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Flow chart for portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE). APC argon plasma coagulation, GAVE gastric antral vascular ectasia, NSBBs non-selective beta blockers, PHG portal hypertensive gastropathy, TIPS transjugular intrahepatic portosystemic shunt
Source publication
The Billroth III guidelines were developed during a consensus meeting of the Austrian Society of Gastroenterology and Hepatology (ÖGGH) and the Austrian Society of Interventional Radiology (ÖGIR) held on 18 February 2017 in Vienna. Based on international guidelines and considering recent landmark studies, the Billroth III recommendations aim to hel...
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Purpose of Review
To provide an overview of the classifications and clinical hallmarks of common cancer-related conditions that contribute to the high incidence of portal hypertension in this population and provide an update on currently available interventional radiology therapeutic approaches.
Recent Findings
In the last few decades, there have...
Citations
... В метаанализе сравнительных исследований лапароскопической и открытой деваскуляризации желудка и пищевода продемонстрировано, что мини-инвазивные эндовидеохирургические вмешательства характеризуются меньшей интраоперационной кровопотерей (p = 0,003) и меньшим периодом госпитализации (p < 0,001), а частота послеоперационных осложнений была одинаковой в обеих группах. Рецидива желудочного кровотечения в раннем послеоперационном периоде не наблюдали, что позволяет считать ЛДЖ и абдоминального отдела пищевода безопасным и эффективным альтернативным минимально инвазивным методом лечения и профилактики желудочных кровотечений портального генеза у больных с СПГ [3,[31][32][33]. Согласно собственным данным, рецидив желудочного кровотечения в раннем периоде после ЛДЖ и абдоминального отдела пищевода развился в 10,7% наблюдений, а в отдаленномв 42,3%. ...
Aim . To analyze the results of modern prevention and treatment strategies applied for bleeding from gastric varices in patients with portal hypertension syndrome.
Materials and methods . The study enrolled 276 patients with portal hypertension, including 187 cases of liver cirrhosis and 89 cases of extrahepatic portal hypertension. 24% of the patients with liver cirrhosis were classified as Child-Turcotte-Pugh Class A, 50% as Class B, and 26% as Class C. The portal vein thrombosis was confirmed in 80% of extrahepatic portal hypertension cases, while isolated splenic vein thrombosis was observed in 20%. Varices GOV1 (Sarin classification) were identified in 126 patients (45.7%), GOV2 in 110 patients (39.8%), and IGV-1 in 40 patients (14.5%). The following interventions were performed: endoscopic ligation, endoscopic sclerotherapy, endovascular techniques (transjugular intrahepatic portosystemic shunt, balloon-occluded retrograde transvenous obliteration), laparoscopic gastric devascularization, and distal splenorenal anastomosis.
Results . Following endoscopic procedures, recurrence of gastric varices was noted in 20% of cases, and bleeding occurred in 7%. The efficacy of endoscopic treatment amounted to 71%; endoscopic ligation for bleeding from GOV1 varices appeared effective in 94.4% of cases. Early recurrence of bleeding developed in 29.4% of patients. The efficacy of endoscopic sclerotherapy for bleeding from GOV2/IGV1 varices comprised 96.7% with early recurrence occurring in 12.9% of patients. The secondary prevention involved multiple endoscopic interventions that led to complete eradication of gastric varices in 34% of cases with recurrent bleeding noted in 9.3% of patients, while persistent recurrence of gastric varices was observed in 66%. A splenorenal anastomosis provided reliable prevention of recurrent bleedings. No shunt thrombosis or mortality was recorded; however, the incidence of post-shunt encephalopathy comprised 16.5%. Transjugular intrahepatic portosystemic shunt facilitated a significant reduction in portal pressure and the enlargement of esophageal and gastric varices. Post-shunt encephalopathy occurred in 48.6% of patients. In the long-term follow-up, a recurrence of esophagogastric bleeding was recorded in one patient. Laparoscopic azygoportal disconnection contributed to the regression of varices in the esophagus and stomach; however, a recurrence of gastric varices developed in 30% of cases and a recurrence of bleeding in 12.5%.
Conclusion . Current medicine obtains a sufficient arsenal of modern methods for the treatment and prevention of bleeding from gastric varices. The choice of treatment and prevention strategies for bleeding in portal hypertension necessitates a differentiated approach, taking into account the etiology and degree of disease decompensation.
... Ascites, a common complication in patients with decompensated cirrhosis, serves as a significant indicator of disease progression throughout the natural course of cirrhosis. Once ascites appears, the 1-year mortality rate is reported to be approximately 20%, and the 5-year mortality rate is approximately 44% [1,2]. The prevention and treatment of ascites remain common challenges in clinical practice. ...
... We have very little confidence in the effect estimate: the true effect is very likely to be substantially different from the estimate of effect Strength of the recommendations Strong (1) The desirable effects of an intervention clearly outweigh the undesirable effects, or clearly do not Weak (2) The balance between the benefits and harms is uncertain, or evidence of any quality shows that the desirable and undesirable effects are closely balanced Ascites can be colorless and transparent, turbid, purulent, hemorrhagic, or chylous. Routine laboratory tests for ascites include cell count and classification, concentration of albumin and total protein. ...
In 2023, Chinese Society of Hepatology of Chinese Medical Association convened a panel of experts to update the Chinese guidelines on the management of ascites and associated complications in cirrhosis which was launched in 2017 and renamed this guidelines as “Guidelines on the Management of Ascites in Cirrhosis.” This comprehensive resource offers essential recommendations for the diagnosis and treatment of cirrhotic ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome.
... VNT was defined as medium or large varices, or small varices with high-risk stigmata. Varices not needing treatment (VNNT) were defined as small varices without high-risk stigmata or no EV [13,14]. ...
Background
Treatment with atezolizumab and bevacizumab has become standard of care for advanced unresectable hepatocellular carcinoma (HCC) but carries an increased gastrointestinal bleeding risk. Therefore, patients are often required to undergo esophagogastroduodenoscopy (EGD) to rule out esophageal varices (EV) prior to initiating therapy, which can delay care and lead to unnecessary procedural risks and health care costs. In 2019, the EVendo score was created and validated as a noninvasive tool to accurately screen out patients who were at low risk for having EV that required treatment. We sought to validate whether the EVendo score could be used to accurately predict the presence of EV and varices needing treatment (VNT) in patients with HCC.
Methods
This was a retrospective multicenter cohort study of patients with HCC from 9/2004 to 12/2021. We included patients who underwent EGDs within 1 year after their HCC diagnosis. We collected clinical parameters needed to calculate an EVendo score at the time of EGD and compared the EVendo model prediction to the gold standard endoscopic report in predicting presence of VNT.
Results
112 with HCC were recruited to this study, with 117 qualifying EGDs. VNT occurred in 39 (33.3%) patients. The EVendo score had a sensitivity of 97.4% and a negative predictive value of 96.9%, supporting the validity in applying EVendo in predicting VNT in HCC.
Conclusion
In this study, we validated the use of the EVendo score in ruling out VNT in patients with HCC. The application of the EVendo score could safely defer about 30% of EGDs for EV screening in HCC patients. Although additional validation cohorts are needed, this suggests that EVendo score can potentially be applied in patients with HCC to avoid unnecessary EGDs, which can ultimately mitigate healthcare costs and delays in initiating HCC treatment with atezolizumab and bevacizumab.
... Therefore, primary and secondary prophylactic treatment of portal hypertension is of paramount importance to avoid variceal (re-)bleeding. Current guidelines recommend either non-selective betablockers (NSBBs) or endoscopic band ligation (EBL) for primary prophylaxis, while combined treatment with NSBB and EBL is recommended as a secondary prophylaxis for variceal (re-)rebleeding [5][6][7][8][9][10][11][12][13][14]. Despite these established treatments, there is still a need for more effective treatments to manage patients with portal hypertension. ...
... RASi: 51U/L IQR 36.5 vs. non-co-medications: 52 U/L IQR 59). In primary prophylaxis as well as secondary prophylaxis, the numbers of performed endoscopies per year (statin: 5 non-co-medications: 1 IQR 6.3) were higher in patients with co-medications. In the setting of secondary prophylaxis, more liver transplantations (10.4%) were performed in the group of patients without co-medications. ...
... In the subgroup analyses, we subdivided the study cohort according to primary and secondary prophylaxis settings to accommodate the previously reported differences in clinical characteristics, current therapeutic approaches, and mortality among these two groups [5,9,29,40]. However, our analyses did not provide any support for potential additional clinical effects of the evaluated drugs. ...
Background
Previous experimental and clinical studies suggested a beneficial effect of statins, metformin, angiotensin-converting-enzyme inhibitors and angiotensin II receptor blockers (RASi) on portal hypertension. Still, their effects on hard cirrhosis-related clinical endpoints, such as variceal bleeding and bleeding-related mortality, remain to be investigated.
Methods
Thus, we recorded the use of statins, metformin and RASi in a large cohort of cirrhotic patients undergoing endoscopic band ligation (EBL) for primary (PP, n = 440) and secondary bleeding prophylaxis (SP, n = 480) between 01/2000 and 05/2020. Variceal (re-) bleeding and survival rates were compared between patients with vs. without these co-medications.
Results
A total of 920 cirrhotic patients with varices were included. At first EBL, median MELD was 13 and 515 (56%) patients showed ascites. Statins, metformin and RASi were used by 49 (5.3%), 74 (8%), and 91 (9.9%) patients, respectively. MELD and platelet counts were similar in patients with and without the co-medications of interest. Rates of first variceal bleeding and variceal rebleeding at 2 years were 5.2% and 11.7%, respectively. Neither of the co-medications were associated with decreased first bleeding rates (log-rank tests in PP: statins p = 0.813, metformin p = 0.862, RASi p = 0.919) nor rebleeding rates (log-rank tests in SP: statin p = 0.113, metformin p = 0.348, RASi p = 0.273). Similar mortality rates were documented in patients with and without co-medications for PP (log-rank tests: statins p = 0.630, metformin p = 0.591, RASi p = 0.064) and for SP (statins p = 0.720, metformin p = 0.584, RASi p = 0.118).
Conclusion
In clinical practice, variceal bleeding and mortality rates of cirrhotic patients were not reduced by co-medication with statins, metformin or RASi. Nevertheless, we recommend the use of these co-medications by indication, as they may still exert beneficial effects on non-bleeding complications in patients with liver cirrhosis.
... 30,31 Presence and size of gastroesophageal varices was recorded according to Austrian Billroth III guidelines. 32 According to the BAVENO VII recommendations 26 ...
Background and Aims
Wilson's disease may progress to cirrhosis and clinically significant portal hypertension (CSPH). We aimed to assess the prevalence and prognostic impact of CSPH‐related features on hepatic decompensation and transplant‐free survival in patients with Wilson's disease.
Methods and Results
About 137 patients with Wilson's disease (Leipzig score ≥4), followed for a median observation period of 9.0 (3.9–17.7) years at the Vienna General Hospital, were included in this retrospective study. Overall, 49 (35.8%) developed features of CSPH: 14 (10.2%) varices, 40 (29.2%) splenomegaly, 20 (14.6%) ascites, 18 (13.1%) hepatic encephalopathy and 3 (2.2%) experienced acute variceal bleeding. Overall, 8 (5.8%) patients died, including three deaths caused by CSPH‐related complications. Within 10 years, compensated patients with features of CSPH developed more decompensation events (8.3% vs. 1.5% in patients without CSPH, p = 0.3) and had worse transplant‐free‐survival (91.7% vs. 98.6%), which further declined in patients with hepatic decompensation (26.7%, log‐rank: p < 0.0001). Patients with liver stiffness <15 kPa and normal platelets (≥150 G/L) were less likely to decompensate within 10 years (2.6% vs. 8.4%, p = 0.002) and had a better 10‐year transplant‐free‐survival (97.7% vs. 83.9%, p = 0.006).
Conclusions
Patients with Wilson's disease developing features of CSPH are at an increased risk for hepatic decompensation and liver‐related mortality, warranting for regular screening and timely initiation of effective CSPH‐directed treatments.
... A widely used approach to diagnosis PHT in adults is by direct measurement of hepatic venous pressure gradient (HVPG), but this may not be routine practice in children due to its invasive nature. 5,13 In adults, PHT is defined as an HVPG measurement > − 6 mmHg and clinically significant portal hypertension (CSPH), the pressure at which varices begin to form, as an HVPG measurement > − 10 mmHg. In children, the diagnosis of PHT is commonly based on clinical/haematological findings of PHT complications such as splenomegaly, thrombocytopenia and ascites. ...
Background & Aims
Von Willebrand factor antigen (vWFAg), a protein measured to test the level of vWF released from the vascular endothelium has gained much attention as a marker for portal hypertension (PHT) severity. The objectives of this study were to investigate the use of vWFAg as a biomarker along with liver and spleen stiffness measurements by transient elastography as potential predictors of clinically significant varices (CSV), variceal bleeding (VB) and decompensation in children with PHT.
Methods
This observational prospective cohort study included 117 children (median age 10 [IQR 6-14] years) who underwent oesophagogastroduodenoscopy between January’2012 to November’2021 and a validation group of 33 children who underwent the same procedure between December’2021 to March’2023. Measurements of vWFAg and glycoprotein Ib binding activity of VWF (GPIbR) were available in 97 patients in the study group and in all patients in the validation group.
Results: vWFAg and GPIbR were significantly higher in children with CSV (223 IU/dl and 166 IU/dl; p = 0.015 and p = 0.04, respectively) and VB (218 IU/dl and 174 IU/dl; p = 0.077 and p = 0.03, respectively) than in those without CSV or VB, respectively. Ninety-six patients had liver and spleen stiffness measurements. Spleen stiffness was significantly higher in patients with CSV compared to those without CSV (p = 0.003). In a chronic liver disease subgroup, a predictive scoring tool based on vWFAg, GPIbR, platelet count, and spleen/liver stiffness measurements could predict CSV with an AUROC of 0.76 (p = 0.04).
Conclusions
This study suggests the predictive value of vWF for CSV and VB increases when combined with spleen stiffness, with AUROCs of 0.88 and 0.82, respectively. Hence, a combination of biomarkers could assist clinicians in diagnosing CSV, preventing unnecessary invasive procedures.
Impacts and implications
Surveillance endoscopies in children with portal hypertension (PHT) have their own risks and non-invasive markers, such as von Willebrand factor antigen, glycoprotein Ib binding activity of VWF (GPIbR), and transient elastography could be used to predict clinically significant varices, variceal bleeding and disease compensation in children with PHT. Such non-invasive markers for PHT and varices are lacking in the paediatric population. The results show that von Willebrand factor and GPIbR along with transient elastography can be used to formulate a scoring system which can be used as a clinical tool by paediatric hepatologists to monitor the progression of PHT and risk of bleeding, and hence to stratify the performance of invasive endoscopic procedures under general anaesthesia. However, there is a need to validate the scoring system in children with portal vein thrombosis and for hepatic decompensation in a multi-centre registry in the future.
... Furthermore, patients with HVPG non-response showed a smaller reduction in heart rate and a post-treatment resting heart rate that was higher than that recommended by guidelines (55-60 / min). 3 These findings suggest that, in patients with fatty liver disease, it may be necessary to consider increasing the dose of NSBB or prolonging the duration of treatment before repeat HVPG measurement. However, further research is still needed to validate these findings. ...
LINKED CONTENT
This article is linked to Paternostro et al papers. To view these articles, visit https://doi.org/10.1111/apt.17653 and https://doi.org/10.1111/apt.17702
... Data regarding ascites was recorded according to clinical description in medical records, need for diuretics, imaging results, or ascites laboratory work. Spontaneous bacterial peritonitis was defined as a polymorphonuclear neutrophil count (PMN) >250x10 6 cells/L [26]. ...
... Dyslipidemia, defined by either low HDL or high LDL levels or high levels of serum triglycerides, is commonly found in all chronic liver disease [47][48][49][50]. In our cohort, we found that low HDL levels were most prominent in the ALD cohort and that low HDL correlated with increased MELD and CPS, and was predictive of a limited prognosis during follow-up, suggesting low HDL as a "red flag" of chronic liver disease [26]. Although we found significant differences in LDL levels across etiologies, the main driver behind this were the elevated levels among patients with primary biliary cholangitis (PBC) in comparison to other etiologies-a well-known effect of the disease [51]. ...
Introduction
Liver cirrhosis accounts for considerable morbidity and mortality worldwide and late presentation limits therapeutic options. We aimed to assess characteristics of patients with liver cirrhosis at the time of first presentation and during their clinical course.
Methods
Patients with cirrhosis as evident by presence of varices at endoscopy, liver stiffness ≥15kPa at elastography, or ascites requiring paracentesis between Q1/2015-Q2/2020 were retrospectively included. Clinical, laboratory, and imaging data were collected from medical records at presentation and last follow-up.
Results
476 patients were included (alcohol-related liver disease, ALD: 211, 44.3%; viral hepatitis: 163, 34.2%). Of these, 106 patients (22.3%) and 160 patients (33.6%) presented already with Child-Pugh C and MELD >15, respectively, and decompensation events were registered in 50% (238 patients) at baseline, and even in 75.4% of ALD patients.
During a median follow-up of 11.0 (IQR 4–24) months, 116 patients died. Two-year survival was worse for patients with ALD than for viral hepatitis (71.1% vs. 90.2%, log rank p<0.001). We observed the highest percentage of portal-vein thrombosis (30.0%), hepatocellular carcinoma (15.0%), and death (45.0%) in the MAFLD group (n = 20). Patients cured from hepatitis C showed significant improvements in platelet count (147 to 169 G/L, p<0.001) and liver stiffness (26.2 to 17.7 kPa, p<0.001), while ALD patients improved in Child-Pugh score (8.6 to 7.6, p<0.001) during follow-up. With increasing Child Pugh score and MELD, we found increasing serum concentrations of CRP (p<0.001) and an inverse correlation with serum HDL (Spearman’s ρ = -0.573 and -0.529, respectively, p<0.001).
Conclusion
Half of the patients with cirrhosis had decompensated cirrhosis at presentation. This calls for increased awareness and strategies for earlier diagnosis of chronic liver disease and cirrhosis.
... Several etiological factors of anemia in patients with ACLD have been described ( Figure 1): acute or chronic blood loss due to gastroesophageal varices bleeding [5], portal hypertensive gastropathy, gastric antral vascular ectasia (GAVE) [6], or peptic ulcer [7,8], which aggravates anemia in ACLD. Defects of the lipid membrane of erythrocytes (functional and structural) can lead to the formation of acanthocytes, which have a short life, due to an increased susceptibility to degradation in the spleen [9,10]. ...
... Several etiological factors of anemia in patients with ACLD have been described (Figure 1): acute or chronic blood loss due to gastroesophageal varices bleeding [5], portal hypertensive gastropathy, gastric antral vascular ectasia (GAVE) [6], or peptic ulcer [7,8], which aggravates anemia in ACLD. Defects of the lipid membrane of erythrocytes (functional and structural) can lead to the formation of acanthocytes, which have a short life, due to an increased susceptibility to degradation in the spleen [9,10]. ...
Hematological abnormalities are frequently linked to chronic liver disease of any etiology. About 75% of patients with advanced chronic liver disease experience anemia. The causes of anemia are complex and multifactorial, particularly in cirrhotic patients. Acute and long-term blood loss from the upper gastrointestinal tract, malnutrition, an enlarged spleen brought on by portal hypertension, hemolysis, and coagulation issues are the main causes of anemia. Alcohol, a common cause of chronic liver disease, determines anemia through direct toxicity on the bone marrow, with the suppression of hematopoiesis, through vitamin B6, B12, and folate deficiency due to low intake and malabsorption. In patients with chronic hepatitis C virus infection, antiviral drugs such as pegylated interferon and ribavirin can also cause significant anemia. The use of interferon has been linked to bone marrow toxicity, and hemolytic anemia brought on by ribavirin is a well-known dose-dependent side effect. Within six months of the infection with hepatitis B, hepatitis C, and Epstein–Barr viruses, aplastic anemia associated with hepatitis is seen. This anemia is characterized by pancytopenia brought on by hypocellular bone marrow. Esophageal varices, portal hypertensive gastropathy, and gastric antral vascular ectasia can all cause acute and chronic blood loss. These conditions can progress to iron deficiency anemia, microcytic anemia, and hypochromic anemia. Another common hematologic abnormality in liver cirrhosis is macrocytosis, with multifactorial causes. Vitamin B12 and folate deficiency are frequent in liver cirrhosis, especially of alcoholic etiology, due to increased intestinal permeability, dysbiosis, and malnutrition. Many chronic liver diseases, like viral and autoimmune hepatitis, have a chronic inflammatory substrate. Proinflammatory cytokines, including tumor necrosis factor and interleukin 1, 6, and 10, are the main factors that diminish iron availability in progenitor erythrocytes and subsequent erythropoiesis, leading to the development of chronic inflammatory, normochromic, normocytic anemia.
... HVPG-guided NSBB therapy was performed according to our local standardised protocol, as previously published 7,14 : After BL-HVPG-measurement, NSBB therapy with either propranolol or carvedilol (choice of agent was at the discretion of the physician) was initiated, in accordance with the effective guidelines at that time. 2 The NSBB dose was titrated according to tolerance, systolic blood pressure and heart rate, as applicable. RE-HVPG was performed within a median of 35 (25th; 75th percentile: 28; 57) days. ...
... Then a balloon catheter (7F, Ferlitsch HVPG catheter, Pejcl Medizintechnik) was used to cannulate a hepatic vein via the transjugular access. 22Varices were graded according to size and presence/absence of red spot signs, as recommended by the respective guidelines.2 ...
Background
Non‐selective betablockers (NSBBs) reduce the risk of hepatic decompensation in patients with compensated advanced chronic liver disease (cACLD). Metabolic co‐morbidities (MetC) are increasingly observed in cACLD patients.
Aims
To investigate the impact of MetC on the haemodynamic effects of NSBB and hepatic decompensation in cACLD.
Methods
cACLD patients undergoing paired hepatic venous pressure gradient (HVPG) measurements before/under NSBB therapy were retrospectively considered for this study. We recorded baseline characteristics on MetC (obesity, dyslipidaemia and diabetes), as well as hepatic decompensation and liver‐related mortality during follow‐up.
Results
We included 92 patients (Child‐A n = 80, 87%; Child‐B n = 12, 13%). MetC were found in 34 (37%) patients: 19 (20.7%) with obesity, 14 (15.2%) with dyslipidaemia and 23 (34.8%) with diabetes. The median baseline HVPG of 18 (IQR:15–21) mmHg decreased to 15 (IQR:9–12) mmHg under NSBB. HVPG‐response (decrease ≥10% or to ≤12 mmHg) was achieved in 60 (65.2.%) patients. Patients with diabetes (OR: 0.35, p = 0.021) and higher BMI (OR: 0.89 per kg/m², p = 0.031) were less likely to achieve HVPG‐response.
During a median follow‐up of 2.3 (0.5–4.2) years, 18 (19.5%) patients experienced hepatic decompensation. Child‐B (adjusted subdistribution hazard ratio, aSHR: 4.3 [95% CI:1.5–12.2], p = 0.006), HVPG‐response (aSHR: 0.3 [95% CI:0.1–0.9], p = 0.037) and diabetes (aSHR: 2.8 [95% CI:1.1–7.2], p = 0.036) were independently associated with hepatic decompensation.
Conclusions
In patients with cACLD, diabetes and a higher BMI impair the HVPG‐response to NSBB. Furthermore, diabetes‐independently from Child B and lack of HVPG‐response‐increases the risk of hepatic decompensation.
