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Biomedical subjects

M Weatherall

Publications and source records attributed to M Weatherall.

At least 55 records · Page 3Linked to original sources
PubMed1992

Medications and their monitoring in Parkinson's disease in Dunedin.

AIMS: to establish the patterns of drug administration and monitoring in people with Parkinson's disease. METHOD: a total community sample was obtained. One hundred and one of the 116 people with Parkinson's disease in Dunedin, who were alive on 31 July 1990, had a full medical assessment. RESULTS: the general practitioner made the diagnosis in 51%, a neurologist in 22%, a geriatrician in 18%, and other in 9%. The general practitioner provided prescriptions for 51 of the 68 people living in the community, a neurologist for 11, and a geriatrician in six cases. The general practitioner provided prescriptions for 23 of the 33 living in an institution, and a geriatrician in ten cases. Medical review took place more frequently than three monthly in 49 cases. There were 81 general practitioners in practice on the prevalence day in the study area. Thirty-six had no patients with Parkinson's disease, 30 had one or two, and the other 15 had varying numbers. Fifty-eight of the 90 patients taking levodopa were taking it as the only therapy. Eight patients were taking phenothiazines. There was a high incidence of side effects and 70 patients had long term complications including loss of effectiveness over time, the end of dose and the on-off phenomena, and dyskinesias. CONCLUSIONS: monitoring of treatment appeared satisfactory but major concerns about drug management included the high use of levodopa monotherapy and the concurrent use by general practitioners of phenothiazines in eight cases. Because most general practitioners have very few patients with Parkinson's disease they will not develop the experience to manage complicated drug regimens in people whose management tends to become more difficult with time. With selegiline and controlled release levodopa only being available on specialist prescription, we suggest that all people with Parkinson's disease should have the benefit of a specialist review at least every two years.

Aged↗
PubMed1992

Is the prevalence of Parkinson's disease in New Zealand really changing?

The prevalence of idiopathic Parkinson's Disease (IPD) in Dunedin, New Zealand on 31st July 1990 was 110.4/100,000. When corrected to a standard population based on the 1960 U.S. census, the prevalence fell to 76.0/100,000 due to changes in the age structure of the population. The corrected prevalence in Wellington (another New Zealand city), in 1962 was 99.6 (before the introduction of levodopa), and in Aberdeen, Scotland in 1984 was 102.7. The principal difference was fewer people under 65 years of age in our study. Case finding methods and diagnostic criteria were similar in all three studies, and case ascertainment was adequate. Under representation of younger people could be due to either a lower incidence rate or poorer survival due to treatment with high doses of levodopa compounds. Prospective research is required to explain our findings.

Adult↗
PubMed1985

The effect of tiaprofenic acid on blood pressure control in treated hypertensive patients.

Eleven patients with osteoarthritis and mild hypertension completed an 8-week, double-blind crossover study in which 200 mg tiaprofenic acid 3-times daily or placebo were substituted for their normal non-steroidal anti-inflammatory therapy. Systolic blood pressure was significantly higher on tiaprofenic acid therapy than on placebo and plasma renin activity was significantly lower on active treatment. No significant changes were seen in biochemical parameters, though the weight of the patient was also higher on tiaprofenic acid than on placebo. Duration of morning stiffness was also lower on tiaprofenic acid than on placebo. Blood pressure on tiaprofenic acid was not different from baseline readings on other non-steroidal anti-inflammatory drug therapy. This study suggests that tiaprofenic acid, like other non-steroidal anti-inflammatory agents, may interfere with blood pressure control in treated hypertensive patients.

Aged↗
PubMed1982

Inhibition of human lymphocyte transformation by two aryloxyalkylamidines.

The incorporation of [3H]thymidine into human lymphocytes stimulated by phytohaemagglutinin (PHA) was inhibited by anilino-N-2-m-chlorophenoxypropylacetamidine (501C) and xylamidine. These amidines antagonize 5-HT, but 5-HT did not alter [3H]thymidine incorporation. 501C inhibited PHA-induced lymphocyte transformation as observed by [3H]thymidine incorporation, [3H]uridine incorporation, [3H]leucine incorporation, DNA content, potassium content, and histological examination. 501C also inhibited increased [3H]thymidine incorporation in human mixed lymphocyte cultures. The IC50 of 501C for inhibition of these processes lay between 4 and 8 microM. When added late in culture (after 6-8 h) 501C was less effective. Possible mechanisms by which 501C inhibits transformation are discussed.

Amidines↗
PubMed1981

Inhibition of lymphocyte transformation by mepacrine and chloroquine.

Mepacrine inhibited uptake and the incorporation of leucine, thymidine and uridine into acid-insoluble material in human lymphocytes stimulated by phytohaemagglutinin (PHA) in vitro. The IC50 for each uptake was of the order of 2 microM. Mepacrine was inhibitory if applied at any time up to 48 h after PHA. The inhibition differed from that produced by colchicine and prostaglandin E1. The dose-response curve was steep, nearly all incorporation being inhibited by 2 x IC50. Chloroquine also had a steep dose-response curve, was about one-fifth as potent as mepacrine and was maximally effective in the first 6 h after PHA.

1-Methyl-3-isobutylxanthine↗
PubMed1978

Mathematical prediction of drug distribution in vivo: studies with doxantrazole in rats.

A pharmacokinetic model incorporating 14 compartments and 29 transfer coefficients has been developed from experimental data obtained after intravenous administration of a single dose to describe the distribution of doxantrazole in the rate. The distribution calculated from the model agreed closely with that determined experimentally. In addition, the model was able to predict with considerable accuracy the distribution of doxantrazole after repeated dosing.

Animals↗