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Biomedical subjects

E Henderson

Publications and source records attributed to E Henderson.

180 records · Page 10Linked to original sources
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Serum antibody levels against T mycoplasmas in two North American Indian populations predisposed to spondylitis.

Serum antibody levels against T mycoplasmas (Ureaplasma urealyticum) were determined by the metabolic inhibition method in several populations. A higher prevalence of antibody was found in Haida Indians and Bella Coola Indians than in blood donors, patients with rheumatoid arthritis, and patients attending a VD clinic. Antibody levels did not correlate with the presence of spodylitis or the histocompatibility antigen HLA-B27, although both these Indian populations have a high prevalence of spondylitis and HLA-B27.

Antibodies, Bacterial↗
PubMedDate not supplied

Yersinia-related arthritis in the Pacific Northwest.

Serologic evidence of Yersinia enterocolitica infection was sought by agglutination testing in serum samples from several populations, including Haida Indians, Red Cross blood donors, and Caucasian patients with rheumatoid arthritis, ankylosing spondylitis, and Reiter's syndrome. No evidence was found to indicate that yersinial infection was etiologically related to Haida spondylitis or Reiter's syndrome. Four of 28 patients with acute arthritis were diagnosed from serologic evidence as having Yersinia-related arthritis.

Adult↗
PubMedDate not supplied

Treating rheumatoid arthritis early with disease modifying drugs reduces joint damage: a randomised double blind trial of sulphasalazine vs diclofenac sodium.

BACKGROUND: Current disease management in rheumatoid arthritis (RA) has moved towards "inverting the therapeutic pyramid" by introducing disease-modifying anti-rheumatic drugs (DMARDs) early. Despite the logic of early DMARD therapy, there is a dearth of supportive evidence for this approach. We report a randomised controlled trial comparing sulphasalazine monotherapy with diclofenac monotherapy in early RA. The primary aim was to provide unequivocal evidence that early DMARDs prevent erosive damage. The secondary aim was to evaluate if sulphasalazine used alone has comparable symptomatic benefits to NSAIDs. METHODS: 117 patients with RA for under 12 months of diagnosis (mean 2 months) were randomised (62 sulphasalazine; 55 diclofenac). Sulphasalazine patients comprised 76% women, and 58% were rheumatoidfactor positive. Diclofenac patients comprised 74% women, and 54% were seropositive. 36% completed 12 months of therapy (16 sulphasalazine; 26 diclofenac); sulphasalazine was given for a mean period of 21 weeks and diclofenac for a mean period of 33 weeks. Results were analysed on an intention to treat basis. RESULTS: After 12 months the mean number of new erosions in patients randomised to receive sulphasalazine was 2.0 (95%CI 0.9, 3.1) and in patients randomised to receive diclofenac was 7.5 (95%CI 4.1, 10.9; p = 0.002 by Student's unpaired t-test). An analysis of valid compliant completers showed the mean number of new erosions in patients who received 12 months therapy with sulphasalazine was 2.3 (95%CI 0.6, 4.0) and in patients who received 12 months diclofenac was 10.5 (95%CI 5.0, 15.9; p = 0.018 by Student's unpaired t-test). The Ritchie articular index, swollen joint counts and pain scores decreased with both sulphasalazine and diclofenac, with mean falls in both groups of 15-20% at 2 weeks and 30-40% at 4 and 8 weeks. There were no differences between treatments. Disease activity scores showed similar highly significant mean decreases within both treatment groups (P < 0.001 in all cases) of 0.5 at 2 weeks and 1.0 at 4 weeks; at 12 and 26 weeks they were significantly lower with sulphasalazine (p = 0.036 and 0.045). 75% of the patients given sulphasalazine and 65% of those given diclofenac had one or more adverse events with no major differences between treatments. CONCLUSIONS: These results show that an accelerated dosing schedule of sulphasalazine has identical effects to diclofenac in reducing symptoms, indicating it is a rapidly effective DMARD. They also provide unequivocal evidence, analysed on an intention to treat basis, that early treatment with sulphasalazine significantly reduces the extent of radiological progression in active RA.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Clinical experience with thrombolytic agents.

It is now possible through the administration of thrombolytic therapy to dissolve an obstructive thrombus in the coronary artery. On the basis of the pathophysiology of acute MI, this should translate into interruption of the ischemic process and benefit to the patient. Clinical trials with t-PA and SK have supported this concept by demonstrating preservation of LVF, reduction in congestive heart failure, and reduction in mortality. All clinical data point to the importance of early intervention and treatment in attaining maximal patient benefit. Studies have shown the safety and feasibility of early treatment in the emergency setting. In the era of thrombolytic therapy, there is an opportunity for the emergency physician and nurse to play a significant role in the treatment of the patient with acute MI. Prompt intervention with thrombolytic therapy in the emergency department will offer the patient the greatest opportunity for benefit.

Clinical Trials as Topic↗
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Behind the scenes.

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Congresses as Topic↗