Rapidly fatal Addison's disease: three case reports

Ringstad, Jetmund; Rodge, S.; Løland, W.; Rode, L

doi:10.1111/j.1365-2796.1991.tb00475.x

Cited by 10 publications

(5 citation statements)

References 4 publications

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“…Furthermore, even if the time targets are kept, a delay of 60 min from the perceived need of parenteral glucocorticoids until their administration is considered acceptable, which increases to 120 min if the time limits are fully used. It is well known that within this time serious clinical deterioration may occur in individual cases . In particular, for children, shorter time frames may be warranted.…”

Section: Discussionmentioning

confidence: 99%

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Timelines in the management of adrenal crisis – targets, limits and reality

Hahner

Hemmelmann

Quinkler

et al. 2014

Clinical Endocrinology

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Section: Discussionmentioning

confidence: 99%

“…It is well known that within this time serious clinical deterioration may occur in individual cases. 19,20 In particular, for children, shorter time frames may be warranted. Thus, efforts are needed to substantially reduce the time to parenteral administration of glucocorticoids after arrival of the emergency health professionals.…”

Section: Discussionmentioning

confidence: 99%

Timelines in the management of adrenal crisis – targets, limits and reality

Hahner

Hemmelmann

Quinkler

et al. 2014

Clinical Endocrinology

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“…A large body of evidence supports the hypothesis that, in Western countries, most cases of idiopathic Addison's disease are caused by autoimmune destruction of the adrenal cortex [1,2]. Although the prevalence of Addison's disease is very low, only 39-60 per million individuals [3,4], the observation that acute adrenal insufficiency associated with mononuclear cell infiltration of the adrenal cortex may be life-threatening [5] strengthens the importance of developing simple and reliable diagnostic assays to identify accurately individuals at high risk for Addison's disease. This is particularly important in the clinical management of adult patients with endocrine autoimmune disorders often associated with Addison's disease, such as Hashimoto's thyroiditis, Graves' disease (GD), insulin-dependent diabetes mellitus (IDDM), or premature menopause [4,[6][7][8].…”

Section: Introductionmentioning

confidence: 99%

21-hydroxylase autoantibodies in adult patients with endocrine autoimmune diseases are highly specific for Addison's disease

Falorni

Laureti

Nikoshkov

et al. 1997

Clinical and Experimental Immunology

111

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SUMMARYThe diagnostic specificity of recombinant 21-hydroxylase autoantibodies (21OH-Ab) for Addison's disease was tested in adult patients with either Graves' disease (GD), insulin-dependent diabetes mellitus (IDDM), or polyendocrinopathy, as well as in healthy controls. Using a radiobinding assay with in vitro translated recombinant human 21-hydroxylase, we found 21OH-Ab in 24/28 (86%) idiopathic Addison patients, and using an immunofluorescence assay we found adrenal cortex autoantibodies (ACA) in 12/28 (43%) patients (P ¼ 0·002). All the 12 ACA-positive sera were also positive for 21OH-Ab and ACA were found in 11/15 (73%) patients with less than 15 years and in 1/13 (8%) patients with 15-38 years of disease duration (P ¼ 0·002). 21OH-Ab were present in 3/92 (3%) patients with GD, in 1/180 (0 . 6%) with IDDM and in 0/106 healthy subjects. The 21OH-Ab-positive GD and IDDM patients were also positive for ACA. None of 17 patients with polyendocrinopathy, but without Addison's disease, had 21OH-Ab. None of the 180 Belgian IDDM patients had Addison's disease or developed an adrenal insufficiency at follow up. In two out of three Graves patients, the presence of 21OH-Ab was associated with clinical and biochemical signs of adrenal insufficiency. Of the 89 21OH-Ab-negative patients with GD none had Addison's disease at the time of blood sampling, and 79 were followed up for 5 . 6-7 . 5 years and none developed clinical signs of adrenal insufficiency. We conclude that the presence of 21OH-Ab in patients with endocrine autoimmune diseases is highly specific for Addison's disease.

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“…Primary adrenal insufficiency, also known as Addison's disease, may present with acute adrenocortical crisis with hypotension and shock, which is invariably fatal if not treated immediately 1,2 . It can also develop slowly and the manifestations may be non‐specific (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Acute Adrenocortical Crisis: Three Different Presentations

Bhattacharyya¹,

MacDonald²,

Lakhdar³

2001

Int J Clinical Practice

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SUMMARYThe adrenal cortex normally produces three principal steroid hormones: the glucocorticoid cortisol, the mineralocorticoid aldosterone, and a small quantity of sex steroids. In primary adrenocortical insufficiency, there is a deficiency of both cortisol and aldosterone with characteristic clinical and laboratory findings. In contrast, with a pituitary disorder there is isolated hypocortisolism, because its production is dependent on pituitary adrenocorticotropic hormone (ACTH), whereas aldosterone production is controlled by extracellular fluid volume, renin and serum potassium. Acute adrenocortical crisis is an absolute medical emergency and its presentation is not always typical. We describe three recent cases of acute adrenocortical crisis in our hospital who presented in three different ways in three different wards.

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Rapidly fatal Addison's disease: three case reports

Cited by 10 publications

References 4 publications

Timelines in the management of adrenal crisis – targets, limits and reality

Timelines in the management of adrenal crisis – targets, limits and reality

21-hydroxylase autoantibodies in adult patients with endocrine autoimmune diseases are highly specific for Addison's disease

Acute Adrenocortical Crisis: Three Different Presentations

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