Chronic acalculous cholecystitis:correlation of clinical assessment,laboratory data and final histopathology

Objective:To summarize and analyze the clinical and histopathological features of chronic acalculous cholecystitis (CAC) and to investigate the diagnosis and surgical treatment of chronic acalculous cholecystit.Methods:The study subjects were 39 patients with chronic biliary symptoms but no evidence of stones in the gallbladder by B ultrasonography and magnetic resonance cholopancreatography (MRCP) (CAC group).The CCC group consisted of 66 patients taken randomly from concurrent all patients of chronic calculous cholecystitis (CCC).All patients accepted fibergastroscopy,B ultrasonography,MRCP,laboratory examination preoperatively.We retrospectively analyzed the clinical features,B ultrasonography and MRCP findings,histopathological results and clinical outcomes between the two groups.Results:All the 39 patients were diagnosed by clinical symptoms,B ultrasonography,fatty meal gallbladder contractability studies under ultrasound,fibergastroscopy and magnetic resonance cholangiopancreatography (MRCP),what's more,they were pathologically verified postoperatively.In all patients,there was a complete absence of gallbladder wall contractability.Mucosa epithelial defect was found in 21 patients in CAC group (53.8%) and 16 patients in CCC group (24.2%) respectively (P<0.005).Thickened arteriole wall was found in 29 patients in CAC group (74.4%) and none patient in CCC group (P<0.0001).Thickened gallbladder wall (4 mm or more in thickness) was found in 33 patients in CAC group (84.6%) and 28 patients in CCC group (42.4%) respectively (P<0.005).Bile stasis was found in 23 patients in CAC group (59.0%) and 14 patients in CCC group (21.2%) respectively by ultrasonography preoperatively and confirmed in operation (P<0.005).The outcomes of cholecystectomy,expressed as total or near total relief,was similar in the two groups.No statistically significant differences were observed between patients with CAC (90%) and CCC (80%),the P-value >0.05.Conclusion:Chronic acalculous cholecystitis could be diagnosed by symptoms,ultrasound,fatty meal gallbladder contractability studies under untrasoundand MRCP.The optimal treatment of chronic acalculous cholecystitis characterized by thickened arteriole wall and mucosa epithelial defect is cholecystectomy.

The role of TRPP2 in agonist-induced gallbladder smooth muscle contraction

TRPP2 channel protein belongs to the superfamily of transient receptor potential(TRP) channels and is widely expressed in various tissues, including smooth muscle in digestive gut. Accumulating evidence has demonstrated that TRPP2 can mediate Ca^(2+) release from Ca^(2+) stores. However, the functional role of TRPP2 in gallbladder smooth muscle contraction still remains unclear. In this study, we used Ca^(2+) imaging and tension measurements to test agonist-induced intracellular Ca^(2+) concentration increase and smooth muscle contraction of guinea pig gallbladder, respectively. When TRPP2 protein was knocked down in gallbladder muscle strips from guinea pig, carbachol(CCh)-evoked Ca^(2+) release and extracellular Ca^(2+) influx were reduced significantly, and gallbladder contractions induced by endothelin 1 and cholecystokinin were suppressed markedly as well. CCh-induced gallbladder contraction was markedly suppressed by pretreatment with U73122, which inhibits phospholipase C to terminate inositol 1,4,5-trisphosphate receptor(IP3) production, and 2-aminoethoxydiphenyl borate(2APB), which inhibits IP3 recepor(IP3R) to abolish IP3R-mediated Ca^(2+) release. To confirm the role of Ca^(2+) release in CCh-induced gallbladder contraction, we used thapsigargin(TG)-to deplete Ca^(2+) stores via inhibiting sarco/endoplasmic reticulum Ca^(2+)-ATPase and eliminate the role of store-operated Ca^(2+) entry on the CCh-induced gallbladder contraction. Preincubation with 2 μmol L^(-1) TG significantly decreased the CCh-induced gallbladder contraction. In addition, pretreatments with U73122, 2APB or TG abolished the difference of the CCh-induced gallbladder contraction between TRPP2 knockdown and control groups. We conclude that TRPP2 mediates Ca^(2+) release from intracellular Ca^(2+) stores, and has an essential role in agonist-induced gallbladder muscle contraction.