Biomedical subjects
B E Bourke
Publications and source records attributed to B E Bourke.
An open study of oxpentifylline in early rheumatoid arthritis.
Explore the source record for details and available documents.
A detailed lectin analysis of IgG glycosylation, demonstrating disease specific changes in terminal galactose and N-acetylglucosamine.
Serum IgG from rheumatoid arthritis patients contains a decreased number of oligosaccharide structures ending in galactose and thus there is an increase in N-acetylglucosamine as the terminal sugar, compared with healthy individuals. The relationship between these two sugars varies depending on the disease examined: IgG from patients with rheumatoid arthritis, juvenile onset chronic arthritis and Crohn's disease are at one extreme, and exhibit a reciprocal galactose:N-acetylglucosamine relationship, while Sjögren's syndrome and osteoarthritis IgG are at the other extreme, exhibiting a parallel increase in the expression of both galactose and N-acetylglucosamine. These results may occur as a consequence of more than one glycosylation site which is differentially glycosylated, but more likely by changes in the level of bisecting N-acetylglucosamine.
Reduction in heart rate variability in patients with systemic lupus erythematosus.
OBJECTIVE: To determine whether heart rate variability and cardiovascular reflex tests are abnormal in patients with systemic lupus erythematosus (SLE). METHODS: We measured heart rate variability (24 h ambulatory recordings), and used baroreflex sensitivity testing and cardiovascular reflex tests in a cross sectional, case-control study. Those taking drugs with cardiovascular activity were excluded. RESULTS: Determination of heart rate variability was simple to perform, well tolerated, and found to be reduced in the patients with lupus, but not strongly related to disease activity or duration. CONCLUSION: This may reflect underlying autonomic dysfunction; longitudinal studies will determine full clinical relevance.
Lymphatic function in inflammatory arthritis.
Explore the source record for details and available documents.
Systemic lupus erythematosus: an occasional misdiagnosis.
Explore the source record for details and available documents.
Favourable outcome of scleroderma renal crisis.
Severe hypertension and rapidly progressive acute renal failure is a well recognized complication of scleroderma, often referred to as the renal crisis, and widely thought to cause irreversible deterioration in renal function. With the advent of angiotensin-converting-enzyme inhibitors (ACE-I) the outlook for patients with this condition has dramatically improved. We report here one such patient.
Antigen specificity of ANCA in systemic vasculitis.
Explore the source record for details and available documents.
Sulphasalazine-induced autoimmune abnormalities in patients with rheumatic disease.
Sulphasalazine is a commonly used second line agent in rheumatoid arthritis (RA) and other inflammatory joint diseases and is reported to be one of the least toxic of this group of drugs. Recently a severe allergic reaction and cases of lupus-like disease have been described in patients with RA after treatment with sulphasalazine. We describe five patients, all with inflammatory arthropathy who developed cutaneous vasculitis, lupus-like disease or atypical serology after exposure to sulphasalazine. Three of four cases investigated were found to have the slow acetylator phenotype. These reactions can complicate the diagnosis and delay discontinuation of the drug. Moreover, present guidelines for the diagnosis of drug-induced lupus do not apply to the majority of patients with sulphasalazine-induced lupus.
Cerebral venous thrombosis and acquired protein S deficiency: an uncommon cause of headache in systemic lupus erythematosus.
A 42-yr-old woman with hypertension and renal involvement due to systemic lupus erythematosus (SLE) developed unilateral headache followed by the sudden onset of confusion and a grand mal convulsion. Cerebral computed tomography was normal. A magnetic resonance imaging angiogram revealed cerebral venous thrombosis and a venous infarct. Nephrotic syndrome had resulted in an acquired protein S deficiency. A review of previous cases suggests that either renal disease with proteinuria or features of the antiphospholipid syndrome are prerequisites for the development of cerebral venous thrombosis in SLE. Low free-protein S levels may be an additional risk factor. Furthermore it is likely that this condition is underdiagnosed.
Upper limb lymphatic function in inflammatory arthritis.
OBJECTIVE: To determine the effect of inflammatory arthritis on lymphatic function in the upper limb. METHODS: Lymphoscintigraphy was used to measure lymphatic drainage in the upper limbs of 3 groups of patients: Group 1, inflammatory arthritis and edema (N = 10); Group 2, inflammatory arthritis and no edema (N = 18); and Group 3, healthy controls (N = 11). RESULTS: Lymphatic drainage was reduced significantly in Group 1 but was the same in Groups 2 and 3. Multiple regression analysis failed to show any effect of arthritis on lymphatic drainage. CONCLUSION: Inflammatory arthritis alone does not impair lymphatic drainage in the upper limbs. The results suggest that the presence of edema is primarily attributable to an unrelated abnormality influencing lymphatic function.
Upper limb lymphedema associated with polyarthritis of rheumatoid type.
OBJECTIVE: To determine the cause of upper limb edema in 8 patients with peripheral polyarthritis of rheumatoid-type. METHODS: Objective assessment of lymph function using quantitative lymphoscintigraphy. RESULTS: Seven cases with either rheumatoid or psoriatic arthritis were found to have impaired lymph drainage associated with edema. All cases shared a distal rheumatoid pattern of arthritis but showed no relation between severity of lymphatic impairment and either duration or severity of arthritis. CONCLUSION: Polyarthritis of rheumatoid-type may be associated with lymphedema due to impaired lymphatic function.
Central nervous system involvement in systemic lupus erythematosus. Are we any further forward?
Explore the source record for details and available documents.
Reversal of gold-induced neutropenia with granulocyte colony-stimulating factor (G-CSF).
We have successfully overcome severe neutropenia in an RA patient treated with gold salts, using granulocyte colony-stimulating factor (G-CSF), reducing the duration of neutropenia and risk of infection. The patient suffered no side effects, and use of G-CSF represents an important addition to the management of a life-threatening drug reaction.
Prevalence of Helicobacter pylori infection and its effect on symptoms and non-steroidal anti-inflammatory drug induced gastrointestinal damage in patients with rheumatoid arthritis.
Non-steroidal anti-inflammatory drugs (NSAIDs) and Helicobacter (H pylori) are both associated with an increased risk of peptic ulceration and gastropathy. It is not known, however, if there is an interaction between these two agents, and thus whether or not screening for H pylori before NSAID treatment is of value. The aim of this study was to find out if H pylori potentiates the damaging effects of NSAIDs. Fifty two patients with rheumatoid arthritis requiring longterm NSAID treatment were studied. Dyspeptic symptoms were assessed according to a standardised questionnaire. Gastroscopy was performed after a one week washout period during which NSAIDs were discontinued. Gastric and duodenal mucosal damage was graded endoscopically. H pylori was identified by biopsy urease test and by histological tests. Investigations were repeated after one month's treatment with an NSAID. Patients with H pylori infection (n = 26) had a higher dyspeptic symptom score (p < 0.05). One patient with duodenal ulcer (H pylori +ve) and two with endoscopic gastritis (both H pylori +ve) were excluded from further study. Forty two subjects completed the study. After treatment there was a rise in the gastric damage score both in the H pylori +ve (p = 0.06) and the H pylori -ve (p < 0.005) groups. There was no difference in the extent of increase in grade or the final grade at the end of the treatment period between the H pylori +ve and -ve patients. It is concluded that H pylori infection is associated with increased dyspeptic symptoms in patients receiving NSAIDs but that it does not potentiate NSAID gastropathy.
Haemarthrosis due to fracture through amyloid deposits in bone in Portuguese familial amyloidosis.
A patient with Portuguese familial amyloid polyneuropathy who developed haemarthroses secondary to pathological fractures is described. Amyloid material was demonstrated on bone biopsy and confirmed immunohistochemically to be transthyretin (prealbumin). Although amyloid deposits in bone have been described in other types of amyloid, this is believed to be the first proved case of amyloid deposition resulting in pathological fracture in familial amyloidosis.
Haemophilia and rheumatoid arthritis.
Explore the source record for details and available documents.