Secondary adrenal insufficiency historical perspective
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Historical Perspective
Discovery
- Primary adrenal insufficiency was first discovered by Thomas Addison, an English physician and scientist, when he described adrenocortical atrophy in 1849 on autopsy of the adrenal glands of patients, some of which had vitiligo.
- In 1926, Schmidt was the first to discover the association between adrenalitis and thyroiditis, called Schmidt's syndrome, which was expanded by Carpenter in 1964 to include type 1 diabetes mellitus.
- In 1956, whitaker found an association between hypoadrenocortisism, hypothyroidism and candidiasis.
- In 1997, AIRE gene mutations were first implicated in the pathogenesis of APS (autoimmune polyglandular syndrome).
Outbreaks
- There have been several outbreaks of [disease name], which are summarized below:
Landmark Events in the Development of Treatment Strategies
- In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].
Impact on Cultural History
Famous Cases
- The following are a few famous cases of disease name:
Primary adrenal insufficiency was first described in 1849 by Thomas Addison, demonstrating that the adrenal cortex is essential for life. On Thursday, March 15, 1849 almost a century ago, President John Hilton requested that, Dr. Addison, describe his latest medical findings before the South London Medical Society. These were Dr. Addison’s introductory comments, "A remarkable form of anemia, which, although incidentally noticed by various writers, had not attracted, as he thought, by any means the attention it really deserved…It was a state of general anemia incident to adult males, and had for several years past been with him a subject of earnest inquiry and of deep interest. It usually occurs between the ages of 20 and 60; sometimes proceeding to an extreme degree in a few weeks, but more frequently commencing insidiously, and proceeding very slowly, so as to occupy a period of several weeks, or even months, before any very serious alarm is taken either by the patient or by the patient's friends. Its approach is first indicated by a certain amount of languor and restlessness, to which presently succeed a manifest paleness of the countenance, loss of muscular strength, general relaxation or feebleness of the whole frame, and indisposition to, or incapacity for, bodily or mental exertion. These symptoms go on increasing with greater or less rapidity: the face, lips, conjunctive, and external surface of the body, become more and more bloodless; the tongue appears pale and flabby; the heart's action gets exceedingly enfeebled, with a weak, soft, unusually large, but always strikingly compressible pulse; the appetite may or may not be lost; the patient experiences a distressing and increasing sense of helplessness and faintness; the heart is excited, or rendered tumultuous in its action, the breathing painfully hurried by the slightest exertion, whilst the whole surface bears some resemblance to a bad wax figure: the patient is no longer able to rise from his bed; slight edema perhaps shows itself about the ankles; the feeling of faintness and weakness becomes extreme, and he dies either from sheer exhaustion, or death is preceded by signs of passive effusion or cerebral compression.” [1]