PubMed Health⌕ Search

Biomedical subjects

J J Manson

Publications and source records attributed to J J Manson.

5 recordsLinked to original sources
PubMed2006

Association of antinucleosome antibodies with disease flare in serologically active clinically quiescent patients with systemic lupus erythematosus.

OBJECTIVE: To identify the prevalence of serologically active clinically quiescent (SACQ) patients in a cohort of 290 patients with systemic lupus erythematosus (SLE). We investigated if the presence of anti-double-stranded DNA (anti-dsDNA) or antinucleosome (anti-NCS) antibodies during the SACQ period was associated with future flares. METHODS: SACQ patients defined as clinically inactive for 6 months (global British Isles Lupus Activity Group index [BILAG] scores <6) and serologically active (anti-dsDNA antibodies >50 units/ml on at least 2 occasions by enzyme-linked immunosorbent assay [ELISA]) were identified. Patient sera collected during the defined SACQ period were also tested for anti-NCS antibodies (ELISA). We retrospectively reviewed patient clinical details and episodes of flare using the BILAG activity index. RESULTS: Twenty-seven (9%) patients were SACQ. Seventeen (81%) patients experienced a flare (total of 91 flares, up to 12 flares per person) in the next 5 years. Median duration to first flare was 15 months (range 2-46). Time to first flare after SACQ period was significantly correlated with the presence of anti-NCS (P = 0.0012), high anti-NCS antibody titers (P = 0.0006), and anti-dsDNA titers 5 times above the normal limit (P = 0.02). Patients with higher absolute anti-NCS antibody titers showed a significant correlation with the number of flares (r = 0.57, P = 0.007). CONCLUSION: A minority of patients with SLE are SACQ. The majority of these patients experience a flare in the next 5 years and close followup is recommended. Anti-NCS antibodies may be a better predictor than anti-dsDNA antibodies for future flares.

Adult↗
PubMed2003

Antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is defined as the presence of venous or arterial thromboses, and/or recurrent miscarriage, with evidence of antiphospholipid antibodies (aPL). Central to the disease, is the development of the antibodies to phospholipid molecules themselves, or to their binding proteins. The production of these antibodies may depend upon the unusual exposure of cytoplasmic molecules seen during the process of apoptosis. The exact pathogenesis of antiphospholipid syndrome remains unclear, but various putative models exist. These include the up-regulation of endothelial cell adhesion molecules, membrane disruption during lipid peroxidation, a dysfunction of endogenous anticoagulants, or abnormal platelet aggregation. The mainstay of treatment is with aspirin or warfarin, and more research is required to discover novel, and safer, therapies.

Animals↗
PubMed2003

The pathogenesis of systemic lupus erythematosus.

SLE is a complex, heterogeneous disease, the precise pathogenesis of which remains something of a mystery. In recent years our understanding has been advanced by the development of novel genetic and immunological techniques. Susceptibility to SLE has a genetic component and multiple putative genes are being investigated. The genes involved are likely to play a part in immune regulation. Central to the immune dysfunction seen in SLE is the presence of autoreactive B cells, which predominantly target nuclear antigens. In addition to evidence of aberrant B and T cell behaviour, lupus is associated with complement deficiencies, and abnormal cytokine function. A number of environmental triggers exist, and likely candidates include viral infection and exposure to UV light. Finally, evidence is accumulating that implicates apoptosis as a mechanism by which disease may be provoked and propagated.

Humans↗