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Biomedical subjects

A D Blann

Publications and source records attributed to A D Blann.

At least 19 recordsLinked to original sources
PubMed1992

Plasma, platelet and erythrocyte glutathione peroxidases as risk factors in ischaemic heart disease in man.

1. Plasma, platelet and erythrocyte glutathione peroxidase activities and serum lipid concentrations were measured in patients with ischaemic heart disease and matched control subjects. 2. Mean plasma and platelet glutathione peroxidase activities were significantly lower in the patients with ischaemic heart disease. Erythrocyte glutathione peroxidase activities and serum lipid concentrations were similar in patients with ischaemic heart disease and control subjects. 3. No correlations between plasma, platelet and erythrocyte glutathione peroxidase activities were observed. 4. The combination of plasma and platelet glutathione peroxidase activities provided an 86% discrimination between patients with ischaemic heart disease and matched control subjects. 5. Our data suggest that plasma and platelet glutathione peroxidases may be significant risk factors for ischaemic heart disease. Plasma glutathione peroxidase is a previously unrecognized risk factor.

Adult↗
PubMed1992

Endothelial cell damage in primary biliary cirrhosis: influence of cholestasis and immunological mechanisms.

In a study looking for evidence of endothelial cell damage in primary biliary cirrhosis, serum from patients was found to be significantly more cytotoxic to cultured endothelial cells in vitro than normal control serum (P less than 0.001). Serum also contained higher levels of von Willebrand factor antigen (vWFAg, a specific product of the endothelium) than control serum (P less than 0.001). Cytotoxicity correlated with serum levels of vWFAg (P less than 0.05) and with serum bilirubin (P less than 0.05). No correlations were found between cytotoxicity and circulating immune complexes, C-reactive protein or CH50. The study was controlled by serum from patients with other liver diseases. In these samples vWFAg (P less than 0.003), and bilirubin levels (P less than 0.001) were also raised relative to normal controls. vWFAg levels again correlated with levels of bilirubin (P less than 0.05). Tissue culture experiments showed that purified bilirubin was cytotoxic to human umbilical vein endothelial cells and induced the release of vWFAg. The case report of a patient with obstructive jaundice again indicated that levels of bilirubin and vWFAg were related. These results suggest that endothelial cell damage occurs in both primary biliary cirrhosis and to a lesser extent in other liver diseases, and may be mediated by cholestasis, not by humoral immunological mechanisms.

Bilirubin↗
PubMed1992

Damage to the endothelium in Sjögren's syndrome: lack of correlation with antinuclear antibody titre and presence of antibodies to SSA or SSB autoantigens.

Serum levels of von Willebrand factor antigen (as an index of damage to the endothelium) and tissue antinuclear antibodies and antibodies to SSA (Ro) (which have been associated with vasculitis) and SSB (La) autoantigens were measured in patients with Sjögren's syndrome. Although high levels of all indices were recorded, there were no intercorrelations. This provides evidence that although tissue autoantibodies may be useful in confirming a diagnosis, they have no place in the pathological course of the disease and so may be an epiphenomenon.

Antibodies, Antinuclear↗
PubMed1992

Plasma and serum von Willebrand factor antigen concentrations in connective tissue disorders.

Concentrations of serum and plasma von Willebrand factor antigen were measured in over 200 patients with a variety of connective tissue diseases, and in control samples from over 200 asymptomatic individuals. This comprehensive study found the highest concentrations of von Willebrand factor antigen in patients with vasculitis, Sjögren's syndrome, Felty's syndrome, giant cell arteritis and polyarteritis nodosum. Raised values were also found in rheumatoid arthritis, systemic lupus erythematosus, polymyalgia rheumatica, systemic sclerosis, Raynaud's syndrome, Takayasu's arteritis and Wegener's granulomatosis, but not in oesteoarthritis. It is possible that the difference in von Willebrand factor antigen concentrations in two sub-groups of systemic necrotising arteritis (Wegener's granulomatosis and polyarteritis nodosum) may imply different disease processes. The large numbers involved have allowed us to confirm or question smaller studies of the role of this molecule in connective tissue disease.

Biomarkers↗
PubMed1992

von Willebrand factor antigen: a radial immunodiffusion method evaluated and compared with an ELISA method.

A new commercial kit method for the quantification of von Willebrand factor antigen (vWFAg) by radial immunodiffusion was compared to an established ELISA technique. Major discrepancies were found between the two methods. The radial immunodiffusion method had poorer intra- and inter-assay coefficients of variation than the ELISA method, although there was adequate inter-method agreement when 100 plasma samples from controls and patients were compared. However, there was a great difference in values obtained for vWFAg in the reference sample supplied with the commercial kit and that obtained directly from the National Institute for Biological Standards and Controls. There were also differences in levels of significance when vWFAg was measured by the two techniques in different clinical groups, and standard deviations were larger when the kit method was used. It is suggested that on scientific and economic grounds, the commercial radial immunodiffusion kit does not offer a competitive advantage over the ELISA method.

Autoantigens↗
PubMed1991

Activated, cytotoxic lymphocytes in systemic vasculitis.

Peripheral blood lymphocytes from some patients with rheumatoid vasculitis and giant cell arteritis were cytotoxic in vitro towards endothelial cells, but not fibroblasts. Use of cell surface markers and cell density showed that cytotoxicity correlated with numbers of HLA-DR bearing cells, but not with cells bearing CD3, the transferrin receptor, or less dense lymphocytes. We concluded that activated, cytotoxic lymphocytes were present in the peripheral blood of a sub-set of patients with vasculitis.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1991

Increased release of von Willebrand factor antigen by endothelial cells whilst in active growth phase.

Human umbilical vein endothelial cells and fibroblasts were grown in tissue culture (with and without added endothelial cell growth supplement) to confluence. von Willebrand factor antigen was measured in supernatants every 24 hours. Cells grown in medium with growth supplement reached confluence before those grown without the supplement. von Willebrand factor antigen release was greatest under both sets of conditions when cells were in their most active growth phase, and rate of release slowed when cells were confluent. Fibroblasts grew more rapidly, showed a small response to the growth supplement, but supernatant von Willebrand factor antigen could not be detected. The implications of these findings for atherogenesis are discussed.

Animals↗
PubMed1991

Venostasis, subclinical vasculitis and von Willebrand factor antigen.

Von Willebrand factor antigen (VW FAg) has been used as a marker for vasculitis and raised levels have been shown to correlate with active disease. The use of VW FAg levels in the diagnosis of vasculitic disorders has been proposed. However, certain cases of vasculitis have normal VW FAg levels and are difficult to diagnose; this is of importance because of the high mortality associated with these disorders. It has been suggested that venostatic stress can be used as a provocative test for stimulating VW FAg release, thereby improving the speed and sensitivity of diagnosis. We tested this hypothesis in a mixed group of 35 patients with vasculitis, systemic lupus erythematosus and rheumatoid arthritis and 16 controls. At baseline, although the levels were not outside the laboratory range, the disease groups had raised VW FAg compared with the simultaneously tested controls. Venostatic stress increased VW FAg activity in all disease groups, control levels also increased and differences between controls and disease groups diminished in significance. Therefore venostatic stress with VW FAg measurement does not produce a more sensitive test for vasculitis. Venostasis should be avoided when measuring VW FAg levels.

Adult↗