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Corticosteroids are the most potent anti-inflammatory agents used to treat chronic inflammatory diseases such as bronchial asthma. However, there are a small number (<5%) of asthmatic patients who do not respond well, or at all, to corticosteroid therapy - the corticosteroid-resistant and corticosteroid-dependent patients. Although this phenomenon is relatively uncommon, it poses a difficult therapeutic problem because few alternative therapies are available and these patients account for >50% of the health care costs of asthma. If the mechanisms for corticosteroid insensitivity are understood they may, in turn, provide insight into the key mechanism of corticosteroid action and allow a rational way to treat these individuals whose disease tends to be severe. Corticosteroid insensitivity is not limited to asthma and is a feature of other inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease. Thus, elucidation of the cause for the relative lack of corticosteroid response in this subgroup of asthmatic individuals may have important implications for other diseases.
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players and phases involved in the stress response and their interactions with each other. Corticosteroids play a major role in the response of the brain to stress. For many years, they were believed to be only responsible for the delayed and prolonged
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Introduction Pick up any endocrinology text published in the last 60 years, and if it deals with the actions of the corticosteroids, you will usually read something to the effect that deoxycorticosterone (DOC, 11-deoxycorticosterone, cortexone, 21
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Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom
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Introduction Corticosteroid-binding globulin (CBG) transports glucocorticoids and progesterone in human blood and regulates their access to target tissues ( Hammond 2016 a ). Human CBG is also known as SERPINA6 because it shares structural
Department of Obstetrics and Gynaecology, University of British Columbia, Vancouver, British Columbia, Canada
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Department of Obstetrics and Gynaecology, University of British Columbia, Vancouver, British Columbia, Canada
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Introduction Produced primarily by the liver, corticosteroid-binding globulin (CBG) is a plasma glycoprotein that binds ~90% of circulating glucocorticoids, and regulates their bioavailability in target tissues ( Lin et al. 2010 ). Plasma
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A technique for the extraction of urinary corticosteroids and their estimation by copper reduction is described.
Results of the application of this technique to the determination of corticosteroid excretion in normal and diseased subjects are given.
The method may be of value in clinical investigations in revealing gross abnormality in the excretion of corticosteroids.
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SUMMARY
Corticosteroid secretion and excretion by the Australian monotreme Tachyglossus aculeatus was investigated by assay of peripheral blood, adrenal venous blood, urine and faeces.
Free corticosteroids could be demonstrated in only one out of five samples of peripheral whole blood, in which trace amounts of cortisol and corticosterone were detected at concentrations of the order of 0·1–0·2 μg./100 ml.
Quantitatively, the major corticosteroid detected in adrenal venous blood of three males and one female was identified as corticosterone, at concentrations of 8–25 μg./100 ml. whole blood. Lesser amounts of cortisol were detected in samples of adrenal venous blood from two males and the female, the ratios 'F:B' being 0·25 and 0·40 in the males, and 0·13 in the female. The highest rate of corticosterone secretion was only 2·6 μg./100 mg. adrenal/hr. or 1·17 μg./kg. body weight/hr.
No free or conjugated corticosteroids were detected in either urine or faeces. Zimmermann chromogens were found in both urine and faeces, and total daily excretion varied unpredictably from undetectable levels to a maximum of only 25 μg./kg. body weight/day.
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inflammatory/immune responses, and synthetic glucocorticoids (corticosteroids) are widely used therapeutically for this purpose ( Schimmer & Parker 1996 , Baxter 2000 ). The pathologies for which anti-inflammatory or immune-suppressing interventions by
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Nuffield Institute for Medical Research, University of Oxford, Headley Way, Headington, Oxford, 0X3 9DS
(Received 14 September 1976)
It is now well established that corticosteroids can act as negative feedback regulators of adrenocorticotrophin (ACTH) secretion (Yates & Maran, 1974), although unbound steroid is probably much more effective than protein-bound steroid in depressing ACTH secretion (Kawai & Yates, 1966). There are very high plasma corticosteroid concentrations in the foetal sheep during late pregnancy (Bassett & Thorburn, 1969) and although much of this is protein-bound the free corticosteroid concentration is also high (Fairclough & Liggins, 1975). Despite this the plasma ACTH concentration in the foetal sheep at this time is not depressed but may be raised (Rees, Jack, Thomas & Nathanielsz, 1975; Jones, Boddy & Robinson, 1977a). This suggests that the corticosteroids may not act as negative feedback regulators of ACTH secretion in the foetal sheep and the present experiments investigate this
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Prolonged pregnancy following foetal hypophysectomy or adrenalectomy (Liggins, Kennedy & Holm, 1967; Drost & Holm, 1968) and premature parturition following injection of corticotrophin or corticosteroids into the ovine foetus (Van Rensburg, 1967; Halliday & Buttle, 1968; Liggins, 1968) implicate the foetal adrenal cortex in the initiation of parturition in sheep. Consequently, foetal plasma corticosteroid concentrations and corticosteroid secretion by the foetal adrenal should be greatly increased towards term. Observations during acute studies on anaesthetized sheep suggest this (Alexander, Britton, James, Nixon, Parker, Wintour & Wright, 1968), but there is no information about blood concentrations or secretion rates of corticosteroids in normal undisturbed sheep foetuses in utero.
We cannulated the carotid artery and the facial branch of the jugular vein of four single Merino foetuses with polyvinyl chloride tubing (o.d. 1·27 mm., i.d. 0·86 mm.) with the ewes under general anaesthesia (pentobarbitone sodium (20 mg./kg., i.v.) followed by halothane and oxygen).
