Analysis Of Stomach Mucosal Diseases Related Factors In Liver Cirrhosis

BackgroundLiver cirrhosis due to various factors lead to liver cells damage, deformation, necrosis, and thus regeneration of liver cells and fibrous connective tissue hyperplasia, fibrosis formation, is the late stage in the development of a variety of chronic liver disease, decreased liver function and portal hypertension as the main clinical manifestation. Liver blood circulation disorder is the pathological basis of the formation of portal hypertension. In addition to liver damage of liver cirrhosis, other organs also can appear the corresponding change. Due to chronic congestion, spleen enlargement, and gastric mucosal visible hyperemia, edema, erosion, when see a Mosaic or snakeskin change we call portal hypertension gastropathy, Upper gastrointestinal bleeding is the most common complication of cirrhosis, esophageal varices bleeding in the first place, with the development of endoscopic techniques, bleeding caused by liver cirrhosis gastric mucosal lesions, aroused people’s more and more attention.Portal hypertension gastropathy refers to the gastric mucosa lesions associated with portal hypertension, is considered a different special type in patients with a non portal hypertension gastritis, its histologic characteristics are mucosa and submucosal blood capillary dilate, twisted, irregular hemal wall, intimal thickening focal, and no obvious change of inflammation. PHG more found in cirrhotic portal hypertension (PHT), and about65%of patients could appear, is one of the common causes of upper gastrointestinal bleeding in PHT patients with second only to stomach esophagus varicosity burst hemorrhage, and in severe cases can be life-threatening. Due to cirrhosis of the liver can cause the body to a variety of metabolic and endocrine changes, cirrhosis of the liver of PHG mechanism will also be affected by various factors, and more complex pathological physiological process.A survey found, such as liver cirrhosis portal hypertension in patients with gastric mucosa pathological changes compared with the general population increased significantly. Increased portal pressure is a necessary condition of the PHG The portal vein pressure makes the gastric mucosa more susceptible to damage, but the rise in the portal venous pressure can not directly cause gastric mucosal injury, to induce gastric mucosal damage, may also have other factors play a role. In patients with liver cirrhosis is often accompanied by severe liver function damage, low albumin synthesis and detoxification function, clotting mechanism dysfunction, infection and hepatitis virus itself of direct and indirect infringement damage such as gastric mucosal barrier, reduce capacity to gastric mucosal repair and defense ability, very prone to gastric mucosal erosion, ulcer, bleeding and other lesions. A number of studies that the incidence of PHG associated with liver function damage and the degree of esophageal varices, increased with the grade of liver function and the degree of esophageal varices, but also has the research draw the opposite conclusion, another study found that PHG associated with the location and severity of esophageal gastric varices, especially closely with the degree of gastric varices. A variety of gastrointestinal endocrine hormone and vascular active substances, such as glucagon, vasoactive intestinal peptide and nitric oxide, increased in patients with PHG, which are mainly involved in the formation of the portal hypertension; at the same time also play an important role in movement and metabolism of the digestive system. Cytokines, inflammatory reaction neurotransmitter and so on can cause endothelial cell damage directly, activate mononuclear macrophages and lymphocytes, cause inflammation and immune reaction and damage the blood vessels wall, leading to dysfunction, and also can activate the vascular smooth muscle cell at the same time, the release of a variety of vascular active substances, decreased blood vessel compliance, increased blood flow resistance, these changes is confirmed in portal vein hypertension. Endotoxin blood disease, H.pylori infection, treatment of portal hypertension etc also has certain relation with the incidence of PHG in liver cirrhosis patients.In recent years, people found that the serum pepsinogen detection has important significance to screen and diagnose gastric diseases, and can reduce the patients with endoscopy, upper gastrointestinal of the pain. As early as the early nineteenth century, researchers found in gastric juice, one can decompose protein material so named pepsin. Halfa century after the study found, pepsin is secreted in the form of inactive proenzyme, in order to protect the stomach tissue from damage, referred to as pepsinogen (PG). PG is a precursor of pepsin, including PG Ⅰ, PGⅡ. PG I is mainly secreted by gastric chief cells and mucous neck cells, PGII in addition to the above two kinds of cells, can also be secreted by pyloric gland, gastric cardiac, duodenal Brunner’s gland. Because the stomach is almost the only source of pepsinogen, when the gastric mucosal lesions, the content of serum PG I, PG II also will change. So, in a certain extent, serum pepsinogen level can reflect different parts of gastric mucosal morphology, function and damage degree, has certain significance to the diagnosis of gastric diseases.At present, on gastric mucosal lesions in patients with cirrhosis has been researched widely, but less research related to the secretion of gastric mucosal. This study detected by gastroscopy, B ultrasonic of abdomen, and other related serological detection of cirrhosis, analysis the possible influence factors in patients with cirrhosis appears PHG, with latex immune enhancement method for determining the levels of serum pepsinogen, observe the secretion function of stomach mucous membrane, and deepen the understanding of liver cirrhosis PHG, look for sensitive clinical predictor of gastric mucosal lesions, in order to relieve the suffering of the patients gastroscope and other invasive examination, so as to make guidance to the clinical diagnosis and treatment.Part1:Analysis of stomach mucosal diseases and its clinically relevant factors in liver cirrhosis Objective:To investigate the relationship between gastric mucosal lesions occurred in liver cirrhosis and liver function, hypersplenism, esophageal gastric varices and other related factors.Methods:A total of114cirrhotic patients were studied by gastroscopy.114cirrhotic patients were divided into PHG group and without PHG group according to gastroscope with Mosaic or snakeskin changes (51patients were PHG group,63patients were without PHG group). We would clear if there was a gastrointestinal bleeding, and then record gastric mucosal lesions in morphological characteristics, degree of esophageal gastric varices, and presence of bile reflux, observe H.pylori infection through rapid urease test or exhale carbon13experimental. All of the patients were conducted detection of routine blood, kidney and liver function, coagulation function before treatment. Patients with liver cirrhosis ascites underwent abdominal ultrasound assessment the degree of ascitic. Liver function according to the Child-Pugh and MELD classification standard. Data were expressed as mean±SD. Comparison between liver cirrhosis group with or no PHG was performed by two-sample t-test. Comparison between PHG group, without PHG group and control group was performed by a standard one-way analysis of variance. The Spearman correlation was used to analysis the relationship between different factors. A p value <0.05(two-tailed) was considered to be significant. All calculations were processed using the SPSS13.0software package.Results:114patients with cirrhosis of the liver under gastroscope performance can appear mucosal hyperemia, edema, erosion, ulcer, Mosaic sample changes, scarlet fever, snakeskin, diffuse hemorrhage, PHG were found in51cases, the incidence rate was44.7%. The lesions mainly located in the fundus and body of stomach, and its occurrence related to the degree of esophageal varicose veins, hepatic function damage, kidney function, severity, ascites, splenomegaly, active bleeding and bile reflux, and no related with the degree of gastric varices, H.pylori infection. We separated analysis of total serum bilirubin, albumin, globulin, prothrombin time, serum transaminase level, the level of albumin lower in PHG group, no significant difference between the others. Conclusion:Cirrhosis of the liver has different degrees of gastric mucosal injury. Liver cirrhosis PHG endoscopic characteristics obviously, portal hypertension is the necessary condition for the formation of PHG The occurrence of PHG in patients with liver cirrhosis is related to the esophageal varices, the damage of liver function, large ascites, and hypersplenism. Cirrhosis of the PHG will increase risk for bleeding significantly. Part2:The significance of serum pepsinogen changes of portal hypertensive gastropathy in liver cirrhosisObjective:Determination of serum pepsinogen levels in patients with liver cirrhosis, analysis of changes of serum pepsinogen level when hepatocirrhosis with PHG, to investigate the function of gastric mucosa in gastric mucosa lesion of liver cirrhosis.Methods:A total of51cirrhotic patients22healthy controls were studied by gastroscopy.51cirrhotic patients were divided into PHG group and without PHG group according to gastroscope with Mosaic or snakeskin changes. Cirrhotic patients were divided into group A, B and C according to the Child-Pugh score (15patients were Child class A,23patients were Child class B,13patients were Child class C). We observed helicobacter pylori infection through rapid urease test or exhale carbon13experimental. At the same time, we detected the serum pepsinogen Ⅰ and Ⅱ of51cirrhotic patients and22healthy controls by latex-enhanced immunoturbidimetry. The PG Ⅰ/PG Ⅱ ratio (PGR) was calculated. Data were expressed as mean±SD. Comparison between liver cirrhosis group and control group was performed by two-sample t-test. Comparison between PHG group, without PHG group and control group was performed by a standard one-way analysis of variance. Comparison between Child A group, Child B group and Child C group was performed by a standard one-way analysis of variance. The Spearman correlation was used to analysis the relationship between different factors. A p value<0.05(two-tailed) was considered to be significant. All calculations were processed using the SPSS13.0software package.Results:Comparison between cirrhotic patients and healthy controls the levels of serum PG I (61.92±29.81μg/1<99.45±15.25μg/1,P=0.000),PGR(5.07±2.00<7.68±2.83, P=0.000), in cirrhotic patients was lower than that in healthy controls. Then comparison the levels of serum PG between cirrhotic PHG group and no PHG group, PHG group(49.48±23.86μg/l)<no PHG group(74.85±30.27μg/l), P=0.000; but there were no significant difference between the two groups for PG Ⅱ and PGR, Cirrhosis of the PHG appear in different parts of the gastric mucosa, there were no obvious difference between serum PG level. There were no significant difference between the A, B and C group for the levels of serum PG, also between alcoholic liver cirrhosis and hepatitis b cirrhosis. But we found significant differences between H.pylori infection and no H.pylori infection group for PⅡI(16.90±7.09μg/1vs.11.39±5.24μg/l, P=0.003)and PGR(4.12±1.60μg/1vs.5.55±2.03μg/1, P=0.015).Conclusion:The level of serum PG Ⅰ decreased obviously in hepatocirrhosis with portal hypertension gastropathy, gastric mucosa lamina propria would damage, glandular stomach mucosa damaged, the secretion function reduced;. H.pylori infection may affect the level of PG Ⅱ. There were no significant correlation between serum PG level and liver function. In a certain extent, serum PG level especially PG I can reflect the function of gastric mucosa in patients of liver cirrhosis.