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Biomedical subjects

C D Pusey

Publications and source records attributed to C D Pusey.

At least 109 records · Page 6Linked to original sources
PubMed1991

Ganciclovir treatment for cytomegalovirus infection in immunocompromised patients with renal disease.

The safety and efficacy of a 10-day course of ganciclovir therapy was assessed in 17 consecutive patients with proven cytomegalovirus infection. The patients were receiving immunosuppressive therapy for a variety of non-malignant renal conditions, including renal transplantation (seven patients), small vessel vasculitis (six patients), systemic lupus erythematosus (three patients) and Goodpasture's disease (one patient). Fifteen patients were pyrexial at the time of their cytomegalovirus infection. Twelve patients had pneumonitis manifesting as a pulmonary parenchymal infiltrate or a reduction in gas transfer. Fourteen patients had a significant lymphopenia (lymphocyte count less than 1 x 10(9)/l), nine were leucopenic (white cell count less than 3.5 x 10(9)/l) and nine had abnormal liver biochemistry. One patient had an infection of the ileum and one an infection of the larynx. All these disease manifestations responded completely to a single course of ganciclovir therapy. There were no clinical relapses and no side effects were observed. Ganciclovir is a safe and effective therapy when administered early in the course of cytomegalovirus infection in immunosuppressed patients with renal impairment.

Adolescent↗
PubMed1990

Towards a more rapid diagnosis of rapidly progressive glomerulonephritis.

An attempt was made to provide simple practical guidelines to alert general practitioners to the diagnosis of rapidly progressive glomerulonephritis and lead to early referral to hospital. The duration of illness before referral to this hospital and its effect on outcome in patients with crescentic nephritis were assessed retrospectively from the case notes of 24 patients referred over two years. Four patients had Goodpasture's syndrome, 11 Wegener's granulomatosis, seven microscopic polyarteritis, and two idiopathic progressive glomerulonephritis. The duration of symptoms before referral to the local hospital was similar in the four groups of patients and varied from one week to 28 months (mean 10 months). The duration of stay in the local hospital was two, nine, 11, and 180 days in the patients with Goodpasture's syndrome and a mean of four days (range one to eight) in those with Wegener's granulomatosis and 10 days (one to 18 days) in those with microscopic polyarteritis. In the local hospital the diagnosis was based on the results of renal biopsy and detection of antibodies to glomerular basement membrane in two patients with Goodpasture's syndrome and on the results of renal biopsy in seven of the other patients aided by the detection of antibodies to the cytoplasm of neutrophils (ANCA) in 10. Three of the 24 patients died and four required maintenance haemodialysis. Patients who present to their general practitioners with persistent non-specific symptoms should have a urine dipstick test and then blood tests and emergency referral to hospital if necessary. Hospital physicians should be aware of the speed and accuracy with which current assays can confirm a diagnosis of rapidly progressive glomerulonephritis.

Adult↗
PubMed1990

Renal involvement in Churg-Strauss syndrome.

Churg-Strauss syndrome is part of the spectrum of systemic vasculitis, but can be distinguished from the other necrotising vasculitides on the basis of clinical and histological criteria. Renal involvement is not regarded as a prominent feature and is generally mild. We report a series of 19 patients with Churg-Strauss syndrome referred to the Hammersmith Hospital between 1976 and 1986. Renal involvement was common (84%) and often severe: three patients had nephrotic syndrome; four presented with serum creatinine greater than 500 mumol/l; and two required dialysis. Focal segmental glomerulonephritis was the predominant lesion on biopsy (85%), often with necrotising features and crescent formation. Extravascular granulomata and eosinophilic infiltrates were uncommon. Treatment with high-dose prednisolone was generally successful in milder cases, but was not always sufficient to halt the progression of more severe vasculitis. In these cases, additional immunosuppressive therapy with azathioprine, cyclophosphamide or plasma exchange was of benefit. Renal disease improved in 14 of 16 patients, ten of whom have maintained normal renal function on follow-up. Only one patient died, as a result of progressive cardiac disease.

Adolescent↗
PubMed1990

Plasma exchange in refractory cutaneous vasculitis.

Eight patients with intractable cutaneous leucocytoclastic vasculitis were given a trial of plasma-exchange therapy. All but one improved, five substantially. Four have been successfully treated by intermittent plasma exchange for periods of 5-12 years. Apart from one episode of hepatitis B, possibly related to administration of fresh frozen plasma, no major adverse effects have occurred. Plasma exchange can be a valuable therapeutic option in patients with severe refractory cutaneous vasculitis.

Adult↗
PubMed1990

Kinetics and pathogenicity of autoantibodies induced by mercuric chloride in the brown Norway rat.

Repeated low-dose injections of mercuric chloride (HgCl2) in the brown Norway (BN) rat result in polyclonal activation which includes the induction of anti-glomerular basement membrane (GBM) autoantibodies. We examined the kinetics of various autoantibodies produced in vivo, general features of polyclonal activation such as total IgG levels and immune complex formation, and the relationship between organ specific autoimmunity and tissue injury in the kidney and thyroid. The production of immune complexes and autoantibodies to GBM and thyroglobulin was short lived, and the increase in levels of total IgG and antibodies to ssDNA and dsDNA was prolonged; the antibody response to collagen types I and II was intermediate in duration. Autoantibodies induced by HgCl2 caused only mild and variable tissue injury in the kidneys and did not induce abnormalities in the thyroid. These studies demonstrate that immunostimulation by mercury may result in the formation of a range of autoantibodies, with variable kinetics and pathogenicity.

Animals↗
PubMed1990

Erythroid HLA class I expression in 300 patients with haematological, renal and rheumatological disorders.

The expression of HLA class I was assessed on erythrocytes by haemagglutination with monoclonal antibodies to monomorphic epitopes on the heavy and light (beta 2-microglobulin) chains. Previously, enhancement of HLA class I expression was observed on erythrocytes of many patients with systemic lupus erythematosus (SLE) and chronic lymphatic leukaemia (CLL), and we have now tested erythrocytes from patients (and 130 normal controls) with other auto-immune diseases and renal and haematological disorders. The striking enhancement in patients with SLE and CLL was confirmed. A significant increase in expression was also observed in aplastic anaemia patients following bone marrow transplantation and in renal patients with primary glomerulonephritis who had received a transplant. No class I was expressed by erythrocytes from many patients with inherited haemoglobinopathies and high reticulocyte counts, which suggests that the enhancement in SLE patients cannot be accounted for by immature or young erythrocyte populations. The distribution of HLA-A and -B types in the patients with enhanced class I expression did not relate to those antigens previously detected more frequently on erythrocytes, B7(Bga), B17(Bgb), A28(Bgc), B8 or A10, and the enhancement was not associated with any particular HLA types.

Antibodies, Monoclonal↗
PubMed1990

Aortic dissection masquerading as systemic disease--the post-dissection syndrome.

Three patients presented with a prolonged illness accompanied by fever, weight loss, high ESR, neutrophilia, abnormal liver function tests, urinary abnormalities and, in one case, splinter haemorrhages and impairment of renal function. Aortic dissection was diagnosed 3-12 weeks after the onset of the illness, and probably accounted for the entire syndrome. All abnormalities resolved spontaneously over the following months. There are few similar cases in the literature, and the syndrome could easily pass unrecognized. Aortic dissection should be considered as a possible cause of any systemic illness of sudden onset, but especially if there is an initial history of chest or abdominal pain, or evidence of previous hypertension or other risk factors.

Aortic Dissection↗
PubMed1989

Modulation of antibody-mediated glomerular injury in vivo by bacterial lipopolysaccharide, tumor necrosis factor, and IL-1.

We have investigated the effects of LPS, human rTNF (hrTNF) and human rIL-1 beta (hrIL-1 beta) pretreatment on the intensity of antibody-mediated injury in vivo by using a passive model of anti-glomerular basement membrane (GBM) antibody-mediated nephritis in rats. The experiments show that all three pretreatments exacerbate injury in this model whether judged by albuminuria or the prevalence of glomerular capillary thrombi. The effect on albuminuria was dose dependent with all three treatments. The lowest effective dose of LPS was 0.025 microgram while those for hrTNF and hrIL-1 beta were 0.4 microgram and 0.5 microgram, respectively. All three pretreatments also increased the prevalence of glomerular capillary thrombi which were rare in rats injected with anti-GBM antibodies without pretreatment. LPS pretreatment appeared to be more effective in causing glomerular capillary thrombi than hrTNF or hrIL-1 beta and this was reflected in the correlations between albuminuria and the proportion of glomeruli with capillary thrombi. This relation was linear for all three pretreatments but the slope was appreciably greater for rats pretreated with LPS (0.37) when compared with results from rats given either hrTNF (0.22) or hrIL-1 beta (0.29). Pretreatment of nephritic rats with both cytokines increased the slope to 0.42 demonstrating a synergistic effect. The synergism of hrTNF with hrIL-1 beta was also demonstrated by the effective doses needed to induce albuminuria which was evident in rats treated with 0.05 microgram of IL-1 beta and 0.4 microgram of TNF. Neither the cytokines nor LPS caused clinical, morphologic, or biochemical evidence of renal toxicity when given alone in the dose used here but they did cause a transient increase in the number of neutrophils marginated in glomerular capillaries. Pretreatment of rats with LPS or cytokines increased the glomerular neutrophil influx after anti-GBM antibodies by roughly sixfold. Our experiments show that TNF and IL-1 can increase the severity of glomerular injury in nephritis; they may be important in modulating glomerular injury clinically.

Albuminuria↗
PubMed1989

Reactivity of monoclonal antibody P1 with glomerular basement membrane in thin-membrane nephropathy.

A monoclonal antibody, P1, possessing antiglomerular basement membrane specificity similar to that of naturally-occurring Goodpasture antibody, was used to study renal biopsy material from patients with thin-membrane nephropathy. Immunofluorescence and immunoperoxidase techniques were employed to detect tissue localisation after sections had been incubated with P1. Staining of glomerular and tubular basement membranes in the 14 patients with thin-membrane nephropathy was similar to that in 10 subjects with various other renal diseases, whereas three patients with Alport's syndrome all gave diminished or absent staining, as has been reported previously. These observations confirm that Goodpasture antigen is present in the basement membranes in thin-membrane nephropathy and that it reacts normally with P1 antibody. They also add to the evidence that the lesions of thin-membrane nephropathy and Alport's syndrome are fundamentally different. The staining method may be used as a differential diagnostic test.

Adult↗