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Sirazum Choudhury, Tricia Tan, Katharine Lazarus, and Karim Meeran

-fold increase in mortality when associated with adrenal insufficiency ( 8 ). Taken together, these data suggest that the mortality gap in hypoadrenalism is not just limited to primary disease. Possible causes of the mortality gap The cause of the

Open access

Salem A Beshyah, Khawla F Ali, and Hussein F Saadi

–10 hypoadrenal patients per year, while 22.1% see 11–25 patients per year ( Table 3 ). Most respondents (78.6%) prescribed hydrocortisone, while the minority prescribed other preparations for replacement therapy ( Table 3 ). The glucocorticoid doses were

Open access

Thabiso R P Mofokeng, Salem A Beshyah, Fazleh Mahomed, Kwazi C Z Ndlovu, and Ian L Ross

survey, manage patients with hypoadrenalism (Supplementary Appendix 1). The respondents were mostly non-endocrine specialists (48.8%) and primary care doctors (33.3%) and the minority (17.6%) were specialist endocrinologists. The proportion who identified

Open access

C E Higham, A Olsson-Brown, P Carroll, T Cooksley, J Larkin, P Lorigan, D Morganstein, P J Trainer, and the Society for Endocrinology Clinical Committee

, mineralocorticoid replacement (fludrocortisone) may be needed once daily glucocorticoid dose is below 50 mg hydrocortisone/24 h or equivalent. This is not required for hypophysitis and other causes of secondary hypoadrenalism. A short Synacthen test may be

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Aleksandra Gilis-Januszewska, Łukasz Kluczyński, and Alicja Hubalewska-Dydejczyk

). Since hypoadrenalism is potentially life-threatening, hormone replacement therapy should be introduced immediately. It should be noted that cortisolemia may be affected by drugs (i.e. etomidate, propofol) that were administered in the intensive care

Open access

David J F Smith, Hemanth Prabhudev, Sirazum Choudhury, and Karim Meeran

Addisonian crises without recognising the side effects of the excess ( 6 ). However, we now see an increased risk of cardiovascular death in hypoadrenal patients, probably due to excess cortisol administration, and consequently there has been a fall in the

Open access

Marloes L P Langelaan, Jérôme M H Kisters, Mirjam M Oosterwerff, and Arjen-Kars Boer

analysis was insufficient to separate hypoadrenal from normal subjects, considering the overlap between the groups ( 16 ). A more recent study using RIA analyses, however, found that a morning salivary cortisol value below 7.31 nmol/L distinguished patients

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M S Elston, V B Crawford, M Swarbrick, M S Dray, M Head, and J V Conaglen

adrenal blockade and watch for the development of hypoadrenalism ( 10 ). In a multicentre study of 195 patients including 37 patients with EAS, where 164 patients received metyrapone monotherapy, biochemical monitoring showed improvement in all cases with

Open access

Maria Stelmachowska-Banaś and Izabella Czajka-Oraniec

irAEs TD T1DM TD TD TD T1DM Hypoadrenalism Hypoadrenalism T1DM T1DM Hypoadrenalism Hypophysitis HLA type DRB1*04 DRB1*04 – DRB1*09 DR3-DQ2 DQB1*02 DQB1*03 DQB1*03 DR4-DQ8 DQA1

Open access

V Guarnotta, C Di Stefano, A Santoro, A Ciresi, A Coppola, and C Giordano

mortality and morbidity in patients with hypoadrenalism compared to the general population, likely due to negative effects on metabolism ( 1 , 15 , 16 , 17 , 18 ). The effects of GCs on cardiovascular risk factors, such as obesity, hypertension, diabetes