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Biomedical subjects

C D Pusey

Publications and source records attributed to C D Pusey.

At least 145 records · Page 8Linked to original sources
PubMed1983

The treatment of quinine poisoning with charcoal haemoperfusion.

Quinine poisoning is rare but serious. Attempts at treatment by active removal have proved unsuccessful because of its high degree of protein binding. We describe two cases of non-accidental overdose of quinine (19.5 g and 15 g) with potentially fatal serum quinine levels. Both patients were treated by 2 periods of charcoal haemoperfusion during which quinine clearances of up to 125 ml/min were obtained. Both patients recovered, though one had some residual visual disturbance. We suggest that in cases of quinine poisoning, charcoal haemoperfusion may be a safe and effective method of drug removal, to be used with stellate ganglion block.

Adult↗
PubMed1983

Effects of cyclophosphamide on autoantibody synthesis in the Brown Norway rat.

The effects of cyclophosphamide on autoantibody synthesis were studied in an experimental model of glomerulonephritis due to autoantibodies to the glomerular basement membrane (GBM). Brown Norway rats develop anti-GBM antibodies, as part of a polyclonal response, when repeatedly injected with mercuric chloride (HgCl2). Anti-GBM antibody levels peak between days 11 and 14 and thereafter rapidly fall; convalescent animals show a time-dependent resistance to rechallenge with HgCl2 which remains significant for up to 3 months. The administration of cyclophosphamide, as a single intramuscular injection at day 0, has three distinct dose-dependent effects on anti-GBM antibody production. Firstly, lower doses (2.5 mg/kg) increase antibody levels at the time of peak response; secondly, higher doses (greater than or equal to 20 mg/kg) prevent antibody synthesis following HgCl2; and thirdly, the higher doses also reduce the response to rechallenge with HgCl2 3-4 months later. These effects of cyclophosphamide also apply to the polyclonal response to HgCl2, as judged by measurement of total IgG concentrations. Further investigation of the mechanisms of action of cyclophosphamide in this model should provide information relevant to the treatment of human autoimmune disease.

Animals↗
PubMed1983

Gastrointestinal manifestations of systemic vasculitis.

Systemic vasculitis is known to affect the gastrointestinal tract but the nature of the complication is poorly characterized. Out of 65 patients with systemic vasculitis, the majority of whom had renal disease, the intestine was found to be affected in 18. These comprised four of eight patients with polyarteritis nodosa, nine of seventeen with microscopic polyarteritis, four of thirty-six with Wegener's granulomatosis and one of four with Churg-Strauss syndrome. The features included abdominal pain (85 per cent), diarrhoea (50 per cent), gut haemorrhage (44 per cent) and abnormal liver function tests (50 per cent). Manifestations of gastrointestinal disease were evident at presentation in half the patients and led to a fetal outcome in five. Ileus, mucosal abnormalities, perforation and slow transit were evident radiographically, and selective visceral angiography showed aneurysms or organ infarcts in five patients. Histological assessment of gut biopsies (chiefly rectal) revealed non-specific inflammation or ulceration in nine patients and intramucosal haemorrhage in two. Focal areas of necrosis and ulceration in colonoscopic biopsies were highly suggestive of vasculitis whereas arteritis was only found in one full thickness biopsy. Hence the diagnosis of gastrointestinal complications depends largely on clinical evidence. In patients who survived, the gastrointestinal features remitted as the systemic illness improved following treatment with steroids, cyclophosphamide or plasma exchange.

Abdomen↗
PubMed1983

Drug associated acute interstitial nephritis: clinical and pathological features and the response to high dose steroid therapy.

Nine episodes of drug associated acute interstitial nephritis, in seven patients, were treated between 1972 and 1980. The drugs implicated were cotrimoxazole (three times), ampicillin, Magnapen (ampicillin and flucloxacillin), penicillin, gentamicin, paracetamol and bendrofluazide. The time from exposure to the onset of symptoms ranged from one to 30 days. Presentation was with acute renal failure, which was non-oliguric in five cases, accompanied by rash (four), fever (four), and loin pain (two). Renal biopsy was carried out in all cases, and showed a characteristic interstitial infiltrate comprising substantial numbers of lymphocytes and plasma cells, with a variable number of neutrophils, eosinophils and histiocytes. Immunofluorescence was negative in all four cases studied in the acute phase, and showed scattered deposits of IgG, IgM, IgA and C3 on the tubular basement membrane in one patient during recovery. Significant proteinuria and an abnormal urine deposit were present in all cases, and seven of nine had radiological evidence of enlarged kidneys. Seven episodes were treated with high doses of methyl prednisolone and in all there was a response with a diuresis or spontaneous fall in serum creatinine within 72 hrs, and recovery of virtually normal renal function. Of two cases who did not initially receive steroids, one improved more slowly and one developed chronic renal impairment.

Acetaminophen↗
PubMed1983

Production of a monoclonal antibody to autoantigenic components of human glomerular basement membrane.

We describe a mouse monoclonal antibody which reacts on immunoblotting with those components of collagenase digested human glomerular basement membrane (GBM) that are also recognized by autoantibodies in sera from patients with anti-GBM nephritis. Competition between the monoclonal antibody and anti-GBM autoantibodies was demonstrated in a solid phase radioimmunoassay, suggesting that both are directed against the same autoantigen.

Animals↗
PubMed1983

Plasma exchange and immunosuppressive drugs in the treatment of glomerulonephritis due to antibodies to the glomerular basement membrane.

Glomerulonephritis due to autoantibodies to the glomerular basement membrane (GBM) usually results in the rapid development of renal failure in untreated patients. We report our experience of the use of plasma exchange and immunosuppressive drugs in the management of this condition. Treatment consisted of daily 4 litre plasma exchanges for plasma protein fraction, together with prednisolone 60 mg daily (reducing to 20 mg daily by 4 weeks), cyclophosphamide 3 mg/kg daily and azathioprine 1 mg/kg daily. It was found that plasma exchange was generally required for 2 weeks, and cytotoxic drugs for 8 weeks. Forty four patients, aged 4 to 72 years, were treated. Anti-GBM antibody production was rapidly controlled, and in 21 of 34 patients antibody was undetectable within 8 weeks. Of 22 oliguric patients, none recovered renal function, 16 remained dialysis-dependent and 6 died; of 5 patients whose initial plasma creatinine was greater than 600 mumol/l, one improved and 4 proceeded to dialysis; and of 17 patients whose creatinine was less than 600 mumol/l, 15 recovered renal function, one became dialysis-dependent and one died. Long term follow-up of those who improved revealed that 2/16 subsequently deteriorated. Our results represent a great improvement in the prognosis of anti-GBM disease, and demonstrate that the majority of patients will recover renal function if treated before irreversible glomerular damage has occurred.

Adolescent↗
PubMed1983

Metabolism of IgG in type II mixed essential cryoglobulinaemia--autologous cryoprecipitated and normal homologous IgG are incorporated into complexes and metabolized in vivo at similar rates.

The metabolism of autologous cryoprecipitated and normal homologous IgG was studied in four patients with type II mixed essential cryoglobulinaemia. 131I-autologous IgG purified from each patient's cryoglobulin (Cryo-IgG), and 125I-pooled normal homologous IgG (N-IgG) were studied simultaneously to compare the extent of their incorporation into complexes with IgM in vitro and in vivo, and their turnover in vivo. A proportion of each preparation of IgG was incorporated into macromolecular complexes in vitro and in vivo in all patients, the Cryo-IgG only slightly more so than N-IgG. Results of the turnover studies were heterogeneous, but the common finding was the absence of any significant difference in the metabolism of Cryo-IgG and N-IgG. In two patients the fractional catabolic rates (FCR) of Cryo-IgG and N-IgG were increased and in one they were normal. The fourth patient was also hypogammaglobulinaemic (IgG 0.52 mg/ml) and it was shown that in vivo virtually all his IgG was combined with IgM; despite this the FCR of both types of IgG was reduced. These results suggest (1) that the IgG component of the cryoglobulins in these patients is unlikely to differ significantly from normal IgG and (2) that, contrary to expectation, complexed IgG is not necessarily rapidly eliminated from the circulation.

Aged↗
PubMed1983

Defective natural killer (NK) and killer (K) cell function in systemic lupus erythematosus.

Two aspects of lymphocyte function, natural killer (NK) and killer (K) cell activity have been studied in 21 normal subjects, 20 patients with systemic lupus erythematosus (SLE) and 6 patients with uraemia caused by non-immunological disorders. NK cell function was assessed by lymphocyte cytotoxicity of K 562 and Molt 4 target cells, and K cell function by killing of antibody coated Chang cells. Severely impaired NK and K cell activity was found in SLE (p = less than 0.001 for all target cells). In patients with uraemia (non SLE) NK cell cytotoxicity was normal, and K cell cytotoxicity was reduced but not as much as in the SLE group. Good correlation was found in normal subjects between NK and K cell activity. These results could not be directly related to disease activity, although NK and K cell function was lower in patients with active SLE than in patients with inactive disease, nor to treatment, for impaired killing was found in untreated patients in relapse and in patients in remission of all therapy. There was also no correlation between the level of circulating immune complexes and the defect in killing. These NK and K cell abnormalities could contribute to the pathogenesis of SLE by, for example, impairing mechanisms responsible for elimination of virus infected cells.

Adolescent↗
PubMed1980

Extreme right ventricular hypoplasia after relief of severe pulmonary stenosis. Use of balloon catheter occlusion of atrial septal defect in assessing right ventricular function.

A patient is described in whom extreme right ventricular hypoplasia and right-to-left shunting through an atrial septal defect occurred after relief of severe pulmonary stenosis. The ability of the hypoplastic right ventricle to deal with an increased volume load was assessed at cardiac catheterisation by occluding the atrial septal defect with a balloon tipped catheter.

Adult↗
PubMed1979

Leptospirosis and acute renal failure--clinical experiences and a review of the literature.

About 50 cases of leptospirosis are diagnosed each year in the United Kingdom, with an overall mortality of 5%. Renal failure, in association with jaundice, is commonly held responsible for this figure. Over a period of 18 years, 6 cases of leptospirosis complicated by renal failure were treated at the Royal Air Force Renal Unit; there were 4 survivors. The 2 deaths occurred before the unit policy of daily haemodialysis and total parenteral nutrition, and were both from haemorrhagic complications. The authors believe that patients with leptospirosis and progressive renal impairment should be managed in renal units experienced in the management of the hypercatabolic patient, and that this should improve their prognosis.

Acute Kidney Injury↗