Causal associations between gastroesophageal reflux disease and essential hypertension: A bidirectional Mendelian randomization study

BACKGROUND Clinical studies have reported that patients with gastroesophageal reflux disease(GERD)have a higher prevalence of hypertension.AIM To performed a bidirectional Mendelian randomization(MR)analysis to investi-gate the causal link between GERD and essential hypertension.METHODS Eligible single nucleotide polymorphisms(SNPs)were selected,and weighted median,inverse variance weighted(IVW)as well as MR egger(MR-Egger)re-gression were used to examine the potential causal association between GERD and hypertension.The MR-Pleiotropy RESidual Sum and Outlier analysis was used to detect and attempt to reduce horizontal pleiotropy by removing outliers SNPs.The MR-Egger intercept test,Cochran’s Q test and“leave-one-out”sen-sitivity analysis were performed to evaluate the horizontal pleiotropy,heterogen-eities,and stability of single instrumental variable.RESULTS IVW analysis exhibited an increased risk of hypertension(OR=1.46,95%CI:1.33-1.59,P=2.14E-16)in GERD patients.And the same result was obtained in replication practice(OR=1.002,95%CI:1.0008-1.003,P=0.000498).Meanwhile,the IVW analysis showed an increased risk of systolic blood pressure(β=0.78,95%CI:0.11-1.44,P=0.021)and hypertensive heart disease(OR=1.68,95%CI:1.36-2.08,P=0.0000016)in GERD patients.Moreover,we found an decreased risk of Barrett's esophagus(OR=0.91,95%CI:0.83-0.99,P=0.043)in essential hypertension patients.CONCLUSION We found that GERD would increase the risk of essential hypertension,which provided a novel prevent and therapeutic perspectives of essential hypertension.

Pyrrolizidine alkaloids-induced hepatic sinusoidal obstruction syndrome: Pathogenesis, clinical manifestations, diagnosis,treatment, and outcomes

Hepatic sinusoidal obstruction syndrome (HSOS) can be caused by the intake of pyrrolizidine alkaloids (PAs). To date, PAs-induced HSOS has not been extensively studied. In view of the difference in etiology of HSOS between the West and China, clinical profiles, imaging findings, treatment, and outcomes of HSOS associated with hematopoietic stem cell transplantation or oxaliplatin might be hardly extrapolated to PAs-induced HSOS. Reactive metabolites derived from PAs form pyrrole-protein adducts that result in toxic destruction of hepatic sinusoidal endothelial cells. PAs-induced HSOS typically manifests as painful hepatomegaly, ascites, and jaundice. Laboratory tests revealed abnormal liver function tests were observed in most of the patients with PAs-induced HSOS. In addition, contrast computed tomography and magnetic resonance imaging scan show that patients with PAs-induced HSOS have distinct imaging features, which reveal that radiological imaging provides an effective noninvasive method for the diagnosis of PAs-induced HSOS. Liver biopsy and histological examination showed that PAs-induced HSOS displayed distinct features in acute and chronic stages. Therapeutic strategies for PAs-induced HSOS include rigorous fluid management, anticoagulant therapy, glucocorticoids, transjugular intrahepatic portosystemic shunt, liver transplantation, etc. The aim of this review is to describe the pathogenesis, clinical profiles, diagnostic criteria, treatment, and outcomes of PAs-induced HSOS.

Difference between type 2 gastroesophageal varices and isolated fundic varices in clinical profiles and portosystemic collaterals

BACKGROUND There is significant heterogeneity between gastroesophageal varices(GOV2)and isolated gastric varices(IGV1).The data on the difference between GOV2 and IGV1 are limited.AIM To determine the etiology,clinical profiles,endoscopic findings,imaging signs,portosystemic collaterals in patients with GOV2 and IGV1.METHODS Medical records of 252 patients with gastric fundal varices were retrospectively collected,and computed tomography images were analyzed.RESULTS Significant differences in routine blood examination,Child-Pugh classification and MELD scores were found between GOV2 and IGV1.The incidence of peptic ulcers in patients with IGV1(26.55%)was higher than that of GOV2(11.01%),while portal hypertensive gastropathy was more commonly found in patients with GOV2(22.02%)than in those with IGV1(3.54%).Typical radiological signs of cirrhotic liver were more commonly observed in patients with GOV2 than in those with IGV1.In patients with GOV2,the main afferent vessels were via the left gastric vein(LGV)(97.94%)and short gastric vein(SGV)(39.18%).In patients with IGV1,the main afferent vessels were via the LGV(75.61%),SGV(63.41%)and posterior gastric vein(PGV)(43.90%).In IGV1 patients with pancreatic diseases,spleno-gastromental-superior mesenteric shunt(48.15%)was a major collateral vessel.In patients with fundic varices,the sizes of gastric/esophageal varices were positively correlated with afferent vessels(LGVs and PGVs)and efferent vessels(gastrorenal shunts).The size of the esophageal varices was negatively correlated with gastrorenal shunts in GOV2 patients.CONCLUSION Significant heterogeneity in the etiology and vascular changes between GOV2 and IGV1 is useful in making therapeutic decisions.

Unusual cause of lesions in the descending duodenum and liver:A case report and review of literature

The descending duodenum is rarely involved in Schistosoma japonicum(S. japonicum) infection. Here, we report a case of acute Schistosoma infection, which presented with abdominal pain, abdominal distension and irregular fever. Tumor-like lesions were observed in the descending duodenum. Simultaneously, heterogeneity in hepatic perfusion was demonstrated by dynamic computed tomography scanning. Biopsy of the descending duodenum showed the deposition of Schistosoma eggs. Following administration of the antihelminthic drug praziquantel, the patient showed rapid clinical improvement. In conclusion, we report a patient with acute S. japonicum infection presenting as tumor-like lesions in the descending duodenum and heterogeneity of blood perfusion in liver parenchyma.