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Biomedical subjects

P Burra

Publications and source records attributed to P Burra.

At least 55 records · Page 3Linked to original sources
PubMed1995

Energy expenditure (EE) and substrate utilization (SU) in the perioperative period in orthotopic liver transplantation (OLTX).

12 patients were investigated with IC (Datex, Deltatrac) preoperatively and during the surgical procedure of OLTX, VO2, VCO2 were continuously measured and RQ, EE and SU were calculated considering the different periods of the procedure: preoperative resting EE: (PREE), anaesthesiological procedures (ANEE), liver preparation EE (LPEEE), liver removal EE (LREE), anhepatic phase EE (APEE), reperfusion, EE (RPEE) and end of operation EE (EOEE). EE were expressed as % respect value calculated with H.B. (Harris-Benedict) formula. Data were analyzed with Student T-test and p < 0.01** or < 0.05* PREE is typical in end stage liver disease with low RQ values and increased EE. Energy production depends on lipid utilization since liver gluconeogenesis and glycogen stores are impaired. Anesthesia reduces energy needs and production up to 50% of the preoperative values, reducing VO2 more than VCO2 and therefore an augmented RQ value over 1.0. SU analysis indicates an increased glucose and aminoacid utilization coupled with high nitrogen catabolism that continues in the postoperative period (from 0.08 0.01 gN/kg b.w. to 0.20 0.06 gN/kg b.w.). When the new liver is reperfused, VO2 increases more than VCO2 indicating the risk of reperfusion injury.

Calorimetry, Indirect↗
PubMed1994

Endothelial activation and circulating vascular adhesion molecules in alcoholic liver disease.

Alcoholic hepatitis is characterized by hepatocyte necrosis associated with infiltration of the liver parenchyma by neutrophils. The mechanisms responsible for recruiting neutrophils to the liver are unknown. We report high circulating levels and tissue expression of the endothelial adhesion molecule E-selectin in alcoholic hepatitis. Because expression of E-selectin is involved in neutrophil transmigration into inflamed tissue, it may play a crucial role in the recruitment of neutrophils to the liver in alcoholic hepatitis. By contrast, we detected high levels of vascular cell adhesion molecule-1, the endothelial counter-receptor for the lymphocyte adhesion molecule very late antigen-4, in alcoholic cirrhosis, which is associated with a predominantly mononuclear cell infiltrate. Both diseases were associated with high levels of circulating intercellular adhesion molecule-1, which is released by activated lymphocytes, providing further evidence of immune activation in alcoholic liver disease.

Cell Adhesion↗
PubMed1994

Aprotinin efficacy on intraoperative bleeding and transfusion requirements in orthotopic liver transplantation.

BACKGROUND: Bleeding complications frequently occur during orthotopic liver transplantation (OLT), particularly in patients with liver cirrhosis. Enhanced fibrinolytic activity in plasma was seen to play a key role in the development of the hemostatic disorder and of hemorrhages. Aprotinin, a serine protease inhibitor, has been used in the prevention and/or treatment of hyperfibrinolytic states. STUDY DESIGN AND METHODS: In the present study, the effect of aprotinin on bleeding complications and transfusion requirements was investigated in OLT patients with liver cirrhosis. Seven consecutive cirrhotic patients undergoing OLT were infused with aprotinin following an original protocol (1,000,000-KIU intravenous loading dose plus 500,000 kallikrein-inhibitory units per hour until skin closure). Seven previous cirrhotic OLT patients not receiving aprotinin were used as controls. RESULTS: In the treated group, a significant decrease in the number of transfused units of packed red cells (48.7%, p < 0.01), fresh-frozen plasma (24.4%, p < 0.05), platelets (35.9%, p < 0.01), and autologous blood (55.2%, p < 0.01) was observed as compared with the control group. Moreover, the mean length of operation was significantly shorter in the aprotinin-infused patients than in untreated patients (8.3 +/- 1.2 vs. 10.1 +/- 1.8 hours, respectively; p < 0.01)). In the aprotinin-treated group, the antifibrinolytic efficacy was confirmed by the lack of increase in D-dimer levels and decrease of fibrinogen in plasma; on the contrary, these changes were always seen in the group not receiving aprotinin. CONCLUSION: Infusion of aprotinin during OLT in cirrhotic patients can be recommended for the prevention of hyperfibrinolysis-triggered bleeding, thus reducing transfusion requirements. A possible protective effect on the primary nonfunction of the grafted liver is suggested.

Adult↗
PubMed1993

Managing severe alcoholic hepatitis complicated by renal failure.

We examined the management and outcome of 15 patients admitted consecutively to a specialist Liver Unit with severe alcoholic hepatitis complicated by renal failure. Fourteen patients were managed conservatively. Of these, 11/14 underwent renal dialysis for a mean of 24 days. Three patients, including two requiring dialysis, recovered renal function. Despite intensive care, 12/14 patients died. Death was frequently associated with bacterial and fungal sepsis. One patient underwent liver transplantation with prompt post-operative recovery of renal function. He was discharged from hospital 16 days later, and remains abstinent from alcohol with normal liver function after one year. Most patients with renal failure complicating severe alcoholic hepatitis will die, despite intensive care including renal dialysis. Selected patients may be suitable for liver transplantation.

Adult↗
PubMed1993

11 beta-Hydroxysteroid dehydrogenase deficiency and glucocorticoid status in patients with alcoholic and non-alcoholic chronic liver disease.

11 beta-Hydroxysteroid dehydrogenase (11 beta HSD), found predominantly in liver and kidney, is responsible for the shuttling of active cortisol to cortisone. A defect in this shuttle mechanism, e.g. after liquorice ingestion, results in an increase in the ratio of urinary cortisol [tetrahydrocortisol (THF)] to cortisone [tetrahydrocortisone (THE)] metabolites. The plasma cortisol half-life is prolonged, but concentrations remain normal because of a concomitant fall in cortisol production. Alcohol-induced pseudo-Cushing's syndrome is an ill defined cause of Cushing's syndrome. Because many of the documented cases have abnormal liver function tests, we have investigated whether abnormal hepatic 11 beta HSD activity may play a role in the pathogenesis of the condition. Fourteen patients with alcoholic (ALD) and 14 patients with non-alcoholic (CLD) chronic liver disease had marked deficiency of 11 beta HSD [5 alpha-THF + THF/THE: ALD, 1.94 +/- 0.38 (+/- SEM); CLD, 1.82 +/- 0.20] compared to controls (0.94 +/- 0.04; P < 0.01 and 0.001, respectively). In the CLD group, the daily cortisol production rate (as assessed by summation of principal cortisol metabolites) was reduced appropriately [median, 3,510; range, 1,101-8,940 micrograms/24 h; controls, 5,492 (range, 3,818-14,996) micrograms/24 h; P < 0.001], and normal 0900 h plasma cortisol and urinary free cortisol levels were maintained. However, in the ALD group, there was no concomitant fall in the cortisol production rate (sum of cortisol metabolites, 5,043 micrograms/24 h; range, 520-27,344). As a consequence, 0900 h plasma cortisol in the ALD group was significantly elevated (633 +/- 52 nmol/L) compared to values in the CLD group (487 +/- 48 nmol/L; P < 0.05) and controls (432 +/- 27 nmol/L; P < 0.001). Our findings of glucocorticoid excess in patients with chronic ALD may indicate that alcohol-induced pseudo-Cushing's syndrome develops as a result of continuing normal cortisol secretion in the face of impaired cortisol metabolism. The latter is mediated by defective hepatic 11 beta HSD activity; the former by either abnormal glucocorticoid feedback or stimulation of cortisol secretion at the level of the hypothalamus/pituitary.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1993

Serum malondialdehyde and mitochondrial aspartate aminotransferase activity as markers of chronic alcohol intake and alcoholic liver disease.

Since lipid peroxidation is a well-know mechanism of alcohol-related liver damage, the aim of the present study was to assess the role of serum malondialdehyde (MDA), a secondary product of lipoperoxidation, in the detection of alcoholism and different stages of alcoholic liver disease and to correlate serum levels of malondialdehyde with other markers. Sixty-five patients with a mean alcohol intake of 151 gr/day, were divided into three groups: alcoholics with normal liver function (ANLF, 7 pts), non-cirrhotic alcoholic liver disease (NCALD, 26 pts) and alcoholic cirrhosis (ALC, 32 pts). The control group consisted of 15 healthy subjects. Serum MDA was measured by the thiobarbituric acid reaction test, and mitochondrial aspartate aminotransferase (mAST) with immunochemical assay. MDA had a higher sensitivity (70% vs 37.5%) and specificity (100% vs 93%) than mAST in detecting alcohol abuse, irrespective of the presence of liver disease. Serum MDA levels were significantly higher in all three groups than in controls (2.3 +/- 0.1 nmol/ml), the highest value being found in NCALD (4.6 +/- 0.4). Serum MDA levels were correlated with prothrombin time (p < 0.005) and blood alcohol levels (p < 0.05). mAST serum activity was also significantly higher in all three groups than in controls. A significant correlation was found between serum MDA and mAST only when the whole group was considered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Detection of circulating intercellular adhesion molecule-1 in chronic liver diseases.

The leucocyte adhesion molecule intercellular adhesion molecule-1 is induced on bile ducts in patients with primary biliary cirrhosis and primary sclerosing cholangitis and may be involved in targeting immune damage to these structures. It has recently been reported that, when activated, in vitro lymphocytes release a soluble form of intercellular adhesion molecule-1 that can also be detected in human serum. Because it is functionally active, this circulating intercellular adhesion molecule-1 might play a role in regulating inflammation by blocking adhesion. We used an enzyme-linked immunosorbent assay to detect circulating intercellular adhesion molecule-1 in the serum of patients with primary biliary cirrhosis and primary sclerosing cholangitis. Levels of circulating intercellular adhesion molecule-1 were markedly elevated in primary biliary cirrhosis and primary sclerosing cholangitis when compared with other chronic liver diseases. Circulating intercellular adhesion molecule-1 is probably derived from activated lymphocytes rather than from bile ducts because biliary epithelial cells from patients with primary biliary cirrhosis did not release circulating intercellular adhesion molecule-1 when stimulated to express the membrane-bound molecule in vitro. These studies are the first to demonstrate circulating intercellular adhesion molecule-1 in chronic inflammatory diseases that are characterized by strong tissue expression of intercellular adhesion molecule-1 and as such suggest a potential immunoregulatory role for circulating adhesion molecules. The very high levels detected in primary biliary cirrhosis and primary sclerosing cholangitis probably reflect lymphocyte activation, which is further evidence of immune pathogeneses for these diseases.

Bilirubin↗
PubMed1992

Is the intercellular adhesion molecule-1/leukocyte function associated antigen 1 pathway of leukocyte adhesion involved in the tissue damage of alcoholic hepatitis?

Alcoholic hepatitis is characterised histologically by an intense inflammatory cell infiltrate made up predominantly of neutrophils but including other cell types, particularly lymphocytes. Leukocyte cytotoxicity requires cell adhesion, which is mediated via receptors on the leukocyte surface including leukocyte function associated antigen-1 (LFA-1) which binds to the ligand intercellular adhesion molecule-1 (ICAM-1) on the target cell. The distribution of ICAM-1 and LFA-1 expression in liver biopsy specimens from patients with alcoholic liver disease was examined to ascertain whether this pathway of leukocyte adhesion is involved in the tissue damage of alcoholic hepatitis. Specimens were stained for ICAM-1 and LFA-1 by a three step immunoalkaline-phosphatase method using monoclonal antibodies against ICAM-1 and LFA-1. LFA-1 staining on portal tract inflammatory cells and parenchymal inflammatory cells and ICAM-1 staining on liver components were examined. ICAM-1 expression on hepatocytes was significantly greater in alcoholic hepatitis compared with fatty liver (p less than 0.001) and normal controls (p less than 0.01). ICAM-1 expression correlated with the histological degree of hepatocellular damage (tau = 0.79; p = 0.0005) and parenchymal inflammation (tau = 0.65; p less than 0.001, and with LFA-1 expression on parenchymal leukocytes (tau = 0.63; p = 0.01). The ICAM-1/LFA-1 pathway may therefore be involved in leukocyte mediated tissue damage during alcoholic hepatitis.

Antibodies, Monoclonal↗
PubMed1992

Severity of alcoholic liver disease and markers of thyroid and steroid status.

Alcoholic liver disease is associated with abnormalities in circulating levels of thyroid, adrenal and gonadal steroid hormones. The relative importance of ethanol consumption and severity of liver disease in the aetiology of these changes and their relationship to clinical abnormalities are unclear. We studied 31 subjects with alcohol-induced liver disease divided into three groups according to the severity of histological features: fatty change, hepatitis and cirrhosis. Circulating concentrations of thyroid, adrenal and gonadal steroid hormones, together with their major binding proteins, were measured in all subjects, and changes related to histology and tests of liver function, as well as clinical endocrine status. A reduction in circulating free tri-iodothyronine (fT3) was seen in subjects with alcoholic hepatitis and cirrhosis, in association with normal or reduced levels of thyrotrophin (TSH). The absence of abnormalities in subjects with fatty change despite similar ethanol intake to the other groups, and correlations between fT3 and liver function tests, suggest that changes in fT3 reflect the severity of underlying liver disease. Similarly, marked increases in circulating cortisol in the hepatitis and cirrhosis groups, and correlations between cortisol and liver function, suggest that changes largely reflect hepatic disease. The absence of clinical features of hypothyroidism or Cushing's syndrome in these groups, despite abnormalities of fT3 and cortisol, suggest an altered tissue sensitivity to hormone effects. In contrast, increases in circulating oestradiol and reductions in testosterone were found in all three groups in males. These findings suggest that both direct effects of ethanol and hepatic dysfunction determine changes in gonadal steroids in males.

Adrenal Cortex Hormones↗
PubMed1991

[Ulcer and hepatic cirrhosis. Epidemiologic and clinical correlations].

Peptic ulcer has been reported with increased frequency in patients with liver cirrhosis, its prevalence ranging form 5% to 20%. The aim of the present study is twofold: 1) to define the frequency of peptic ulcer in chronic liver disease in a large sample of cirrhotic patients, 2) to investigate the epidemiological and clinical features of a group of subjects affected by both peptic ulcer and liver cirrhosis. Two years of admission have been retrospectively investigated to define the frequency of peptic ulcer in chronic liver disease. In 237 subjects affected by both cirrhosis and peptic ulcer, epidemiological and clinical data were collected. Peptic ulcer was present in 16% of cirrhotic patients. There were no differences between ulcer subjects who drank and those did not. A linear positive correlation between smoking habit and frequency of ulcer disease has been found in the words. A positive history for peptic ulcer was described in a little subgroup of the studied sample, suggesting a low importance of the genetic factor in the pathophysiological pattern of ulcer disease in chronic hepatitis.

Adult↗
PubMed1990

[A clinico-endoscopic study on cicatrization of lesions and prevention of recurrences in patients with liver cirrhosis and peptic ulcer].

Seventy-four and five cirrhotic patients with acute peptic ulcer were respectively treated with H2-blockers and cytoprotective drugs for 4-6 weeks; after this period 49 (62.2%) healed and 14 (17.7%) did not heal after further 2 months with the same therapy. In order to observe the effectiveness of H2-blockers in preventing peptic ulcer recurrences, 77 cirrhotic patients were followed-up for a mean period of 12 months (range 3-48 months) after ulcer scarring; 51.2% under H2-blockers maintenance treatment and 54.8% who took antiacid in case of need, relapsed. The therapeutical response, as regards short-term treatment in cirrhotic patients, seems not to differ from the usual outcome of the general ulcer population; on the contrary, the relapses, also during a maintenance therapy, appears increased.

Adult↗
PubMed1990

[Peptic ulcer and liver cirrhosis. Clinico-epidemiologic considerations].

A significant increase in associated liver disease has been confirmed in duodenal ulcer cases, with various studies showing a 5-14% incidence of the ulcers in patients with cirrhosis. The present study was undertaken to discover the incidence of peptic ulcer in such patients, to investigate a series of epidemiological data in a group cirrhosis patients with ulcers and to establish an adequate protocol for the treatment of the ulcer in both its acute and post-healing stage. The incidence of peptic ulcers in cirrhosis patients was calculated in a retrospective study of 377 hospitalised patients in two consecutive years (1986, 1987). The epidemiological data are based on 99 of them. Acute ulcer treatment was given in 31, while 41 with healed ulcers were put on maintenance therapy. Ulcers were found in 16-17% of the cirrhosis patients; the cirrhosis was caused by alcohol abuse in 61.53% and was post-necrotic in 21.79%. Endoscopy revealed duodenal ulcers in 60.6%, gastric ulcers in 32.3%. In this sample, 39.39% were non-smokers, while 23.23% smoked over 20 cigarettes a day.

Age Factors↗