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The classical clinical picture of untreated\n                      <jats:styled-content style=\"fixed-case\">AAD<\/jats:styled-content>\n                      is well\u2010described, but methodical investigations are scarce.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      Perform a retrospective audit of patient records with the aim of identifying biochemical markers for early diagnosis of\n                      <jats:styled-content style=\"fixed-case\">AAD<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Material and Methods<\/jats:title>\n                    <jats:p>\n                      A multicentre retrospective study including 272 patients diagnosed with\n                      <jats:styled-content style=\"fixed-case\">AAD<\/jats:styled-content>\n                      at hospitals in Norway and Sweden during 1978\u20132016. Scrutiny of medical records provided patient data and laboratory values.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Low sodium occurred in 207 of 247 (84%), but only one\u2010third had elevated potassium. Other common nonendocrine tests were largely normal.\n                      <jats:styled-content style=\"fixed-case\">TSH<\/jats:styled-content>\n                      was elevated in 79 of 153 patients, and hypoglycaemia was found in 10%. Thirty\u2010three per cent were diagnosed subsequent to adrenal crisis, in whom electrolyte disturbances were significantly more pronounced (\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.001). Serum cortisol was consistently decreased (median 62 nmol L\n                      <jats:sup>\u22121<\/jats:sup>\n                      [1\u2013668]) and significantly lower in individuals with adrenal crisis (38 nmol L\n                      <jats:sup>\u22121<\/jats:sup>\n                      [2\u2013442]) than in those without (81 nmol L\n                      <jats:sup>\u22121<\/jats:sup>\n                      [1\u2013668],\n                      <jats:italic>P<\/jats:italic>\n                      &lt; 0.001).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      The most consistent biochemical finding of untreated\n                      <jats:styled-content style=\"fixed-case\">AAD<\/jats:styled-content>\n                      was low sodium independent of the degree of glucocorticoid deficiency. Half of the patients had elevated\n                      <jats:styled-content style=\"fixed-case\">TSH<\/jats:styled-content>\n                      levels. Only a minority presented with marked hyperkalaemia or other nonhormonal abnormalities. Thus, unexplained low sodium and\/or elevated\n                      <jats:styled-content style=\"fixed-case\">TSH<\/jats:styled-content>\n                      should prompt consideration of an undiagnosed\n                      <jats:styled-content style=\"fixed-case\">AAD<\/jats:styled-content>\n                      , and on clinical suspicion bring about assay of cortisol and\n                      <jats:styled-content style=\"fixed-case\">ACTH<\/jats:styled-content>\n                      . Presence of 21\u2010hydroxylase autoantibodies confirms autoimmune aetiology. Anticipating additional abnormalities in routine blood tests may delay diagnosis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/joim.12699","type":"journal-article","created":{"date-parts":[[2017,11,3]],"date-time":"2017-11-03T08:14:14Z","timestamp":1509696854000},"page":"190-199","source":"Crossref","is-referenced-by-count":49,"title":["Clues for early detection of autoimmune Addison's disease \u2013 myths and realities"],"prefix":"10.1111","volume":"283","author":[{"given":"\u00c5. B.","family":"S\u00e6vik","sequence":"first","affiliation":[{"name":"Department of Clinical Medicine University of Bergen Bergen Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.\u2010K.","family":"\u00c5kerman","sequence":"additional","affiliation":[{"name":"Department of Medicine \u00d6rebro University Hospital \u00d6rebro Sweden"},{"name":"Department of Molecular Medicine and Surgery Karolinska Institutet Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Gr\u00f8nning","sequence":"additional","affiliation":[{"name":"Division of Medicine Akershus University Hospital L\u00f8renskog Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I.","family":"Nermoen","sequence":"additional","affiliation":[{"name":"Division of Medicine Akershus University Hospital L\u00f8renskog Norway"},{"name":"Institute of Clinical Medicine Akershus University Hospital University of Oslo L\u00f8renskog Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. 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