scholarly journals Observations on epinephrectomized cats treated with adrenal cortex hormone. Hartman F.A., Griffith F.R. Ir and W.I. Hartman (Am. J. of Physiol. 86, 360, 1928)

1929 ◽  
Vol 25 (10) ◽  
pp. 1111-1112
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenal Cortex ◽  
The State ◽  
Daily Injection

The state of chronic adrenal insufficiency was observed in 108 bilaterally epinephrectomized cats with daily injection of an extract from the adrenal cortex. The symptoms were similar to those of acute insufficiency, but in general they tended to develop more gradually.

Effect of cholesterol on the state of the adrenal cortex in severe stress

1978 ◽  
Vol 85 (5) ◽  
pp. 569-572 ◽  
Author(s):  
B. Ya. Ryzhavskii ◽  
M. T. Lutsenko
Keyword(s):  
Adrenal Cortex ◽  
The State ◽  
Severe Stress

Adrenal gland disorders

2011 ◽  
Author(s):  
Gary Butler ◽  
Jeremy Kirk
Keyword(s):  
Adrenal Gland ◽  
Adrenal Insufficiency ◽  
Steroid Hormones ◽  
Adrenal Cortex ◽  
Renin Angiotensin System ◽  
Cortisol Secretion ◽  
Aldosterone Secretion ◽  
Angiotensin System ◽  
Adrenal Steroid ◽  
Endocrine Axis

Physiology 236Adrenal insufficiency 238Adrenal steroid excess 246Further reading 247The adrenal cortex, which produces steroid hormones, is under the control of both the hypothalamo–pituitary–adrenal (HPA) endocrine axis, which regulates cortisol secretion, and the renin–angiotensin system, which regulates aldosterone secretion (Figs 8.1 and ...

scholarly journals MON-LB038 Isolated Hypoaldosteronism Due to Autoimmune Adrenalitis in a Patient With Autoimmune Polyglandular Syndrome

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Dheera Grover ◽  
Chenxiang Cao ◽  
Sarika Rao
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenal Cortex ◽  
Time Course ◽  
Serum Cortisol ◽  
Diabetes Mellitus Type 1 ◽  
Normal Serum ◽  
Serum Cortisol Level ◽  
Autoimmune Polyglandular Syndrome ◽  
Loss Of Appetite ◽  
Autoimmune Adrenalitis

Abstract BACKGROUND At the initial presentation of autoimmune adrenal insufficiency, most patients present with hormonal deficiencies from all three layers of adrenal cortex. However, isolated aldosterone deficiency causing a true partial adrenal insufficiency in the setting of autoimmune adrenalitis remains underrecognized. CASE REPORT A 67-year old female patient with a known history of diabetes mellitus type 1 since the age of 13 and morphea, presented with progressively worsening symptoms of confusion and hallucinations, fatigue, and loss of appetite over the past 5 years. During this time, she has had frequent and recurrent episodes of mild intermittent hyponatremia with hyperkalemia requiring intravenous fluids and ingested salt tablets, especially when she felt more symptomatic. On her initial evaluation here, she presented with hyponatremia (125 mmol/l, n: 135-145 mmol/l), low osmolality (264 mOsm/kg, n: 275-295 mOsm/kg), and normal potassium level (3.6 mmol/l, n: 3.6-5.2 mmol/l). Further investigations drawn at the same time revealed a low aldosterone (<4 ng/dL), normal renin (5.3 ng/mL/hr, ref 2.9-10.8), normal serum cortisol level (and normal response to Cortrosyn stimulation), though all in the setting of positive antibodies against 21-hydroxylase. Pan-imaging revealed no evidence of malignancy that can be causing ectopic SIADH production. Additional testing showed presence of auto antibodies contributing to pernicious anemia and thyroid disease. Treatment was started with fludrocortisone 0.1 mg tablet daily and she was advised to take the salt tablets only if she has any symptoms. The patient’s symptoms have resolved 8 months since this diagnosis, with normalized sodium and potassium levels. CONCLUSION Autoimmune primary adrenal insufficiency usually affects all three layers of the adrenal cortex, where patients present with deficiencies in cortisol and aldosterone. Isolated hypoaldosteronism has rarely been reported, however because it can cause life-threatening hyponatremia, it is an important entity to recognize. It is important to work up in such patients as they may be in the initial stages of autoimmune Addison’s disease and can progress to developing cortisol deficiency, though the time course to this progression is not well known.

scholarly journals Primary adrenal insufficiency replacement therapy

2000 ◽  
Vol 46 (3) ◽  
pp. 31-45
Author(s):  
V. V. Fadeev ◽  
G. A. Melnichenko
Keyword(s):  
Heart Failure ◽  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Adrenal Cortex ◽  
Adrenal Glands ◽  
Pathological Process ◽  
Clinical Syndrome ◽  
Primary Adrenal Insufficiency ◽  
Adrenal System ◽  
System 2

Adrenal insufficiency is a clinical syndrome caused by insufficient secretion of hormones by the adrenal cortex, which is the result of a malfunction of one or more parts of the hypothalamic-pituitary-adrenal system [2]. Primary chronic adrenal insufficiency (1-CNI) develops as a result of the destruction of more than 90% of the cortex of both adrenal glands by a pathological process. The main causes of 1-CNN are currently autoimmune (80–85%) and tuberculosis (5–10%) destruction of the adrenal cortex [2, 3]. 1-CNN of the indicated etiology is better known as "Addison's disease." 1-CNN is a relatively rare disease (40-110 new cases per 1 million people per year) [2, 3], but it is of considerable importance in the practice of endocrinology. Without exception, all patients with a diagnosis of 1-chronic heart failure need lifelong replacement therapy with corticosteroids (CS), which will be discussed in this work.

scholarly journals CHANGES IN CIRCULATING LEUKOCYTES INDUCED BY THE ADMINISTRATION OF PITUITARY ADRENOCORTICOTROPHIC HORMONE (ACTH) IN MAN

Blood ◽  
1948 ◽  
Vol 3 (7) ◽  
pp. 755-768 ◽  
Author(s):  
A. GORMAN HILLS ◽  
PETER H. FORSHAM ◽  
CLEMENT A. FINCH
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenal Cortex ◽  
Human Subjects ◽  
Normal Subjects ◽  
Adrenocorticotrophic Hormone ◽  
Adrenal Hormones ◽  
Intramuscular Dose ◽  
Circulating Lymphocytes ◽  
Initial Depression ◽  
Stimulation Of

Abstract 1. Pituitary adrenocorticotrophic hormone (ACTH), when administered in a single intramuscular dose of 25 mg. to human subjects with unimpaired adrenal function, results in a characteristic alteration of the leukocytic pattern. This consists of an increase of circulating neutrophils and a decrease of circulating lymphocytes and eosinophils. 2. The decrease in circulating lymphocytes and eosinophils is contingent upon the stimulation of a functionally competent adrenal cortex, and does not occur in its absence. The neutrophilic response is present but somewhat diminished in adrenal insufficiency. 3. The entire pattern of leukocytic alterations found in normal subjects after administration of ACTH can be induced in patients with Addison’s disease by 17-hydroxycorticosterone (20 mg.) but not with desoxycorticosterone glucoside (30 mg.). 4. Prolonged adrenal stimulation by ACTH, given over a four day period in a dose of 10 mg. every six hours, results in a sustained and striking elevation of neutrophils and depression of eosinophils; the lymphocytes, after an initial depression lasting not more than twenty-four hours, may increase above their initial levels in spite of the continued increased secretion of adrenal hormones. 5. The relation of the adrenal cortex to the characteristic nonspecific leukocyte pattern, observed as a response of the organism to any type of insult, is discussed.

scholarly journals Suprarenal cortical extract against adrenal insufficiency (Addison's disease)

2021 ◽  
Vol 25 (11) ◽  
pp. 1232-1232
Author(s):  
N. Kramov
Keyword(s):  
Blood Pressure ◽  
Adrenal Insufficiency ◽  
Adrenal Cortex ◽  
Adrenal Medulla ◽  
Adrenal Glands ◽  
Addison’S Disease ◽  
Gastrointestinal Disorders ◽  
Addison's Disease ◽  
Case Histories

Contrary to the generally accepted view that Addison's disease develops as a result of insufficient epinephrine secretion by the adrenal medulla Rogoff and Stewart (A. MA, 1929, 11 / V) see the cause of this disease in the insufficiency of the adrenal cortex. The product interrenalin isolated from this layer, which was used by the authors on dogs with removed adrenal glands and on patients with Addison's disease, gave extremely favorable results. Interrenaline was administered intravenously to dogs, per os in humans. The authors cite 7 case histories where, after the administration of this drug, the symptoms of Addison's disease improved or disappeared: blood pressure increased, bronze color disappeared, gastrointestinal disorders stopped and weakness disappeared, etc.

scholarly journals Pediatric Adrenal Insufficiency: Diagnosis, Management, and New Therapies

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Sasigarn A. Bowden ◽  
Rohan Henry
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenal Cortex ◽  
Clinical Management ◽  
Current Treatment ◽  
Treatment Recommendations ◽  
Morbidity And Mortality ◽  
Secondary Adrenal Insufficiency ◽  
Primary Adrenal Insufficiency ◽  
New Therapies ◽  
Timely Diagnosis

Adrenal insufficiency may result from a wide variety of congenital or acquired disorders of hypothalamus, pituitary, or adrenal cortex. Destruction or dysfunction of the adrenal cortex is the cause of primary adrenal insufficiency, while secondary adrenal insufficiency is a result of pituitary or hypothalamic disease. Timely diagnosis and clinical management of adrenal insufficiency are critical to prevent morbidity and mortality. This review summarizes the etiologies, presentation, and diagnosis of adrenal insufficiency utilizing different dynamic hormone testing and describes current treatment recommendations and new therapies.

scholarly journals Looking beyond the thyroid: advances in the understanding of pheochromocytoma and hyperparathyroidism phenotypes in MEN2 and of non-MEN2 familial forms

2018 ◽  
Vol 25 (2) ◽  
pp. T15-T28 ◽  
Author(s):  
Carole Guerin ◽  
Pauline Romanet ◽  
David Taieb ◽  
Thierry Brue ◽  
André Lacroix ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Adrenal Insufficiency ◽  
Adrenal Cortex ◽  
Recent Literature ◽  
Age At Diagnosis ◽  
Familial Hypocalciuric Hypercalcemia ◽  
Phenotypic Features ◽  
Optimal Quality

Over the last years, the knowledge of MEN2 and non-MEN2 familial forms of pheochromocytoma (PHEO) has increased. In MEN2, PHEO is the second most frequent disease: the penetrance and age at diagnosis depend on the mutation ofRET. Given the prevalence of bilateral PHEO (50% by age 50), adrenal sparing surgery, aimed at sparing a part of the adrenal cortex to avoid adrenal insufficiency, should be systematically considered in patients with bilateral PHEO. Non-MEN2 familial forms of PHEO now include more than 20 genes: however, only small phenotypic series have been reported, suggesting that phenotypic features of isolated hereditary PHEO must be better explored, and follow-up series are needed to better understand the outcome of patients carrying mutations of these genes. The first part of this review will mainly focus on these points. In the second part, a focus will be given on MEN2 and non-MEN2 familial forms of hyperparathyroidism (HPTH). Again, the management of MEN2 HPTH should be aimed at curing the disease while preserving an optimal quality of life by a tailored parathyroidectomy. The phenotypes and outcome of MEN1-, MEN4- and HRPT2-related HPTH are briefly described, with a focus on the most recent literature data and is compared with familial hypocalciuric hypercalcemia.

scholarly journals Latent Adrenal Insufficiency: From Concept to Diagnosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Nada Younes ◽  
Isabelle Bourdeau ◽  
Andre Lacroix
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenal Cortex ◽  
Standard Dose ◽  
Signs And Symptoms ◽  
Serum Cortisol ◽  
Zona Glomerulosa ◽  
Adrenocortical Function ◽  
Adrenal Crisis ◽  
Zona Fasciculata ◽  
Adrenal Androgen

Primary adrenal insufficiency (PAI) is a rare disease and potentially fatal if unrecognized. It is characterized by destruction of the adrenal cortex, most frequently of autoimmune origin, resulting in glucocorticoid, mineralocorticoid, and adrenal androgen deficiencies. Initial signs and symptoms can be nonspecific, contributing to late diagnosis. Loss of zona glomerulosa function may precede zona fasciculata and reticularis deficiencies. Patients present with hallmark manifestations including fatigue, weight loss, abdominal pain, melanoderma, hypotension, salt craving, hyponatremia, hyperkalemia, or acute adrenal crisis. Diagnosis is established by unequivocally low morning serum cortisol/aldosterone and elevated ACTH and renin concentrations. A standard dose (250 µg) Cosyntropin stimulation test may be needed to confirm adrenal insufficiency (AI) in partial deficiencies. Glucocorticoid and mineralocorticoid substitution is the hallmark of treatment, alongside patient education regarding dose adjustments in periods of stress and prevention of acute adrenal crisis. Recent studies identified partial residual adrenocortical function in patients with AI and rare cases have recuperated normal hormonal function. Modulating therapies using rituximab or ACTH injections are in early stages of investigation hoping it could maintain glucocorticoid residual function and delay complete destruction of adrenal cortex.

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