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Biomedical subjects

R D Sturrock

Publications and source records attributed to R D Sturrock.

At least 91 records · Page 5Linked to original sources

Clinical analysis in intact erythrocytes using 1H spin echo NMR.

A new method of clinical analysis based on 1H spin echo NMR spectroscopy is presented. It is capable of providing information on six metabolites within viable erythrocytes, directly and without any preparative procedures prior to analysis except for cell separation and washing. Erythrocytes from patients with rheumatoid arthritis and Graves' disease are compared with cells obtained from healthy volunteers. The NMR detectable species in the cytosol of the cells are glutathione, ergothioneine, choline, creatine, glycine, lactate and to a lesser extent alanine and valine. Significant differences are observed between the ergothioneine pools in the rheumatoid group (P less than 0.01) compared to the control group. The glutathione: di-glutathione ratio can be assessed from the ratio, g2 to g4, taken from different signals in the glutathione molecule. The total concentration of glutathione present is easily assessed qualitatively but is more difficult to quantitate.

Adult↗

Enteroscopic diagnosis of small bowel ulceration in patients receiving non-steroidal anti-inflammatory drugs.

15 patients with rheumatoid arthritis who were receiving non-steroidal anti-inflammatory drugs (NSAIDs) and who had chronic occult gastrointestinal bleeding underwent extended small bowel examination with a Sonde enteroscope. 7 patients (47%) were found to have jejunal or ileal ulceration. Small bowel enteroscopy may be a valuable technique for the investigation of undiagnosed gastrointestinal bleeding.

Adult↗

Hematologic disorders in rheumatic disease.

The 1990 literature relating to hematologic disorders in rheumatic disease is reviewed. Two main subject areas of general interest are identified. The anemia of chronic disease has been reviewed and shown to be associated with a variety of medical conditions. Generalized reticuloendothelial hyperplasia associated with heavy-chain disease is a poorly recognized complication associated with rheumatoid arthritis and may be mistaken for underlying sepsis in these patients.

Hematologic Diseases↗

Increased intestinal permeability in ankylosing spondylitis--primary lesion or drug effect?

We have found increased small intestinal permeability to 51Cr-ethylenediaminetetra acetate in patients with ankylosing spondylitis compared with controls. There is no significant difference between patients with ankylosing spondylitis and patients with rheumatoid arthritis taking non-steroidal anti-inflammatory drugs (NSAID). The increased intestinal permeability in ankylosing spondylitis is independent of disease activity. These findings suggest that the increased permeability is caused by NSAID treatment and is probably not a primary lesion of small bowel mucosa.

Adult↗

Nonsteroidal peptic damage in rheumatoid patients receiving second-line drugs.

Using endoscopy, we assessed the prevalence of peptic ulceration in 281 rheumatoid patients receiving nonsteroidal antiinflammatory drugs alone, or in combination with second-line agents. Ulcers were found in 33 of 96 patients who took nonsteroidals only (33/96, 34%), compared with 8/33 (24%) on hydroxychloroquine, 10/30 (33%) on penicillamine, 13/46 (28%) on sulphasalazine, but only 11/76 (14%) on intramuscular gold plus nonsteroidals (chi 2 = 7.95, 0.001 less than p less than 0.01, p less than 0.05 using Bonferroni correction). Second-line drugs do not seem to increase the prevalence of ulcers related to nonsteroidal antiinflammatory drugs; on the contrary, fewer ulcers were found in patients receiving gold therapy, and this might have therapeutic implications.

Anti-Inflammatory Agents, Non-Steroidal↗

Is the beneficial effect of sulfasalazine due to inhibition of synovial neovascularization?

Angiogenesis is fundamental to support the continued synovial proliferation observed in rheumatoid arthritis. We investigated the effects of sulfasalazine and its metabolites on endothelial cell proliferation, a prerequisite to angiogenesis. At concentrations achieved in vivo sulfapyridine inhibited basal and endothelial cell growth factor stimulated endothelial cell proliferation. Sulfasalazine and 5 amino salicylic acid had no effect.

Aminosalicylic Acids↗

Prevalence of vertebral compression fractures due to osteoporosis in ankylosing spondylitis.

OBJECTIVE: To determine the prevalence of vertebral compression fractures due to osteoporosis in patients with ankylosing spondylitis. DESIGN: Prospective study of 111 consecutive patients; patients with vertebral compression fractures were entered into a case-control study. SETTING: Outpatient clinic at the centre for rheumatic diseases, Glasgow. PATIENTS: 111 Consecutive patients with ankylosing spondylitis. Patients with compression fractures were matched for age and sex with two controls selected from the rest of the group. Patients with biconcave vertebral fractures were also studied. MAIN OUTCOME MEASURES: Assessments of spinal deformity and mobility and analysis of lateral radiographs of spines for presence of syndesmophytes. RESULTS: Fifteen patients with compression fractures and five with biconcave fractures were studied. Compared with the controls the patients with compression fractures had increased formation of syndesmophytes in the lumbar spine, whereas those with biconcave fractures had increased formation throughout the spine. Patients with compression fractures also had a greater degree of spinal deformity (distance from wall to tragus 24.5 cm v 12.7 cm in controls), less spinal mobility (20 v 45.6 degrees of flexion), and reduced chest expansion (2 cm v 3cm). CONCLUSION: Vertebral compression fractures due to osteoporosis are a common but frequently unrecognised complication of ankylosing spondylitis and may contribute to the pathogenesis of spinal deformity and back pain.

Adolescent↗

Evaluation of sulphasalazine in ankylosing spondylitis--an interventional study.

Sulphasalazine has recently been shown to have an effect in ankylosing spondylitis but the clinical indication for its use is controversial. We have used an 'interventional' study design to investigate the clinical and laboratory effects of sulphasalazine in a group of 20 patients with active ankylosing spondylitis and peripheral joint disease. Following an initial assessment period, patients were treated with sulphasalazine for 24 weeks and the drug was then withdrawn and the patients monitored for a further 12 weeks. Significant improvements were observed in chest expansion, number of active joints, ESR and CRP which deteriorated after withdrawal of sulphasalazine. No change in spinal mobility was demonstrated. The 'interventional' design may be a useful screening procedure for identifying potential second line drugs in ankylosing spondylitis.

Adult↗

Hypercalcaemia in rheumatoid arthritis revisited.

The prevalence and mechanisms of hypercalcaemia were studied in a series of patients attending a regional referral centre for rheumatic diseases. In a prospective study one case of hypercalcaemia due to primary hyperparathyroidism was found in 251 consecutive patients who were screened over a three month period. In a retrospective study of 39 patients who had been discovered to be hypercalcaemic during the preceding 12 months known cases of hypercalcaemia were found in 38 (97%) cases. Primary hyperparathyroidism was the most common cause (n = 24; 62%), followed by thiazide treatment in five (13%), cancer in three (8%), immobility in three (8%), vitamin D toxicity in two (5%), and chronic liver disease in one (3%). In one case the diagnosis remained unclear after full investigation. This study shows that the causes of hypercalcaemia in rheumatological patients are similar to those in the general population. These observations contrast with previous reports, which suggested that hypercalcaemia may be a complication of rheumatoid arthritis itself.

Adult↗

Rheumatology at the general practitioner/hospital interface: a study of prevalence and access to specialist care.

Four general practices with a combined population of 23,300 in the west of Scotland participated in a record research and questionnaire assessment of 551 patients with rheumatic diseases. The study describes the prevalence, levels of disability found, and the types of service used. Even with this number of patients it was not possible to detect any significant differences in disability levels, use of second line drugs, or aids/appliances when comparing practices with adequate or inadequate access to rheumatological facilities (general practitioner perception). General practice is an appropriate setting in which to investigate the effect of service provision, but larger studies will be needed to reach more definite conclusions.

Disability Evaluation↗

Effect on gastric and duodenal mucosal prostaglandins of repeated intake of therapeutic doses of naproxen and etodolac in rheumatoid arthritis.

The synthesis of gastric and duodenal mucosal prostaglandin E2, prostaglandin I2, and thromboxane B2 during a 60 minute incubation of biopsy specimens, the degree of endoscopic and histological damage, and the anti-inflammatory response were all studied after a four week, double blind study of therapeutic doses of two non-steroidal anti-inflammatory drugs, naproxen and etodolac, received by 27 patients with active rheumatoid arthritis (13 receiving naproxen, 14 etodolac). Prostaglandin values after treatment did not differ from the baseline levels when all the patients were analysed as one group. Subgroup analysis showed that naproxen suppressed gastric prostaglandin E2 from a median of 29 to 9 ng/mg protein, duodenal prostaglandin E2 from 34 to 11 ng/mg, and duodenal prostaglandin I2 from 62 to 15 ng/mg protein. No overall suppression occurred with etodolac. Also, on the second assessment patients receiving naproxen had lower gastric and duodenal prostaglandin E2 and prostaglandin I2, but higher values of duodenal thromboxane B2, than patients receiving etodolac. Both drugs had comparable anti-arthritic activity and caused microscopic gastritis in similar proportions of patients. No correlation was detected between prostaglandin values and the mucosal damage which developed in seven patients receiving naproxen (54%) and three receiving etodolac (21%). These findings indicate that, unlike naproxen, etodolac does not seem to affect gastric or duodenal prostaglandin synthesis; other mechanisms of injury need to be considered.

Adolescent↗