This study was aimed at investigating the presence of Helicobacter hepaticus(Hh)infection in patients with digestive tract diseases and evaluating Helicobacter pylori(Hp)infection status in patients with digestive tract cancers other than gastric cancer.Fecal samples were collected from 197 patients with digestive tract diseases at the Affiliated Cancer Hospital of Guizhou Medical Uni-versity and from 149 healthy volunteers residing in Guiyang.Hp stool antigen(HpSA)was detected with the colloidal gold method.Af-ter the extraction of fecal DNA,the Hp specific ureA gene and the Hh specific 16S rRNA gene were amplified via nested PCR,and the amplified products were subsequently confirmed through sequencing analysis.The study included 197 patients with digestive system diseases,comprising 135 cases of colorectal cancer,32 cases of chronic gastritis,22 cases of gastric cancer,5 cases of liver cancer,and 3 cases of cholangiocarcinoma.The detection rate of HpSA was 31.5%(62/197).HpSA was detected across all five disease catego-ries,and the highest detection rate was observed in patients with gastric cancer,at 50.0%(11/22),or colorectal cancer,at 24.4%(33/135).The positivity rate of Hp ureA gene PCR was 7.6%(15/197),and sequencing confirmed that the amplified products were in-deed Hp ureA gene fragments.Notably,the highest detection rate was observed in patients with colorectal cancer,at 8.9%(12/135).The positivity rate of Hh 16S rRNA gene PCR was 11.2%(22/197),and sequencing confirmed that the amplified products were in-deed Hh 16S rRNA gene fragments.Hh 16S rRNAgene presence was detected in patients with all five diseases,and the highest detec-tion rate was observed in patients with colorectal cancer,at 11.1%(15/135).Among 149 healthy volunteers,the detection rate of HpSA was 11.4%(17/149),only one case tested positive for the Hp ureA gene,and the Hh 16S rRNA gene was undetectable in all samples.In conclusion,Hh infection was detected in patients with digestive tract diseases.Beyond patients with gastric cancer,the prevalence of Hp infection was also notably high among patients with colorectal cancer,liver cancer,and cholangiocarcinoma.Further investigation is warranted to elucidate the roles of the two species of Helicobacter in the occurrence and progression of digestive tract cancers.

This study was aimed at investigating the presence of Helicobacter hepaticus(Hh)infection in patients with digestive tract diseases and evaluating Helicobacter pylori(Hp)infection status in patients with digestive tract cancers other than gastric cancer.Fecal samples were collected from 197 patients with digestive tract diseases at the Affiliated Cancer Hospital of Guizhou Medical Uni-versity and from 149 healthy volunteers residing in Guiyang.Hp stool antigen(HpSA)was detected with the colloidal gold method.Af-ter the extraction of fecal DNA,the Hp specific ureA gene and the Hh specific 16S rRNA gene were amplified via nested PCR,and the amplified products were subsequently confirmed through sequencing analysis.The study included 197 patients with digestive system diseases,comprising 135 cases of colorectal cancer,32 cases of chronic gastritis,22 cases of gastric cancer,5 cases of liver cancer,and 3 cases of cholangiocarcinoma.The detection rate of HpSA was 31.5%(62/197).HpSA was detected across all five disease catego-ries,and the highest detection rate was observed in patients with gastric cancer,at 50.0%(11/22),or colorectal cancer,at 24.4%(33/135).The positivity rate of Hp ureA gene PCR was 7.6%(15/197),and sequencing confirmed that the amplified products were in-deed Hp ureA gene fragments.Notably,the highest detection rate was observed in patients with colorectal cancer,at 8.9%(12/135).The positivity rate of Hh 16S rRNA gene PCR was 11.2%(22/197),and sequencing confirmed that the amplified products were in-deed Hh 16S rRNA gene fragments.Hh 16S rRNAgene presence was detected in patients with all five diseases,and the highest detec-tion rate was observed in patients with colorectal cancer,at 11.1%(15/135).Among 149 healthy volunteers,the detection rate of HpSA was 11.4%(17/149),only one case tested positive for the Hp ureA gene,and the Hh 16S rRNA gene was undetectable in all samples.In conclusion,Hh infection was detected in patients with digestive tract diseases.Beyond patients with gastric cancer,the prevalence of Hp infection was also notably high among patients with colorectal cancer,liver cancer,and cholangiocarcinoma.Further investigation is warranted to elucidate the roles of the two species of Helicobacter in the occurrence and progression of digestive tract cancers.

Objective:To explore the disease spectrum and corresponding clinical indicators of infantile cholestasis so as to provide a basis for the diagnosis of this type of disease at an early stage.Methods:The clinical data was collected from 203 hospitalized children diagnosed with infantile cholestasis at the Department of Gastroenterology of Maternal and Child Health Care, Guiyang City, from January 2018 to March 2023, including 130 males and 73 females. Patients general condition, personal history, and blood biochemical test indicators, including liver and coagulation function, blood ammonia, blood lipid profile, blood sugar, TORCH, thyroid function, and others, were retrospectively analyzed after admission. Cholangiography and high-throughput gene sequencing were performed in certain patients. The etiology of the enrolled cases were analyzed. Children's clinical data were compared with distinct inherited metabolic liver diseases (Group A) and biliary atresia (Group B). The statistical analysis was conducted using the t-test, Mann-Whitney test, Kruskal-Wallis test, or χ2 test, according to different data. Results:In 33 cases, infectious factors—primarily CMV infection—were the etiology of cholestasis. Forty cases had aberrant bile duct development, primarily biliary atresia, choledochal cysts, and intrahepatic bile duct dysplasia. In 26 cases, genetic metabolic factors mainly included citrin protein deficiency, sodium-taurocholate co-transporting polypeptide deficiency, and Alagille syndrome. 11 cases had drug/poisoning factors (parenteral nutrition-associated cholestasis). 19 cases had idiopathic infantile cholestasis. Three cases had other factors; however, all of them had Kawasaki disease. 71 cases had an unclear diagnosis. There was no statistically significant difference in terms of gender and age between groups A and B ( P>0.05). The alkaline phosphatase (ALP) and bile acid levels were significantly higher in Group A than Group B, with a P<0.05, while the gamma glutamyltransferase (GGT), direct bilirubin (DBil), and albumin levels were lower than those in Group B, with a P<0.05. The cytomegalovirus infection rate was higher in Group B (62.50%) than Group A (34.62%), and the difference between the two groups was statistically significant ( χ2=3.89, P<0.05). The alanine aminotransferase, aspartate aminotransferase, GGT, DBil, and albumin were significantly lower in patients with citrin protein deficiency than those in patients with biliary atresia, while ALP, bile acid, and blood ammonia were higher than those in patients with biliary atresia. Patients with sodium-taurocholate co-transporting polypeptide deficiency had higher bile acid than patients with biliary atresia, while the DBil was lower than that in patients with biliary atresia, and the difference was statistically significant ( P<0.05). Conclusion:Infantile cholestasis etiology is diverse. ALP, bile acids, GGT, DBil, and albumin levels can serve as simple indicators for early-stage differentiation between inherited metabolic liver disease and biliary atresia. The cholestasis etiology should be determined as early as possible following biliary atresia exclusion by actively completing genetic metabolic gene detection.