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Nodular regenerative hyperplasia: Evolving concepts on underdiagnosed cause of portal hypertension  [cached]
Marek Hartleb, Krzysztof Gutkowski, Piotr Milkiewicz
World Journal of Gastroenterology , 2011,
Abstract: Nodular regenerative hyperplasia (NRH) is a rare liver condition characterized by a widespread benign transformation of the hepatic parenchyma into small regenerative nodules. NRH may lead to the development of non-cirrhotic portal hypertension. There are no published systematic population studies on NRH and our current knowledge is limited to case reports and case series. NRH may develop via autoimmune, hematological, infectious, neoplastic, or drug-related causes. The disease is usually asymptomatic, slowly or non-progressive unless complications of portal hypertension develop. Accurate diagnosis is made by histopathology, which demonstrates diffuse micronodular transformation without fibrous septa. Lack of perinuclear collagen tissue distinguishes NRH from typical regenerative nodules in the cirrhotic liver. While the initial treatment is to address the underlying disease, ultimately the therapy is directed to the management of portal hypertension. The prognosis of NRH depends on both the severity of the underlying illness and the prevention of secondary complications of portal hypertension. In this review we detail the epidemiology, pathogenesis, diagnosis, management, and prognosis of NRH.
Portal hypertensive colopathy is associated with portal hypertension severity in cirrhotic patients  [cached]
Antonio Diaz-Sanchez, Oscar Nu?ez-Martinez, Cecilia Gonzalez-Asanza, Ana Matilla, Beatriz Merino, Diego Rincon, Inmaculada Beceiro, Maria Vega Catalina, Magdalena Salcedo, Rafael Ba?ares, Gerardo Clemente
World Journal of Gastroenterology , 2009,
Abstract: 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 was alcoholism (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 ± 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.
Gastrointestinal Bleeding in Cirrhotic Patients with Portal Hypertension  [PDF]
Erwin Biecker
ISRN Hepatology , 2013, DOI: 10.1155/2013/541836
Abstract: Gastrointestinal bleeding related to portal hypertension is a serious complication in patients with liver cirrhosis. Most patients bleed from esophageal or gastric varices, but bleeding from ectopic varices or portal hypertensive gastropathy is also possible. The management of acute bleeding has changed over the last years. Patients are managed with a combination of endoscopic and pharmacologic treatment. The endoscopic treatment of choice for esophageal variceal bleeding is variceal band ligation. Bleeding from gastric varices is treated by injection with cyanoacrylate. Treatment with vasoactive drugs as well as antibiotic treatment is started before or at the time point of endoscopy. The first-line treatment for primary prophylaxis of esophageal variceal bleeding is nonselective beta blockers. Pharmacologic therapy is recommended for most patients; band ligation is an alternative in patients with contraindications for or intolerability of beta blockers. Treatment options for secondary prophylaxis include variceal band ligation, beta blockers, a combination of nitrates and beta blockers, and combination of band ligation and pharmacologic treatment. A clear superiority of one treatment over the other has not been shown. Bleeding from portal hypertensive gastropathy or ectopic varices is less common. Treatment options include beta blocker therapy, injection therapy, and interventional radiology. 1. Introduction One of the main complications of liver cirrhosis is portal hypertension. Portal hypertension is defined as an hepatic venous pressure gradient (HVPG) above 5?mmHg. Clinical significant complications of portal hypertension like development of ascites and/or esophageal and gastric varices usually develop at an HVPG above 10?mmHg [1]. Bleeding from esophageal or gastric varices still carries a significant morbidity and mortality risk. The prevention of a first bleeding episode and the management of acute bleeding have markedly improved over the last years. This paper gives a concise overview of the current recommendations for the prevention and treatment of bleeding from esophageal, gastric, and ectopic varices as well as bleeding from portal hypertensive gastropathy. 2. Natural History of Esophageal Varices At the first diagnosis, about 30 to 40% of patients with compensated cirrhosis of the liver and 60% of patients with ascites present with esophageal varices. The annual incidence for the development of new varices in patients who were diagnosed with liver cirrhosis without varices is between 5 and 10% [2–5]. Once varices have developed, they have
Hepatocellular carcinoma in cirrhotic patients with portal hypertension: Is liver resection always contraindicated?  [cached]
Andrea Ruzzenente,Alessandro Valdegamberi,Tommaso Campagnaro,Simone Conci
World Journal of Gastroenterology , 2011, DOI: 10.3748/wjg.v17.i46.5083
Abstract: AIM: To analyze the outcome of hepatocellular carcinoma (HCC) resection in cirrhosis patients, related to presence of portal hypertension (PH) and extent of hepatectomy. METHODS: A retrospective analysis of 135 patients with HCC on a background of cirrhosis was submitted to curative liver resection. RESULTS: PH was present in 44 (32.5%) patients. Overall mortality and morbidity were 2.2% and 33.7%, respectively. Median survival time in patients with or without PH was 31.6 and 65.1 mo, respectively (P = 0.047); in the subgroup with Child-Pugh class A cirrhosis, median survival was 65.1 mo and 60.5 mo, respectively (P = 0.257). Survival for patients submitted to limited liver resection was not significantly different in presence or absence of PH. Conversely, median survival for patients after resection of 2 or more segments with or without PH was 64.4 mo and 163.9 mo, respectively (P = 0.035). CONCLUSION: PH is not an absolute contraindication to liver resection in Child-Pugh class A cirrhotic patients, but resection of 2 or more segments should not be recommended in patients with PH.
Life-threatening hypersplenism due to idiopathic portal hypertension in early childhood: case report and review of the literature
Jan D?britz, Jennifer Worch, Ulrike Materna, Bernward Koch, Gabriele Koehler, Christina Duck, Michael C Frühwald, Dirk Foell
BMC Gastroenterology , 2010, DOI: 10.1186/1471-230x-10-122
Abstract: We report the first case of uncontrolled splenic hyperperfusion and enlargement with subsequent hypersplenism leading to life-threatening complications of IPH in infancy and emergent splenectomy.Our results suggest that splenic NO and VCAM-1, rather than ET-1, have a significant impact on the development of IPH, even at a very early stage of disease. The success of surgical interventions targeting the splenic hyperperfusion suggests that the primary defect in the regulation of splenic blood flow seems to be crucial for the development of IPH. Thus, beside other treatment options splenectomy needs to be considered as a prime therapeutic option for IPH.Non-cirrhotic portal hypertension (NCPH) comprises a group of diseases with increased portal pressure in the absence of cirrhosis, most of which have portal hypertension as a late manifestation of the disease. Common causes of NCPH include extrahepatic portal venous obstruction, non-cirrhotic portal fibrosis or idiopathic portal hypertension (IPH) [1]. IPH is a rare disorder, characterized clinically by portal hypertension, splenomegaly, and hypersplenism accompanied by pancytopenia. Intrahepatic or prehepatic lesions are generally vascular, either in the portal vein, its branches or in the perisinusoidal area ('obliterative portovenopathy') and cause an increase in portal pressure.The underlying etiology and pathogenesis are poorly understood. It has been proposed that infectious, toxic (exposure to trace metals or chemicals), immunological and immunogenetic factors may play a role [1]. As hepatosplenomegaly is the leading symptom, other causes of organomegaly such as infections, malignancy, malformations and metabolic disorders, must be ruled out. In particular, childhood onset points to inherited conditions involved in early hepatic fibrosis, with special emphasis on storage disorders. On the other hand, IPH is not associated with hepatic cirrhosis but portal vein thrombosis, non-thrombotic causes, and parenchymal at
Idiopathic portal hypertension in a twin treated with TIPS and consequent splenectomy
I.A. Mouzas,A.A. Hatzidakis,Erminia Matrella,Maria Roussomoustakaki
Annals of Gastroenterology , 2008,
Abstract: Background: Idiopathic portal hypertension is a disorder of unknown aetiology characterized by portal hypertension secondary to splenomegaly, without cirrhosis. There are no reports on idiopathic portal hypertension occurring in twins. Variceal haemorrhage, a life threatening manifestation of portal hypertension may be treated with transjugular intrahepatic portosystemic shunt in the acute setting. Case presentation: A 36-year-old woman with severe variceal haemorrhage and ascites due to idiopathic portal hypertension was admitted to the Gastroenterology Department. Her twin sister underwent a splenectomy at the age of 12 due to splenomegaly and haemolytic episodes without further complications. The patient, like her twin sister, had also a history of splenomegaly since her childhood, with haemolytic episodes and need for multiple transfusions. Splenectomy was not preferred for her. In the following years, blood group incompatibilities developed after multiple transfusions that precluded any further blood transfusions. A β-thalassemia trait was also present. At admission, because of active variceal haemorrhage we performed a transjugular intrahepatic portosystemic shunt (TIPS) in an emergency setting. A decline of the portosystemic pressure gradient from 26 to 12 mmHg resulted with no further bleeding and with a subsequent reduction of the spleen size from 35 cm to 20 cm in diameter. A transjugular liver biopsy, a few months after TIPS, revealed a mild chronic hepatitis that was attributed to hepatitis C virus infection acquired from transfusions before 1990. A splenectomy was performed and the haematological parameters improved significantly. Despite TIPS obstruction that occurred later, no further oesophageal varices developed, and there was no need for further transfusions. Conclusions: In this patient, idiopathic portal hypertension may have had splenomegaly possibly related to haemolytic episodes as an initial cause, whereas later increased portal vascular resistance developed. In her twin sister, who also had splenomegaly at childhood, there was no development to portal hypertension due to an early splenectomy. Emergency treatment of the portal hypertension with TIPS, followed by a later surgical splenectomy was an effective management option for a follow up period of six years.
Idiopathic portal hypertension complicating systemic sclerosis: a case report
John Moschos, Grigoris I Leontiadis, Clive Kelly, James Henry, Savvas Kadis
BMC Gastroenterology , 2005, DOI: 10.1186/1471-230x-5-16
Abstract: An 82-year-old man with known systemic sclerosis presented with melaena. Urgent gastroscopy revealed oesophageal varices, which re-started bleeding during the procedure and were treated ensocopically, with Sengstaken tube and glypressin. Liver function tests and coagulation were normal. Non-invasive liver screen (including hepatitis viral serology and autoantibodies) was negative. Ultrasound scan of the abdomen revealed a small liver with coarse texture and no focal lesion. Hepato-portal flow was demonstrated in the portal vein. The spleen was enlarged. A moderate amount of free peritoneal fluid was present. A CT scan confirmed the absence of portal vein thrombosis. One month following discharge the patient had a liver biopsy. Histological examination showed essentially normal liver tissue; there was no evidence of any excess inflammation and no features to suggest cirrhosis or drug-induced liver disease. Taking into account the above evaluation we concluded that the patient had idiopathic portal hypertension.Both male and female patients with systemic sclerosis may – rarely – develop idiopathic portal hypertension.Systemic sclerosis (SSc) is a multisystem disease of unknown cause. The incidence of the disease is 10/million population per year. The female/male ratio is 4:1. A few cases of idiopathic portal hypertension (IPH) associated with SSc have been reported, all in females.We report a case of an 82-year-old man admitted to the hospital with melaena and dizziness on standing.He had a past medical history of SSc diagnosed 3 years before and pulmonary fibrosis. He was on prednisolone and azathioprine. There was no history of liver disease or alcohol abuse.On examination his blood pressure of 95/65 mmHg, pulse 90/min. He had bilateral fine inspiratory crackles. The abdomen was soft and non-tender. Rectal examination revealed melaena.White blood count was 12,700/mm3, haemoglobin 10.9 g/dl, platelets 186,000/mm3 and MCV 99.4 fl. Blood urea was 12.5 mmol/l, creatinin
Association Between Portal Vein Color Doppler Findings and the Severity of Disease in Cirrhotic Patients With Portal Hypertension
Puneet Mittal,Ranjana Gupta,Gaurav Mittal,Vishal Kalia
Iranian Journal of Radiology , 2011,
Abstract: Background: Doppler ultrasound is the accepted gold standard for assessing direction of flow in the portal vein (PV). Moreover, it is non-invasive; therefore, it is well accepted by the patients and does not interfere with flow hemodynamics.Objectives: The present study was aimed to evaluate the association between color Doppler findings and the severity of portal hypertension in patients with cirrhosis.Patients and Methods: The study group included 50 patients referred for ultrasound (US) evaluation over a period of six months from March to August, 2007. The patients were divided into three groups (Child’ A, B and C) based on Child Pugh classification. The direction of flow in the main portal vein (hepatopetal or nonhepatopetal) and peak venous velocity (PVV) in the main portal vein were measured and correlated with the presence or absence of ascites, splenomegaly, splenic and esophageal varices (assessed by Doppler US). These findings were correlated with clinical features and laboratory findings (using Child Pugh’s criteria).Results: There was significant association between the decrease of peak portal venous velocity (PVV) and the increase in Child Pugh score. Hepatofugal flow was seen only in patients with more advanced disease. There was also significant association between PVV and splenic varices and ascites, while PVV was not affected by the presence or absence of esophageal varices or splenomegaly. Presence of a recanalized umbilical vein (UV) was associated with increased PVV even in advanced disease.Conclusions: Color Doppler is an excellent modality for detecting and characterizing the complex hemodynamics of portal hypertension in cirrhosis and they correlate with the clinical stage of disease.
Non-cirrhotic portal hypertension with large regenerative nodules: A diagnostic challenge  [cached]
Umberto Vespasiani Gentilucci,Paolo Gallo,Giuseppe Perrone,Riccardo Del Vescovo
World Journal of Gastroenterology , 2011, DOI: 10.3748/wjg.v17.i20.2580
Abstract: Non-cirrhotic portal hypertension is a poorly understood condition characterized by portal hypertension in the absence of conventional hepatic cirrhosis and described in association with blood coagulation disorders, myeloproliferative and immunological diseases and with exposure to toxic drugs. Very recently, precise classification criteria have been proposed in order to define four distinct subcategories. The present case highlights how the clinical presentation, the confounding results from imaging studies, and the difficulties in the histological evaluation often render cases of non-cirrhotic portal hypertension a real diagnostic challenge. It also underscores the classification problems which can be faced once this diagnosis is performed. Indeed, the different subcategories proposed result from the prevalent subtypes in a spectrum of hepatic regenerative responses to a variety of injuries determining microcirculatory disturbances. More flexibility in classification should derive from this etiopathogenic background.
Severe bleeding from esophageal varices resistant to endoscopic treatment in a non cirrhotic patient with portal hypertension
Roberto Caronna, Mario Bezzi, Monica Schiratti, Maurizio Cardi, Giampaolo Prezioso, Michele Benedetti, Federica Papini, Simona Mangioni, Gabriele Martino, Piero Chirletti
World Journal of Emergency Surgery , 2008, DOI: 10.1186/1749-7922-3-24
Abstract: Recent advances in interventional radiology, especially the introduction of endovascular portosystemic shunts, have brought about rapid changes in therapy for the complications of portal hypertension [1]. Although the preferred treatment for a patient with variceal bleeding related to portal hypertension remains endoscopic sclerotherapy, when this option fails, as it does in about 15% of the cases, the only alternative is an emergency portosystemic shunt [2]. A surgical shunt procedure is indicated in patients with Child-Pugh A cirrhosis, the transjugular intrahepatic portosystemic shunt (TIPS) in those with Child-Pugh B-C cirrhosis scheduled for liver transplantation [3]. The treatment of variceal bleeding raises different problems in cirrhotic and non cirrhotic patients with portal vein thrombosis. Whereas from 0.6 to 2.6% of patients with cirrhosis have spontaneous portal thrombosis, those without cirrhosis generally do not (Table 1) [4]. The major causes of portal thrombosis in these patients are hereditary or acquired coagulation defects and local factors that include intraabdominal infections (in particular close to hepatic hilum) and surgical or traumatic portal vein damage.We describe a case of severe recurrent hemorrhage from esophageal varices in a patient without cirrhosis who had undergone open cholecystectomy 12 months earlier. The failure of endoscopic therapy raised complex problems in deciding how to manage portal hypertension.A 58-year-old non alcoholic patient was admitted to hospital for investigation of hematemesis and melena. Twelve months earlier he had undergone elective open cholecystectomy for chronic calculous cholecystitis complicated by a biliary fistula that had resolved spontaneously. An esophagogastroduodenoscopy disclosed bloody esophageal varices and the bleeding was successfully controlled by endoscopic sclerotherapy. During repeated endoscopic sessions the varices were progressively eradicated by ligation. Laboratory serum screenin
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