Hepatic venous pressure gradient: Inaccurately estimates portal venous pressure gradient in alcoholic cirrhosis and portal hypertension

BACKGROUND Portal hypertension(PHT)in patients with alcoholic cirrhosis causes a range of clinical symptoms,including gastroesophageal varices and ascites.The hepatic venous pressure gradient(HVPG),which is easier to measure,has replaced the portal venous pressure gradient(PPG)as the gold standard for diagnosing PHT in clinical practice.Therefore,attention should be paid to the correlation between HVPG and PPG.METHODS Between January 2017 and June 2020,134 patients with alcoholic cirrhosis and PHT who met the inclusion criteria underwent various pressure measurements during transjugular intrahepatic portosystemic shunt procedures.Correlations were assessed using Pearson’s correlation coefficient to estimate the correlation coefficient(r)and determination coefficient(R^(2)).Bland-Altman plots were constructed to further analyze the agreement between the measurements.Disagreements were analyzed using paired t tests,and P values<0.05 were considered statistically significant.RESULTS In this study,the correlation coefficient(r)and determination coefficient(R2)between HVPG and PPG were 0.201 and 0.040,respectively(P=0.020).In the 108 patients with no collateral branch,the average wedged hepatic venous pressure was lower than the average portal venous pressure(30.65±8.17 vs.33.25±6.60 mmHg,P=0.002).Hepatic collaterals were identified in 26 cases with balloon occlusion hepatic venography(19.4%),while the average PPG was significantly higher than the average HVPG(25.94±7.42 mmHg vs 9.86±7.44 mmHg;P<0.001).The differences between HVPG and PPG<5 mmHg in the collateral vs no collateral branch groups were three cases(11.54%)and 44 cases(40.74%),respectively.CONCLUSION In most patients,HVPG cannot accurately represent PPG.The formation of hepatic collaterals is a vital reason for the strong underestimation of HVPG.

Osteopontin: A non-invasive parameter of portal hypertension and prognostic marker of cirrhosis

AIM: To investigate the relationship between osteopontin plasma concentrations and the severity of portal hypertension and to assess osteopontin prognostic value.METHODS: A cohort of 154 patients with confirmed liver cirrhosis (112 ethylic, 108 men, age 34-72 years) were enrolled in the study. Hepatic venous pressure gradient (HVPG) measurement and laboratory and ultrasound examinations were carried out for all patients. HVPG was measured using a standard catheterization method with the balloon wedge technique. Osteopontin was measured using the enzyme-linked immunosorbent assay (ELISA) method in plasma. Patients were followed up with a specific focus on mortality. The control group consisted of 137 healthy age- and sex- matched individuals.RESULTS: The mean value of HVPG was 16.18 &#x000b1; 5.6 mmHg. Compared to controls, the plasma levels of osteopontin in cirrhotic patients were significantly higher (P &#x0003c; 0.001). The plasma levels of osteopontin were positively related to HVPG (P = 0.0022, r = 0.25) and differed among the individual Child-Pugh groups of patients. The cut-off value of 80 ng/mL osteopontin distinguished patients with significant portal hypertension (HVPG above 10 mmHg) at 75% sensitivity and 63% specificity. The mean follow-up of patients was 3.7 &#x000b1; 2.6 years. The probability of cumulative survival was 39% for patients with HVPG &#x0003e; 10 mmHg and 65% for those with HVPG &#x02264; 10 mmHg (P = 0.0086, odds ratio (OR), 2.92, 95% confidence interval (CI): 1.09-7.76). Osteopontin showed a similar prognostic value to HVPG. Patients with osteopontin values above 80 ng/mL had significantly lower cumulative survival compared to those with osteopontin &#x02264; 80 ng/mL (37% vs 56%, P = 0.00035; OR = 2.23, 95%CI: 1.06-4.68).CONCLUSION: Osteopontin is a non-invasive parameter of portal hypertension that distinguishes patients with clinically significant portal hypertension. It is a strong prognostic factor for survival.

Clinical effects and complications of TIPS for portal hypertension due to cirrhosis:A single center

AIM:To determine the clinical effects and complications of transjugular intrahepatic portosystemic shunt(TIPS)for portal hypertension due to cirrhosis.METHODS:Two hundred and eighty patients with portal hypertension due to cirrhosis who underwent TIPS were retrospectively evaluated.Portal trunk pressure was measured before and after surgery.The changes in hemodynamics and the condition of the stent were assessed by ultrasound and the esophageal and fundic veins observed endoscopically.RESULTS:The success rate of TIPS was 99.3%.The portal trunk pressure was 26.8±3.6 cmH2O after surgery and 46.5±3.4 cmH2O before surgery(P<0.01).The velocity of blood flow in the portal vein increased.The internal diameters of the portal and splenic veins were reduced.The short-term hemostasis rate was100%.Esophageal varices disappeared completely in68%of patients and were obviously reduced in 32%.Varices of the stomach fundus disappeared completely in 80%and were obviously reduced in 20%of patients.Ascites disappeared in 62%,were markedly reduced in 24%,but were still apparent in 14%of patients.The total effective rate of ascites reduction was 86%.Hydrothorax completely disappeared in 100%of patients.The incidence of post-operative stent stenosis was 24%at 12 mo and 34%at 24 mo.The incidence of post-operative hepatic encephalopathy was 12%at3 mo,17%at 6 mo and 19%at 12 mo.The incidence of post-operative recurrent hemorrhage was 9%at 12mo,19%at 24 mo and 35%at 36 mo.The cumulative survival rate was 86%at 12 mo,81%at 24 mo,75%at 36 mo,57%at 48 mo and 45%at 60 mo.CONCLUSION:TIPS can effectively lower portal hypertension due to cirrhosis.It is significantly effective for hemorrhage of the digestive tract due to rupture of esophageal and fundic veins and for ascites and hydrothorax caused by portal hypertension.

Abnormal splenic artery diameter/hepatic artery diameter ratio in cirrhosis-induced portal hypertension

AIM:To determine an optimal cutoff value for abnormal splenic artery diameter/proper hepatic artery diameter(S/P) ratio in cirrhosis-induced portal hypertension.METHODS:Patients with cirrhosis and portal hypertension(n = 770) and healthy volunteers(n = 31) underwent volumetric computed tomography threedimensional vascular reconstruction to measure the internal diameters of the splenic artery and proper hepatic artery to calculate the S/P ratio.The cutoff value for abnormal S/P ratio was determined using receiver operating characteristic curve analysis,and the prevalence of abnormal S/P ratio and associations between abnormal S/P ratio and major complications of portal hypertension were studied using logistic regression.RESULTS:The receiver operating characteristic analysis showed that the cutoff points for abnormal splenic artery internal diameter and S/P ratio were > 5.19 mm and > 1.40,respectively.The sensitivity,specificity,positive predictive value,and negative predictive value were 74.2%,45.2%,97.1%,and 6.6%,respectively.The prevalence of an abnormal S/P ratio in the patients with cirrhosis and portal hypertension was 83.4%.Patients with a higher S/P ratio had a lower risk of developing ascites [odds ratio(OR) = 0.708,95%CI:0.508-0.986,P = 0.041] and a higher risk of developing esophageal and gastric varices(OR = 1.483,95%CI:1.010-2.175,P = 0.044) and forming collateral circulation(OR = 1.518,95%CI:1.033-2.230,P = 0.034).After splenectomy,the portal venous pressure and maximum and mean portal venous flow velocities were reduced,while the flow rate and maximum and minimum flow velocities of the hepatic artery were increased(P < 0.05).CONCLUSION:The prevalence of an abnormal S/P ratio is high in patients with cirrhosis and portal hypertension,and it can be used as an important marker of splanchnic hemodynamic disturbances.

Contemporary concepts of the medical therapy of portal hypertension under liver cirrhosis

Severe complications of liver cirrhosis are mostly related to portal hypertension. At the base of the pathogenesis of portal hypertension is the increase in hepatic vascular resistance to portal blood flow with subsequent development of hyperdynamic circulation, which, despite of the formation of collateral circulation, promotes progression of portal hypertension. An important role in its pathogenesis is played by the rearrangement of vascular bed and angiogenesis. As a result, strategic directions of the therapy of portal hypertension under liver cirrhosis include selectively decreasing hepatic vascular resistance with preserving or increasing portal blood flow, and correcting hyperdynamic circulation and pathological angiogenesis, while striving to reduce the hepatic venous pressure gradient to less than 12 mm Hg or 20% of the baseline. Over the last years, substantial progress in understanding the pathophysiological mechanisms of hemodynamic disorders under liver cirrhosis has resulted in the development of new drugs for their correction. Although the majority of them have so far been investigated only in animal experiments, as well as at the molecular and cellular level, it might be expected that the introduction of the new methods in clinical practice will increase the efficacy of the conservative approach to the prophylaxis and treatment of portal hypertension complications. The purpose of the review is to describe the known methods of portal hypertension pharmacotherapy and discuss the drugs that may affect the basic pathogenetic mechanisms of its development.

Laparoscopic splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension

Since the first laparoscopic splenectomy(LS)was reported in 1991,LS has become the gold standard for the removal of normal to moderately enlarged spleens in benign conditions.Compared with open splenectomy,fewer postsurgical complications and better postoperative recovery have been observed,but LS is contraindicated for hypersplenism secondary to liver cirrhosis in many institutions owing to technical difficulties associated with splenomegaly,well-developed collateral circulation,and increased risk of bleeding.With the improvements of laparoscopic technique,the concept is changing.This article aims to give an overview of the latest development in laparoscopic splenectomy for hypersplenism secondary to liver cirrhosis and portal hypertension.Despite a lack of randomized controlled trial,the publications obtained have shown that with meticulous surgical techniques and advanced instruments,LS is a technically feasible,safe,and effective procedure for hypersplenism secondary to cirrhosis and portal hypertension and contributes to decreased blood loss,shorter hospital stay,and less impairment of liver function.It is recommended that the dilated short gastric vessels and other enlarged collateral circulation surrounding the spleen be divided with the LigaSure vessel sealing equipment,and the splenic artery and vein be transected en bloc with the application of the endovascular stapler.To support the clinical evidence,further randomized controlled trials about this topic are necessary.

Liver surgery in cirrhosis and portal hypertension

The prevalence of hepatic cirrhosis in Europe and the United States, currently 250 patients per 100000 inhabitants, is steadily increasing. Thus, we observe a significant increase in patients with cirrhosis and portal hypertension needing liver resections for primary ormetastatic lesions. However, extended liver resections in patients with underlying hepatic cirrhosis and portal hypertension still represent a medical challenge in regard to perioperative morbidity, surgical management and postoperative outcome. The Barcelona Clinic Liver Cancer classification recommends to restrict curative liver resections for hepatocellular carcinoma in cirrhotic patients to early tumor stages in patients with Child A cirrhosis not showing portal hypertension. However, during the last two decades, relevant improvements in preoperative diagnostic, perioperative hepatologic and intensive care management as well as in surgical techniques during hepatic resections have rendered even extended liver resections in higher-degree cirrhotic patients with portal hypertension possible. However, there are few standard indications for hepatic resections in cirrhotic patients and risk stratifications have to be performed in an interdisciplinary setting for each individual patient. We here review the indications, the preoperative risk-stratifications, the morbidity and the mortality of extended resections for primary and metastatic lesions in cirrhotic livers. Furthermore, we provide a review of literature on perioperative management in cirrhotic patients needing extrahepatic abdominal surgery and an overview of surgical options in the treatment of hepatic cirrhosis.

Antiangiogenic therapy for portal hypertension in liver cirrhosis: Current progress and perspectives

Developing medicines for hemodynamic disorders that are characteristic of cirrhosis of the liver is a relevant problem in modern hepatology. The increase in hepatic vascular resistance to portal blood flow and subsequent hyperdynamic circulation underlie portal hypertension(PH) and promote its progression, despite the formation of portosystemic collaterals. Angiogenesis and vascular bed restructurization play an important role in PH pathogenesis as well. In this regard, strategic directions in the therapy for PH in cirrhosis include selectively decreasing hepatic vascular resistance while preserving or increasing portal blood flow, and correcting hyperdynamic circulation and pathological angiogenesis. The aim of this review is to describe the mechanisms of angiogenesis in PH and the methods of antiangiogenic therapy. The Pub Med database, the Google Scholar retrieval system, and the reference lists from related articles were used to search for relevant publications. Articles corresponding to the aim of the review were selected for 2000-2017 using the keywords: "liver cirrhosis", "portal hypertension", "pathogenesis", "angiogenesis", and "antiangiogenic therapy". Antiangiogenic therapy for PH was the inclusion criterion. In this review, we have described angiogenesis inhibitors and their mechanism of action in relation to PH. Although most of them were studie donly in animal experiments, this selective therapy for abnormally growing newly formed vessels is pathogenetically reasonable to treat PH and associated complications.

Cirrhosis and portal hypertension: The importance of risk stratification, the role of hepatic venous pressure gradient measurement

Portal hypertension is the main prognostic factor in cirrhosis. The recent emergence of potent antiviral drugs and new algorithm of treatment for the management of complications due to portal hypertension have sensibly changed our perception of cirrhosis that can be now considered as a multistage liver disease whose mortality risk can be reduced by a tailored approachfor any stage of risk. Experts recommend to move toward a pathophysiological classification of cirrhosis that considers both structural and functional changes. The hepatic venous pressure gradient HVPG, is the reference gold standard to estimate the severity of portal hypertension in cirrhosis. It correlates with both structural and functional changes that occur in cirrhosis and carries valuable prognostic information to stratify the mortality risk. This article provides a general overview of the pathophysiology and natural course of cirrhosis and portal hypertension. We propose a simplified classification of cirrhosis based on low, intermediate and high mortality stage. The prognostic information provided by HVPG is presented according to each stage. A comparison with prognostic models based on clinical and endoscopic variables is discussed in order to evidence the additional contribute given by HVPG on top of other clinical and instrumental variables widely used in clinical practice.

Combined Laparoscopic Splenectomy and Esophagogastric Devascularization versus Open Splenectomy and Esophagogastric Devascularization for Portal Hypertension due to Liver Cirrhosis

This study was conducted to compare the feasibility,safety and effectiveness of the combined-laparoscopic splenectomy and esophagogastric devascularization(C-LSED)with open splenectomy and esophagogastric devascularization surgery(OSED)in patients with portal hypertension due to liver cirrhosis.From February 2014 to June 2018,68 patients with portal hypertension were diagnosed as having serious gastroesophageal varices and/or hypersplenism in our center.Thirty patients underwent C-LSED and 38 patients received OSED.Results and outcomes were compared retrospectively.No patients of C-LSED group required an intraoperative conversion to open surgery.Significantly shorter operating time,less blood loss,lower transfusion rates,shorter postoperative hospital stay,lower rates of complications were found in C-LSED group than in C-LSED group(P<0.05).No death and rebleeding were documented in both groups during the follow-up periods of one year Postoperative endoscopy revealed that varices in the patients of both groups were alleviated significantly from severe to mild,and in a part of cases,the varices disappeared.The final results suggest that the C-LSED technique is superior to open procedure,due to slightly invasive,simplified operative procedure,significantly shorter operating time,less intraoperative bleeding and lower post-operative complication rates.And C-LSED offers comparable long-term effects to open surgery.

Attenuation of portal hypertension by natural taurine in rats with liver cirrhosis

AIM： To investigate the inhibitory effect of natural taurine （NTau） on portal hypertension （PHT） in rats with experimentally-induced liver cirrhosis （LC）. METHODS： Experimentally-induced LC Wistar rats （20 rats/group） were treated with either oral saline or oral NTau for 6 consecutive weeks. Evaluation parameters included portal venous pressure （PVP）, portal venous resistance （PVR）, portal venous flow （PVF）, splanchnic vascular resistance （SVR） and mean arterial pressure （NAP）. Vasoactive substance levels including nitric oxide （NO）, nitric oxide synthase （NOS） and cyclic guanosine monophosphate （cGMP） were also measured. Histological investigation of type Ⅰ and Ⅲ collagen （COL Ⅰ and Ⅲ） and transforming growth factor-β1 （TGF-β1） was also performed. RESULTS： Treatment with NTau （1） significantly decreased PVP, PVR and PVF, and increased MAP and SVP; （2） markedly increased the vascular compliance and reduced the zero-stress of the portal vein; （3） markedly decreased the amount of NO and cGMP and activity of NOS; and （4） improved the pathological status of the liver tissue and reduced the expression of COL Ⅰ, COL Ⅲ and TGF-β1. CONCLUSION： NTau inhibited the LC-induced PHT by improving hyperdynamic circulation, morphology of liver and biomechanical properties of the portal vein in experimentally-induced LC rats.

Selection of a TIPS stent for management of portal hypertension in liver cirrhosis: An evidence-based review

Nowadays,transjugular intrahepatic portosystemic shunt(TIPS)has become a mainstay treatment option for the management of portal hypertension-related complications in liver cirrhosis.Accumulated evidence has shown that its indications are being gradually expanded.Notwithstanding,less attention has been paid for the selection of an appropriate stent during a TIPS procedure.Herein,we attempt to review the current evidence regarding the diameter,type,brand,and position of TIPS stents.Several following recommendations may be considered in the clinical practice:(1)a 10-mm stent may be more effective than an 8-mm stent for the management of portal hypertension,and may be superior to a 12-mm stent for the improvement of survival and shunt patency;(2)covered stents are superior to bare stents for reducing the development of shunt dysfunction;(3)if available,Viatorr stent-grafts may be recommended due to a higher rate of shunt patency;and(4)the placement of a TIPS stent in the left portal vein branch may be more reasonable for decreasingthe development of hepatic encephalopathy.However,given relatively low quality of evidence,prospective well-designed studies should be warranted to further confirm these recommendations.

Effect of increased hepatic platelet activating factor and its receptor portal hypertension in CCl_4-induced liver cirrhosis

AIM： To evaluate the changes in hepatic platelet activating factor （PAF） and its receptors and their effect on portal pressure of cirrhotic rats induced by CCh. METHODS： A model of liver cirrhosis was replicated in rats by intra-peritoneal injection of CCh for 8 wk. We determined the effect of hepatic PAF and its receptor level on portal and arterial pressure by EIA, saturation binding and RT-PCR technique. RESULTS： Compared to control rats, cirrhotic rats had higher hepatic PAF levels and output as well as higher plasma PAF levels （P〈0.01, P〈0.01, P〈0.05, respectively）. Both hepatic PAF receptor mRNA levels and PAF binding were nearly 3-fold greater in cirrhotic rats （P〈0.01）. Portal injection of PAF （1 g/kg WT） increased the portal pressure by 22% and 33% in control and cirrhotic rats, respectively. In contrast, the arterial pressure was decreased in the both groups （54% in control rats and 42% in cirrhotic rats）. Injection of the PAF antagonist BN52021 （5 mg/kg WT） decreased the portal pressure by 16% in cirrhotic rats but had no effect in the control rats. CONCLUSION： The upregulation of the PAF system contributes to hepatic hemodynamic and metabolic abnormalities in drrhosis, and the increased release of PAF into the circulation has impacts on the systemic hemodynamics.

Rethinking the role of non-selective beta blockers in patients with cirrhosis and portal hypertension

Non-selective beta blockers(NSBB) are commonly used to prevent portal hypertensive bleeding in cirrhotics.Nevertheless, in the last years, the use of NSBB in critically decompensated patients, especially in those with refractory ascites, has been questioned, mainly for an increased risk of mortality and worsening of systemic hemodynamics. Moreover, even if NSBB have been reported to correlate with a higher risk of renal failure and severe infection in patients with advanced liver disease and hypotension, their use has been associated with a reduction of risk of spontaneous bacterial peritonitis, modification of gut permeability and reduction of bacterial translocation. This manuscript systematically reviews the published evidences about harms and benefits of the use of NSBB in patients with decompensated cirrhosis.

Histological abnormalities of the small bowel mucosa in cirrhosis and portal hypertension

AIM: To study the small bowel (SB) mucosa on biopsy in cirrhotic patients with portal hypertension and in non-cirrhotic controls and grade fi ndings according to the Marsh criteria. METHODS: We prospectively enrolled 51 consecutive patients undergoing an upper endoscopy for their routine medical care. Twenty f ive patients with cirrhosis and portal hypertension were compared to 26 controls. We obtained coeliac serology and multiple upper small bowel biopsies on all 51 patients. A GI pathologist interpreted biopsies and graded fi ndings according to the Marsh criteria. We assessed equivalence in Marsh grade between cirrhotic and non-cirrhotic controls using the Mann-Whitney test for equivalence. RESULTS: Gender, ethnicity and age were similar between both groups. Marsh grades were equivalent between the groups. Grade of 0 was present in 96% and grade of 1 was present in 4% of both groups and there was no villus atrophy or decrease in villus/crypt ratio in patients with portal hypertension. CONCLUSION: This study provides evidence for the lack of villus atrophy in patients with cirrhosis and portal hypertension, and supports the continuous reliance on the Marsh criteria when the diagnosis of coeliac disease is to be made in the presence of cirrhosis.

Role of Injury of Gastric Parietal Vessels by Immunocomplexes in the Mechanism of Gastric Mucosal Lesion in Portal Hypertension with Cirrhosis

The present experiment employed the immunohistochemical technique and morphological observation to investigate the expression and distribution of C3, C4, IgG, IgE and 5-HT in portal hypertensive pigs with pathological change of gastric mucosa and gastric parietal vessels. The wall of gastric mucosal microvessels in portal hypertensive pigs had a positive or strong positive reaction of C3,C4, IgG, IgE and 5-HT with obvious injury of gastric mucosa normal pigs imparted negative or feeble positive reaction, suggesting that during portal hypertension, the gastric mucosal micr0-vessels has deposit of immunocomplexes resulting in the injury of the micro-vessels. It might be a factor inv01ved in the pathogenesis of the gastric mucosal lesion during portal hypertension with cirrhosis.

Analysis of the nitric oxide-cyclic guanosine monophosphate pathway in experimental liver cirrhosis suggests phosphodiesterase-5 as potential target to treat portal hypertension

AIM To investigate the potential effect of inhibitors of phosphodiesterase-5(PDE-5) for therapy of portal hypertension in liver cirrhosis.METHODS In the rat model of thioacetamide-induced liver fibrosis/cirrhosis the nitric oxide-cyclic guanosine monophosphate(NO-cGMP) pathway was investigated. Expression and localization of PDE-5, the enzyme that converts vasodilating cGMP into inactive 5'-GMP, was in the focus of the study. Hepatic gene expression of key components of the NO-cGMP pathway was determined by qRT-PCR: Endothelial NO synthase(eNOS), inducible NO synthase(iNOS), soluble guanylate cyclase subunits α1 and β1(sGCa1, sGCb1), and PDE-5. Hepatic PDE-5 protein expression and localization were detected by immunohistochemistry. Serum cGMP concentrations were measured using ELISA. Acute effects of the PDE-5 inhibitor Sildenafil(0.1 mg/kg or 1.0 mg/kg) on portal and systemic hemodynamics were investigated using pressure transducers.RESULTS Hepatic gene expression of eNOS(2.2-fold; P = 0.003), sGCa1(1.7-fold; P = 0.003), sGCb1(3.0-fold; P = 0.003), and PDE-5(11-fold; P = 0.003) was increased in cirrhotic livers compared to healthy livers. Overexpression of PDE-5(7.7-fold; P = 0.006) was less pronounced in fibrotic livers. iNOS expression was only detected in fibrotic and cirrhotic livers. In healthy liver, PDE-5 protein was localized primarily in zone 3 hepatocytes and to a lesser extent in perisinusoidal cells. This zonation was disturbed in cirrhosis: PDE-5 protein expression in perisinusoidal cells was induced approximately 8-fold. In addition, PDE-5-expressing cells were also found in fibrous septa. Serum cGMP concentrations were reduced in rats with cirrhotic livers by approximately 40%. Inhibition of PDE-5 by Sildenafil caused a significant increase in serum cGMP concentrations [+ 64% in healthy rats(P = 0.024), + 85% in cirrhotic rats(P = 0.018)]. Concomitantly, the portal venous pressure was reduced by 19% in rats with liver cirrhosis. CONCLUSION Overexpression and abrogated zonation of PDE-5 likely contribute to the pathogenesis of cirrhotic portal hypertension. PDE-5 inhibition may therefore be a reasonable therapeutic approach for portal hypertension.

Spontaneous rupture of splenic hamartoma in a patient with hepatitis C virus-related cirrhosis and portal hypertension:A case report and review of the literature

Spontaneous rupture is a rare complication of splenic hamartoma. A review of the literature revealed only four such cases. To the best of our knowledge, this is the first report of spontaneous rupture of splenic hamartoma associated with liver cirrhosis and portal hypertension. A 53-year-old woman, who was followed up for aortic dissection and hepatitis C virus （HCV）-related liver cirrhosis, was referred with sudden left chest and shoulder pain. An abdominal ultrasound showed intraabdominal bleeding, and computed tomography indicated rupture of a splenic tumor. Emergent splenectomy was carried out. The postoperative course was uneventful, and the patient was discharged on the 13th postoperative day. Pathology revealed the tumor to be a ruptured splenic hamartoma. The non-tumorous splenic parenchyma revealed congestive changes. We consider that the presence of liver cirrhosis and portal hypertension are risk factors for spontaneous rupture of the splenic hamartoma.

Effects of asymmetric dimethylarginine on renal arteries in portal hypertension and cirrhosis

AIM To evaluate the effects of asymmetric dimethylarginine(ADMA) in renal arteries from portal hypertensive and cirrhotic rats.METHODS Rat renal arteries from Sham(n = 15), pre-hepatic portal hypertension(PPVL; n = 15) and bile duct ligation and excision-induced cirrhosis(BDL; n = 15) were precontracted with norepinephrine, and additional contractions were induced with ADMA(10-6-10-3 mol/L), an endogenous inhibitor of nitric oxide(NO) synthase. Concentration-response curves to acetylcholine(1 × 10-9^(-3) × 10^(-6) mol/L) were determined in precontractedrenal artery segments with norepinephrine in the absence and in the presence of ADMA. Kidneys were collected to determine the protein expression and activity of dimethylarginine dimethylaminohydrolase(DDAH), an enzyme that catabolizes ADMA. RESULTS In renal arteries precontracted with norepinephrine, ADMA caused endothelium-dependent contractions. The pD 2 values to ADMA were similar in the Sham and PPVL groups(4.20 ± 0.08 and 4.11 ± 0.09, P > 0.05, respectively), but were lower than those of the BDL group(4.79 ± 0.16, P < 0.05). Acetylcholine-induced endothelium-dependent relaxation that did not differ, in terms of p D2 and maximal relaxation, among the 3 groups studied. Treatment with ADMA(3 × 10^(-4) mol/L) inhibited acetylcholine-induced relaxation in the 3 groups, but the inhibition was higher(P < 0.05) in the BDL group compared with that for the Sham and PPVL groups. The m RNA and protein expression of DDAH-1 were similar in kidneys from the three groups. Conversely, DDAH-2 expression was increased(P < 0.05) in PPVL and further enhanced(P < 0.05) in the BDL group. However, renal DDAH activity was significantly decreased in the BDL group. CONCLUSION Cirrhosis increased the inhibitory effect of ADMA on basal- and induced-release of NO in renal arteries, and decreased DDAH activity in the kidney.

Role of Portal Hypertension in Prediction of Bacterial Infection in Decompensated Cirrhosis

Background: Bacterial infection in cirrhotic patients is a fatal complication. The high incidence of bacterial infections in those patients may be related to several alterations in the defensive mechanisms against infections and increased intestinal permeability with bacterial translocation. Aim: To evaluate the role of portal hypertension (PH) in predicting the occurrence of bacterial infections in decompensated cirrhosis. Patients and Methods: In this retrospective cohort study, 99 patients—56 males and 43 females, with decompensated liver cirrhosis were included. Diagnosis of liver cirrhosis was based on clinical, laboratory and ultrasonographic examinations. Patients were classified according to the presence of bacterial infection into patients with infection—Group 1, and those without infection—Group 2. Laboratory, abdominal US and upper endoscopic data for all patients were collected. Logistic regression analysis was done to detect the independent factors for prediction of bacterial infection. Results: The mean age of patients was 50.5 ± 14.2 years. Bacterial infection was found in 41 patients (41.4%) and no infection in 58 patients (58.6%). Infected patients showed statistically significant higher values in the level of bilirubin, PT and Child-Pugh score (P value = 0.000) and lower values in the level of albumin, total serum protein and PC than those without infection (P value = 0.006, 0.000 and 0.000 respectively). Portal vein diameter (PVD) and splenic diameter (SD) showed statistically significant higher values in infected patients than in those without infection (P value = 0.028 and 0.000 respectively), also infection was more significantly prevalent in patients with varices than those without varices (P value = 0.000). The independent predictors for bacterial infection were: the age, total serum bilirubin, serum albumin, PT, PC, child score, PVD, SD and the presence of varices. Conclusion: Presence of varices (as a complication of PH) is an independent risk factor for the development of bacterial infection in decompensated cirrhotic patients and reduction of PH by any way could decrease this fatal complication.