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Biomedical subjects

B D Williams

Publications and source records attributed to B D Williams.

At least 127 records · Page 7Linked to original sources
PubMed1985

Meningococcal endocarditis with profound acquired hypocomplementaemia.

A patient is described who presented with chronic endocarditis, due to Neisseria meningitidis, affecting a previously normal mitral valve. The illness was associated with glomerulonephritis that caused renal impairment and the nephrotic syndrome. Despite antibiotic treatment and replacement of the mitral valve, serum complement values remained very low, only returning to normal when immune complexes and a type III cryoglobulin disappeared from the circulation three months after resection of the valve vegetation. Such acquired hypocomplementaemia may have contributed to the chronicity of the disease process in this patient.

Adult↗
PubMed1985

The penetration of ceftriaxone into synovial fluid of the inflamed joint.

Fifteen patients with acute exacerbation of rheumatoid arthritis each received a 1 g bolus intravenous injection of ceftriaxone. Serum and synovial fluid was sampled at intervals between 1 h and 24 h later and assayed for ceftriaxone. Synovial fluid leucocyte counts and albumin content were measured concomitantly. Detectable levels of ceftriaxone were found in synovial fluid and serum 24 h after injection. Synovial fluid ceftriaxone concentration ranged between 66% and 100% of the concomitant serum levels. No correlation was observed between synovial fluid ceftriaxone concentration and synovial fluid leucocyte count and albumin concentration.

Arthritis, Rheumatoid↗
PubMed1985

Reticuloendothelial Fc function in normal individuals and its relationship to the HLA antigen DR3.

Reticuloendothelial Fc function was examined in 24 normal individuals by determining the clearance rates of erythrocytes coated with rhesus antibody (IgG RBC) or chemically modified by treatment with n-ethyl malemide (NEM). The mean clearance times for the IgG RBC (52.1 +/- 10.3 min) and the NEM cells (87.5 +/- 14.7 min) in the 10 individuals who possessed the HLA antigen DR3 did not differ significantly from the mean clearance times observed in the 14 non-DR3 controls (IgG RBC 51.5 +/- 6.9 min and NEM cells 77.6 +/- 4.5 min). Two individuals with prolonged clearance times for the IgG RBC were identified in each group, the values observed being 80, 103, 119 and 137 min. These prolonged clearance times could not be attributed to lower numbers of antibody molecules bound to the red cell surface. The prolonged clearance times were reproducible but the putative Fc receptor defect in these individuals could be abolished by using IgG RBC obtained from different donors. When IgG RBC, prepared from a single donor were used to assess Fc function, no difference in the clearance rates of DR3 positive and DR3 negative individuals was found. Our results indicate that differences in the distribution of the rhesus antigen on the red cell surface can markedly influence the fate of these cells in vivo. We suggest that this is the explanation for our failure to confirm the association between Fc receptor defects and the HLA antigen DR3.

Erythrocytes↗
PubMed1985

Reticuloendothelial Fc receptor function in patients with Sjogren's syndrome.

The functional status of the reticuloendothelial Fc receptor in patients with Sjogren's Syndrome was examined by determining the clearance from the circulation of IgG coated erythrocytes which had been obtained from a single donor. 18 patients with Sjogren's Syndrome were studied and the results compared with those obtained from 18 patients with Rheumatoid Arthritis and 27 healthy controls. Abnormal Fc mediated clearance was observed in 3 individuals with Sjogren's Syndrome and 2 patients with Rheumatoid Arthritis. Extraglandular disease was not associated with abnormal Fc function and there was no correlation between the clearance rates and the immune complex levels, complement levels or rheumatoid factor titre. A comparison of the clearance rates obtained using the patients own red cells with those derived from using a single donor showed that the source of cells used had a significant effect on the clearance rate. Our findings provide no support for the idea that defective Fc function may be of pathogenic significance in the development of more extensive disease in patients with Sjogren's Syndrome.

Adult↗
PubMed1984

Deposition of eosinophil cationic protein in granulomas in allergic granulomatosis and vasculitis: the Churg-Strauss syndrome.

Biopsy specimens and tissues obtained at necropsy from two women who died after developing the Churg-Strauss syndrome were analysed to see whether granulomas in these patients contained activated eosinophils or secreted eosinophil cationic proteins, or both. Immunocytochemical studies with monoclonal antibody EG2 showed large amounts of eosinophil cationic protein and eosinophil protein-X (which are toxic for heart cells and other tissues) in the granulomas. Many activated and degranulating eosinophils were seen to be migrating from the blood into these areas. Eosinophils may play a central part in the development of lesions in the heart and other tissues in the Churg-Strauss syndrome.

Adolescent↗
PubMed1983

Immune complexes in Hodgkin's disease: isolation, immunochemical and physico-chemical analysis.

Immune complexes (IC) present in sera from patients with Hodgkin's disease (HD) were isolated using three different affinity columns: C1q-degalan, anti-C1q sepharose and conglutinin (K)-degalan. The isolated IC were analysed by immunoprecipitation, SDS-PAGE and sucrose density gradients and compared with IC similarly isolated from patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and in vitro prepared BSA-anti-BSA complexes. Isolated material from each disease, and BSA-anti-BSA complexes contained proteins compatible with true immune complexes--IgM, IgG, C1q and C3 breakdown components. Albumin, fibronectin and CRP, whose affinity for IgM, C1q and C3 are known, were co-isolated along with IC material. The size of isolated IC in HD ranged from 8-40S on sucrose density gradients. Despite the operational difference in detecting and isolating HD complexes via the C1q ligand (C1q-degalan or anti-C1q column) and C3bi (K-degalan), material purified by both methods showed remarkable similarity on SDS-PAGE and immunoprecipitation analysis. Although IC isolated from different diseases showed disparate banding patterns on SDS-PAGE this was attributed to a variation in the relative concentrations of constituent proteins--IgM, IgG and C3 breakdown products. IgM, IgG and C3 bind loosely, and non-specifically, to macromolecular aggregates formed around immune complexes. Using the anti-C1q column, most of this material could be eluted using 0.02M EDTA. Least protein, yet the most specific for antigen and antibody was eluted at pH 3.0.

Antigen-Antibody Complex↗
PubMed1982

Anti-C1q column: ligand specific purification of immune complexes from human serum or plasma. Analysis of the interaction between C1q and immune complexes.

An efficient and reproducible procedure has been developed for the specific isolation of immune complexes. PEG precipitation of EDTA serum or plasma was an essential preliminary step to separate complex-bound from free C1q. PEG had no discernible effect on the molecular weight size of the extracted complexes. Redissolved complexes were incubated with a Sepharose-4B column coated with anti-human C1q antibodies and following removal of unbound material the bound complexes were sequentially eluted with 0.02 M EDTA, 0.5 M NaCl and 1 M propionic acid. Characteristics of the affinity column were established by the purification of 125I-labelled BSA-anti-BSA complexes and heat-aggregated IgG (HAGG) incubated in normal human serum (NHS). EDTA and NaCl eluted complexes were of similar molecular size and contained antigen, specific antibody, as well as human IgM, IgG, albumin, C3, C3c, C3d and C1q. Acid eluted complexes contained the highest yield of specific antigen and antibody and comprised in addition human C1q and C3d. Activation of complement components after C1q made the bond between C1q and immune complexes resistant to 0.5 M NaCl and interfered with the binding between solid phase anti-C1q and complex bound C1q. Using BSA-anti-BSA complexes and HAGG activated in NHS it was apparent that only a minority of the complexed material was isolated via the C1q ligand and this probably applies to the C1q binding assay. Most complexed material could be isolated using an anti-C3 affinity column.

Antigen-Antibody Complex↗
PubMed1980

Circulating immune complexes in patients with ankylosing spondylitis.

EDTA plasma samples from 13 patients with ankylosing spondylitis (AS) were fractionated on Sephadex G-200 and the quantities of C3 and IgG within the first protein peak determined by a sensitive haemagglutination-inhibition assay. Seven patients with AS had G3 detectable in the first peak and this was associated with an increased concentration of IgG in the corresponding fraction. These 7 patients had more active disease but did not have more peripheral arthritis. Our results indicate that circulating immune complexes capable of initiating complement activation are present in the circulation of patients with ankylosing spondylitis.

Antigen-Antibody Complex↗
PubMed1979

Inhibition of reticuloendothelial function by gold and its relation to postinjection reactions.

A patient with rheumatoid arthritis developed severe exacerbation of symptoms 18 hours after an injection of gold thiomalate (sodium aurothiomalate). Immune complexes were present in his serum and synovial fluid; in the synovial fluid they were associated with intense complement activation. The effect of gold salts on splenic reticuloendothelial function was determined by measuring the clearance of heat-damaged erythrocytes from the circulation. Gold thiomalate (50 mg) substantially delayed clearance in the patient but had no effect in four other patients with rheumatoid arthritis who had not had a postinjection reaction. Severely impaired clearance also occurred in three out of four healthy people given 100 mg gold but they remained asymptomatic. The postinjection reaction may be an immune-complex disease that is triggered in certain patients because gold transiently inhibits reticuloendothelial function.

Arthritis, Rheumatoid↗
PubMed1979

Defective reticuloendothelial system function in rheumatoid arthritis.

The function of the splenic reticuloendothelial system in patients with rheumatoid arthritis (R.A.) was assessed by determining the clearance of autologous heat-damaged erythrocytes from the circulation. 11/13 patients with active R.A. had a defect in the clearance of red cells and there was a significant inverse correlation between splenic function and the level of circulating immune complexes detected by a Clq-binding assay. Splenic function was normal in 13 patients with inactive disease who had been treated with either gold or prednisone. A serial study on 1 patient with active R.A. showed a clear correlation between fluctuations in disease activity, splenic function, and the level of circulating immune complexes.

Adult↗
PubMed1979

The complement system.

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Complement Pathway, Alternative↗
PubMed1978

Immunoradiometric assay of salivary anti-c3 antibodies.

By an immunoradiometric assay IgA and IgG anti-C3 antibodies were found in adult parotid salivas. The binding of the IgA antibodies to complement coated red cells could be reversed by washing in buffer containing 0.01 M EDTA but IgG antibodies were unaffected. The binding of IgA antibodies was inhibited by small quantities of purified C3. This assay may prove useful in the detection of anti-C3 antibodies in other body fluids.

Adult↗
PubMed1978

Detection of immune complexes in serum of patients with ankylosing spondylitis.

Immune complexes were measured in the sera of 18 patients iwth ankylosing spondylitis and 5 normal control subjects by their ability to inhibit antibody-mediated lymphocyte-induced cytotoxicity. 11 of the spondylitis and none of the control sera contained circulating complexes. Fractionation of sera on Sephadex G-200 showed that complexes were of two molecular sizes, one of intermediate and the other of large molecular weight. The presence of immune complexes did not correlate with activity of disease or the presence of peripheral arthritis although the one patient with polyarthritis had the highest level of complexes detected in this study. The nature of the antigen in these antigen-antibody complexes is of great interest since it may provide evidence of the aetiological agent in the disease.

Adult↗
PubMed1978

Comparative clinical study of protein SAP (amyloid P component) and C-reactive protein in serum.

The serum concentration of protein SAP (amyloid P component) has been measured for the first time in a substantial series of normal individuals and patients with various diseases, and the results contrasted with the levels of the related protein C-reactive protein (CRP). The mean +/- s.d. concentration of protein SAP was 43 +/- 14 microgram/ml in seventy-six normal men, 33 +/- 10 microgram/ml in eighty-six normal women and 4 +/- 2 microgram/ml in thirty-six normal cord sera. Unlike CRP, whick is a major acute phase reactant, protein SAP was only slightly elevated in inflammatory and neoplastic diseases in which CRP was greatly increased. The level of protein SAP was significantly depressed in patients with hepatic disease, suggesting that its measurement might be of value in their management.

Amyloid↗