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Biomedical subjects

B A Pussell

Publications and source records attributed to B A Pussell.

At least 55 records · Page 3Linked to original sources
PubMed1982

Failure to detect brain reactivity of lymphocytotoxins in cerebral lupus.

Lymphocytotoxic activity (LCA) was examined in the sera of 29 patients with systemic lupus erythematosus (SLE), including eight with cerebral involvement. LCA was elevated in 80% of samples and was significantly higher in the group with cerebral disease (P less than 0.001). No correlations were observed between LCA and immune complexes or complement components. Sera from 10 patients (six with cerebral SLE) were absorbed with homogenates of normal human frontal cortex and liver using protein standards to control for dilutional effects. No serum sample showed selective depletion of LCA following incubation with brain homogenate. It is concluded that no single parameter, including brain absorption of LCA, is effective in monitoring disease activity in cerebral lupus.

Absorption↗
PubMed1981

Proliferative glomerulonephritis in mice given intravenous Corynebacterium parvum.

Mice given a killed suspension of Corynebacterium parvum (C.p.) developed nephritis as part of an immune complex disease. The nephritis was dose-related. After a single dose of 70 microgram (a human-equivalent dose) or of 466 microgram there was a mesangiopathic glomerulonephritis and after repeated human-equivalent doses there was a mesangiocapillary glomerulonephritis. Antibodies to C.p. increased and circulating immune complexes were detected. Mice receiving repeated doses also developed an arteritis. Study of this model may help in the understanding of human immune complex disease and the pathogenesis of glomerulonephritis.

Animals↗
PubMed1981

Lymphocytotoxic activity in primary glomerulonephritis: evidence for immune complex-mediated cytotoxicity.

Sera from 84 patients with primary glomerulonephritis (GN) were tested for lymphocytotoxic activity (LCA) against panels of (a) normal peripheral lymphocytes and (b) B-lymphocytes obtained from patients with chronic lymphatic leukaemia (CLL). Significant LCA was found particularly in minimal change GN, acute post-streptococcal GN (AGN-PS) and mesangiocapillary GN (MCGN) where 62%, 75% and 45% respectively of samples were positive. No correlation was observed between LCA and levels of C3 or immune complexes. All but three positive sera showed reactivity against T and B cells; these three showed only T cell cytotoxicity. Fractionation of 6 sera (2 minimal change GN; 2 AGN-PS; 2 MCGN) on Sephadex G200 showed cell killing to reside in the exclusion peak. When samples were separated under dissociating conditions at pH 3.0, there was significant reduction in LCA (P less than 0.001) compared to that of fractions collected at pH 7.2. The same protocol did not affect the lymphocytotoxicity of anti-human lymphocyte globulin. The data suggest that lymphocyte killing in GN is mediated at least in part by antigen/antibody complex activity. The reaction is immunochemically similar to that seen in systemic lupus erythematosus and may have comparable implications for antibody regulation in GN.

Antigen-Antibody Complex↗
PubMed1980

Relapses in Wegener's granulomatosis: the role of infection.

Out of 20 relapses that occurred in patients with Wegener's granulomatosis, nine were provoked by bacterial or viral infection. Seven of these occurred during maintenance treatment in response to infection with common pathogens, and treatment of the infection alone was insufficient to produce remission. Circulating immune complexes were seen only in relapses due to infection and rarely in infections that occurred without relapse. A possible mechanism for infection-provoked relapses is that infection-derived complexes reactivate disease; alternatively, the acute-phase or cellular response to infection may enhance quiescent disease. Infection may exacerbate Wegener's granulomatosis and other autoallergic diseases, but whether it does so by a common mechanism is not known and further study is required.

Antigen-Antibody Complex↗
PubMed1980

Complement deficiency and nephritis. A report of a family.

A family is described in which three children had homozygous deficiency of C3 and in which both parents and two other children were heterozygous for the C3 null gene. One child with heterozygous C3 deficiency was found to have membranoproliferative glomerulonephritis; proteinuria and/or microscopical haematuria was present in all three homozygous C3-deficient children. All children with homozygous or heterozygous C3 deficiency were, to a varying degree, susceptible to infection. The only child of the family with normal complement had no increased risk of infection and no renal disease. This family study provides further support for the proposal that C3 deficiency predisposes to nephritis.

Adolescent↗
PubMed1980

The C1q binding assay in systemic lupus erythematosus: discordance with disease activity.

To investigate the relationship of C1q binding assay (C1qBA) to disease activity in systemic lupus erythematosus (SLE), a retrospective study was carried out on 232 C1qBA performed in 33 patients with SLE. When initial values were assessed (33 tests in 33 patients), there was no relationship between positive and negative C1qBA and abnormal renal function (P = 0.482, Fisher exact test). Of 87 tests performed during active renal disease, 34 (39%) were positive; of 48 tests during active non-renal disease, 25 (52%) were positive; of 83 tests when the disease was inactive, 45 (54%) were positive; and of 14 tests during episodes of infection, 10 (71%) were positive. Corresponding means for the C1qBA were follows: renal 65.66, non-renal 78.02, inactive 56.04, infection 135.79 (no significant differences by Student's t-test). There was no significant relationship with the C1qBA when comparing active disease (renal and non-renal) with inactive disease (chi 2 Yates = 1.875, P = 0.171). When renal function abnormalities were analyzed separately, the C1qBA values were independent of azotemia or proteinuria (chi 2 Yates = 1.399, P = 0.237). Patients were seen with progressive renal disease who had consistently negative C1qBA, as well as patients with benign clinical courses despite elevated C1qBA. The discordance of the C1qBA results with disease activity in SLE highlights the limitations of immune complex (IC) determinations by a single technique, and stresses the importance of evaluating such tests in terms of both their specificity and sensitivity. These data further suggest that the relationship of IC to the disease process in SLE may be a complex one.

Complement C1↗
PubMed1980

Immune-complex disease in mice and humans given C. parvum.

The present studies in mice and cancer-bearing patients, treated with C. parvum (CP) immunotherapy, were to determine the effects of CP on the production of immune complexes (IC) and associated disease. Using the Clq-binding assay, circulating immune complexes were detected in mice given a single high dose of CP (466 microgram) and repeated human-equivalent doses (70 microgram). All mice treated with CP developed proliferative glomerulonephritis, the severity of which was dose-related. The histological and immunofluorescent patterns of the nephritis were those attributed to immune-complex disease. The mice had haematuria but were not in renal failure. Fifty patients with inoperable lung cancer were studied. All received radiotherapy. Twenty-two had no other treatment (controls) and 28 were treated with infusions of CP. Using 2 immune-complex assays (Clq binding and monoclonal rheumatoid-factor binding) IC were found in 10/22 control patients but these did not develop haematuria or proteinuria. Twenty-four of the 28 patients treated with CP developed transient haematuria and/or proteinuria with red-cell and hyaline casts, the changes resolving over 5 days. Immune complexes were detected in 5 of these 28 patients before CP treatment. Although 16/28 had IC at the time of haematuria and proteinuria, these findings were difficult to interpret because IC may occur in response to the tumour, the radiotherapy, or the CP. Although no patient developed renal failure, we believe that those treated with CP should have regular assessment of their renal function.

Adult↗
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

Metabolism of human beta 1H: studies in man and experimental animals.

Metabolic studies were performed with a purified, functionally-active preparation of human beta 1H. In seven normal human subjects, the half-life ranged from 66--87 hr with fractional catabolic rates (FCR) of 1.04--1.63%/hr. Synthesis rates were 0.22--0.57 mg/kg/hr and extravascular distribution ratios were 0.34--0.67. There was evidence of extra-vascular catabolism in each subject. In sixteen patients with immunological disease four showed hypercatabolism of beta 1H. However, three patients with C3 mephritis factor (NeF) had normal beta 1H turnover despite profound reduction in C3 concentration; it is suggested that the reaction of beta 1H with the C3b. Bb convertase exposes it to a catabolic site and that in the NeF patients the NeF stabilized convertase prevents such exposure. Studies of the acute phase response were carried out in nine patients following elective surgery, with C-reactive protein (CRP) used as the control protein: six patients showed no rise in beta 1H levels and three showed a small (20%) rise whereas all exhibited a gross rise in CRP. Pre-incubation of 125I- beta 1H with NHS, with NHS in the presence of NeF and with C3b+C3b 1NA caused no change in beta 1H turnover in animals despite demonstrable total C3 conversion with the NeF.

Animals↗
PubMed1978

Value of immune-complex assays in diagnosis and management.

Two complement-dependent assays for circulating immune complexes, the C1q-binding assay and the conglutinin binding, were used to study patients with suspected immune-complex disease. Complexes were detected most frequently in multisystem disease such as infective endocarditis (69%) and systemic lupus erythematosus (60%), and less frequently in isolated nephritis (26% of membrano-proliferative nephritis). Sequential estimations in 32 patients showed that concentrations of circulating immune complexes correlated with disease activity and were useful in monitoring therapy.

Adolescent↗
PubMed1977

The Nail Patella syndrome--a report of a family.

This report describes two cases of the Nail Patella Syndrome with renal involvement. Pathological studies include immunochemistry, light microscopy, immunofluorescence and electron microscopy. The possibility of secondary immune damage to altered glomerular basement membrane is suggested as a cause of the progressive renal disease which occurs in some of these cases.

Adolescent↗
PubMed1977

The complement system in infectious mononucleosis.

The complement system was investigated in 34 patients with infectious mononucleosis. Three had specific complications: one haemolytic anaemia, one severe arthralgia/myalgia and one proliferative glomerulonephritis. Complement changes consistent with classical pathway consumption were seen in ten of the uncomplicated group and the patients with haemolytic anaemia and arthralgia/myalgia. The patient with glomerulonephritis showed evidence of alternative pathway utilisation including C3 splitting activity and the deposition of properdin on renal biopsy. The complement findings suggest that circulating immune complexes are common in such patients and are likely to play a role in the pathogenesis of the complications. It is proposed that both complement pathways may be required for the effective clearance of viral material from the circulation.

Complement C1 Inactivator Proteins↗
PubMed1976

Measles infection. Involvement of the complement system.

The complement system was examined in fifty patients with acute, apparently uncomplicated measles; forty-six were children less than 10 years old. Twenty showed evidence of pathological complement activation. In thirteen of these the pattern was consistent with activation of the classical pathway while in the other seven data suggested utilization of an alternative pathway. An additional eleven patients had isolated reduction in Clq without alteration in concentration of other components; these were excluded from the classical pathway group. No patient had detectable immune complexes or C3 splitting activity in serum; however, it is suggested that the abnormal complement patterns observed are likely to indicate the presence of circulating immune complexes in a high percentage of patients with this infection.

Antigen-Antibody Complex↗