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Biomedical subjects

N J Sheehan

Publications and source records attributed to N J Sheehan.

At least 19 recordsLinked to original sources
PubMed1993

Polyautoimmunity in a young woman.

A young woman with the HLA phenotype A1, A2, B5, B8, DR3, DR4 developed RA, idiopathic thrombocytopenic purpura (ITP), pernicious anaemia (PA), Hashimoto's thyroiditis (HT), systemic sclerosis (SS), pancreatic exocrine insufficiency (PEI) and coeliac disease (CD) before dying from vasculitic complications. A family study revealed RA, PA and insulin-dependent diabetes mellitus (IDDM) amongst her first degree relatives. Her case emphasizes the clinical and immunogenetic links between the autoimmune diseases.

Adult↗
PubMed1991

Arthritis artefacta: factitious disease in rheumatology.

Self-induced disease can be difficult to diagnose and costly of time and money to investigate. The key is to think of the possibility. Five patients in whom the evidence for factitious rheumatological illness was strong are discussed and their histories, physical signs and family backgrounds are explored in relationship to factitious disease presenting in other fields. Young immature individuals seem most at risk and the discrepancy between physical signs and understandable pathological mechanisms may suggest the diagnosis. The outlook seems frequently poor.

Adolescent↗
PubMed1987

Adherence of rheumatoid polymorphonuclear cells (PMNs) to cultured endothelial cell monolayers.

Blood polymorphonuclear cells (PMNs) from 40 patients with rheumatoid arthritis (RA) and 40 normal subjects were incubated with confluent cultures of porcine aortic endothelium and their adherence assessed by either a microscopic or radiometric enumeration assay. There was no difference between the number of rheumatoid and control PMNs adhering. The synovial fluid PMNs from patients with RA were less adherent than their paired blood samples when autologous serum was present in the incubation medium and more adherent when serum was absent. Most of the RA sera tested inhibited the adhesion of normal PMNs, an effect that was not due to an increase in PMN aggregation. A similar inhibition was seen with sera obtained from patients with Felty's syndrome. These findings suggest that there is no intrinsic difference between the adhesiveness of rheumatoid PMNs and normal PMNs but that there are soluble factors present in RA serum which inhibit the attachment of normal PMNs to vascular endothelium.

Arthritis, Rheumatoid↗
PubMed1987

Rheumatoid blood decreases the adherence of polymorphonuclear cells (PMNs) to cultured endothelium.

Rheumatoid sera and plasma inhibited the adherence of normal blood polymorphonuclear cells (PMNs) to cultured porcine endothelium. This inhibition of adhesion was not seen when PMNs were treated with the plasma or serum from normal subjects or patients with other inflammatory arthropathies. The abrogation of PMN adherence was directly related to the levels of circulating immune complexes and was not dependent upon the type of anti-inflammatory therapy that the patients were receiving nor on any of the recorded clinical parameters. A similar inhibition of adhesion was seen with heat induced aggregated human IgG (HAGG) provided that serum was present in the culture medium. In view of these results we propose that circulating immune complexes in RA may have a significant role in controlling the interaction of PMNs with vascular endothelium and in perpetuating the entry of these cells into the synovial fluid of the inflamed joints.

Antigen-Antibody Complex↗
PubMed1986

Lack of correlation between clinical disease activity and erythrocyte sedimentation rate, acute phase proteins or protease inhibitors in ankylosing spondylitis.

Disease activity was assessed clinically and erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), orosomucoid, alpha 1-antitrypsin (alpha 1AT) and alpha 2-macroglobulin (alpha 2M) were measured in 65 patients with ankylosing spondylitis (AS). Positive correlations were found between ESR and the acute phase proteins (APP), CRP, orosomucoid and alpha 1AT, but none of these variables correlated with the clinical assessment of activity. No relationship was demonstrated between the protease inhibitor, alpha 2M and clinical activity, ESR or any of the APP. While the treatment of AS remains predominantly symptomatic, routine management of patients should continue to be founded on the clinical assessment of disease activity rather than on laboratory indices of inflammation.

Acute-Phase Proteins↗
PubMed1985

[111In]oxine labelling of polymorphonuclear leucocytes: doubts concerning elution and effects on cell behaviour.

Polymorphonuclear leucocytes (PMN) from normal human subjects were labelled with [111In]oxine (20 muCi 10(8) cells). In the presence of 20% autologous serum (AS), dissociation of 111In from the cells resulted in mean losses of radioactivity of 13% at 3 h and 30% at 24 h. Adherence of 111In-labelled PMN to cultured porcine endothelial monolayers was increased by 40.7 +/- 31.6% after 60 min incubation in 20% AS at 37 degrees C when compared with unlabelled cells. Phagocytosis and intracellular killing of Candida albicans were unaltered by labelling. Elution of 111In from labelled PMN together with enhanced adhesiveness may have important implications for the study of PMN kinetics and the investigation of inflammatory disease.

Cell Adhesion↗
PubMed1984

A radiometric assessment of phagocytosis and intracellular killing by blood polymorphonuclear leucocytes in rheumatoid arthritis.

Disagreement persists about the phagocytic function of blood polymorphonuclear leucocytes (PMN) in rheumatoid arthritis (RA). Many of the experimental data have been generated by subjective methods of assessment. Using a radiometric assay, we found no difference in the phagocytosis and intracellular killing of Candida albicans by blood PMN from 18 patients with RA when compared with PMN from 21 healthy control subjects. We infer that the increased incidence of non-articular infection reported in RA is not related to impaired phagocytic function of blood PMN.

Arthritis, Rheumatoid↗