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Prävalenz eines polyglandulären Autoimmunsyndroms bei Patienten mit Diabetes mellitus Typ 1

Prevalence of Polyglandular Autoimmune Syndrome in Patients with Diabetes Mellitus Type 1

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Zusammenfassung

Hintergrund und Ziel:

Bei Patienten mit Diabetes mellitus Typ 1 treten gehäuft weitere endokrine Autoimmunerkrankungen (AIEK) auf. In dieser Studie wurden die Häufigkeit pathologischer Autoantikörper-(AAK-)Befunde und das Auftreten einer klinisch manifesten endokrinen AIEK (Hypophysitis, Adrenalitis, Thyreopathie, Perniziosa, Sprue) bei Patienten mit Diabetes mellitus Typ 1 im Verlauf 1 Jahres untersucht.

Patienten und Methodik:

Bei 139 Patienten mit Diabetes mellitus Typ 1 (Alter 44 ± 14 Jahre; Diabetesmanifestationsalter 26 ± 15 Jahre; Diabetesdauer 18 ± 12 Jahre; Body-Mass-Index 26 ± 4 kg/m2; HbA1c 7,5% ± 1,1% [Normalbereich 4,4–5,9%]), die in einer Universitätsklinik behandelt wurden, erfolgten ein AAK-Screening und bei pathologischem AAK-Titer eine Diagnostik hinsichtlich o.g. AIEK. Eine Befundkontrolle wurde 1 Jahr später durchgeführt.

Ergebnisse:

2003 zeigten 63% der Patienten mit Diabetes mellitus Typ 1 mindestens einen pathologischen AAK-Titer (2004: 60%) Bei 32% waren erhöhte AAK-Titer klinisch nicht relevant. Bei 31% der Patienten lag 2003 neben dem Typ-1-Diabetes mindestens eine weitere therapiepflichtige AIEK vor (2004: +3,6%): Dabei zeigten 22,3% zwei AIEK (2004: +2,2%) und 8,6% ≥ 3 AIEK (2004: +1,5%). Folgende positive AAK-Titer/Erkrankungsprävalenzen lagen vor (Vergleich 2004): positive Schilddrüsen-AAK: 47,5% (–0,7%)/Autoimmunthyreoiditis 24,5% (+2,8%) bzw. Morbus Basedow 4,3% (+0,7%), Nebennierenrinden-AAK 0,7% (+1,5%)/Morbus Addison 1,4% (±0), Gliadin-AAK bzw. Gewebsglutaminase-IgA positiv: 18,7% (–5,0%)/Sprue 1,4% (+0,8%), Parietalzellantikörper positiv: 15,8% (+7,2%)/Perniziosa 7,2% (+1,4%), Hypophysitis 0,7% (±0), Hypogonadismus 0,7% (±0). Alle Neuerkrankungen 2004 zeigten bereits im Vorjahr einen mindestens zehnfach erhöhten AAK-Titer. Zwischen Patienten mit versus ohne polyglanduläres Autoimmunsyndrom (PAS) fanden sich keine signifikanten Unterschiede bezüglich Alter (43 ± 14 vs. 46 ± 13 Jahre), Diabetesdauer (17 ± 13 vs. 18 ± 12 Jahre) und HbA1c (7,3% ± 0,9% vs. 7,6% ± 1,1%).

Schlussfolgerung:

In dieser Untersuchung wies mehr als die Hälfte der Patienten mit Diabetes mellitus Typ 1 mindestens einen weiteren pathologischen AAK-Titer auf, der jedoch keinen sicheren Rückschluss auf eine klinisch relevante AIEK zuließ. Bei 31% der Patienten lag mindestens eine weitere therapiepflichtige AIEK vor (Prävalenzanstieg um 3,6% innerhalb 1 Jahres). Bei Patienten mit Diabetes mellitus Typ 1 sollte an ein PAS gedacht werden. Eine Thyreopathie war am häufigsten und zeigte einen Prävalenzanstieg um 3,5% innerhalb 1 Jahres.

Abstract

Background and Purpose:

The aim of this study was to examine the prevalence of autoimmune antibodies (autoimmune hypophysitis, adrenalitis, thyropathy, pernicious anemia, celiac disease) and clinically relevant endocrine autoimmune disease (AIEK) in patients with type 1 diabetes in the course of 1 year.

Patients and Methods:

Antibody screening was performed in 139 diabetic patients (age 44 ± 14 years; years since diagnosis 26 ± 15 years; duration of diabetes 18 ± 12 years; body mass index 26 ± 4 kg/m2; HbA1c 7.5% ± 1.1% [normal range 4.4–5.9%]) who completed a routine clinic visit in 2003. Patients with pathologically increased antibody titers were further examined regarding the clinically relevant AIEKs. Reexamination was performed 1 year later.

Results:

In 2003, 63% of diabetic patients showed at least one pathologically increased antibody titer (2004: 60%). In 32% of the patients, increased antibody titers were clinically inapparent. Apart from diabetes mellitus type 1, in 2003, 31% suffered from other AIEK requiring therapy (2004: +3.6%): 22.3% harbored two additional AIEKs (2004: +2.2%) and 8.6% even ≥ 3 AIEKs (2004: +1.5%). The following pathologically increased antibody titers/prevalences of clinically relevant AIEKs were found (in comparison with 2004): increased antithyroid autoantibodies: 47.5% (–0.7%)/autoimmune thyroiditis 24.5% (+2.8%) and Graves’ disease 4.3% (+0.7%), respectively; adrenal cortex autoantibodies 0.7% (+1.5%)/Addison’s disease 1.4% (±0), gliadin peptide antibodies and IgA to tissue transglutaminase, respectively: 18.7% (–5.0%)/celiac disease 1.4% (+0.8%), parietal cell antibodies: 15.8% (+7.2%)/pernicious anemia 7.2% (+1.4%), hypophysitis 0.7% (±0), hypogonadism 0.7% (±0). All new AIEK manifestations in 2004 had had an at least tenfold increased antibody titer in 2003. Comparing patients with and without polyglandular autoimmune syndrome (PAS), no difference in age (43 ± 14 vs. 46 ± 13 years), duration of diabetes (17 ± 13 vs. 18 ± 12 years), and HbA1c (7.3% ± 0.9% vs. 7.6% ± 1.1%) could be found.

Conclusion:

In this study, more than half of the patients with diabetes mellitus type 1 had at least one pathologically increased antibody titer apart from diabetes without clinical sign of an additional AIEK. 31% of patients with increased antibodies presented with symptoms of another AIEK (increase by 3.6% within 1 year). Patients with diabetes mellitus type 1 should be screened for other AIEKs. Thyropathy had the greatest prevalence and increased by 3.5% within 1 year’s time.

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Authors and Affiliations

  1. Klinik für Innere Medizin III, Universitätsklinikum Jena, Jena, Germany

    Wilgard Hunger-Battefeld, Alexandra Mandecka, Christof Kloos, Ulrich Alfons Müller & Gunter Wolf

  2. Medizinische Fakultät, Universitätsklinikum Jena, Jena, Germany

    Katharina Fath

  3. Institut für Klinische Chemie und Laboratoriumsdiagnostik, Universitätsklinikum Jena, Jena, Germany

    Michael Kiehntopf

  4. Klinik für Innere Medizin III, Universitätsklinikum Jena, Erlanger Allee 101, 07740, Jena, Germany

    Wilgard Hunger-Battefeld

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  1. Wilgard Hunger-Battefeld
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  2. Katharina Fath
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Correspondence to Wilgard Hunger-Battefeld.

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Hunger-Battefeld, W., Fath, K., Mandecka, A. et al. Prävalenz eines polyglandulären Autoimmunsyndroms bei Patienten mit Diabetes mellitus Typ 1. Med Klin 104, 183–191 (2009). https://doi.org/10.1007/s00063-009-1030-x

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