Biomedical subjects
Publications and source records attributed to M L Snaith.
A patient with systemic lupus erythematosus (SLE)/erosive arthritis overlap is described who was also shown to have late latent treponemal infection. The possibility of serological reactivation is discussed. Since antiphospholipid antibodies are the basis of the reagin tests for syphilis as well as being present in patients with SLE, difficulties with diagnosis may ensue.
Twenty five patients with idiopathic myositis attended this department for long term follow up from 1980 to 1989. Twelve patients had primary polymyositis (four men, eight women) and six had primary dermatomyositis (three men, three women); five women had an overlap syndrome. Two patients had a malignant condition associated with the myositis. The mean age at diagnosis was 40 years. All of the patients had proximal muscle weakness, 18/25 had a raised creatine kinase value (mean 2325 IU/l), 19/20 had an abnormal electromyogram, and 19/24 had positive muscle biopsy samples. Of the disease specific antibodies, anti-Jo-1 was detected in only 1/21 patients tested (three patients with fibrosing alveolitis were negative for this antibody), but the 56 kDa antibody was detected in 12/17 patients. The HLA data analysed in the white patients (17/25) showed that 6/8 of those tested were HLA-DR3 positive. All patients were treated with prednisolone and azathioprine was used for 14/25 patients. Only three deaths occurred during the eight year follow up, but there was a substantial morbidity, which may reflect the referral pattern. Muscle strength tests and creatine kinase levels were useful in recording the response to treatment in some patients. These data emphasise that careful long term follow up of patients with myositis is mandatory and that although the present treatment strategy has substantially reduced the death rate, morbidity associated with the disease remains a major problem.
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A prospective, double blind, cross over study assessing the effects of a low fat, high marine oil diet in 27 patients with active systemic lupus erythematosus has been performed. The patients were given 20 g daily of MaxEPA (eicosapentaenoic acid) or 20 g of olive oil (placebo) in matching capsules added to a standardised isoenergetic low fat diet. When individual outcome measures of the 17 patients who completed the full 34 week study were considered 14 who were receiving MaxEPA achieved useful or ideal status, whereas 13 receiving placebo were rated as worse or no change. The difference between the two types of capsule was statistically significant. No major side effects were noted, and it is suggested that dietary modification with additional marine oil may be a useful way of modifying disease activity in systemic lupus erythematosus.
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Dual energy x ray absorptiometry and a wide range of blood and urine tests were used to assess the propensity of patients with systemic lupus erythematosus to develop an impairment of bone mineral density. Surprisingly, in this preliminary study no significant differences in bone mineral density were found when patients taking 10 mg or more of prednisolone for six months or longer were compared with those who had never taken prednisolone.
Clinical features and immunogenetics were assessed in 100 SLE patients attending a rheumatology clinic for periods ranging from six months to 11 years (mean five years). Five-year survival was 88 per cent. Joint problems (94 per cent), rash (90 per cent) and haematological abnormalities (89 per cent) were the most common clinical features; neuropsychiatric disturbance (45 per cent) and renal disease (29 per cent) were seen less frequently. A range of serological abnormalities was found, including antinuclear antibodies (98 per cent) and antibodies to phospholipids (38 per cent). Anti-Sm antibodies (7 per cent) showed a marked ethnic bias. Tissue typing confirmed the importance of genetic factors by demonstrating significant increases in A1, B8 and DR3 in white Caucasians. The composite phenotype A1,B8,DR3 was present in 35 per cent of white Caucasian patients with SLE. The A1,B8 phenotype was associated with a relative risk of 8.0 and B8,DR3 with a relative risk of 8.32.
Twelve female patients with severe secondary Raynaud's phenomenon were treated in a randomized order with both placebo and Iloprost infusions. Infusions were for 5 hours on 3 consecutive days and Iloprost was administered at variable dosage from 1.0 to 3.0 ng/kg/min. A 6-week follow-up period was used between the two sets of infusions. A significant number of patients reported Iloprost had improved Raynaud's symptomatology compared with placebo and this effect lasted for up to 6 weeks. The number of attacks of Raynaud's as recorded by patients in diary books was similarly reduced after Iloprost. Digital and nail-bed blood flows measured by laser-Doppler methods were increased for up to 6 weeks after Iloprost, but not after placebo infusions. Iloprost may be a useful therapeutic agent in the treatment of severe secondary Raynaud's syndrome.
A detailed retrospective study of 105 patients with Sjögren's syndrome (50 primary and 55 secondary cases), showed that 31 had vasculitis and 18 had neurological abnormalities which after full investigation were not attributable to other causes. Most of the neurological symptoms were mild and when found in patients with secondary Sjögren's syndrome were more characteristic of the underlying autoimmune rheumatic disease. We found no significant association between the frequency of either vasculitis or any autoantibodies and the presence of neurological disease, but did confirm a significant association between vasculitis and the presence of antibodies to extractable nuclear antigens. We therefore question whether severe and relapsing neurological disease is common in patients with Sjögren's syndrome.
A disturbance in endothelial cell (EC) function may be pathogenetic in the thrombotic tendency of patients with the lupus anticoagulant (LA). The ability of serum from normal subjects and patients with systemic lupus erythematosus (SLE), with and without the LA, to modulate the release of prostacyclin (PGI2) and the expression of procoagulant activity by cultured human EC was investigated. Only the 10% and 20% serum concentrations from patients with SLE-LA produced a significantly greater inhibition of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) release (the stable metabolite of PGI2) than control serum. However, when patients with SLE-LA having Raynaud's phenomenon were excluded from this group, there was then no significant difference between the effect of the patient and control serum. Serum from patients with SLE +/- LA caused a significant increase in EC procoagulant activity compared to healthy controls. The two-stage partial thromboplastin time expressed in seconds decreased from 66 (normal) to 34 (SLE - LA) and 31 (SLE + LA), but there was no significant difference between the patients with and without the LA. The significantly increased EC procoagulant activity induced by serum from patients with SLE +/- LA may account for the observed increased incidence of thrombotic events in patients with SLE. Our data suggest that factors other than decreased prostacyclin release are responsible for the altered hemostasis observed in patients with SLE + LA.
Reduced in vitro anti-influenza antibody response by peripheral blood mononuclear cells (PBMs) after vaccination was confirmed in a group of 28 patients with systemic lupus erythematosus (SLE), and also in 16 patients with some other autoimmune syndromes. This group of patients with SLE had higher serum anti-DNA binding, but there was no evidence of increased autoantibody production after vaccination, nor any clinical or laboratory evidence of flares in disease activity that are sometimes seen to follow intercurrent infection. Although a reduced in vitro antibody response may, to some extent, reflect redistribution of antibody producing cells, there appears to be more generalised impairment of the immune response in these patients, which cannot be accounted for by steroid/immunosuppressive therapy.
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Five centres in Great Britain and the Republic of Ireland have collaborated to produce a computerized index of clinical disease activity in systemic lupus erythematosus, based on the principle of the physician's intention to treat. The index assesses separately eight organ-based systems. The index has proved quick and easy to use despite a comprehensive database and compares favourably with two other indices of disease activity. It has great potential for use in multicentre studies of disease outcome and new therapies in systemic lupus erythematosus.
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Twenty one patients with severe systemic lupus erythematosus (SLE) were treated with three daily infusions of either 100 mg or 1 g of methylprednisolone on a randomised double blind basis. Nine patients with unsatisfactory outcome subsequently received the alternative therapy. Patients were rated for improvement on a four point scale using individualised criteria. On three occasions patients improved to 'ideal', on 12 there was 'useful' improvement, on 11 the patient remained static, and on four occasions there was deterioration. There was no significant difference between the clinical states after the two doses. The results suggest that any additional benefit of 1 g of methylprednisolone over 100 mg by repeated infusion in the treatment of active SLE is probably not enough to justify the potential hazards and cost involved.
Thirteen haematological parameters were measured in 44 patients with rheumatoid arthritis (RA) and 39 disease control patients with ankylosing spondylitis (AS). Using a 10 000 cells per sample automated differential counter the most frequent abnormalities found were monocytopenia, low numbers of large unstained cells, basophilia and increased numbers of cells with high peroxidase activity (HPX). The total white cell count, lymphocyte and monocyte counts, the HPX count, platelet distribution width and erythrocyte sedimentation rate were able to distinguish RA from AS at a statistically significant level. Discriminant function analysis showed that a maximum of 55% of RA patients could be correctly classified into disease state when combinations of six out of seven laboratory tests were used.
111Indium leucocyte scans were performed on 26 patients with active rheumatoid arthritis. An abnormal localization of radioactivity was observed in the gut of 12 of these patients, generally in the region of the terminal ileum, caecum and ascending colon. No difference was found in the intake of nonsteroidal anti-inflammatory drugs between those with positive and negative scans. Two patients with positive scans were on no medication. These observations suggest the possibility of a primary role for a gastrointestinal lesion in the aetiology of rheumatoid arthritis, although these abnormalities could be secondary or unrelated.