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Biomedical subjects

D M Reid

Publications and source records attributed to D M Reid.

At least 181 records · Page 10Linked to original sources

Hydroxyapatite associated disease in an elderly female: differentiation from aseptic necrosis.

The crystal arthropathies caused by monosodium urate and calcium pyrophosphate dihydrate are commonly recognised, but the destructive arthropathy associated with the deposition of calcium hydroxy-apatite is less well known in general clinical practice. We describe a case with many of the classical features of hydroxy-apatite associated disease and discuss the features differentiating the condition from aseptic necrosis.

Aged↗

Intravenous gammaglobulin therapy for neonatal alloimmune thrombocytopenia.

A clinical experience with the combined use of intravenous gammaglobulin and platelet transfusions in a neonate with alloimmune thrombocytopenia secondary to PLA1 incompatibility is described and compared to a previously affected sibling treated with a conventional regimen of corticosteroids, random donor platelet transfusions, and exchange transfusion for neonatal alloimmune thrombocytopenia.

Antibodies↗

Drug purpura due to surreptitious quinidine intake.

Three patients had recurrent episodes of thrombocytopenia that resembled drug purpura, but the drug history in each case did not support the diagnosis. Although the patients specifically denied taking quinidine, serologic testing with this drug was done because the patients had access to it, and it is the commonest cause of drug purpura. Highly specific quinidine-dependent antiplatelet antibodies were found in the sera of all three patients. After being informed of the laboratory findings, the patients have had no recurrences of purpura. Serologic tests for quinidine- or quinine-dependent antibodies can help elucidate some obscure cases of purpura that may be self-induced.

Aged↗

EB-virus transformed human lymphocytes from uveitis and retinitis pigmentosa patients secrete antibodies to retinal antigens.

Autoimmunity to retinal antigens has been implicated in the pathogenesis of both endogenous posterior uveitis and retinitis pigmentosa. Recent studies, however, suggest that low levels of antibodies to retinal antigens occur generally in the population. We have attempted to maximize antibody secretion by peripheral blood lymphocytes from patients and normal healthy controls using the polyclonal activator, Epstein-Barr virus, to stimulate lymphocytes in vitro. Whereas cells from controls and uveitis patients showed a level of anti-retinal antibody secretion which corresponded with their serum titres of antibodies, patients with retinitis pigmentosa showed a greater tendency to produce high secretor lymphocytes after EB-virus stimulation despite having low serum titres of antibody. This strategy for studying antibody secretion may be of value in unmasking low levels of autoimmune responsiveness in conditions such as retinitis pigmentosa where low grade tissue damage occurs over many years and antigen release is correspondingly too low to initiate a measurable autoimmune reaction.

Autoantibodies↗

Electron immunocytochemical localization of retinal S-antigen with a rat monoclonal antibody.

This report describes the ultrastructural localization of S-antigen in pig and human retinas by means of a highly specific rat IgG monoclonal antibody, S2.4.C5, followed by a secondary antibody adsorbed to colloidal gold. This monoclonal antibody gave definitive staining with negligible background. The protein was detected in both the rod outer and inner segments. Connecting cilia and the rod outer segment disc membranes were labelled. The outer segment plasma membrane was not obviously labelled. Cones were labelled at background level. S-Antigen was not detected in any other cells of the neural retina. The fate of S-antigen was also followed to the pigment epithelial phagosomes where intracytoplasmic ROS debris was stained with the antibody. No label, however, was detected in the choroid, suggesting that trans-cellular transport of the S-antigen did not occur.

Animals↗

Binding of quinine- and quinidine-dependent drug antibodies to platelets is mediated by the Fab domain of the immunoglobulin G and is not Fc dependent.

The antibody domain controlling reactions between platelet membranes and drug-dependent (dd) antibodies from patients with thrombocytopenia induced by cinchona alkaloids was studied using F(ab')2, Fab, and Fc fragments made from purified dd-IgG. By direct binding radioimmunoassay (RIA) measurements, 20,000 to 50,000 antibody molecules bound per platelet equivalent of purified platelet membranes at apparent saturation with three different antibodies. F(ab')2 and Fab fragments bound to platelet membranes drug dependently but Fc fragments did not. The ability of dd-IgG fragments to compete with intact IgG was quantitatively measured by RIA and by complement fixation. F(ab')2 and Fab competed with intact IgG at an 8:1 and greater than 50:1 molar ratio, respectively, in RIA, and at a 1.6-3:1 and 44-75:1 ratio, respectively, by complement fixation assays. Fc did not compete with IgG in either assay. We conclude that the Fab domain supports attachment of dd antibody to the platelet surface.

Autoantibodies↗

Is there a humoral autoimmune response to retinal antigens in the RCS rat?

The naturally occurring humoral immune response of Campbell and Hunter strains of Royal College of Surgeons (RCS) rat to bovine retinal S-antigen and bovine rod outer segments was tested by a sensitive ELISA (enzyme linked immunosorbent assay) in animals up to the age of 9 weeks. Controls of Piebald Virol Glaxo, Wistar and DA rats were also employed. The ELISA results indicate that rats of all strains had a response to both antigens. The magnitude of the response in any particular strain varied with the age of the animal and the antigen and serum dilution employed in the assay. Considerable variation in response was observed among animals of the same strain at any one particular age. Immunoblot analysis of the strongest ELISA positive sera detected S-antigen and other autoantigenic proteins in both RCS and Wistar rats. The data suggest that the antibody response observed may have little significance to the retinal degeneration observed with RCS rats.

Animals↗

Corticosteroids and bone mass in asthma: comparisons with rheumatoid arthritis and polymyalgia rheumatica.

Bone mass has previously been shown to be reduced at peripheral bone sites in patients with bronchial asthma receiving corticosteroids. To assess whether total bone mass is reduced in asthma total body calcium was measured by in vivo neutron activation analysis in patients receiving various treatments for asthma and compared with results from normal controls and patients with rheumatoid arthritis and polymyalgia rheumatica. Compared with controls total body calcium was reduced by 13.6% (p less than 0.001) in patients with asthma receiving daily oral corticosteroids but by only 9.0% (p less than 0.005) in a similar group of patients who had received oral calcium supplements at the start of their corticosteroid treatment. Total body calcium was also reduced in a group of patients receiving only inhaled corticosteroids (8.8%; p less than 0.001) but not significantly reduced in a small group of patients with asthma who had never received these drugs. When compared with controls a group of patients matched for age and for dose of corticosteroids given for rheumatoid arthritis had a similar reduction in total body calcium to the patients with asthma receiving daily oral treatment (17.7%; p less than 0.001), but no such reduction was shown in patients with polymyalgia rheumatica. These findings suggest that the risk of bone loss with low dose oral corticosteroids in similar in asthma and rheumatoid arthritis. Further work is required to assess the clinical relevance of small losses of bone associated with the use of inhaled corticosteroids.

Administration, Oral↗

Total and peripheral bone mass in patients with psoriatic arthritis and rheumatoid arthritis.

Psoriatic arthritis is thought to be associated with periarticular osteoporosis while rheumatoid arthritis may be associated with generalised as well as periarticular bone loss. To assess the extent of total and peripheral bone loss in these two diseases, total body calcium was measured by in vivo neutron activation analysis and peripheral bone mass was assessed by metacarpal indices in age-matched patients with psoriatic arthritis and rheumatoid arthritis treated with nonsteroidal anti-inflammatory drugs alone. In comparison with age and sex-matched normal controls, total and peripheral bone mass was normal in psoriatic arthritis. There were significant reductions in total (6.2% in men; 7.9% in women) and peripheral (10.9% in men; 12.8% in women) bone mass in patients with rheumatoid arthritis compared with controls. Peripheral bone mass was significantly correlated with the degree of radiographic damage in male and female patients with rheumatoid arthritis. The mean annual loss of total body calcium was insignificant in psoriatic arthritis (0.6% in men; 1.9% in women) but markedly greater in rheumatoid arthritis (4.4% in men; 2.7% in women). The data suggested that total and peripheral bone loss is greater in rheumatoid arthritis than psoriatic arthritis. Substantial reductions in peripheral bone mass in patients with rheumatoid arthritis not receiving corticosteroids may account in part for the small reductions in total bone mass.

Adult↗

The seasonal variation of total body calcium.

Total body calcium was measured using in vivo neutron activation analysis in 156 patients with rheumatic diseases at six-month intervals. Evidence of seasonal variation was sought by relating deviation from a linear change to the month in which the measurement was made. A cyclic regression fitted to the data had an amplitude of 0.25% but a significance of only P = 0.08. The calcium balance studies of Malm were re-analysed to quantify the seasonal variation he had demonstrated in one group of men. The deduced variations of body calcium were highly significant, with a phase and amplitude very similar to the regression of our data. Both analyses differed from two previous reports of seasonal variations of part-body bone mineral of much greater amplitude and different phase.

Calcium↗

Bone loss in rheumatoid arthritis and primary generalized osteoarthrosis: effects of corticosteroids, suppressive antirheumatic drugs and calcium supplements.

The annual rate of bone loss in rheumatoid arthritis (RA) and primary generalized osteoarthrosis (PGOA) was determined by measurement of total body calcium (TBCa). The mean annual rate of bone loss in 24 patients with RA treated with nonsteroidal anti-inflammatory drugs (NSAIDs) alone was 3.4%. This rate of bone loss was not reduced in ten RA patients responding to suppressive antirheumatic drugs (4.3%) or seven patients receiving oral calcium supplements (4.5%). The mean annual rate of loss of TBCa in 19 patients with PGOA was 1.6%, a figure which probably represents age-associated bone loss. The rate of bone loss in PGOA was significantly less than that in RA patients not receiving corticosteroids. The mean annual rate of change of TBCa in 30 RA patients receiving corticosteroids (+0.7%) was significantly less than that in any of the other RA groups despite an initial normalized bone mass which was significantly less than in those RA patients receiving NSAIDs alone. The data supported the hypothesis that bone loss occurred early in the course of corticosteroid therapy and thereafter the drugs might have a protective effect on the loss of bone in RA.

Adrenal Cortex Hormones↗

Monoclonal autoantibodies from rats with inherited retinal dystrophy.

The Royal College of Surgeons (RCS) rat carries a recessive gene for retinal dystrophy and is used as an experimental model for human retinal degenerative conditions such as retinitis pigmentosa (RP). It has been suggested that an autoimmune response to retinal antigens may contribute to the retinal degenerative processes. In this study, fusions of RCS rat splenic lymphocytes with the rat Y3 Ag 1.2.3 myeloma cell line, resulted in primary fusion cultures, some of which were positive to retinal S-antigen and others to insoluble components of rod outer segments. Three fully cloned IgM monoclonal antibodies were generated and the reaction of 2 of them to S-antigen and opsin was confirmed by immunoblotting.

Animals↗

Bone mass in ankylosing spondylitis.

To assess bone mass in ankylosing spondylitis (AS) we have measured total body calcium, bone mineral content of the lumbar spine and metacarpal indices in groups of patients with AS. Mean total body calcium was reduced by 5.3% (p less than 0.05) in 20 patients compared with controls. The mean annual loss of bone, assessed over an 18 month period in 17 patients, was 2.9% (p less than 0.001). Compared to controls, bone mineral content was increased by 28% (p less than 0.05) in 8 male patients while metacarpal indices were normal in 18 male and female patients. The results of total body calcium measurements give support to the hypothesis of a minor increase in bone turnover in AS. The increased bone mineral content in the male patients may relate to syndesmophyte formation.

Adult↗