| Background And AimLiver cirrhosis is a common disease in our country. The main cause is viral hepatitis whose morbidity is decreasing while the alcoholic, non-alcoholic, autoimmune cirrhosis are increasing. Portal hypertension appears in the patients with decompensated cirrhosis and causes hemodynamic changes in the liver and gastrointestinal tract, etc, which result in esophageal and gastric varices, portal hypertensive gastropathy and a series of complications. There have been many studies about esophageal and gastric varices, however, the research about portal hypertensive gastropathy, especially about its hemodynamics, is relatively weak. According to the PHG consensus on the Milan, Italy in 1992, it is a kind of independent gastropathy, and the definition is that portal hypertension patients appear with special gastric mucosal pathological changes in the endoscopy along with mucosal and submucosal vessels dilated, but without obvious inflammation histologically. Its pathogenesis is still unclear and the diagnosis mainly relies on the endoscopy.Its pathophysiology mainly related to the dysfunction of gastric mucosa microcirculation, but at the moment there was big difference among the research results about the changes in blood flow and micro vascular diameter. And most of the research objects were the specimens of human body in vitro or animal model. Also, the detection methods, such as laser Doppler, pathological specimens, influenced the results. So, it lacked of clinical research data real-time in vivo. The probe-confocal laser endomicroscopy, pCLE, could observe the change of the capillary network real-time in vivo and showed the vascular wall and morphology and flow condition of blood cells clearly. Therefore, it was a new tool to study the microcirculation.The aim of this study is to observe gastric mucosa microcirculation real-time with pCLE, and then to measure and to analyze gastric mucosa microcirculatory hemodynamic change with the hope to offer help to the research of its pathophysiological mechanisms and therapy based on that in the future in patients withPHG.MethodsPHG (experimental group) and chronic non-atrophic gastritis (control group) patients from outpatient and ward of department of gastroenterology in Qilu Hospital of Shandong University were rolled in the study from March 2014 to March 2015. With the clinical data collected, the patients underwent white light gastroscopy in intravenous anesthesia to collect and store typical images.Then all patients were given intravenous injections of fluorescein sodium, and if it was safe, then we obtained and stored the pCLE images and videos(effective observation time of every part not less than 15 seconds). The observation sites included the fundus of stomach*1, four walls of body of stomach*1 and some typical parts. Finally we measured and analyzed the data with Cellvizio Viewer and Adobe PhotoShop CS6 softwares. The main indicators were microvascular diameter, micro vascular area. Other pCLE indicators included vascular morphology, blood flow state, fluorescein leakage, gastric pit changes. The other indicators were white light gastroscopy appearance and clinical indicators (etiology proportion, etc.). Chinese version SPSS 19.0 was used for the statistical analysis in this study. The p< 0.05 showed significant statistical difference, and p< 0.001 showed very significant statistical difference.ResultsThere were 25 patients in the experimental group in which there were 17 males and their ages were 52.5+9.8 years. There were 3 hypertension patients. The main causes of portal hypertension were cirrhosis and there were 2 idiopathic portal hypertension patients. The etiologies of cirrhosis included hepatitis B virus, alcoholic, autoimmune and hepatitis C virus. There were 33 patients in the control group in which there were 23 males and their ages were 49.1±11.1 years. Some of them were mixed with gastric polyps or bile reflux and there were 3 hypertension patients. There were no statistical difference in gender, age, history of hypertension in the two groups and the pvalues were 0.890ã€0.223ã€1.000,respectively.In white light endoscopy, the typical features of most PHG patients were mosaic-like pattern, erythema, red pattern lesions and cherry red spots that were mostly seen in the fundus and body of the stomach and the most common was mosaic-like pattern. But some patients showed relatively light changes. The gastric mucosa in the control group patients was chronic inflammation change and some were active.The gastric mucosal micro vascular diameter of PHG patients were greater than that of the control group in gastric fundus, greater curvature and lesser curvature of gastric body, the p values were 0.001,< 0.001,0.016 respectively. However, there was no statistical significance about the difference of microvascular diameter between the two groups in anterior and posterior wall of gastric body, and the p values were 0.126, 0.061 respectively. The gastric mucosal microvascular areas in PHG patients in gastric fundus and four body walls were greater than that of the control group, the p values were less than 0.001.In the experimental group patients, the blood flow states mostly slowed down which were mainly particle flow, slowly particle flow and particle linear flow. Some were even long or short particle of pendulum flow and stagnate. Some blood cells were aggregated into a mass in the micro vessels. But a few were characterized by line flow and line particle flow, which were similar to the normal state of microcirculation blood flow. Some were distortion, deformation and sodium fluorescein leakage increased. The changes of gastric pits in the PHG patients were not obvious. But the leakage of fluorescein sodium increases and some are like inflammation changes. In the control group patients, the blood flow states mainly were linear flow, linear particle flow and particle linear flow. Several were particle of pendulum flow, but there was no stagnate.ConclusionspCLE observes the microvascular changes and microcirculatory dynamics of PHG patients and overall they present with microvessels hyperplasia and expansion. Some are distortion, deformation and permeability increases. The microcirculation blood flow slow down and tends to be stasis and we can see some blood cells are aggregated into a mass. The changes of gastric pits in the PHG patients are not obvious. But the epithelial permeability increases and some are like inflammation changes. |