Frida Dalin1,2, Gabriel Nordling Eriksson3, Per Dahlqvist4, Åsa Hallgren1, Jeanette Wahlberg5, Olov Ekwall6, Stefan Söderberg4, Johan Rönnelid7, Per Olcén8, Ola Winqvist9, Sergiu-Bogdan Catrina3,10, Berit Kriström11, Maria Laudius4, Magnus Isaksson12, Maria Halldin Stenlid13, Jan Gustafsson13, Gennet Gebre-Medhin13, Sigridur Björnsdottir3,10, Annika Janson14, Anna-Karin Åkerman8, Jan Åman15, Karel Duchen16, Ragnhildur Bergthorsdottir17,18, Gudmundur Johannsson17,18, Emma Lindskog6, Mona Landin-Olsson19, Maria Elfving20, Erik Waldenström19, Anna-Lena Hulting3, Olle Kämpe1,10, Sophie Bensing3,10. 1. Centre for Molecular Medicine, Department of Medicine (Solna). 2. Science for Life Laboratory, Department of Medical Sciences, and. 3. Department of Molecular Medicine and Surgery, and. 4. Department of Public Health and Clinical Medicine and. 5. Division of Endocrinology, Department of Medical and Health Sciences, Faculty of Health Sciences, and. 6. Department of Pediatrics, Institute of Clinical Sciences. 7. Departments of Immunology, Genetics and Pathology. 8. Department of Laboratory Medicine and. 9. Translational Immunology, Department of Medicine (Solna), and. 10. Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Karolinska Institutet, Stockholm SE-17176, Sweden. 11. Institution of Clinical Science, Pediatrics, Umeå University, Umeå SE-90736, Sweden. 12. Medical Sciences, and. 13. Women's and Children's Health, Uppsala University, Uppsala SE-75236, Sweden. 14. Department of Women's and Children's Health, Karolinska Institutet, Stockholm SE-17176, Sweden. 15. Department of Pediatrics, Faculty of Medicine and Health, Örebro University, Örebro SE-70281, Sweden. 16. Division of Pediatrics, Department of Clinical and Experimental Medicine, Linköping University, Linköping SE-58183, Sweden. 17. Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, and. 18. Department of Endocrinology, Sahlgrenska University Hospital, Sahlgrenska Academy, University of Gothenburg, Gothenburg SE-40530, Sweden. 19. Department of Endocrinology, Skåne University Hospital, Lund SE-22362, Sweden; and. 20. Department of Pediatrics, Pediatric Endocrinology, Clinical Sciences, Lund University, Lund SE-22362, Sweden.
Abstract
Context: Studies of the clinical and immunological features of autoimmune Addison disease (AAD) are needed to understand the disease burden and increased mortality. Objective: To provide upgraded data on autoimmune comorbidities, replacement therapy, autoantibody profiles, and cardiovascular risk factors. Design, Setting, and Participants: A cross-sectional, population-based study that included 660 AAD patients from the Swedish Addison Registry (2008-2014). When analyzing the cardiovascular risk factors, 3594 individuals from the population-based survey in Northern Sweden, MONICA (monitoring of trends and determinants of cardiovascular disease), served as controls. Main Outcome Measures: The endpoints were the prevalence of autoimmune comorbidities and cardiovascular risk factors. Autoantibodies against 13 autoantigens were determined. Results: The proportion of 21-hydroxylase autoantibody-positive patients was 83%, and 62% of patients had ≥1 associated autoimmune diseases, more frequently coexisting in females (P < 0.0001). AAD patients had a lower body mass index (P < 0.0001) and prevalence of hypertension (P = 0.027) compared with controls. Conventional hydrocortisone tablets were used by 89% of the patients, with a mean dose of 28.1 ± 8.5 mg/d. The mean hydrocortisone equivalent dose normalized to the body surface was 14.8 ± 4.4 mg/m2/d. A greater hydrocortisone equivalent dose was associated with a greater incidence of hypertension (P = 0.046). Conclusions: Careful monitoring of AAD patients is warranted to detect associated autoimmune diseases. Contemporary Swedish AAD patients did not have an increased prevalence of overweight, hypertension, type 2 diabetes mellitus, or hyperlipidemia. However, high glucocorticoid replacement doses could be a risk factor for hypertension.
Context: Studies of the clinical and immunological features of autoimmune Addison disease (AAD) are needed to understand the disease burden and increased mortality. Objective: To provide upgraded data on autoimmune comorbidities, replacement therapy, autoantibody profiles, and cardiovascular risk factors. Design, Setting, and Participants: A cross-sectional, population-based study that included 660 AAD patients from the Swedish Addison Registry (2008-2014). When analyzing the cardiovascular risk factors, 3594 individuals from the population-based survey in Northern Sweden, MONICA (monitoring of trends and determinants of cardiovascular disease), served as controls. Main Outcome Measures: The endpoints were the prevalence of autoimmune comorbidities and cardiovascular risk factors. Autoantibodies against 13 autoantigens were determined. Results: The proportion of 21-hydroxylase autoantibody-positive patients was 83%, and 62% of patients had ≥1 associated autoimmune diseases, more frequently coexisting in females (P < 0.0001). AAD patients had a lower body mass index (P < 0.0001) and prevalence of hypertension (P = 0.027) compared with controls. Conventional hydrocortisone tablets were used by 89% of the patients, with a mean dose of 28.1 ± 8.5 mg/d. The mean hydrocortisone equivalent dose normalized to the body surface was 14.8 ± 4.4 mg/m2/d. A greater hydrocortisone equivalent dose was associated with a greater incidence of hypertension (P = 0.046). Conclusions: Careful monitoring of AAD patients is warranted to detect associated autoimmune diseases. Contemporary Swedish AAD patients did not have an increased prevalence of overweight, hypertension, type 2 diabetes mellitus, or hyperlipidemia. However, high glucocorticoid replacement doses could be a risk factor for hypertension.
Authors: Hanna Nowotny; S Faisal Ahmed; Sophie Bensing; Johan G Beun; Manuela Brösamle; Irina Chifu; Hedi Claahsen van der Grinten; Maria Clemente; Henrik Falhammar; Stefanie Hahner; Eystein Husebye; Jette Kristensen; Paola Loli; Svetlana Lajic; Nicole Reisch Journal: Endocrine Date: 2021-03-04 Impact factor: 3.633
Authors: S Puglisi; A Rossini; I Tabaro; S Cannavò; F Ferrau'; M Ragonese; G Borretta; M Pellegrino; F Dughera; A Parisi; A Latina; A Pia; M Terzolo; G Reimondo Journal: J Endocrinol Invest Date: 2020-08-10 Impact factor: 4.256