Hem-o-lok clip migration to duodenal bulb post-cholecystectomy:A case report

BACKGROUND Hem-o-lok clips are typically used to control the cystic duct and vessels during laparoscopic cholecystectomy(LC)and common bile duct exploration for stones in the bile duct and gallbladder.Here,we report a unique example of Hem-o-lok clip movement towards the duodenal bulb after LC,appearing as a submucosal tumor(SMT).Additionally,we provide initial evidence of gradual and evolving endoscopic manifestations of Hem-o-lok clip migration to the duodenal bulb wall and review the available literature.CASE SUMMARY A 72-year-old man underwent LC for gallstones,and Hem-o-lok clips were used to ligate both the cystic duct and cystic artery.Esophagogastroduodenoscopy(EGD)2 years later revealed an SMT-like lesion in the duodenal bulb.Due to the symptomatology,the clinical examination did not reveal any major abnormalities,and the patient was followed up as an outpatient.A repeat EGD performed 5 months later revealed an SMT-like lesion in the duodenal bulb with raised edges and a central depression.A third EGD was conducted,during which a Hem-o-lok clip was discovered connected to the front side of the duodenum.The clip was extracted easily using biopsy forceps,and no complications occurred.Two months after the fourth EGD,the scar was surrounded by normal mucosa.CONCLUSION Clinicians should be aware of potential post-LC complications.Hem-o-lok clips should be removed if symptomatic.

Angiotensin-converting enzyme 2 improves liver fibrosis in mice by regulating autophagy of hepatic stellate cells

BACKGROUND Liver fibrosis is the common pathological process associated with the occurrence and development of various chronic liver diseases.At present,there is still a lack of effective prevention and treatment methods in clinical practice.Hepatic stellate cell(HSC)plays a key role in liver fibrogenesis.In recent years,the study of liver fibrosis targeting HSC autophagy has become a hot spot in this research field.Angiotensin-converting enzyme 2(ACE2)is a key negative regulator of reninangiotensin system,and its specific molecular mechanism on autophagy and liver fibrosis needs to be further explored.AIM To investigate the effect of ACE2 on hepatic fibrosis in mice by regulating HSC autophagy through the Adenosine monophosphate activates protein kinases(AMPK)/mammalian target of rapamycin(mTOR)pathway.METHODS Overexpression of ACE2 in a mouse liver fibrosis model was induced by injection of liver-specific recombinant adeno-associated virus ACE2 vector(rAAV2/8-ACE2).The degree of liver fibrosis was assessed by histopathological staining and the biomarkers in mouse serum were measured by Luminex multifactor analysis.The number of apoptotic HSCs was assessed by terminal deoxynucleoitidyl transferase-mediated dUTP nick-end labeling(TUNEL)and immunofluorescence staining.Transmission electron microscopy was used to identify the changes in the number of HSC autophagosomes.The effect of ACE2 overexpression on Wu Y et al.ACE2 improves liver fibrosis through autophagy WJG https://www.wjgnet.com 4976 September 7,2023 Volume 29 Issue 33 autophagy-related proteins was evaluated by multicolor immunofluorescence staining.The expression of autophagy-related indicators and AMPK pathway-related proteins was measured by western blotting.RESULTS A mouse model of liver fibrosis was successfully established after 8 wk of intraperitoneal injection of carbon tetrachloride(CCl4).rAAV2/8-ACE2 administration reduced collagen deposition and alleviated the degree of liver fibrosis in mice.The serum levels of platelet-derived growth factor,angiopoietin-2,vascular endothelial growth factor and angiotensin II were decreased,while the levels of interleukin(IL)-10 and angiotensin-(1-7)were increased in the rAAV2/8-ACE2 group.In addition,the expression of alpha-smooth muscle actin,fibronectin,and CD31 was down-regulated in the rAAV2/8-ACE2 group.TUNEL and immunofluorescence staining showed that rAAV2/8-ACE2 injection increased HSC apoptosis.Moreover,rAAV2/8-ACE2 injection notably decreased the number of autophagosomes and the expression of autophagy-related proteins(LC3I,LC3II,Beclin-1),and affected the expression of AMPK pathway-related proteins(AMPK,p-AMPK,p-mTOR).CONCLUSION ACE2 overexpression can inhibit HSC activation and promote cell apoptosis by regulating HSC autophagy through the AMPK/mTOR pathway,thereby alleviating liver fibrosis and hepatic sinusoidal remodeling.