Publications by authors named "Rector W"

Background And Aims: To assess the effect of warfarin anticoagulation therapy (AC) on the incidence of colon bleeding after elective colonoscopy with polypectomy and to identify independent predictors of post-polypectomy colon bleeding.

Methods: This was a retrospective cohort analysis. Patients interrupting warfarin AC therapy for polypectomy (AC group) were matched on age (+/- 3 years) with up to two patients who underwent polypectomy but were not receiving AC (non-AC group).

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Objectives: Elevation of plasma norepinephrine concentration in patients with cirrhosis and ascites is attributed to sympathetic activation due to arterial underfilling. Plasma norepinephrine should thus be normal in patients without sodium retention. We examined the prevalence and determinants of elevated plasma norepinephrine concentration in compensated cirrhosis.

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Sodium retention is triggered in rats with experimental liver injury at a critical threshold of liver function. We compared liver function and sodium retention in serially studied patients with alcoholic cirrhosis to determine whether a similar threshold exists in human beings. Antipyrine, caffeine, and cholic acid clearance were measured in 35 men with alcoholic liver disease.

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Purpose: To test the peripheral arterial vasodilation hypothesis of sodium retention in cirrhosis. This states that sodium retention is triggered by arterial underfilling and predicts that development of sodium retention will be associated with significant and related declines in indices of arterial filling that reverse when sodium retention resolves.

Design: Longitudinal evaluation of a cohort of patients with alcoholic liver disease.

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Purpose And Patients And Methods: The relationship of plasma renin activity (PRA) to indices of circulatory filling and other possible determinants of renin secretion was studied in 31 men with alcoholic liver disease. Characteristics of patients with normal and increased PRA values were examined. Significant differences guided subsequent simple and multiple regression analysis.

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A pathological state of arterial vasodilation has been postulated to cause the increased cardiac output commonly observed in cirrhosis. Further, subsequent arterial underfilling has been proposed as the stimulus to sodium retention and ascites formation. Left ventricular size during the cycle of a cardiac contraction is predictably altered by a decrease in afterload.

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Less complex methods of measuring hepatic metabolic capacity are needed. A simplified caffeine clearance test was evaluated in 23 patients with stable alcoholic liver disease. First, saliva caffeine concentrations were measured over a 24-h caffeine-free interval.

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We investigated the occurrence of alcoholic autonomic dysfunction in patients with alcoholic cirrhosis in order to define its prevalence and relationship to renal sodium retention. Forty-seven alcoholics and 16 age-matched normal subjects were evaluated. Thirty-seven patients had liver disease (13 with and 24 without ascites), and 10 patients had normal hepatic function.

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Vasopressin is often used to treat variceal hemorrhage. However, its efficacy is uncertain, and its portal hemodynamic effects in this setting are unknown. Eleven patients with alcoholic liver disease and bleeding varices were given vasopressin (0.

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Portal pressure was monitored by means of an indwelling hepatic vein balloon catheter in patients with alcoholic cirrhosis and bleeding varices to determine the safety and feasibility of the technique and its value in predicting recurrence of bleeding. Forty patients were enrolled. Central venous access could not be achieved in 4 patients (10%).

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We tested the hypothesis that increased plasma glucagon concentration resulting from portal-systemic shunting or liver dysfunction causes arterial vasodilation and thereby stimulates sodium retention in cirrhosis. Twenty-seven studies were performed in patients with alcoholic liver disease, 11 of whom had ascites. Liver function was quantitated as the elimination rate of antipyrine, caffeine, and stable isotopes of cholic acid administered both orally (2,2,4,4-2H) and intravenously (24-13C).

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The aim of this study was to determine whether liver function and portosystemic shunting are related to renal sodium retention in alcoholic liver disease. Twenty-three studies were performed; 10 patients had ascites. Liver function was assessed from the plasma elimination rates of antipyrine, caffeine and stable isotopes of cholic acid, the latter administered both orally [2,2,4,4-2H] and intravenously [24-13C].

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Increased blood volume, atrial size, and plasma concentration of atrial natriuretic factor are described in cirrhosis. Their interrelationships were examined in 17 men with alcoholic liver disease, 7 with and 10 without ascites. Atrial size was determined by two-dimensional echocardiography.

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Nitroglycerin is reportedly an effective treatment for portal hypertension. However, the effects of graded doses have not been examined. We administered nitroglycerin intravenously to 10 patients with alcoholic cirrhosis, beginning at 10 micrograms/min and doubling the dose every 10 min thereafter until mean arterial pressure fell 10-15 mmHg.

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The pathogenesis of variceal hemorrhage is not well understood. Portal pressure and gastroesophageal collateral (azygous) blood flow are similar in patients with cirrhosis with or without a history of variceal bleeding. However, acute increases in these parameters in individual patients might predispose them to variceal rupture.

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Immunologic syndromes are associated with hepatitis B viral (HBV) infection. However, mononeuropathy multiplex (MM), a syndrome in which immune factors may play a role, is rare in acute HBV infection. Few cases of MM associated with HBV infection have been reported.

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Purpose: Pica, particularly ice-eating (pagophagia), is a recognized symptom of iron deficiency. The value of pica as a clue to the etiology of blood loss has never been studied.

Patient Population: Fifty-five unselected patients with iron-deficiency anemia due to gastrointestinal blood loss evaluated by a gastroenterology referral service at a city hospital.

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We measured the coronary, systemic, and splanchnic effects of vasopressin and vasopressin plus nitroglycerin in 8 stable patients with alcoholic cirrhosis. Vasopressin (0.1-0.

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Budd-Chiari syndrome secondary to membranous obstruction of the intrahepatic inferior vena cava is a treatable form of chronic liver disease. I report a patient with portal hypertension in whom distortion of the inferior vena cava by cirrhosis and increased intraabdominal pressure initially suggested this condition. The correct diagnosis was made by obtaining lateral views during inferior vena cavography, which demonstrated a tapered, rather than membranous, obstruction, along with normal hepatic venous anatomy and pressure and markedly increased portal vein pressure during transhepatic puncture with a thin needle.

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Portal hypertension occurs in several aetiologically distinct disease states associated with either increased flow or increased resistance in the portal venous system. The morbidity and mortality observed are the result of ascites formation, impaired hepatic metabolism, encephalopathy and, most ominously, variceal haemorrhage. Patients with conditions in which there is relatively little hepatic parenchymal damage (non-cirrhotic portal hypertension) tend to have fewer episodes of encephalopathy and are better able to tolerate bleeding episodes than those patients with underlying cirrhosis.

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We measured total blood volume (125I-albumin), cardiac dimensions and function (echocardiography with Doppler), systemic hemodynamics (blood pressure and pulse), and plasma renin activity and norepinephrine levels in cirrhotic patients with and without ascites to assess the likelihood that either diminished central or arterial filling is the stimulus to sodium retention. Patients with ascites (n = 9) had significantly increased total blood volume, cardiac output, pulse rate, plasma renin activity, and plasma norepinephrine concentration, as well as decreased systemic vascular resistance and arterial blood pressure compared with patients without ascites (n = 8). Left atrial size was similar in the two groups but significantly larger than in normal control subjects.

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Cirrhosis is frequently associated with increased arterial plasma renin activity. This could be the result of increased renin production or diminished renin clearance. We measured plasma renin activity in simultaneous portal, hepatic vein, and femoral artery blood samples in 7 patients with clinically stable alcoholic cirrhosis to determine whether hepatic extraction of renin is reduced and whether, as has been suggested, there is a splanchnic source of plasma renin activity in this condition.

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The prevalence of hepatitis D virus (HDV) infection in patients with hepatitis B virus (HBV) infection in the mid-United States is not well defined. We tested 65 patients seen between 1983 and 1986 with HBV infection in Denver for evidence of coexisting HDV infection. Five patients had anti-delta (delta) antibody.

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