Search Results

You are looking at 1 - 5 of 5 items for

  • Author: Klaus Badenhoop x
  • All content x
Clear All Modify Search
Free access

Gesine Meyer, Kathrin Neumann, Klaus Badenhoop, and Roland Linder


Our objective was to investigate the epidemiology of autoimmune Addison's disease (AD) in Germany.


Routine data were analyzed from the Statutory Health Insurance (SHI) database of the Techniker Krankenkasse (TK) for an observation period from 01/01/2008 to 31/12/2012. The TK is one of the largest German health care insurance providers covering more than 10% of the German population.

Subjects and methods

Between 2008 and 2012, a total of 2477 diagnoses of primary adrenal failure were recorded in the SHI database. After exclusion of secondary, iatrogenic or other non-idiopathic forms and after adjustment for incomplete data sets, 1364 diagnoses of autoimmune-mediated AD remained.


The prevalence of AD in our cohort showed a steady increase from 82 per million in 2008 to 87 per million in 2012. On average, the prevalence rose about 1.8% per year, and due to a pronounced increase (2.7%) in females. The prevalence was lower in men (63–68 per million) than in women (96–108 per million). Autoimmune comorbidities were found in 46.5% of AD patients. Adrenal crises were documented with a frequency of 14–17/100 patient years.


These data provide a first epidemiological profile of this rare and perilous endocrine disease in Germany. Although the prevalence of AD appears lower than in the Scandinavian countries, the increasing figures in females over the last 5 years warrant further investigations. Furthermore, adrenal crises pose a considerable burden. Hereby, we can show that health insurance data provide a valuable tool for epidemiological studies in the absence of national registries.

Free access

Heinrich Kahles, Elizabeth Ramos-Lopez, Britta Lange, Oliver Zwermann, Martin Reincke, and Klaus Badenhoop

Background: Endocrine autoimmune disorders share genetic susceptibility loci, causing a disordered T-cell activation and homeostasis (HLA class II genes, CTLA-4). Recent studies showed a genetic variation within the PTPN22 gene to be an additional risk factor.

Materials and Methods: Patients with type 1 diabetes (n = 220), Hashimoto’s thyroiditis (n = 94), Addison’s disease (n = 121) and healthy controls (n = 239) were genotyped for the gene polymorphism PTPN22 1858 C/T.

Results: Our study confirms a significant association between allelic variation of the PTPN22 1858 C/T polymorphism and type 1 diabetes mellitus (T1D). 1858T was observed more frequently in T1D patients (19.3% vs 11.3%, P = 0.0009; odds ratio for allele T = 1.88, 95% confidence interval [1.3–2.7]). Furthermore, we found a strong association in female patients with T1D (P = 0.0003), whereas there was no significant difference between male patients with type 1 diabetes and male controls. No significant difference was observed between the distribution of PTPN22 C/T in patients with Hashimoto’s thyroiditis or Addison’s disease and healthy controls.

Conclusion: The PTPN22 polymorphism 1858 C/T may be involved in the pathogenesis of type 1 diabetes mellitus by a sex-specific mechanism that contributes to susceptibility in females.

Free access

Grigoris Effraimidis, Klaus Badenhoop, Jan G P Tijssen, and Wilmar M Wiersinga


Vitamin D deficiency has been identified as a risk factor for a number of autoimmune diseases including type 1 diabetes and multiple sclerosis.


We hypothesized that low levels of vitamin D are related to the early stages of autoimmune thyroid disease (AITD).


Two case–control studies were performed. In the cross-sectional study A, euthyroid subjects with genetic susceptibility for AITD but without thyroid antibodies were compared with controls. Cases were subjects from the Amsterdam AITD cohort (euthyroid women who had first- or second-degree relatives with overt AITD) who at baseline had normal TSH and no thyroid antibodies; controls were healthy women examined at the same period. In the longitudinal study B, subjects who developed de novo thyroid peroxidase antibody (TPO-Ab) were compared with those who did not. Cases and controls were subjects from the Amsterdam AITD cohort who at baseline had normal TSH and no thyroid antibodies and during follow-up developed TPO-Ab (cases) or remained without thyroid antibodies (controls). Controls in both studies were matched for age, BMI, smoking status, estrogen use, month of blood sampling, and in study B for the duration of follow-up.


Serum 25(OH)D levels were as follows: study A: 21.0±7.9 vs 18.0±6.4 ng/ml (78 cases vs 78 controls, P=0.01); study B: baseline, 22.6±10.3 vs 23.4±9.1; follow-up 21.6±9.2 vs 21.2±9.3 ng/ml (67 cases vs 67 controls, NS).


Early stages of thyroid autoimmunity (in study A genetic susceptibility and in study B development of TPO-Ab) are not associated with low vitamin D levels.

Free access

Giovanna Muscogiuri, Joanna Mitri, Chantal Mathieu, Klaus Badenhoop, Gonca Tamer, Francesco Orio, Teresa Mezza, Reinhold Vieth, Annamaria Colao, and Anastassios Pittas


It has been suggested that vitamin D may play a role in the pathogenesis of several endocrine diseases, such as hyperparathyroidism, type 1 diabetes (T1DM), type 2 diabetes (T2DM), autoimmune thyroid diseases, Addison's disease and polycystic ovary syndrome (PCOS). In this review, we debate the role of vitamin D in the pathogenesis of endocrine diseases.


Narrative overview of the literature synthesizing the current evidence retrieved from searches of computerized databases, hand searches and authoritative texts.


Evidence from basic science supports a role for vitamin D in many endocrine conditions. In humans, inverse relationships have been reported not only between blood 25-hydroxyvitamin D and parathyroid hormone concentrations but also with risk of T1DM, T2DM, and PCOS. There is less evidence for an association with Addison's disease or autoimmune thyroid disease. Vitamin D supplementation may have a role for prevention of T2DM, but the available evidence is not consistent.


Although observational studies support a potential role of vitamin D in endocrine disease, high quality evidence from clinical trials does not exist to establish a place for vitamin D supplementation in optimizing endocrine health. Ongoing randomized controlled trials are expected to provide insights into the efficacy and safety of vitamin D in the management of endocrine disease.

Restricted access

Marissa Penna-Martinez, Gesine Meyer, Anette Bøe Wolff, Beate Skinningsrud, Corrado Betterle, Alberto Falorni, William Er Ollier, Dag Undlien, Eystein Sverre Husebye, Simon H S Pearce, Anna L Mitchell, and Klaus Badenhoop


While vitamin D regulates immune cells, little is known about it in autoimmune Addison´s disease (AAD). We investigated the vitamin D status in AAD patients from five European populations to assess its deficiency. In addition, we studied two case-control cohorts for vitamin D metabolism and pathway genes.


Cross-sectional study


A total of 1028 patients with AAD from Germany (n=239), Italy (n=328), Norway (n=378), UK (n=44) and Poland (n=39) and 679 controls from Germany (n=301) and Norway (n=378) were studied for 25(OH)D3 (primary objective). Secondary objectives (1,25(OH)2D3 and pathway genes) were examined in case-controls from Germany and Norway correlating 25(OH)D3 and single nucleotide polymorphisms within genes encoding the vitamin D receptor (VDR), 1-α-hydroxylase (CYP27B1), 25-hydroxylase (CYP2R1); 24-hydroxylase (CYP24A1) and vitamin D binding protein (GC/DBP).


Vitamin D deficiency (25(OH)D3 10-20 ng/ml) was highly prevalent in AAD patients (34-57%), 5-22% were severely deficient (<10 ng/ml), 28-38% insufficient (20-30 ng/ml) and only 7-14% sufficient (>30 ng/ml). Lower 25(OH)D3 and 1,25(OH)2D3 levels were observed both in Norwegian and German AAD (p = 0.03/0.003 and p = 1 x 10-5/< 1 x 10-7, respectively) the former was associated with CYP2R1 (rs1553006) genotype G. Whereas controls achieved sufficient median 25(OH)D3 in summers (21.4 to 21.9 ng/ml), AAD patients remained largely deficient (18.0 to 21.2 ng/ml) and synthesize less 1,25(OH)2D3.


Vitamin D deficiency and insufficiency are highly prevalent in AAD patients. The vitamin D status of AAD may be influenced by genetic factors and suggests individual vitamin D requirements throughout the year.