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Stephen Gough

Publications and source records attributed to Stephen Gough.

8 recordsLinked to original sources
PubMed2005

HLA , CTLA-4 and PTPN22 : the shared genetic master-key to autoimmunity?

Several genetic loci appear to be involved in susceptibility to autoimmune disease. Some loci are disease specific, whereas others appear to exert a general effect on the autoimmune disease process. Despite a large number of studies of many different diseases, consistent associations with multiple autoimmune disorders have been restricted to three gene regions: the human leukocyte antigen (HLA) class II region on chromosome 6p21, the gene encoding cytotoxic T lymphocyte-associated 4 (CTLA-4) on chromosome 2q33, and the PTPN22 gene encoding lymphoid tyrosine phosphatase (LYP) on chromosome 1p13. Each of these loci is likely to encode molecules that are crucial in the immune cascade and are actively involved in T-cell activation. Moreover, gene polymorphisms that affect function might contribute to the triggering of autoimmune disease by as-yet-unknown mechanisms. This review summarises recent developments and current understanding of the way in which molecules encoded by these susceptibility loci contribute to T-cell activation, and hypothesises how aberrant function of these molecules might trigger autoimmunity.

Antigens, CD↗
PubMed2005

Post-marketing surveillance: a UK/European perspective.

The granting of regulatory approval allows medical practitioners to prescribe a drug in a controlled way to a group of patients defined within the licence. Prior to this, the new product may have been evaluated often in less than 5000 patients and usually in a selected environment in which many patients have been excluded, including for example, women of childbearing potential, the elderly and children. Co-existent disease and the concomitant use of a number of common drug treatments also frequently exclude patients from pre-licensing trials. It is hardly surprising, therefore, that many adverse drug reactions are only detected once the product has been prescribed to the general population. National and international regulatory bodies, therefore, provide systems for post-marketing pharmacosurveillance, although participation in these by clinicians is generally voluntary and under-reporting is widespread. Post-marketing surveillance (PMS) studies are not generally an integral component to launching a new drug and many clinicians are sceptical over data generated in trials which do not conform to the 'gold standard' randomised control trial (RCT) design. However, in dismissing such studies, a great opportunity to obtain information, often from many thousands of subjects, is being missed. This article discusses post-marketing pharmacovigilance and the role of PMS studies in the context of current UK and European legislation.

Drug-Related Side Effects and Adverse Reactions↗
PubMed2004

The thyroglobulin gene: the third locus for autoimmune thyroid disease or a false dawn?

Genetic studies have identified the HLA and CTLA4 regions as susceptibility loci for the development of common autoimmune thyroid diseases (AITDs), including Graves' disease and autoimmune hypothyroidism. Despite numerous studies, the identification of a third locus has remained elusive. Genetic-linkage studies have implicated chromosome 8q24 as a susceptibility locus for AITD. The gene encoding thyroglobulin (Tg), which encodes a major thyroid autoantigen, maps to this region, and a recent study has reported the association of several exonic single-nucleotide polymorphisms (SNPs) with disease. Although these preliminary data are potentially exciting, caution needs to be exercised, and replication of the data sought before Tg can be designated as the third locus for AITD.

Autoimmune Diseases↗
PubMed2004

Diabetes and its prevention: pragmatic solutions for people with schizophrenia.

BACKGROUND: Patients with schizophrenia have an increased risk of developing diabetes. However, no pragmatic pathway of care has ever been proposed in order to identify individuals at risk and manage that risk effectively. AIMS: To develop practical recommendations for the screening and management of diabetes in schizophrenia. METHOD: Staged review of evidence for the under recognition of diabetes in people with schizophrenia and of the applicability of current screening strategies to this population. Recommendations for pragmatic pathways of care were developed. RESULTS: All patients with schizophrenia should be screened and managed as a high-risk group for the development of diabetes. Psychiatrists should be responsible for screening and diabetes risk management; primary care physicians and/or diabetologists should be responsible for managing diabetes. Choice of antipsychotics should be based on achieving good control of schizophrenia, which may improve compliance with diabetes risk reduction strategies. CONCLUSIONS: Effective multidisciplinary team working should reduce the burden of diabetes in schizophrenia.

Critical Pathways↗
PubMed2003

'Loss of self': a psychosocial study of the quality of life of adults with diabetic foot ulceration.

At present, recognition of the importance of psychosocial factors in the care of individuals with diabetes is still in its infancy. Understanding of the specific psychosocial factors relating to diabetic foot ulceration is embryonic. The study reported in this paper begins to raise awareness of psychosocial quality of life issues for patients living with diabetic foot ulceration, as narrated by the patients themselves. Findings revealed a range of restrictions on daily life that profoundly affected the individual's sense of self. These findings have implications for patients' adherence to treatment. Implications of these findings for health promotion are also reported.

Diabetic Foot↗
PubMed2002

Autoimmunity in thyroid disease.

The autoimmune thyroid diseases, Graves' disease and autoimmune hypothyroidism, represent the two ends of a disease spectrum where an immune response is directed against the thyroid gland. In Graves' disease, antibodies directed against the thyrotropin receptor (TSH-R) lead to the development of glandular overactivity, while in autoimmune hypothyroidism, cell-mediated and humoral thyroid injury leads to destruction of thyroid tissue and thyroid hormone deficiency. The mechanisms by which these diseases develop are unknown, although it is likely that both diseases occur in genetically susceptible individuals exposed to a permissive environment. A number of environmental factors have been postulated to be involved in the development of autoimmune thyroid disease. There is, however, no direct evidence to support clear causality. Susceptibility loci within immune response genes have been identified although a significant component of the genetic predisposition to disease remains unknown. This review will focus on some of the studies designed to identify genes that confer susceptibility to the autoimmune disease process within the thyroid gland.

Abatacept↗