In-kind assistance for medical research

The ADSHG is proud to have assisted a number of UK endocrine units to recruit for medical research projects over the years, including:

• A 12 month clinical trial of DHEA at Addenbrooke’s Hospital, Cambridge
• Ongoing genetic studies, involving DNA analysis of blood samples, to better understand the genetic origins of autoimmune Addison's disease at the Institute of Genetic Medicine, Newcastle University
• An ongoing clinical trial of Rituximab, which suppresses one part of the immune system, and ACTH which stimulates the adrenal glands, to see if adrenal function can be improved in people with autoimmune Addison's disease, at the Royal Victoria Infirmary, Newcastle
• An ongoing clinical trial of physiological cortisol replacement using 24 hour pulsatile pump therapy, at the Bristol Royal Infirmary.
• An ongoing qualitative research project exploring the psychological impacts of living with a long term condition and the experience of adrenal crisis, coordinated through the Royal Sussex County Hospital.

You can read the outcomes of some of this research in the journal articles listed below.

Anyone wishing to make a charitable donation towards the work of the ADSHG in supporting medical research, may do so through our dedicated Just Giving appeal, here.

If you are interested in recruiting participants from among the ADSHG’s membership for a research project of any type, please read the explanation of our research application process here.

Scientific articles derived from research assisted by the ADSHG through member recruiting

• Role of the X-linked gene GPR174 in autoimmune Addison's disease Napier C et al. 2015, J Clin Endocrinol Metab 100 E187-90
• Linkage analysis in autoimmune Addison’s disease: NFATC1 as a potential novel susceptibility locus, Mitchell AL et al. 2015 PLoS One 10 e0123550
• CTLA-4 as a genetic determinant in autoimmune Addison's disease. Wolff AS et al. 2015 Genes Immun 16 430-6
• Subcutaneous pulsatile glucocorticoid replacement therapy. Russell GM et al. 2014 Clin Endocrinol 81 289-93
• Spontaneous and tetracosactide-induced anti-ACTH antibodies in man. Gan EH et al. 2015 Clin Endocrinol 84 489–95
• High frequency of cytolytic 21-hydroxylase–specific CD8+ T cells in autoimmune Addison’s disease patients, Dawoodji A et al. 2014 J. Immunol. 193 2118-26
• Association of autoimmune Addison's disease with alleles of STAT4 and GATA3 in European cohorts. Mitchell AL et al. 2014 PLoS One 9 e88991
• Residual adrenal function in autoimmune Addison's disease: improvement after tetracosactide (ACTH1–24) treatment Gan EH et al. 2014 J Clin Endocrinol Metab. 99 111-8
• Adrenal steroidogenesis after B lymphocyte depletion therapy in new-onset Addison's disease Pearce SHS et al. 2012 J. Clin Endocrinol. Metab. 97 E1927-32
• The role of functionally defective rare germline variants of sialic acid acetylesterase (SIAE) in autoimmune Addison's disease, Gan EH et al. 2012 Eur J Endocrinol 167 825-8
• Quality of life in European patients with Addison's disease: validity of the disease-specific questionnaire AddiQoL, Øksnes M et al, J Clin Endocrinol Metab. 2012 Feb;97(2):568-76
• The role of a non-synonymous CD226 (DNAX-accessory molecule-1) variant (Gly 307Ser) in isolated Addison’s disease and autoimmune polyendocrinopathy type 2 pathogenesis. Gan EH et al. 2011 Clin Endocrinol 75 165-8
• Development of a disease-specific quality of life questionnaire in Addison's, Løvås K et al, J Clin Endocrinol Metab. 2010 Feb;95(2):545-51
• Glucocorticoid replacement therapy and pharmacogenetics in Addison's disease: effects on bone, Løvås K et al, Eur J Endocrinol 2009 Jun;160(6):993-1002
• Programmed death ligand 1 (PD-L1) gene variants contribute to autoimmune Addison's disease and Graves' disease susceptibility. Mitchell AL et al. 2009 J Clin Endocrinol Metab. 94 5139-45
• Long-term DHEA replacement in primary adrenal insufficiency: a randomized, controlled trial. Gurnell EM et al. 2008 J Clin Endocrinol Metab. 93 400-9
• Dehydroepiandrosterone replacement in patients with Addison's disease has a bimodal effect on regulatory (CD4+CD25hi and CD4+FoxP3+) T cells. Coles AJ et al. 2005 Eur J Immunol. 35 3694-703