Plasma 17-Hydroxycorticosteroids in Cushing's Syndrome*

Ekman, H; Håkansson, Britt; McCarthy, Jack D.; Lehmann, Jörgen; Sjögren, Björn

doi:10.1210/jcem-21-6-684

Cited by 54 publications

(12 citation statements)

References 17 publications

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“…Some workers have reported relatively lower mean P-S chromogens in plasma for the obese than the lean (Szenas & Pattee, 1959); others have found that they are within the normal range (Migeon et al, 1963;Schultz et al, 1964). The observation that some subjects with Cushing's syndrome may have values within the normal range confirms the studies of several other workers (Ekman et al, 1961 ;Kornel, 1969). Similarly the finding that a few subjects with Cushing's syndrome may maintain day-night variation of plasma corticosteroids, and that it may be absent in some apparently normal subjects and in cases of obesity, has been noted (Ekman et al, 1961 ;Schultz et al, 1964;McHardy-Young et al, 1967;Jackson & Mowatt, 1970;Hankin et al, 1972).…”

Section: Discussionsupporting

confidence: 87%

“…Elevated urinary 17-OHCS have been reported in a significant number of obese subjects (Simkin, 1961;Baird, 1963;McHardy-Young, Harris, Lessof & Lyne, 1967) and in most instances of Cushing's syndrome (Ekman et al, 1961 ;Ernest, 1966). However, a marked daily variation in urinary 17-OHCS excretion can occur and repeated estimations show that the value may be within the control range on some days (Ernest, 1966).…”

mentioning

confidence: 99%

“…However, some subjects with Cushing's syndrome may maintain a normal rhythm (Schteingart et al, 1963;Ernest, 1966;Espiner, 1966) and the variation may be absent in some apparently normal subjects and some with obesity (Ekman et al, 1961;McHardy-Young et al, 1967;Jackson & Mowatt, 1970;Hankin et al, 1972).…”

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confidence: 99%

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Adrenocortical Function in Obesity and Cushing's Syndrome

1974

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S U M M A R Y1. The 24 h urinary excretions of Porter-Silber (P-S) chromogens, 17-hydroxycorticosteroids (17-OHCS) and free cortisol, and day-night variation of plasma P-S chromogens, were studied in normal and obese women and patients with a confirmed diagnosis of Cushing's syndrome.2. The mean absolute values of P-S chromogens, 17-OHCS and free cortisol were similar for the normal and obese subjects and elevated in Cushing's syndrome. With the exception of the 17-OHCS there was some overlapping of the individual values within the three groups. All the subjects with Cushing's syndrome and several of the obese subjects had values of 17-OHCS which were outside the normal range. 3.The 24 h urinary 17-OHCS and free cortisol excretion expressed per kg body weight were significantly lower for the obese than for the control subjects and subjects with Cushing's syndrome. The values were significantly higher for the subjects with Cushing's syndrome than for the obese and normal subjects. There was some overlapping of the individual values. 4. Two normal and two obese subjects failed to show significant day-night variation, whereas only four of the patients with Cushing's syndrome had significant daynight variation of plasma P-S chromogens.5. The urinary 17-OHCS for four of the obese subjects with some symptoms of adrenocortical hyperactivity were suppressed normally on a low dose of dexamethasone whereas those with Cushing's syndrome failed to do so.Porter-Silber (p-S) chromogens comprise the 17,21-dihydroxy-20-oxocorticosteroids which react with phenylhydrazine hydrochloride in ethanol-sulphuric acid to give a yellow colour. In plasma, cortisol and tetrahydrocortisone are the major steroids estimated by this reaction

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Section: Discussionsupporting

confidence: 87%

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confidence: 99%

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Adrenocortical Function in Obesity and Cushing's Syndrome

1974

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“…Yet when these assays are taken as a group, the mean value (0.62 mU per 100 ml) is significantly greater than the mean value (0.25 mU per 100 ml) of a group of normal subjects at 6 a.m. Patients with Cushing's disease lack diurnal variation in plasma 17-OHCS (21). Since 17-OHCS secretion is apparently a function of ACTH in these patients, probably they also lack normal diurnal variation in ACTH secretion.…”

Section: Discussionmentioning

confidence: 80%

Correlation of Plasma Acth Concentration With Adrenocortical Response in Normal Human Subjects, Surgical Patients, and Patients With Cushing's Disease*

Ney¹,

Shimizu²,

Nicholson³

et al. 1963

J. Clin. Invest.

122

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The role of ACTH in various clinical disorders has been difficult to ascertain because the available assay methods have lacked the sensitivity necessary for valid quantitation of the hormone in the plasma of normal subjects (1-4). Even the method of Lipscomb and Nelson (5), the most sensitive practical bioassay procedure now available, usually requires the injection of at least 0.05 mU of ACTH per rat, if responses are to be elicited that will be statistically significant without the use of a prohibitive number of animals. It is usually impractical to inject more than 5 ml of crude human plasma into a single rat. Therefore, in order to be accurately measurable by this procedure, the concentration of ACTH in the plasma must be at least 0.05 mU per 5 ml, or 1 mU per 100 ml.Numerous studies indicate that normal plasma levels of ACTH are well below this concentration. Byr the adrenal ascorbic acid depletion assay method, Sydnor, Sayers, Brown, and Tyler (1) were unable to detect ACTH in plasma of normal subjects, even after attempting to extract the hormone with oxvcellulose in preparation for the bioassay. These workers concluded that blood ACTH concentrations of normal human subjects were less than 0.5 mU per 100 ml. Using a similar procedure, Fujita (3) estimated the normal level of ACTH to be about 1 mU per L, i.e., 0.1 mU per 100 ml. Cooper and Nelson (6) were able to detect ACTH in the plasma of only 3 of 10 patients before surgery, by a method that they

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“…INTRODUCTION During the last few years it has become apparent that there are a number of characteristic abnormalities in the control of adrenocortical function in patients with Cushing's syndrome associated with bilateral adrenal hyperplasia (Cushing's disease). These include the observation that the normal diurnal changes of plasma cortisol levels may be absent in these patients (Ekman, Hakansson, McCarthy, Lehmann & Sjogren, 1961) and that they have a diminished sensitivity to the suppressive effects of exogenous corticosteroids on corticotrophin release (Liddle, 1960). More 16 V. H. T. James, J. Landon, V. Wynn and F. C. Greenwood it has been found that they do not have a normal adrenal response to insulin-induced hypoglycaemia (Landon, James & Stoker, 1965;Bethge, Winklemann & Zimmer¬ mann, 1966).…”

mentioning

confidence: 99%

A Fundamental Defect of Adrenocortical Control in Cushing's Disease

James¹,

Landon²,

Wynn³

et al. 1968

Journal of Endocrinology

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SUMMARY The plasma sugar, 11-hydroxycorticosteroid, and growth hormone responses to insulin have been studied in patients with Cushing's disease. They showed an impaired or absent plasma 11-hydroxycorticosteroid and growth hormone rise during the test, as compared with control subjects, despite the injection of amounts of insulin which produced a similar degree of hypoglycaemia. This test proved of value in differentiating between these patients and those with 'simple ' obesity since the latter usually showed a normal growth hormone and adrenal response provided an adequate amount of insulin was administered. The patients with Cushing's disease also had an impaired adrenal response to pyrogen and to dexamethasone administration and failed to show a normal plasma 11-hydroxycorticosteroid circadian rhythm. Their response to corticotrophin, lysine vasopressin, and metyrapone, however, was normal or enhanced. It is suggested that these findings imply an abnormality of hypothalamic or cerebral control and not a primary defect of pituitary function as proposed originally by Harvey Cushing. The growth hormone response to insulin remained impaired in four out of six patients totally adrenalectomized for Cushing's disease but was normal in three patients adrenalectomized for other reasons. It is suggested that the defect which impairs the adrenal response to insulin may, on occasions, also impair the mechanism normally operative for growth hormone secretion.

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Plasma 17-Hydroxycorticosteroids in Cushing's Syndrome*

Cited by 54 publications

References 17 publications

Adrenocortical Function in Obesity and Cushing's Syndrome

Adrenocortical Function in Obesity and Cushing's Syndrome

Correlation of Plasma Acth Concentration With Adrenocortical Response in Normal Human Subjects, Surgical Patients, and Patients With Cushing's Disease*

A Fundamental Defect of Adrenocortical Control in Cushing's Disease

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