 1, a direct correlation was fixed between H. pylori infection and GBC development, the level of H. pylori antibodies and the value of the atherogenic index. In subgroup 2, atherogenic dyslipidemia (58,6%), atherosclerotic changes in BCA (28,3%) were detected. An increase in ultrasensitive CRP in 50% of patients in subgroup 2 correlated with the thickness of the intima-media complex (IMC) and LDL levels. In subgroup 1 prevailed polyposis (87%), in subgroup 2 – polyposis and reticular- polyposis (91,4%) forms of GBC, which indicates at the diffuse lesion of gallbladder wall. Contractile function of this organ was reduced in both subgroups.

Conclusion. In patients with normal body weight, H. pylori is probably playing the role in the pathogenesis of the polyposis form of GBC in the absence of systemic metabolic changes. In overweight patients, GBC is associated with impaired lipid metabolism, an increase in the thickness of IMT in the carotid arteries, atherogenic dyslipidemia, and a high level of subclinical inflammation. H. pylori is probably one of the triggers, but not the leading factor in the development of GBC in this subgroup.