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Clues for early detection of autoimmune Addison's disease - myths and realities.

Artikel i vetenskaplig tidskrift
Författare Å B Saevik
A-K Åkerman
K Grønning
I Nermoen
S F Valland
T E Finnes
M Isaksson
P Dahlqvist
Ragnhildur Bergthorsdottir
Olov Ekwall
J Skov
B G Nedrebø
A-L Hulting
J Wahlberg
J Svartberg
C Höybye
I H Bleskestad
A P Jørgensen
O Kämpe
M Øksnes
S Bensing
E S Husebye
Publicerad i Journal of internal medicine
Volym 283
Nummer/häfte 2
Sidor 190–199
ISSN 1365-2796
Publiceringsår 2018
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition
Sidor 190–199
Språk en
Länkar dx.doi.org/10.1111/joim.12699
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämneskategorier Endokrinologi

Sammanfattning

Early detection of autoimmune Addison's disease (AAD) is important as delay in diagnosis may result in a life-threatening adrenal crisis and death. The classical clinical picture of untreated AAD is well-described, but methodical investigations are scarce.Perform a retrospective audit of patient records with the aim of identifying biochemical markers for early diagnosis of AAD.A multicentre retrospective study including 272 patients diagnosed with AAD at hospitals in Norway and Sweden during 1978-2016. Scrutiny of medical records provided patient data and laboratory values.Low sodium occurred in 207 of 247 (84%), but only one-third had elevated potassium. Other common nonendocrine tests were largely normal. TSH was elevated in 79 of 153 patients, and hypoglycaemia was found in 10%. Thirty-three per cent were diagnosed subsequent to adrenal crisis, in whom electrolyte disturbances were significantly more pronounced (P < 0.001). Serum cortisol was consistently decreased (median 62 nmol L(-1) [1-668]) and significantly lower in individuals with adrenal crisis (38 nmol L(-1) [2-442]) than in those without (81 nmol L(-1) [1-668], P < 0.001).The most consistent biochemical finding of untreated AAD was low sodium independent of the degree of glucocorticoid deficiency. Half of the patients had elevated TSH levels. Only a minority presented with marked hyperkalaemia or other nonhormonal abnormalities. Thus, unexplained low sodium and/or elevated TSH should prompt consideration of an undiagnosed AAD, and on clinical suspicion bring about assay of cortisol and ACTH. Presence of 21-hydroxylase autoantibodies confirms autoimmune aetiology. Anticipating additional abnormalities in routine blood tests may delay diagnosis.

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