Acute upper gastrointestinal bleeding due to portal hypertension in a patient with primary myelofibrosis:A case report

BACKGROUND Acute upper gastrointestinal bleeding is a common medical emergency that has a 10%hospital mortality rate.According to the etiology,this disease can be divided into acute varicose veins and nonvaricose veins.Bleeding from esophageal varices is a life-threatening complication of portal hypertension.Portal hypertension is a clinical syndrome defined as a portal venous pressure that exceeds 10 mmHg.Cirrhosis is the most common cause of portal hypertension,and thrombosis of the portal system not associated with liver cirrhosis is the second most common cause of portal hypertension in the Western world.Primary myeloproliferative disorders are the main cause of portal venous thrombosis,and somatic mutations in the Janus kinase 2 gene(JAK2 V617F)can be found in approximately 90% of polycythemia vera,50% of essential thrombocyrosis and 50% of primary myelofibrosis.CASE SUMMARY We present a rare case of primary myelofibrosis with gastrointestinal bleeding as the primary manifestation that presented as portal-superior-splenic mesenteric vein thrombosis.Peripheral blood tests revealed the presence of the JAK2 V617F mutation.Bone marrow biopsy ultimately confirmed the diagnosis of myelofibrosis(MF-2 grade).CONCLUSION In patients with acute esophageal variceal bleeding due to portal hypertension and vein thrombosis without cirrhosis,the possibility of myeloproliferative neoplasms should be considered,and the JAK2 mutation test should be performed.

Triplex operation for portal hypertension with esophageal variceal bleeding:report of 140 cases

BACKGROUND:Portal hypertension is a common dis ease. The surgical therapy of this disease focuses on the re sultant upper digestive tract bleeding, which can imperi patients' life directly. This study was to evaluate the effect of triplex operation ( mesocaval C shunt with artificia graft, ligation of the coronary vein and splenic artery) on portal hypertension and its associated upper digestive tract bleeding. METHODS: A retrospective study was made on clinical da- ta of 140 patients undergoing triplex operation, who had suffered from portal hypertension and upper digestive tract bleeding. RESULTS: Postoperative portal pressure was 25-43 cmH2 O ( preoperative portal pressure 27-45 cmH2 O ) with the average reduction of 10 cmH2O. One patient (0.7%) died of cerebrovascular disease. Five patients (3.5%) suffered from mild hepatic encephalopathy, which was ameliorated through conservative treatment. Lymphatic fistula occurred in 3 patients (2.1% ) who recovered without treatment 5, 10 days and 3 months after operation respectively. One hundred patients were followed up for 1 month to 6 years without recurrent hemorrhage or hepatic encephalopathy. Hypersplenism and ascites disappeared in 70 patients (70% ) and 80 patients (80% ) respectively. A significant reduction of ascites was seen in 12 patients(12% ). The arti- ficial vessels remained unblocking detected by B type ultra- sonography and Doppler sonography in 95 patients (95% ). CONCLUSION: Triplex operation is suitable for patients with the following portal hypertensions; portal hyperten- sion caused by simple occlusion of the hepatic vein (a patho- logical type of Budd-Chiari syndrome); thrombosis of the portal vein or prehepatic portal hypertension because of cavernous transformation; intrahepatic portal hypertension with rebleeding after splenectomy or non-operation, and those patients with liver function in grade A or B according to the Child-Pugh classification.

Noninvasive methods for prediction of esophageal varices in pediatric patients with portal hypertension

AIM: To evaluate clinical and laboratory parameters for prediction of bleeding from esophageal varices (EV) in children with portal hypertension. METHODS: Retrospective study of 103 children (mean age: 10.1 ± 7.7 years), 95.1% with intrahepatic portal hypertension. All patients had no history of bleeding and underwent esophagogastroduodenoscopy for EV screening. We recorded variceal size (F1, F2 and F3), red-color signs and portal gastropathy, according to the Japanese Research Society for Portal Hypertension classification. Patients were classified into two groups: with and without EV. Seven noninvasive markers were evaluated as potential predictors of EV: (1) platelet count; (2) spleen size z score, expressed as a standard deviation score relative to normal values for age; (3)platelet count to spleen size z score ratio; (4) platelets count to spleen size (cm) ratio; (5) the clinical prediction rule (CPR); (6) the aspartate aminotransferase to platelet ratio index (APRI); and (7) the risk score. RESULTS: Seventy-one children had EV on first endoscopy. On univariate analysis, spleen size, platelets, CPR, risk score, APRI, and platelet count to spleen size z score ratio showed significant associations. The best noninvasive predictors of EV were platelet count [area under the receiver operating characteristic curve (AUROC) 0.82; 95%CI: 0.73-0.91], platelet: spleen size z score (AUROC 0.78; 95%CI: 0.67-0.88), CPR (AUROC 0.77; 95%CI: 0.64-0.89), and risk score (AUROC 0.77; 95%CI: 0.66-0.88). A logistic regression model was applied with EV as the dependent variable and corrected by albumin, bilirubin and spleen size z score. Children with a CPR < 114 were 20.7-fold more likely to have EV compared to children with CPR > 114. A risk score > -1.2 increased the likelihood of EV (odds ratio 7.47; 95%CI: 2.06-26.99). CONCLUSION: Children with portal hypertension with a CPR below 114 and a risk score greater than -1.2 are more likely to have present EV. Therefore, these two tests can be helpful in selecting children for endoscopy.

Multiple esophageal variceal ruptures with massive ascites due to myelofibrosis-induced portal hypertension

A 75-year old man had been diagnosed at 42 years of age as having polycythemia vera and had been monitored at another hospital. Progression of anemia had been recognized at about age 70 years, and the patient was thus referred to our center in 2008 where secondary myelofibrosis was diagnosed based on bone marrow biopsy findings. Hematemesis due to rupture of esophageal varices occurred in January and February of 2011. The bleeding was stopped by endoscopic variceal ligation. Furthermore, in March of the same year, hematemesis recurred and the patient was transported to our center. He was in irreversible hemorrhagic shock and died. The autopsy showed severe bone marrow fibrosis with mainly argyrophilic fibers, an observation consistent with myelofibrosis. The liver weighed 1856 g the spleen 1572 g, indicating marked hepatosplenomegaly. The liver and spleen both showed extramedullary hemopoiesis. Myelofibrosis is often complicated by portal hypertension and is occasionally associated with gastrointestinal hemorrhage due to esophageal varices. A patient diagnosed as having myelofibrosis needs to be screened for esophageal/gastric varices. Myelofibrosis has a poor prognosis. Therefore, it is necessary to carefully decide the therapeutic strategy in consideration of the patient's concomitant conditions, treatment invasiveness and quality of life.

Computed tomography combined with gastroscopy for assessment of pancreatic segmental portal hypertension

BACKGROUND Pancreatic segmental portal hypertension(PSPH) is the only type of portal hypertension that can be completely cured. However, it can easily cause varicose veins in the esophagus and stomach and hemorrhage in the digestive tract.AIM To explore the application of computed tomography(CT) to examine the characteristics of PSPH and assess the risk level.METHODS This was a retrospective analysis of CT images of 22 patients diagnosed with PSPH at our center. Spearman correlation analysis was performed using the range of esophageal and gastric varices(measured by the vertical gastric wall), the ratio of the width of the splenic portal vein to that of the compression site(S/C ratio), the degree of splenomegaly, and the stage determined by gastroscopy. This study examined whether patients experienced gastrointestinal bleeding within 2 wk and combined CT and gastroscopy to explore the connection between bleeding and CT findings.RESULTS The range of esophageal and gastric varices showed the best correlation in the diagnosis of PSPH(P < 0.001), and the S/C ratio(P = 0.007) was correlated with the degree of splenomegaly(P = 0.021) and PSPH(P < 0.05). This study revealed that male patients were more likely than females to progress to grade 2 or grade 3 as determined by gastroscopy. CT demonstrated excellent performance, with an area under the curve of 0.879.CONCLUSION CT can be used to effectively analyze the imaging signs of PSPH, and CT combined with gastroscopy can effectively predict the risk level of gastrointestinal bleeding.

Portal hypertension and gastrointestinal bleeding:Diagnosis,prevention and management

Bleeding from esophageal varices is a life threatening complication of portal hypertension.Primary prevention of bleeding in patients at risk for a first bleeding episode is therefore a major goal.Medical prophylaxis consists of non-selective beta-blockers like propranolol or carvedilol.Variceal endoscopic band ligation is equally effective but procedure related morbidity is a drawback of the method.Therapy of acute bleeding is based on three strategies:vasopressor drugs like terlipressin,antibiotics and endoscopic therapy.In refractory bleeding,self-expandable stents offer an option for bridging to definite treatments like transjugular intrahepatic portosystemic shunt(TIPS).Treatment of bleeding from gastric varices depends on vasopressor drugs and on injection of varices with cyanoacrylate.Strategies for primary or secondary prevention are based on non-selective beta-blockers but data from large clinical trials is lacking.Therapy of refractory bleeding relies on shuntprocedures like TIPS.Bleeding from ectopic varices,portal hypertensive gastropathy and gastric antral vascular ectasia-syndrome is less common.Possible medical and endoscopic treatment options are discussed.

Clinical role of non-invasive assessment of portal hypertension

Measurement of portal pressure is pivotal in the evaluation of patients with liver cirrhosis. The measurement of the hepatic venous pressure gradient represents the reference method by which portal pressure is estimated. However, it is an invasive procedure that requires significant hospital resources, including experienced staff, and is associated with considerable cost. Non-invasive methods that can be reliably used to estimate the presence and the degree of portal hypertension are urgently needed in clinical practice. Biochemical and morphological parameters have been proposed for this purpose, but have shown disappointing results overall. Splanchnic Doppler ultrasonography and the analysis of microbubble contrast agent kinetics with contrast-enhanced ultrasonography have shown better accuracy for the evaluation of patients with portal hypertension. A key advancement in the non-invasive evaluation of portal hypertension has been the introduction in clinical practice of methods able to measure stiffness in the liver, as well as stiffness/congestion in the spleen. According to the data published to date, it appears to be possible to rule out clinically significant portal hypertension in patients with cirrhosis (i.e., hepatic venous pressure gradient &#x02265; 10 mmHg) with a level of clinically-acceptable accuracy by combining measurements of liver stiffness and spleen stiffness along with Doppler ultrasound evaluation. It is probable that the combination of these methods may also allow for the identification of patients with the most serious degree of portal hypertension, and ongoing research is helping to ensure progress in this field.

Right liver lobe/albumin ratio:Contribution to non-invasive assessment of portal hypertension

AIM： To study the value of biochemical and ultrasonographic parameters in prediction of presence and size of esophageal varices.METHODS： The study includes selected cirrhotic patients who underwent a complete biochemical workup, upper digestive endoscopic and ultrasonographic examinations. Albumin/right liver lobe diameter and platelet count/spleen diameter ratios were calculated. The correlation between calculated ratio and the presence and degree of esophageal varices was evaluated.RESULTS： Ninety-four subjects （62 males, 32 females）, with a mean age of 52.32 ± 13.60 years, were studied. Child-Pugh class A accounted for 42.6%, class 13 37.2%, whereas class C 20.2%. Esophageal varices （OE） were not demonstrated by upper digestive endoscopy in 24.5%, while OE grade Iwas found in 22.3% patients, grade Ⅱ in 33.0%, grade m in 16.0%, and grade iV in 4.3%. The mean value of right liver lobe diameter/ albumin ratio was 5.51± 1.82 （range from 2.76 to 11.44）, while the mean platelet count/spleen diameter ratio was 1017.75 ± 729.36 （range from 117.39 to 3362.50）, respectively. Statistically significant correlation was proved by Spearman＇s test between OE grade and calculated ratios. The P values were 0.481 and -0.686, respectively.CONCLUSION： The right liver lobe diameter/albumin and platelet count/spleen diameter ratios are noninvasive parameters providing accurate information pertinent to determination of presence of esophageal varices, and their grading in patients with liver cirrhosis.

Role of endoscopy in management of gastrointestinal complications of portal hypertension

The management of patients with gastrointestinal complications of portal hypertension is often complex and challenging. The endoscopy plays an important role in the management of these patients. The role of endoscopy is both diagnostic and interventional and in the last years the techniques have undergone a rapid expansion with the advent of different and novel endoscopic modalities, with consequent improvement of investigation and treatment of these patients. The choice of best therapeutic strategy depends on many factors: baseline disease, patient's clinical performance and the timing when it is done if in emergency or a prophylactic approaches. In this review we evaluate the endoscopic management of patients with the gastrointestinal complications of portal hypertension.

Portal hypertension exacerbates intrahepatic portosystemic venous shunt and further induces refractory hepatic encephalopathy: A case report

BACKGROUND Intrahepatic portosystemic venous shunt(IPSVS)is a rare hepatic disease with different clinical manifestations.Most IPSVS patients with mild shunts are asymptomatic,while the patients with severe shunts present complications such as hepatic encephalopathy.For patients with portal hypertension accompanied by intrahepatic shunt,portal hypertension may lead to hemodynamic changes that may result in exacerbated portal shunt and increased shunt flow.CASE SUMMARY A 57-year-old man,with the medical history of chronic hepatitis B and liver cirrhosis,was admitted to our hospital with abnormal behavior for 10 mo.He had received the esophageal varices ligation and entecavir therapy 1 year ago.Comparing with former examination results,the degree of esophageal varices was significantly reduced,while the right branch of the portal vein was significantly expanded and tortuous.Meanwhile,abdominal ultrasound presented the right posterior branch of portal vein connected with the retrohepatic inferior vena cava.The imaging findings indicated the diagnosis of IPSVS and hepatic encephalopathy.Instead of radiologic interventions or surgical therapies,this patient had only accepted symptomatic treatment.No recurrence of hepatic encephalopathy was observed during 1-year follow-up.CONCLUSION Hemodynamic changes may exacerbate intrahepatic portosystemic shunt.The intervention or surgery should be carefully applied to patients with severe portal hypertension due to the risk of hemorrhage.

Non-invasive splenic parameters of portal hypertension:Assessment and utility

BACKGROUND Portal hypertension is a major complication of cirrhosis that is associated with significant morbidity and mortality.The present gold-standard method to risk stratify and observe cirrhosis patients with portal hypertension is hepatic venous pressure gradient measurement or esophagogastroduodenoscopy.However,these methods are invasive,carry a risk of complications and are associated with significant patient discomfort.Therefore,non-invasive splenic parameters are of clinical interest as potential useful markers in determining the presence of portal hypertension.However,diagnostic accuracy and reproducibility remains unvalidated.AIM To assess the diagnostic accuracy of spleen stiffness,area and diameter in predicting the presence of portal hypertension.METHODS Of 50 patients with varying liver disease pathologies were prospectively recruited from the St.Mary’s Hospital Liver Unit in London;25 with evidence of portal hypertension and 25 with no evidence of portal hypertension.Liver stiffness,spleen stiffness,spleen diameter and spleen area were measured using the Philips Affiniti 70 elastography point quantification point shear wave elastography system.The aspartate aminotransferase-to-platelet-ratio-index(APRI)score was also calculated.Performance measures,univariate and multivariate logistic regression were used to evaluate demographic,clinical and elastography variables.Interclass correlation coefficient was used to determine the reproducibility of splenic area and diameter.RESULTS On univariate and individual performance,platelet count[area under the receiver operating characteristic(AUROC)0.846,P value<0.001],spleen area(AUROC 0.828,P value=0.002)and APRI score(AUROC 0.827,P value<0.001)were the most accurate variables in identifying the presence of portal hypertension.On multivariate logistic regression models constructed,the combination of spleen area greater than 57.90 cm2 and platelet count less than 126×10^9 had 63.2%sensitivity and 100%specificity,100%positive predictive value and 100%negative predictive value.An alternative combination of spleen stiffness greater than 29.99 kPa and platelet count less than 126×10^9 had 88%sensitivity,75%specificity,78.6%positive predictive value and 85.7%negative predictive value.An interclass correlation coefficient value of 0.98(95%CI:0.94-0.99,P value<0.001)and 0.96(95%CI:0.91-0.99,P value<0.001)were determined for inter-operator variability for spleen area and diameter respectively.CONCLUSION Spleen area,spleen stiffness and platelet count may be useful markers to assess the presence of portal hypertension in patients of various etiologies.

Splenic artery ligature associated with endoscopic banding for schistosomal portal hypertension

AIM: To propose a less invasive surgical treatment for schistosomal portal hypertension.

CA-125 Significance in Cirrhosis and Correlation with Disease Severity and Portal Hypertension: A Retrospective Study

Background and Aims:To evaluate the prevalence and significance of elevated cancer antigen-125(CA-125)levels in patients with cirrhosis being treated in a tertiary care liver center and its correlation with objective markers of disease severity.Methods:We retrospectively reviewed medical records of 172 adult patients with cirrhosis(due to any etiology)after obtaining CA-125 serum analysis.Demographics,etiology of cirrhosis,model of end-stage liver disease(MELD)score,Child's Turcotte-Pugh classification,albumin bilirubin(ALBI)score,degree of ascites,presence of esophageal varices,serum CA-125 level and various other parameters were collected.Statistical analysis was performed using SPSS software and descriptive statistics.Results:Elevated CA-125 levels were noted in 147 patients(85%)of the study population.Higher MELD score was associated with higher CA-125 levels(p=0.001).Statistically significant correlation was observed between elevated CA-125 levels and degree of ascites(p<0.001),ALBI score(p<0.001)and Child's Turcotte-Pugh class(p<0.001).No correlation was observed with presence or absence of esophageal varices.Near-normal CA-125 levels were noted in patients with cirrhosis but undetectable ascites on ultrasound imaging.No differences were observed in mean values between male and female patients(p=0.207).Regression analysis confirmed that CA-125 levels had a better correlation with degree of ascites than MELD score or ALBI score.Conclusions:Elevated CA-125 levels were noted in 85%of patients with cirrhosis at our center.Our study establishes that the more advanced the degree of decompensation based on MELD score,Child's Turcotte-Pugh classification and ALBI score,the higher the elevation in CA-125.Absence of ascites was associated with normal CA-125 level,with a direct correlation between high levels and worsening ascites,but there was no statistically significant correlation with esophageal varices,indicating that elevated CA-125 levels could be related to mechanical stretch of the peritoneum rather than portal hypertension itself.Further multi-centered studies are required to confirm and validate these findings.

Per rectal portal scintigraphy as a useful tool for predicting esophageal variceal bleeding in cirrhotic patients

AIM: To investigate potential roles of per rectal portal scintigraphy in diagnosis of esophageal varices and predicting the risk of bleeding.METHODS: Fifteen normal subjects and fifty cirrhotic patients with endoscopically confirmed esophageal varices were included. Patients were categorized into bleeder and non-bleeder groups according to history of variceal bleeding. All had completed per rectal portal scintigraphy using 99mTechnetium pertechnetate. The shunt index was calculated from the ratio of 99mTechnetium pertechnetate in the heart and the liver. Data were analyzed using Student’s t-test and receiver operating characteristics.RESULTS: Cirrhotic patients showed a higher shunt index than normal subjects (63.80 ± 25.21 vs 13.54 ± 6.46, P < 0.01). Patients with variceal bleeding showed a higher shunt index than those without bleeding (78.45 ± 9.40 vs 49.35 ± 27.72, P < 0.01). A shunt index of over 20% indicated the presence of varices and that of over 60% indicated the risk of variceal bleeding.CONCLUSION: In cirrhotic patients, per rectal portal scintigraphy is a clinically useful test for identifying esophageal varices and risk of variceal bleeding.

Computed tomography for prediction of esophageal variceal bleeding

This letter to the editor relates to the study entitled“The role of computed tomography for the prediction of esophageal variceal bleeding:Current status and future perspectives”.Esophageal variceal bleeding(EVB)is one of the most common and severe complications related to portal hypertension(PH).Despite marked advances in its management during the last three decades,EVB is still associated with significant morbidity and mortality.The risk of first EVB is related to the severity of both PH and liver disease,and to the size and endoscopic appearance of esophageal varices.Indeed,hepatic venous pressure gradient(HVPG)and esophagogastroduodenoscopy(EGD)are currently recognized as the“gold standard”and the diagnostic reference standard for the prediction of EVB,respectively.However,HVPG is an invasive,expensive,and technically complex procedure,not widely available in clinical practice,whereas EGD is mainly limited by its invasive nature.In this scenario,computed tomography(CT)has been recently proposed as a promising modality for the non-invasive prediction of EVB.While CT serves solely as a diagnostic tool and cannot replace EGD or HVPG for delivering therapeutic and physiological information,it has the potential to enhance the prediction of EVB more effectively when combined with liver disease scores,HVPG,and EGD.However,to date,evidence concerning the role of CT in this setting is still lacking,therefore we aim to summarize and discuss the current evidence concerning the role of CT in predicting the risk of EVB.

Comprehensive approach to esophageal variceal bleeding:From prevention to treatment

Esophageal variceal bleeding is a severe complication often associated with portal hypertension,commonly due to liver cirrhosis.Prevention and treatment of this condition are critical for patient outcomes.Preventive strategies focus on reducing portal hypertension to prevent varices from developing or enlarging.Primary prophylaxis involves the use of non-selective beta-blockers,such as propranolol or nadolol,which lower portal pressure by decreasing cardiac output and thereby reducing blood flow to the varices.Endoscopic variceal ligation(EVL)may also be employed as primary prophylaxis to prevent initial bleeding episodes.Once bleeding occurs,immediate treatment is essential.Initial management includes hemodynamic stabilization followed by pharmacological therapy with vasoactive drugs such as octreotide or terlipressin to control bleeding.Endoscopic intervention is the cornerstone of treatment,with techniques such as EVL or sclerotherapy applied to directly manage the bleeding varices.In cases where bleeding is refractory to endoscopic treatment,transjugular intrahepatic portosystemic shunt may be considered to effectively reduce portal pressure.Long-term management after an acute bleeding episode involves secondary prophylaxis using betablockers and repeated EVL sessions to prevent rebleeding,complemented by monitoring and managing liver function to address the underlying disease.In light of new scientific evidence,including the findings of the study by Peng et al,this editorial aims to review available strategies for the prevention and treatment of esophageal varices.

Non-invasive assessment of esophageal varices:Status of today

With increasing burden of compensated cirrhosis,we desperately need noninvasive methods for assessment of clinically significant portal hypertension.The use of liver and spleen stiffness measurement helps in deferring unnecessary endoscopies for low risk esophageal varices.This would reduce cost and patient discomfort.However,these special techniques may not be feasible at remote areas where still we need only biochemical parameters.More prospective studies validating the non-invasive risk prediction models are definitely needed.

Platelet counts to spleen diameter ratio:A promising noninvasive tool for predicting esophageal varices in cirrhosis patients

BACKGROUND Liver cirrhosis is the end stage of progressive liver fibrosis as a consequence of chronic liver inflammation,wherein the standard hepatic architecture is replaced by regenerative hepatic nodules,which eventually lead to liver failure.Cirrhosis without any symptoms is referred to as compensated cirrhosis.Complications such as ascites,variceal bleeding,and hepatic encephalopathy indicate the onset of decompensated cirrhosis.Gastroesophageal varices are the hallmark of clini-cally significant portal hypertension.AIM To determine the accuracy of the platelet count-to-spleen diameter(PC/SD)ratio to evaluate esophageal varices(EV)in patients with cirrhosis.METHODS This retrospective observational study was conducted at Tikur Anbessa Specia-lized Hospital and Adera Medical Center from January 1,2019,to December 30,2023.Data were collected via chart review and direct patient interviews using structured questionnaires.The data were exported to the SPSS software version 26 for analysis and clearance.A receiver operating characteristic curve was plotted for splenic diameter,platelet count,and PC/SD ratio to obtain sensitivity,speci-ficity,positive predictive value,negative predictive value,positive likelihood ratio,and negative likelihood ratio.RESULTS Of the 140 participants,67%were men.Hepatitis B(38%)was the most common cause of cirrhosis,followed by cryptogenic cirrhosis(28%)and hepatitis C(16%).Approximately 83.6%of the participants had endoscopic evidence of EV,whereas 51.1%had gastric varices.Decompensated cirrhosis and PC were associated with the presence of EV with adjusted odds ratios of 12.63(95%CI:3.16-67.58,P=0.001)and 0.14(95%CI:0.037-0.52,P=0.004),respectively.A PC/SD ratio<1119 had a sensitivity of 86.32%and specificity of 70%with area under the curve of 0.835(95%CI:0.736-0.934,P<0.001).CONCLUSION A PC/SD ratio<1119 predicts EV in patients with cirrhosis.It is a valuable,noninvasive tool for EV risk assess-ment in resource-limited settings.

Portal hypertensive gastropathy:A systematic review of thepathophysiology,clinical presentation,natural history andtherapy

AIM: To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy(PHG) based on a systematic literature review.METHODS: Computerized search of the literature was performed via Pub Med using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS: PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG.PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt or liver transplantation is highly successful ultimate therapies because they reduce the underlying portal hypertension.CONCLUSION: PHG is important to recognize in patients with cirrhotic or non-cirrhotic portal hypertension because it can cause acute or chronic GI bleeding that often requires pharmacologic therapy.

Endoscopic management of esophageal varices

The rupture of gastric varices results in variceal hemorrhage, which is one the most lethal complications of cirrhosis. Endoscopic therapies for varices aim to reduce variceal wall tension by obliteration of the varix. The two principal methods available for esophageal varices are endoscopic sclerotherapy (EST) and band ligation (EBL). The advantages of EST are that it is cheap and easy to use, and the injection catheter fits through the working channel of a diagnostic gastroscope. Endoscopic variceal ligation obliterates varices by causing mechanical strangulation with rubber bands. The following review aims to describe the utility of EBL and EST in different situations, such as acute bleeding, primary and secondary