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Biomedical subjects

A K Burroughs

Publications and source records attributed to A K Burroughs.

At least 235 records · Page 13Linked to original sources
PubMed1991

Liver transplantation for chronic viral hepatitis.

Liver transplantation remains a problem for end stage liver disease due to chronic viral hepatitis, in contrast to the success with fulminant hepatitis B, D and C in which recurrence of viraemia is relatively rare. Following transplantation for chronic HCV disease recurrence of hepatitis C is infrequent and does not appear to be an important clinical problem. The complete picture will only be described when a suitable HCV-RNA test becomes routinely available. Patients with cirrhosis due to hepatitis B, with low levels of viraemia, or patients with hepatitis D are less likely to develop reinfection than those with high levels of HBV viraemia. The use of hepatitis B immunoglobulin in high doses for prolonged periods delays rather than prevents recurrence. It is a very expensive ancillary treatment. Patients with chronic hepatitis D related cirrhosis in whom levels of hepatitis B replication are suppressed, have a low recurrence rate even without immunoglobulin prophylaxis although HDAg remains in the liver. Hepatitis only reoccurs with recurrence of HBV infection. Unfortunately transplantation of HBV DNA and HBeAg positive patients has many shortcomings, and reinfection of the engrafted liver and subsequent development of hepatitis B is common. Survival rates are reduced in this latter group. At present there are no firm recommendations that can be given to prevent recurrence: HBIG in large doses and for prolonged periods would appear to be insufficient to prevent reinfection and these patients often die of recurrent disease. A major challenge for transplant groups will be the prevention of viral reinfection particularly in this latter group.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed1991

Prognosis in primary biliary cirrhosis. A review.

Recent progress has been made in estimating prognosis in primary biliary cirrhosis using Cox models. These models have also demonstrated the therapeutic value of liver transplantation by comparing the observed survival for a group after transplantation with the expected survival without transplantation calculated from the Cox prognostic model. However, good risk patients and those not transplanted principally for hepatocellular failure may not have a survival advantage for many years. Cox models have several limitations: the selection criteria for the patient populations used to derive the models, the selection of the time at which the patients are evaluated, the poor prognostic accuracy for individual patients rather than patient groups and lastly the fact that they use variables derived at only one time point-time independent Cox models. Thus new statistical tools must be used to improve prediction of survival in individual patients with PBC in order to optimize timing of liver transplantation. In addition a more precise definition of the natural history of both symptomatic and asymptomatic forms of this disease is needed to evaluate the efficacy of therapeutic agents in randomized clinical trials. However, although use and timing of therapeutic intervention, including liver transplantation, still requires good clinical experience and judgement, statistical modelling does give some objective measurement of prognosis, which is useful for the clinician treating patients with PBC. At the same time that new treatments are being evaluated, there is an obvious need to improve prognostic tools for application to individual patients with PBC. This may be achieved by using serial data in a different form of modelling-time dependent Cox models.

Humans↗
PubMed1990

Bleeding time in patients with hepatic cirrhosis.

OBJECTIVE: To determine the frequency of an abnormal bleeding time in patients with cirrhosis and to relate this to known factors that affect primary haemostasis and to the severity of liver disease. DESIGN: Prospective clinical and laboratory study in patients admitted for complications or investigations of liver disease. SETTING: Royal Free Hospital hepatobiliary and liver transplantation unit. SUBJECTS: 100 Consecutive inpatients aged 17-74 with various forms of cirrhosis, including alcoholic, biliary, autoimmune, viral, and cryptogenic. At least 10 days had elapsed since any episodes of bleeding, resolution of sepsis, or alcohol intake. No patient was taking any drug known to affect primary haemostasis. MAIN OUTCOME MEASURES: Bleeding time as measured with the Simplate double blade template device. A bleeding time longer than 10 minutes was considered abnormal. Other measures were platelet count, prothrombin time, partial thromboplastin time, packed cell volume, and blood urea, serum bilirubin, and serum albumin concentrations, all measured on each subject at the same time by standard laboratory methods. RESULTS: A weak but significant correlation existed between the bleeding time and the platelet count (rs = 0.483; p less than 0.001). There were significantly lower platelet counts, longer prothrombin times, and higher blood urea and serum bilirubin concentrations in the 42 patients with bleeding times of 10 minutes or more compared with the 58 patients with bleeding times less than 10 minutes. Multiple linear regression analysis showed that the bilirubin concentration as well as the platelet count was independently correlated with the bleeding time. The combination of a platelet count greater than 80 x 10(9)/l and a prothrombin time less than 17 seconds (usually taken as safe limits for performing routine liver biopsy) did not predict a normal bleeding time. Ten of 39 patients fulfilling these criteria had a prolonged bleeding time. CONCLUSIONS: Prolonged bleeding time is common in patients with cirrhosis, even in those with prothrombin times and platelet counts within "safe limits" for invasive procedures. The severity of liver disease as assessed by the bilirubin concentration plays an important part in determining the bleeding time in cirrhosis. The bleeding time should be measured when assessing patients for invasive procedures who have a raised bilirubin concentration or poor hepatic function, even if the platelet count and prothrombin time are considered adequate.

Adolescent↗
PubMed1990

Randomized, double-blind, placebo-controlled trial of somatostatin for variceal bleeding. Emergency control and prevention of early variceal rebleeding.

A randomized, double-blind, placebo-controlled trial of somatostatin was conducted among 120 patients admitted for bleeding esophageal varices (59 placebo, 61 somatostatin). An initial 250-micrograms bolus of somatostatin followed by a 5-day continuous infusion of 250 micrograms/h and an identical administration of placebo were evaluated for both the control of bleeding and prevention of early rebleeding from varices. Failure to control bleeding occurred in 22 (36%) somatostatin patients vs. 35 (59%) placebo patients, with time to failure occurring earlier with placebo (P = 0.036). blood and plasma transfused per hour during drug infusion of trial drug was reduced in the somatostatin group: median 0.033 vs. 0.105 unit/h (P = 0.025). Use of balloon tamponade was halved in somatostatin-treated patients. The average effect of somatostatin was a 41% reduction in the hazard of failure (95% confidence interval, -1% to 65%, P = 0.0545) after adjustment for the severity of liver disease, which was the only other variable having a significant influence on time to failure. There was no difference in 30-day mortality per admission (7 placebo, 9 somatostatin) or complications. It is concluded that somatostatin is safe and more effective than placebo for the control of variceal bleeding.

Adolescent↗
PubMed1990

Haemodynamic effect of triglycyl-lysine-vasopressin (glypressin) on intravascular oesophageal variceal pressure in patients with cirrhosis. A randomized placebo controlled trial.

A double-blind random administration of 2 mg glypressin intravenously (i.v.) or placebo was given to 20 volunteer patients suffering from liver cirrhosis with portal hypertension and oesophageal varices. Experimental protocol required two basal intravascular oesophageal variceal pressure (IOVP) measurements, before and after bolus i.v. drug injection. The second measurement was taken as reference to determine whether the treatment was effective. Other measurements were taken 1, 3, 5 and 10 min after drug administration. The fall in IOVP at 3, 5 and 10 min in the patients who had been administered glypressin proved statistically significant (p less than 0.01) with mean percentage variations of -22.3%, -24.4% and -27.9%, respectively. In conclusion, the administration of glypressin in portal hypertensive patients brought about a marked reduction in transmural oesophageal variceal pressure in over 70% of the cases. This decrease may prove to be of clinical importance both as a first line therapy and as a possible aid to emergency sclerotherapy in the presence of active variceal bleeding.

Adult↗
PubMed1990

The effect of non-protein liquid meals on the hepatic venous pressure gradient in patients with cirrhosis.

It has been suggested that protein feeding increases portal pressure in cirrhotic patients, but that carbohydrate and fat have little effect. We examined the relationship between feeding and portal pressure, using different liquid test meals (250 or 500 ml non-protein, 250 ml protein-containing, 500 ml water), in 29 alcoholic patients with cirrhosis and portal hypertension. The mean hepatic venous pressure gradient (HVPG) increased significantly 30 min after the protein meal (10% increase; p = 0.009) and returned to basal levels at 60 min. The mean HVPG also increased significantly after the non-protein meal: after 500 ml the increase was 23% at 30 min (p = 0.046) and 17% at 60 min (p = 0.12); and after 250 ml it was 15% at 30 min (p = 0.012) and 7% at 60 min (p = 0.05). Ingestion of 500 ml water caused a small, non-significant, increase in mean HVPG. Plasma glucagon levels increased significantly at 30 and 60 min after the protein meal, but did not change significantly after the non-protein meal or water. Both protein-containing and non-protein meals significantly elevate HVPG in alcoholic patients with cirrhosis and portal hypertension.

Adult↗
PubMed1990

Long-term pharmacologic therapy of portal hypertension.

Beta-blockers modify splanchnic hemodynamics in cirrhotic patients. Nonselective beta-blockers are more effective than selective beta-blockers. Azygos blood flow, as a measure of collateral circulation, including that through varices, is always reduced, but the effects on portal pressure, whether measured directly or by the wedged hepatic venous pressure, are variable. The initial reported correlation between a 25% reduction of resting pulse rate and similar percentage reduction in the wedged free hepatic venous gradient has not been reproduced in subsequent studies. Therefore, to study the effect of changes in hemodynamic indices and the likelihood of variceal bleeding, direct measurements of such indices need to be made in clinical trials. At present, only one primary-prevention trial of propranolol suggests that a hemodynamic index can be used to identify patients given propranolol who will not bleed. Some clinical factors may be important in identifying nonresponders in trials of secondary prevention, but these are not universally recognized. The results of secondary-prevention studies are very heterogeneous, and it is difficult to understand why this is so. However, comparative studies versus sclerotherapy suggest that reductions in rebleeding and mortality are similar. Pharmacologic treatment, including beta-blockade, is ideal for primary prevention of variceal bleeding. The initial results from randomized studies are more homogeneous regarding the benefit of beta-blockers than in the secondary-prevention studies, although there is still doubt about the response in cirrhotics with ascites. No fatal complications due to propranolol administration have been reported in cirrhotic patients, and the complications are reversible. The future of pharmacologic therapy for portal hypertension lies in combination therapy. The addition of vasodilators to beta-blockers appears to potentiate their effect on portal pressure reduction. The results of clinical trials are awaited with great interest.

Adrenergic beta-Antagonists↗
PubMed1990

Intravenous albumin infusion is an effective therapy for hyponatraemia in cirrhotic patients with ascites.

The treatment of moderate to severe hyponatraemia in patients with decompensated liver disease is unsatisfactory. We report our preliminary experience using intravenous infusion of albumin to treat this condition. Three patients with cirrhosis, ascites, and hyponatraemia responded satisfactorily to treatment; one patient with fulminant hepatitis B did not respond. Intravenous albumin infusion is a safe and effective therapy for patients with cirrhosis complicated by hyponatraemia. Its main role may be in preparing patients for surgery, particularly liver transplantation.

Aged↗
PubMed1990

Pancreatic pseudocyst causing portal vein thrombosis and pancreatico-pleural fistula.

Portal vein thrombosis and pancreatico-pleural fistula are unusual complications of chronic pancreatitis. We describe a patient with chronic alcoholic pancreatitis in whom erosion of the splenic vein led to portal vein thrombosis and to the development of a pancreatico-pleural fistula. We suggest that fistula formation may occur over a considerable time period as the portal vein thrombosis was diagnosed three years before the amylase-rich pleural effusions.

Adult↗
PubMed1990

Metabolism of exogenous S-adenosyl-L-methionine in patients with liver disease.

S-Adenosyl-L-methionine (SAMe) is an important methyl group donor for many biochemical reactions. It is widespread in body tissues, including the liver, and is metabolised via 3 main metabolic pathways: transmethyltion, trans-sulphuration and amino-propylation. In chronic liver disease these pathways are impaired, the major abnormality being a reduction in SAMe-synthetase activity. Exogenous SAMe may overcome the effects of impaired SAMe-synthetase activity. Exogenous SAMe is stable in digestive juices and, although well absorbed orally, bioavailability is reduced because of a significant first pass effect in the liver. Dose-dependent peak plasma levels are achieved within 3 to 6 hours of oral administration and plasma levels approach baseline after 24 hours. Volumes of distribution are small. The metabolism of exogenous SAMe appears to follow the known pathways of endogenous SAMe metabolism and the initial data suggest that the process is largely unaffected in patients with chronic liver disease.

Animals↗
PubMed1990

Hemodynamic evaluation of portal hypertension.

The portal circulation has long been relatively inaccessible to clinical investigation, a fact which has hindered the management of patients with portal hypertension. In recent years an increasing number of techniques have become available for hemodynamic evaluation of the portal circulation. This review discusses the most important of these, and attempts to highlight clinical situations in which hemodynamic assessment may be of value to the individual patient.

Azygos Vein↗
PubMed1990

How to insert a Sengstaken-Blakemore tube.

The Sengstaken-Blakemore (SB) tube is a valuable tool in the emergency treatment of patients with bleeding oesophageal varices. However, as its use may be associated with a number of serious complications it should be used judiciously and inserted with care. Once bleeding has been controlled with an SB tube, definitive treatment for the bleeding varices should be urgently considered.

Esophageal and Gastric Varices↗