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D A Brewerton

Publications and source records attributed to D A Brewerton.

At least 19 recordsLinked to original sources
PubMed1991

Increased calcitonin gene-related peptide (CGRP), substance P, and enkephalin immunoreactivities in dorsal spinal cord and loss of CGRP-immunoreactive motoneurons in arthritic rats depend on intact peripheral nerve supply.

The distribution of peptides thought to be involved in pain modulation--substance P, calcitonin gene-related peptide (CGRP), and enkephalin--were studied in the spinal cord and dorsal root ganglia of polyarthritic rats and in rats with one sciatic nerve sectioned prior to induction of arthritis. In arthritic rats there was a bilateral increase of CGRP- and substance P-immunoreactive fibers and appearance of enkephalin-immunoreactive cell bodies in the dorsal horn of the lumbar (L4) spinal cord when compared to controls. In the corresponding dorsal root ganglia there were significant increases of CGRP- (P less than 0.02) and substance P- (P less than 0.001) immunoreactive cell bodies compared to controls. In the ventral horn of the control rats CGRP-immunoreactive motoneurons were abundant but were significantly (P less than 0.001) reduced in the arthritic spinal cord. Less pronounced changes were seen in the contralateral L4 spinal cord of arthritic rats with unilateral sciatic nerve section. In the ipsilateral dorsal horn, however, CGRP- and substance P-immunoreactive fibers were markedly depleted, and no enkephalin cell bodies were present. Furthermore, a number of CGRP-immunoreactive motoneurons were observed. In the ipsilateral L4 ganglia CGRP- (P less than 0.02) and substance P- (P less than 0.02) immunoreactive cells were significantly decreased compared to the contralateral side. The data suggest that pain perception is linked to complex interactions between CGRP, substance P, and enkephalin in sensory pathways and an intact peripheral input. The loss of CGRP-immunoreactive motoneurons may reflect muscular dysfunction associated with the arthritic condition.

Animals↗
PubMed1991

Echocardiographic diastolic abnormalities of the left ventricle in inflammatory joint disease.

Echocardiographic early diastolic abnormalities have been shown recently in 50% of men with ankylosing spondylitis. Similar techniques were used to investigate subjects with rheumatoid arthritis and psoriatic arthritis with or without spondylitis. These subjects had no clinical, radiographic, or electrocardiographic evidence of cardiac or respiratory disease. Echocardiographic abnormalities seen resembled those of ankylosing spondylitis in that the interval between minimum left ventricular dimension and mitral valve opening was prolonged in 12 of 22 subjects with rheumatoid arthritis and in seven of 11 subjects with psoriatic arthritis. Isovolumic relaxation time was significantly prolonged in four subjects with rheumatoid arthritis and one with psoriatic arthritis. Unlike ankylosing spondylitis, however, there was consistent reduction in peak rate of left ventricular dimension increase in subjects with rheumatoid arthritis and psoriatic arthritis. In addition, the dimension increase during atrial systole was greater than normal in nine subjects with rheumatoid arthritis and two with psoriatic arthritis. The most likely cause of these abnormalities is increased connective tissue deposition in the myocardium.

Adult↗
PubMed1991

Regional distribution of mast cells and peptide containing nerves in normal and adjuvant arthritic rat synovium.

Simultaneous visualization of nerves and mast cells in the rat synovium was possible with double staining. Thus, a direct comparison could be made of nerves and mast cells in the ankle joints of healthy rats and in those with severe adjuvant induced polyarthritis. Nerves were studied with avidin-biotin-peroxidase complex (ABC) immunostaining, using heterologous antisera to protein gene product 9.5 (PGP 9.5), a recently discovered neural protein, and the neuropeptides substance P and calcitonin gene related peptide (CGRP). Mast cells were visualized by metachromatic staining of granule heparin. With double staining of sections, a parallel distribution of mast cells and nerves in all parts of the normal synovium was noted. In rats with adjuvant induced arthritis, a near total parallel disappearance of mast cells and nerves in the synovium occurred. In the arthritic rat such mast cell/nerve "units" were only present in the region where synovium attaches to bone. The observed regional depletion of both nerves and mast cells in arthritis may be of importance in the pathophysiology of arthritis.

Animals↗
PubMed1990

Introduction: B27-associated diseases.

As an introduction, a hypothesis for the causation of ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and rheumatoid arthritis is outlined. It comprises ten basic mechanisms. With that hypothesis as a background, a further ten issues based on clinical evidence are presented for discussion. Finally, four questions are presented on behalf of the clinicians.

Arthritis, Infectious↗
PubMed1990

Nerves in inflammatory synovium: immunohistochemical observations on the adjuvant arthritis rat model.

Previous evidence has been presented that neurogenic input may influence adjuvant induced arthritis (AA) in rats. We now present evidence of alterations in synovial nerves in AA. Nerves were studied in well perfused and fixed rats, using immunohistochemistry with the sensitive avidin-biotin peroxidase complex (ABC) method and heterologous antisera to cytoskeletal protein gene product 9.5 (PGP) and the neuropeptides substance P and calcitonin gene related peptide (CGRP). The innervation of synovium was compared in normal rats and rats with AA. Observations concordant with what has been reported for neuropeptide nerves in the synovium of patients with rheumatoid arthritis (RA) are presented. It has been suggested that neural peptide substances are reduced in nerves of synovium from patients with RA. In the AA rat a specific reduction of lining zone and sublining nerves in the synovium was noted. The AA rat model is very suitable for studying the involvement of synovial nerves in arthritis, permitting optimal preservation of immunoreactive neural epitopes.

Animals↗
PubMed1989

Polymorphonuclear leucocyte motility in men with ankylosing spondylitis.

The polymorphonuclear leucocyte (PMN) response to a chemotactic or chemokinetic stimulus is enhanced in men with ankylosing spondylitis (AS). This effect does not parallel the severity of disease activity or the size of the acute phase response, and it is independent of non-steroidal anti-inflammatory drug treatment. Polymorph function is normal in HLA-B27 positive brothers of probands with AS and in other HLA-B27 positive individuals in the absence of disease. Polymorph motility is also normal in patients with psoriasis vulgaris or Crohn's disease, indicating that enhanced PMN motility is not a non-specific consequence of all inflammatory disorders.

Adult↗
PubMed1979

Degenerative joint disease in the hip and spine.

Clinical and radiographic assessment of the spine was carried out in 75 patients with osteoarthrosis (OA) of the hip and in 75 controls without hip disease. Radiographic degenerative changes in the spine were more frequent in the patients with OA hips, occurring in both the dorsal and lumbar spine. Moderate or severe changes were found in the dorsal spine in 29 patients with OA hips (compared with 12 controls), and in the lumbar spine in 32 patients with OA hips (compared with 10 controls).

Adult↗
PubMed1977

alpha 1-antitrypsin phenotypes in fibrosing alveolitis and rheumatoid arthritis.

alpha 1-antitrypsin (alpha 1-A.T.) phenotypes were determined in 55 patients with rheumatoid arthritis (R.A.), 33 patients with R.A. and either obstructive airways disease or recurrent chest infections, 49 patients with fibrosing alveolitis (F.A.), 22 patients with R.A. and F.A., and 200 healthy controls. A highly significant increase in the frequency of MZ phenotype was found among patients with F.A., both with and without R.A. Patients with R.A. alone had a normal distribution of phenotypes. Inherited modification of immune function may predispose to F.A. Alternatively, lowered levels of alpha 1-A.T. associated with non-M phenotypes may predispose to tissue damage with subsequent fibrosis.

Alleles↗
PubMed1977

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