Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.461741
Title: Bone loss in rheumatoid arthritis : a clinical, radiological and biochemical study
Author: Kennedy, Alastair Cathcart
ISNI:       0000 0001 3597 1331
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1978
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Abstract:
The first patient I saw when 1 took up my clinical duties at the Centre for Rheumatic Diseases in Glasgow was a 59 year old spinster who had rheumatoid arthritis for 39 years. She had been bedridden for eight years and had received oral corticosteroid therapy for 15 years. The patient was in severe agony from multiple vertebral body collapse and from rib and long bone fractures. On x-ray the bones were almost transparent, and extensive biochemical tests revealed no evidence of osteomalacia. The patient's problem of osteoporosis intrigued me and on reading the literature I was surprised to find that very little had been done to study the problem of bone loss in patients with rheumatoid arthritis. For example, it was not clear from reading the literature how much oral corticosteroid therapy was responsible for bone loss compared to the disease itself. Chapter I of this thesis describes an extensive radiological investigation of osteoporosis in patients with rheumatoid arthritis in order to assess its extent and severity. The results show that osteoporosis in rheumatoid arthritis is a generalised phenomenon, which is particularly evident in patients of both sexes over the age of 45 years. In addition to the duration of the arthritis, corticosteroid therapy was shown to be the other important variable in producing this osteoporosis. Chapter II describes an extensive clinical study of calcium metabolism in patients with rheumatoid arthritis in an attempt to explore further possible factors in the bone loss occuring in this disease. One of the surprising results of this investigation indicated that hypercalcaemia is a not uncommon feature in rheumatoid arthritis. Circumstantial evidence pertaining to serum and urine biochemistry together with tentative conclusions from a calcium absorption study suggested that the hypercalcaemia might be part of a "hyperparathyroid-like" state. However, immunoassay of serum parathyroid hormone levels clearly indicated that this hormone was not elevated and was thus not responsible for these biochemical abnormalities. Similarly serum 25-hydroxyvitamin D levels were normal but an interesting trend towards elevation of serum calcitonin levels was noted. The study was then extended to examine the effects of rheumatoid sera on a bone culture in vitro. Bone resorption activity was demonstrated in the sera of those patients who were hypercalcaemic. It is tentatively concluded that this bone resorption is due to a substance, as yet unidentified, which has some, but not all, of the properties associated with osteoclast activating factor. These observations may subsequently be shown to have therapeutic implications in the treatment of rheumatoid arthritis.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.461741  DOI: Not available
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