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Biomedical subjects

A J Rees

Publications and source records attributed to A J Rees.

At least 127 records · Page 7Linked to original sources
PubMed1982

Infection and immunosuppression. A study of the infective complications of 75 patients with immunologically-mediated disease.

We have studied the infective complications in a group of 75 patients with immunologically-mediated disease who required high dose immunosuppression. There were 22 patients with anti-glomerular basement membrane antibody disease, 19 patients with systemic lupus erythematosus, 18 with wegener's granulomatosis and 16 patients with other forms of systemic vasculitis. The infection rate was 3.69 infections/patient, or 0.74 infections/patient/week of immunosuppression. Bacteria were the commonest infecting organisms (76.1 per cent); serious opportunist viral and fungal infections were less frequent (10.7 per cent) but opportunist pneumonias were an important cause of death. Sixteen patients died (21 per cent) and in 10 of these (62.5 per cent) death was considered to be primarily due to infection. Analysis of six aspects of host susceptibility to infection (age, renal function, dose of prednisolone, cyclophosphamide and azathioprine, and number of plasma exchanges) revealed no single factor as predisposing to infection in the whole group, but in 23 patients who suffered severe infective complications, renal impairment and increasing doses of prednisolone were associated significantly, particularly in combination (p = 0.06). Cyclophosphamide was associated with infection only in the presence of neutropenia, which was rare (13 infections in nine patients). The duration of plasma exchange was not related to the frequency of infection. Fifty patients needed an arteriovenous shunt to provide vascular access for haemodialysis or plasma exchange, and septicaemia occurred in 13; only two episodes of septicaemia were seen in patients without a shunt.

Adolescent↗
PubMed1982

Renal failure in familial lecithin: cholesterol acyltransferase deficiency.

Familial lecithin cholesterol acyltransferase (LCAT) deficiency is a rare inherited enzyme deficiency characterized by widespread disturbance of lipid metabolism and infiltration of many organs, including kidneys by lipids; usually it results in death from renal failure in the fourth or fifth decades. We have described a new family with LCAT deficiency and have studied three sisters with characteristic corneal opacities and no detectable plasma LCAT activity, together with eight obligate heterozygotes who have reduced LCAT activity but are phenotypically normal. All three sisters had the typical lipid abnormalities including large molecular weight particles in the low density lipoprotein (LDL) fraction of plasma previously described only in LCAT deficient patients with renal disease. However, only the youngest sister had proteinuria and renal failure. Renal biopsies from two of the sisters were infiltrated with lipid but the biopsy from the youngest contained electron dense deposits indistinguishable from those seen in immune complex disease. These findings cast doubt on the concept that large molecular weight LDL particles are the sole determinants of renal failure in LCAT deficiency.

Adult↗
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

Amyloid P-component in human glomerular basement membrane. Abnormal patterns of immunofluorescent staining in glomerular disease.

Serum amyloid P-component (SAP) is a normal plasma protein and is a constituent of normal human glomerular basement membrane. Immunofluorescence with anti-SAP antibody produced characteristic linear staining along the glomerular basement membrane in normal kidney. Distinctive abnormal staining patterns were seen in renal biopsy specimens from patients with diabetes, membranous glomerulonephritis, mesangiocapillary nephritis, systemic vasculitis, Goodpasture's syndrome.

Amyloid↗
PubMed1978

Strong association between HLA-DRW2 and antibody-mediated Goodpasture's syndrome.

In a study of HLA types in Caucasian patients with nephritis due to antibodies to glomerular basement membrane, antigen frequencies at A, B, or CW loci were normal. However, 15 out of 17 (88%) patients to whom DRW types were definitely assigned had HLA-DRW2 compared with 32 out of 100 Caucasian blood-donors. This difference is highly significant.

Anti-Glomerular Basement Membrane Disease↗
PubMed1977

Enhanced allergic tissue injury in Goodpasture's syndrome by intercurrent bacterial infection.

Studies of 16 relapses in seven patients receiving treatment for Goodpasture's syndrome showed that intercurrent bacterial infection seemed to be the precipitating event in 13 cases, whereas a rising antibody titre to glomerular basement membrane was responsible in only one. This association between infection and relapse in Goodpasture's syndrome has several implications for the pathogenesis of antibody-mediated tissue damage, and, clearly, more experiments are needed. Whatever the explanation, however, prevention and early diagnosis and treatment of infection in anti-GBM disease are important.

Adolescent↗
PubMed1977

Plasma-exchange and immunosuppression in the treatment of fulminating immune-complex crescentic nephritis.

Nine patients with fulminating immune-complex crescentic nephritis were treated by a regimen of intensive plasma-exchange, steroids, and cytotoxic drugs. In five patients with severe renal failure there was early and rapid improvement in renal function; in one patient an early but extensive focal necrotising glomerulitis was arrested; in two patients improvement was delayed for 3 and 7 weeks and could not confidently be attributed to therapy; one patient, anuric at presentation, did not recover renal function. Follow-up renal biopsy specimens, obtained in three patients, showed no evidence of active disease. With the Clq-deviation test, circulating immune complexes were detected in five patients before treatment and had disappeared when renal function had improved and stabilised: these patients showed the best response to therapy. In three patients temporary withdrawal of plasma-exchange was followed by the reappearance of immune complexes in the circulation and was accompanied in two patients by deterioration in renal function; reintroduction of plasma-exchange was followed by elimination of immune complexes and further improvement in renal function.

Adult↗
PubMed1976

Immunosuppression and plasma-exchange in the treatment of Goodpasture's syndrome.

Seven patients with Goodpasture's syndrome induced by anti-glomerular-basement-membrane (anti-G.B.M.) antibody were treated by a regimen of intensive plasma-exchange, cytotoxic drugs, and steroids. In the three patients retaining some renal function at presentation, this regimen led to suppression and eventual termination of antibody synthesis with improvement in renal function. In four patients, all anuric at presentation, antibody to G.B.M. persisted with variable reduction in the circulating levels. No return of renal function occurred in this group, all of whom had extensive changes on renal biopsy. Pulmonary haemorrhage, life-threatening in one patient, was rapidly controlled in all five patients in whom it was a presenting feature. In addition to its effect on antibody levels, plasma-exchange, using volume-replacement with plasma-protein fraction (P.P.F.), resulted in substantial depletion of complement and fibrinogen, mediators possibly contributing to the antibody-induced injury.

Adolescent↗
PubMed1975

Experimental drug intoxication: treatment with charcoal haemoperfusion.

Dogs were given large doses of barbiturates, glutethimide, ethanol, methaqualone, ethchlorvynol, meprobamate, chloral hydrate, paracetamol and aspirin. These were treated by haemoperfusion using a column packed with charcoal coated with an acrylic hydrogel. Clearances for most drugs were significantly higher than those reported for haemodialysis. Minimal clearances of common biochemical entities were observed and although leucocyte and platelet counts were diminished, no deleterious effects attributable to this were encountered. Careful histological examination of tissues derived from perfused dogs revealed no evidence of charcoal emboli.

Acetaminophen↗