Hypoadrenia or "a bit of Addison's disease".

نویسنده

  • R B Tattersall
چکیده

In the fully developed form of Addison's disease, first described in 1855 and now usually called acute adrenocortical failure or adrenal insufficiency, the signs and symptoms are unmistakable. They are weakness, tiredness, low blood pressure and pigmentation which is especially prominent in scars, flexures and inside the mouth. By the end of the nineteenth century it was generally agreed that the adrenal glands were essential to life and that they consisted of two glands, the medulla and cortex, in a single capsule. The discovery of the pressor effects of adrenal extracts in 1895, and isolation and synthesis of adrenaline in the subsequent decade diverted the attention of clinicians and physiologists away from the adrenal cortex.1 Adrenaline raised the blood pressure and increased muscular strength and, since these were the antithesis of the symptoms of Addison's disease, many concluded that Addison's disease was adrenaline deficiency. Final proof that Addison's disease was due to failure of the adrenal cortex did not come until the early 1930s,2 and even then there were major difficulties in diagnosis in patients with "doubtful pigmentation, loss of weight, fatigability, weakness and hypotension".3 These, with the exception of pigmentation, are common and non-specific and in the context of neurasthenia form part of what Sicherman has described as "the staggering variety of symptoms that had long taxed the ingenuity and patience of physicians".4 They were seized on by some pioneer endocrinologists in the period 1902-1925 to construct a disease, "hypoadrenia", or aformefruste of Addison's disease. The history of medicine is replete with "new" diseases which, like comets, have made a dramatic entry, shone brightly for a time in the medical firmament, and then faded and died (or had their symptoms reconstructed in a different way). Examples from the last century include visceroptosis, suppressed gout, autointoxication and neurasthenia, while An early version of this paper was presented at a symposium, 'Medicine and the glandular vision of life', held at the Wellcome Institute for the History of Medicine in June 1997. I thank the discussants at that meeting and the anonymous referees for much helpful criticism. My major debt is to Mrs Pat Lister for her invaluable editorial assistance. 1 Throughout this paper I have used the modem English spelling "adrenaline" for the hormone of the adrenal medulla. The name "Adrenalin" was the registered trade name of Parke, Davis and Co. from 1901 onwards. In the period 1895-1925 many other names …

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Auto-Immune Addison\'s Disease Associated with Hyperprolactinemia

SUMMARY Three cases ofauto-immune addison's disease are reported in association with hyperprolactilinemia. All of them had galactorrhea. In three cases complete resolution of hyperprolactitinemia occurred with corticosteroid replacement. We suggest that hyperprolactinemia was due to cortisol deficiency operating directly or indirectly at the level of the pituitary.  

متن کامل

Increase Serum Aminotransferases in Addison\'s Patients

SUMMARY Three pa ticnts admitted because of slightly increased serum amino trans fcrases were found to have Addison's disease. A review of 16 other patients with addison 's disease who had serum aminotransferase activity (aspartate aminotrans­ferase (ASAT) and alanine aminotransferase (ALAT) J determined prior to treatment revealed one more patient with slightly increased aminotransferase acti...

متن کامل

Cure of Psoriasis and Arthritis when Addison's Disease Was Detected

INTRODUCTION: Corticoid therapy is well-known to improve the symptoms of psoriasis. Addison's disease is an autoimmune disease which leads to a loss of cortisol production in the adrenal glands. This case report describes a patient with wide-spread psoriasis for 34 years who was cured when Addison's disease was detected and substitution to reach normal biological cortisol levels was introduced....

متن کامل

DRB1*04 and DQ alleles: expression of 21-hydroxylase autoantibodies and risk of progression to Addison's disease.

Of 957 patients with type 1 diabetes without known Addison's disease 1.6% (n = 15) were positive for 21-hydroxylase autoantibodies. Among DQ8/DQ2 heterozygous patients, the percentage expressing 21-hydroxylase autoantibodies was 5% (10 of 208) vs. less than 0.5% of patients with neither DQ8 nor DQ2. Three of the diabetic patients found to have 21-hydroxylase autoantibodies on screening were sub...

متن کامل

No Difference in Mood and Quality of Life in DHEA-S Deficient Adults with Addison’s Disease vs. Type 2 Diabetes Patients with Normal DHEA-S Levels: Implications for Management of These Conditions

Patients with Addison's disease have relatively high rates of depression and anxiety symptoms compared with population-based reference samples. Addison's disease results in deficiency of dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEA-S). There is considerable debate about the specific effects of DHEA deficiency on energy level and mood. We measured emotional well-being in 16 patients with...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Medical History

دوره 43  شماره 

صفحات  -

تاریخ انتشار 1999