Medical decompressive therapy for prophylaxis of rebleeding.
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Adrenergic beta-Antagonists↗
Biomedical subjects
D Lebrec
Publications and source records attributed to D Lebrec.
Pulmonary vascular disorders in portal hypertension.
The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance is elevated. Since hepatopulmonary syndrome and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the common factor that determines their development must be portal hypertension. The clinical presentations are very different, with gas exchange impairment in the hepatopulmonary syndrome and haemodynamic failure in portopulmonary hypertension. The severity of hepatopulmonary syndrome seems to parallel the severity of liver failure, whereas no simple relationship has been identified between hepatic impairment and the severity of portopulmonary hypertension. Resolution of hepatopulmonary syndrome is common after liver transplantation, which has an uncertain effect in portopulmonary hypertension. The pathophysiology of both syndromes may involve vasoactive mediators and angiogenic factors.
Hemodynamics↗
[Clinical and Biological Gastroenterology: evaluation of Hepatology division, 1995 to 1997].
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France↗
In vitro and in vivo vascular responses to the L-type calcium channel activator, Bay K 8644, in rats with cirrhosis.
A substance which increases the entry of extracellular calcium into arterial smooth muscle may decrease cirrhosis-induced vasodilation. The aim of the present study was to measure the effects of the L-type Ca2+ channel activator, Bay K 8644, on the haemodynamics of rats with cirrhosis. Vascular reactivity to this substance was also investigated. Splanchnic and systemic haemodynamic responses to Bay K 8644 (50 microg/kg) were measured in cirrhotic and normal rats. Contraction induced by 0.1 micromol/L Bay K 8644 was measured in arterial rings (aorta and superior mesenteric artery) from cirrhotic and normal rats. In cirrhotic rats, Bay K 8644 significantly decreased portal pressure (15%) and portal tributary blood flow (24%), significantly increased portal territory vascular resistance (54%) and did not significantly change hepatocollateral vascular resistance. Bay K 8644 significantly increased arterial pressure (7%) and systemic vascular resistance (24%) and did not change the cardiac index. In normal rats, Bay K 8644 significantly increased vascular resistance (150%) in portal, hepatocollateral and systemic territories and significantly decreased the cardiac index (44%). Changes in portal territory, hepatocollateral and systemic vascular resistances were significantly less marked in cirrhotic than in normal rats. In rings from the aorta and superior mesenteric artery, Bay K 8644-induced contraction was significantly lower in cirrhotic than in normal rats. In conclusion, in rats with cirrhosis, Bay K 8644 administration reduced vasodilation in splanchnic and systemic arteries and did not affect hepatocollateral vascular resistance. The Bay K 8644-induced reduction in splanchnic vasodilation caused a decrease in portal hypertension. This study also shows that Bay K 8644-induced vascular contraction was less marked in cirrhotic than in normal rats, in systemic and splanchnic vascular beds.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
Studies of portal hemodynamics and hepatic oxygen consumption during acute liver allograft rejection.
Hemodynamics and oxygen variables, plasma cytokines, and histological features of a liver tissue sample obtained by transvenous biopsy were evaluated during 65 episodes of acute rejection. The hepatic venous pressure gradient was significantly higher in patients with acute rejection than in those without (5.1+/-0.3 vs. 3.1+/-0.2 mmHg, P<0.01). The increase in pressure gradient was related to the severity of rejection lesions. Hepatic blood flow was significantly lower in patients with than in those without acute graft rejection (1.28+/-0.11 vs. 1.75+/-0.13 L/min, P<0.05). Plasma interleukin-6 levels were significantly increased in patients with acute rejection and positively correlated with pressure gradient values. In patients with acute rejection, a significant decrease in hepatic venous oxygen content (-16%) was associated with a significant increase in hepatic oxygen consumption (+24%), whereas hepatic oxygen transport did not change significantly. In treated patients with a favorable response, the pressure gradient decreased significantly by 46%, but it remained elevated in patients who later developed chronic graft rejection. In conclusion, this study confirms that acute graft rejection may induce an increase in portal pressure, which is related to the severity of rejection lesions. It also shows that acute rejection decreases hepatic blood flow and increases hepatic oxygen consumption. In addition, it suggests that the hepatic venous pressure gradient might be useful to determine the outcome of rejection.
Acute Disease↗
Propranolol and sclerotherapy in the prevention of gastrointestinal rebleeding in patients with cirrhosis: a meta-analysis.
BACKGROUND/AIMS: A meta-analysis of nine selected randomized trials was performed to compare the effects of propranolol and sclerotherapy in the prevention of rebleeding and on survival in patients with cirrhosis. METHODS: Five end points were assessed: rebleeding, esophageal rebleeding, death, death due to bleeding, and adverse events. Analyses were performed according to the intention-to-treat method. For each end point, heterogeneity and treatment efficacy were assessed by the Der Simonian and Peto methods. When a significant difference was observed, sensitivity analyses were performed by successive stratification according to treatment duration, type of publication, severity of cirrhosis, and methodological quality. RESULTS: The mean percentage of patients free of rebleeding, the mean survival rate and the mean percentage of patients free of death from bleeding were not significantly different between patients treated with propranolol and those treated by sclerotherapy. The mean percentage of patients free of variceal rebleeding was 39% in propranolol group and 55% in sclerotherapy group (mean difference: 17%, 95% confidence interval: 9-25%, p < 0.001). The mean percentage of patients free of adverse events was significantly higher in the propranolol group than in the sclerotherapy group (mean difference: 22%, 95% confidence interval: 6-38%, p < 0.007). CONCLUSION: In patients with cirrhosis and esophageal varices, endoscopic sclerotherapy is more effective than propranolol in preventing variceal rebleeding, but the incidence of adverse events is significantly higher with sclerotherapy. There was no difference in survival between the treatments. Propranolol should be considered as a first choice treatment for preventing rebleeding.
Adult↗
Vascular hyporesponsiveness to vasodilators in rats with cirrhosis.
BACKGROUND/AIMS: In cirrhosis, the activation of nitric oxide and prostacyclin contributes to vasodilation, and ATP-sensitive K+ (KATP) channel activation or L-type calcium (Ca2+) channel inhibition may also play a role in this process. At the same time in cirrhosis, certain endogenous mechanisms may be stimulated which limit the influence of vasodilator mechanisms on vascular tone, thus altering vascular responses to exogenous substances such as nitric oxide donors, exogenous prostacyclin, KATP channel openers or L-type Ca2+ channel blockers. The aim of the present study was to examine the arterial depressor to these exogenous substances in normal rats and in rats with secondary biliary cirrhosis. METHODS: Arterial depressor dose-response curves to nitroprusside (a nitric oxide donor, 5-60 micrograms.kg-1.min-1), prostacyclin (0.5-5 micrograms.kg-1) and aprikalim (a KATP channel opener, 10-200 micrograms.kg-1) were obtained in both groups. The effects of different L-type Ca2+ channel blockers, i.e. nicardipine (a dihydropyridine, 0.02-0.5 mg.kg-1), diltiazem (a benzothiazepine, 0.5-5 mg.kg-1) and verapamil (a phenylalkylamine, 0.02-0.2 mg.kg-1. min-1), were also studied. RESULTS: Cirrhosis produced hyporeactivity to the arterial depressor effect of all doses of nitroprusside, the lowest dose of prostacyclin and the highest doses of aprikalim or diltiazem. Cirrhosis did not significantly change depressor responses to nicardipine or verapamil. CONCLUSIONS: Rats with cirrhosis are hyporeactive to exogenous nitric oxide, prostacyclin, KATP channel opener and benzothiazepine (an L-type Ca2+ channel blocker). Therefore, cirrhosis-induced mechanisms seem to limit the decrease in vascular tone by most vasodilators. However, these mechanisms appear to be more marked in nitric oxide-mediated vasodilation than in other vasorelaxation mechanisms.
Animals↗
Induction of nitric oxide synthase II does not account for excess vascular nitric oxide production in experimental cirrhosis.
BACKGROUND/AIMS: Excess production of nitric oxide (NO) reduces vasoconstriction of cirrhotic rat aorta. Expression of the inducible nitric oxide synthase (NOS II) in endothelial cells or vascular smooth muscle could account for this, as described with endotoxin or lipopolysaccharide (LPS) treatment. Alternatively, the endothelial NOS enzyme (NOS III) could be activated by an as-yet undescribed mechanism. Here we describe a combined study of the basal release of NO and quantitative measurement of the mRNA for NOS II and NOS III from thoracic aorta of an animal model of cirrhosis. METHODS: Thoracic aortas of six normal, six cirrhotic (secondary biliary cirrhosis) and six intra-peritoneal LPS-treated (15 mg/kg) rats were removed. Dissected aortic rings were precontracted with norepinephrine (NE; 10(-6) M) and relaxed with acetylcholine (Ach; 10(-6) M) with or without pre-incubation with the specific NOS inhibitor (L-NNA, 10(-5) M). Total RNA was extracted from aorta, reverse transcribed (RT) and used in polymerase chain reaction (PCR) amplification with primers specific for NOS II, NOS III and beta-actin. PCR products were hybridized with fluorescein labelled cDNA probes and the relative intensity on film was analyzed by densitometry. RESULTS: Compared to normal, NE caused 32% less contraction in cirrhotic and 43% less contraction in LPS-treated aortic rings. This response was corrected to normal by L-NNA pre-incubation. All the contracted rings relaxed with Ach. NOS II mRNA, was expressed only in LPS-treated aorta and not in aorta from normal and cirrhotic rats. NOS III mRNA levels were the same in normal, cirrhotic and LPS-treated rats: 1176 +/- 170, 1233 +/- 626 and 979 +/- 423, in arbitrary densitometry units, respectively. CONCLUSIONS: NO is overproduced by aorta from cirrhotic and LPS-treated rats. In LPS-treated rats this could result from expression of NOS II, but this was not the case in the cirrhotic rat aorta. Comparable amounts of NOS III mRNA suggest that, in cirrhosis, increased activity of this enzyme and not increased NOS III expression is responsible for the overproduction of NO.
Animals↗
Hypoxemia in patients with cirrhosis: relationship with liver failure and hemodynamic alterations.
BACKGROUND/AIMS: The relationship between hypoxemia, liver failure and the hemodynamic alterations in cirrhosis are unknown. This study examined the relationship between arterial hypoxemia, the severity of liver disease and hyperkinetic circulation in patients with cirrhosis. METHODS: Arterial blood gases, the severity of cirrhosis (Child-Pugh score), and splanchnic and systemic hemodynamics were measured in 120 patients with cirrhosis and without cardiopulmonary disease. Hypoxemia was considered to be present when PaO2 was < or = 70 mmHg. RESULTS: Seventeen patients had hypoxemia (14%). Hypoxemic patients had significantly lower pulmonary vascular resistance and a significantly higher alveolar-arterial oxygen gradient, Child-Pugh score and hepatic venous pressure gradient than non-hypoxemic patients. Cardiac index and right atrial and pulmonary pressures did not significantly differ between the two groups. CONCLUSIONS: Hypoxemia occurs mainly in patients with severe liver disease and is associated with pulmonary vasodilation.
Adult↗
Diuretic requirements after therapeutic paracentesis in non-azotemic patients with cirrhosis. A randomized double-blind trial of spironolactone versus placebo.
BACKGROUND/AIMS: Diuretic requirements after mobilization of ascites by paracentesis have never been assessed in cirrhosis. It is also unknown whether diuretics increase the incidence of postparacentesis circulatory dysfunction. The aim of this study was to investigate these features and to assess whether measurement of plasma renin activity and aldosterone prior to paracentesis predicts diuretic response after this procedure. METHODS: Thirty-six patients with non-azotemic cirrhosis and ascites treated by total paracentesis plus i.v. albumin were randomly assigned to receive placebo (n=17) or spironolactone 225 mg/day (n=19) immediately after paracentesis and followed-up for 4 weeks. RESULTS: Five patients (three in the placebo and two in the spironolactone group) abandoned the treatment prior to ascites recurrence or the end of the study due to complications or lack of compliance. The analysis was performed in the remaining 31 patients. Ascites recurrence was more common in the placebo group (13 cases, 93%) than in the spironolactone group (3 cases, 18%) (p<0.0001) and occurred within the first 2 weeks of follow-up in more than 50% of patients. Patients developing ascites in the spironolactone group had higher levels of renin (14.1, 20.6, 32.4 ng/ml per h) and aldosterone (120, 149, 288 ng/dl) than those who did not develop ascites (renin: 2.0+/-2.1 ng/ml per h; range 0.1-6.8; aldosterone: 43+/-38 ng/dl; range 4-116). Three patients in the placebo group and two in the spironolactone group developed postparacentesis circulatory dysfunction (defined as an increase in renin at the third day after paracentesis greater than 50% over baseline levels up to a value higher than 4 ng/ml per h). CONCLUSIONS: Patients with cirrhosis treated by paracentesis should receive diuretics immediately after this procedure to prevent early recurrence of ascites. The administration of 225 mg/day of spironolactone is a good empiric treatment for non-azotemic patients with cirrhosis, because it is effective in most cases and does not increase the incidence of postparacentesis circulatory dysfunction. The determination of plasma levels of renin or aldosterone prior to paracentesis predicts the efficacy of spironolactone in the prevention of ascites recurrence.
Aldosterone↗
Acute effects of propylthiouracil on hemodynamics and oxygen content in patients with alcoholic cirrhosis.
BACKGROUND/AIMS: The antithyroid drug propylthiouracil has been suggested for the treatment of alcoholic liver disease. Its beneficial effects could be due to either a decrease in hepatic oxygen consumption or an increase in hepatic blood flow. The aim of this study was to test these two hypotheses in patients with proven alcoholic cirrhosis. METHODS: The pharmacokinetic parameters after intravenous administration of 300 mg of propylthiouracyl were first determined in four patients. Then, the effects on systemic and splanchnic hemodynamics, and oxygen content were measured 45 and 90 min after the intravenous administration of 300 mg (n=6) or 600 mg (n=6) of propylthiouracil. RESULTS: Systemic hemodynamics (heart rate, arterial pressure, cardiac output and systemic vascular resistance) and splanchnic hemodynamics (hepatic venous pressure gradient, hepatic and azygos blood flows) were not modified 45 and 90 min after the administration of 300 mg or 600 mg of propylthiouracil. Moreover, neither oxygen content in the radial artery, pulmonary artery or hepatic vein, nor systemic oxygen uptake was modified after propylthiouracyl administration. The absence of effect of propylthiouracyl administration was also confirmed in patients with cirrhosis with proven acute alcoholic hepatitis (n=7). CONCLUSIONS: In patients with alcoholic cirrhosis, acute administration of propylthiouracyl has no effect on systemic and splanchnic hemodynamics or on oxygen contents. The presence of acute alcoholic hepatitis does not modify these results.
Adult↗
Endothelial calcium-calmodulin dependent nitric oxide synthase in the in vitro vascular hyporeactivity of portal hypertensive rats.
BACKGROUND/AIMS: Increased nitric oxide production has been implicated in impaired vascular responsiveness to vasoconstrictors in portal hypertension. However, there is no firm evidence concerning the involved nitric oxide synthase isoform. The present study investigated the possible contribution of one nitric oxide synthase isoform, the endothelial constitutive Ca2+-calmodulin dependent, in the overproduction of nitric oxide in portal hypertension. METHODS: Vascular responses to norepinephrine and acetylcholine were evaluated in isolated thoracic aortic rings from normal and portal vein stenosed rats. RESULTS: An impaired concentration-dependent contraction to norepinephrine was observed in intact rings from portal hypertensive rats compared to controls. The hyporeactivity to norepinephrine was reversed after endothelium denudation, the inhibition of nitric oxide synthase with L-NOARG or the inhibition of calmodulin with W-7, but not after pre-incubation with indomethacin. Stimulation of intact rings with norepinephrine after the inhibition of calmodulin with calmidazolium was followed by a decreased vascular response in vessels from normal rats but not in those from portal hypertensive rats. Stimulation of intact rings with norepinephrine in a Ca2+-free medium was followed by a decreased vascular response in vessels from both portal hypertensive and normal rats. No difference in vasoconstrictive responses was observed between the two groups after calmidazolium or in a Ca2+-free medium. Relaxation induced by acetylcholine in norepinephrine-precontracted rings was more marked in rings from portal hypertensive rats than in controls. No differences in the vasodilator responses were observed after relaxations had been inhibited by the removal of the endothelium, pre-incubation with L-NOARG, indomethacin, W-7 or calmidazolium and in a Ca2+-free medium. CONCLUSIONS: This study demonstrates the involvement of the endothelial constitutive Ca2+-calmodulin dependent nitric oxide synthase isoform in the overproduction of nitric oxide in portal hypertension.
Animals↗
Natriuretic response to the combination of atrial natriuretic peptide and terlipressin in patients with cirrhosis and refractory ascites.
BACKGROUND/AIMS: Refractory ascites, which occurs in certain patients with cirrhosis, is associated with a blunted natriuretic response to exogenous atrial natriuretic peptide (ANP). Since this blunting seems to be related to ANP-induced arterial hypotension, a vasoconstrictor, such as terlipressin (a vasopressin analogue), may restore natriuresis to exogenous ANP. Moreover, since cirrhosis-elicited vasodilation is thought to play a role in sodium retention, a vasoconstriction caused by terlipressin alone may lead to an increase in sodium excretion. This study aimed to evaluate the natriuretic response to either a combination of ANP with terlipressin or terlipressin alone in patients with cirrhosis and refractory ascites. METHODS: Sixteen consecutive patients with cirrhosis and refractory ascites were randomly assigned to receive either a combination of terlipressin (1-2 mg, i.v. bolus) with ANP (35 ng/kg, i.v. bolus followed by 15 ng x kg(-1) x min(-1) for 60 min) (n=8) or terlipressin alone (1-2 mg, i.v. bolus) (n=8). Sodium excretion and urine output, systemic, splanchnic and renal hemodynamics and renal oxygen consumption were measured before and during treatments. RESULTS: Combined therapy did not change arterial pressure but significantly increased urinary sodium excretion and urine output. These effects were associated with a significant increase in glomerular filtration rate and a decrease in renal oxygen consumption. Terlipressin alone significantly increased arterial pressure but did not change urinary sodium excretion or urine output. Moreover, terlipressin did not change either glomerular filtration rate or renal oxygen consumption. CONCLUSIONS: The combination of exogenous ANP with terlipressin, but not terlipressin alone, increases sodium excretion in patients with cirrhosis and refractory ascites.
Adult↗
Evaluation of patients with portal hypertension.
Patients with suspected portal hypertension must first be evaluated by physical examination, upper digestive endoscopy and ultrasonography with Doppler. Moreover, the evaluation of patients with portal hypertension depends on the cause of portal hypertension, the presence of complications and the specific treatment considered. Haemodynamic assessment with measurement of the hepatic venous pressure gradient is useful in confirming the origin of portal hypertension. This technique is the 'gold-standard' for evaluating haemodynamic treatments. Splanchnic and systemic circulation must also be measured. Quantitative evaluation of the splanchnic territory by Doppler sonography and other non-invasive investigations, may be performed. Further clinical studies are, however, needed to determine their interest in portal hypertension.
Diagnosis, Differential↗
Noncirrhotic portal hypertension.
This article reviews the different conditions leading to noncirrhotic intrahepatic portal hypertension, describes the related vascular lesions, and provides a review of the clinical characteristics, diagnosis, and treatment options available. Diseases associated with noncirrhotic portal hypertension are also specifically discussed.
Female↗
Haemodynamic effects of octreotide in portal hypertensive rats receiving propranolol.
BACKGROUND: The aim of this study was to investigate short-term effects of propranolol (a non-selective beta-adrenergic antagonist), octreotide (a long-acting somatostatin analogue), or a combination of these substances on splanchnic and systemic haemodynamics and arterial blood gases in rats with portal vein stenosis. METHODS: Splanchnic and systemic haemodynamics were measured using the radioactive microspheres method. Eight rats first received an i.v. infusion of isotonic saline (10 microL/min for 15 min) and then an i.v. infusion of octreotide (8 micrograms.h/kg for 15 min). Eight other rats first received a bolus i.v. injection of propranolol (2 mg) and an i.v. infusion of octreotide 15 min later. RESULTS: Propranolol or octreotide alone significantly decreased portal pressure (both by 23%), portal tributary blood flow (35 and 10%, respectively) and cardiac index (36 and 26%, respectively). Octreotide administration in rats pretreated with propranolol significantly decreased cardiac index but did not change portal and arterial pressures or portal tributary blood flow. Propranolol significantly increased arterial oxygen tension. Octreotide alone or combined with propranolol significantly decreased oxyhaemoglobin saturation and pH and increased carbon dioxide tension. CONCLUSIONS: In rats with portal vein stenosis, the somatostatin analogue, octreotide, accentuates the short-term decrease in cardiac index due to propranolol. In addition, octreotide altered arterial blood gases and acid-base status. In contrast, octreotide does not further decrease portal pressure in animals receiving propranolol.
Adrenergic beta-Antagonists↗
Haemodynamic responses to a combination of terlipressin and octreotide in portal hypertensive rats.
BACKGROUND: An enhancement of the haemodynamic effects of terlipressin by octreotide (and vice versa) may be useful in the treatment of portal hypertension. The aim of this study was to investigate the short-term effects of terlipressin, octreotide or a combination of these substances on splanchnic and systemic haemodynamics in rats with portal vein stenosis. METHODS: Eight rats received an intravenous (i.v.) infusion of isotonic saline (10 microL/min for 15 min). Eight rats received terlipressin first (0.05 mg/kg) and then an i.v. infusion of octreotide (8 micrograms.h/kg for 15 min) 15 min later. Eight other rats first received an i.v. infusion of octreotide and then terlipressin 15 min later. Splanchnic and systemic haemodynamics (radioactive microsphere method) were measured after saline, after terlipressin or octreotide alone, and after the combined treatments. RESULTS: Terlipressin and octreotide alone significantly decreased portal pressure, portal tributary blood flow and cardiac index. Terlipressin, but not octreotide, significantly increased heptocollateral vascular resistance and arterial pressure. Octreotide administration in rats pre-treated with terlipressin did not change portal pressure, caused portal tributary blood flow to increase and decreased hepatocollateral vascular resistance; it also decreased arterial pressure but not cardiac index. Terlipressin administration in rats pre-treated with octreotide further decreased portal pressure, portal tributary blood flow and increased hepatocollateral vascular resistance; terlipressin increased arterial pressure and further decreased cardiac index. CONCLUSIONS: In rats with portal vein stenosis, octreotide decreased short-term splanchnic and systemic vasoconstriction due to terlipressin. In contrast, terlipressin enhanced the splanchnic and systemic vasoconstriction due to octreotide. Thus, the haemodynamic responses to the combination of octreotide and terlipressin depend on the order of administration of these substances.
Animals↗
The treatment of oesophageal varices: a debate and a discussion.
At the Biennial Meeting of the International Association for the Study of the Liver, in Cape Town, South Africa, 20-24 February 1996, the treatment of oesophageal varices was selected as a subject for the discussion of controversies in portal hypertension. This review gives a summary of that discussion. Dr Didier LeBrec gave a broad overview of the medical management of oesophageal varices by presenting a list of 52 pharmacological agents that reduce portal venous pressure and presented the advantages and disadvantages of each. He emphasized that recent randomized clinical trials (RCT) have demonstrated that propranolol delays and decreases the occurrence of haemorrhage from varices in patients who have not previously suffered such complications. He also reported that isosorbidemononitrate is equally effective and further enhances the effect of propranolol. He also reported that the effects of propranolol plus endoscopic sclerotherapy (EST) were more effective than EST alone in preventing haemorrhage, but not in improving survival. Finally he noted that propranolol in high dosage did not prevent the development of large varices in cirrhotic patients with small or undetectable varices. Dr John Terblanche compared the efficacy of EST and endoscopic ligation of varices (ELV) and reported that all four RCTs found ELV to be superior. He discussed portacaval anastomosis (PCA) and concluded that only emergency PCA as reported by Orloff, is thought to be truly beneficial, and suggested that EST, plus ELV may be the treatment of choice. Dr Harold O. Conn, who served as the moderator of this session summarized the presentations and pointed out that liver transplantation is the most effective form of therapy of all, albeit extremely complex and expensive. He discussed transjugular intrahepatic portosystemic shunts (TIPS), the newest form of therapy, and emphasized its virtues (immediate reduction of portal venous pressure) and its limitations (frequent portosystemic encephalopathy and frequent spontaneous stenoses). He presented a brief discussion of the prevention of the development of the varices themselves, currently termed "pre-primary prophylaxis', a hope for the future. He ended with "Predictions' which if proven correct will give a preview of portal hypertension in the 21st century.
Esophageal and Gastric Varices↗