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Biomedical subjects

F J Dudley

Publications and source records attributed to F J Dudley.

89 records · Page 5Linked to original sources
PubMed1971

The serum concentration of the third component of complement beta-1C-beta-1A in liver disease.

Serum C(3) (beta(1C)/beta(1A)) has been measured in normal individuals and the range found is in agreement with findings of other authors (85-370 mg/100 ml). In 18 patients with acute hepatitis and massive necrosis serum C(3) was consistently reduced to below 50% of normal. In other patients with acute hepatitis the serum C(3) concentration was normal. In the majority of the 150 patients with chronic liver disease serum C(3) concentration was normal. However, 10 patients (six with active chronic hepatitis, four with cryptogenic cirrhosis) had hypocomplementaemia. The reason for the depression is not clear but could reflect either decreased synthesis or increased consumption, or a combination of the two.

Acute Disease↗
PubMedDate not supplied

Hepatorenal syndrome without avid sodium retention.

A urinary sodium concentration [U(Na)] of less than 10 mmoles per liter is considered important in differentiating hepatorenal syndrome from other causes of progressive renal impairment in patients with liver disease. However, occasionally, patients with hepatorenal syndrome have been recognized in whom the U(Na) is consistently greater than 10 mmoles per liter. Eight such patients, in all of whom there was no clinical or laboratory evidence to implicate other causes of progressive renal impairment, were identified. The clinical features, hepatic and renal status and hospital course were compared with eight other patients who had hepatorenal syndrome and a U(Na) consistently less than 10 mmoles per liter. The mean U(Na) was 24 +/- 4 mmoles per liter in the high U(Na) group and 3.7 +/- 1.8 mmoles per liter in the low U(Na) group. All patients in both groups had acutely decompensated alcoholic hepatitis of similar severity and activity. The high U(Na) group had significantly less clinical ascites and peripheral edema and higher serum levels of sodium and chloride both at the onset of the hepatorenal syndrome and throughout the clinical course. Significant differences in the serum potassium and blood urea nitrogen levels became apparent between the two groups of patients as renal failure progressed, and the mean average blood urea nitrogen to serum creatinine ratio was significantly higher (p less than 0.025) in the low U(Na) group (13.8 +/- 0.9 vs. 10.1 +/- 1.1). Mean urinary potassium concentration was significantly higher in the high U(Na) patients but urinary creatinine concentrations, specific gravity and sediment were similar in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMedDate not supplied

Renal sodium retention in cirrhosis: tubular site and relation to hepatic dysfunction.

Renal sodium handling, assessed by the response to acute saline loading, was investigated in 14 well-compensated, nonascitic alcoholic cirrhotics and six normal controls. Urinary sodium excretion in cirrhotic patients (199 +/- 141 mumoles per min) was significantly lower than in controls (387 +/- 104 mumoles per min; p less than 0.01) at 3 hr postinfusion. In contrast to controls, renal plasma flow and glomerular filtration rate did not increase in the cirrhotics in response to acute saline loading. Proximal fractional reabsorption of sodium was estimated by clearance techniques in the presence of a hypotonic diuresis. Cirrhotic subjects with impaired functional liver cell mass as assessed by antipyrine clearance were unable to decrease proximal fractional reabsorption of sodium significantly in response to saline loading. Assessment in the cirrhotics included measurement of hepatic vein pressure gradient, indocyanine green extraction ratio, indocyanine green clearance, and antipyrine clearance as indices of portal pressure, intrahepatic shunting, hepatic blood flow and functional hepatocellular mass, respectively. Urinary sodium excretion in the cirrhotics correlated strongly with antipyrine clearance (r = 0.839, p less than 0.0001) and weakly with portal pressure (r = 0.562, p = 0.037). No correlation was seen with the other indices of hepatic blood flow and shunting. The findings of this study suggest that alcoholic cirrhosis is associated with a decline in hepatocellular function which results in either a decreased clearance of a salt-retaining hormone or decreased synthesis of a natriuretic hormone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Detection of interferon-alpha expression by PCR in patients with chronic hepatitis C and hepatitis non-A, non-B.

The polymerase chain reaction (PCR) was used to examine expression of interferon-alpha (IFN A) genes in general and the expression of messenger RNA (mRNA) encoding the subtypes IFN-alpha-2 and IFN-alpha-4 in blood and liver biopsy samples from patients with chronic hepatitis C or hepatitis non-A, non-B (HC/HNANB) infection entered into a trial of IFN-alpha-2a therapy. Peripheral blood mononuclear cells (PBMC) from healthy controls and HC/HNANB infected patients were studied for their capacity to produce transcripts encoding IFN-alpha after stimulation with Sendai virus. Expression at the level of mRNA for IFN A and the subtypes IFN A2 and A4 was detected in both controls and HC/HNANB infected patients PBMC and no significant difference was seen in expression of IFN A transcripts or level of total IFN-alpha secreted into culture supernatants between controls and patients. Interferon A, and specifically IFN A2 and IFN A4 transcripts were detected in a high proportion of liver biopsies from patients with HC/HNANB infection. The presence of IFN A mRNA (and specifically IFN A2 and IFN A4) showed no correlation to histological improvement nor response to therapy. The use of PCR to detect those IFN A genes that are not expressed, thereby identifying subtypes that may be lacking, could be the key to the choice of IFN-alpha subtypes that are used for effective therapy.

Adult↗
PubMedDate not supplied

The management of acutely bleeding varices by injection sclerotherapy.

Acutely bleeding varices present a therapeutic dilemma because of the limited efficacy and high complication rates of conventional treatments. Over a period of 26 months, 56 episodes of acutely bleeding varices were treated with injection sclerotherapy as the initial management. Immediate control of haemorrhage was achieved in 91% of patients and control of bleeding during the hospital admission in 84%. Balloon tamponade and surgery were reserved for those patients in whom bleeding was not controlled by sclerotherapy; in 66% of patients the bleeding was controlled by sclerotherapy alone. Of the 56 episodes, 75% survived their admission to hospital. Acute injection sclerotherapy is as least as effective as conventional therapies in the control of bleeding with a low incidence of complications. The technique can be used in all patients irrespective of the severity of their liver disease and, when bleeding is controlled, allows the physician the choice of all the available prophylactic therapies.

Acute Disease↗
PubMedDate not supplied

Relapse of duodenal ulceration after healing with omeprazole.

The subsequent recurrence rate after duodenal ulcers were healed with omeprazole, 10 mg or 30 mg a day, was documented during a 12-month period in 55 patients. Endoscopy was performed if patients developed symptomatic recurrence; those patients who remained symptom-free at 12 months were also requested to undergo endoscopy to assess the incidence of asymptomatic recurrence. The proportion with symptomatic recurrence during the year was 56%. The median times (life-table analysis) to relapse were 50 and 39 weeks in the group that was treated initially with 30 mg and 10 mg of omeprazole, respectively, although this trend to slower relapse in the higher-dose group was not statistically significant. Five asymptomatic ulcers were detected in 11 asymptomatic subjects who agreed to a final endoscopy. The over-all recurrence rate was similar to previously-reported recurrence rates after the cessation of histamine H2-receptor antagonist drugs.

Clinical Trials as Topic↗