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Biomedical subjects

B Willems

Publications and source records attributed to B Willems.

At least 73 records · Page 4Linked to original sources
PubMed1993

Isometric maximal and submaximal trunk extension at different flexed positions in standing. Triaxial torque output and EMG.

Thirty-one healthy men were tested for the effects of trunk-flexion positions (0 degrees, 15 degrees, and 35 degrees) in standing on triaxial torques and electromyogram of 10 trunk muscles during voluntary maximal and submaximal isometric trunk extension. At a more flexed position, both erector spinae and latissimus dorsi showed significantly higher RMS-EMG. The abdominal obliques were coactivated only during 100% maximum voluntary exertion at each posture. In all tests, the rectus abdomini were quiet. Mean maximum extension torque increased significantly at 15 degrees and 35 degrees of trunk flexion. The ratio of extension torque over RMS-EMG of the trunk extensor muscles, called the neuromuscular efficiency ratio (NMER), also increased in the more flexed posture. However, NMER has to be interpreted with caution because it is affected both by posture and exertion levels. The effects of posture on the torque generation capability of the trunk question the validity of the current lifting recommendations.

Abdominal Muscles↗
PubMed1992

Transjugular intrahepatic portacaval stent shunt as a rescue treatment for life-threatening variceal bleeding in a cirrhotic patient with severe liver failure.

Variceal bleeding in cirrhotic patients with severe liver failure that is not controllable by endoscopic sclerotherapy is a life-threatening situation. We report the case of a patient with decompensated cirrhosis (Pugh class C) who bled repeatedly from gastric varices despite multiple sessions of sclerotherapy. The portal vein was catheterized by a transjugular approach. A tract between a hepatic vein and the portal vein was created after balloon dilatation, and this opening was stented with an expandable stainless steel Palmaz stent. The portal vein pressure decreased from 35 mm Hg to 19 mm Hg after shunting. Gastric varices also were embolized. Two months later, bleeding had not recurred; the shunt remained opened and the marked decrease in portal pressure still persisted. Endoscopy showed the disappearance of gastric varices. This procedures could become a life-saving therapeutic option for such critically ill cirrhotic patients.

Catheterization↗
PubMed1990

Isolated perfused cirrhotic human liver obtained from liver transplant patients: a feasibility study.

Cirrhotic livers obtained from eight patients who underwent orthotopic liver transplantation were perfused through the portal vein and hepatic artery in a closed recycling system for periods ranging from 2 to 7 hr. An average perfusion flow of 451 ml/min was used, with about 80% coming from the portal vein and 20% from the hepatic artery. The livers appeared to remain viable as assessed by gross appearance, stable portal vein and hepatic artery pressures, oxygen consumption and bile production. The extraction ratio of indocyanine green by the perfused livers averaged 0.098 (range = 0.023 to 0.168); that of propranolol averaged 0.445 (range = 0.126 to 0.813). Using the multiple-indicator dilution-curve method, shunts greater than 15 microns in diameter were demonstrated between the portal and hepatic veins in six of eight cases, whereas shunts from the hepatic artery to the hepatic veins were absent. Perfusion of human livers obtained during hepatic transplantation is a fairly simple procedure that will allow researchers to gain new insights into cirrhosis in humans.

Angiography↗
PubMed1990

Isolation and partial characterization of an unusual human immunodeficiency retrovirus from two persons of west-central African origin.

An unusual human retrovirus was isolated from two patients with persistent generalized lymphadenopathy who originate from West-Central Africa and are currently residing in Belgium. Although the virus shared a number of the same biological and morphological properties as human immunodeficiency retrovirus type 1 (HIV-1) and HIV-2, significant antigenic differences could be demonstrated. Several of the viral proteins also differed in molecular weight from the corresponding HIV-1 and HIV-2 proteins. Partial chemical cleavage of the most highly conserved viral proteins resulted in patterns which differed from those of HIV-1 and HIV-2. Furthermore, nucleic acid hybridization experiments were capable of discriminating between the virus types. Sequence analysis of the viral U3 region revealed a unique enhancer organization not found in other immunodeficiency viruses. The data indicated that the new isolate is more closely related to HIV-1 than to HIV-2 but clearly differs in a number of important respects.

Africa, Central↗
PubMed1989

Pharmacokinetics of benzodiazepine antagonist Ro 15-1788 in cirrhotic patients with moderate or severe liver dysfunction.

Ro 15-1788, a benzodiazepine antagonist, has been advocated as a new treatment for hepatic encephalopathy. This drug is extensively metabolized by the liver in normal subjects. In the present study, we examined Ro 15-1788 disposition in eight healthy controls (Group I), eight cirrhotic patients with moderately impaired liver function (Pugh score less than 10, Group II) and eight patients with severe liver dysfunction (Pugh score greater than 10, Group III). The subjects of each group were age and sex matched. After an intravenous infusion of 2 mg Ro 15-1788 over 5 min, blood samples were taken at fixed intervals up to 7 hr after the infusion. Plasma levels of the drug were determined by capillary gas chromatography. In controls, Ro 15-1788 had a high plasma clearance [16.3 +/- 2.6 ml per min per kg (mean +/- S.D.)], a short half-life (45.7 +/- 8.5 min), a large volume of distribution (0.62 +/- 0.09 liter per kg) and a low plasma protein binding (45 +/- 6%). Plasma clearance was reduced markedly in both groups of cirrhotic patients (-57 and -74%, respectively); the volume of distribution was unchanged in Group II and moderately increased in Group III (+37%). The elimination half-life was markedly prolonged in Groups II and III (+66 and +210%, respectively). Plasma clearance and Pugh score were highly correlated in cirrhotic patients (r = 0.830, p less than 0.001). The plasma protein binding of Ro 15-1788 was lower in cirrhotics, resulting in a significant increase in the free fraction of the drug (+16% in Group II; +44% in Group III).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Systemic and hepatic hemodynamics after variceal hemorrhage: effects of propranolol and placebo.

Hepatic and systemic hemodynamics were measured in 19 cirrhotic patients with variceal bleeding enrolled in a controlled trial of propranolol for the prevention of rebleeding. The patients were studied on three separate occasions. The first study was performed before randomization within 24 h of the bleeding episode, once hemodynamic stabilization had been achieved. The second study was performed after 10 days of treatment, and the third after 6 mo without rebleeding. Propranolol dosage was titrated according to blood levels. Wedged and free hepatic venous pressures and the hepatic venous pressure gradient were recorded. Hepatic blood flow and cardiac output were also measured. Before treatment, the groups of patients treated with propranolol (n = 11) or placebo (n = 8) were comparable according to clinical, biochemical, and hemodynamic parameters. After 10 days, hepatic venous pressure gradient decreased similarly in the two groups (-20% in the propranolol group, -25% in the placebo group). Cardiac output fell only in the propranolol group (-40%). Hepatic blood flow remained unchanged in either group. After 6 mo, hepatic venous pressure gradient remained lower than the values from the first (within 24 h of bleeding) study in both the propranolol group (n = 5) and the placebo group (n = 6). Our results suggest that portal pressure increases shortly after hemorrhage with a return to baseline values 10 days later, and that propranolol does not further magnify these changes. Spontaneous changes in hepatic hemodynamics after variceal hemorrhage must be taken into account when evaluating the effect of pharmacologic agents on portal pressure.

Adult↗
PubMed1987

Emergency portacaval shunt for variceal hemorrhage. A prospective study.

Emergency portacaval shunt for variceal bleeding is associated with a high operative mortality, particularly if used as a last resort. Because of this, a strong case has been made against emergency shunt. This report describes an experience with emergency portacaval shunt for the treatment of variceal bleeding when used systematically after hemodynamic stabilization and control of the bleeding episode with balloon tamponade, if necessary, in patients with mild or moderate liver disease. The population studied comprised 62 consecutive patients who rebled from varices while participating in a controlled trial of propranolol for the prevention of rebleeding. Of the 62 patients, nine died of massive hemorrhage and 53 survived the hemorrhage. Of the 53 survivors, 11 had severe liver disease and were not considered for shunt surgery. Of the remaining 42 patients with mild or moderate liver disease, 36 had emergency central portacaval shunt. The interval between endoscopic diagnosis of variceal bleeding and surgery averaged 19 +/- 3 hours (mean +/- SE). The operative mortality rate, defined as in-hospital mortality, was 19%. One- and 2-year survival rates were 78% and 71%, respectively. The incidence of postoperative hepatic encephalopathy was 36%; all patients responded favorably to protein restriction and lactulose. Thus, under specific conditions, emergency portacaval shunt results in an acceptable long-term survival rate. In patients with mild or moderate liver disease, emergency portacaval shunt should be considered when other forms of treatment for the prevention of variceal rebleeding have failed.

Emergencies↗
PubMedDate not supplied

Presinusoidal portal hypertension in non-alcoholic cirrhosis.

The simultaneous measurement of wedged hepatic vein pressure (WHVP) and portal vein pressure (PVP) was performed in 156 cirrhotic patients. In the 110 alcoholic cirrhotic patients (97 micronodular and 13 macronodular cirrhosis), WHVP and PVP were closely related (25.8 +/- 6.3 vs. 25.9 +/- 6.3 mm Hg; p = not statistically significant). The difference between the two parameters was greater than 4 mm Hg in only six patients. In the 46 patients with nonalcoholic cirrhosis (41 macronodular and 1 micronodular cirrhosis; 4 primary biliary cirrhosis), PVP was significantly higher than was WHVP (25.8 +/- 6.2 vs. 21.7 +/- 6.8 mm Hg; p less than 0.001); in 20 patients, PVP exceeded WHVP by more than 4 mm Hg, and the mean difference was 7.5 mm Hg. There was no correlation between the porto-hepatic gradient and total hepatic blood flow measured by the indocyanine green single injection method or the portal fraction of total hepatic blood flow measured by indicator dilution curves. It is concluded that: (i) measurement of WHVP in alcoholic cirrhosis provides a reliable estimate of the severity of the portal hypertension, and (ii) hemodynamic evaluation of nonalcoholic cirrhosis should include PVP measurement in order to avoid underestimation of the porto-hepatic gradient.

Hepatic Veins↗
PubMedDate not supplied

Effect of propranolol on hepatic and systemic hemodynamics in dogs with chronic bile duct ligation.

Propranolol has been reported to reduce portal and wedged hepatic vein pressures in man and may be useful for the prevention of variceal bleeding. However, its mechanism of action remains unclear. We have examined the effect of propranolol on the systemic and hepatic circulations in dogs with chronic bile duct ligation and secondary biliary cirrhosis. Under anesthesia, eight dogs received four increasing doses of propranolol as an i.v. bolus followed by continuous infusion. Systemic and hepatic hemodynamic parameters were measured in basal conditions and after a 30 min infusion for each dose. Portal vein and hepatic artery blood flows were measured with electromagnetic flow meters. All dogs had portal hypertension (portal venous pressure 15.3 +/- 0.8 mm Hg), a hyperdynamic circulation and severe liver disease resulting in a marked decrease of propranolol systemic clearance (8.75 ml per min per kg) and extraction (40%). The first dose of propranolol induced a decrease in heart rate (-27%) and in cardiac index (-21%), and an increase in systemic vascular resistance (+20%). With increasing doses, the systemic vascular resistance decreased with an increase in the cardiac index. Propranolol was not associated with significant modifications of hepatic hemodynamics: portal, wedged and free hepatic venous pressures and hepatic artery blood flow were stable, and portal blood flow decreased slightly at very high propranolol levels. In seven dogs studied without dissection of the hepatic vessels, there was a small decrease in portal pressure, but not in wedged and free hepatic venous pressures with increasing doses of propranolol. Thus, in dogs with intrahepatic portal hypertension, propranolol has significant effects on systemic hemodynamics, but only minimal effects on the hepatic circulation.

Animals↗
PubMedDate not supplied

Propranolol for the prevention of recurrent variceal hemorrhage: a controlled trial.

We conducted a prospective, randomized single-blind trial of propranolol for the prevention of recurrent variceal bleeding. Seventy-nine patients shown to have variceal hemorrhage at endoscopy were included in the study within 72 hr following diagnosis. Fifty-seven patients had alcoholic cirrhosis, 10 cryptogenic cirrhosis, 6 posthepatitic cirrhosis, 4 biliary cirrhosis, 1 portal vein thrombosis without cirrhosis and 1 idiopathic portal hypertension. The severity of liver disease at inclusion was assessed according to the Pugh modification of the Child-Turcotte classification: 9 (11%) had Class A; 41 (52%) Class B, and 29 (37%) Class C disease. Patients were randomly assigned by sealed envelope to the propranolol group (42 patients) or the placebo group (37 patients). Propranolol dosage was titrated in order to produce plasma concentrations of propranolol of 50 to 150 ng per ml. beta-blockade was also confirmed by isoproterenol testing. The cumulative percentages of patients free of rebleeding 1 and 2 years after inclusion were 31 and 21% in the propranolol group, and 25 and 17% in the placebo group; both differences were not significant. Cumulative 1 and 2 years survival were also comparable: 64 and 54% in the propranolol group vs. 70 and 63% in the placebo group. There was no evidence for a therapeutic effect of propranolol after adjusting for potential confounding variables by multiple logistic regression. We conclude that propranolol is not effective for the prevention of variceal rebleeding, when administered early following the initial bleed, in cirrhotics unselected with respect to the severity of the liver disease.

Clinical Trials as Topic↗
PubMedDate not supplied

Intrahepatic pressure measurement: not an accurate reflection of portal vein pressure.

Previous studies have established the reliability of percutaneous portal venous pressure measurement using a Chiba needle, a procedure requiring fluoroscopic guidance. Intrahepatic pressure has been advocated by some as a simple and safe index of portal venous pressure. The aim of this study was to examine the reliability of intrahepatic pressure measurement and its relationship to portal venous pressure. Fifty patients requiring liver biopsy were included: 29 with cirrhosis (n = 20 micronodular, n = 9 macronodular) and 21 with various hepatic disorders but no cirrhosis. The procedure was performed under fluoroscopic guidance, using a Chiba needle connected to a manometer by a saline-filled catheter. Immediately prior to biopsy, each patient underwent measurement of: (i) 3 to 5 separate intrahepatic pressures, the intraparenchymal site being inferred by the lack of blood or bile return; and (ii) portal and hepatic venous pressures, the intravascular position of the needle being ascertained by the reflux of blood and the vessel identified with injection of contrast. Intrahepatic pressure measurements showed great intraindividual variability (variation coefficient up to 115%). Mean intrahepatic pressure (13.19 +/- 8.32 mm Hg) was similar to portal venous pressure (14.43 +/- 6.10 mm Hg) in the noncirrhotics but significantly lower in the cirrhotics (intrahepatic pressure = 18.34 +/- 8.82 mm Hg, portal venous pressure = 22.52 +/- 9.47 mm Hg; p less than 0.01). The difference between these two parameters exceeded 3 mm Hg in 50% of patients (mean = 9 mm Hg, range = 4 to 19 mm Hg), both in cirrhotics and noncirrhotics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Severe cholestasis leads to vitamin D depletion without perturbing its C-25 hydroxylation in the dog.

The role of the liver as a contributory factor in the vitamin D deficiency of cholestatic liver disease has been studied in vivo in dogs with chronic bile duct ligation, whereas controls underwent diversion of the bile flow through the urinary bladder via a choledococystostomy anastomosis. The hepatic extraction of vitamin D3 was evaluated by the multiple indicator dilution technique, and the formation of 25-hydroxyvitamin D3 was assessed by directly sampling the hepatic effluent for up to 150 min after vitamin D3 administration. The serum and hemodynamic data indicate that dogs with chronic bile duct ligation had severe cholestasis and hepatocellular injury; histologically, macronodular cirrhosis was present. Dogs with choledococystostomy anastomosis had normal livers and normal liver function. The data indicate that the absence of normal bile flow into the intestinal lumen led to a progressive depletion of vitamin D reserve in both animals with choledococystostomy anastomosis and those with chronic bile duct ligation. However, neither the hepatic fractional extraction of vitamin D3, its hepatic clearance nor its transformation into 25-hydroxyvitamin D3 was significantly changed by chronic bile duct ligation. The results of the present studies indicate that the hepatic handling of vitamin D3 including its C-25 hydroxylation, is well preserved in the presence of severe cholestasis. They also suggest that the state of vitamin D depletion which often accompanies chronic cholestatic liver disease can largely be accounted for by factors such as secondary malabsorption of the vitamin due to the absence of adequate amounts of bile salts in the intestinal lumen, or by other factors which seem independent of the hepatic metabolism of vitamin D.

Animals↗
PubMedDate not supplied

Surgical treatment of severe postshunt hepatic encephalopathy.

Hepatic encephalopathy is a major complication of portal-systemic shunts with an incidence ranging up to 52%. A small fraction of these patients are refractory to medical therapy. Shunt ligation and colonic procedures are the main surgical approaches. The goal of the latter is to diminish the colonic absorption of nitrogenous substances which are involved in the pathophysiology of hepatic encephalopathy. Six patients, whose average age was 55.7 +/- 2.6 years, were operated for severe postshunt encephalopathy requiring 4.3 +/- 0.9 admissions for a total duration of 76 +/- 26 days over 1-11 years. One patient had undergone a splenoral shunt and 5 had a portacaval shunt. One ligation of the shunt and 5 colon exclusions were performed. The average postoperative hospital stay was 21.5 +/- 3.9 days. The mean follow-up was 47 +/- 20 months. The patient with the shunt ligation remains free of encephalopathy 94 months after the procedure and has not bled from his esophageal varices. Among the 5 colon exclusion patients, there were 1 death and 3 complications. Three patients were completely relieved of their hepatic encephalopathy. One of those 3 died of a subarachnoid hemorrhage 28 months after the surgery. The fourth still needs medication to control a persistent, although improved, encephalopathy that required 2 further hospitalizations. Colon exclusion is a useful intervention in very selected cases. It has a lower operative mortality than total colectomy and the advantage over shunt ligation of not reestablishing hypertension in the portal system.

Hepatic Encephalopathy↗
PubMedDate not supplied

Smokers can learn to influence their urge to smoke.

Forty heavy smokers participated in a within-subject experiment in which the association between smoking-related cues and nicotine intake was made conditional on two neutral stimuli. Two colored cards indicated whether smoking-related cues, placed on the cards, would or would not be followed by nicotine intake. In the presence of each card, subjects were asked to rank their urge to smoke before and during the exposure to the smoking cues. The results of the present study revealed that the predictive value of a cue, in regard to the occurrence of nicotine intake, strongly determines its ability to generate craving. It was concluded that participants learned a modified predictive value of smoking cues, through a process of conditioning, and in this way influenced their urge to smoke. Furthermore, the findings suggest the reconditioning of CS-US associations as an aid in the treatment of smoking addiction.

Adult↗