Plasma Adrenocorticotrophic Hormone in Addison's Disease and its Modification by the Administration of Adrenal Steroids

PEDIATRICS ◽  
1958 ◽  
Vol 21 (4) ◽  
pp. 660-660

Adrenal steroids exert a depressant effect on the release of pituitary adrenocorticotrophic hormone. It is therefore of interest to ascertain whether there is an increased secretion of ACTH in Addison's disease because of the deficiency of adrenal steroids in the plasma in this condition. The concentration of ACTH was determined by measuring the production of corticosteroids in the hypophysectomized dog as a measure of the amount of ACTH in plasma obtained from humans. In normal adults the amount of ACTH circulating in the plasma is so small that 20 to 31 ml of plasma does not contain sufficient ACTH to cause a significant increase in adrenal corticosteroids in adrenal venous blood collected from the test animal. Fifty-one determinations in 32 patients with adrenal insufficiency revealed a mean concentration of ACTH in the plasma which was significantly elevated over that found for plasma from 16 controlled samples obtained from normal subjects. The increased concentration of ACTH found in 10 patients with Addison's disease was significantly reduced by the intravenous infusion of hydrocortisone. It was not possible to correlate the increased concentration of ACTH in the plasma of patients with Addison's disease with the clinical manifestations or duration of the disease. The relative suppressive effect of various amounts and kinds of corticosteroids was studied.

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hong Ouyang ◽  
Bo Chen ◽  
Na Wu ◽  
Ling Li ◽  
Runyu Du ◽  
...  

Abstract Background Most patients with congenital adrenal hypoplasia (AHC) develop symptoms during infantile and juvenile periods, with varying clinical manifestations. AHC is a disease that is easily misdiagnosed as Addison’s disease or congenital adrenal hyperplasia (CAH). There was also a significant time difference between the age at which patients developed symptoms and the age at which they were diagnosed with AHC. Most patients showed early symptoms during infantile and juvenile periods, but were diagnosed with AHC many years later. Case presentation We are currently reporting a male patient who developed systemic pigmentation at age 2 and was initially diagnosed with Addison’s disease. At 22 years of age, he experienced a slipped capital femoral epiphysis (SCFE), a disease mostly seen in adolescents aged 8–15 years, an important cause of which is endocrine disorder. Testes evaluated using color Doppler Ultrasonography suggested microcalcifications. Further genetic testing and auxiliary examinations revealed that the patient had hypogonadotropic hypogonadism (HH) and DAX-1 gene disorders, at which time he was diagnosed with AHC complicated by HH. He was given hormone replacement therapy, followed by regular outpatient review to adjust the medication. Conclusions The typical early symptoms of AHC are hyperpigmentation and ion disturbance during infantile and juvenile periods, while few patients with AHC develop puberty disorders as early symptoms. AHC is prone to being misdiagnosed as Addison’s disease, and then gradually develops the symptoms of HH in adolescence. The definitive diagnosis of AHC ultimately is based on the patient’s clinical presentation, laboratory results and genetic testing results.


Blood ◽  
1949 ◽  
Vol 4 (5) ◽  
pp. 646-652 ◽  
Author(s):  
JACQUES L. GABRILOVE ◽  
MARIO VOLTERRA ◽  
MILDRED D. JACOBS ◽  
LOUIS J. SOFFER

Abstract Ten normal subjects and 11 patients with Addison’s disease were studied as to their leukocyte response following the subcutaneous administration of epinephrin. The pattern of response was found to be similar in both groups, diphasic curves being noted. In general, the patients with Addison’s disease differ from normal individuals in having: (1) a lower and less labile white count, (2) a lower and less labile neutrophile count, (3) a higher lymphocyte count, (4) a slightly lesser percentage fall in absolute number of lymphocytes, and (5) a higher lymphocyte percentage. The use of this method to demonstrate adrenal cortical destruction is not feasible with the dosage of epinephrin employed in this study.


BMJ ◽  
1988 ◽  
Vol 296 (6635) ◽  
pp. 1489-1491 ◽  
Author(s):  
P. Kendall-Taylor ◽  
A. Lambert ◽  
R. Mitchell ◽  
W. R Robertson

2018 ◽  
Vol 56 (6) ◽  
pp. 896-900 ◽  
Author(s):  
Jacopo Manso ◽  
Raffaele Pezzani ◽  
Riccardo Scarpa ◽  
Nicoletta Gallo ◽  
Corrado Betterle

Abstract Autoimmune Addison’s disease (AAD) is the most frequent cause of adrenocortical insufficiency. The natural history of AAD usually comprises five consecutive stages with the first stage characterized by the increase of plasma renin consistent with the impairment of pars glomerulosa, which is usually the first affected layer of the adrenal cortex. We describe a 19-year-old female with Hashimoto’s thyroiditis (HT) who underwent an autoantibody screening due to having the personal and family history of other autoimmune diseases in the absence of relevant clinical manifestations. She was positive for adrenal cortex autoantibodies (ACA) and steroid 21-hydroxylase autoantibodies (21-OH Ab) at high titers. She had increased basal levels of ACTH with normal basal cortisol not responding to ACTH stimulation, reduced levels of dehydroepiandrosterone-sulfate but normal levels of orthostatic renin and aldosterone. This scenario was consistent with a subclinical AAD presenting with first impairments in pars fasciculata and reticularis and conserved pars glomerulosa function. Only subsequently, progressive deficiency in pars glomerulosa function has become evident. Review of the literature showed that there was only one case, reported to date, with a similar atypical natural history of AAD. The strategies for screening for ACA/21-OH Ab in patients with HT are discussed.


1974 ◽  
Vol 15 (1) ◽  
pp. 21-31 ◽  
Author(s):  
J.C. Gillin ◽  
L.S. Jacobs ◽  
F. Snyder ◽  
R.I. Henkin

1969 ◽  
Vol 60 (3) ◽  
pp. 486-490
Author(s):  
H. J. Faarvang ◽  
D. Francis ◽  
O. Buus

ABSTRACT A case of lymphangiomatous adrenal cyst containing 30 ml of cyst fluid, found at autopsy, is reported. The cyst wall contained islands of intact adrenocortical tissue just below the endothelium suggesting the possibility of a direct secretion of hormones into the cyst fluid. The content of cortisol, cortisone, corticosterone and deoxycortisol in the cyst fluid was 250, 7.5, 30 and 7.5 μg per 100 ml, respectively. The ratios between the concentrations of cortisol and corticosterone and cortisol and deoxycortisol were a little below the lower range limits for those found in mixed venous blood from normal subjects, whereas the ratio between cortisol and cortisone in the cyst fluid was much larger than the same ratio in mixed venous blood from normal subjects.


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