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1. A progressive increase in cardiovascular risk assessed by coronary angiography in non-diabetic patients at sub-diabetic glucose levels

Author

Schott Matthias, Willenberg Holger S, Martin Stephan, Kempf Kerstin, Füth Reiner, Schinner Sven, Dinh Wilfried, Scherbaum Werner A, and Lankisch Mark

Subjects
impaired glucose tolerance, impaired fasting glucose, diabetes mellitus, oral glucose tolerance test, cardiovascular disease, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Abstract Objective Diabetes mellitus type 2 (DM2) is a risk factor for coronary heart disease (CHD). While there is a clear correlation of fasting blood glucose (FBG) and 2 h post-challenge blood glucose values (2h-BG) with microvascular complications, the risk for CHD conferred by glucose dysregulation antecedent to DM2 is less clear. Therefore, we investigated associations of FBG and 2h-BG values with the prevalence of CHD assessed by coronary angiography as the most sensitive diagnostic tool. Research Design and Methods Coronary angiography was performed in 1394 patients without known DM. Capillary blood glucose was analyzed before and 2 h after an oral glucose tolerance test. Associations between FBG as well as 2h-BG levels and the risk for CHD were assessed by logistic regression analysis. Results 1064 (75%) of patients were diagnosed with CHD. 204 (15%) were diagnosed with so far unknown DM2, 274 (20%) with isolated impaired fasting glucose (IFG), 188 (13%) with isolated impaired glucose tolerance (IGT) and 282 (20%) with both, IGT and IFG. We found a continuous increase in the risk for CHD with fasting and post-challenge blood glucose values even in the subdiabetic range. This correlation did however not suggest clear cut-off values. The increase in risk for CHD reached statistical significance at FBG levels of > 120 mg/dl (Odds Ratio of 2.7 [1.3-5.6] and 2h-BG levels > 140 mg/dl (141-160 mg/dl OR 1.8 [1.1-2.9], which was however lost after adjusting for age, sex and BMI. Conclusions In our study population we found a continuous increased risk for CHD at fasting and 2h-BG levels in the sub-diabetic glucose range, but no clear cut-off values for cardiovascular risk.

Published
2011
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2. Insulin gene polymorphisms in type 1 diabetes, Addison's disease and the polyglandular autoimmune syndrome type II

Author

Hahner Stefanie, Reisch Nicole, Penna-Martinez Marissa, Meyer Gesine, Willenberg Holger S, Kahles Heinrich, Lange Britta, Ramos-Lopez Elizabeth, Seissler Jürgen, and Badenhoop Klaus

Subjects
Internal medicine, RC31-1245, Genetics, QH426-470
Abstract

Abstract Background Polymorphisms within the insulin gene can influence insulin expression in the pancreas and especially in the thymus, where self-antigens are processed, shaping the T cell repertoire into selftolerance, a process that protects from β-cell autoimmunity. Methods We investigated the role of the -2221Msp(C/T) and -23HphI(A/T) polymorphisms within the insulin gene in patients with a monoglandular autoimmune endocrine disease [patients with isolated type 1 diabetes (T1D, n = 317), Addison's disease (AD, n = 107) or Hashimoto's thyroiditis (HT, n = 61)], those with a polyglandular autoimmune syndrome type II (combination of T1D and/or AD with HT or GD, n = 62) as well as in healthy controls (HC, n = 275). Results T1D patients carried significantly more often the homozygous genotype "CC" -2221Msp(C/T) and "AA" -23HphI(A/T) polymorphisms than the HC (78.5% vs. 66.2%, p = 0.0027 and 75.4% vs. 52.4%, p = 3.7 × 10-8, respectively). The distribution of insulin gene polymorphisms did not show significant differences between patients with AD, HT, or APS-II and HC. Conclusion We demonstrate that the allele "C" of the -2221Msp(C/T) and "A" -23HphI(A/T) insulin gene polymorphisms confer susceptibility to T1D but not to isolated AD, HT or as a part of the APS-II.

Published
2008
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3. Feasibility of Imaging-Guided Adrenalectomy in Young Patients With Primary Aldosteronism

Author

Rossi, Gian Paolo, Crimì, Filippo, Rossitto, Giacomo, Amar, Laurence, Azizi, Michel, Riester, Anna, Reincke, Martin, Degenhart, Christoph, Widimsky, Jiri, Naruse, Mitsuhide, Deinum, Jaap, Kool, Leo Schultze, Kocjan, Tomaz, Negro, Aurelio, Rossi, Ermanno, Kline, Gregory, Tanabe, Akiyo, Satoh, Fumitoshi, Rump, Lars Christian, Vonend, Oliver, Willenberg, Holger S., Fuller, Peter J., Yang, Jun, Chee, Nicholas Yong Nian, Magill, Steven B., Shafigullina, Zulfiya, Quinkler, Marcus, Oliveras, Anna, Wu, Vin Cent, Kratka, Zuzana, Barbiero, Giulio, Battistel, Michele, and Seccia, Teresa Maria

Published
2022
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4. Impact of Dietary Isoflavones in Standard Chow on Reproductive Development in Juvenile and Adult Female Mice with Different Metabolic Phenotypes.

Author

Meyer, Zianka, Soukup, Sebastian T., Lubs, Anna, Ohde, Daniela, Walz, Christina, Schoen, Jennifer, Willenberg, Holger S., Hoeflich, Andreas, and Brenmoehl, Julia

Abstract

Two factors influencing female reproduction have been repeatedly studied in different animal species and humans, namely, 1. secondary plant compounds, especially phytoestrogens (mainly isoflavones (IFs)), and 2. the physical constitution/metabolic phenotype (e.g., obesity). So far, these research results have only been considered separately. In this study, we investigated the influence on reproduction of both phytochemicals, mainly dietary IFs, and the metabolic phenotype represented by three mouse models considered as three distinct genetic groups (a control group, a mouse model with high metabolic activity, and a mouse line with obese body weight). The IF content in different investigated standard chows with similar macronutrient profiles varied significantly (p < 0.005), leading to high mean total plasma IF levels of up to 5.8 µmol/L in juvenile and 6.7 µmol/L in adult female mice. Reproductive performance was only slightly affected; only an IF dose-dependent effect on gestation length was observed in all genetic groups, as well as an effect on pregnancy rate in obese mice. Dietary IF exposure, however, caused earlier onset of vaginal opening by 4–10 days in juvenile mice (p < 0.05), dependent on the genetic group, resulting in a slight acceleration of sexual maturation in the already precocious obese model and to a strong earlier maturation in the otherwise late-maturing sporty model, bred for high treadmill performance. Therefore, our results may help to draw the missing line between the effect of dietary secondary plant constituents, such as IFs, and metabolic phenotype on sexual development. [ABSTRACT FROM AUTHOR]

Published
2024
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5. THU593 Unilaterally Selective Adrenal Vein Sampling For Identification Of Surgically Curable Primary Aldosteronism

Author

Paolo Rossi, Gian, primary, Bagordo, Domenico, additional, Amar, Laurence, additional, Azizi, Michel, additional, Riester, Anna, additional, Reincke, Martin, additional, Degenhart, Christoph, additional, Widimský, Jiří, additional, Naruse, Mitsuhide, additional, Deinum, Jaap, additional, Kocjan, Tomaz, additional, Negro, Aurelio, additional, Rossi, Ermanno, additional, Kline, Gregory, additional, Tanabe, Akiyo, additional, Satoh, Fumitoshi, additional, Christian Rump, Lars, additional, Vonend, Oliver, additional, Willenberg, Holger S, additional, Fuller, Peter J, additional, Yang, Jun, additional, Nian Chee, Nicholas Yong, additional, Magill, Steven B, additional, Shafigullina, Zulfiya, additional, Quinkler, Marcus, additional, Oliveras, Anna, additional, Lee, Bo-Ching, additional, Chang, Chin-Chen, additional, Wu, Vin-Cent, additional, Krátká, Zuzana, additional, Battistel, Michele, additional, Rossitto, Giacomo, additional, and Seccia, Teresa M, additional

Published
2023
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6. Unilaterally Selective Adrenal Vein Sampling for Identification of Surgically Curable Primary Aldosteronism

Author

Rossi, Gian Paolo, primary, Bagordo, Domenico, additional, Amar, Laurence, additional, Azizi, Michel, additional, Riester, Anna, additional, Reincke, Martin, additional, Degenhart, Christoph, additional, Widimský, Jiří, additional, Naruse, Mitsuhide, additional, Deinum, Jaap, additional, Kocjan, Tomaz, additional, Negro, Aurelio, additional, Rossi, Ermanno, additional, Kline, Gregory, additional, Tanabe, Akiyo, additional, Satoh, Fumitoshi, additional, Rump, Lars Christian, additional, Vonend, Oliver, additional, Willenberg, Holger S., additional, Fuller, Peter J., additional, Yang, Jun, additional, Chee, Nicholas Yong Nian, additional, Magill, Steven B., additional, Shafigullina, Zulfiya, additional, Quinkler, Marcus, additional, Oliveras, Anna, additional, Lee, Bo-Ching, additional, Chang, Chin-Chen, additional, Wu, Vin-Cent, additional, Krátká, Zuzana, additional, Battistel, Michele, additional, Rossitto, Giacomo, additional, and Seccia, Teresa Maria, additional

Published
2023
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7. Clinical Outcomes of 1625 Patients With Primary Aldosteronism Subtyped With Adrenal Vein Sampling

Author

Rossi, Gian Paolo, Rossitto, Giacomo, Amar, Laurence, Azizi, Michel, Riester, Anna, Reincke, Martin, Degenhart, Christoph, Widimsky, Jiri, Jr, Naruse, Mitsuhide, Deinum, Jaap, Schultze Kool, Leo, Kocjan, Tomaz, Negro, Aurelio, Rossi, Ermanno, Kline, Gregory, Tanabe, Akiyo, Satoh, Fumitoshi, Christian Rump, Lars, Vonend, Oliver, Willenberg, Holger S., Fuller, Peter J., Yang, Jun, Chee, Nicholas Yong Nian, Magill, Steven B., Shafigullina, Zulfiya, Quinkler, Marcus, Oliveras, Anna, Dun Wu, Kwan, Wu, Vin-Cent, Kratka, Zusana, Barbiero, Giulio, Battistel, Michele, Chang, Chin-Chen, Vanderriele, Paul-Emmanuel, and Pessina, Achille C.

Published
2019
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17. Mass Spectrometry–Based Adrenal and Peripheral Venous Steroid Profiling for Subtyping Primary Aldosteronism

Author

Eisenhofer, Graeme, primary, Dekkers, Tanja, primary, Peitzsch, Mirko, primary, Dietz, Anna S, primary, Bidlingmaier, Martin, primary, Treitl, Marcus, primary, Williams, Tracy A, primary, Bornstein, Stefan R, primary, Haase, Matthias, primary, Rump, L C, primary, Willenberg, Holger S, primary, Beuschlein, Felix, primary, Deinum, Jaap, primary, Lenders, Jacques W M, primary, and Reincke, Martin, primary

Published
2016
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18. Major prognostic role of Ki67 in localized adrenocortical carcinoma after complete resection

Author

Beuschlein, Felix, Weigel, Jens, Saeger, Wolfgang, Kroiss, Matthias, Wild, Vanessa, Daffara, Fulvia, Libé, Rosella, Ardito, Arianna, Ghuzlan, Abir Al, Quinkler, Marcus, Oßwald, Andrea, Ronchi, Cristina L., De Krijger, Ronald, Feelders, Richard A., Waldmann, Jens, Willenberg, Holger S., Deutschbein, Timo, Stell, Anthony, Reincke, Martin, Papotti, Mauro, Baudin, Eric, Tissier, Frédérique, Haak, Harm R., Loli, Paola, Terzolo, Massimo, Allolio, Bruno, Müller, Hans Helge, Fassnacht, Martin, Beuschlein, Felix, Weigel, Jens, Saeger, Wolfgang, Kroiss, Matthias, Wild, Vanessa, Daffara, Fulvia, Libé, Rosella, Ardito, Arianna, Ghuzlan, Abir Al, Quinkler, Marcus, Oßwald, Andrea, Ronchi, Cristina L., De Krijger, Ronald, Feelders, Richard A., Waldmann, Jens, Willenberg, Holger S., Deutschbein, Timo, Stell, Anthony, Reincke, Martin, Papotti, Mauro, Baudin, Eric, Tissier, Frédérique, Haak, Harm R., Loli, Paola, Terzolo, Massimo, Allolio, Bruno, Müller, Hans Helge, and Fassnacht, Martin

Published
2015

19. Major prognostic role of Ki67 in localized adrenocortical carcinoma after complete resection

Author

Pathologie patiënten zorg, Beuschlein, Felix, Weigel, Jens, Saeger, Wolfgang, Kroiss, Matthias, Wild, Vanessa, Daffara, Fulvia, Libé, Rosella, Ardito, Arianna, Ghuzlan, Abir Al, Quinkler, Marcus, Oßwald, Andrea, Ronchi, Cristina L., De Krijger, Ronald, Feelders, Richard A., Waldmann, Jens, Willenberg, Holger S., Deutschbein, Timo, Stell, Anthony, Reincke, Martin, Papotti, Mauro, Baudin, Eric, Tissier, Frédérique, Haak, Harm R., Loli, Paola, Terzolo, Massimo, Allolio, Bruno, Müller, Hans Helge, Fassnacht, Martin, Pathologie patiënten zorg, Beuschlein, Felix, Weigel, Jens, Saeger, Wolfgang, Kroiss, Matthias, Wild, Vanessa, Daffara, Fulvia, Libé, Rosella, Ardito, Arianna, Ghuzlan, Abir Al, Quinkler, Marcus, Oßwald, Andrea, Ronchi, Cristina L., De Krijger, Ronald, Feelders, Richard A., Waldmann, Jens, Willenberg, Holger S., Deutschbein, Timo, Stell, Anthony, Reincke, Martin, Papotti, Mauro, Baudin, Eric, Tissier, Frédérique, Haak, Harm R., Loli, Paola, Terzolo, Massimo, Allolio, Bruno, Müller, Hans Helge, and Fassnacht, Martin

Published
2015

20. The rs1990760 polymorphism within the IFIH 1 locus is not associated with Graves' disease, Hashimoto's thyroiditis and Addison's disease

Author

Penna Martinez, Marissa, Ramos-Lopez, Elizabeth, Robbers, Inka, Kahles, Heinrich, Hahner, Stefanie, Willenberg, Holger S., Reisch, Nicole, Seidl, Christian, Segni, Maria, and Badenhoop, Klaus

Subjects
endocrine system, endocrine system diseases, ddc:610
Abstract

Background: Three genes have been confirmed as major joint susceptibility genes for endocrine autoimmune disease:human leukocyte antigen class II, cytotoxic T-lymphocyte antigen 4 and protein tyrosine phosphatase non-receptor type 22. Recent studies showed that a genetic variation within the interferon induced helicase domain 1 (IFIH1) locus (rs1990760 polymorphism) is an additional risk factor in type 1 diabetes and Graves' disease (GD). Methods: The aim of the present study was to investigate the role of the rs1990760 polymorphism within the IFIH1 gene in German patients with GD (n=258), Hashimoto's thyroiditis (HT,n=106), Addison's disease (AD,n=195) and healthy controls (HC,n=227) as well as in 55 GD families (165 individuals, German) and 100 HT families (300 individuals, Italian). Furthermore, the interaction between rs1990760 polymorphism with human leukocyte antigen (HLA) risk haplotype DQ2(DQA*0501-DQB*0201), the risk haplotypes DQ2/DQ8 (DQA*0301-DQB*0302) and the status of thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb) and TSH receptor antibody (TRAb) in patients and families were analysed. Results:No significant differences were found between the allele and genotype frequencies for rs1990760 IFIH1 polymorphism in patients with GD, HT, AD and HC. Also no differences were observed when stratifying the IFIH1 rs1990760 polymorphism for gender, presence or absence of thyroid antibodies (GD:TRAb and HT:TPOAb/TgAb) and HLA risk haplotypes (DQ2:for GD and HT, DQ2/DQ8:for AD). Furthermore the transmission analysis in GD and HT families revealed no differences in alleles transmission for rs1990760 IFIH1 from parents with or without HLA risk haplotype DQ2 to the affected offspring. In contrast, by dividing the HT parents according to the presence or absence of thyroid Ab titers, mothers and fathers both positive for TPOAb/TgAb overtransmitted the allele A of IFIH1 rs1990760 to their HT affected offspring (61.8% vs 38.2%;p=0.05;corrected p [pc]=0.1). However, these associations did not remain statistically significant after correction of the p-values. Conclusion: In conclusion, our data suggest, no contribution from IFIH1 rs1990760 polymorphism to the pathogenesis of either Graves' disease, Hashimoto's thyroiditis or Addison's disease in our study populations. However, in order to exclude a possible influence of the studied polymorphism in specified subgroups within patients with autoimmune thyroid disease, further investigations in larger populations are needed.

Published
2009

21. Insulin gene polymorphisms in type I diabetes, Addison's disease and the polyglandular autoimmune syndrome type II

Author

Ramos-Lopez, Elizabeth, Lange, Britta Kristina, Kahles, Heinrich, Willenberg, Holger S., Meyer, Gesine, Penna Martinez, Marissa, Reisch, Nicole, Hahner, Stefanie, Seissler, Jürgen, and Badenhoop, Klaus

Subjects
endocrine system diseases, ddc:610
Abstract

Background: Polymorphisms within the insulin gene can influence insulin expression in the pancreas and especially in the thymus, where self-antigens are processed, shaping the T cell repertoire into selftolerance, a process that protects from ß-cell autoimmunity. Methods: We investigated the role of the -2221Msp(C/T) and -23HphI(A/T) polymorphisms within the insulin gene in patients with a monoglandular autoimmune endocrine disease [patients with isolated type 1 diabetes (T1D, n = 317), Addison´s disease (AD, n = 107) or Hashimoto´s thyroiditis (HT, n = 61)], those with a polyglandular autoimmune syndrome type II (combination of T1D and/or AD with HT or GD, n = 62) as well as in healthy controls (HC, n = 275). Results: T1D patients carried significantly more often the homozygous genotype "CC" -2221Msp(C/T) and "AA" -23HphI(A/T) polymorphisms than the HC (78.5% vs. 66.2%, p = 0.0027 and 75.4% vs. 52.4%, p = 3.7 × 10-8, respectively). The distribution of insulin gene polymorphisms did not show significant differences between patients with AD, HT, or APS-II and HC. Conclusion: We demonstrate that the allele "C" of the -2221Msp(C/T) and "A" -23HphI(A/T) insulin gene polymorphisms confer susceptibility to T1D but not to isolated AD, HT or as a part of the APS-II.

Published
2008

22. Recurrent activating mutation in PRKACA in cortisol-producing adrenal tumors

Author

Goh, Gerald, Scholl, Ute, Healy, James, Choi, Murim, Prasad, Manju L, Nelson-Williams, Carol, Kuntsman, John W, Korah, Reju, Suttorp, Anna-Carinna, Dietrich, Dimo, Haase, Mathias, Willenberg, Holger S, Stålberg, Peter, Hellman, Per, Åkerström, Göran, Björklund, Peyman, Carling, Tobias, Lifton, Richard P, Goh, Gerald, Scholl, Ute, Healy, James, Choi, Murim, Prasad, Manju L, Nelson-Williams, Carol, Kuntsman, John W, Korah, Reju, Suttorp, Anna-Carinna, Dietrich, Dimo, Haase, Mathias, Willenberg, Holger S, Stålberg, Peter, Hellman, Per, Åkerström, Göran, Björklund, Peyman, Carling, Tobias, and Lifton, Richard P

Abstract

Adrenal tumors autonomously producing cortisol cause Cushing's syndrome1, 2, 3, 4. We performed exome sequencing of 25 tumor-normal pairs and identified 2 subgroups. Eight tumors (including three carcinomas) had many somatic copy number variants (CNVs) with frequent deletion of CDC42 and CDKN2A, amplification of 5q31.2 and protein-altering mutations in TP53 and RB1. Seventeen tumors (all adenomas) had no somatic CNVs or TP53 or RB1 mutations. Six of these had known gain-of-function mutations in CTNNB1 (β-catenin)5, 6 or GNAS (Gαs)7, 8. Six others had somatic mutations in PRKACA (protein kinase A (PKA) catalytic subunit) resulting in a p.Leu206Arg substitution. Further sequencing identified this mutation in 13 of 63 tumors (35% of adenomas with overt Cushing's syndrome). PRKACA, GNAS and CTNNB1 mutations were mutually exclusive. Leu206 directly interacts with the regulatory subunit of PKA, PRKAR1A9, 10. Leu206Arg PRKACA loses PRKAR1A binding, increasing the phosphorylation of downstream targets. PKA activity induces cortisol production and cell proliferation11, 12, 13, 14, 15, providing a mechanism for tumor development. These findings define distinct mechanisms underlying adrenal cortisol-producing tumors., Correction in: Nature Genetics, vol. 46, article nr. 759 (2014), doi: 10.1038/ng0714-759b

Published
2014
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23. Comprehensive Re-Sequencing of Adrenal Aldosterone Producing Lesions Reveal Three Somatic Mutations near the KCNJ5 Potassium Channel Selectivity Filter

Author

Åkerström, Tobias, Crona, Joakim, Verdugo, Alberto Delgado, Starker, Lee F., Cupisti, Kenko, Willenberg, Holger S., Knoefel, Wolfram T., Saeger, Wolfgang, Feller, Alfred, Ip, Julian, Soon, Patsy, Anlauf, Martin, Alesina, Pier F., Schmid, Kurt W., Decaussin, Myriam, Levillain, Pierre, Wangberg, Bo, Peix, Jean-Louis, Robinson, Bruce, Zedenius, Jan, Backdahl, Martin, Caramuta, Stefano, Iwen, K. Alexander, Botling, Johan, Stålberg, Peter, Kraimps, Jean-Louis, Dralle, Henning, Hellman, Per, Sidhu, Stan, Westin, Gunnar, Lehnert, Hendrik, Walz, Martin K., Åkerström, Göran, Carling, Tobias, Choi, Murim, Lifton, Richard P., Björklund, Peyman, Åkerström, Tobias, Crona, Joakim, Verdugo, Alberto Delgado, Starker, Lee F., Cupisti, Kenko, Willenberg, Holger S., Knoefel, Wolfram T., Saeger, Wolfgang, Feller, Alfred, Ip, Julian, Soon, Patsy, Anlauf, Martin, Alesina, Pier F., Schmid, Kurt W., Decaussin, Myriam, Levillain, Pierre, Wangberg, Bo, Peix, Jean-Louis, Robinson, Bruce, Zedenius, Jan, Backdahl, Martin, Caramuta, Stefano, Iwen, K. Alexander, Botling, Johan, Stålberg, Peter, Kraimps, Jean-Louis, Dralle, Henning, Hellman, Per, Sidhu, Stan, Westin, Gunnar, Lehnert, Hendrik, Walz, Martin K., Åkerström, Göran, Carling, Tobias, Choi, Murim, Lifton, Richard P., and Björklund, Peyman

Abstract

Background: Aldosterone producing lesions are a common cause of hypertension, but genetic alterations for tumorigenesis have been unclear. Recently, either of two recurrent somatic missense mutations (G151R or L168R) was found in the potassium channel KCNJ5 gene in aldosterone producing adenomas. These mutations alter the channel selectivity filter and result in Na+ conductance and cell depolarization, stimulating aldosterone production and cell proliferation. Because a similar mutation occurs in a Mendelian form of primary aldosteronism, these mutations appear to be sufficient for cell proliferation and aldosterone production. The prevalence and spectrum of KCNJ5 mutations in different entities of adrenocortical lesions remain to be defined. Materials and Methods: The coding region and flanking intronic segments of KCNJ5 were subjected to Sanger DNA sequencing in 351 aldosterone producing lesions, from patients with primary aldosteronism and 130 other adrenocortical lesions. The specimens had been collected from 10 different worldwide referral centers. Results: G151R or L168R somatic mutations were identified in 47% of aldosterone producing adenomas, each with similar frequency. A previously unreported somatic mutation near the selectivity filter, E145Q, was observed twice. Somatic G151R or L168R mutations were also found in 40% of aldosterone producing adenomas associated with marked hyperplasia, but not in specimens with merely unilateral hyperplasia. Mutations were absent in 130 non-aldosterone secreting lesions. KCNJ5 mutations were overrepresented in aldosterone producing adenomas from female compared to male patients (63 vs. 24%). Males with KCNJ5 mutations were significantly younger than those without (45 vs. 54, respectively; p < 0.005) and their APAs with KCNJ5 mutations were larger than those without (27.1 mm vs. 17.1 mm; p < 0.005). Discussion: Either of two somatic KCNJ5 mutations are highly prevalent and specific for aldosterone producing lesions

Published
2012
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24. Combination chemotherapy in advanced adrenocortical carcinoma

Author

Fassnacht, Martin, Terzolo, Massimo, Allolio, Bruno, Baudin, Eric, Haak, Harm, Berruti, Alfredo, Welin, Staffan, Schade-Brittinger, Carmen, Lacroix, André, Jarzab, Barbara, Sorbye, Halfdan, Torpy, David J, Stepan, Vinzenz, Schteingart, David E, Arlt, Wiebke, Kroiss, Matthias, Leboulleux, Sophie, Sperone, Paola, Sundin, Anders, Hermsen, Ilse, Hahner, Stefanie, Willenberg, Holger S, Tabarin, Antoine, Quinkler, Marcus, de la Fouchardière, Christelle, Schlumberger, Martin, Mantero, Franco, Weismann, Dirk, Beuschlein, Felix, Gelderblom, Hans, Wilmink, Hanneke, Sender, Monica, Edgerly, Maureen, Kenn, Werner, Fojo, Tito, Müller, Hans-Helge, Skogseid, Britt, Fassnacht, Martin, Terzolo, Massimo, Allolio, Bruno, Baudin, Eric, Haak, Harm, Berruti, Alfredo, Welin, Staffan, Schade-Brittinger, Carmen, Lacroix, André, Jarzab, Barbara, Sorbye, Halfdan, Torpy, David J, Stepan, Vinzenz, Schteingart, David E, Arlt, Wiebke, Kroiss, Matthias, Leboulleux, Sophie, Sperone, Paola, Sundin, Anders, Hermsen, Ilse, Hahner, Stefanie, Willenberg, Holger S, Tabarin, Antoine, Quinkler, Marcus, de la Fouchardière, Christelle, Schlumberger, Martin, Mantero, Franco, Weismann, Dirk, Beuschlein, Felix, Gelderblom, Hans, Wilmink, Hanneke, Sender, Monica, Edgerly, Maureen, Kenn, Werner, Fojo, Tito, Müller, Hans-Helge, and Skogseid, Britt

Abstract

BACKGROUND: Adrenocortical carcinoma is a rare cancer that has a poor response to cytotoxic treatment. METHODS: We randomly assigned 304 patients with advanced adrenocortical carcinoma to receive mitotane plus either a combination of etoposide (100 mg per square meter of body-surface area on days 2 to 4), doxorubicin (40 mg per square meter on day 1), and cisplatin (40 mg per square meter on days 3 and 4) (EDP) every 4 weeks or streptozocin (streptozotocin) (1 g on days 1 to 5 in cycle 1; 2 g on day 1 in subsequent cycles) every 3 weeks. Patients with disease progression received the alternative regimen as second-line therapy. The primary end point was overall survival. RESULTS: For first-line therapy, patients in the EDP-mitotane group had a significantly higher response rate than those in the streptozocin-mitotane group (23.2% vs. 9.2%, P<0.001) and longer median progression-free survival (5.0 months vs. 2.1 months; hazard ratio, 0.55; 95% confidence interval [CI], 0.43 to 0.69; P<0.001); there was no significant between-group difference in overall survival (14.8 months and 12.0 months, respectively; hazard ratio, 0.79; 95% CI, 0.61 to 1.02; P=0.07). Among the 185 patients who received the alternative regimen as second-line therapy, the median duration of progression-free survival was 5.6 months in the EDP-mitotane group and 2.2 months in the streptozocin-mitotane group. Patients who did not receive the alternative second-line therapy had better overall survival with first-line EDP plus mitotane (17.1 month) than with streptozocin plus mitotane (4.7 months). Rates of serious adverse events did not differ significantly between treatments. CONCLUSIONS: Rates of response and progression-free survival were significantly better with EDP plus mitotane than with streptozocin plus mitotane as first-line therapy, with similar rates of toxic events, although there was no significant difference in overall survival.

Published
2012
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26. Plasma Metanephrine for Assessing the Selectivity of Adrenal Venous Sampling

Author

Dekkers, Tanja, primary, Deinum, Jaap, additional, Schultzekool, Leo J., additional, Blondin, Dirk, additional, Vonend, Oliver, additional, Hermus, Ad R.R.M., additional, Peitzsch, Mirko, additional, Rump, Lars C., additional, Antoch, Gerald, additional, Sweep, Fred C.G.J., additional, Bornstein, Stefan R., additional, Lenders, Jacques W.M., additional, Willenberg, Holger S., additional, and Eisenhofer, Graeme, additional

Published
2013
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27. Comprehensive Re-Sequencing of Adrenal Aldosterone Producing Lesions Reveal Three Somatic Mutations near the KCNJ5 Potassium Channel Selectivity Filter

Author

Åkerström, Tobias, primary, Crona, Joakim, additional, Delgado Verdugo, Alberto, additional, Starker, Lee F., additional, Cupisti, Kenko, additional, Willenberg, Holger S., additional, Knoefel, Wolfram T., additional, Saeger, Wolfgang, additional, Feller, Alfred, additional, Ip, Julian, additional, Soon, Patsy, additional, Anlauf, Martin, additional, Alesina, Pier F., additional, Schmid, Kurt W., additional, Decaussin, Myriam, additional, Levillain, Pierre, additional, Wängberg, Bo, additional, Peix, Jean-Louis, additional, Robinson, Bruce, additional, Zedenius, Jan, additional, Bäckdahl, Martin, additional, Caramuta, Stefano, additional, Iwen, K. Alexander, additional, Botling, Johan, additional, Stålberg, Peter, additional, Kraimps, Jean-Louis, additional, Dralle, Henning, additional, Hellman, Per, additional, Sidhu, Stan, additional, Westin, Gunnar, additional, Lehnert, Hendrik, additional, Walz, Martin K., additional, Åkerström, Göran, additional, Carling, Tobias, additional, Choi, Murim, additional, Lifton, Richard P., additional, and Björklund, Peyman, additional

Published
2012
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31. Deficits in the Management of Patients With Adrenocortical Carcinoma in Germany

Author

Johanssen, Sarah, primary, Hahner, Stefanie, additional, Saeger, Wolfgang, additional, Quinkler, Marcus, additional, Beuschlein, Felix, additional, Dralle, Henning, additional, Haaf, Michaela, additional, Kroiss, Matthias, additional, Jurowich, Christian, additional, Langer, Peter, additional, Oelkers, Wolfgang, additional, Spahn, Martin, additional, Willenberg, Holger S., additional, Mäder, Uwe, additional, Allolio, Bruno, additional, and Fassnacht, Martin, additional

Published
2010
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32. High Diagnostic and Prognostic Value of Steroidogenic Factor-1 Expression in Adrenal Tumors

Author

Sbiera, Silviu, primary, Schmull, Sebastian, additional, Assie, Guillaume, additional, Voelker, Hans-Ullrich, additional, Kraus, Luitgard, additional, Beyer, Melanie, additional, Ragazzon, Bruno, additional, Beuschlein, Felix, additional, Willenberg, Holger S., additional, Hahner, Stefanie, additional, Saeger, Wolfgang, additional, Bertherat, Jerome, additional, Allolio, Bruno, additional, and Fassnacht, Martin, additional

Published
2010
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33. Expression of excision repair cross complementing group 1 and prognosis in adrenocortical carcinoma patients treated with platinum-based chemotherapy

Author

Ronchi, Cristina L, primary, Sbiera, Silviu, additional, Kraus, Luitgard, additional, Wortmann, Sebastian, additional, Johanssen, Sarah, additional, Adam, Patrick, additional, Willenberg, Holger S, additional, Hahner, Stefanie, additional, Allolio, Bruno, additional, and Fassnacht, Martin, additional

Published
2009
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35. Dendritic Cell Vaccination with Xenogenic Polypeptide Hormone Induces Tumor Rejection in Neuroendocrine Cancer

Author

Papewalis, Claudia, primary, Wuttke, Margret, additional, Seissler, Jochen, additional, Meyer, Yvonne, additional, Kessler, Caroline, additional, Jacobs, Benedikt, additional, Ullrich, Evelyn, additional, Willenberg, Holger S., additional, Schinner, Sven, additional, Baehring, Thomas, additional, Scherbaum, Werner A., additional, and Schott, Matthias, additional

Published
2008
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36. Long-term recurrence after parathyroidectomy in primary hyperparathyroidism-do predictors exist?

Author

Müller-Graff I, Müller-Graff FT, Reichenbach K, Leuchter M, Willenberg HS, Schafmayer C, and Philipp M

Abstract

Background: Primary hyperparathyroidism (pHPT) is the third most common endocrine disease, affecting predominantly postmenopausal women. About 85% of cases are caused by a solitary parathyroid adenoma which leads to a hypersecretion of the parathyroid hormone (PTH) and consequently to elevated serum calcium concentrations. Parathyroidectomy is the only curative treatment. While a very low recurrence rate of 0.4-1.3% was previously thought, recent long-term studies have shown significantly higher recurrence rates at longer follow-up intervals of more than 6 months to several years, posing new challenges for surgeons. In addition, laboratory dynamics may occur in the early postoperative period that cannot yet be adequately explained in terms of long-term outcomes. Therefore, the aim of this study was to evaluate the long-term outcome after parathyroidectomy for pHPT at the Department of General Surgery at the University Medical Center Rostock with regard to late recurrences., Methods: This retrospective long-term follow-up evaluated the postoperative course after parathyroidectomy for pHPT. Based on 111 patients who underwent surgery at the Department of General Surgery at the University Medical Center Rostock between 2007 and 2017, 65 patients were followed for a median postoperative period of 41 months., Results: In addition to normocalcemic PTH fluctuations in the early postoperative period, which is a well-known phenomenon, the result shows an elevated calcium or PTH concentration during a follow-up of more than 10 years. These results may predict late recurrence. Furthermore, it is not the preoperative PTH and calcium, but rather the preoperative serum creatinine that plays a role in late follow-up, contrary to expectations., Conclusions: The results emphasise the importance of long-term follow-up of patients who have undergone parathyroidectomy and may help to guide the development of institutional postoperative surveillance., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://gs.amegroups.com/article/view/10.21037/gs-24-116/coif). The authors have no conflicts of interest to declare., (2024 AME Publishing Company. All rights reserved.)

Published
2024
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