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Biomedical subjects

E Begg

Publications and source records attributed to E Begg.

12 recordsLinked to original sources
PubMed2001

Fifteen years of drug information in Christchurch Hospital.

AIM: To determine changes in numbers, demography and type of questions posed to the drug information service (DIS) at Christchurch Hospital over the last fifteen years. METHODS: The database of the DIS was used to retrieve data for one-year periods including the period of establishment in 1985/1986, 1993/1994 and 1999/2000. RESULTS: The number of questions per month increased from 26 in 1985/1986 to 284 in 1999/2000. The majority of questions have related to adverse drug reactions, contraindications/precautions, drug selection, interactions, and administration/dosage. Questions on drug interactions showed the greatest relative increase, from 8% to 19% of all questions. A disproportionate increase in requests came from primary care, which provided 14% of questions in 1985/1986 and 38% in 1999/2000. Computer databases are the major resource used currently whereas journal articles and textbooks dominated in 1985/1986. CONCLUSIONS: There has been a marked increase in use of the DIS despite a relatively constant population base. This may reflect an increased awareness of both the availability of the service and recognition of the complexity of medicines. The computer database is a useful reference source, decreasing repetition of search pathways and allowing audit to assist in the ongoing improvement of the service.

Data Interpretation, Statistical↗
PubMed1997

The effects of pathophysiological increments in brain natriuretic peptide in left ventricular systolic dysfunction.

Plasma levels of brain natriuretic peptide (BNP) are raised in patients with left ventricular impairment and may play a role in the adaptation to left ventricular impairment. Manipulation of BNP levels may have therapeutic potential. The effects of BNP have not been well studied in patients with left ventricular impairment. We studied the effects of low-dose BNP infusion, reproducing the increment in plasma BNP seen with progression from mild to severe heart failure in patients with impaired left ventricular systolic function. BNP was infused in a placebo-controlled, single-blind, crossover design at a rate of 3.3 pmol x kg(-1) x min(-1) over 4 hours to 8 patients with a history of congestive heart failure and persistent impairment of left ventricular systolic function (left ventricular ejection fraction <35%). Endocrine, renal, and hemodynamic effects were measured. Compared with time-matched placebo-control, BNP infusion decreased mean systemic arterial pressure (peak decrease, 17.1 mm Hg; P=.04), mean pulmonary artery pressure (peak decrease, 6.1 mm Hg; P=.007), mean pulmonary capillary wedge pressure (peak decrease, 5.5 mm Hg; P=.04), and systemic vascular resistance (peak decrease, 1400 dyne s(-1) cm(-5); P=.015), but cardiac output and heart rate were unchanged. Urinary volume and urinary excretion of sodium and potassium were not altered. BNP infusion increased plasma cGMP (2.3-fold change, P=.002). Plasma atrial natriuretic peptide levels were increased for the first hour of BNP infusion (peak increase, 11.5 pmol/L; P=.005). Plasma aldosterone levels were unchanged during but increased over time-matched control levels after the end of the BNP infusion (peak increase, 90 pmol/L; P=.02). Plasma renin activity and cortisol and catecholamine levels were unchanged. Low-dose infusion of BNP causes favorable hemodynamic changes and relative neurohormonal suppression but has attenuated renal effects in patients with impaired left ventricular systolic function.

Aged↗
PubMed1994

Dose proportionality of bisoprolol enantiomers in humans after oral administration of the racemate.

Dose proportionality of racemic bisoprolol and the stereoselectivity of its enantiomers were studied after single oral dosing of 5 to 40 mg of bisoprolol hemifumarate in eight healthy male volunteers in an open-label, randomized, four-way cross-over trial. There were dose-proportional increases in mean peak plasma concentration (Cmax) and area under the plasma concentration versus time curve (AUC) values for the racemate and the individual enantiomers. No statistically significant differences were detected between the mean half life (t 1/2), Cmax, and time to reach Cmax (tmax) of the R- and S-isomers at each of the four dose levels studied. These findings support dose proportionality and absence of stereoselective pharmacokinetics for bisoprolol in the dose range studied.

Administration, Oral↗
PubMed1989

A prospective randomised trial comparing individualised pharmacokinetic dosage prediction for aminoglycosides with prediction based on estimated creatinine clearance in critically ill patients.

A prospective randomised trial was conducted in critically ill patients to evaluate a computer aided pharmacokinetic method of aminoglycoside dose prediction based on 3 measured plasma concentrations following the loading dose. The ability of this method to achieve therapeutic plasma aminoglycoside concentrations early in the course of treatment was compared with that of a nomogram approach based on creatinine clearance estimated using the formula of Cockroft and Gault. Ninety-two percent of patients in the computer group achieved peak plasma concentrations within the optimum range of 6-10 mg/l at 48-72 h compared with 21% of control group patients (p = 0.0009). The mean peak plasma concentration of 7.45 mg/l at 48-72 h in the computer group was closer to the target concentration of 8 mg/l than was the 5.14 mg/l in the control group (p = 0.0004). There was no significant difference between the groups in measured indices of renal function, both groups showing an improvement in mean estimated creatinine clearance from the beginning to the end of the course of treatment. Dosing based on individualised pharmacokinetic data is therefore a more reliable method of achieving therapeutic blood concentrations early in the course of treatment than is nomogram based dosing. Other studies suggest that this should be associated with a reduction in mortality in severe infections.

Adult↗
PubMed1983

Effects of phenytoin, phenobarbital, and ascorbic acid on misonidazole elimination.

The kinetics of an oral dose (1.0 gm/m2) of the 2-nitroimidazole radiosensitizer misonidazole were studied in three groups of six healthy subjects before and after a 1-wk course of phenytoin, phenobarbital, or ascorbic acid. Phenytoin and phenobarbital decreased mean misonidazole half-life by 27% and 23% and the decrease was associated with the respective increases in mean clearance of 42% and 31%. The area under the plasma concentration-time curve for the metabolite O-desmethylmisonidazole increased correspondingly. Volume of distribution of misonidazole was unchanged. After treatment with ascorbic acid there was a very small increase in the mean clearance of misonidazole, but there was no significant change in other kinetic parameters. Induction by phenytoin and phenobarbital of the oxidative metabolism of misonidazole is the most likely mechanism responsible. Deliberate induction of a patient's metabolism may help to reduce the neurotoxicity associated with the use of the drug. The efficacy of the radiosensitizing action of the drug is unlikely to be compromised under these conditions since peak plasma concentrations of misonidazole were not affected by treatment with either phenytoin or phenobarbital. The potentiation of the cytotoxic effects of misonidazole by ascorbic acid is unlikely to be related to a direct effect on the oxidative metabolism of misonidazole.

Adult↗
PubMed1980

Plasma and urine concentrations of acebutolol and its acetyl metabolite in patients with renal functional impairment.

This study was undertaken to examine the elimination of orally administered acebutolol and its major acetyl metabolite in four healthy controls and seven patients with varying degrees of renal functional impairment. Analysis of acebutolol and its metabolites was undertaken using a high performance liquid chromatographic method. Plasma concentrations of acebutolol and the acetyl metabolite were greater in patients with renal functional impairment than in controls. The elimination of acebutolol did not appear to be influenced by impaired renal function. However the elimination of the acetyl metabolite decreased as renal function diminished. Acebutolol has a major non-renal route of elimination, but the acetyl metabolite (also a beta-adrenoreceptor blocking drug) is primarily excreted by the kidney and may accumulate in renal failure.

Acebutolol↗
PubMed1979

Acebutolol in the treatment of patients with hypertension and renal functional impairment.

Eleven patients with hypertension and varying degrees of stable renal functional impairment were treated with the beta adrenoreceptor blocking drug, acebutolol (Sectral). Parameters of renal, cardiovascular and respiratory function were measured immediately prior to treatment and again after four and 12 weeks. In five patients the blood pressure was well controlled throughout the 12-week period on 400mg of acebutolol each morning, in three the blood pressure was satisfactory after four weeks treatment with 400mg each morning but control had been lost by 12 weeks, while in the remaining three patients 800mg each morning was ineffective. There was no significant change in the mean glomerular filtration rate of the 11 patients but in two of these patients with severe, but stable, chronic renal failure the introduction of acebutolol was associated with a decline in renal function and the onset of uraemic symptoms. One of these patients showed an improvement when the acebutolol was discontinued but the other required regular dialysis treatment. Beta adrenoreceptor blockers should be used cautiously in severe renal failure.

Acebutolol↗