Concomitant Portal Hypertension Research Articles

Analysis of prognostic predictors and differences between subgroups of pulmonary arterial hypertension associated with portal hypertension and HIV infection

Abstract Background Pulmonary arterial hypertension (PAH) represents a complication of both portal hypertension (Po-PAH) and HIV infection (HIV-PAH). Due to overlapping risk factors, it is frequent to have an overlap PAH form associated with both portal hypertension and HIV (HIV/Po-PAH). Methods We enrolled 204 patients with Po-PAH (128), HIV-PAH (41) and HIV/Po-PAH (35), with the aim of comparing the characteristics and identifying the prognostic determinants. At baseline, in patients with Po-PAH and HIV/Po-PAH, the severity of liver disease was estimated using the Child-Turcotte-Pugh (CTP) score, MELD score (Model for End-stage Liver Disease); instead, in patients with HIV-PAH and HIV/Po-PAH it was defined whether they received HAART (Highly Active Anti-Retroviral Therapy) and the CD4+ lymphocytes number. Data are expressed as median (interquartile range) and compared with Dunn’s test. Prognostic determinants were identified by univariate and multivariate Cox-regression analysis. Survival was assessed using Kaplan Meier method. Results HIV-infected patients [40 (37-43) years] and HIV/Po-PAH [44 (39-48) years] are younger than Po-PAH patients [53 (44-60) years]; the exercise capacity assessed by the 6-minute walking test of patients with HIV/Po-PAH [516 (432-571) m] was superior to both patients with Po-PAH [426 (366-504) m] and HIV-PAH [448 (370-510) m], presumably justified by the demographic and haemodynamic differences between these groups. In fact, patients with concomitant portal hypertension (Po-PAH and HIV/Po-PAH) have a better haemodynamic profile than patients with HIV-PAH, specifically, lower pulmonary vascular resistance [6.2 (4.9-8.8) and 7.0 (5.5-11.2) WU vs 8.9 (7.5-12.2) WU] and higher cardiac index [3.1 (2.6-3.8) and 3.0 (2.7-3.7) l/min/m2 vs 2.6 (2.2-2.9) l/min/m2] and mixed venous oxygen saturation [70 (65-75) and 67 (62-71) % vs 61 (55-66)%] values. Despite these differences, the survival of the three groups of patients was not statistically different (5-year survival of patients with Po-PAH was 41%; of patients with HIV/Po-PAH was 46%; and of patients with HIV-PAH was 51%; log-rank test p-value= 0.059) and the prognostic factors that emerge at the multivariate analysis are only parameters associated with the underlying disease. In particular, the parameters independently associated with prognosis are, in patients with Po-PAH, only the CTP score [HR 1.665 (CI 1.153-2.403), p= 0.007]; in patients with HIV-PAH only the treatment with HAART [HR 0.283 (CI 0.119-0.675), p= 0.004]; in patients with HIV/Po-PAH both MELD-Na+ [HR 1.224 (CI 1.064-1.408), p= 0.005] and trans-hepatic venous gradient [HR 1.125 (CI 1.026-1.235), p= 0.013]. Conclusions In patients with Po-PAH, HIV-PAH, and HIV/Po-PAH adequately treated with PAH medications, the prognosis seems to be related to the underlying disease. This may explain why their survival is not statistically different despite significant demographic, exercise and hemodynamic differences.

100 ANALYSIS OF PROGNOSTIC PREDICTORS AND DIFFERENCES BETWEEN SUBGROUPS OF PULMONARY ARTERIAL HYPERTENSION ASSOCIATED WITH PORTAL HYPERTENSION AND HIV INFECTION

Abstract Background Pulmonary arterial hypertension (PAH) represents a rare complication of both portal hypertension (Po-PAH) and HIV infection (HIV-PAH). Due to overlapping risk factors, in the latter patients there may frequently be a hepatic involvement that can cause portal hypertension, resulting in an overlap PAH form associated with both portal hypertension and HIV (HIV/Po-PAH). Methods A retrospective analysis was conducted on 204 patients with Po-PAH (128), HIV-PAH (41) and HIV/Po-PAH (35) referred to our centre from 1993 to 2021, with the aim of describing the clinical, functional and haemodynamic characteristics and identifying the prognostic determinants. At baseline, in patients with Po-PAH and HIV/Po-PAH, the severity of liver disease was estimated using the Child-Turcotte-Pugh (CTP) score, MELD score (Model for End-stage Liver Disease); instead, in patients with HIV-PAH and HIV/Po-PAH it was defined whether they received HAART (Highly Active Anti-Retroviral Therapy) and the CD4+ lymphocytes number. Data are expressed as median (interquartile range) and compared with Dunn's test. Prognostic determinants were identified by univariate and multivariate Cox-regression analysis. Survival was assessed using Kaplan Meier method. Patients were treated according to ESC/ERS guidelines. Results HIV-infected patients [40 (37-43) years] and HIV/Po-PAH [44 (39-48) years] are younger than Po-PAH patients [53 (44-60) years]; the exercise capacity assessed by the 6-minute walking test of patients with HIV/Po-PAH [516 (432-571) m] was superior to both patients with Po-PAH [426 (366-504) m] and HIV-PAH [448 (370-510) m], presumably justified by the demographic and haemodynamic differences between these groups. In fact, patients with concomitant portal hypertension (Po-PAH and HIV/Po-PAH) have a better haemodynamic profile than patients with HIV-PAH, specifically, lower pulmonary vascular resistance [6.2 (4.9-8.8) and 7.0 (5.5-11.2) WU vs 8.9 (7.5-12.2) WU] and higher cardiac index [3.1 (2.6-3.8) and 3.0 (2.7-3.7) l/min/m2 vs 2.6 (2.2-2.9) l/min/m2] and mixed venous oxygen saturation [70 (65-75) and 67 (62-71) % vs 61 (55-66)%] values. Despite these differences, the survival of the three groups of patients was not statistically different (5-year survival of patients with Po-PAH was 41%;of patients with HIV/Po-PAH was 46%; and of patients with HIV-PAH was 51%; log-rank test p-value= 0.059) and the prognostic factors that emerge at the multivariate analysis are only parameters associated with the underlying disease. In particular, the parameters independently associated with prognosis are, in patients with Po-PAH, only the CTP score [HR 1.665 (CI 1.153-2.403), p= 0.007]; in patients with HIV-PAH only the treatment with HAART [HR 0.283 (CI 0.119-0.675), p= 0.004]; in patients with HIV/Po-PAH both MELD-Na+ [HR 1.224 (CI 1.064-1.408), p= 0.005] and trans-hepatic venous gradient [HR 1.125 (CI 1.026-1.235), p= 0.013]. Conclusions in patients with Po-PAH, HIV-PAH, and HIV/Po-PAH adequately treated with PAH medications, the prognosis seems to be related to the underlying disease. This may explain why their survival is not statistically different despite significant demographic, exercise and hemodynamic differences.

Study of the effect of vascular endothelial growth factor (VEGF) C(+405)G (rs2010963) single nucleotide polymorphism on the development of esophageal and gastric varices and risk of variceal bleeding in cirrhotic hepatitis C virus (HCV) patients (VEGF) C(+405)G IN esophageal and gastric varices

BackgroundHCV infection is a major worldwide cause of chronic liver diseases. Esophageal and gastric varices are common in cirrhotic patients due to concomitant portal hypertension. Variceal hemorrhage is a major decompensating event with high morbidity and mortality. Endothelial dysfunction, occurring in cirrhosis, facilitates the development of liver cirrhosis, portal hypertension and contributes to increased intrahepatic vascular resistance..VEGF family members are major regulators of blood vessel development and function.ResultsThe study was conducted on 90 subjects admitted to Tropical Medicine Department, Alexandria Main University Hospital: 30 cirrhotic patients with endoscopically proven varices (group A), 30 cirrhotic patients without varices (group B), and 30 healthy controls (group C). All patients was subjected to detailed history taking and thorough clinical examination, laboratory investigations, ultrasound abdomen, upper gastrointestinal endoscopy, and genotyping for VEGF C(+405)G (rs2010963) by 5′ nuclease assay. The VEGF C(+405)G (rs2010963) GG genotype was associated with higher prevalence of esophageal and gastric varices and higher bleeding risk.ConclusionVEGF C(+405)G (rs2010963) is an important genetic determinant of esophageal varices, gastric varices, and correlates with variceal bleeding risk. Genetic testing of this SNP would be useful in prediction of esophageal and gastric varices and bleeding risk.

Pregnancy outcomes in women with Budd–Chiari syndrome or portal vein thrombosis – a multicentre retrospective cohort study

ObjectiveTo evaluate current practice and outcomes of pregnancy in women previously diagnosed with Budd–Chiari syndrome and/or portal vein thrombosis, with and without concomitant portal hypertension.Design and settingMulticentre retrospective cohort study between 2008 and 2021.PopulationWomen who conceived in the predefined period after the diagnosis of Budd–Chiari syndrome and/or portal vein thrombosis.Methods and main outcome measuresWe collected data on diagnosis and clinical features. The primary outcomes were maternal mortality and live birth rate. Secondary outcomes included maternal, neonatal and obstetric complications.ResultsForty‐five women (12 Budd–Chiari syndrome, 33 portal vein thrombosis; 76 pregnancies) were included. Underlying prothrombotic disorders were present in 23 of the 45 women (51%). Thirty‐eight women (84%) received low‐molecular‐weight heparin during pregnancy. Of 45 first pregnancies, 11 (24%) ended in pregnancy loss and 34 (76%) resulted in live birth of which 27 were at term (79% of live births and 60% of pregnancies). No maternal deaths were observed; one woman developed pulmonary embolism during pregnancy and two women (4%) had variceal bleeding requiring intervention.ConclusionsThe high number of term live births (79%) and lower than expected risk of pregnancy‐related maternal and neonatal morbidity in our cohort suggest that Budd–Chiari syndrome and/or portal vein thrombosis should not be considered as an absolute contraindication for pregnancy. Individualised, nuanced counselling and a multidisciplinary pregnancy surveillance approach are essential in this patient population.Tweetable abstractBudd–Chiari syndrome and/or portal vein thrombosis should not be considered as an absolute contraindication for pregnancy.

Портальная гипертензивная гастропатия (Обзор литературы)

Статья посвящена портальной гипертензивной гастропатии (ПГГ) — вторичному изменению слизистой оболочки и подслизистого слоя желудка на фоне цирроза печени (ЦП) любой этиологии и сопутствующей ему портальной гипертензии. В обзоре представлены данные, касающиеся истории изучения данной патологии, эпидемиологии, патогенеза, клинических проявлений, методов диагностики и лечения. Показано, что в основе заболевания лежит портальная гипертензия, приводящая к нарушению микроциркуляции в слизистой желудка, и как следствие — к полнокровию и венозному застою. Клиническое течение ПГГ в большинстве случаев бессимптомное. Основным методом диагностики является эндоскопический, базирующийся на определенных макроскопических признаках. В обзоре рассмотрены основные эндоскопические классификации ПГГ. Основные гистологические изменения при ПГГ включают расширение капилляров и венул в слизистом и подслизистом слое без существенного воспаления. Течение ПГГ динамичное. К осложнениям ПГГ относятся хронические и, реже, острые кровотечения. Лечение медикаментозное, с использованием неселективных бета-блокаторов

Long-term survival and recurrence after curative resection for hepatocellular carcinoma in patients with chronic hepatitis C virus infection: a multicenter observational study from China

BackgroundHepatocellular carcinoma (HCC) is a recognized sequalae of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection. This study aimed to identify long-term survival and prognostic factors after curative resection for HCC among patients with chronic HCV infection. MethodsFrom a Chinese multicenter database, the data of consecutive patients with HCV infection undergoing curative liver resection for initial HCC between 2006 and 2015 were retrospectively reviewed. Postoperative 30-day mortality and morbidity, long-term overall survival (OS) and recurrence-free survival (RFS) were evaluated. ResultsAmong 382 HCC patients with HCV infection, 68 (18%) had concurrent HBV infection and 110 (29%) had portal hypertension. Postoperative 30-day morbidity and mortality rates were 45% and 2.9%, respectively. The 5-year OS and RFS rates were 45% and 34%, respectively. Multivariable Cox-regression analyses identified that concurrent HBV infection, presence of portal hypertension, largest tumor size > 5 cm, and macrovascular and microvascular invasion were independently associated with worse OS and RFS, while postoperative regular anti-HCV therapy was independently associated with better OS. ConclusionLong-term prognosis after HCC resection among patients with HCV infection was worse in those with concurrent HBV infection and concomitant portal hypertension. Postoperative regular anti-HCV therapy was associated with better OS.

1804 An Unusual Presentation of Mallory-Weiss Syndrome (MWS)

INTRODUCTION: Mallory-Weiss syndrome (MWS) is characterized as longitudinal mucosal tears of the esophagus, most often located in the gastro-esophageal junction that may extendproximally into the distal and even mid- esophagus or distally into the stomach. Risk factors for bleeding as a result of a tear include alcohol abuse and concomitant portal hypertension. Incidence is highest among the male gender and between the ages of 40-60. The proposed mechanism of the tearing is an increase in intra-abdominal pressure leading to a tear through the mucosa and underlying esophageal venous and/or arterial plexus. We present a unique case of MWS that originated in the mid-esophagus with no extended involvement of the distal esophagus. CASE DESCRIPTION/METHODS: A 51-year-old male with a past medical history of alcohol dependence presented to the ER for hematemesis. In the ER, the patient’s respiratory status rapidly declined and the patient was intubated. The lab values and chest xrays were all normal. After intubation, the patient continued with heavy retching that contained frank blood and clots. Emergent endoscopy was performed and a large mid-esophageal Mallory Wiess tear was identified and treated with epinephrine injections. There was also an ulceration of the GE junction that was treated with epinephrine and hemoclip placement. The patient recovered without further incident and was discharged several days later. DISCUSSION: Initial management of MWS with concomitant upper GI bleed includes: airway management, IV PPI, IV antiemetic, and upper endoscopy for evaluation of the tear with therapeutic interventions that may involve thermal coagulation, hemoclips, epinephrine injection, and/or band ligation. Complications often occur if bleeding cannot be controlled, and surgery may ultimately be necessary. As mentioned, MWS usually involves the gastro-esophageal junction. In a literature review, no previous cases involving a tear limited solely to the mid-esophagus were described until now. It is unclear as to what the pathophysiology behind this particular presentation is or if the location of the tear changes the prognosis and/or complication rate of the case. With no previous cases to review, recommendations are limited; however prompt management remains vital for all MWS cases.

Update on transarterial approaches to locoregional treatment in hepatocellular carcinoma.

This review explores current knowledge and recent data about vascular-centered locoregional treatments and proposes alternate algorithms. Hepatocellular carcinoma represents the sixth most common neoplasm worldwide. Currently, the Barcelona Clinic Liver Cancer (BCLC) staging is the most commonly used in Europe for treatment allocation. According to this classification, European Society for Medical Oncology (ESMO) guidelines currently recommend transarterial chemoembolization for intermediate stage HCC and systemic treatments, such as, sorafenib in more advanced stages. However, strong evidences are still lacking to conclude to the superiority of one technique over another, as the optimal treatment choice remains challenging and should take into consideration more clinical, biological and imaging findings than reported in the BCLC staging system, such as patient age or clinical status, tumor characteristics (including distribution and heterogeneity), tumor vascularization and concomitant portal hypertension or biliary anomalies. Many controversies remain, in particular, the relative place of bland embolization versus chemoembolization, the clinical benefit of drug-eluting bead chemoembolization (DEB-TACE) over conventional chemoembolization (cTACE), as well as the real place of radioembolization in general setting as well as innovative applications, such as radiation segmentectomy and radiation lobectomy.

Visceral artery aneurysms - classification, diagnosis and treatment.

Although visceral artery aneurysms are rare, mortality due to their rupture is high, estimated at even 25–75%. That is why it is significant to detect each such lesion. Visceral artery aneurysms are usually asymptomatic and found incidentally during examinations performed for other indications. Autopsy results suggest that most asymptomatic aneurysms remain undiagnosed during lifetime. Their prevalence in the population is therefore higher. The manifestation of a ruptured aneurysm depends on its location and may involve intraperitoneal hemorrhage, gastrointestinal and portal system bleeding with concomitant portal hypertension and bleeding from esophageal varices. Wide access to diagnostic tests, for example ultrasound, computed tomography or magnetic resonance imaging, helps establish the correct diagnosis and a therapeutic plan as well as select appropriate treatment. After a procedure, the same diagnostic tools enable assessment of treatment efficacy, or are used for the monitoring of aneurysm size and detection of potential complications in cases that are ineligible for treatment. The type of treatment depends on the size of an aneurysm, the course of the disease, risk of rupture and risk associated with surgery or endovascular procedure. Endovascular treatment is preferred in most cases. Aneurysms are excluded from the circulation using embolization coils, ethylene vinyl alcohol, stents, multilayer stents, stent grafts and histoacryl glue (or a combination of these methods).

Association Between Changes in Splanchnic Hemodynamics and Risk Factors of Portal Venous System Thrombosis After Splenectomy with Periesophagogastric Devascularization.

BackgroundThe purpose of this study was to investigate splanchnic hemodynamic changes and determine an optimal cutoff value for risk factors of portal venous system thrombosis (PVST) after splenectomy with periesophagogastric devascularization (SPD) in cirrhotic patients with esophageal and gastric variceal bleeding (EGVB) and portal hypertension (PH).Material/MethodsData on patients who underwent SPD were collected retrospectively from January 2013 to December 2017. Color Doppler ultrasound was performed to detect hemodynamic changes of the hepatic artery, splenic artery, splenic vein, and portal vein in included patients (n=60) and healthy volunteers (n=30). Outcomes were compared between preoperative and postoperative biochemical indicators. The cutoff values for hemodynamics were identified using receiver operating characteristic (ROC) curve analysis, and univariate and multivariate analyses of risk factors of PVST were performed.ResultsIn our series, hemodynamic indexes of splenic artery, spleen vein, and portal vein in the study group were significantly higher than that of the control group (P<0.05). Multivariate analysis revealed that the portal vein flow and the internal diameter of the portal vein were significantly correlated with PVST. The ROC analysis revealed that the cutoff points for portal vein flow and internal diameter of the splenic vein and portal vein were ≥1822.32 ml/min, ≥1.37 cm, and ≥1.56 cm, respectively.ConclusionsSPD is an effective treatment in cirrhotic patients with concomitant EGVB and PH by increasing hepatic artery flow and decreasing portal vein flow. High portal vein flow and wider diameters of the portal vein and splenic vein are important markers of PVST.

Left-sided portal hypertension revisited

Background: Splenic vein obstruction can lead to left-sided portal hypertension, which is a rare segmental portal hypertension condition, often caused by inflammatory or neoplastic disease of the pancreas. Today, adequate study by cross-sectional imaging, e.g., ultrasound and computed tomography, allows the identification of particular features of the venous collateral pathways that favor the development of gastroesophageal varices. Methods: A retrospective study of 15 cases of left-sided portal hypertension secondary to complete thrombosis of the splenic vein was performed, with special attention to the morphodynamic conditions predicting the development of gastroesophageal varices. Results: In patients with left-sided portal hypertension, gastroesophageal varices were greatly favored by two conditions: collateral pathways directed to the gastric fundus and hypertension in the left gastric vein. This last condition typically occurs when the left gastric vein inflows into an already obstructed splenic trunk, or in the case of concomitant portal hypertension. On the contrary, patients with left-sided portal hypertension and collaterals connected with the left renal or adrenal veins have minor risk of gastroesophageal varices. Conclusions: In every case of left-sided portal hypertension, upper digestive endoscopy and close follow-up are recommended. Besides, computed tomography can demonstrate particular conditions directly favoring gastroesophageal varices, and aid in selection of the appropriate therapeutic decisions.

Relationship between portal vein pressure and FibroScan score in cirrhotic patients with concomitant portal hypertension

Relationship between portal vein pressure and FibroScan score in cirrhotic patients with concomitant portal hypertension

Outcomes of pregnancies complicated by liver cirrhosis, portal hypertension, or esophageal varices

Objective: To evaluate pregnancy outcomes in women with liver cirrhosis, portal hypertension, or esophageal varices.Study design: We analyzed a retrospective cohort of 2 284 218 pregnancies in 2005–2009 recorded in the California Birth Registry database. Utilizing ICD-9 codes we analyzed the following outcomes for liver cirrhosis, portal hypertension, or esophageal varices in pregnancy: preeclampsia (PET), preterm delivery (PTD; <37 weeks), cesarean section, low birth weight (LBW; <2500 g), small for gestational age (SGA; <10th percentile), neonatal death (NND), and postpartum hemorrhage (PPH).Results: Cirrhosis in pregnancy conferred an increased risk of PET, PTD, CS in multiparous women, LBW, and NND. Portal hypertension in pregnancy was associated with PTD, LBW, NND, and PPH. Non-bleeding esophageal varices in pregnancy were not associated with the outcomes assessed in a statistically significant manner. One case of bleeding esophageal varices was observed, resulting in PTD with a LBW infant. There were three cases of concomitant portal hypertension or concomitant esophageal varices with cirrhosis in pregnancy.Conclusion: Pregnancy in women with concomitant liver cirrhosis, portal hypertension, or esophageal varices can be successful. However, pregnancy outcomes are worse and may warrant closer antenatal monitoring and patient counseling. Cirrhosis in pregnancy with concomitant portal hypertension or esophageal varices is rare.

Peripancreatic Enhancing Lesion in a Cirrhotic Patient

Question: A 74-year-old white man with a history of decompensated alcoholic liver disease was referred to our clinic for further management of his cirrhosis. The patient initially presented to an outside hospital 2 months prior with increasing abdominal girth and confusion. Small, nonbleeding esophageal varices were visualized on upper endoscopy. Doppler ultrasonography revealed a portal vein thrombus with cavernous transformation. The patient was initiated on warfarin. He presented to us for a second opinion. Physical examination revealed an elderly, ill-appearing gentleman with anicteric sclera, shifting dullness and bilateral lower extremity edema. Laboratory testing was notable for a total bilirubin of 0.8 mg/dL, alanine and aspartate aminotransferases 190 and 150 U/L, respectively, and alkaline phosphatase 1000 U/D. International Normalized Ratio was prolonged (on warfarin) at 4.2; creatinine was 1.1 mg/dL and albumin 3.2 g/dL. Triphasic computed tomography of the abdomen and pelvis demonstrated a large peripancreatic lesion enhancing on portal venous phase with resultant mass effect on adjacent structures (Figure A). What is the diagnosis? Look on page 324 for the answer and see the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. Triphasic computed tomography of the abdomen reveals an 8.2 × 6.5-cm portal vein aneurysm containing subacute thrombi. Compression of the remnant thrombosed portal vein demonstrates mass effect from the aneurysm (Figure A). Cavernous transformation of the liver secondary to portal vein thrombosis can be seen distal to the aneurysm (Figure B). Coronal and sagittal views further demonstrate the extent of the aneurysm (Figures C, D). Portal vein aneurysm is a rare clinical entity that mainly occurs at bifurcations and confluences of the portal venous system, both intra- and extrahepatically. In patients without preexisting liver disease, it may result from congenital malformations, such as intrinsic weakness of the vein wall or diverticular remnant of a primitive portal precursor.1Lau H. Chew D.K. Belkin M. Extrahepatic portal vein aneurysm: a case report and review of the literature.Cardiovasc Surg. 2002; 10: 58-61Crossref PubMed Scopus (0) Google Scholar In cases of acquired portal vein aneurysm, portal hypertension secondary to cirrhosis is the most frequently reported cause. Portal hypertension initially leads to compensatory medial hypertrophy that is eventually replaced by fibrous tissue with weak tensile strength.2Rafiq S.A. Sitrin M.D. Portal vein aneurysm: case report and review of the literature.Gastroenterol Hepatol. 2007; 3: 296-298PubMed Google Scholar However, portal vein aneurysms are still rare in patients with known cirrhosis, suggesting that an existing congenital abnormality may be present for portal hypertension to result in aneurysmal dilation.1Lau H. Chew D.K. Belkin M. Extrahepatic portal vein aneurysm: a case report and review of the literature.Cardiovasc Surg. 2002; 10: 58-61Crossref PubMed Scopus (0) Google Scholar Because most patients are asymptomatic, portal vein aneurysms are generally found incidentally on abdominal imaging. Conservative management with serial imaging is appropriate for small aneurysms in asymptomatic patients without concomitant portal hypertension or cirrhosis. Complications from portal vein aneurysm include thrombosis, rupture, and symptoms related to compression on adjacent organs such as the common bile duct, duodenum, and vena cava. Rupture of portal vein aneurysm is unusual because of low portal venous pressure, but the risk of rupture does increase in the presence of portal hypertension. Patients with portal hypertension and portal vein thrombosis may benefit from surgical shunts to reduce portal pressure and prevent progressive dilation of the aneurysm.3Brock P.A. Jordan P.H. Barth M.H. et al.Portal vein aneurysm: a rare but important vascular condition.Surgery. 1997; 121: 105-108Abstract Full Text PDF PubMed Scopus (69) Google Scholar This particular patient had several risk factors for acquired portal vein aneurysm, including decompensated alcoholic cirrhosis with portal hypertension as well as radiographic evidence of chronic pancreatitis. Given the patient's age, multiple comorbidities, and rapid deterioration, it was the family's request not to pursue aggressive measures. His anticoagulation with warfarin was discontinued.

Colonic venous malformation and portal hypertension: association, management, and review of the literature

We present a case of an adolescent with lower gastrointestinal bleeding caused by a colorectal venous malformation (VM) with concomitant portal hypertension. After an episode of massive gastrointestinal bleeding, we performed an extended right hemicolectomy and resection of the VM and selective portosystemic shunt. Here, we present the case and review the literature regarding portal hypertension and gastrointestinal vascular malformations. Additionally, we discuss the physiologic and hemodynamic effects of gastrointestinal vascular malformations on the portal system.

An Interesting Case of Chronic Idiopathic Non-cirrhotic Portal Vein Thrombosis

Purpose: Introduction: Portal vein thrombosis was first reported in 1868 by Balfour and Stewart. It is a rare condition that typically presents in non-cirrhotic patients. Inherited (Factor V Leiden and Prothrombin gene mutation G201210A, Protein C, S, Anti thrombin III deficiency) and acquired thrombophilias (Lupus Anticoagulant, myeloproliferative diseases, malignancy, surgery and trauma) account for majority of the cases of portal vein thrombosis. Doppler ultrasound studies are usually the initial test of choice. Case Report: 63 year old Hispanic Female with history of hypertension, Diabetes Mellitus, coronary artery disease presented with complaints of epigastric pain & bloody vomiting. She initially had epigastric discomfort & 2 episodes of hematemesis. She denied alcohol use. Abdominal examination was unremarkable except for mild epigastric tenderness. Laboratory analysis revealed hemoglobin of 10.5 mg/dl with normal liver function tests and aminotransferases. An upper gastrointestinal endoscopic examination was done which revealed grade 4 esophageal varices with fresh blood in the distal esophagus which were subsequently ligated. She was started on octreotide and propranolol. She had another episode of GI bleed requiring emergent endoscopic intervention. She underwent a liver biopsy. Pathology revealed focal mild portal fibrosis with mild micro & macro vesicular steatosis but no cirrhosis. A Doppler Ultrasound revealed portal vein thrombosis and concomitant portal hypertension. An extensive hypercoaguable work up was done which included protein C & S levels, anti thrombin III, Prothrombin gene mutation G20210A, Factor V Leiden, Lupus anticoagulant, Anticardiolipin antibodies, Homocysteine level & they were all negative. We also tested her blood for flow-cytometry for CD 55 and CD 59 but the test was normal and in the process effectively ruled out paroxysmal nocturnal hemoglobinuria. She also was also tested for the JAK 2 mutation. It was negative. We gave her the clinical diagnosis of chronic idiopathic non-cirrhotic portal vein thrombosis. She subsequently had a meso-caval shunt done to relieve the portal hypertension. She was started on warfarin anticoagulation 3 days later with close monitoring for bleeding. She clinically got better and was then discharged home. Discussion: Non-cirrhotic portal vein thrombosis can be acute or chronic. Acute cases need at least 3 months of anticoagulation. Chronic cases needs porto-systemic shunting. The use of anticoagulation in chronic cases should be decided upon on a case by case basis weighing the risk of bleeding versus thrombosis. We opted to give longterm anticoagulation to our patient to prevent re-thrombosis of the mesocaval shunt/graft.

P62 Bacterial translocation in human immunodeficiency virus-infected patients with hepatitis C virus-related cirrhosis: implication in haemodynamic alterations and mortality

IntroductionHepatitis C virus (HCV)-related liver disease follows an accelerated course in patients with human immunodeficiency virus (HIV) co-infection. Liver fibrosis progression to cirrhosis is faster in HIV/HCV coinfected individuals than...

Hematochezia in a patient with liver cirrhosis

Although commonly detectable in patients with cirrhosis, rectal varices only infrequently cause significant hematochezia (0.5–3.6%). While they may be expected to resolve with treatment of the concomitant portal hypertension, there is currently no standardized approach to their management in isolation. Therefore many authorities recommend transjugular intrahepatic portosystemic shunting (TIPS) as a means of alleviating otherwise recalcitrant bleeding. Conceptually, however, rectal varices should be as amenable to local therapies as are their counterparts occurring at the esophagogastric junction. In this report, we describe the use of endoscopic banding per ano to alleviate significant rectal bleeding in a patient with poorly controlled portal hypertension. This allowed medical optimisation so that the underlying pathology could be controlled without recourse to TIPS or other means of creating a formal portosystemic shunt.

Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension.

Altered small bowel motility and a high prevalence of small intestinal bacterial overgrowth (SIBO) has been observed in patients with liver cirrhosis. Our aim was to explore the relationship between motility abnormalities, portal hypertension, and SIBO. Twenty-four patients with liver cirrhosis were included. Twelve had portal hypertension (PH) and 12 had liver cirrhosis (LC) alone. Child-Pugh score was the same in the groups. Antroduodenojejunal pressure recordings were performed, and noninvasive variceal pressure measurements were undertaken. Thirty-two healthy volunteers served as a reference group. Bacterial cultures were obtained from jejunal aspirates. The PH group had a higher proportion of individual pressure waves that were retrograde in the proximal duodenum during phase II (52% vs 13% vs 8% of propagated contractions; p < 0.001) as well as postprandially (49% vs 18% vs 13%; p < 0.01) compared with LC and controls, respectively. Long clusters were more common in PH than in controls (9.1 +/- 2.1 vs 4.9 +/- 0.8; p < 0.05), and a higher motility index in phase III in the proximal and distal duodenum was seen in the PH as compared with the other groups. The mean variceal pressure was 21 +/- 1 mm Hg. Motor abnormalities were not correlated to the level of variceal pressure. Thirty-three percent of the patients in the PH group but none in the LC group had SIBO. Abnormal small bowel motility and SIBO is common in patients with liver cirrhosis with concomitant portal hypertension. Portal hypertension per se might be significantly related to small bowel abnormalities observed in patients with liver cirrhosis.

Small intestinal motility disturbances and bacterial overgrowth in patients with liver cirrhosis and portal hypertension

Objectives Altered small bowel motility and a high prevalence of small intestinal bacterial overgrowth (SIBO) has been observed in patients with liver cirrhosis. Our aim was to explore the relationship between motility abnormalities, portal hypertension, and SIBO. Methods Twenty-four patients with liver cirrhosis were included. Twelve had portal hypertension (PH) and 12 had liver cirrhosis (LC) alone. Child-Pugh score was the same in the groups. Antroduodenojejunal pressure recordings were performed, and noninvasive variceal pressure measurements were undertaken. Thirty-two healthy volunteers served as a reference group. Bacterial cultures were obtained from jejunal aspirates. Results The PH group had a higher proportion of individual pressure waves that were retrograde in the proximal duodenum during phase II (52% vs 13% vs 8% of propagated contractions; p < 0.001) as well as postprandially (49% vs 18% vs 13%; p < 0.01) compared with LC and controls, respectively. Long clusters were more common in PH than in controls (9.1 ± 2.1 vs 4.9 ± 0.8; p < 0.05), and a higher motility index in phase III in the proximal and distal duodenum was seen in the PH as compared with the other groups. The mean variceal pressure was 21 ± 1 mm Hg. Motor abnormalities were not correlated to the level of variceal pressure. Thirty-three percent of the patients in the PH group but none in the LC group had SIBO. Conclusions Abnormal small bowel motility and SIBO is common in patients with liver cirrhosis with concomitant portal hypertension. Portal hypertension per se might be significantly related to small bowel abnormalities observed in patients with liver cirrhosis.