Development Of Portal Hypertensive Gastropathy Research Articles

CORRELATION BETWEEN HELICOBACTER PYLORI INFECTION AND RISK OF ESOPHAGOGASTRIC VARICEAL BLEEDING IN LIVER CIRRHOSIS

Background: Bleeding from esophageal and gastric varices is a fatal event in patients with liver cirrhosis and portal hypertension. Objective: Evaluation the correlation between Helicobacter Pylori infection and risk of esophagogastric variceal bleeding in liver cirrhosis. Patients and Methods: This study was carried out on one hundred (100) patients, suffering from post hepatitic cirrhosis and portal hypertension: fifty (50) of them presented with esophageogastric varices without bleeding selected from patients coming for screening of esophagogastric varices for anti-hepatitis c virus treatment, and the other fifty (50) presented with acute variceal bleeding. All patients attending to Internal Medicine outpatient’s clinic and Internal Medicine Department of Al-Azhar University Hospital at new Damietta during the period from September 2018, to April 2020. All patients were subjected to complete history, clinical assessment, abdominal ultrasonography, upper GIT endoscope and laboratory investigations. Results: There was a significant relation between H.Pylori infection and the presence of esophagogastric variceal hemorrhage and H. Pylori infection was positive in 92% of the patients in group II, and 24% patients was grade II oseophageal varices, 70% grade III oseophagogastric varices, and 6% grade IV oseophagogastric varices, There was a statistically significant correlation of increased esophageal varices (grade three) in positive H pylori in group II, while in group I detection of H.pylori showed 24% patients were positive, and 76% patients were negative. Endoscopic examination showed 40 patients without esophagogastric varices (80%), 8% patients grade I, 4% patients grade II, 6% patients grade III, 2% patients grade IV, and there was a statistically significant increase on esophageal varices (grade zero) in negative H pylori in group I. Conclusion: Helicobacter Pylori infection helped in the development of portal hypertensive gastropathy as well as its severity, and increased risk of esophagogastric variceal bleeding in patients with liver cirrhosis. So, eradication and treatment of Helicobacter Pylori in all patients with liver cirrhosis helped to decrease risk of esophagogastric variceal bleeding in these patients.

Helicobacter Pylori Infection is Associated with Portal ‎Hypertensive Gastropathy in Patients with Liver Cirrhosis ‎

Background and study aims‎: Portal hypertensive gastropathy (PHG) is a complication of portal hypertension in patients with liver cirrhosis, and it is considered one of the causes of upper gastrointestinal bleeding. Helicobacter pylori (H. Pylori) is one of the most common pathogenic organism worldwide because it infects 50% of the population all over the world. The role of H. Pylori infection in the development of PHG and its severity is controversial. The aim of this study is to determine the frequency of H. pylori infection in cirrhotic patients with PHG, and to find out the possible association of H.pylori infection with PHG severity. Method: This study was carried out on 90 patient with cirrhotic liver. Patients were divided into two groups according to the presence or absence of PHG diagnosed by upper endoscopy. Child's Pugh score, MELD, uMELD and detection of H.Pylori by histopathological examination were done for all patients. Results: The studied patients 47 were males and 43 were females their mean age was 51.96 ± 7.02 years (ranging between 38-66 years). H.Pylori infection was significantly more frequent in patients with PHG than patients without PHG (P= 0.001). H.Pylori infection was significantly more frequent in patients with severe PHG than those with mild PHG (P=0.012). By multi-variant analysis, splenomegaly, presence of esophageal varices, gastric varices and H. Pylori infection were independent predictors for PHG presence. Conclusion: H. Pylori infection could be an independent predictor for PHG development and ‎associated with its severity.

Association of Helicobacter pylori Infection with Portal Hypertensive Gastropathy in Patients with Liver Cirrhosis

Portal hypertensive gastropathy(PHG) is a complication of portal hypertension and considered one of the causes of upper gasterointestinal bleeding. Helicobacter pylori as one of the most common pathogenic organism worldwide because it infects 50% of the population all over the world. The role of H. Pylori infection in the development of PHG and its severity is controversal. The aim of this study is to determine the frequency of H. pylori infection in cirrhotic patients with PHG and to find out the possible association of H. pylori infection with PHG severity. This study was carried out on 90 patient with cirrhotic liver, divided into two groups according to prescence or absence of PHG diagnosed by upper endoscopy. H.Pylori infection was significantly more frequent in patients with PHG than patients without PHG. H.Pylori infection was significantly more frequent in patients with sever PHG than patients with mild PHG .Splenomegaly, presence of esophageal varices, gastric varices and H.Pylori infection are independent predictors for PHG presence.

Esophageal variceal ligation in the secondary prevention of variceal bleeding: result of long term follow-up

IntroductionLong-term outcome of patients after band ligation have been poorly defined. Therefore, we conducted a long-term follow-up study to delineate the outcome of ligation in patients with portal hypertension in the Hassan II university hospital, Fes, Morocco.MethodsOver 118 months patients treated by endoscopic variceal ligation were received regular follow- up and detailed clinical assessment of at least 24 months.ResultsOne hundred twenty five patients were followed up for a mean of 31 months (range 12-107 months). Obliteration of the varices was achieved in 89.6 % (N = 112) of patients, with 3 +/-1.99 (range 1-8) endoscopy sessions over a period of 14 + /-6.8 weeks (range 3-28). The percentage of variceal recurrence during follow-up after ligation was 20.5 % (N = 23). Recurrence were observed in a mean of 22 months +/- 7.3 (range 3-48). Bleeding rate from recurrent varices was 30.4 % (7/23). Rebleeding from esophageal ulcers occurred in 5.6 % (7/125) of patients. Portal hypertensive gastropathy before and after eradication of varices was 17.6% (N = 22) and 44.6% (N = 50) respectively; p< 0.05. Fundal gastric varices was 30.4% (N = 38) and 35.7% (N = 40) before and after eradication of varices respectively; p> 0.05. The overall mortality was 4 % (N = 5).ConclusionBand ligation was an effective technical approach for variceal obliteration with low rates of variceal recurrence, rebleeding and development of gastric varices. Furthermore, it was associated with frequent development of portal hypertensive gastropathy.

Effect of early propranolol administration on portal hypertensive gastropathy in cirrhotic rats.

To investigate any protective effect of early propranolol administration in the development of portal hypertensive gastropathy in cirrhotic rats. For the development of liver cirrhosis and portal hypertensive gastropathy, 60 rats underwent ligation of the left adrenal vein and complete devascularization of the left renal vein, followed by phenobarbital and carbon tetrachloride (CCl(4)) administration. After two weeks of CCl(4) administration, the rats were randomly separated into two groups. In group A, propranolol was continuously administered intragastrically throughout the study, whereas in group B normal saline (placebo) was administered instead. Hemodynamic studies and vascular morphometric analysis of gastric sections were performed after complete induction of cirrhosis. Vascular morphometric studies showed higher numbers of vessels in all mucosal layers in the control group. Statistical analysis revealed a significantly higher total vascular surface in the control group compared to the propranolol group, but with no statistically significant difference between the mean vascular surfaces between the groups. Our study clearly shows that the increased mucosal blood flow is manifested by a marked increase of vessel count. Early propranolol's administration in portal hypertensive cirrhotic rats seems to prevent intense gastric vascular congestion that characterizes portal hypertensive gastropathy.

PORTAL HYPERTENSIVE GASTROPATHY (literature review)

This article reviews the current literature in order to evaluate clinical and experimental data on the portal hypertensive gastropathy. In the last two decades, portal hypertensive gastropathy (PHG) has emerged as a new nosological entity that can be included among the complications of liver cirrhosis. Pathogenesis of PHG is not clearly defined, but there is very close relationship between portal hypertension and development of PHG. PHG is a potential source of gastrointestinal bleeding in patients with cirrhosis and portal hypertension. In this reason PHG attract attention of investigators.

Pathogenesis in Portal Hypertensive Gastropathy Due to Liver Cirrhosis

The recent advances of endoscopic examination had proven that source of upper gastrointestinal bleeding in liver cirrhosis is not always caused by esophageal varices rupture but also gastric mucosal lesion. The prevalence of gastric ulcer in patients with liver cirrhosis is higher than healthy individuals. Imbalance of defensive and aggressive factors of gastric mucosa may involve in development of portal hypertensive gastropathy (PHG). Several studies reported hemodynamic changes associated wuth portal hypertension causing decreased mucus layer thickness as one of mechanism of PHG. Other etiologic factors of PHG were hypoacidity, hypergastrinemia, reduced hexosamin concentration, mucus metabolic function associated with decreased prostaglandin E2 (PGE2), and increased nitric oxyde (NO) which had caused mucus wall thickness changes. Gastric mucus damage induced by portal hypertension has important role in the pathogenesis of gastric ulcer in liver cirrhosis. Keywords : Pathogenesis, PHG, liver cirrhosis

Portal Hypertensive gastropathy.

Portal hypertensive gastropathy (PHG), a term used to describe the endoscopic appearance of gastric mucosa with a characteristic mosaic-like pattern with or without red spots, is a common finding in patients with portal hypertension. Current classification systems that describe the severity of PHG have many limitations, but it appears that simple grading systems have better inter- and intraobserver agreement. The wide variation in the reported prevalence of PHG is probably related to selection bias, absence of uniform criteria and classification, and more importantly, the differences in inter- and intraobserver variation. Pathogenesis of PHG is not clearly defined, but there is a very close relationship between portal hypertension and development of PHG. GAVE is a separate entity from PHG, but patients with severe PHG may have a GAVE-like appearance in the gastric antrum. Acute bleeding from PHG, seen usually in the presence of severe PHG, is often mild and self-limiting. Currently, the only treatment that could be recommended for prophylaxis of bleeding from PHG is nonselective B-blockers.

CAUSES AND MANAGEMENT OF PORTAL HYPERTENSION IN THE PEDIATRIC POPULATION

Therapeutic options for children with portal hypertension now include a broad range of pharmacologic, endoscopic, and surgical procedures. Thoughtful application of all of these options can improve quality of life by decreasing the complications of portal hypertension and can decrease mortality by preventing the consequences of variceal hemorrhage. The development of portal hypertensive gastropathy following palliative procedures such as endoscopic sclerotherapy and band ligation may limit their long-term success in children. The excellent results now obtained with selective portosystemic shunts and liver transplantation assure that definitive surgical treatments will continue to be important components in the treatment of children with portal hypertensive complications or progressive liver disease. Evolving procedures, such as TIPS, represent excellent short-term life-preserving techniques to stabilize critically ill patients while awaiting liver transplantation. Their role in the future, long-term management of children is yet to be defined.

Do alterations in the rate of gastric emptying after injection sclerotherapy for oesophageal varices play any role in the development of portal hypertensive gastropathy?

Bleeding from portal hypertensive gastropathy (PHG) has been estimated to account for upto 30% of all upper gastrointestinal haemorrhage in patients with cirrhosis and portal hypertension. Although portal hypertension seems to be an essential prerequisite, the precise mechanisms responsible for the development of PHG are unknown. The aim of this study was to examine the role of injection sclerotherapy of oesophageal varices in the development of PHG. Gastric emptying was studied using a radionuclide test meal with the emptying characteristics of a slow liquid in 57 patients with cirrhosis and/or portal hypertension (median age 53 yrs), of whom 34 had received injection sclerotherapy for their oesophageal varices and 20 normal healthy volunteers (median age 42 yrs). As vagal damage is associated with more rapid emptying of liquids, despite hold up of solids, this technique might be expected to demonstrate such damage if gastric emptying was accelerated. The results indicated that there was no difference in the rate of gastric emptying between normal healthy volunteers and portal hypertensive patients. However, patients who had received injection sclerotherapy emptied their stomachs faster than those who had not (p<0.05). Furthermore, the speed of gastric emptying correlated directly with the number of injections (r=0.41; p=0.02) and the volume of sclerosant injected (r=0.39; p=0.03). These observations suggest that injection sclerotherapy for oesophageal varices results in disturbances of gastric emptying that may contribute to the pathogenesis of portal hypertensive gastropathy.

静脈瘤供血路と食道静脈瘤に対する内視鏡的結紮術後のportal hypertensive gastropathyの進展

静脈瘤供血路と食道静脈瘤に対する内視鏡的結紮術後のportal hypertensive gastropathyの進展

Chronic administration of octreotide ameliorates portal hypertension and portal hypertensive gastropathy in rats with cirrhosis.

1. Portal hypertension and hyperdynamic circulation have been postulated to play a role in the pathogenesis of portal hypertensive gastropathy. Administration of octreotide to portal hypertensive rats has been shown to reduce portal pressure and ameliorate hyperdynamic circulation. 2. This study investigated the effects of chronic administration of octreotide on systemic and portal haemodynamics and the development of portal hypertensive gastropathy in carbon tetrachloride-induced cirrhotic rats. 3. After 12 weeks of carbon tetrachloride induction, cirrhotic rats were randomly assigned to receive either placebo (5% dextrose in water) or octreotide (65 micrograms/kg in 5% dextrose in water) subcutaneously twice daily for 10 days. Haemodynamic studies with a thermodilution technique and gastric morphometric analyses were performed at 10 days after treatment. 4. In cirrhotic rats, octreotide treatment induced a significant increase in systemic vascular resistance (2.7 +/- 0.2 versus 3.4 +/- 0.2 mmHg/ml.min-1.100 g-1, P < 0.05) and decrease in portal pressure (12.5 +/- 1.2 versus 9.9 +/- 0.5 mmHg, P < 0.05) compared with placebo-treated rats. In addition, octreotide treatment significantly reduced the mean cross-sectional area of gastric mucosal vessels (2290 +/- 145 versus 1810 +/- 101 micron 2, P < 0.05). 5. This study shows that chronic octreotide treatment ameliorates the development of portal hypertensive gastropathy in cirrhotic rats. The effect of octreotide on portal hypertensive gastropathy may, at least partly, be due to the alleviation of portal hypertension and hyperdynamic circulation.

Variceal inflow vessels and the development of portal hypertensive gastropathy after endoscopic ligation therapy for esophageal varices

Variceal inflow vessels and the development of portal hypertensive gastropathy after endoscopic ligation therapy for esophageal varices

Role of extravariceal collateral channels in the development of portal-hypertensive gastropathy before and after sclerotherapy.

We investigated whether extravariceal collateral pattern contributed to the development of portal-hypertensive gastropathy (PHG) before and after sclerotherapy. Ninety-nine patients with cirrhosis and large esophageal varices were examined in this retrospective study. They were divided into four groups according to transhepatic portographic findings: group A (with neither paraesophageal veins nor gastrorenal shunt; n = 46), group B (with paraesophageal veins; n = 27), group C (with gastrorenal shunt; n = 14), and group D (with paraesophageal veins and gastrorenal shunt; n = 12). To assess PHG, endoscopic examinations were carried out before and 1 week and 1 month after sclerotherapy. The severity of PHG was classified according to a modified McCormack's classification and scored as: absence, 0; mild, 1; severe, 2. There were no significant differences in age, sex, cause of cirrhosis, severity of liver dysfunction, and extent of esophageal varices in the four groups. The PHG score before sclerotherapy was significantly higher in group A than in either group C (P < 0.05) or group D patients (P < 0.05). The calculated, integrated incremental change in PHG score after sclerotherapy was significantly higher in group A than in group C (P < 0.01) and group D patients (P < 0.01). Although the integrated change in PHG score was lower in group B than in group A patients, the difference was not significant (P = 0.68). These results suggest that gastrorenal shunt, but not paraesophageal veins, may play a protective role in the development of PHG before and after sclerotherapy.

Endoscopic and ultrasound criteria predicting less development of portal-hypertensive gastropathy in hepatic cirrhosis

Endoscopic and ultrasound criteria predicting less development of portal-hypertensive gastropathy in hepatic cirrhosis

Tumor necrosis factor-alpha regulates inducible nitric oxide synthase gene expression in the portal hypertensive gastric mucosa of the rat

Increased expression of both nitric oxide synthase (NOS) and tumor necrosis factor-alpha (TNF-α) have been implicated in the hyperdynamic circulation of portal hypertension. Since overexpression of these proteins would affect gastric mucosal defenses, which are impaired in portal hypertension, we examined the expression and interrelationships of TNF-α and NOS in the gastric mucosa of portal hypertensive rats. Following staged portal vein ligation, gastric strips from portal hypertensive rats were incubated in organ culture medium with or without TNF-α antibody. The expression of TNF-α and NOS mRNAs was assessed by reverse transcription—polymerase chain reaction (RT-PCR) at baseline and after 1, 2, and 6 hours of incubation. RT-PCR demonstrated a threefold increase in inducible NOS mRNA and a 50% increase in TNF-α mRNA expression at baseline in portal hypertensive animals as compared to sham-operated animals. In tissue incubated with TNF-α neutralizing antibody, inducible NOS mRNA expression was significantly decreased by 40%, 70%, and 80% after 1, 2, and 6 hours, respectively. Since increased TNF-α and NOS production could potentially impair gastric mucosal defenses, our findings suggest a major role for these proteins in the development of portal hypertensive gastropathy.

Aminoguanidine corrects hyperdynamic circulation without ameliorating portal hypertension and portal hypertensive gastropathy in anesthetized portal hypertensive rats

Background/Aims: Portal hypertension and hyperdynamic circulation (i.e. generalized vasolidation and increased cardiac output and regional organ blood flows) may play an important role in the development of portal hypertensive gastropathy. This study investigated the effect of chronic administration of aminoguanidine, a selective inducible nitric oxide synthase inhibitor, to portal hypertensive rats on hemodynamics and the development of portal hypertensive gastropathy. Methods: Partial portal vein-ligated or sham-operated rats were randomly assigned to receive either placebo (distilled water) or aminoguanidine (∼100 mg/kg per day subcutaneously) for 2 days prior to and 14 days. Hemodynamic studies with a thermodilution technique and gastric morphometric analysis were performed at 14 days after the operation. Results: In rats given placebo, portal vein-ligated rats had a significantly lower mean arterial pressure and systemic vascular resistance associated with a significantly higher cardiac index and portal pressure than sham-operated rats ( p<0.05). In portal vein-ligated rats aminoguanidine induced a significant increase in mean arterial pressure and systemic vascular resistance accompanied by a significant decrease in cardiac index ( p<0.05) without changes in portal pressure ( p<0.05). Despite persistence of portal hypertension, the aminoguanidine-treated portal vein-ligated rats had similar mean arterial pressure, cardiac index, and systemic vascular resistance as seen in placebo-treated sham-operated rats. The mean cross-sectional area of gastric mucosal vessels was significantly higher in placebo-treated portal vein-ligated than in placebo-treated sham-operated rats ( p<0.05). Treatment with aminoguadinidine did not induce changes in the mean cross-sectional area of gastric mucosal vessels in either portal vein-ligated or sham-operated rats ( p<0.05). Conclusion: The results show that in portal hypertensive rats long-term aminoguanidine therapy corrects the hyperdynamic circulation without inducing changes in portal pressure and ameliorating the development of portal hypertensive gastropathy. This study suggests that, instead of correcting hyperdynamic circulation, treatment of portal hypertensive gastropathy should be aimed at reducing portal pressure.

F4-6 Large gastric varices protect development of portal-hypertensive gastropathy: A study of 510 cirrhotic patients

F4-6 Large gastric varices protect development of portal-hypertensive gastropathy: A study of 510 cirrhotic patients

食道静脈瘤合併肝硬変例における胃粘膜病変と門脈血行動態の検討

We evaluated the association between portal hypertensive gastropathy and portal hemodynamics. The subjects were 35 patients with liver cirrhosis complicated by esophageal varices in whom the clinical course were observed for 3 years. They were classified into the group who developed a spleno-renal shunt during the course and that who did not. The incidence of portal hypertensive gastropathy before observation was similar between the two groups. Changes in portal hypertensive gastropathy during the course were slighter in the spleno-renal shunt group than the non-shunt group. Since no difference were observed in the size of spleen, the diameter of the main trunk of the portal vein, or blood biochemical findings between the two groups during the observation period, the development of the spleno-renal shunt, ie, the state of the development of the collateral circulation seems to be involved in the development of portal hypertensive gastropathy.

Diagnosis and treatment using endoscopy

Percutaneous endoscopic gastrostomy feeding has continued to gain popularity with a 12-fold increase in its use in the United Kingdom in the past 4 years. There is now a large body of literature detailing the outcome and complications of percutaneous endoscopic gastronomy feeding. A recent randomized controlled study comparing percutaneous endoscopic gastrostomy feeding with nasogastric feeding in patients requiring long-term nutritional support indicates that percutaneous endoscopic gastrostomy feeding is superior in improving nutritional status and is better tolerated. Portal hypertensive gastropathy is being increasingly recognized as a cause of upper gastrointestinal hemorrhage. Recent studies have highlighted the role of variceal sclerotherapy and the anatomic pattern of the blood supply to the stomach as factors that promote the development of portal hypertensive gastropathy. β-Blockers decrease the incidence of bleeding from portal hypertensive gastropathy and should be used in most patients both prophylactically and after variceal sclerotherapy. Further evidence has accumulated indicating that endoscopic injection of ulcers with visible vessels decreases the risk of rebleeding. Endoscopic therapy is also beneficial for the treatment of Dieulafoy's lesions. A steady flow of publications continues to point to endosonography as a powerful tool in the diagnosis and staging of upper gastrointestinal malignancy, and for the detection of residual tumor tissue after therapy. Current Opinion in Gastroenterology 1993, 9:917-921