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Biomedical subjects

A S Dixon

Publications and source records attributed to A S Dixon.

At least 19 recordsLinked to original sources
PubMed1992

Euthanasia.

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Ethics, Medical↗
PubMed1990

The evolution of clinical policies.

Physicians use clinical policies as guidelines in the day-to-day management of patients. Some policies, by reducing otherwise complicated dilemmas to simple rules, encourage improved patient outcomes, but some are adopted without any evidence of benefit; some may be extended beyond their proper limitations and others are used despite accumulating data that they are at best useless and at worst dangerous. Four stages, development, diffusion, domination, and disillusionment, may be recognized in the evolution of clinical policies. Social rather than scientific forces play a central role, and at each step characteristic errors in both reasoning and research may occur. Attempts to improve patient outcomes by encouraging more appropriate research methodology and increasing the ability of physicians to critically appraise published studies may not be successful unless account is also taken of the social forces that influence the use and abuse of clinical policies.

Attitude of Health Personnel↗
PubMed1988

A prospective endoscopic study of the effect of Orudis and Oruvail on the upper gastrointestinal tract, in patients with osteoarthritis.

The effect of ketoprofen, a nonsteroidal anti-inflammatory drug, was tested on the upper gastrointestinal tract (UGIT) in patients with osteoarthritis. The drug was given in two forms; as simple ketoprofen (Orudis) and as a slow release preparation (Oruvail), when the drug was not released into the stomach, but into the small intestine. These formulations were compared with indomethacin for endoscopically proven damage to the UGIT. Orudis and Oruvail produced similar damage to previously normal UGITs over 56 days; each formulation produced about a 50% incidence of ulceration and inflammation. Indomethacin, by comparison produced less damage. The results suggested that the direct action of ketoprofen (barrier breaking effect) adds little to the mechanism of gastric cytotoxicity of this drug, which may be assumed to be predominantly caused by a systemic effect of ketoprofen on gastric cytoprotective mechanisms.

Administration, Oral↗
PubMed1988

Clinical trial of intra-articular injection of sodium hyaluronate in patients with osteoarthritis of the knee.

A multi-centre randomized, double-blind, parallel-group clinical trial was carried out in 63 patients with osteoarthritis of the knee to compare the efficacy and tolerability of a course of intra-articular injections of 20 mg sodium hyaluronate with a similar course of injections of placebo. Treatment consisted of up to 11 injections over a 23-week period. Evaluation was by means of subjective symptom and activity assessments, serially during the course of treatment and also 25 weeks thereafter. Ten patients (5 of 30 on active treatment; 5 of 33 on placebo) were withdrawn prematurely. Pain on movement, assessed by visual analogue scale (VAS) showed statistically significant (p less than 0.05 to p less than 0.0001) reductions in mean scores throughout the first 11 weeks of treatment with sodium hyaluronate but smaller, non-significant, reductions with placebo treatment. The difference between treatments was significant (p less than 0.05) at 5 weeks. Pain at rest, also assessed by VAS, showed little change in mean scores with placebo but with sodium hyaluronate there was a progressive reduction which was significant (p less than 0.01) throughout the period from 5 to 23 weeks. The difference between sodium hyaluronate and placebo was significant (p less than 0.05 to p less than 0.002) at Weeks 5, 11, 15, 19 and 23. 'Activities of daily living' were assessed using a standard scale. There were small improvements with both treatments, significant at some assessments and somewhat greater with sodium hyaluronate than placebo, but there were no statistically significant differences between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

'There's a lot of it about': clinical strategies in family practice.

Is there a difference in the way family physicians and specialists deal with clinical problems? Family physicians, in contrast to specialists, work in a practice environment in which there is a high prevalence of symptomatic discomfort, but a low prevalence of frank disease. These circumstances result in clinical strategies that are very different to those used in secondary and tertiary levels of care, and which run counter to what are usually accepted as medical norms. The primary care physician must often diagnose what things are not, rather than what they are, must make management decisions prior to, or instead of, diagnostic decisions and must resist the temptation to be ;thorough' These imperatives are reflected in the language family physicians sometimes use in their conversations with patients. Clinical reasoning in primary care involves important but poorly understood intellectual processes which may be of significance to all levels of medicine.

Family Practice↗
PubMed1984

Giant cell (temporal) arteritis presenting with syncope.

Giant cell (temporal) arteritis presenting with syncope due to carotid sinus hypersensitivity is described. Although the association of giant cell (temporal) arteritis and carotid sinus hypersensitivity is known, there are no previous reports of syncope as the presenting feature of giant cell (temporal) arteritis.

Carotid Sinus↗
PubMed1984

Osteoporosis. An update on management.

Osteoporosis is the reduction of expected bone mass. This results in structural failure with an increased risk of fracture and it is the most common bone disorder encountered. Bone mass declines with age, and in some people will fall below the threshold for easy fracture. This loss is accelerated in the postmenopausal period. Trauma and the internal trabecular structure of bone are additional determinants of risk of fracture. Effective management of osteoporosis depends on identifying and treating those at risk before reaching the critical bone mass and presenting with skeletal failure. There are limitations to methods available for assessing bone loss, and the final arbiter of any treatment is prevention of fracture. Primary prevention involves maximising peak adult bone mass and reducing the rate of bone loss. This may be attained by exercise, adequate dietary calcium, and the identification and treatment of risk factors such as postmenopausal hormone replacement. Once skeletal failure has occurred, long term treatment is required to have a clinically significant effect. Increasing bone mass cannot be assumed to reduce the risk of fracture, and such a reduction has not been directly demonstrated for several agents. Calcium supplements, hormone replacement therapy and fluoride are probably effective in reducing fracture rate, particularly when used in combination, whereas the efficacy of anabolic steroids, calcitonin and diphosphonates is yet to be established. Vitamin D is only of use in coexistent osteomalacia. The limitation of significantly strengthening the skeleton during the life expectancy of the elderly must be realised.

Adult↗