Is there ileopathy in portal hypertension?

BACKGROUND AND AIMS: Portal hypertensive gastropathy and colopathy are well described endoscopic abnormalities in patients with portal hypertension. Endoscopic abnormalities in the ileum in patients with portal hypertension have not been well described. The aim of the present study was to evaluate endoscopic abnormalities in the ileum of patients with portal hypertension. METHODS: Patients with portal hypertension of various etiologies were included in the study. Upper gastrointestinal endoscopy was performed to record esophageal varices, gastric varices and portal hypertensive gastropathy. Colonoscopy with retrograde intubation of the ileum was performed and the presence of colorectal varices, colopathy and mucosal findings in the ileum were noted. RESULTS: Forty-one patients (age 16-80 years, 33 men) were studied. Esophageal varices were present in all. Portal hypertensive gastropathy was present in 27/41 (66%) patients. Rectal varices were noted in 22/41 (54%) patients and 17/41 (42%) patients had features suggestive of colopathy. Ileum could be intubated in 38 patients (93%). Endoscopic abnormalities in the ileum were noted in 13/38 (34%) patients. Ileopathy as evident by endoscopic mucosal abnormalities was observed in 10/38 (26%) patients. Ileal varices were present in 8/38 (21%) patients. Three of these had ileal varices alone while the remaining five patients also had associated ileopathy The presence of ileopathy was significantly associated with the presence of portal hypertensive gastropathy and colopathy but not with esophageal, gastric or rectal varices. CONCLUSIONS: Ileopathy occurs in one-third of patients with portal hypertension and is significantly associated with the presence of portal hypertensive gastropathy and colopathy.     

Endoscopic Evaluation of Rectal Mucosal Reddening in Patients with Liver Cirrhosis

Background: Colonic mucosal lesions observed in patients with portal hypertension have been reported as portal hypertensive colopathy. We studied the rectal mucosa in patients with liver cirrhosis to evaluate the prevalence of mucosal reddening which looks like gastric red spots in the portal hypertensive gastropathy and to determine whether there is a correlation between this lesion and portal hypertension or the severity of liver disease. Methods: Seventy‐two patients with liver cirrhosis and 50 control subjects were examined. Colonoscopy was performed to evaluate the presence of mucosal reddening in the rectum. We investigated the relations between rectal mucosal reddening and esophageal varices, portal hypertensive gastropathy and the severity of liver cirrhosis. Results: Rectal mucosal reddening was observed in eight of 72 patients with liver cirrhosis but in none of the 50 control subjects; its prevalence in cirrhosis patients was significantly higher than that in the control subjects (P < 0.05). Cirrhosis patients with esophageal varices were more likely to have rectal mucosal reddening than cirrhosis patients without esophageal varices (P < 0.05). In addition, the occurrence of rectal mucosal reddening correlated with the severity of cirrhosis, based on Child–Pugh's classification (P < 0.05). Conclusion: We have shown that rectal mucosal reddening develops in patients with liver cirrhosis and is associated with the existence of esophageal varices and the severity of liver cirrhosis. These results suggest the possibility that portal hypertension and impaired liver function may play an important role in the pathogenesis of rectal mucosal reddening in patients with cirrhosis.     

Mucosal abnormalities of the colon in patients with portal hypertension: an endoscopic study

BACKGROUND: Controversy still exists regarding colonic mucosal abnormalities in patients with portal hypertension (portal colopathy). The aims of this study were to better define portal colopathy and to identify risk factors for these colonic mucosal abnormalities. METHODS: We reviewed the medical records of 437 patients with cirrhosis and portal hypertension and 224 with irritable bowel syndrome (control patients) who underwent colonoscopy over a 6-year period. RESULTS: Individuals with portal hypertension were significantly more likely than control patients to have colitis-like abnormalities (38% vs. 3%, p < 0.001) and vascular lesions (13% vs. 3%, p < 0.001). In the multivariate model, portal hypertensive gastropathy (odds ratio 5.64: 95% CI [3.39, 9.41]; p < 0.001), 2+ or larger esophageal varices (odds ratio 4.76: 95% CI [2. 78, 8.15]; p < 0.001), and Child-Pugh class C cirrhosis (odds ratio 2.64: 95% CI [1.40, 4.97]; p = 0.003) were independently associated with an increased risk of having portal colopathy, whereas the use of beta-blockers independently decreased the risk of having these findings (odds ratio 0.23: 95% CI [0.13, 0.40]; p < 0.001). Mucosal biopsies of the colon in patients with colitis-like abnormalities revealed a mild, nonspecific inflammatory infiltrate with edema and vascular ectasias in the majority of cases. CONCLUSIONS: Mucosal abnormalities in portal colopathy include edema, erythema, granularity, friability, and vascular lesions, findings that may be confused with colitis. A standardized grading system to classify the endoscopic appearance and severity of portal colopathy should be adopted.     

Portal hypertensive colopathy in patients with liver cirrhosis

AIM: In patients with liver cirrhosis and portal hypertension, portal hypertensive colopathy is thought to be an important cause of lower gastrointestinal hemorrhage. In this study, we evaluated the prevalence of colonic mucosal changes in patients with liver cirrhosis and its clinical significance. METHODS: We evaluated the colonoscopic findings and liver function of 47 patients with liver cirrhosis over a 6-year period. The main cause of liver cirrhosis was post-viral hepatitis (68%) related to hepatitis B (6%) or C (62%) infection. All patients underwent upper gastrointestinal endoscopy to examine the presence of esophageal varices, cardiac varices, and congestive gastropathy, as well as a full colonoscopy to observe changes in colonic mucosa. Portal hypertensive colopathy was defined endoscopically in patients with vascular ectasia, redness, and blue vein. Vascular ectasia was classified into two types: type 1, solitary vascular ectasia; and type 2, diffuse vascular ectasia. RESULTS: Overall portal hypertensive colopathy was present in 31 patients (66%), including solitary vascular ectasia in 17 patients (36%), diffuse vascular ectasia in 20 patients (42%), redness in 10 patients (21%) and blue vein in 6 patients (12%). As the Child-Pugh class increased in severity, the prevalence of portal hypertensive colopathy rose. Child-Pugh class B and C were significantly associated with portal hypertensive colopathy. Portal hypertensive gastropathy, esophageal varices, ascites and hepatocellular carcinoma were not related to occurrence of portal hypertensive colopathy. Platelet count was significantly associated with portal hypertensive colopathy, but prothrombin time, serum albumin level, total bilirubin level and serum ALT level were not related to occurrence of portal hypertensive colopathy. CONCLUSION: As the Child-Pugh class worsens and platelet count decreases, the prevalence of portal hypertensive colopathy increases in patients with liver cirrhosis. A colonoscopic examination in patients with liver cirrhosis is indicated, especially those with worsening Child-Pugh class and/or decreasing platelet count, to prevent complications such as lower gastrointestinal bleeding.     

Portal hypertensive colopathy is associated with portal hypertension severity in cirrhotic patients

AIM： To assess the prevalence of portal hypertension （PH） related colorectal lesions in liver transplant candidates, and to evaluate its association with the severity of PH. METHODS： Between October 2004 and December 2005, colonoscopy was performed in 92 cirrhotic liver transplant candidates. We described the lesions resulting from colorectal PH and their association with the grade of PH in 77 patients who underwent measurement of hepatic venous pressure gradient （HVPG）. RESULTS： Mean age was 55 years and 80.7% of patients were men. The main etiology of cirrhosis wasalcoholism （45.5%）. Portal hypertensive colopathy （PHC） was found in 23.9%, colonic varices in 7.6% and polyps in 38% of patients （adenomatous type 65.2%）. One asymptomatic patient had a well-differentiated adenocarcinoma. The manifestations of colorectal PH were not associated with the etiology of liver disease or with the Child-Pugh grade. Ninety percent of patients with colopathy presented with gastroesophageal varices （GEV）, and 27.5% of patients with GEV presented with colopathy （P = 0.12）. A relationship between higher values of HVPG and presence of colopathy was observed （19.9：1：6.2 mmHg vs 16.8 ± 5.4 mmHg, P = 0.045）, but not with the grade of colopathy （P = 0.13）. Preneoplastic polyps and neoplasm （P = 0.02） and spontaneous bacterial peritonitis （P = 0.006） were more prevalent in patients with colopathy. We did not observe any association between previous β-blocker therapy and the presence of colorectal portal hypertensive vasculopathy. CONCLUSION： PHC is common in cirrhotic liver transplant candidates and is associated with higher portal pressure.     

The prevalence and spectrum of colonic lesions in patients with cirrhotic and noncirrhotic portal hypertension

Portal hypertension diffusely affects the gastrointestinal tract. The frequency and profile of distinct colonic mucosal lesions (portal colopathy) and rectal varices (RV; veins >4 cm above the anal verge) is not well studied. Fifty consecutive patients with portal hypertension (25 with cirrhosis, 10 with noncirrhotic portal fibrosis [NCpf], and 15 with extrahepatic portal vein obstruction [EHPVO]) were assessed clinically and by upper and lower gastrointestinal (GI) endoscopy. Colorectal lesions were seen in 35 (70%) patients, significantly more often in bleeders than in nonbleeders. Rectal varices were detected in 22 (44%) patients; larger and more often seen in EHPVO (80%) than in cirrhosis (28%) and NCPF (30%) (P < .01) patients. Portal colopathy was seen in 26 (52%) patients, with nearly similar frequency in cirrhotics, NCPF, and EHPVO patients. Previous sclerotherapy or presence of gastric varices had little influence on the development of these lesions. An association (P < .01) was, however, seen between the presence of colopathy and portal gastropathy. Overt bleeding was seen in 8% and 4% of patients with RV and colopathy, respectively. In conclusion, our results demonstrate that colorectal lesions are present in about two thirds of patients with portal hypertension. Patients with portal hypertension and lower GI bleeding should be colonoscoped. Patients with extrahepatic portal vein obstruction may in turn benefit from baseline sigmoidoscopic examination to define the presence and size of rectal varices.     

Observation of thoracic duct morphology in portal hypertension by endoscopic ultrasound

Background:Thoracic duct dilation has been demonstrated in portal hypertension and hepatic cirrhosis by lymphangiography and laparotomy and at autopsy. It is thought to be secondary to increased hepatic lymph flow and has been described in the absence of ascites or esophageal varices. The aim of the present study was to observe thoracic duct morphology by endoscopic ultrasound in various subsets of patients with portal hypertension and hepatic cirrhosis and also to validate existing radiologic/surgical data. Methods:The thoracic duct of 33 patients with cirrhosis and portal hypertension was studied by endoscopic ultrasound. Patients were divided into four groups: 1, patients with ascites and esophageal varices; 2, esophageal varices without ascites; 3, without esophageal varices or ascites; 4, extrahepatic portal hypertension due to pancreatic malignancy. The thoracic duct diameter was also measured in 14 control subjects (group 5). Results:When the thoracic duct diameter for the five groups was compared with analysis of variance, significance was p < 0.0001; by pairwise comparison, group 1 differed from the other four groups (p < 0.05). Thoracic duct dilation (5.61 mm) was seen in group 1 patients, whereas no dilation was present in groups 2 through 4. Additionally, thoracic duct diameter in 33 portal hypertensive and/or cirrhotic patients was significantly different from that in the 14 control subjects (p = 0.003). Conclusion:The thoracic duct can be reliably identified by EUS in patients with hepatic cirrhosis and portal hypertension. Dilation of the duct is seen only in patients with hepatic cirrhosis, ascites, and esophageal varices. No thoracic duct dilation is present in extrahepatic portal hypertension. Contrary to existing radiologic/surgical data, thoracic duct dilation is not seen in all patients with hepatic cirrhosis and portal hypertension signifying advanced disease. A dilated thoracic duct by endoscopic ultrasound should be considered yet another sign of portal hypertension. (Gastrointest Endosc 1998;48:588-92.)     

Frequency and factors influencing portal hypertensive gastropathy and duodenopathy in cirrhotic portal hypertension

Portal hypertensive gastropathy and duodenopathy are distinct clinical and endoscopic entities. Data on factors influencing the development of these lesions are still emerging. Data on portal hypertensive duodenopathy are scarce. We prospectively studied 230 patients with liver cirrhosis and oesophageal varices attending the liver clinic of the Sanjay Gandhi Post Graduate Institute of Medical Sciences. One hundred and forty-two patients had no history of upper gastrointestinal bleeding, while the remainder had bled in the past. Endoscopic appearances were recorded before starting patients on a sclerotherapy programme. Forty-four patients were re-evaluated after variceal eradication. The frequency of portal hypertensive gastropathy (PHG) and duodenopathy (PHD) was 61 and 14%, respectively. Mild PHG was present in 85% and was severe in the rest. Portal hypertensive duodenopathy was mild in 50%, while in the other half it was severe. There was no relationship of PHG and PHD to: (i) a history of upper gastrointestinal bleed; (ii) size of oesophageal varices; (iii) aetiology of liver cirrhosis; or (iv) liver function status as assessed by Child Pugh's scores (P=NS for all). The prevalence of PHG was higher in those patients with oesophagogastric varices (74 of 107; 69%) compared with patients with oesophageal varices alone (68 of 123; 55%; P<0.05). However, no such increase in frequency of PHD was noted in patients with oesophagogastric varices. Sclerotherapy increased the frequency of PHG. Twenty-four patients had PHG before starting sclerotherapy, while it was noted in 33 patients 1–3 months after variceal eradication (P< 0.05). In contrast, there was no increase in the prevalence of portal hypertensive duodenopathy after sclerotherapy (P=NS). There was no correlation between endoscopic and histological changes of PHG and PHD. In conclusion, PHG is quite frequent in patients with cirrhosis and its frequency increases with the presence of oesophagogastric varices and after sclerotherapy. However, the frequency of PHD is low and is not affected by the factors studied.     

Severe acute bleeding from portal colopathy controlled by somatostatin: a case report.

Portal hypertensive colopathy (PHC) is a recently described entity in patients with portal hypertension which can cause even life-threatening lower gastrointestinal bleeding. In contrast to variceal bleed, there is no standardized treatment for the control of bleeding from these lesions. We report a case of alcoholic cirrhosis with portal hypertension, in whom bleeding from colonic angiodysplasia-like lesions was effectively controlled by somatostatin infusion.     

Effect of Portal Hypertension in the Small Bowel: An Endoscopic Approach

BACKGROUND AND AIM: The effects of portal hypertension in the small bowel are largely unknown. The aim of the study was to prospectively assess portal hypertension manifestations in the small bowel. METHODS: We compared, by performing enteroscopy with capsule endoscopy, the endoscopic findings of 36 patients with portal hypertension, 25 cirrhotic and 11 non-cirrhotic, with 30 controls. RESULTS: Varices, defined as distended, tortuous, or saccular veins, and areas of mucosa with a reticulate pattern were significantly more frequent in patients with PTH. These two findings were detected in 26 of the 66 patients (39%), 25 from the group with PTH (69%) and one from the control group (3%) (P < 0.0001). Among the 25 patients with PTH exhibiting these patterns, 17 were cirrhotic and 8 were non-cirrhotic (P = 0.551). The presence of these endoscopic changes was not related to age, gender, presence of cirrhosis, esophageal or gastric varices, portal hypertensive gastropathy, portal hypertensive colopathy, prior esophageal endoscopic treatment, current administration of beta-blockers, or Child-Pugh Class C. More patients with these endoscopic patterns had a previous history of acute digestive bleeding (72% vs. 36%) (P = 0.05). Active bleeding was found in two patients (5.5%). CONCLUSIONS: The presence of varices or areas of mucosa with a reticulate pattern are manifestations of portal hypertension in the small bowel, found in both cirrhotic and non-cirrhotic patients. The clinical implications of these findings, as regards digestive bleeding, are uncertain, although we documented acute bleeding from the small bowel in two patients (5.5%).     

Association of liver cirrhosis related IgA nephropathy with portal hypertension

A high incidence of IgA nephropathy has been reported in patients with liver cirrhosis, though, clinically evident nephrotic syndrome is very uncommon. Impaired hepatic clearance of circulating IgA immune complexes and subsequent deposition in renal glomeruli has been considered principally in the pathogenesis of liver cirrhosis associated IgA nephropathy. Here we report on a patient with cryptogenic liver cirrhosis and splenic vein thrombosis, who presented with nephrotic syndrome. Renal biopsy showed findings consistent with IgA nephropathy. Lower endoscopy showed features of portal hypertensive colopathy. Following initiation of propranolol and anticoagulant treatment to reduce portal pressure, a gradual decrease of proteinuria and hematuria to normal range was noted. The potential pathogenetic role of portal hypertension in the development of IgA nephropathy in cirrhotic patients is discussed.     

Alterations in colonic mucosal lesions in patients with portal hypertension

Background and study aimsPortal hypertensive colopathy (PHC) is a clinical entity in liver cirrhosis. The frequency and profile of colonic mucosal lesions of this entity are not well studied. The aim of this study is to evaluate the prevalence of colonic mucosal changes in patients with liver cirrhosis and their clinical significance.Patients and methodsForty patients with post-viral liver cirrhosis and portal hypertension (PHT) underwent upper gastrointestinal endoscopy as well as a full length colonoscopy to detect changes in colonic mucosa. PHC was diagnosed endoscopically by the presence of vascular ectasia, diffuse hyperaemic mucosa and rectal varices. Biopsies were obtained from the recto-sigmoid area as well as from any abnormal mucosal lesions apart from angiodysplastic areas.ResultsDiffuse hyperaemia, angiodysplasia and rectal varices were found in 40%, 32.5% and 17.5% of patients while haemorrhoids in 42.5%, respectively. The prevalence of PHC increased with worsening Child-Pugh class, the mere presence of oesophageal varices while platelet count was significantly associated with angiodysplastic lesions only. None of other upper endoscopic features of PHT was significantly related to PHC. Moreover, history of lower gastrointestinal (GI) bleeding was significantly associated with the presence of rectal varices and haemorrhoids. Colonoscopic features of PHC were significantly associated with the histopathological diagnosis revealing 79% sensitivity and 66.6% specificity.ConclusionPHC is a frequent finding in patients with PHT. Colonoscopic features suggestive of PHC were in concordance with the histopathological evidence. Although the presence of haemorrhoids is not a feature of colopathy, yet it should be considered together with anorectal varices as a cause of lower GI bleeding.     

Anorectal varices--their frequency in cirrhotic and non-cirrhotic portal hypertension.

Anorectal varices in portal hypertension have been little studied: Seventy eight per cent of 72 patients with portal hypertension had anorectal varices shown at flexible sigmoidoscopy. Significantly more patients with noncirrhotic portal hypertension had these varices than patients with cirrhosis (89% v 56%, p less than 0.01).     

Mucosal abnormalities of the small bowel in patients with cirrhosis and portal hypertension: a capsule endoscopy study

BACKGROUND: The frequency of small-bowel mucosal changes in patients with portal hypertension is not known. The objective of the study is to better define the mucosal abnormalities of portal hypertensive enteropathy (PHE) and to determine whether these findings are associated with the severity of liver disease, esophageal varices, portal gastropathy, portal colonopathy, or other clinical characteristics. METHODS: We compared the medical records of 37 patients with cirrhosis and portal hypertension with 34 control patients who underwent capsule endoscopy over a 3-year period. RESULTS: Mucosal changes were found to be significantly more common in the cirrhotic patients than in the control patients (67.5% vs. 0, p < 0.001). The lesions included telangiectasias or angiodysplastic-like lesions in 9 (24.3%) patients, red spots in 23 (62.2%), and varices in 3 (8.1%). Active bleeding was seen during endoscopic examinations in 4 (10.8%) patients. A comparison of patients with and those without PHE showed that grade 2+ or larger esophageal varices, portal gastropathy, portal colonopathy, and Child-Pugh class C cirrhosis were all significantly associated with PHE. There were no differences between these two groups of patients with regard to the etiology of cirrhosis, gender, or history of esophageal variceal bleeding. CONCLUSIONS: Mucosal abnormalities in portal jejunopathy include edema, erythema, and vascular lesions findings. A standardized grading system to classify the endoscopic appearance and the severity of portal enteropathy is proposed. The clinical import of these changes remains to be explained.     

The natural history of portal hypertensive gastropathy in patients with liver cirrhosis and mild portal hypertension

BACKGROUND: Portal hypertensive gastropathy is a potential cause of bleeding in patients with liver cirrhosis. Studies on its natural history have often included patients submitted to endoscopic or pharmacological treatment for portal hypertension. PATIENTS AND METHODS: A total of 222 cirrhotic patients with mild degree of portal hypertension (i.e., with no or small varices at entry, without previous gastrointestinal bleeding and medical, endoscopic, or angiographic treatment) were followed up with upper endoscopy every 12 months for 47 +/- 28 months. RESULTS: Upon enrollment 48 patients presented portal hypertensive gastropathy (43 mild and 5 severe) and the presence of esophageal varices was the only independent predictor of the presence of this gastric lesion at multivariate analysis. The incidence of portal hypertensive gastropathy was 3.0% (1.1-4.9%) at 1 yr and 24% (18.1-29.9%) at 3 yr, while the progression was 3% (1-6.9%) at 1 yr and 14% (4.2-23.8%) at 3 yr. The presence of esophageal varices and the Child-Pugh class B or C at enrollment were predictive of the incidence of portal hypertensive gastropathy, while only Child-Pugh class B or C was correlated with the progression from mild to severe, at multivariate analysis. During follow-up 16 patients bled from portal hypertensive gastropathy (9 acutely and 7 chronically) and one patient died of exsanguination from this lesion. CONCLUSIONS: The natural history of portal hypertensive gastropathy is significantly influenced by the severity of liver disease and severity of portal hypertension. Acute bleeding from portal hypertensive gastropathy is infrequent but may be severe.     

Prevalence of upper and lower gastrointestinal tract findings in liver transplant candidates undergoing screening endoscopic evaluation

OBJECTIVE: The incidence of esophageal and gastric varices and portal hypertensive gastropathy (PHG) has been well studied in cirrhotic patients. Because little is known of the prevalence of other upper and lower gastrointestinal tract pathology in pre-liver transplant candidates, we retrospectively studied the prevalence of and factors associated with these findings. METHODS: One hundred and twenty pre-liver transplant candidates underwent esophagogastroduodenoscopy to evaluate for varices, and 71 of them also underwent flexible sigmoidoscopy to screen for colorectal carcinoma. The association of upper and lower GI tract pathology with Child-Pugh Class, etiology of cirrhosis, and signs of portal hypertension, including presence and size of esophageal varices, presence of gastric varices, PHG, ascites, and splenomegaly, was analyzed using univariate and multivariate analysis. RESULTS: Etiology of cirrhosis among 87 men and 33 women (mean age, 52 yr) included 25% hepatitis C, 27% hepatitis C/alcohol, 15% alcohol, 10% primary sclerosing cholangitis/primary biliary cirrhosis, 9% cryptogenic, 8% metabolic, and 6% hepatitis B. Prevalence of Child-Pugh Classes A, B, and C were 34%, 49%, and 17%, respectively; 73% of patients had esophageal varices (23% were large), 62% PHG (23% were severe), and 16% gastric varices. Excluding varices and PHG, endoscopic findings in the upper GI tract (n = 120) included: 13% esophagitis/ulcers, 7.5% gastritis, 8% duodenitis, 2% Barrett's esophagus, 3% duodenal ulcers, and 2% gastric ulcers. Findings in the lower gastrointestinal tract (n = 71) included 21% adenomatous polyps, 21% internal hemorrhoids, 15% diverticulosis, 7% rectal varices, 3% colopathy, and 3% vascular ectasias. Univariate analysis revealed that there was a significant association between rectal varices and severe PHG (p < 0.05). This association was not maintained when multivariate analysis was performed. CONCLUSIONS: Among all the findings, only rectal varices and colopathy were of higher prevalence in the pre-liver transplant population than that reported for the general population. No significant associations were found between these gastrointestinal tract lesions and patient characteristics.     

Digestive endoscopy and portal hypertension. North Italian Endoscopic Club

Improved knowledge of pathophysiology of portal hypertension and technological progress have contributed to development of new endoscopic techniques and pharmacological approaches to treatment of this condition. To put the role of endoscopy in the right perspective, it is important to consider that liver transplantation has greatly modified prognosis of cirrhosis. Because of the increase of indications for transplantation, these complications are no longer regarded as the last, but rather as an intermediate stage before a possible transplantation. We have reviewed some pathophysiologic, diagnostic and therapeutic aspects on portal hypertension, especially the role of endoscopy in diagnosis, natural history and therapeutic options for complications of cirrhosis. In addition to sclerotherapy, new endoscopic methods have been developed, with a low complication rate and possibility of being applied for treatment of gastric varices, i.e. injection of tissue adhesives and rubber band ligation. Besides oesophageal varices, gastric varices and portal hypertensive gastropathy (and portal colopathy) are important findings in cirrhosis. Further information is needed on natural history and treatment of these conditions. Digestive haemorrhage is the most important consequence of portal hypertension, so treatment should be aimed at controlling acute bleeding, rebleeding and, more important, at preventing first haemorrhagic episode. Good results will probably be obtained using a combination of drugs, a combination of endoscopic methods or a combination of both. All will need evaluation in randomised, controlled trials. These considerations renew interest in strategies for diagnosis and treatment of portal hypertension and a multidisciplinary approach may be necessary, involving gastroenterologists, endoscopists, interventionist radiologists and surgeons, ideally in a departmental environment.     

Superior mesenteric artery impedance in chronic liver diseases: relationship with disease severity and portal circulation

Objective: The increase of splanchnic blood flow volume in liver cirrhosis is attributed to decreased arterial resistance. The aim of this study was to noninvasively investigate superior mesenteric artery impedance in patients with chronic liver diseases and to assess its relationship with portal hemodynamics and with clinical parameters.
Methods: Superior mesenteric artery (SMA) pulsatility (SMA-PI) and resistance (SMA-RI) indices and portal vein flow parameters (velocity, volume, and congestion index) were measured by duplex-Doppler ultrasound in 14 patients with chronic hepatitis, in 73 cirrhotics, in 30 liver transplant recipients, and in 31 control subjects.
Results: SMA-PI significantly differed among the five groups (   p < 0.0001  ), being lower in cirrhotics (2.55 ± 0.70) and transplanted patients (2.77 ± 0.69) than in chronic hepatitis (3.28 ± 0.57) and control subjects (3.42 ± 0.92). SMA-PI was lower in ascitic cirrhosis (2.40 ± 0.71) than in compensated cirrhosis (2.71 ± 0.70) (   p < 0.01  ) and in cirrhotics with large varices (2.30 ± 0.67) than in those without varices (2.75 ± 0.65) (   p < 0.05  ). Moreover SMA-PI correlated with numeric Child-Pugh score (  r =−0.28  ) and portal vein congestion index (  r =−0.36  ).
Conclusion: Hyperdynamic splanchnic circulation, noninvasively assessed by a decrease of mesenteric artery impedance, occurs in cirrhosis since the early stage of the disease and tends to worsen in relation to liver failure and the severity of portal hypertension. Furthermore, the persistent SMA-PI decrease in transplant recipients suggests a consistent contribution to this circulatory alteration from a patent portosystemic collateral circulation.     

Prevalence of portal hypertensive duodenopathy in cirrhosis: clinical and haemodynamic features

OBJECTIVES: To estimate the prevalence of portal hypertensive duodenopathy (PHD) in patients with cirrhosis and portal hypertension, and to evaluate its relationship with clinical and haemodynamic parameters. PATIENTS AND METHODS: Endoscopy reports and clinical history of 549 consecutive patients with cirrhosis and portal hypertension were evaluated retrospectively. A diagnosis of PHD was obtained in those patients with a congestive vascular pattern of the duodenum. RESULTS: PHD was found in 46 patients (8.4%). Previous endoscopic band ligation and coexistence of severe gastropathy were significantly more frequent in PHD group. Systemic and hepatic haemodynamic evaluations were performed in 20 patients with PHD and 160 without PHD: the mean hepatic venous pressure gradient was higher in those cases with PHD (22.5 (5.4) vs. 19.8 (5.5) mmHg, P=0.045). Hypertensive colopathy was found in seven out of the 10 patients with PHD and a colonoscopic evaluation. In five of six patients PHD disappeared after liver transplant. CONCLUSIONS: PHD is an uncommon finding of portal hypertension in cirrhotic patients. It is associated with previous endoscopic band ligation, to manifestations of portal hypertension in other sites of the gastrointestinal tract and to greater values of hepatic venous pressure gradient. The clinical relevance of this syndrome remains to be determined.     

Prevalence of autonomic dysfunction in cirrhotic and noncirrhotic portal hypertension

OBJECTIVE: Autonomic dysfunction is common in patients with cirrhosis of the liver, but more so in patients with decompensated state, and is associated with increased mortality. We evaluated the presence and extent of autonomic dysfunction in patients with extrahepatic portal venous obstruction (EHPVO) and noncirrhotic portal fibrosis (NCPF), diseases with relatively preserved liver functions. METHODS: Heart rate variability in response to standing, deep breathing, and Valsalva maneuver and blood pressure response to sustained handgrip and standing were studied in 18 patients with EHPVO (13 mol/L, 5 F, mean age 15.2 +/- 6 yr), 12 patients with NCPF (5 mol/L, 7 F, mean age 26.4 +/- 8 yr), 15 patients with cirrhosis (7 mol/L, 8 F, mean age 12.6 +/- 6 yr), and 17 healthy controls (11 mol/L, 6 F, mean age 18.6 +/- 3 yr). Time-domain parameters of heart rate variability on 24-h ambulatory monitoring were assessed in all the patients. RESULTS: Autonomic dysfunction was observed in 67% of EHPVO, 25% of NCPF, and 80% of cirrhotic subjects but none of the healthy controls (p < 0.05). Four of five time-domain heart rate variability indices showed significant abnormalities in patients with EHPVO (p < 0.05) and cirrhosis (p < 0.05), when compared with patients with NCPF and healthy controls. CONCLUSIONS: Autonomic dysfunction is frequently encountered in patients with EHPVO and cirrhosis, and the presence of autonomic dysfunction in patients with noncirrhotic portal hypertension suggests a primary role of portal hypertension per se in the dysfunction.