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Antibodies to gluta...
Antibodies to glutamic acid decarboxylase and insulin-dependent diabetes in patients with autoimmune polyendocrine syndrome type I
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- Tuomi, Tiinamaija (författare)
- Lund University,Lunds universitet,Translationell muskelforskning,Forskargrupper vid Lunds universitet,Wallenberglaboratoriet, Malmö,Medicinska fakulteten,Translational Muscle Research,Lund University Research Groups,The Wallenberg Laboratory, Malmö,Faculty of Medicine
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- Björses, Petra (författare)
- Helsinki University Central Hospital
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- Falorni, Alberto (författare)
- Karolinska Institute
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Partanen, Jukka (författare)
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- Perheentupa, Jaakko (författare)
- Helsinki University Central Hospital
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- Lernmark, Åke (författare)
- University of Washington
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- Miettinen, Aaro (författare)
- University of Helsinki Haartman Institute
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(creator_code:org_t)
- The Endocrine Society, 1996
- 1996
- Engelska.
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 81:4, s. 1488-1494
- Relaterad länk:
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http://dx.doi.org/10...
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https://academic.oup...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- To evaluate the association of autoimmunity to glutamic acid decarboxylase (GAD) with insulin-dependent diabetes mellitus (IDDM) and IDDM-associated human leukocyte antigen (HLA) types, we studied a unique group of 47 patients with autoimmune polyendocrine syndrome type 1, a recessive disease not associated with HLA. GAD65 antibodies (GAD65-Ab), GAD67-Ab, islet cell antibodies, and HLA-DQA1, -DQB1, and -DRB1 were analyzed in relation to IDDM or a decreased insulin secretory capacity. GAD65-Ab were found in six of the eight diabetic patients 0.9-8.0 yr before the onset of IDDM and in 16 (41%) nondiabetic patients during a follow-up of 2.4-19.5 yr. Eleven (28%) nondiabetic patients had GAD67-Ab and islet cell antibodies. Fasting C peptide (mean ± SD, 0.5 ± 0.24 vs. 1.03 ± 0.49 nmol/L; P = 0.003) and first phase insulin response (75.6 ± 37.9 vs. 166.4 ± 112.7 mU/L; P = 0.019) were lower in patients with than in those without GAD65-Ab. No HLA genotype predominated in the IDDM patients or GAD65-Ab-positive nondiabetic patients, but the IDDM high risk genotypes were decreased in frequency among the patients with GAD65-Ab. In conclusion, nondiabetic autoimmune polyendocrine syndrome type 1 patients frequently have GAD65-Ab together with a decreased insulin secretory capacity, suggesting subclinical islet cell inflammation not invariably progressing to diabetes. This is not associated with HLA haplotypes conferring susceptibility to or protection from IDDM.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)
Publikations- och innehållstyp
- art (ämneskategori)
- ref (ämneskategori)
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