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PubMed1991

The biochemical assessment of sympathoadrenal activity in man.

Sympathoadrenal activity in man can be assessed by measuring catecholamines in plasma or by recording impulses in sympathetic nerves to skin and muscles by microneurography. Several studies have indicated that forearm venous plasma noradrenaline concentration and muscle sympathetic nerve activity are closely correlated in normal subjects at rest as well as during various conditions with increased or decreased sympathetic activity. Both parameters are influenced by baroreceptors and increase with age. Plasma adrenaline should preferably be measured in arterial blood because the extraction of adrenaline in organs and tissues may increase considerably when plasma adrenaline increases. The problem of studying the metabolic clearance rate of noradrenaline but not of adrenaline is discussed. It is emphasized that sympathetic activity is highly differentiated and it should therefore be measured in specific organs and tissues. Sympathetic activity in internal organs can be studied by measuring the release of noradrenaline from these organs. Imaging technique may, however, prove useful in future studies. The significance of microdialysis, measurements of plasma catecholamine metabolites, dopa and dopamine, plasma neuropeptide Y, catecholamines in urine and in the cerebrospinal fluid is discussed. Furthermore, it is emphasized that adrenergic agonist and antagonist drugs are important tools to study sensitivity and responsiveness to catecholamines preferably in specific organs and tissues. Finally, a few examples are given of the values in human research of the techniques described.

Adrenal Cortex Function Tests↗
PubMed2003

[Adrenal crisis. Diagnostic and therapeutic management of acute adrenal cortex insufficiency].

Acute adrenal insufficiency is a rare but life-threatening disorder that develops as a result of inadequate adrenal steroid production. Early diagnosis is key for effective and life-saving treatment of the affected patients. The main clinical features are non-specific, thus often leading to misdiagnosis and invasive diagnostic work up, in particular in patients with previously unknown disease. Adrenal crisis in patients with known chronic adrenal insufficiency is nowadays rare, but can only be prevented by structured patient education on stress-related glucocorticoid dose adjustment. Outcome of adrenal crisis is crucially determined by the physician's clinical competence and immediate initiation of specific treatment.

Acute Disease↗
PubMed2006

Adrenal insufficiency: diagnosis and management.

Adrenal insufficiency is a disorder characterized by hypoactive adrenal glands resulting in insufficient production of the hormones cortisol and aldosterone by the adrenal cortex. This disorder may develop as a primary failure of the adrenal cortex or be secondary to an abnormality of the hypothalamic-pituitary axis. Patients with adrenal insufficiency often are asymptomatic or they may present with fatigue, muscle weakness, weight loss, low blood pressure, and sometimes darkening of the skin. The presentation of adrenal insufficiency varies dramatically and poses a major diagnostic dilemma. This review focuses on the diagnosis and treatment of primary and secondary adrenal insufficiency.

Adrenal Cortex Function Tests↗
PubMed1978

Familial glucocorticoid deficiency with achalasia of the cardia and deficient tear production.

Isolated glucocorticoid failure associated with achalasia of the cardia is described in two pairs of siblings in separate families. Defective tear production is also present in three of the patients, and one shows other signs of autonomic dysfunction. Two other families with adrenal insufficiency and achalasia are known. This unusual association probably represents a familial disorder of as yet unknown aetiology.

Adrenal Cortex Function Tests↗
PubMed1991

[Role of vitamin C on adrenocortical effects of etomidate].

This study was carried out to assess whether the adrenal inhibition induced by etomidate could be prevented by associating ascorbic acid with etomidate, as a protective effect of ascorbic acid administered three hours after etomidate has been described. Sixteen ASA 1 or 2 patients, less than 65 years old, free of endocrine disease, were included. At induction of anaesthesia, eight of them (group B) were given an infusion of ascorbic acid 1 g, in 500 ml of 5% glucose. Group A patients (n = 8) were given 500 ml of 5% glucose. Anaesthesia was induced with etomidate 0.3 mg.kg-1, fentanyl 0.005 mg.kg-1 and vecuronium 0.1 mg.kg-1. Maintenance was carried out using a continuous infusion of etomidate (0.1 mg.kg-1.h-1 for 10 min, followed by 0.01 to 0.02 mg.kg-1.h-1). Additional boluses of fentanyl or diazepam (10 mg) were administered when arterial blood pressure or heart rate were 20% greater than preanaesthetic values. The number of injections required was the same in both groups. Plasma cortisol concentrations were measured by radioimmunoassay (RIA) before anaesthesia (T0), 4 h (T4) and 24 h (T24) after the end of surgery. Blood ACTH levels were also assessed by RIA at T0 and T4. The adrenal insufficiency at T4 had completely ended at T24. In fact, the relative decrease in cortisol levels was greater in patients treated with ascorbic acid (T4/T0: 47.6 +/- 9% in group A vs 76.5 +/- 33% in group B, p less than 0.05); this was suggestive of a higher degree of adrenal inhibition in patients receiving ascorbic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1979

Adrenal-cortical function in patients with medullary carcinoma of the thyroid and pheochromocytoma.

Medullary carcinoma of the thyroid (MCT) is reported to synthesize ACTH. This ACTH is believed to be responsible for the development of Cushing's syndrome in some patients with MCT. To determine the frequency of occurrence of adrenal cortical overactivity in patients with MCT, we measured plasma cortisol concentration and the urinary excretion of 17-hydroxycorticosteroids, 17-ketosteroids and urinary free cortisol in 22 patients with MCT and 7 patients with MCT plus pheochromocytomas. The patients with MCT and MCT plus pheochromocytoma had similar adrenal cortical function to age and sex matched normal subjects. We conclude that adrenal cortical function is usually normal in patients with MCT.

17-Hydroxycorticosteroids↗
PubMed1992

Two cases of adrenal myelolipoma.

We report myelolipoma found in two patients, of whom one had hormonal abnormalities related to adrenal function. The first patient was a 36-year-old woman, who was found incidentally to have a left adrenal tumor by CT scan during admission for treatment of Guillain-Barré syndrome. Obesity, hirsutism and osteoporosis were also evident, and the patient was forwarded for additional endocrine function analysis, which revealed elevation of serum cortisol, urine 17-OHCS and 17-KS, and a decreased level of ACTH. These abnormalities returned to normal after excision of the tumor. Pathologically, the tumor was composed of mature fat cells and hematopoietic components, and was diagnosed as myelolipoma. The second patient was a 63-year-old woman, who was receiving follow-up care for hyperthyroidism. A right adrenal tumor was noted incidentally in a routine examination by CT scan. Endocrinologically, she was found to have no abnormalities of adrenal function. The tumor was excised, and diagnosed pathologically as myelolipoma, being composed of mature fat cells and hematopoietic components. Generally, although most myelolipomas have no endocrine function, our first patient showed features of Cushing's syndrome. Thus it is suggested that an interrelationship may exist between myelolipoma and endocrinological alteration.

Adrenal Cortex Function Tests↗
PubMed1975

Effect on adrenal function of topically applied clobetasol propionate (Dermovate).

Thirty-nine patients (15 outpatients and 24 inpatients) with a variety of skin diseases affecting variable areas of the body surface were treated with clobetasol propionate ointment (Dermovate). Before and after treatment the adrenal response to an intramuscular injection of tetracosactrin was rested and additional 9 am plasma cortisol levels were measured at intervals during treatment. A satisfactory initial therapeutic response was achieved in almost all cases during the trial period. When more than 50 g of ointment a week was used a significant number of patients developed adrenal suppression. WHen less than 50 g per week was used any suppression tended to be transtion. These cysts may be the cause of this condition, producing abnormal amounts of ovarian steroids which modify the pituitary response. Futher studies are needed, however, to determine this possibility.

Adolescent↗
PubMed1977

Urinary free 11-hydroxycorticosteroid/creatinine ratios in early morning urine samples as an index of adrenal function.

Urinary free 11-hydroxycorticosteroid/creatinine ratios were determined in early morning urine samples from 113 females (age range 20-45 years) and 65 males (age range 22-45 years). Basal values in normal subjects fluctuated between 5 and 55 mumol/mol creatinine. In four patients in whom Cushing's syndrome was diagnosed, urinary free 11-hydroxycorticosteroid/creatinine ratios were greater than 85 mumol/mol creatinine. Administration of dexamethasone (0.5 mg/q.i.d.) to nine normal laboratory staff for two days resulted in a suppression of the urinary free 11-hydroxycorticosteroid/creatinine ratio to less than 50% of the mean basal value in all cases. This degree of suppression did not occur in two cases of Cushing's syndrome due to adrenal tumours.

11-Hydroxycorticosteroids↗
PubMed2004

Adrenal sensitivity to adrenocorticotropin 1-24 is reduced in patients with autoimmune polyglandular syndrome.

Autoimmune polyglandular syndromes are fairly common diseases that are classified into four constellations based on the clinical clustering of the various component diseases. In types 1, 2, and 4, primary adrenal insufficiency due to an autoimmune process is usually present, but its diagnosis is often delayed because it is difficult to detect in a subclinical phase. It is widely accepted that the classical dose of 250 microg ACTH(1-24) is supramaximal, whereas 0.06 microg has been shown to be one of the lowest ACTH doses that is able to stimulate adrenal secretion in normal young subjects. The aim of this study was to clarify the sensitivity and maximal secretory response of the adrenal gland to ACTH in a group of patients with at least two autoimmune diseases, without clinical signs and symptoms of overt or subclinical hypocortisolism. Cortisol (F), aldosterone (A), and dehydroepiandrosterone (DHEA) responses to the sequential administration of very low and supramaximal ACTH(1-24) doses [0.06 microg followed by 250 microg ACTH(1-24) i.v. at 0 and +60 min] were studied in 18 patients with at least two autoimmune diseases (AP; age, 20-40 yr; body mass index, 22-26 kg/m(2)). The results in the patients were compared with the results recorded in 12 normal age-matched control subjects (CS; age, 22-34 yr; body mass index, 20-25 kg/m(2)). At baseline, ACTH levels in AP were within the normal range but higher (P < 0.05) than in CS, whereas F, A, DHEA, urinary-free F, and plasma renin activity were similar in both groups. F, A, and DHEA responses to ACTH were dose dependent in both groups. However, in AP, F, A, and DHEA levels showed no response to the 0.06- micro g ACTH dose, which, in turn, elicited clear responses (P < 0.01) in CS. On the other hand, F, A, and DHEA responses to 250 microg ACTH in AP were not different from those in CS. In conclusion, patients with autoimmune diseases who displayed a normal basal adrenal function showed a loss of F, A, and DHEA response to the very low ACTH dose, although they were normal responders to the high ACTH dose. These data are likely to indicate that a reduced sensitivity to ACTH in all adrenal zones occurs in patients with different types of autoimmune disease.

Adrenal Cortex Function Tests↗