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At least 19 recordsLinked to original sources
PubMed1979

Pulmonary hypertension complicating portal hypertension.

We report 9 patients with pulmonary hypertension complicating portal hypertension. The cause of portal hypertension was cirrhosis in 7 patients, nodular regenerative hyperplasia of the liver in 1, and portal vein obstruction in 1. Six patients had been treated by portal-systemic shunting before the clinical onset of pulmonary hypertension. The interval between the first manifestation of portal hypertension and the recognition of pulmonary hypertension ranged from 2 to 15 years. Histologic examination in 1 of these patients revealed medial hypertrophy, concentric intimal proliferation, and plexiform lesions affecting the small pulmonary arteries. Pulmonary hypertension might result from the effect of a vasoconstrictive agent on the small pulmonary arteries or of a substance toxic to the walls of these vessels that is produced in the splanchnic territory, destroyed by the liver in normal subjects, and reaches the pulmonary arteries through portal-systemic shunts in these patients.

Adult↗
PubMed1979

Primary pulmonary hypertension presenting as portal hypertension.

A two and a half-year old child is described who presented with signs of portal hypertension (hematemesis, hepatosplenomegaly, ascites). Her subsequent work-up revealed that the "pressure-head" originated within the pulmonary arterial bed. Indeed, severe changes of primary pulmonary hypertension were found at autopsy. What is unique about this case is the absence of cardiopulmonary symptoms prior to the development of suprahepatic portal hypertension. In addition, the pulmonary disease developed in the absence of underlying chronic hepatic disease or extrahepatic portal vein thrombosis which, reportedly, can lead to pulmonary hypertension.

Autopsy↗
PubMed2024

Serum proteomic profiling of patients with compensated advanced chronic liver disease with and without clinically significant portal hypertension.

INTRODUCTION: Portal hypertension (PH) drives the progression of liver cirrhosis to decompensation and death. Hepatic venous pressure gradient (HVPG) measurement is the standard of PH quantification, and HVPG≥10 mmHg defines clinically significant PH (CSPH). We performed proteomics-based serum profiling to search for a proteomic signature of CSPH in patients with compensated advanced chronic liver disease (cACLD). MATERIALS AND METHODS: Consecutive patients with histologically confirmed cACLD and results of HVPG measurements were prospectively included. Serum samples were pooled according to the presence/absence of CSPH and analysed by liquid chromatography-mass spectrometry. Gene set enrichment analysis was performed, followed by comprehensive literature review for proteins identified with the most striking difference between the groups. RESULTS: We included 48 patients (30 with, and 18 without CSPH). Protein CD44, involved in the inflammatory response, vascular endothelial growth factor C (VEGF-C) and lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1), both involved in lymphangiogenesis were found solely in the CSPH group. Although identified in both groups, proteins involved in neutrophil extracellular traps (NET) formation, as well as tenascin C, autotaxin and nephronectin which mediate vascular contractility and lymphangiogenesis were more abundant in CSPH. DISCUSSION AND CONCLUSION: We propose that altered inflammatory response, including NET formation, vascular contractility and formation of new lymph vessels are key steps in PH development. Proteins such as CD44, VEGF-C, LYVE-1, tenascin C, Plasminogen activator inhibitor 1, Nephronectin, Bactericidal permeability-increasing protein, Autotaxin, Myeloperoxidase and a disintegrin and metalloproteinase with thrombospondin motifs-like protein 4 might be considered for further validation as potential therapeutic targets and candidate biomarkers of CSPH in cACLD.

Humans↗
PubMed1979

Chronic oral arsenic intoxication as a possible aetiological factor in idiopathic portal hypertension (non-cirrhotic portal fibrosis) in India.

Estimates were made of the arsenic concentration in liver specimens from nine patients having idiopathic portal hypertension (IP), and in four livers these were found to be significantly higher than those in patients with cirrhosis and in control subjects. The splenovenogram revealed extensive portosystemic collateral circulation. Corrected sinusoidal pressure and blood flow studies showed higher levels in four patients than in normal subjects. Microscopic examination of liver tissues revealed periportal fibrosis. The higher hepatic arsenic levels that were found were due to the inadvertent drinking of water contaminated with arsenic, adulterated opium, and indigenous medicines. A history of opium intake was not forthcoming but two patients had drunk water contaminated with arsenic and two others had taken bhasams (Ayurvedic medicines prepared by repeated oxidation of ores). Though the aetiology of idiopathic portal hypertension is not known, it is possible that arsenic intake may be one of the factors.

Adolescent↗
PubMed1978

[Gastrointestinal bleeding and emergency endoscopy in portal hypertension (author's transl)].

Portal hypertension is found in about one quarter of the cases with upper gastrointestinal bleeding. 57 patients with portal hypertension underwent endoscopy for gastrointestinal haemorrhage. Despite visible varices in all cases varice rupture underlies only 50% of the bleeding episodes. Conditions other than rupture were found to bleed in 50%. Superficial mucosal erosions, which escape radiological detection, were the most frequent other bleeding sources.

Adult↗
PubMed1979

Extrahepatic portal hypertension due to congenital obstruction of the portal vein and associated gross hepatic lobulation.

A 10-233k old girl presented with splenomegaly and recurrent hematemesis from esophageal varices. Splenoportography revealed a dilated extrahepatic portion of the portal vein with nonvisualization of its intrahepatic tributaries. The child died following an episode of hematemesis and was found to have a dilated portal vein which ended blindly. In addition, there was abnormal lobulation of the inferior surface of the liver which was not cirrhotic. The portal vascular anomaly, which presumably was responsible for the portal hypertension, was probably due to failure of communication between the embryonic vitelline veins or to atresia of the portal vein secondary to pressure from the abnormal hepatic lobulation in utero. It would appear that congenital factors may be significant in the etiology and pathogenesis of some cases of extrahepatic portal hypertension in early life and recognition of such developmental anomalies is of importantance in management.

Female↗
PubMed1978

Portal hypertension following renal transplantation.

Portal hypertension and variceal hemorrhage may be found in the renal transplant patient with chronic liver disease. The development of portal hypertension was found to occur after long-term graft survival without significant rejection. The development of positive cytomegalic virus and negative hepatitis-associated antigen appeared to be common. Splenomegaly and prominent venous collateral were the most frequent physical findings, while ascites and hepatomegaly were less frequent. Portasystemic decompression can be performed successfully, however, the mortality and morbidity appear to be higher for this group than for other cirrhotic patients with comparable hepatic reserve.

Adult↗
PubMed1979

The pathophysiology and surgical management of portal hypertension.

1. A classification of portal hypertension is given which relates better to the disordered pathophysiology than the older anatomical classification. 2. A review of the various procedural approaches to solution of the problems associated with portal hypertension has been given. 3. Based on our existing knowledge, a suggested approach to portal hypertension is described in which the various procedures and various types of shunts suggested over the years may be selectively applied to the appropriate patients.

Budd-Chiari Syndrome↗
PubMed1979

Effect of phenoxybenzamine (POB) on portal venous pressure in patients with portal hypertension.

In order to assess an effect of phenoxybenzamine (POB) on portal circulation, POB (0.5-1.0 mg./kg.) was administered intravenously to six patients with portal hypertension and two patients without portal hypertension. In patients with portal hypertension, POB reduced portal venous pressure (PVP) from 362.5 +/- 53.8 mm. H2O to 282.5 +/- 50.4 mm. H2O (P less than 0.001) where central venous pressure (CVP) was maintained constant. In patients without portal hypertension, change in PVP was in parallel with that in CVP where the decrease in PVP was regarded as not specific. This preferential reduction of PVP in portal hypertension seemed to implicate functional vasoconstriction of the portal venous system. In the treatment of bleeding esophageal varices, use of POB with blood transfusion after decompression of the Sengstaken-Blakemore tube should be beneficial because of its prolonged effect of lowering PVP and preventing ischemic liver damage.

Adult↗
PubMed1978

[Drainage of the thoracic lymphatic duct and lymphovenous anastomosis in treating portal hypertension].

To correct the portal blood flow 52 operations on the thoracic lympheduct (TLD) were performed on 43 patients with decompensated portal hypertension syndrome. The external drainage of the TLD (lymphaticostomy) was carried out upon 22 patient and the internal drainage of TLD (lympho-venous anastomosis-LVA) upon 26 patients. 4 patients underwent other operations. The authors conclude that the selection of a LVA variant should be individual, depending on peculiarities of topographo-anatomical correlations between TLD and the anastomosed vein.

Adolescent↗
PubMed1979

Portal hypertension after bile duct obstruction: effect of bile diversion on portal pressure in the rat.

Biliary obstruction of 14 and 28 days induced in the rat an increase of portal pressure (PP) and wedge hepatic vein pressure (WHVP); the higher these were, the longer was the obstruction. Occurrence of portal hypertension seemed related to portal and periportal fibrosis. Relief of obstruction after 14 days by bilioduodenal anastomosis brought back to normal PP and WHVP. In rats with longer obstruction periods, bilioduodenal anastomosis failed to lower PP and WHPV although biological signs of cholestasis returned to normal levels. These results suggest that portal hypertension may arise very shortly after biliary obstruction in rats and that it may persist in animals with a prolonged biliary obstruction despite an efficient bile drainage. In clinical conditions, such results would favor early treatment of lesions that usually cause prolonged bile duct obstruction, such as postoperative bile duct stenosis.

Animals↗
PubMed1979

Subcutaneous transposition of the spleen: a method for treatment of complications in portal hypertension?

Eleven patients with portal hypertension were treated with subcutaneous transposition of a resected spleen. In eight of the patients the operation was performed after variceal bleeding. In this group there was one operative mortality--a 77-year-old woman. Another patient died after 28 months in upper gastrointestinal bleeding. Autopsy showed varices in the gastric fundus and a cancer in the cardia. The other six patients are alive and in good health after 41--60 months. The operation was performed in another three patients, who had not bled. The indication was hypersplenism and esophageal varices in two and severe thrombocytopenia in one. Two of these patients (both with advanced hepatic disease) died postoperatively. The operation is proposed as an alternative method in the treatment of portal hypertension--especially when the main problem is hypersplenism. The operation has no negative effects on liver function and does not cause encephalopathy. Hypersplenism is cured. The survival time and freedom from postoperative bleeding among those who bled preoperatively is in the present material very satisfactory. However, the operation cannot be recommended for the prophylactic treatment of patients with esophageal varices who have not bled--at least not in the patient with advanced hepatid dysfunction.

Adolescent↗
PubMed1978

Correlation between percutaneous transhepatic portography and clinical findings in 56 patients with portal hypertension.

56 consecutive patients with portal hypertension were studied with percutaneous transhepatic portography and the results were correlated to clinical findings and the number of upper gastrointestinal haemorrhages and the size of the individual bleeding. An abundance of collateral paths was noted in most patients. No regularity in development of these collaterals was found. It was not correlated to liver disease etiology, sex or liver function parameters. Portal pressure was not correlated to the size or amount of collaterals. In four patients with liver cirrhosis hepato-fugal flow in one segment of the liver was noted proving that portal flow through the liver is not uniform in this disease. The size of the haemorrhages was only correlated to presence of hepato-fugal flow in the main stem of the portal vein. It was not correlated to the estimated size of the oesophageal varices or to portal pressure. Percutaneous transhepatic portography seems to be of little help in selecting "high risk bleeders" in portal hypertension. Other factors may be of greater help in this task as indicated by the findings in this investigation that patients with alcohol cirrhosis had larger haemorrhages than those with cirrhosis of another etiology and that patients with none or few bleeding episodes had higher thrombocyte count than those with several haemorrhages.

Aged↗
PubMed1979

Portal hypertension secondary to choledochal cyst.

Two patients with portal hypertension secondary to choledochal cyst are reported and combined with four others previously reported in the literature. Choledochal cysts may, by extrensic compression, cause partial or complete portal vein obstruction, portal hypertension and esophageal varices. Needle biopsy of the liver is probably not a reliable means of differentiating choledochal cyst from other intrahepatic causes of portal hypertension. Internal drainage of the choledochal cyst has been performed in four patients and in each instance resulted in satisfactory portal decompression.

Adolescent↗
PubMedDate not supplied

[Percutaneous splenoportogammagraphy in the study of patients with portal hypertension].

Percutaneous esplenoportogammagraphy in 28 patients with portal hypertension, was carried out; in three patients studies were done before and after a derivative operation; in nine only after operation for portal hypertension and thirteen patients were not surgically treated. Hepatic maximal opacification was obtained in 4.35 seconds. In the operated patients the tecnesium reached right cardiac chambers in 2.91 seconds. In three of the thirteen patients with the test, there were intrahepatic circulatory pattern changes, average spleen-liver was 6 seconds and spleen-heart, 7 seconds, that is, esplenoportal perfussion was poor. In all the operated patients the decreased circulation time spleen-heart and the typical image showed anastomosis permeability.

Humans↗
PubMed1977

[Surgical procedures in portal hypertension (author's transl)].

Successful therapy of portal hypertension and especially bleeding oesophageal varices can only be achieved by decompressing surgical measures. An emergency porto-caval shunt has the advantage of short operating time and optimal decompression. Blocking procedures are only indicated in rare cases. In the time free of bleeding spleno-renal-anastomosis is the procedure of choice. Postoperative encephalopathy is still a menace in surgery of portal hypertension.

Age Factors↗
PubMed1979

New pathways in portal hypertension surgery.

An individualized treatment of portal hypertension is advocated. The treatment is suggested to be based upon the presence of complications to the disease: bleeding oesophageal varices, insufficient cardia function, regurgitation and oesophagitis, hyperacidity, stomach and duodenal ulcer, ascites and hypersplenism. The choice of method of treatment of the patient depends on the presence of the symptoms. There are several methods available. These can be divided in methods directed against one symptom - unisymptomatic treatment - and methods directed against several symptoms - polysymptomatic treatments. The author advocates a more frequent use of decongestion operations and pexi operations. For acute control of bleeding varices it seems that sclerotherapy is the preferred choice at present.

Brain Diseases↗