Islet autoantibodies in clinically diagnosed type 2 diabetes: prevalence and relationship with metabolic control (UKPDS 70)

Aims/hypothesis: we examined the prevalence of islet autoantibodies and their relationship to glycaemic control over 10 years in patients diagnosed clinically with new-onset type 2 diabetes.

Methods: patient clinical characteristics and autoantibody status were determined at entry to the UK Prospective Diabetes Study (UKPDS) before randomisation to different glucose control policies. Patients were followed for 10 years. Results: Data available on 4,545 of the 5,102 UKPDS patients showed that 11.6% had antibodies to at least one of three antigens: islet cell cytoplasm, glutamic acid decarboxylase and islet autoantibody 2A (IA-2A). Autoantibody-positive patients were younger, more often Caucasian and leaner, with lower beta cell function and higher insulin sensitivity than autoantibody-negative patients. They also had higher HbA₁c, and HDL-cholesterol levels, and lower blood pressure, total cholesterol and plasma triglyceride levels. Despite relative hyperglycaemia, autoantibody-positive patients were less likely to have the metabolic syndrome (as defined by the National Cholesterol Education Program Adult Treatment Program III), reflecting a more beneficial overall risk factor profile. Of 3,867 patients with post-dietary run-in fasting plasma glucose (FPG) values between 6.0 and 14.9 mmol/l and no hyperglycaemic symptoms, 9.4% were autoantibody-positive, compared with 25.1% of 678 patients with FPG values of 15.0 mmol/l or higher, or hyperglycaemic symptoms. In both groups, no differences were seen between those with and without autoantibodies in changes to HbA₁c over time, but autoantibody-positive patients required insulin treatment earlier, irrespective of the allocated therapy (p<0.0001).

Conclusions/interpretation: autoantibody-positive patients can be treated initially with sulphonylurea, but are likely to require insulin earlier than autoantibody-negative patients.

GADA, Glycaemia, ICA, Type 2 diabetes, UKPDS

10.1007/s00125-005-1690-x

0012-186X

695-702

Davis, T.M.E.

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Wright, A.D.

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Mehta, Z.M.

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Cull, C.A.

ae95233f-ce25-4c32-a5b9-368419e07826

Stratton, I.M.

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Bottazzo, G.F.

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Bosi, E.

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MacKay, I.R.

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Holman, R.R.

d03ac9f9-2f1d-40c9-827f-939b8b05b25f

April 2005

Davis, T.M.E.

6193a548-b3f0-468c-9d39-abe971b4d3bc

Wright, A.D.

ba7005fd-7d2d-4e9f-a796-b265dc3b17a0

Mehta, Z.M.

85f7dd33-f6c3-4518-91e6-d9e4d7512e02

Cull, C.A.

ae95233f-ce25-4c32-a5b9-368419e07826

Stratton, I.M.

772f25b9-23c0-4240-a3f6-1e76b03b172f

Bottazzo, G.F.

6d33f51a-1266-439b-88e9-c68a47e9dc2d

Bosi, E.

c1c777a2-4fba-47ff-8ee2-0f75b08b2a44

MacKay, I.R.

a58d52bb-761d-4663-b7b5-5367da612f70

Holman, R.R.

d03ac9f9-2f1d-40c9-827f-939b8b05b25f

Davis, T.M.E., Wright, A.D., Mehta, Z.M., Cull, C.A., Stratton, I.M., Bottazzo, G.F., Bosi, E., MacKay, I.R. and Holman, R.R. (2005) Islet autoantibodies in clinically diagnosed type 2 diabetes: prevalence and relationship with metabolic control (UKPDS 70). Diabetologia, 48 (4), 695-702. (doi:10.1007/s00125-005-1690-x).

Record type: Article

Abstract

Aims/hypothesis: we examined the prevalence of islet autoantibodies and their relationship to glycaemic control over 10 years in patients diagnosed clinically with new-onset type 2 diabetes.

Conclusions/interpretation: autoantibody-positive patients can be treated initially with sulphonylurea, but are likely to require insulin earlier than autoantibody-negative patients.

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More information

Accepted/In Press date: 30 November 2004

e-pub ahead of print date: 24 February 2005

Published date: April 2005

Additional Information: Funding Information: Acknowledgements The cooperation of the patients and many National Health Service (NHS) and non-NHS staff at the centres is much appreciated. The major grants for this study were from the UK Medical Research Council, British Diabetic Association, The British Heart Foundation, The UK Department of Health, The Italian Ministry of Health, The National Eye Institute and The National Institute of Digestive, Diabetes and Kidney Disease in the National Institutes of Health USA, Novo-Nordisk, Bayer, Bristol Myers Squibb, Hoechst, Lilly, Lipha and Farmitalia Carlo Erba. Other funding companies and agencies, the supervising committees and all participating staff are acknowledged in an earlier paper [6]. We are also grateful to the Wellcome Trust for a grant for the measurement of ICA and GADA. We thank Marion Shattock for the ICA assay, Dr Merrill Rowley for supervision, and Ray Spark for the technical performance of GADA assays in the Monash University Laboratory. We thank Dr Mattia Locatelli for helpful review of the manuscript. Participating UK Centres Radcliffe Infirmary, Oxford; Royal Infirmary, Aberdeen; University Hospital, Birmingham; St. George’s Hospital, Hammersmith Hospital and Whittington Hospital, London; City Hospital and Royal Victoria Hospital, Belfast; North Staffordshire Royal Infirmary, Stoke-on-Trent; St. Helier Hospital, Carshalton; Norfolk and Norwich Hospital, Norwich; Lister Hospital, Stevenage; Ipswich Hospital, Ipswich; Ninewells Hospital, Dundee; Northampton General Hospital, Northampton; Torbay Hospital, Torbay; Peterborough General Hospital, Peterborough; Scarborough Hospital, Scarborough; Derbyshire Royal Infirmary, Derby; Manchester Royal Infirmary, Manchester; Hope Hospital, Salford; Leicester General Hospital, Leicester; Royal Exeter & Devon Hospital, Exeter.

Keywords: GADA, Glycaemia, ICA, Type 2 diabetes, UKPDS