Biomedical subjects
Publications and source records attributed to A C Klestov.
We describe the case of a young male who manifested Brucella suis osteomyelitis after a 5-year period of relapsing monoarthritis. We discuss some of the difficulties regarding the diagnosis of osteoarticular brucellosis and review presentation patterns of the disease.
BACKGROUND: Because of several similar features in the pathobiology of periodontitis and rheumatoid arthritis, in a previous study we proposed a possible relationship between the two diseases. Therefore, the aims of this study were to study a population of rheumatoid arthritis patients and determine the extent of their periodontal disease and correlate this with various indicators of rheumatoid arthritis. METHODS: Sixty-five consecutive patients attending a rheumatology clinic were examined for their levels of periodontitis and rheumatoid arthritis. A control group consisted of age- and gender-matched individuals without rheumatoid arthritis. Specific measures for periodontitis included probing depths, attachment loss, bleeding scores, plaque scores, and radiographic bone loss scores. Measures of rheumatoid arthritis included tender joint analysis, swollen joint analysis, pain index, physician's global assessment on a visual analogue scale, health assessment questionnaire, levels of C-reactive protein, and erythrocyte sedimentation rate. The relationship between periodontal bone loss and rheumatological findings as well as the relationship between bone loss in the rheumatoid arthritis and control groups were analyzed. RESULTS: No differences were noted for the plaque and bleeding indices between the control and rheumatoid arthritis groups. The rheumatoid arthritis group did, however, have more missing teeth than the control group and a higher percentage of these subjects had deeper pocketing. When the percentage of bone loss was compared with various indicators of rheumatoid arthritis disease activity, it was found that swollen joints, health assessment questionnaire scores, levels of C-reactive protein, and erythrocyte sedimentation rate were the principal parameters which could be associated with periodontal bone loss. CONCLUSIONS: The results of this study provide further evidence of a significant association between periodontitis and rheumatoid arthritis. This association may be a reflection of a common underlying disregulation of the inflammatory response in these individuals.
AIM: The aim of this study was to determine whether there is a relationship between disease experience of rheumatoid arthritis and periodontal disease. METHODS: 1,412 individuals attending the University of Queensland's School of Dentistry were assessed for the prevalence of periodontal disease and rheumatoid arthritis. Analysis of data obtained from a self-reported health questionnaire and dental records was carried out and included: number of individuals referred for advanced periodontal care (test group); number of individuals attending for routine dentistry; determination of rheumatoid arthritis, cardiovascular disease and diabetes mellitus through self-reporting and assessment of prescription medications; assessment of periodontal disease through assessment of existing oral radiographs. RESULTS: In patients referred for periodontal treatment, the prevalence of self-reported rheumatoid arthritis was 3.95% which is significantly higher than that seen in patients not referred for periodontal treatment (0.66%) and also that reported in the general population (1%). Of those referred patients with rheumatoid arthritis, 62.5% had advanced forms of periodontal disease. These results were mirrored in the results of the self-reported prevalence of cardiovascular disease and diabetes mellitus which was consistent with the published higher prevalence in periodontal patients. CONCLUSIONS: Based on data derived from self-reported health conditions, and not withstanding the limitations of such a study, we conclude that there is good evidence to suggest that individuals with moderate to severe periodontal disease are at higher risk of suffering from rheumatoid arthritis and vice versa.
We describe a case of antiphospholipid associated thrombocytopenia in which warfarin, but not heparin, normalized the platelet count. Systemic lupus erythematosus was present in association with chorea, mitral valve stenosis, and renal thrombotic microangiopathy. No evidence of platelet consumption was detected. Low dose aspirin, pulse methylprednisolone, intravenous gammaglobulin, and cyclophosphamide also partially elevated the platelet count. Platelet activation, measured by P selectin assay, was not present during warfarin or aspirin therapy, suggesting that platelet activation may have been decreased by these treatments. We discuss possible mechanisms for correction of thrombocytopenia in antiphospholipid syndrome by warfarin.
We describe 3 patients with severe sensorimotor neuropathy complicating rheumatoid arthritis. Two patients had evidence of vasculitis and an axonal neuropathy. These patients were unusual in that the neuropathy occurred early in the course of rheumatoid arthritis. The third patient had a demyelinating neuropathy with a high cerebrospinal fluid protein level, and is a probable example of a chronic inflammatory neuropathy occurring in rheumatoid arthritis. All patients improved or were stabilized with corticosteroid therapy.
The first-ever controlled study of a therapeutic modality for xerostomia is reported. A recently described formulation for saliva substitute (SS) has been tested against a glycerine mouthwash as a control saliva substitute (placebo) in a double-blind clinical trial in 108 patients with varying grades of xerostomia of Sjögren's syndrome. The results indicate that SS offered significant relief of nocturnal oral discomfort (p less than 0.02) and more patients reported "excellent" improvement (p less than 0.01) on a five-point graded response. In all other respects, the SS was not significantly better than the placebo. Significant adverse effects were not reported. It is suggested that any such current and future therapeutic modalities for Sjögren's syndrome be subjected to similar critical appraisal of their worth.
In search for a practical solution to analyse a large quantity of medical information, rheumatic disease data base system (RDDS) is described. Details of data configuration, data entry and retrieval are discussed in some detail. The system incorporates a range of commonly used statistical tests and provisions for more advanced data analysis are made. Additional facilities include provisions for a variety of printed reports, back up facilities and a word processor. The ease of system operation and flexibility are emphasised. Technical support requirements are minimal even when new applications are being developed. The system is fully operational at present and can be implemented on a number of computer systems.
A 48-year-old male patient with underlying CPT II enzyme deficiency is described. Emotional stress appeared to precipitate recurrent myalgias, rhabdomyolysis and reversible renal impairment over a 40-year period. Our search of the English literature indicates this to be the first time that the emotional stress has been documented to precipitate the CPT II syndrome. Although the pathogenesis of this syndrome has yet to be established, existing knowledge is briefly reviewed and the likely metabolic and neuroendocrine mechanisms which link emotional stress to muscle metabolism are examined. These mechanisms influence the extent of lipolysis or glycolysis that occurs during the process of muscle ATP generation. It is suggested that neuroendocrine and other stress related changes which favour lipolysis over glycolysis adversely affect muscle energy metabolism in patients whose mitochondria are deficient in CPT II enzyme. Possible treatment strategies are those that favour glycolysis over fatty acid metabolism and include a variety of ways of modulating sympathetic and parasympathetic tone. The use of carbohydrate supplementation beta-blockers and anxiolytic agents is discussed.
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