The History of the Discovery of Addison's Disease

Bishop, P. M. F.

doi:10.1177/003591575004300105

Cited by 13 publications

(18 citation statements)

References 12 publications

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“…A “disease” usually has only one cause, and there are many causes of primary adrenal insufficiency (Table 4). When Thomas Addison first described this disorder in the 19 th century, the most common cause was destruction of the adrenal cortex due to tuberculosis (26,52). In the 21 st century in the developed parts of the world, autoimmune destruction of the adrenal cortex is more common, although tuberculosis still exists and can still cause primary adrenal insufficiency (65, 135).…”

Section: Adrenal Insufficiencymentioning

confidence: 99%

Physiological Basis for the Etiology, Diagnosis, and Treatment of Adrenal Disorders: Cushing's Syndrome, Adrenal Insufficiency, and Congenital Adrenal Hyperplasia

Raff

Sharma

Nieman

2014

Comprehensive Physiology

127

105

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The hypothalamic-pituitary-adrenal (HPA) axis is a classic neuroendocrine system. One of the best ways to understand the HPA axis is to appreciate its dynamics in the variety of diseases and syndromes that affect it. Excess glucocorticoid activity can be due to endogenous cortisol overproduction (spontaneous Cushing’s syndrome) or exogenous glucocorticoid therapy (iatrogenic Cushing’s syndrome). Endogenous Cushing’s syndrome can be subdivided into ACTH-dependent and ACTH-independent, the latter of which is usually due to autonomous adrenal overproduction. The former can be due to a pituitary corticotroph tumor (usually benign) or ectopic ACTH production from tumors outside the pituitary; both of these tumor types overexpress the proopiomelanocortin gene. The converse of Cushing’s syndrome is the lack of normal cortisol secretion and is usually due to adrenal destruction (primary adrenal insufficiency) or hypopituitarism (secondary adrenal insufficiency). Secondary adrenal insufficiency can also result from a rapid discontinuation of long-term, pharmacological glucocorticoid therapy because of HPA axis suppression and adrenal atrophy. Finally, mutations in the steroidogenic enzymes of the adrenal cortex can lead to congenital adrenal hyperplasia and an increase in precursor steroids, particularly androgens. When present in utero, this can lead to masculinization of a female fetus. An understanding of the dynamics of the HPA axis is necessary to master the diagnosis and differential diagnosis of pituitary-adrenal diseases. Furthermore, understanding the pathophysiology of the HPA axis gives great insight into its normal control.

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Section: Adrenal Insufficiencymentioning

confidence: 99%

Physiological Basis for the Etiology, Diagnosis, and Treatment of Adrenal Disorders: Cushing's Syndrome, Adrenal Insufficiency, and Congenital Adrenal Hyperplasia

Raff

Sharma

Nieman

2014

Comprehensive Physiology

127

105

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“…His description of the cardinal symptoms—fatigue, weight loss, abdominal irritability and skin hyperpigmentation—has barely been altered since, and remains relevant today thanks to the accuracy and fluency of his findings 15. Despite this, the condition continues to be a diagnostic challenge in the 21st century, mainly due to the slow and non-specific progression of symptoms, which offer a wealth of differential diagnoses 15…”

Section: Discussionmentioning

confidence: 99%

First presentation of Addison's disease as hyperkalaemia in acute kidney injury

et al. 2016

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Addison's disease is a rare endocrine disorder that frequently presents with non-specific symptoms, but may deteriorate rapidly into life-threatening Addisonian crisis if left untreated. Diagnosis can be difficult in patients without a suggestive medical history. We describe a case of a 37-year-old man who was admitted with acute kidney injury and hyperkalaemia, resistant to treatment with insulin/dextrose and calcium gluconate. On clinical examination, he was found to be hyperpigmented; a subsequent random serum cortisol of 49 nmol/L affirmed the preliminary diagnosis of Addison's disease. The patient's hyperkalaemia improved on treatment with hydrocortisone, and a follow-up morning adrenocorticotropic hormone of 1051 ng/L confirmed the diagnosis.

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“…(Brown-Séquard, 1856). In 1901, Takamine and Aldrich isolated adrenaline (Bishop, 1949), and in 1917, Rogoff and Stewart began more detailed research in totally adrenalectomized animals, establishing that cortical adrenal extracts have life-preserving properties (Bishop, 1949). In 1901, Takamine and Aldrich isolated adrenaline (Bishop, 1949), and in 1917, Rogoff and Stewart began more detailed research in totally adrenalectomized animals, establishing that cortical adrenal extracts have life-preserving properties (Bishop, 1949).…”

Section: Historical Aspectsmentioning

confidence: 99%

“…Its approach is indicated by a certain amount of languor and restlessness, paleness, loss of muscular strength, general relaxation or feebleness of the whole frame, and indisposition to, or incapacity for, bodily and mental exertion" (Bishop, 1949). Its approach is indicated by a certain amount of languor and restlessness, paleness, loss of muscular strength, general relaxation or feebleness of the whole frame, and indisposition to, or incapacity for, bodily and mental exertion" (Bishop, 1949).…”

Section: Historical Aspectsmentioning

confidence: 99%