Portal Hypertension In Cirrhosis Research Articles

Impact of catheter tip to hepatic vein ostium distance on the validity and prognostication of hepatic venous pressure gradient in cirrhosis

Hepatic venous pressure gradient (HVPG) is an accurate measure of portal hypertension in cirrhosis. However, the effect of catheter tip distance from hepatic vein ostium (HVO) on HVPG is unknown. We performed a retrospective study on 228 patients with 307 HVPGs in our institution. The objectives of this study were to assess the effect of catheter position on the validity of HVPG and its prognostication in cirrhosis. In this study, free hepatic vein pressure (FHVP) was considered optimal when difference between FHVP and inferior vena cava pressure was ≤ 2 mmHg. HVPG progressively decreased (p < 0.001) when measured at increasing distance from HVO due to an increasing FHVP (p = 0.036) but an unchanged wedged hepatic vein pressure (p = 0.343). Catheter tip distance > 5 to ≤ 8 cm [odds ratio {OR} 0.16 (95% CI 0.05–0.47), p = 0.001] and > 8 cm [OR 0.14 (95% CI 0.04–0.47), p = 0.002] compared to ≤ 3 cm from HVO were independent predictors of not achieving optimal FHVP. Baseline HVPG ≥ 16 mmHg was strongly associated with deaths due to cirrhosis and liver transplantation for end-stage liver disease compared to HVPG < 16 mmHg when FHVP was optimal (p < 0.001) but not when it was suboptimal (p = 0.359). Our study showed that FHVP is spuriously elevated when measured at > 5 cm from HVO, resulting in inaccurately low HVPG.

Esophagoduodenal Varices in Non-cirrhotic Portal Hypertension with Myelodysplastic Syndrome: A Case Report

Background: Esophagogastroduodenal varices are dilated submucosal of distal esophageal, gastric, and duodenal veins connecting the portal and systemic circulation. This case report aims to describe a unique case of a child with esophagoduodenal varices due to myelodysplastic syndrome. Case: We reported a case of 3-year-old girl who came to Hasan Sadikin General Hospital on April 3 2022, complaining of black stools 1 time per day for two days before admission. She had previously been diagnosed with esophagogastroduodenal varices since 2019. On initial examination, the patient was fully conscious and appeared pale. The patient's clinical condition improved after adequate treatment of blood transfusion, octreotide, omeprazole and propanolol. However, patient later developed pancytopenia and underwent bone marrow puncture examination which revealed a myelodysplastic syndrome. Discussion: Myelodysplastic syndrome is a condition where ineffective hematopoiesis occurs and can lead to blood malignancy, especially acute myeloblastic leukemia. In this patient, she presented with unequivocal hypertensive gastroesophageal varices, splenomegaly, absence of fibrosis and thrombocytosis supporting subsequent diagnosis of idiopathic non cirrhosis portal hypertension. On the other hand, non-cirrhotic portal hypertension can also be caused by myelodysplastic syndrome as described in this case report. Conclusion: Myeloproliferative malignancies can be a cause of idiopathic non cirrhosis portal hypertension. Pancytopenia often occurs in patients with portal hypertension due to splenomegaly or myelodysplastic syndrome, which can lead to acute myeloblastic leukemia, an example of a myeloproliferative malignancy.

Portal Hypertension in Nonalcoholic Fatty Liver Disease: Challenges and Paradigms.

Portal hypertension in cirrhosis is defined as an increase in the portal pressure gradient (PPG) between the portal and hepatic veins and is traditionally estimated by the hepatic venous pressure gradient (HVPG), which is the difference in pressure between the free-floating and wedged positions of a balloon catheter in the hepatic vein. By convention, HVPG≥10 mmHg indicates clinically significant portal hypertension, which is associated with adverse clinical outcomes. Nonalcoholic fatty liver disease (NAFLD) is a common disorder with a heterogeneous clinical course, which includes the development of portal hypertension. There is increasing evidence that portal hypertension in NAFLD deserves special considerations. First, elevated PPG often precedes fibrosis in NAFLD, suggesting a bidirectional relationship between these pathological processes. Second, HVPG underestimates PPG in NAFLD, suggesting that portal hypertension is more prevalent in this condition than currently believed. Third, cellular mechanoresponses generated early in the pathogenesis of NAFLD provide a mechanistic explanation for the pressure-fibrosis paradigm. Finally, a better understanding of liver mechanobiology in NAFLD may aid in the development of novel pharmaceutical targets for prevention and management of this disease.

Outcome of pharmacological thromboprophylaxis in hospitalized patients with cirrhosis - a systematic review and meta-analysis.

Portal hypertension in cirrhosis brings about a complex interplay in the risks of bleeding and thrombosis. It is unclear whether hospitalized patients with cirrhosis need pharmacological prophylaxis for venous thromboembolism (VTE), as it may increase the risk of bleeding. We aimed to compare the outcome of hospitalized patients with cirrhosis with and without pharmacological thromboprophylaxis. A comprehensive search of three databases was conducted from inception to August 2022 for studies comparing the outcome of hospitalized patients with cirrhosis with and without pharmacological prophylaxis for VTE. Odds ratios (OR) with 95% confidence intervals (CIs) were calculated for the outcomes of VTE or bleeding. Overall, 12 studies were included in the final analysis. The pooled incidence of VTE in patients with and without thromboprophylaxis was 1.9% (95% CI: 0.8-2.9) and 1.9% (95% CI: 0.9-2.9), respectively. The odds of VTE were comparable between the groups with OR 1.11 (95% CI: 0.76-1.62). The pooled incidence of bleeding events in patients with and without thromboprophylaxis was 6.7% (95% CI: 3.6-9.8) and 10.4% (95% CI: 6.6-14.1), respectively. There was no significant difference in the odds of overall bleeding (OR 0.68; 95% CI: 0.30-1.52) or major bleeding (OR 1.18; 95% CI: 0.55-2.56) between the groups. There was no significant difference in the relative effects on sensitivity analysis. The present analysis could not demonstrate the benefit of pharmacological thromboprophylaxis in reducing in-hospital VTE in patients with cirrhosis. Future studies are required to assess the role of risk prediction models in hospitalized patients with cirrhosis.

Heart rate variability is associated with disease severity and portal hypertension in cirrhosis.

Autonomic nervous system activity in cirrhotic portal hypertension is linked to hyperdynamic circulation. Heart rate variability (HRV) is a validated noninvasive method to assess the sympathovagal balance. To investigate the correlation between HRV parameters and degree of portal hypertension, we studied a cohort of patients with cirrhosis accounting for etiology and treatments. In this cross-sectional, observational cohort study, 157 outpatients of both sex with nonalcoholic cirrhosis were assessed by upper gastrointestinal endoscopy to search for esophagogastric varices. Twenty-four-hour electrocardiogram Holter monitoring with 3 HRV parameters measurement [SD of the NN intervals, root mean square successive difference of NN intervals, and SD of the averages of NN intervals (SDANN)] according to time-domain analysis were performed in all patients. Sixteen patients with large esophagogastric varices underwent measurements of the HVPG and assessment of HRV parameters at baseline and after 45 days on carvedilol. The liver dysfunction, expressed by Child-Pugh class or MELD score, was directly related to root mean square successive difference of NN intervals and inversely related to SDANN. Presence of ascites was inversely related to SDANN and to SD of the NN intervals. Treatment with carvedilol had an inverse relation with SDANN. Presence and size of esophagogastric varices had an inverse relation to SDANN and SD of the NN intervals. Upon multivariate analysis the associations between SDANN and Child-Pugh class, size of varices and ascites were confirmed. In the subgroup of 16 patients undergoing HVPG measurement, pressure gradient was unrelated to heart rate and HRV parameters. Time-domain HRV parameters in patients with cirrhosis, confirm the autonomic nervous system alteration, and their correlation to the degree of portal hypertension suggesting a role of the ANS in hepatic decompensation.

Improving Management of Portal Hypertension: The Potential Benefit of Non-Etiological Therapies in Cirrhosis.

Portal hypertension is the consequence of cirrhosis and results from increased sinusoidal vascular resistance and hepatic blood inflow. Etiological therapies represent the first intervention to prevent a significant increase in portal pressure due to chronic liver damage. However, other superimposed pathophysiological drivers may worsen liver disease, including inflammation, bacterial translocation, endothelial dysfunction, and hyperactivation of hemostasis. These mechanisms can be targeted by a specific class of drugs already used in clinical practice. Albumin, rifaximin, statins, aspirin, and anticoagulants have been tested in cirrhosis and were a topic of discussion in the last Baveno consensus as non-etiological therapies. Based on the pathogenesis of portal hypertension in cirrhosis, our review summarizes the main mechanisms targeted by these drugs as well as the clinical evidence that considers them a valid complementary option to manage patients with cirrhosis and portal hypertension.

Contrast-enhanced ultrasonography for the management of portal hypertension in cirrhosis.

Portal hypertension is a major pathophysiological condition in patients with cirrhosis. This accounts for the occurrence and severity of the various manifestations. The degree is determined by the portal pressure or hepatic venous pressure gradients, both of which are obtained by invasive interventional radiological procedures. Ultrasound (US) is a simple and minimally invasive imaging modality for the diagnosis of liver diseases. Owing to the availability of microbubble-based contrast agents and the development of imaging modes corresponding to contrast effects, contrast-enhanced US (CEUS) has become popular worldwide for the detailed evaluation of hepatic hemodynamics, diffuse liver disease, and focal hepatic lesions. Recent advancements in digital technology have enabled contrast-based demonstrations with improved resolution, leading to a wider range of applications. This review article describes the current role, benefits, and limitations of CEUS in the management of portal hypertension.

FRI224 - Development and validation of a hepatic vascular geometrical model for noninvasive diagnosis of clinically significant portal hypertension in cirrhosis (CHESS1802)

FRI224 - Development and validation of a hepatic vascular geometrical model for noninvasive diagnosis of clinically significant portal hypertension in cirrhosis (CHESS1802)

Mas-related G protein-coupled receptor type D antagonism improves portal hypertension in cirrhotic rats.

Splanchnic vasodilatation contributes to the development and aggravation of portal hypertension (PHT). We previously demonstrated that in cirrhosis, angiotensin‐ mediates splanchnic vasodilatation through the Mas receptor (MasR). In this study, we investigated whether the recently characterized second receptor for angiotensin‐(1–7), Mas‐related G protein‐coupled receptor type D (MrgD), contributes to splanchnic vasodilatation in cirrhotic and noncirrhotic PHT. Splanchnic vascular hemodynamic and portal pressure were determined in two rat models of cirrhotic PHT and a rat model with noncirrhotic PHT, treated with either MrgD blocker D‐Pro7‐Ang‐(1‐7) (D‐Pro) or MasR blocker A779. Gene and protein expression of MrgD and MasR were measured in splanchnic vessels and livers of cirrhotic and healthy rats and in patients with cirrhosis and healthy subjects. Mesenteric resistance vessels isolated from cirrhotic rats were used in myographs to study their vasodilatory properties. MrgD was up‐regulated in cirrhotic splanchnic vessels but not in the liver. In cirrhotic rats, treatment with D‐Pro but not A779 completely restored splanchnic vascular resistance to a healthy level, resulting in a 33% reduction in portal pressure. Mesenteric vessels pretreated with D‐Pro but not with A779 failed to relax in response to acetylcholine. There was no splanchnic vascular MrgD or MasR up‐regulation in noncirrhotic PHT; thus, receptor blockers had no effect on splanchnic hemodynamics. Conclusion: MrgD plays a major role in the development of cirrhotic PHT and is a promising target for the development of novel therapies to treat PHT in cirrhosis. Moreover, neither MrgD nor MasR contributes to noncirrhotic PHT.

TIPSS as a bridge to extrahepatic abdominal surgery: a case report

Severe portal hypertension in cirrhosis is a relative contraindication to major surgical intervention. Pre-surgical placement of a transjugular intrahepatic portosystemic shunt (TIPSS) can potentially reduce portal hypertension and the risk of intraoperative bleeding. Two patients in our service, with cirrhosis and portal hypertension, required abdominal surgery and underwent TIPSS placement as a potential bridging therapy. Patient 1, a 56-year-old female, successfully underwent surgery with no intraoperative complications. Patient 2, a 36-year-old male, experienced liver decompensation post-TIPSS and is currently awaiting a liver and bowel transplant. Prophylactic TIPSS placement may allow some patients with decompensated cirrhosis to successfully undergo major extrahepatic abdominal surgery. However, careful patient selection and preoperative counselling for decompensation is necessary.

ОЦЕНКА ТЯЖЕСТИ ПОРТАЛЬНОЙ ГИПЕРТЕНЗИИ ПРИ ЦИРРОЗЕ ПЕЧЕНИ

Objective. Development of a non-invasive assessing diagnostic and severity grading accuracy of portal hypertension in cirrhosis of the liver. Methods. To identify diagnostically significant indicators, a statistical analysis of the data of laboratory and instrumental diagnostics was carried out in 60 patients with liver cirrhosis. The followingbiochemical indicators weredetermined: general and biochemical blood tests, coagulogram, general urine analysis; the level of interleukin-6 (IL-6), matrix metalloproteinases 1 and 9 (MMP-1, MMP-9), tissue inhibitor of matrix metalloproteinase 1 (TIMP-1), hepatocyte growth factor (HGF); abdominal ultrasound examination, esophagogastroscopy. The index of the ratio of the number of blood platelets (N×10&lt;sup&gt;9&lt;/sup&gt; / L) to the transverse size (D) of the spleen in millimeters (PSR - Platelet count to Spleen diameter Ratio) was calculated: PSR = NTr / D spleen. Results. The following indicators turned out to be diagnostically significant (predictive values based on ROC analysis are presented): blood levels of IL-6 (&gt;19.9 pg/ml), MMP-1 (&gt;8.06 ng/ml), cholesterol (≤4,5mmol/L), portal vein diameter (&gt;13 mm), PSR (≤1.89). Diagnosticmethods for cirrhosis and portal hypertension was developed, based on a point assessment of a set of laboratory and instrumental criteria (AUC = 0.931; p &lt;0.001). The method can be used in a complex of medical services aimed at diagnosis of portal hypertension severity in patients with cirrhosis of the liver, as well as medical prevention of life-threatening complications of the disease. Conclusion. The developed method makes it possible to identify patients with a «severe» form of portal hypertension, to recommend an unscheduled FEGDS with an endoscopic assessment of the risk of bleeding, and to carry out preventive and therapeutic procedures. If a low probability of a “severe” form of PH is identified, FEGDS should be refrained from if the patient has absolute or relative contraindications to the use of this diagnostic method. The method can be used in a complex of medical services aimed at diagnosing the severity of portal hypertension against the background of liver cirrhosis. What this paper adds For the first time, a method for diagnosis of portal hypertension in liver cirrhosis has been developed. It is based on a score assessment of a set of laboratory and instrumental criteria, including blood levels of interleukin-6, matrix metalloproteinase-1, cholesterol, platelet count, portal vein diameter and transverse size of the spleen. The method can be used in a complex of medical services aimed to estimate the severity of portal hypertension in cirrhosis of the liver, as well as medical prevention of life-threatening complications of the disease.

Development and Validation of a Hepatic Vascular Geometrical Model for Noninvasive Diagnosis of Clinically Significant Portal Hypertension in Cirrhosis

Development and Validation of a Hepatic Vascular Geometrical Model for Noninvasive Diagnosis of Clinically Significant Portal Hypertension in Cirrhosis

Update on the diagnosis and management of portal hypertension in cirrhosis according to the Baveno VII Consensus Conference recommendations.

Development of portal hypertension is the most critical hallmark in the natural history of advanced chronic liver disease, as it is responsible for most liver decompensations. Correct risk stratification allows the design of personalized treatment strategies. In addition, the dynamic nature of chronic liver disease requires a refinement of both invasive and non-invasive diagnostic methods at every stage. Treatment with non-selective beta blockers and suppression of the etiologic factor improve portal hypertension and decrease the probability of decompensation in high-risk patients. Patients admitted for variceal hemorrhage also benefit from personalized management, where insertion of a preventive TIPS plays a relevant role.

Risk factors associated with non-malignant portal vein thrombosis in patients with decompensated cirrhosis : a case-control study

Backgrounds and Aim: Portal vein thrombosis (PVT) is defined as thrombosis of the portal vein and branches of spleno-portal axis. Incidence of PVT in compensated liver disease is between 0.6-5% and up to 25% in advanced disease. Presence of PVT in decompensated chronic liver disease (DCLD) is associated with significant morbidity and mortality. We evaluated the proportion and risk factors associated with non-malignant PVT in DCLD patients. Methods: 502 patients with DCLD were enrolled over a period of 1.5 years. Patients underwent detailed clinical history and evaluation, baseline investigation and ultrasonography. CECT Abdomen was performed in patients with USG evidence of PVT or alteration in portal flow dynamics. Results: 39 patients were excluded. 51 of the 463 patients included had PVT (11.0%). Duration of cirrhosis >4years(p<0.01), NASH related etiology (p<0.01), prior history of obesity(p<0.01), dyslipidaemia with high serum cholesterol and LDL(p<0.01), clinically evident sarcopenia (p<0.01), first initial decompensation of cirrhosis as upper gastro-intestinal bleed (UGIB), prior UGIB (p=0.002), poorly controlled ascites (p<0.01), 2 history of episodes of SBP(p<0.01), platelet count <66.5x109/L(p=0.002), leucocyte count <5350/cu mm(p<0.01) were significantly associated with PVT group. There was no difference between CHILD B and C status, among the 2 groups. On multiple logistic regression analysis, prior endoscopic variceal ligation, SAAG >1.95 were found as independent risk factors for development of PVT in DCLD patients. Conclusions: Proportion of non-malignant PVT in decompensated cirrhosis was 11%. Presence of poorly controlled ascites, prior history of UGIB, high SAAG, low Platelet count as markers of severity of portal hypertension in cirrhosis are significantly associated with non-malignant PVT in DCLD. Patients with prior history of obesity and dyslipdemia, with NASH related cirrhosis are at high risk for PVT development.

Additional Benefits Conferred by Endoscopic Sclerotherapy to Liver Cirrhosis Patients Receiving Endoscopic Variceal Ligation.

Objective Gastroesophageal varices are a direct consequence of portal hypertension in cirrhosis. The management of gastroesophageal varices has evolved over the last decade resulting in reduced mortality and morbidity rates. The study was aimed to analyze the short-term and long-term efficacy of different endoscopic methods in the treatment of gastric varices in cirrhotic patients. Methods From January 2016 to December 2019, 135 patients with liver cirrhosis and gastric varices undergoing different endoscopic treatment protocols were retrospectively analyzed. The patients were divided into three groups according to endoscopic variceal ligation, endoscopic sclerotherapy, and a combination of both, respectively. Main outcomes including the overall response rate, hemostasis, short- and long-term rebleeding (3 months before and after treatment), complication, blood pressure, heart rate, portal venous pressure (PVP), portal vein diameter (PVD), portal vein velocity (PVV), portal vein blood flow (PVF) detected by ultrasound, recurrence rate, and mortality were analyzed after treatments. Results The overall response rate in the combined group was higher than that in the ligation group and the sclerotherapy group (P < 0.05). The incidence rate of complications in the combined group and the ligation group was lower than that in the sclerotherapy group (P < 0.05). After treatment, the PVP, PVD, and PVF were reduced in the combined group compared with the ligation group and the sclerotherapy group, while the PVV was not (P < 0.05). Lower rates of long-term rebleeding, recurrence, and mortality were noted in the combined group compared to the ligation group and the sclerotherapy group (P < 0.05). Conclusion Endoscopic variceal ligation combined with endoscopic sclerotherapy is more effective than both alone in treating liver cirrhosis and gastric varices. The combined therapy contributed to reduced short-term and long-term rebleeding rate, decreased long-term recurrence rate, and mortality.

Test-Retest Reliability and Consistency of HVPG and Impact on Trial Design: A Study in 289 Patients from 20 Randomized Controlled Trials.

Portal hypertension (PH) is a major driver for cirrhosis complications. Portal pressure is estimated in practice by the HVPG. The assessment of HVPG changes has been used for drug development in PH. This study aimed at quantifying the test-retest reliability and consistency of HVPG in the specific context of randomized controlled trials (RCTs) for the treatment of PH in cirrhosis and its impact on power calculations for trial design. We conducted a search of published RCTs in patients with cirrhosis reporting individual patient-level data of HVPG at baseline and after an intervention, which included a placebo or an untreated control arm. Baseline and follow-up HVPGs in the control groups were extracted after digitizing the plots. We assessed reliability and consistency and the potential impact of study characteristics. We retrieved a total of 289 before and after HVPG measurements in the placebo/untreated groups from 20 RCTs. The time span between the two HVPG measurements ranged between 20minutes and 730days. Pre-/post-HVPG variability was lower in studies including only compensated patients; therefore, modeled sample size calculations for trials in compensated cirrhosis were lower than for decompensated cirrhosis. A higher proportion of alcohol-associated cirrhosis and unicentric trials was associated with lower differences between baseline and follow-up measurements. The smallest detectable difference in an individual was 26% and 30% in compensated and decompensated patients, respectively. The test-retest reliability of HVPG is overall excellent. Within-individual variance was higher in studies including higher proportions of decompensated patients. These findings should be taken into account when performing power analysis for trials based on the effects on HVPG or when considering HVPG as a tool to guide therapy of PH.

Friend or Foe? Spontaneous Portosystemic Shunts in Cirrhosis-Current Understanding and Future Prospects.

Portal hypertension (PHT) in cirrhosis results from increased resistance to splanchnic blood flow secondary to parenchymal and vascular changes within the liver. In an attempt to counteract the increased portal pressure, two mechanisms simultaneously occur: splanchnic vasodilatation and formation of spontaneous portosystemic shunts (SPSS). Long considered to be a compensatory mechanism to decompress the portal venous system, it is now well established that SPSS are not only inefficient in decreasing the portal pressure but also contribute to reduced hepatocyte perfusion and increased splanchnic blood flow and resistance, associated with worsening PHT. Recent studies have described a high prevalence of SPSS in cirrhosis patients, increasing with liver dysfunction, and observed an association between the presence of SPSS and worse clinical outcomes. In cirrhosis patients with preserved liver functions, the presence of SPSS independently increases the risk of hepatic encephalopathy, variceal bleeding, and ascites, and reduces transplant-free survival. Moreover, the presence of SPSS in patients undergoing transjugular intrahepatic portosystemic shunting and liver transplant has been shown to variably affect the postprocedural outcome. This article provides an overview of the current understanding of the role of SPSS in the natural history of liver cirrhosis and their status as a therapeutic target and an imaging biomarker to identify patients at higher risk of developing complications of PHT.

Nonselective Beta-Blockers in Compensated Cirrhosis: Preventing Variceal Hemorrhage or Preventing Decompensation?

Nonselective Beta-Blockers in Compensated Cirrhosis: Preventing Variceal Hemorrhage or Preventing Decompensation?

Traditional Chinese medicine on treating splenomegaly due to portal hypertension in cirrhosis: A protocol for systematic review and meta-analysis.

Background:Liver cirrhosis is a common clinical chronic progressive disease. Due to the obstruction of blood flow after cirrhosis, it leads to long-term congestion of splenic sinus, hyperplasia of fibrous tissue and proliferation of splenic myeloid cells, resulting in hepatocirrhosis and splenomegaly. At present, western medicine still uses splenectomy and interventional therapy are the main treatment, but the adverse reactions are more and the curative effect is not good. Many clinical trials have proved that Traditional Chinese medicine has a great therapeutic effect on Hepatocirrhosis with splenomegaly, which can effectively delay the development of the disease and improve the survival rate of patients. This systematic review aims to evaluate the efficacy and safety of Traditional Chinese medicine in the treatment of hepatocirrhosis with splenomegaly.Methods:The databases of Pubmed, CENTRAL (The Cochrane Central Register of Controlled Trials), China National Knowledge Infrastructure (CNKI), Wanfang Data Knowledge Service Platform (WANFANG Data), Weipu Information Chinese Periodical Service Platform (VIP), and China Biomedical Literature Service System (SinoMed) will be searched online to collect randomized controlled trials related to the treatment of hepatocirrhosis with splenomegaly with Traditional Chinese medicine The time is limited from the construction of the library to November 2020. We will use the criteria provided by Cochrane 5.1.0 for quality assessment and risk assessment of the included studies, and use the Revman 5.3 and Stata 13.0 software so as to systematically review the effectiveness of Traditional Chinese medicine for hepatocirrhosis with splenomegaly.Ethics and dissemination:This systematic review will evaluate the efficacy and safety of Traditional Chinese medicine for hepatocirrhosis with splenomegaly. Because all data used in this systematic review and meta-analysis have been published, this review does not require ethical approval. In addition, all data will be analyzed anonymously during the review process.Results:In this study, we will evaluate the efficacy of Traditional Chinese medicine in the treatment of cirrhosis with splenomegaly.Conclusion:The conclusion of this study will be evidence to ensure the efficacy of Traditional Chinese medicine© in the treatment of cirrhosis with splenomegaly and provide guidance for its treatment.Trial registration number:INPLASY2020110121.

Лечение и профилактика кровотечений из варикозно расширенных вен пищевода

Liver cirrhosis is the result of various chronic liver diseases. Portal hypertension is a serious complication of cirrhosis. Its consequences, in turn, along with other complications are gastroesophageal varicose bleeding, which cause high mortality rates. The article contains analysis of the results of laparoscopic esophagogastric devascularization without esophageal transsection and splenectomy in a patient with liver cirrhosis portal hypertension and recurrent bleeding from varicose veins of the esophagus. First successful surgery according to this method was introduced in the Grodno Municipal Clinical Hospital No. 4 in November 2011. Immediate and long-term results show a rather high efficiency of using this operation in the treatment and prevention of bleeding from varicose veins of the esophagus with cirrhosis. It is advisable to conduct further studies of the effectiveness of using this operation, despite the encouraging results of the use of this modification of laparoscopic esophagogastric devascularization.