Background <p>Numerous risk factors are linked to gallbladder stone disease (GBSD). Nonetheless, the relationship between <i>Clonorchis sinensis</i> (<i>C. sinensis</i>) and this condition remains to be clarified.</p> Methods <p>The antibody against <i>C. sinensis</i> in serum and the glucose, triglyceride, and cholesterol levels were investigated in 220 patients with GBSD and 251 controls. Bile components were analysed in patients with gallbladder polyps (GP, <i>n</i> = 18), gallstones (GS, <i>n</i> = 265), and GS combined with <i>C. sinensis</i> infection (GSI, <i>n</i> = 243). Additionally, the gallbladder ejection fraction (<i>%E</i>), residual gallbladder volume (RGV) at 1&#xa0;h after a fatty meal, and fasting gallbladder volume (FGV) were compared among the GP (<i>n</i> = 43), GS (<i>n</i> = 311), and GSI (<i>n</i> = 277) groups.</p> Results <p>The results indicated positive antibody against <i>C. sinensis</i> (OR: 1.759, 95% CI: 1.163–2.662) and hyperglycaemia (glucose concentration ≥ 6.10 mmol/L, OR: 2.263, 95% CI: 1.227–4.172) were risk factors for GBSD. There were more non-cholesterol stones in GSI patients (216/241, 89.6%) than in GS patients (137/281, 48.8%) (<i>P</i> &lt; 0.0001). Microscopic observations revealed that mucus containing glycogen coated the <i>C. sinensis</i> eggs and the proportion of dead eggs gradually increased in bile, sediment, and stones alongside rising calcium salt content. Total bile acid and cholesterol concentrations were lower in GSI patients than in GP patients or GS patients (<i>P</i> &lt; 0.05). Moreover, increased FGV and RGV and decreased <i>%E</i> were observed in GSI patients compared with GP patients (<i>P</i> &lt; 0.001).</p> Conclusions <p>The formation of non-cholesterol gallstones in populations residing in endemic areas is related to the deposition, death, and calcification of eggs in the gallbladder, changes in bile components, and decreased gallbladder motility caused by <i>C. sinensis</i> infection.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Formation of non-cholesterol gallstones in populations within clonorchiasis endemic regions is closely related to Clonorchis sinensis infection

  • Xiaobing Luo,
  • Ruihong Ma,
  • Hongying Cai,
  • Xiangyu Su,
  • Sangui Wang,
  • Tie Qiao

摘要

Background

Numerous risk factors are linked to gallbladder stone disease (GBSD). Nonetheless, the relationship between Clonorchis sinensis (C. sinensis) and this condition remains to be clarified.

Methods

The antibody against C. sinensis in serum and the glucose, triglyceride, and cholesterol levels were investigated in 220 patients with GBSD and 251 controls. Bile components were analysed in patients with gallbladder polyps (GP, n = 18), gallstones (GS, n = 265), and GS combined with C. sinensis infection (GSI, n = 243). Additionally, the gallbladder ejection fraction (%E), residual gallbladder volume (RGV) at 1 h after a fatty meal, and fasting gallbladder volume (FGV) were compared among the GP (n = 43), GS (n = 311), and GSI (n = 277) groups.

Results

The results indicated positive antibody against C. sinensis (OR: 1.759, 95% CI: 1.163–2.662) and hyperglycaemia (glucose concentration ≥ 6.10 mmol/L, OR: 2.263, 95% CI: 1.227–4.172) were risk factors for GBSD. There were more non-cholesterol stones in GSI patients (216/241, 89.6%) than in GS patients (137/281, 48.8%) (P < 0.0001). Microscopic observations revealed that mucus containing glycogen coated the C. sinensis eggs and the proportion of dead eggs gradually increased in bile, sediment, and stones alongside rising calcium salt content. Total bile acid and cholesterol concentrations were lower in GSI patients than in GP patients or GS patients (P < 0.05). Moreover, increased FGV and RGV and decreased %E were observed in GSI patients compared with GP patients (P < 0.001).

Conclusions

The formation of non-cholesterol gallstones in populations residing in endemic areas is related to the deposition, death, and calcification of eggs in the gallbladder, changes in bile components, and decreased gallbladder motility caused by C. sinensis infection.