Dataset Information

Erectile dysfunction in cirrhosis is impacted by liver dysfunction, portal hypertension, diabetes and arterial hypertension.

ABSTRACT:

Background

Although several risk factors for erectile dysfunction may be present in patients with cirrhosis, data on the actual prevalence and cause of erectile dysfunction is limited. The International Index of Erectile Function-5 (IIEF-5) is a well-validated survey to determine the presence and severity of erectile dysfunction in men. We assessed (i) the prevalence and severity of erectile dysfunction, and (ii) risk factors for erectile dysfunction in patients with cirrhosis.

Methods

In this prospective study, erectile dysfunction was defined as: absent (>21 IIEF-5-points), mild (12-21) and severe (5-11). Patients with overt hepatic encephalopathy, active alcohol abuse, extrahepatic malignancy, previous urologic surgery, previous liver transplantation and severe cardiac conditions were excluded.

Results

Among n = 151 screened patients, n = 41 met exclusion criteria and n = 30 were sexually inactive. Thus, a final number of n = 80 male patients with cirrhosis were included. Patient characteristics: age: 53 ± 9 years; model for end-stage liver disease score (MELD): 12.7 ± 3.9; Child-Pugh score (CPS) A: 30 (37.5%), B: 35 (43.8%), C: 15 (18.7%); alcohol: 38 (47.5%), viral: 25 (31.3%), alcohol/viral: 7 (8.8%) and others: 10 (12.5%). The presence of erectile dysfunction was found in 51 (63.8%) patients with 44 (55%) and 7 (8.8%) suffering from mild-to-moderate and moderate-to-severe erectile dysfunction. Mean MELD and hepatic venous pressure gradient (HVPG) were significantly higher in patients with erectile dysfunction (P = .021; P = .028). Child-Pugh score C, MELD, creatinine, age, arterial hypertension, diabetes, low libido, low testosterone and high HVPG were associated with the presence of erectile dysfunction. Interestingly, beta-blocker therapy was not associated with an increased risk. In multivariate models, arterial hypertension (OR: 6.36 [1.16-34.85]; P = .033), diabetes (OR: 7.40 [1.31-41.75]; P = .023), MELD (OR: 1.19 [1.03-1.36]; P = .015) and increasing HVPG (n = 48; OR: 1.11 [1.002-1.23]; P = .045) were independent risk factors for the presence of erectile dysfunction.

Conclusion

About two-thirds of male patients with cirrhosis show erectile dysfunction. Severity of liver dysfunction, portal hypertension, arterial hypertension and diabetes were identified as risk factors for erectile dysfunction.

SUBMITTER: Paternostro R

PROVIDER: S-EPMC6766949 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:BackgroundHydrogen sulfide (H(2)S) displays vasodilative, anti-oxidative, anti-inflammatory and cytoprotective activities. Impaired production of H(2)S contributes to the increased intrahepatic resistance in cirrhotic livers. The study aimed to investigate the roles of H(2)S in carbon tetrachloride (CCl(4))-induced hepatotoxicity, cirrhosis and portal hypertension.Methods and findingsSodium hydrosulfide (NaHS), a donor of H(2)S, and DL-propargylglycine (PAG), an irreversible inhibitor of cystathionine ?-lyase (CSE), were applied to the rats to investigate the effects of H(2)S on CCl(4)-induced acute hepatotoxicity, cirrhosis and portal hypertension by measuring serum levels of H(2)S, hepatic H(2)S producing activity and CSE expression, liver function, activity of cytochrome P450 (CYP) 2E1, oxidative and inflammatory parameters, liver fibrosis and portal pressure. CCl(4) significantly reduced serum levels of H(2)S, hepatic H(2)S production and CSE expression. NaHS attenuated CCl(4)-induced acute hepatotoxicity by supplementing exogenous H(2)S, which displayed anti-oxidative activities and inhibited the CYP2E1 activity. NaHS protected liver function, attenuated liver fibrosis, inhibited inflammation, and reduced the portal pressure, evidenced by the alterations of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), albumin, tumor necrosis factor (TNF)-?, interleukin (IL)-1?, IL-6 and soluble intercellular adhesion molecule (ICAM)-1, liver histology, hepatic hydroxyproline content and ?-smooth muscle actin (SMA) expression. PAG showed opposing effects to NaHS on most of the above parameters.ConclusionsExogenous H(2)S attenuates CCl(4)-induced hepatotoxicity, liver cirrhosis and portal hypertension by its multiple functions including anti-oxidation, anti-inflammation, cytoprotection and anti-fibrosis, indicating that targeting H(2)S may present a promising approach, particularly for its prophylactic effects, against liver cirrhosis and portal hypertension.

Project description:BackgroundRecent data suggest that noninvasive liver fibrosis indexes could be useful for predicting esophageal varices (EV) in cirrhotic patients. However, thus far, the diagnostic efficacy of these indexes in predicting portal hypertension (PH) in cirrhotic patients has been poorly evaluated.AimsTo evaluate the diagnostic efficacy of noninvasive liver fibrosis indexes in the diagnosis of PH.MethodsA total of 238 cirrhotic patients underwent hepatic venous pressure gradient (HVPG) evaluation and relevant serum tests to analyze the variables associated with PH grade. Then, the diagnostic performances of seven fibrosis indexes, the aspartate aminotransferase (AST)-to-alanine aminotransferase (ALT) ratio (AAR), AST-to-platelet (PLT) ratio index (APRI), fibrosis index (FI), FIB-4, Forns index, King's score and the Lok index, were evaluated to determine their efficacy in predicting clinically significant PH (CSPH) and severe PH (SPH). In addition, the performances of these fibrosis indexes in different subgroups were investigated.ResultsThe results of a multivariate analysis of serum markers showed that AST values, platelet (PLT) count and albumin (ALB) were associated with PH grade. Among the seven-fibrosis indexes, King's score, APRI and the Lok index showed modest diagnostic accuracy in predicting CSPH and SPH, as indicated by AUC of 0.755 and 0.742, 0.740 and 0.742, and 0.722 and 0.717, respectively. In addition, combination of King's score (cutoff 23.47) and Lok index (cutoff 1.30) predicted presence of CSPH, with the highest PPV (95.38%) and +LR (5.49). A subgroup analysis indicated that the noninvasive screening model may be more applicable to patients with cirrhosis of viral etiology.ConclusionsSerum liver fibrosis indexes exhibited modest diagnostic accuracy for PH in cirrhotic patients. These indexes may not be able to replace HVPG measurements for the diagnosis of PH but may be used as a first-line screening method for CSPH in liver cirrhosis patients.

Project description:Recent studies have indicated that the Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) pathway is closely involved in liver fibrosis and other fibrotic diseases. However, whether targeting the AMPK pathway can rescue liver fibrosis and its complications, such as portal hypertension, is unknown. This study aimed to explore the therapeutic value of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside), an agonist of the AMPK pathway, on liver fibrosis and portal hypertension in bile duct ligation (BDL) rats. In vitro experiments showed that the gene expression levels of TGF-b, a-SMA, and collagen 1 in primary rat hepatic stellate cells (HSCs) were significantly decreased after AICAR treatment. The p-eNOS expression and nitric oxide (NO) production were increased by AICAR administration in sinusoidal endothelial cells (SECs). For in vivo animal studies, AICAR acutely decreased portal pressure in the BDL and CCL4 fibrotic rats, but not in the partial portal vein ligation (PVL) rats, without changes in systemic hemodynamics. It was also observed by using intravital fluorescence microscopy that AICAR led to sinusoidal vasodilation in situ experiment. We propose that the relevant mechanisms may be related to the activation of the AMPK/NO pathway in SECs and that this activation promoted NO production in the liver, thereby promoting hepatic sinusoid microcirculation and decreased intrahepatic resistance. The results were verified using the NO inhibitor L-NAME. Chronic AICAR treatment also showed profound beneficial effects on the BDL model rats. The hemodynamic condition was greatly improved, but the positive effect could be partially blocked by L-NAME. Moreover, AICAR also decreased hepatic fibrogenesis in the BDL rats. KEY MESSAGES: Acute and chronic use of AICAR could alleviate portal pressure without changing systemic hemodynamics. AICAR induced sinusoidal vasodilation by improving NO bioavailability and ameliorating endothelial dysfunction in vivo and in vitro. AICAR could alleviate liver cirrhosis in the BDL model rats.

Project description:Background:Portal hypertensive polyps in patients with portal hypertension are described. Aims:The most significant and serious complication in liver cirrhosis proves to be portal hypertension. Polypoid lesions, which can be seen in the stomach as endoscopic finding in patients with portal hypertension, have not quite been defined in the literature. The aim of this study, therefore, was to define polypoid lesion formation due to portal hypertension in the upper gastrointestinal system in patients with portal hypertension. Study Design. Cross-sectional study. Methods:The study covered a group of patients with liver cirrhosis and a healthy control group that did not have portal hypertension. All individuals covered by the study received upper GI endoscopy, while the endoscopic features and pathological characteristics of the identified polypoid lesions were defined. Standard histological criteria were used in polyp diagnosis. Results:A total of 400 individuals were included in the study. Upper GI endoscopy was performed for 200 patients with liver cirrhosis and another 200 healthy individuals with no portal hypertension in the control group. When the cases were gastroscopically assessed with regard to polypoid lesion presence, it was seen that a total of 87 (21.8%) individuals had polyps. While 67 (33.5%) cirrhotic patients were identified to have polyps, 20 (10%) individuals in the healthy control group had polyps. When the results of those with liver cirrhosis who received esophageal variceal endoscopic band ligation (EVL) and who did not were compared, it was observed that a higher number of individuals in the group with EVL had polypoid lesions. When the patient and control groups were compared as to Helicobacter pylori presence, the results showed that it was slightly higher in the dyspepsia group but the difference was not statistically significant (p > 0.05). Conclusion:Portal hypertension-associated polypoid lesions are common in advanced liver cirrhosis cases. The pathological analyses of these polyps pointed out that they were all benign and no malignant cases were detected. It was argued that these polypoid lesions, referred to as portal hypertensive polyps, were associated with elevated angiogenesis in the gastric mucosa.