Pancreatic function was studied in 29 patients with extrahepatic portal venous obstruction, and 30 age-matched controls. The aetiology of the portal venous obstruction was known in 20 out of 29 patients. No patient had a history of pancreatitis. Serum trypsin, both fasting and for 120 minutes after a Lundh meal, was significantly lower in the patients than in controls (p <0 005). 5/28 (18 %) patients had reduced fasting serum trypsin levels and in 5/14 trypsin was abnormal after a Lundh meal. Mean fasting serum glucose (3.8 ±0 49 mmol/l was significantly higher than in control subjects (mean 3.4 ±0A42 mmol/l) (p <005). After 100 g glucose orally, mean serum glucose at 180 minutes (5.26 ±1.58 mmol/l) was higher than the control value (3.96 +1.45 mmol/l) (p <0 05), and 30 and 60 minutes serum C-peptide values were significantly lower (p <0.005). Pancreatic hypofunction found in these patients probably results from an abnormal portal circulation in association with mild pancreatic damage secondary to chronic venous congestion.

Serum trypsin concentrations within the portal venous system have been measured in man during transhepatic portal venography in an attempt to determine its source. In eight experiments, mean serum trypsin concentration at the splenic hilum was 180±25 ng/ml (mean±sem). Trypsin concentration in the rest of the splenic vein was not significantly different. The mean concentrations in the portal vein (210±32 ng/ml) and within the superior mesenteric vein (233±29 ng/ml) were, however, significantly higher than at the hilum (P<0.05). Following cholecystokinin-pancreozymin (CCK-PZ) and secretin stimulation, marked increases in serum trypsin concentration were seen within the portal vein (two patients) and deep within the superior mesenteric (two out of three patients). We conclude that circulating serum trypsin is derived, at least in part, from intestinal reabsorption.

LiverVolume 1, Issue 1 p. 3-6 The therapy of bleeding oesophageal varices Sheila Sherlock, Corresponding Author Sheila Sherlock Departments of Medicine and Radiology, Royal Free Hospital School of Medicine, University of London, London, EnglandDepartment of Medicine Royal Free Hospital Pond Street Hampstead London NW3 EnglandSearch for more papers by this authorG. Smith-Laing, G. Smith-Laing Departments of Medicine and Radiology, Royal Free Hospital School of Medicine, University of London, London, EnglandSearch for more papers by this authorR. Dick, R. Dick Departments of Medicine and Radiology, Royal Free Hospital School of Medicine, University of London, London, EnglandSearch for more papers by this author Sheila Sherlock, Corresponding Author Sheila Sherlock Departments of Medicine and Radiology, Royal Free Hospital School of Medicine, University of London, London, EnglandDepartment of Medicine Royal Free Hospital Pond Street Hampstead London NW3 EnglandSearch for more papers by this authorG. Smith-Laing, G. Smith-Laing Departments of Medicine and Radiology, Royal Free Hospital School of Medicine, University of London, London, EnglandSearch for more papers by this authorR. Dick, R. Dick Departments of Medicine and Radiology, Royal Free Hospital School of Medicine, University of London, London, EnglandSearch for more papers by this author First published: March 1981 https://doi.org/10.1111/j.1600-0676.1981.tb00017.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume1, Issue1March 1981Pages 3-6 RelatedInformation

One hundred and forty-one attempts at percutaneous transhepatic variceal obliteration were made in 116 patients with portal hypertension complicated by variceal hemorrhage. Varices were successfully obliterated in 80% of procedures and included 37 patients with continuous, acute variceal hemorrhage. Hemorrhage ceased immediately in these patients. Sixty-five percent of patients rebled a mean of 4.6 mo after successful transhepatic variceal obliteration. A randomized controlled trial against conventional medical therapy (29 treatment, 25 control) failed to show a significant reduction in death rate after transhepatic sclerotherapy, although the onset of further variceal hemorrhage was delayed. Follow-up portography in 50 patients demonstrated new vessel formation in 38 patients and recanalization of previously occluded varices in 5 patients. Complications arose in 29 of 141 procedures. There was one death but all the other complications responded to conservative management. Transhepatic variceal obliteration is an excellent, safe emergency treatment for variceal hemorrhage, especially in patients with decompensated liver disease. A high incidence of rebleeding is a long-term disadvantage and means that transhepatic variceal obliteration should not be used for the prophylaxis of variceal hemorrhage. Successful emergency treatment of variceal hemorrhage should be followed by elective portal decompression in suitable patients.

Twenty-five patients with primary biliary cirrhosis undergoing portal decompression have been followed up for a mean of 51 months. Five patients with decompensated cirrhosis died postoperatively. Overall five year survival of 66% is comparable with that for other forms of cirrhosis but none of the long-term survivors, including three patients with a precirrhotic stage of primary biliary cirrhosis at the time of surgery, developed significant portal-systemic encephalopathy. The results suggest that portal decompression may be the therapy of choice for patients with well-compensated primary biliary cirrhosis who suffer recurrent variceal haemorrhage.

Sixty-four transhepatic portograms performed before transhepatic obliteration of varices in patients with variceal hemorrhage have been reviewed. Sixty-two patients had coronary gastroesophageal vessels feeding gastric and esophageal varices and other major collateral circulation was seen in 25 patients. There was no relationship between the presence of major collateral circulation and the height of portal pressure or the severity of hemorrhage from gastroesophageal varices. Failure to opacify the intrahepatic portal venous system was seen in 11 patients and was strongly associated with portal-systemic encephalopathy. In addition to transhepatic portography, 35 patients had a splenic portogram, and 27 patients had coeliac axis angiography. There was poor agreement between the findings of these three techniques. Transhepatic portography was markedly superior in demonstrating the portal-systemic collateral circulation. Because of the excellent anatomical definition obtained, transhepatic portography is a superior technique for visualizing the portal system. However, even this technique may occasionally fail to demonstrate gastroesophageal collateral circulation in patients with endoscopically documented variceal hemorrhage.

The portal vein is formed at the confluence of the splenic and superior mesenteric vein behind the head of the pancreas. Normal blood pressure within the portal system varies between 5 and 10 mmHg. Portal hypertension is defined when the gradient between the portal and systemic venous blood pressure exceeds 5 mmHg. The most common cause of portal hypertension is cirrhosis. In cirrhosis, portal hypertension develops due to extensive fibrosis within the liver parenchyma causing increased vascular resistance. In addition, the inability of the liver to metabolise certain vasodilators leads to hyperdynamic splanchnic circulation resulting in increased portal blood flow. Decompression of the portal pressure is achieved by formation of portosystemic collaterals. In this review, we will discuss the pathophysiology, anatomy, and imaging findings of spontaneous portosystemic collaterals and clinical manifestations of portal hypertension with emphasis on the role of interventional radiology in the management of complications related to portal hypertension.

Plasma glucagon and growth hormone concentrations were measured fasting and after oral glucose in 19 patients with portal vein block with extensive portal-systemic shunting but minimal liver cell damage, 11 cirrhotic patients and 12 matched control subjects. Portal vein block patients and controls had similar fasting glucose and glucagon levels (glucose 3.8 ±0.1 mmol/l vs control 3.4±0.1 mmol/l (mean±SEM); glucagon 57.5 ±9.1 pg/ml vs control 51.3±7.8 pg/ml). Cirrhotic patients were hyperglycaemic (cirrhosis 4.3±0.2 mmol/l vs control 3.4 ±0.1 mmol/l, p < 0.01) with significantly elevated glucagon levels (167.3±61.1 pg/ml vs control 51.3 ±7.8 pg/ml, p < 0.05), which suppressed towards control values after oral glucose. There was no correlation between fasting plasma glucagon levels and the degree of portal-systemic shunting in cirrhotic patients. There was a strong correlation between fasting plasma glucagon concentrations and aspartate transaminase levels (r = 0.68; p < 0.01) in cirrhotic and portal vein block patients. Significant elevations of growth hormone were seen only in cirrhotic patients. It is concluded that hyperglucagonaemia is a feature of hepatocellular damage rather than portalsystemic shunting but the relationship between elevated glucagon and growth hormone concentrations and carbohydrate intolerance in cirrhosis remains unclear.

Plasma glucagon and growth hormone concentrations were measured fasting and after oral glucose in 19 patients with portal vein block with extensive portal-systemic shunting but minimal liver cell damage, 11 cirrhotic patients and 12 matched control subjects. Portal vein block patients and controls had similar fasting glucose and glucagon levels (glucose 3.8 +/- 0.1 mmol/l VS control 3.4 +/- 0.1 mmol/l (mean +/- SEM); glucagon 57.5 +/- 9.1 pg/ml VS control 51.3 +/- 7.8 pg/ml). Cirrhotic patients were hyperglycaemic (cirrhosis 4.3 +/- 0.2 mmol/l VS control 3.4 +/- 0.1 mmol/l, p < 0.01) with significantly elevated glucagon levels (167.3 +/- 61.1 pg/ml VS control 51.3 +/- 7.8 pg/ml, p < 0.05), which suppressed towards control values after oral glucose. There was no correlation between fasting plasma glucagon levels and the degree of portal-systemic shunting in cirrhotic patients. There was a strong correlation between fasting plasma glucagon concentrations and aspartate transaminase levels (r = 0.68; p < 0.01) in cirrhotic and portal vein block patients. Significant elevations of growth hormone were seen only in cirrhotic patients. It is concluded that hyperglucagonaemia is a feature of hepatocellular damage rather than portal-systemic shunting but the relationship between elevated glucagon and growth hormone concentrations and carbohydrate intolerance in cirrhosis remains unclear.

Pancreatic function was studied in 29 patients with extrahepatic portal venous obstruction, and 30 age-matched controls. The aetiology of the portal venous obstruction was known in 20 out of 29 patients. No patient had a history of pancreatitis. Serum trypsin, both fasting and for 120 minutes after a Lundh meal, was significantly lower in the patients than in controls (P less than 0.005). 5/28 (18%) patients had reduced fasting serum trypsin levels and in 5/14 trypsin was abnormal after a Lundh meal. Mean fasting serum glucose (3.8 +/- ).49 mmol/l was significantly higher than in control subjects (mean 3.4 +/- 0.42 mmol/l) (P less than 0.05). After 100 g glucose orally, mean serum glucose at 180 minutes (5.26 +/- 1.58 mmol/l) was higher than the control value (3.96 +/- 1.45 mmol/l) (P less than 0.05), and 30 and 60 minutes serum C-peptide values were significantly lower (P less than 0.005). Pancreatic hypofunction found in these patients probably results from an abnormal portal circulation in association with mild pancreatic damage secondary to chronic venous congestion.

Cirrhosis is complicated by numerous abnormalities of carbohydrate metabolism although these are seldom of clinical importance. Carbohydrate intolerance is extremely common and is accompanied by hyperinsulinaemia, hyperglucagonaemia and elevated levels of gluconeogenic precursors. The hyperinsulinaemia results from impaired hepatic degradation of insulin while recent evidence suggests that pancreatic hypersecretion is responsible for the elevated levels of glucagon in cirrhosis. The role of hepatocellular damage and portal-systemic shunting in the pathogenesis of these abnormalities is controversial but the derangements in carbohydrate metabolism probably reflect hepatocellular damage rather than portal-systemic shunting.

Insulin degradation was measured by the C-peptide/insulin ratio in 19 patients with portal vein block with extensive spontaneous portal-systemic shunting but minimal liver cell damage: 13 patients with biopsy-proved cirrhosis and 12 controls. Blood obtained fasting and for 3 hr after oral glucose was assayed for glucose, insulin, and C-peptide. Fasting C-peptide and insulin levels in patients with portal vein block and those in controls did not differ. Eight of 13 cirrhotic patients had fasting hyperinsulinemia with a significantly reduced C-peptide/insulin ratio. After glucose administration, the C-peptide/insulin ratio in portal vein block patients with normal aspartate transaminase levels did not differ from control values. In portal vein block patients with elevated asparatate transaminase levels, the C-peptide/insulin ratio was significantly reduced only from 60 min onwards. All the cirrhotic patients showed a significantly reduced C-peptide/insulin ratio after glucose administration. It is suggested that portal-systemic shunting of blood in the presence of a normal liver does not influence hepatic insulin metabolism and that the hyperinsulinemia of cirrhosis is a feature of parenchymal liver damage. In addition, insulin degradation was abnormal in all cirrhotic patients at high insulin secretion rates, even when fasting insulin levels were normal.